The Anesthesia Technician & Technologist\'s Manual (2012)
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The Anesthesia Technician & Technologist’s Manual
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The Anesthesia Technician & Technologist’s Manual All You Need to Know for Study and Reference
G R
-V r i 9 . 9 & s r s i n h a i ta s r e p . p i v
Glenn Woodworth, MD
Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Shannon Sayers-Rana, BS, Cer AT Anesthesia Support Manager Oregon Health and Science University Past President, ASATT Portland, Oregon
Jeffrey R. Kirsch, MD Professor and Chair Department of Anesthesiology and Perioperative Medicine Associate Dean for Clinical and Veterans Affairs Oregon Health and Science University Portland, Oregon
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Acquisitions Editor: Brian Brown Product Manager: Tom Gibbons Vendor Manager: Bridgett Dougherty Senior Manufacturing Manager: Benjamin Rivera Marketing Manager: Lisa Lawrence Design Coordinator: Teresa Mallon Production Service: SPi Global © 2012 by LIPPINCOTT WILLIAMS & WILKINS, a WOLTERS KLUWER business Two Commerce Square 2001 Market Street Philadelphia, PA 19103 USA LWW.com All rights reserved. This book is protected by copyright. No part of this book may be reproduced in any form by any means, including photocopying, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. Printed in China
G R
-V r i 9 . 9 & s r s i n h a i ta s r e p . p i v
Library of Congress Cataloging-in-Publication Data The anesthesia technician and technologist’s manual : all you need to know for study and reference / [edited by] Glenn Woodworth, Jeffrey Kirsch. — 1st ed. p. ; cm. Includes bibliographical references and index. ISBN-13: 978-1-4511-4266-2 ISBN-10: 1-4511-4266-8 I. Woodworth, Glenn. II. Kirsch, Jeffrey, 1957[DNLM: 1. Anesthesia. 2. Allied Health Personnel—education. 3. Anesthesiology—methods. WO 18.2] 617.96—dc23 2011040962 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. Application of the information in a particular situation remains the professional responsibility of the practitioner. The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accordance with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new or infrequently employed drug. Some drugs and medical devices presented in the publication have Food and Drug Administration (FDA) clearance for limited use in restricted research settings. It is the responsibility of the health care provider to ascertain the FDA status of each drug or device planned for use in their clinical practice. To purchase additional copies of this book, call our customer service department at (800) 638-3030 or fax orders to (301) 223-2320. International customers should call (301) 223-2300. Visit Lippincott Williams & Wilkins on the Internet: at LWW.com. Lippincott Williams & Wilkins customer service representatives are available from 8:30 am to 6 pm, EST. 10 9 8 7 6 5 4 3 2 1
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Dedication Of course, as an editorial staff, we must dedicate this text to our loving families who put up with our countless hours hunched over our computers when we should have been eating dinner or relaxing at home. Without their love and support, we would have not had the will or energy to complete this text. Finally, we dedicate this text to the community of anesthesia technicians so that they will know of our commitment to their education and our appreciation for their expertise and the role they play in the care of our patients.
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Contributors Kenneth Abbey, MD, JD Clinical Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Mark J. Baskerville, MD, JD, MBA Critical Care Fellow Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Matthew Abrahams, MD Oregon Anesthesiology Group Portland, Oregon
Curtis Bergquist, AB Anesthesia Technician Oregon Health and Science University Portland, Oregon
Diane Alejandro-Harper, Cer AT Administrative Manager O.R. Anesthesia Stanford Hospital and Clinics Stanford, California Ahmed Alshaarawi, CRNA Instructor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Ryan B. Anderson, MD, PhD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Michael S. Axley, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Michael F. Aziz, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Mary A. Blanchette, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Richard Botney, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Valdez G. Bravo, BA Supervisor, Biomedical Engineering Portland VA Medical Center Portland, Oregon Guy Buckman, Cer ATT Certified Anesthesia Technician Portland VA Medical Center Portland, Oregon Mark D. Burno, MD Instructor Department of Anesthesiology Northwestern University Feinberg School of Medicine Chicago, Illinois
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Contributors
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Michelle Cameron, MD, PT Assistant Professor Department of Neurology Oregon Health and Science University Portland, Oregon
Arjun Desai, MD Chief Anesthesia Resident Department of Anesthesia Stanford University School of Medicine Stanford, California
Deborah Carter, RN, BSN Laser Safety Officer/Coordinator Department of Surgical Services Oregon Health and Science University Portland, Oregon
Richa Dhawan, MD Assistant Professor Department of Anesthesia and Critical Care University of Chicago Chicago, Illinois
Lisa Chan, MD Pediatric Anesthesia Fellow Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Dawn Dillman, MD Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Mark A. Chaney, MD Professor Department of Anesthesia and Critical Care University of Chicago Chicago, Illinois
Laura Downey, MD Chief Resident Department of Anesthesiology Stanford University Palo Alto, California
Matthew Chao-Ben Chia, BA Coordinator, Anesthesia Technicians Northwestern Memorial Hospital Chicago, Illinois
Brian N. Egan, MD Pediatric Fellow Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Sue Christian, Cer ATT Manager/Educator Department of Anesthesiology Vanderbilt University Medical Center Nashville, Tennessee Thomas W. Cutter, MD, MA Ed Professor and Associate Chairman Department of Anesthesia and Critical Care Pritzker School of Medicine University of Chicago Chicago, Illinois Shohreh Sadlou Daraee Operating Room Pharmacist Department of Pharmacy Oregon Health and Science University Portland, Oregon Asish Das, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Dalia H. Elmofty, MD Assistant Professor Department of Anesthesia and Critical Care University of Chicago Chicago, Illinois Roy K. Esaki, MD, MS Resident Department of Anesthesiology Stanford University Stanford, California Josh Finkle Medical Student University of Illinois College of Medicine Chicago, Illinois Judith A. Freeman, MB, ChB Associate Professor of Anesthesia Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon tahir99-VRG & vip.persianss.ir
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Contributors
Ryan Goldsmith, MD Department of Anesthesia PGY-2 Resident University of Florida Gainesville, Florida Matthew J. Griffee, MD Assistant Professor Department of Anesthesiology University of Utah Health Care Salt Lake City, Utah Jared D. Grose, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Karen Hand, FRCA Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Casey A. Harper, BA Manager of Anesthesia Services Northwestern Memorial Hospital Chicago, Illinois Matthew Hart, MS, CRNA Chief CRNA Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Izumi Harukuni, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Michael T. Jamond, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Staff Anesthesiologist Portland VA Medical Center Portland, Oregon
Edward A. Kahl, MD Assistant Professor of Cardiac Anesthesia Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Markus Kaiser, MD Assistant Professor Department of Anesthesiology Medical College of Wisconsin Milwaukee, Wisconsin Angela Kendrick, MD Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Shaleha Khalique, BS, Cer AT Certified Anesthesia Technician New York Presbyterian Weill Cornell Medical Center New York, New York Vishal Khemlani, BS Oregon Health and Science University Portland, Oregon Tae W. Kim, MD Clinical Associate Department of Anesthesiology and Critical Care Johns Hopkins Medical Institutions Baltimore, Maryland Aaron Kirsch Medical Student Wayne State University School of Medicine Detroit, Michigan Jeffrey R. Kirsch, MD Professor and Chair Department of Anesthesiology and Perioperative Medicine Associate Dean for Clinical and Veterans Affairs Oregon Health and Science University Portland, Oregon Jodi Heather Kirsch, DC Chiropractic Physician National University of Health Sciences Lombard, Illinois tahir99-VRG & vip.persianss.ir
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Contributors
Pamela Kirwin, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Eve Klein, MD Anesthesia Fellow Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Ramon Larios, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Staff Anesthesiologist Portland VA Medical Center Portland, Oregon Dawn M. Larson, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Delbert K. Macanas Manager, Anesthesia Services Kuakini Medical Center Honolulu, Hawaii Alex Macario, MD, MBA Professor of Anesthesia Program Director, Anesthesia Residency Stanford University School of Medicine Stanford, California Jeffrey Mako, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Kim Mauer, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
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Terrence McGraw, MD, FAAP Associate Professor Department of Anesthesiology and Pediatrics Oregon Health and Science University Doernbecher Children’s Hospital Portland, Oregon Sameer Menda, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Brett Miller, MD Anesthesiology Resident Stanford University Stanford, California Brian Mitchell, MD Staff Anesthesiologist Portland VA Medical Center Portland, Oregon Jeffrey L. Moller, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon MicHael Moore, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Lori Nading, CRNA Instructor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon L. Michele Noles, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
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Contributors
Andrew Oken, MD Staff Anesthesiologist Portland VA Medical Center Portland, Oregon Amy J. Opilla, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Jorge Pineda, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Andrew J. Pittaway, BM, BS, FRCA Attending Anesthesiologist Seattle Children’s Hospital Seattle, Washington Donald S. Prough, MD Professor and Chair Department of Anesthesiology University of Texas Medical Branch Professor and Chair Department of Anesthesiology John Sealy Hospital Galveston, Texas Brenda A. Quint-Gaebel, RHIT, MPA-HA Quality Program Manager Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Bryan J. Read, CRNA Instructor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Victoria Reyes Assistant Director Kaiser Permanente Anesthesia Technology Program Kaiser School of Anesthesia Pasadena, California
Scott W. Richins, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Berklee Robins, MD Assistant Professor of Anesthesia and Pediatrics Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Danny L. Robinson, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Stephen T. Robinson, MD Clinical Professor and Vice-Chair for Clinical Anesthesia Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Henry Rosenberg, MD, CPE Director of Medical Education and Clinical Research Chief Medical Information Officer Saint Barnabas Medical Center Livingston, New Jersey Adjunct Professor of Anesthesiology Columbia University School of Medicine New York, New York Shannon Sayers-Rana, BS, Cer AT Anesthesia Support Manager Oregon Health and Science University Past President, ASATT Portland, Oregon Katie J. Schenning, MD, MPH Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
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Contributors
Eric Schnell, MD, PhD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Staff Anesthesiologist Portland VA Medical Center Portland, Oregon Peter Schulman, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Valerie Sera, MD Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Sarah M. Shabot, MD Assistant Professor Department of Anesthesiology University of Texas Medical Branch Galveston, Texas David M. Sibell, MD Associate Professor Comprehensive Pain Center Oregon Health and Science University Portland, Oregon Wesley Simpson II, BCTS, Cer ATT Clinical Education Specialist Deltex Medical Group, SC San Diego, California Corey Sippel, BS Lead Anesthesia Technician Oregon Health and Science University Portland, Oregon Karen J. Souter, MB, BS, FRCA Associate Professor, Vice Chair for Education, and Residency Program Director Department of Anesthesiology and Pain Medicine University of Washington Seattle, Washington
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M. Christine Stock, MD, FCCP, FCCM James E. Eckenhoff Professor and Chair Department of Anesthesiology Northwestern University Feinberg School of Medicine Chicago, Illinois Anita Stoltenberg, RRT Supervisor of CV Surgical and ICU Respiratory Therapy Mayo Clinic Rochester, Minnesota Esther Sung, MD Staff Anesthesiologist Portland VA Medical Center Portland, Oregon Pedro Paulo Tanaka, MD, PhD Clinical Associate Professor Department of Anesthesia Stanford University School of Medicine Stanford, California Heather Taylor, MD Anesthesiologist Department of Anesthesiology Banner Estrella Medical Center Phoenix, Arizona Norman E. Torres, MD Assistant Professor and Consultant Department of Anesthesia Mayo Clinic St. Mary’s Hospital Rochester, Minnesota Charles A. Vacanti, MD Professor of Anaesthesia Harvard Medical School Chair, Department of Anesthesiology Brigham and Women’s Hospital Boston, Massachusetts Kamila Vagnerova, MD Assistant Professor of Anesthesiology Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
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Contributors
David C. Warltier, MD, PhD John P. Kampine Professor and Chairman Department of Anesthesiology Medical College of Wisconsin Milwaukee, Wisconsin Mary Ellen Warner, MD Associate Professor Department of Anesthesiology Mayo Clinic Rochester, Minnesota
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David Wilson Glenn Woodworth, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
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Acknowledgments
W
e extend our thanks to the many authors who contributed their time and effort to the creation of this text. Although many have written extensively on their respective topics, they enthusiastically embraced the challenge of reworking the material to better serve the
needs of anesthesia technicians. Thanks to Matt Schreiner for his tireless efforts to coordinate our authors and the many tasks associated with bringing a textbook with 65 chapters together. Special thanks to Claudia Woodworth for her monumental editorial efforts.
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Preface
T
he role of the anesthesia technician in the perioperative environment has been expanding to keep pace with the rapid innovations in anesthesiology and surgery. As the responsibilities and complexity of the job have increased, so has the visibility of the role of anesthesia technician within hospitals and other health care institutions. Much like other health care roles, the increased responsibilities and complexity of job requirements have put the role of anesthesia technician on the path of becoming a more widely recognized allied health profession. Associated with this is an increased requirement for education and training ranging from equipment maintenance to medication handling. More and more institutions are scrutinizing the education and training of anesthesia technicians, with some going so far as to require certification as a job requirement. The goal of this text was to fill a critical gap in the material available to support the education and training of anesthesia technicians and technologists. Currently, there is no single text directed specifically at this group of allied health professionals. Community college course students or individuals studying for a certification exam must often utilize textbooks directed at anesthesiologists. Although the material is similar, the focus of these texts is not directed at an anesthesia technician audience. The Anesthesia Technician and Technologist’s Manual is specifically directed at this audience and their background education. Section I provides an overview of the profession, while Section II covers basic anatomy
and physiology with an emphasis on highlighting the principles upon which anesthesia equipment or procedures are based. Section III covers the basic activities of anesthesia to give the technician a solid foundation for understanding the different aspects of performing an anesthetic including airway management, sedation, general anesthesia, regional anesthesia, fluid therapy, and patient positioning. Section IV is the bulk of the text and covers a wide variety of anesthesia equipment and procedures from anesthesia machines and vascular access, to neuromuscular monitoring and ventricular assist devices. This section places a heavy emphasis on anesthesia equipment setup, operation and maintenance— a priority for anesthesia technicians. This section will help anesthesia technicians understand why a procedure is performed, what equipment might be needed and why, as well as how to set up and troubleshoot the equipment. Section IV introduces the anesthesia technician to the operating room and hospital environment covering topics from fire safety to the special needs of performing anesthesia out of the operating room. The final section, Section V, covers several anesthesia emergencies with the goal of familiarizing the anesthesia technician with what is going on, what the priorities are during the crisis, and what equipment or other activities the anesthesia technician should be prepared for. It is our sincere hope that current and future anesthesia technicians and technologists will think of The Anesthesia Technician and Technologist’s Manual as the core resource text for this exciting and growing health care profession.
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Foreword
A
s anesthesiologists, we realize that the safety of the patient and the outcomes of procedures require the coordinated efforts of many individuals. Anesthesiologists need the cooperation of the surgical and nursing personnel to do their jobs and work with us. However, we absolutely depend on anesthesia technicians to skillfully provide the tools we need and the expertise and support we must have to perform our jobs successfully. This book is dedicated to supporting the continuing education of our friends and colleagues, the anesthesia technicians. It will provide the support they need while attending a formal anesthesia technician educational program, studying for certification, or for simply advancing their knowledge to help them better perform their duties. One of the challenges for any textbook is to stay current with the rapid introduction of new information. Of course the pace of the introduction of new equipment and technologies into
the operating room environment is ever accelerating. Because a large portion of this text deals with equipment issues, it will require frequent updates and constant vigilance for developments in our field to maintain its relevancy to anesthesia practice. True to the educational mission of the text, all royalties from the sale of this book are designated to be donated to the Foundation for Anesthesia Education and Research. We hope this book is helpful to all individuals interested in caring for perioperative patients and that it improves the care of our patients. Jeanine Wiener-Kronish, MD Anesthetist-in-Chief Massachusetts General Hospital Henry Isaiah Dorr Professor of Research and Teaching in Anaesthetics and Anaesthesia Harvard Medical School Boston, Massachusetts
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Contents Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vi Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xiv Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xv
SECTION
I
Careers in Anesthesia Technology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 1
The Anesthesia Technician and Technologist Shannon Sayers-Rana and Delbert Macanas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
2
Certification for Anesthesia Technicians and Technologists Sue Christian . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
3
The Surgical Experience Shannon Sayers-Rana and Shaleha Khalique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
SECTION
II
Anatomy, Physiology, and Pharmacology . . . . . . . . . . . . . . . . . . . . 15 4
Pharmacokinetics David Sibell and Ryan Anderson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16
5
Pharmacodynamics Pamela Kirwin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22
6
Efficacy, Toxicity, and Drug Interactions Amy Opilla and Kim Mauer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
7
Cardiovascular Anatomy and Physiology Glenn Woodworth, Asish Das, and Valerie Sera . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
8
Cardiovascular Pharmacology Markus Kaiser and David C. Warltier. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58
9
Cardiovascular Monitoring Richa Dhawan and Mark Chaney. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
10
Mechanical Cardiovascular Support Richa Dhawan and Mark Chaney. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74
11
The Respiratory System Mark Burno, Casey A. Harper, Matthew Chao-Ben Chia, and M. Christine Stock . . . . . . . . . . 79
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Contents
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xvii
Acid and Base Physiology Aaron Kirsch and Jeffrey Kirsch . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101
13
Central Nervous System Josh Finkle and Jeffrey Kirsch . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
14
Autonomic Nervous System Lori Nading and Ahmed Alshaarawi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121
15
Peripheral Nervous System Eve Klein and Michelle Cameron . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
16
Neuromuscular Anatomy and Physiology Jodi H. Kirsch and Jeffrey Kirsch . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138
SECTION
III
Principles of Anesthesia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147 17
Sedation Angela Kendrick and Dawn M. Larson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
18
Principles of Airway Management Michael Aziz . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155
19
Patient Positioning: Common Pitfalls, Neuropathies, and Other Problems Mary Ellen Warner . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165
20
Overview of a General Anesthetic Dalia Elmofty and Thomas Cutter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175
21
Regional Anesthesia for Anesthesia Technicians Michael S. Axley . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190
22
Fluid Therapy Sarah Shabot and Donald Prough . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204
23
Transfusion Medicine Curtis Bergquist and Kamila Vagnerova . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210
SECTION
IV
Equipment Setup, Operation, and Maintenance . . . . . . . . . . . . . . 219 24
Infectious Disease Brett Miller. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220
25
Equipment Contamination and Sanitation and Waste Disposal Katie Schenning and Stephen Robinson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225
26
Overview of Anesthesia Machines Brian Mitchell and Michael Jamond. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
27
Anesthesia Machine Checkout Ramon Larios and Esther Sung . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240
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28
Contents
Vaporizers Roy Esaki and Alex Macario . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247
29
Anesthesia Breathing Systems Charles A. Vacanti . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255
30
Anesthesia Machine Ventilators Eric Schnell and Valdez Bravo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261
31
Anesthesia Machine Operation, Maintenance, and Troubleshooting Andrew Oken and Scott Richins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 270
32
Gas Analyzers Wesley Simpson II . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
33
Basic Monitoring Wesley Simpson II . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 286
34
Vascular Access Equipment and Setup MicHael Moore and Izumi Harukuni . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297
35
Airway Equipment Setup, Operation, and Maintenance Norman E. Torres, Anita Stoltenberg, and Glenn Woodworth . . . . . . . . . . . . . . . . . . . . . . . . 330
36
Infusion Pumps Victoria Reyes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 356
37
Blood Gas Analyzers and Point-of-Care Testing David Wilson and Guy Buckman . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363
38
Ultrasound Matthew Abrahams and Jorge Pineda . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 372
39
Transesophageal Echo Edward A. Kahl and Lisa Chan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391
40
Neuromuscular Blockade Assessment Ryan Goldsmith . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 398
41
Neurophysiologic Monitoring Judith A. Freeman . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403
42
Intra-aortic Balloon Pumps and Ventricular Assist Devices Laura Downey . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411
43
Defibrillators Matthew Griffee and Jeffrey Moller . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 426
44
Pacemakers and Implantable Defibrillators Jeffrey Mako and Peter Schulman . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 434
45
Device Malfunction Pedro Tanaka, Diane Alejandro-Harper, and Arjun Desai . . . . . . . . . . . . . . . . . . . . . . . . . . . . 442
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SECTION
xix
V
Operating Room and Hospital Environment . . . . . . . . . . . . . . . . . 447 46
Pediatric Anesthesiology Brian N. Egan, Terrence McGraw, and Danny L. Robinson . . . . . . . . . . . . . . . . . . . . . . . . . . . 448
47
Obstetric Anesthesia Karen Hand . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 456
48
Anesthesia Considerations for out of Operating Room (OOR) Locations Andrew J. Pittaway and Karen J. Souter. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468
49
Medication Handling Shohreh Sadlou and Corey Sippel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483
50
Patient Transport Matthew Hart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 489
51
Electrical Safety Richard Botney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 495
52
Fire Safety Richard Botney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 502
53
Laser Safety Sameer Menda, Berklee Robins, Deborah Carter, and Vishal Khemlani . . . . . . . . . . . . . . . . . 509
54
Electronic Medical Records Heather Taylor and David Sibell . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 515
55
Legal Aspects of the Operating Room Mark J. Baskerville and Kenneth Abbey . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 520
56
Continuous Quality Improvement and Risk Management Brenda Quint-Gaebel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 523
57
Accreditation Shannon Sayers-Rana . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 528
58
Simulation-based Training Bryan J. Read and Michele Noles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 532
59
BLS and ACLS Certification Glenn Woodworth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 537
SECTION
VI
Operating Room Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 543 60
Airway Emergencies Dawn Dillman . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 544
61
Cardiac Arrest Glenn Woodworth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 554
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Contents
Fire in the Operating Room Richard Botney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 559
63
Malignant Hyperthermia Tae W. Kim and Henry Rosenberg . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 566
64
Anaphylaxis Mary Blanchette . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 575
65
Massive Hemorrhage Jared Grose and Ryan Anderson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 581
Acronyms and Abbreviations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 587 Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 591
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SECTION
I
Careers in Anesthesia Technology
1
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CHAPTER
1
The Anesthesia Technician and Technologist Shannon Sayers-Rana and Delbert Macanas ■ INTRODUCTION What exactly is an anesthesia technician (AT) or anesthesia technologist? This role was first developed in hospitals as the complexity of anesthesia increased and the anesthesia care team required more assistance in and out of the operating room. The first ATs became responsible for the anesthesia equipment and medication cart, stocking supplies, and running small errands for the anesthesia team. Over time, the role has evolved into becoming a significant, integral part of the anesthesia care team with numerous clinical responsibilities. These responsibilities typically include maintaining the anesthesia machine, assisting with vascular access and regional anesthesia procedures, assisting with difficult airways, troubleshooting anesthesia equipment, assisting with resuscitations and other operating room emergencies, and running point-of-care lab tests. In some institutions, ATs operate sophisticated blood collection equipment or even intraaortic balloon pumps to support patients with severe congestive heart failure. The American Society of Anesthesia Technicians and Technologists (ASATT) has a recommended scope of practice for these roles, which are outlined below, but each institution will have its own unique job description and preemployment requirements. What are the qualities of an AT? An AT must possess detailed knowledge of anesthesia procedures; must have solid technical skills to be able to operate numerous electronic devices and equipment; must have good communication skills to interact with anesthesia staff and patients; must be able to think on his or her feet while working in stressful situations; and must be able to work well in a team environment.
■ ANESTHESIA TECHNICIANS AND TECHNOLOGISTS: SCOPE OF PRACTICE The ASATT’s recommended scope of practice details the duties at three levels of practice: the AT, the certified anesthesia technician (Cer.A.T.), and the certified anesthesia technologist (Cer.A.T.T.). As stated on ASATT’s Web site, “Their role is to assist licensed anesthesia providers in the acquisition, preparation and application of the equipment and supplies required for the administration of anesthesia.” Outlined below are the common duties and responsibilities for each position as well as their educational requirements. However, as stated above, job duties may differ depending upon where the AT works. AT Responsibilities • Providing support for routine surgical cases by assisting in the preparation and maintenance of patient equipment and anesthesia delivery systems before, during, and after anesthesia • Assisting the licensed anesthesia providers in various settings • Performing duties under the direct supervision of a licensed anesthesia provider and/or registered nurse (RN) • Performing first-level maintenance on anesthesia equipment, cleaning, sterilizing, disinfecting, stocking, ordering, and maintaining routine anesthesia equipment and supplies AT Education • A high school diploma or 2-year degree and previous work experience are preferred for entry-level employment.
2
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Chapter 1 • The Anesthesia Technician and Technologist
An AT should also show proficiency in basic life support, physiologic monitors relating to the administration of anesthesia, handling of biologic hazards, infection control practices, and safe use and handling of anesthetic gases. The AT should also be aware of the indications for local, regional, and general anesthesia. Cer.A.T. Responsibilities • All of the above for the AT as well as the items listed below • Demonstrate practical knowledge and expertise in all areas of anesthesia with a thorough experience of the setup, operation, and troubleshooting of anesthesia equipment and devices • Knowledge of institutional guidelines, policies, and safety requirements • Understanding of anatomy and physiology as it applies to anesthesia • Administrative duties that include scheduling, evaluations, payroll, job descriptions, etc. • Assisting the licensed anesthesia provider with patient assessments, evaluations, transport, positioning, insertion of intravenous and other invasive lines, as well as airway management and regional anesthesia procedures Cer.A.T. Education • Successful completion of the ASATT certification exam. (To qualify for the exam, you must have a high school diploma or greater, a minimum of 2 years of AT experience, or graduation from an approved AT program.) A Cer.A.T. will show the same proficiencies as an AT, in addition to demonstrating the ability to perform technical duties in complex clinical situations, coordinating daily routines of the AT staff, delegating responsibilities, understanding the expenses incurred for anesthesia procedures, participating in quality improvement, as well as ensuring a safe environment for patient care. Cer.A.T.T. Responsibilities • All of the above duties for the Cer.A.T. in addition to the items listed below • Assisting the anesthesia provider with intraoperative fluid management including volume resuscitation • Operating autotransfusion equipment • Maintaining current basic cardiac life support (BCLS) and/or advanced cardiac life support
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3
(ACLS) certification and maintaining current pediatric advanced life support (PALS) certification if required • Performing inspection and maintenance of the anesthesia gas delivery systems • Setting up and troubleshooting the intraaortic balloon pump • Providing point-of-care laboratory services, following all regulatory guidelines Cer.A.T.T. Education • Currently, the role of the Cer.A.T.T. is distinguished from that of the Cer.A.T. by additional levels of training and education. Successful completion of the technologist exam is required to be designated as a Cer.A.T.T.
■ OTHER ROLES WITHIN THE ANESTHESIA CARE TEAM There can be confusion as to the different nonphysician roles within the anesthesia care team. The two more commonly recognized positions include the anesthesia assistant (AA) and the certified registered nurse anesthetist (CRNA). The AA has completed an advanced degree, specializing in anesthesia. He or she is able to practice anesthesia under the direction of an anesthesiologist. There are currently six schools offering anesthesia assistant programs throughout the United States, with AAs currently practicing in 18 states (and growing). The CRNA is an RN with advanced practice training and a degree from a nurse anesthetist program. CRNAs may practice anesthesia independently in some states. Others require that they practice under the supervision of an anesthesiologist, but not necessarily an anesthesiologist. Individual institutions will further define the local scope of practice through their governing boards and credentialing committees. As of April 2011, there were 111 nurse anesthesia training programs in the United States. To gain additional detailed information about becoming an AT, a Cer.A.T., or a Cer.A.T.T., visit the ASATT Web site at www.asatt.org. To gain further knowledge about the position of AA or CRNA, visit the Web sites at www.anesthesiaassistant.com and www.aana.com, respectively.
■ SUMMARY The operating room is an exciting environment. Incredible advances in the surgical treatment
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4
Section I • Careers in Anesthesia Technology
of patients are being constantly introduced as new technology or techniques become available. Recent advances include robotic surgery, magnetic resonance image–guided neurosurgical procedures, and ultrasound-guided nerve blocks. The introduction of new technology, the complexity of these procedures, and the medical condition of the patients who receive them have increased the complexity of working in the operating room. Nowhere is this more true than providing anesthesia during these procedures. The anesthesia team is responsible for providing safe operating conditions, preventing awareness, controlling pain, and keeping a patient immobile, all the while monitoring multiple physiologic parameters (e.g., blood pressure, inhaled gas concentration, cardiac rhythm, blood oxygen saturation, exhaled carbon dioxide levels, urine output and renal function, and blood glucose and electrolyte levels). The anesthesia technicians/technologists play a critical role on the anesthesia team. They are responsible for the setup, operation, and maintenance of
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the majority of the equipment that the anesthesia team of today and the future will use to care for the patient. The AT must be capable of troubleshooting equipment on the fly, assisting with complex procedures, transporting patients, and assisting with monitoring physiologic parameters. In addition to on-the-job training, there are several educational programs to help prospective ATs obtain the necessary skills and knowledge to enter this field. This text was designed to serve as the go-to source for current and prospective ATs, covering everything from relevant anatomy, physiology, and pharmacology, equipment setup/ operation/maintenance, anesthesia machine function and checkout, procedures for obtaining vascular access, and infection control to operating room emergencies.
SUGGESTED READINGS AA. Retrieved from www.anesthesiaassistant.com. AANA. Retrieved from www.aana.com. ASATT. Retrieved from www.asatt.org.
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CHAPTER
2
Certification for Anesthesia Technicians and Technologists Sue Christian ■ INTRODUCTION The first recorded use of anesthesia support personnel occurred during the late 1930s in England. History of the specialty shows that Sir Robert Macintosh solicited the services of Richard Salt to take care of the equipment and facilitate the administration of anesthesia (McMahon & Thompson, 1987). Since that time, the administration of anesthesia has been supported by dedicated ancillary staff to address the maintenance and operation of equipment and supplies needed to administer a safe anesthetic. Over the years, the number and complexity of surgical interventions have grown. Along with the growth have come significant advances in instrumentation and technology. This has increased the complexity of administering modern anesthetics and increased the demand for qualified support personnel. During the majority of this period, anesthesia technicians lacked a formalized training program and were trained “on the job” (on-thejob training [OJT]).
■ BACKGROUND The American Society of Anesthesia Technologists and Technicians (ASATT) is a nonprofit organization whose primary focus is the education of anesthesia technologists and technicians. The organization was officially founded in October 1989 when a core group of technicians met in New Orleans, Louisiana. Due to the overwhelming need for a formalized training program, the charter leadership was determined to legitimize the profession as well as provide educational support for the professionals practicing in this area. Realizing that they would need the support of the anesthesia providers to succeed, the timing and location for this historical meeting were
fixed in conjunction with the annual meeting of the American Society of Anesthesiologists (ASA). As interest in the ASATT grew and a formalized training program was adopted, it was realized that to gain formal recognition of the importance of anesthesia support personnel, a process would need to be implemented demonstrating these individuals possessed the knowledge and qualifications to be employed as anesthesia technicians. In 1993, ASATT began laying the foundation for the development of a national certification examination. The entire process took 2 years to complete, and in May 1996, ASATT administered its very first written certification examination for anesthesia technicians. Due to the popularity of the certification exam, ASATT members expressed interest in an advanced level of certification, and in 2001, the first technologist-level exam was administered. After several years, interest waned and the exam was put on hiatus. However, as certification became more widely accepted, the technologist exam was reactivated in 2006 due to expressed interest from both technicians and employers. As a condition of employment, the demand for certification has increased, as has the number of individuals seeking certification and taking the exam. To meet this increased demand, the ASATT began to administer the exam via computer in 2003, making it accessible year round. Due to expanded interest on the international level, ASATT began to offer a Web-based exam to those candidates in 2006. ASATT has the only nationally recognized certifications for both anesthesia technologists and technicians. The technologist and technician certifications are endorsed by the ASA and the American Association of Nurse Anesthetists (AANA). 5
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Section I • Careers in Anesthesia Technology
■ CERTIFICATION PROCESS A Certification Test Development and Test Writing Committee evaluates and develops the ASATT certification standards and exam in conjunction with Applied Measurement Professionals (AMP), an organization that develops and administers certification exams. Test development is written in accordance with the standards set forth by the National Organization for Competency Assurance (NOCA), an organization dedicated to providing educational, networking, and advocacy resources for the credentialing community. The Certification Test Development and Test Writing Committee consists of the following: • Anesthesiologists • Certified registered nurse anesthetists (CRNAs) • Certified anesthesia technologists (Cer.A.T.T.s) and certified anesthesia technicians (Cer.A.T.s) • Corporate representatives • A professor of anesthesia education • A member of the professional development company (AMP) Test items are written in accordance with a detailed content outline that is specific to each level of certification. Topics include, but are not limited to, operating room (OR) environment, infection control, types of anesthesia, anesthesia machine and gas delivery, anatomy, monitors and ancillary devices, and intraoperative complications. The test items are taken directly from the suggested study reference books.
■ CERTIFIED TECHNICIAN EXAM The current qualifications to take the technician exam are as follows: the candidate must (1) be actively working as an anesthesia technician with a minimum of 2 years of clinical experience and (2) be proficient in English and possess a high school diploma or equivalent. Interested applicants must complete the registration form, submit a copy of their high school diploma, submit a letter from their employer detailing their work experience, and pay the required fees. Once the application is processed, applicants are notified via e-mail when they may register to take the examination. The applicant will then have 90 days to register for the examination. Candidates who do not register within that time limit will forfeit all fees and have to restart the process.
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The exam consists of 120 questions pulled from a bank of 1,575 questions ensuring that the same exam is not given twice. The candidate is then given 3 hours to complete the test. Candidates are only scored on 100 questions, with the remaining 20 anonymous questions being used for research purposes. These 20 questions are predetermined prior to the candidate taking the exam. Once the candidates have completed the test, they will receive a printout of their score. Candidates will not be given the questions or the answers to the test items that were incorrectly answered. The certification must be renewed every 2 years to the ASATT Certification/Recertification Review Committee. At the end of each two full calendar year period, Cer.A.T.smust show that they have 20 continuing education hours (CEHs) relevant to their level of certification. • Example: You passed the exam in January 2011. Your certification will expire on December 31, 2013 (certification is granted for 2 full years beginning with the year following the year in which the applicant meets all certification requirements). • 20 CEHs must be earned between January 1, 2012, and December 31, 2013. • CEHs’ content must be relevant to the Cer.A.T.
■ CERTIFIED TECHNOLOGIST EXAM Currently, to be eligible for this examination, the candidate must be a certified technician in good standing. The test consists of 125 questions that are randomly drawn from a bank of 700. The candidate is given 3 hours to complete the exam and is scored on all 125 questions. The technologist exam is significantly more difficult than the technician exam. Certification for the technologist is also granted for a 2-year period. In order to maintain certification, a minimum of 30 CEHs must be submitted to the ASATT Certification/ Recertification Review Committee. At the end of each 2-year period, Cer.A.T.T.s must reapply for certification. • Example: You passed the exam in January 2010. Your certification will expire in December 2012. (Certification is granted for two full years beginning with the year following the year in which the applicant meets all certification requirements).
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Chapter 2 • Certification for Anesthesia Technicians and Technologists
• CEHs must be earned between the period of January 1, 2011, through December 31, 2012. • CEHs must come from this 2-year period, and the content must be relevant to the Cer.A.T.T. Since the candidate took the exam earlier in the year, he or she has a longer grace period in which to earn CEHs compared to a candidate who passed the certification exam in November of 2010 because the 2-year certification period begins with the year following the year in which the applicant meets all certification requirements. Both candidates’ certification will expire on December 31, 2012.
■ EDUCATIONAL PROGRAMS In April 2010, the Commission on Accreditation of Allied Health Education Programs (CAAHEP) approved anesthesia technology as an official health science discipline. Schools that offer an associate’s degree in anesthesia technology must become accredited through ASATT and CAAHEP in order for their graduates to be eligible for the certification exam. As an official health science discipline, OJT will be phased out as college graduates enter the workforce. The ASATT has tentatively set a timeline of July 2015 to phase out the certified technician exam. The technologist exam will be the only exam offered after that date. To qualify for the exam, you will need to be a graduate from a CAAHEP-accredited program. While the certified technician designation will continue to be recognized by the society, it will be imperative that these individuals keep their certification status in good standing.
■ CERTIFICATION BENEFITS In the past 7 years, there has been a steady increase of employers requiring certification as a condition of employment. Salaries may be based on whether the technician holds certification for the technician or technologist level. While some employers do not mandate certification as a condition of employment, most have initiated a requirement for certification within a designated time period from the date of hire. In addition, many employers have developed a clinical ladder for advancement based on certification. There is also an added incentive for employers to hire and maintain certified technologists and technicians. These individuals are staying abreast on the latest technology employed in the OR environment and actively participate in
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quality assurance for the monitoring devices in use. This enables the anesthesia department to remain compliant with local and state regulations as well as the Joint Commission (formerly the Joint Commission on Accreditation of Healthcare Organizations) and College of American Pathologists (CAP) accreditation. Certified technologists and technicians are skilled individuals who assist the anesthesia provider in line placement, difficult intubations, and patient monitoring, thus improving patient safety. They reduce operating costs and facilitate room turnovers by properly ensuring that all needed equipment and necessary supplies are readily available. The acronym for ASATT, “Assisting with Safe Anesthesia Today and Tomorrow,” guarantees that these qualified individuals are readily available to assist in both emergent and nonemergent patient situations.
■ SUMMARY The majority of anesthesia technologists and technicians in practice today were trained on the job. Looking at the history of the profession, the complexity of the surgical procedures, the medical acuity of patients, and the advancement in technology, no one can argue that the job has evolved in the last 20 years. Taking these factors into account, many institutions are beginning to question if OJT is feasible in this day and age. Employers are seeking qualified anesthesia technicians, and the demand is currently greater than the supply. This may be attributed to the 2006 recognition from the Association of Operating Room Nurses (AORN) when it included anesthesia technologists and technicians in its position statement on allied health care providers and support personnel in the perioperative practice setting. Several Cer.A.T.T.s and Cer.A.T.s have also been asked to sit on a variety of committees for the Anesthesia Safety Patient Foundation (ASPF). CAAHEP accreditation not only provides opportunities for the profession to excel but also enables the employer to hire qualified individuals as anesthesia technicians, thereby phasing out the costly and time-consuming responsibility of OJT. The society’s original goal was to see certification to fruition. By all indications, this health science discipline will be one of the fastest growing disciplines the medical profession has experienced in the last decade.
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Section I • Careers in Anesthesia Technology
REVIEW QUESTIONS 1. The ASATT was established in this year: A) 1986 B) 1989 C) 1996 D) 2001 E) None of the above Answer: B. ASATT was established in New Orleans, LA, in 1989.
2. The first recorded use of anesthesia support personnel occurred in A) England B) Australia C) Louisiana D) China E) California Answer: A. The first recorded use of anesthesia support personnel occurred in England in the late 1930s.
3. ASATT issued its very first written certification exam for the technician in A) 1889 B) 1993 C) 1996 D) 2001 E) 2010 Answer: C. ASATT offered the first written exam for anesthesia technicians in 1996.
4. The certification exam is administered in accordance with standards developed by A) ASA B) AANA C) APSF D) NOCA E) JCAHO Answer: D. NOCA developed the standards on which the certification exams are administered.
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5. Certification for both the technologist and technician exams is granted on a A) Four-year basis B) Rotation of every other year C) Two-year basis D) Yearly basis E) None of the above Answer: C. Both the technician and the technologist must recertify every 2 years after completing the required number of CEHs for their discipline.
6. The test writing committee is composed of A) Anesthesiologists B) CRNAs C) Corporate representatives D) Anesthesia technicians and technologists E) All of the above Answer: E. The test writing committee consists of anesthesiologists, CRNAs, corporate representatives, anesthesia technicians and technologists, educators, along with a representative from the test writing development company.
7. A certified anesthesia technician must show proof of this number of CEHs in a 2-year period: A) 30 B) 20 C) 120 D) 125 E) 10 Answer: B. The anesthesia technician must show proof of 20 CEHs every 2 years as part of the recertification process. The anesthesia technologist must have 30 CEHs in the same time period.
SUGGESTED READING McMahon DJ, Thompson GE. A survey of anesthesia support personnel in teaching programs. Med Instrum. 1987;21(5):269–274.
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CHAPTER
3
The Surgical Experience Shannon Sayers-Rana and Shaleha Khalique ■ INTRODUCTION In order to better understand the role of the anesthesia technician (AT) as a member of the anesthesia team and the flow of patients through the operating room (OR), it is useful to understand the overall surgical experience. This chapter provides a description of the different phases of care a patient may experience while undergoing a surgical procedure. This will serve as an excellent introduction to the perioperative environment.
■ THE SURGEON’S OFFICE OR CLINIC Mr. Smith has been experiencing abdominal pain for several months. He finally went to his primary care physician. After an examination and preliminary testing, his doctor told him that he had a mass near his pancreas and that surgery would be necessary to remove it and to make a definitive diagnosis. Diagnosis is the identification of a specific disease or an illness gleaned from a history of signs and symptoms, a physical exam, and testing. A surgery patient is usually diagnosed prior to coming to the OR unless it is an emergency or the surgery itself is necessary to make the diagnosis. Once the decision to proceed with surgery has been made, Mr. Smith will consult with the surgeon’s office staff to schedule the surgery. The timing will depend upon the following: • The surgeon’s schedule • The urgency of the procedure • Availability of surgical facilities for which the surgeon has privileges and are appropriate for the planned procedure; that is, an outpatient procedure would not be appropriate for heart surgery. • The patient’s insurance coverage: The insurance may only cover certain facilities or the cost to the patient may differ depending upon which facility is chosen.
• The schedule of the patient and any caregivers who might be involved in the postoperative care of the patient. Prior to surgery, a patient may go through additional testing or consultations to make sure that the medical condition is optimized, as much as time permits, prior to surgery. Standard preoperative (preop) testing may include an electrocardiogram (ECG), lab work, blood pressure, x-ray, urinalysis, etc. The type of testing will depend upon the patient’s medical condition and the scheduled surgery. For many healthy patients, pre-op testing may not be necessary.
■ PREADMISSION: PRE-OP VISIT Preadmission is the period of time prior to admission to the surgical facility. If the procedure will not take place for several days, the patient may be asked to return to the surgeon’s office for a pre-op visit; otherwise, the pre-op instructions will be given during the current visit. At this time, the surgeon will update the history and physical, provide instructions to the patient, and make sure that the patient understands the risks and benefits of the procedure he or she is about to undergo. Most institutions require that a history and physical be performed within the 30 days prior to a surgical procedure. All necessary documentation, such as the consent form and any legal forms, can also be completed at this time. Patients receive pertinent information regarding what needs to be brought with them the day of the surgery, what to avoid (i.e., not have anything to eat or drink 8 hours prior to surgery), what to expect after surgery, whether or not medications should be continued, and also when they should plan on arriving at the hospital or outpatient surgical facility. The patient will often be given prescriptions for medications to be
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Section I • Careers in Anesthesia Technology
taken during the postoperative period and care instructions for the period following the procedure. The vast majority of surgical procedures today are performed on an outpatient basis, and all of the above information is essential to help the patient be prepared for the surgery and the postsurgical period. On rare occasions, an anesthesia consultation may be requested by the surgeon. These are reserved for patients with severe medical conditions or special considerations that affect anesthesia. For example, the patient may have a family history of a rare, but lethal, reaction to a certain anesthetic.
■ ADMISSION Mr. Smith arrives at 5:00 in the morning at Sunnyside Hospital. He proceeds through the admission process where paperwork is filled out and his insurance verified. Mr. Smith had to get up at 3:00 am to get ready and have his wife drive them to the hospital, which was an hour away from their home. They are both tired and anxious. To make matters worse, Mr. Smith is asked about his religious preferences and who to designate for power of attorney should anything bad happen to him during surgery. The admissions personnel give Mr. Smith an identifying wristband. Patients coming in for surgery are asked to arrive 1-2 hours prior to their scheduled surgery time. Upon arrival, the patient will be prepared for the OR. In many cases, the patient will have had an opportunity to fill out admission paperwork in advance. In other cases, the paperwork will need to be filled out at the surgical facility. At the appropriate time, the patient will be referred to the pre-op holding area.
■ PRE-OP HOLDING Mr. Smith and his wife wait in the waiting area for about 3 hours. Mr. Smith’s surgery has been delayed because his doctor, Dr. Martin, has been delayed due to an emergency surgery that was added on this morning. Finally, at 9:00 am, Mr. Smith and his wife are escorted to the pre-op holding area. The nursing staff in the pre-op holding area assign him to a bed and have him change into a hospital gown. The pre-op nurse goes over an exhaustive list of questions about Mr. Smith’s medical history and medications. He is told that someone from the anesthesia department will see him soon.
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In the pre-op area, patients will be asked to change into a hospital gown and wear a cap to cover their hair. They will also be asked to remove any items such as jewelry, hearing aids, contact lenses, glasses, and dentures, which will be stored away. Their identification bracelet will be checked. If there are any allergies, or any precautions, patients will receive an additional band to alert all medical personnel. A nurse will come in and take vitals, measure height and weight, measure body temperature, and note if there are any changes in health. An intravenous (IV) line will also be placed to keep the patient hydrated and also as a place for administering medications. The nurse will also confirm that the paperwork and the surgical consent form are in order and have been signed by the patient and the surgeon. Mr. and Mrs. Smith wait in the pre-op holding area for another 30 minutes. Finally, the surgeon arrives. She apologizes for the long delay and begins reviewing the procedure with the Smith’s. Dr. Martin puts her initials on Mr. Smith’s abdomen. Once all of the Smiths’ questions are answered, Dr. Martin hurries off. Shortly thereafter, Dr. Kirby, the anesthesiologist arrives. Once again, Dr. Kirby reviews Mr. Smith’s medical history with him and performs a brief physical examination, which includes asking him to open his mouth wide and extend his neck. Mr. Smith is given the option of an epidural to help him with pain control after the surgery. The Smith’s are unsure but decide to go ahead with the procedure because the doctor must know best. Dr. Kirby finishes up with a discussion of the risks and benefits of the anesthesia, the invasive lines that will be placed, and the epidural. All of the things that can go wrong are a bit scary to Mrs. Smith, but she says nothing so as not to alarm her husband. Dr. Kirby hurries off and says that he will be right back. Soon the surgical nurse arrives and again asks many of the same medical questions. She also verifies the consent form. Many things happen in the pre-op area. The pre-op nursing staff will take vital signs, go over the patient’s medical history, and start an IV line. They will also record information in the medical record and make sure all the paperwork is in order and up to date. In many cases, the patient will get to briefly meet with the surgeon. The surgeon will answer any last minute questions and “mark” the surgical site on the patient. Marking of the surgical site in cooperation with
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Chapter 3 • The Surgical Experience
the patient is to reduce the risk of wrong-site surgery. In addition to meeting the surgeon, the patient will meet some of the other members of the OR team. The circulating nurse in the OR will stop by and verify that everything is ready for the patient to proceed to surgery. This will also be the time that the patient will meet the anesthesiologist. During the pre-op evaluation, the anesthesia provider reviews the patient’s medical history and inquires if there were any family complications with anesthesia. Part of the pre-op evaluation includes evaluating the patient’s airway and reviewing all labs, x-rays, and all other tests relevant to the surgery. The anesthesiologist will have already formed a preliminary anesthetic plan based upon initial information. After review of the history with the patient, a physical examination, and review of any new test results, the anesthesiologist modifies the plan. Based on the type of procedure, along with the preferences of the anesthesiologist, the patient, and the surgeon, the type of anesthetic is chosen. This may include local, regional, general, or a combination of methods. In addition to the type of anesthesia, any special monitoring or vascular access will also be planned. The patient must participate in the choice of the anesthetic plan and be informed of important risks and potential benefits of the anesthesia type and any special procedures. To prepare the patient for the OR, the anesthesia care provider will inform the patient of what he or she can expect as he or she enters the OR. If a regional block is indicated, the anesthesiologist or the regional block team may place the block in the pre-op holding area before the patient goes to the OR. Procedures performed in the pre-op holding area by the anesthesiologist will be conducted with the assistance of an AT. The pre-op area will be the final destination where family members can be with the patient. After the patient is taken to the OR, family members will wait in the family waiting room. In many institutions, anesthesia functions as a care team with the anesthesiologist supervising a certified registered nurse anesthetist (CRNA). In these cases, the anesthesiologist may be supervising several different CRNAs simultaneously. The anesthesiologist discusses and formulates the anesthetic plan along with the CRNA. The physician is then present for all critical portions of the procedure and is available for consultation if the CRNA needs help with the cases.
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In other institutions, the CRNA may function independently.
■ THE OPERATING ROOM In preparation for a surgical case, the anesthesia provider and the AT will make sure all necessary equipment, medications, monitors, and supplies for the procedure are readily available. This is particularly important if special equipment or supplies will be needed based upon the planned surgical procedure or the medical condition of the patient. The AT should be able to anticipate special needs based upon the planned surgical procedure as described in the surgical schedule. The anesthesia provider should communicate with the AT any other special requirements based upon the patient’s medical condition. Communication between the anesthesia provider and the AT is essential to ensure an efficient and safe anesthetic. The anesthesia provider should also coordinate with the AT if the technician will be required to assist the provider with any procedures. When the OR is ready for the patient, a member of the surgical team will come to the pre-op area and transport the patient to the room. Once in the OR, the appropriate monitors are placed and the anesthesia provider will “induce” anesthesia with IV or inhalational anesthetic agents. The patient’s airway may require intubation or the use of other devices to ensure safe ventilation of the lungs. Invasive lines, such as arterial lines or central lines, are usually placed after the patient is asleep with the assistance of an anesthesia technician. In some cases, due to the patient’s medical status, venous access or monitoring lines may be placed while the patient is still awake. The next phase of the anesthetic is referred to as maintenance. The anesthesia provider will administer anesthetic gases, additional pain medications, and drugs to paralyze muscles as necessary for the procedure. The anesthesiology provider continuously monitors the patient’s vital signs during the procedure. The level of awareness is also monitored through measurement of vital signs and the reaction to surgical stimulation, agent monitoring, or through brain wave monitors. During the operative procedure, the anesthesia provider will assess the need for transfusion of blood products or other fluids. Lab tests drawn and reviewed during the surgery will
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Section I • Careers in Anesthesia Technology
aid in this evaluation. In addition to maintaining the anesthetic, the anesthesia provider will monitor the patient’s respiratory status and in many cases will ventilate the patient with a mechanical ventilator. The final stage of the anesthetic is awakening the patient from anesthesia. This process is referred to as “emergence.” Once the surgical case is coming to an end, the anesthesia provider will slowly reduce the anesthetic medications or even give an IV reversal agent to assist with the waking-up process. Once full strength and awareness is observed in the patient, the anesthesiology provider will remove the breathing tube/device. When the patient is stable, the team can transfer the patient to the postanesthesia recovery room (PACU) or directly to the intensive care unit (ICU). At any point during the surgery, the AT may be asked to come to the OR to assist with a procedure, bring additional medications, equipment, or supplies, or help deal with an equipment problem. In addition, the AT could be called to assist the anesthesia provider with a medical emergency taking place in the OR.
■ POSTANESTHESIA CARE UNIT The next thing Mr. Smith remembers is waking up in an unfamiliar area. He is confused. The PACU nurse is telling him to take a deep breath. He does not have much pain but cannot seem to move his legs. The nurse tells him he is in the recovery room and that he must keep the oxygen mask on. Can he rate his pain on a scale of 1 to 10? Mr. Smith is slowly waking up and he realizes it is early evening. Didn’t he just go into surgery around lunchtime? He is a bit sick to his stomach and dizzy. The nurse tells him he is on his way to the ICU. Following anesthesia, some patients will be transported to the PACU for recovery. This is an area that monitors and supports patients as they recover from the immediate effects of anesthesia and surgery. Patients’ vital signs are continually monitored, and pain medication is administered as needed. Pain medication is given in the form of oral medication, injection, or a patient-controlled analgesia (PCA) pump. In some cases, a nerve block will be performed in the PACU to assist with pain that cannot be controlled with standard measures. When patients are stable, they are either discharged (referred to as “ambulatory” or
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“outpatients”) or transferred to a surgical ward in the hospital or an ICU (inpatients). An ambulatory patient is a patient who comes in for a procedure and leaves the facility the same day. An inpatient is a patient who was either already a patient in the hospital or a patient who was coming in for surgery but expected to stay in the hospital.
■ THE ANESTHESIA TECHNICIAN The anesthesia team consists of several different personnel with different job titles and descriptions who work together in order to provide anesthesia care to patients undergoing medical procedures. An important part of the anesthesia care team is the AT. ATs are the support service providers to the anesthesiologist and/or the nurse anesthetist who provide anesthesia care. The day-to-day tasks of the AT may vary based on the roles defined by each institution. Despite the differences, ATs do have a set of responsibilities that are often associated with them as part of their everyday routine. Some of these include resource planning, anesthesia machine checkout, covering multiple areas, assisting the anesthesia provider, turning over rooms, and supply management.
■ RESOURCE PLANNING Resource planning is a significant part of the job of an AT. It deals with analyzing available resources and making certain that the anesthesia team is fully prepared for the day’s cases as well as for emergencies or unanticipated cases. With experience, the ATs can anticipate what will be needed and prepare accordingly.
■ ANESTHESIA MACHINE CHECKOUT The anesthesia machine checkout is the full inspection of the anesthesia machine according to the manufacturer’s recommended procedure. This complete workup needs to be performed every morning by the AT and/or the anesthesia care provider. See Chapter 27 for details on the anesthesia machine checkout.
■ COVERING MULTIPLE AREAS ATs work in all areas where the anesthesia team is needed. These can include holding areas, ORs, PACUs, block rooms, obstetrics rooms, MRI/ CAT scan rooms, nuclear medicine suites, interventional radiology suites, cardiac procedure suites, electrophysiology labs, gastrointestinal
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Chapter 3 • The Surgical Experience
(GI) procedure areas, special procedure rooms, ICUs, and many more. With advances in modern-day medicine and technology, the areas covered by the anesthesia team are constantly growing; therefore, the areas covered by the AT are also growing. Chapter 48 provides an excellent overview of the special challenges associated with providing care in these areas.
■ ASSISTING THE ANESTHESIA PROVIDER A large part of the AT’s day is taken up by assisting the anesthesia provider directly. This may include assisting with regional blocks, transporting patients, placement of monitoring equipment, airway management, invasive line placement, use of ultrasound devices, and troubleshooting equipment. All of these will be covered individually in later chapters.
■ ROOM TURNOVER Room turnover is the term used to indicate that an OR is being cleaned and prepped for the next case. Room turnovers can be very quick and often require the AT to assist in making sure all disposables that have been used in the last case are discarded. All monitoring cables, screens, and surfaces of the machine and cart need to be cleaned with a hospital-approved disinfectant. Following the appropriate dry time, a new circuit, EKG pads, and suction are placed for the next patient. A leak test should be performed to
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make sure that there are no leaks in the new circuit. The CO2 absorbent should be checked to make sure it is not saturated. Requests for any supplies for the next case should be brought to the room following completion of the room turnover.
■ SUPPLY MANAGEMENT The AT should be involved on a daily basis in making sure adequate supplies are available. This may entail direct ordering or communication of needs to a purchasing department. It is important that there be a process in place that ensures products are continually checked for expiration dates.
■ EQUIPMENT STERILIZATION Nondisposable devices used by anesthesia need to be sterilized between uses. Sterilization means to get rid of any bacteria or virus that may have been exposed to that tool or device. Depending on the product being cleaned, there can be different methods of decontaminating them.
■ SUMMARY This chapter provides an overview of the surgical experience from the perspective of the patient, the anesthesia provider, and the AT. It is intended to introduce what goes on in the pre-op holding area, the OR, and the PACU. In addition, this chapter introduces several routine types of tasks performed in the OR by the anesthesia provider and the AT.
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SECTION
II
Anatomy, Physiology, and Pharmacology
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CHAPTER
4
Pharmacokinetics David Sibell and Ryan Anderson ■ INTRODUCTION The terms pharmacokinetics and pharmacodynamics are often confused or used interchangeably, but they are two distinct concepts. Pharmacodynamics examines how drugs affect the body—induce unconsciousness, relieve pain, increase blood pressure, etc. Pharmacokinetics is the study of how the body affects the drug—the process by which drugs are absorbed, distributed throughout the body, metabolized, and excreted from the body. The practice of anesthesia involves the administration of a large number of drugs that have a significant impact on patients’ physiology and behavior. These effects are influenced not only by dose, route, and timing of administration but also by each patient’s physiology and anatomy, as well as coexisting disease. This chapter introduces some of the more important concepts in pharmacokinetics.
■ ROUTES OF ADMINISTRATION In anesthesia, most drugs are given as intravenous (IV) injections, but they can also be given orally (PO, from Latin per os, or “by mouth”), inhaled into the lungs, or given by other numerous other routes (see Table 4.1). Most drugs are delivered to their sites of action by the bloodstream. Therefore, the initial distribution and onset time of the drug will be determined by how long it takes the drug to get into the bloodstream. This depends on the route of administration. Drugs that are injected intravenously are delivered directly to the bloodstream (intravascular space, central compartment). Inhaled gases are rapidly absorbed into the bloodstream in the alveoli. Sublingual drugs, like nitroglycerin, are absorbed by the oral epithelium and then move quickly into the bloodstream (within seconds). Transdermal and oral routes are much slower. Drug patches must diffuse the drug out of the patch, through the
skin (an excellent barrier to the outside world), through subcutaneous fat and fascial layers, and into the bloodstream, which usually takes hours. The oral route has a unique set of obstacles that must be overcome before a drug can get to its target organs. A tablet of gabapentin must be dissolved by gastric fluid, move to the small intestine where it is absorbed, and then move through the epithelial layers to eventually diffuse into the bloodstream, taking roughly 30-60 minutes. Unlike most other tissues, the venous drainage of the gut does not go directly back to the heart. Instead, it flows into the portal circulation taking nutrients and drugs, which are absorbed from the gut, to the liver where they are processed. One of the main functions of the liver is to detoxify the blood, by chemically altering (metabolizing) foreign substances. Therefore, with oral administration, the liver can remove a portion of drug from the bloodstream before the drug ever makes its way to the systemic circulation and target organs. This is known as first pass clearance. Much of the drug can be lost not only to first pass clearance but also to other factors. Gastric contents are highly acidic and can chemically degrade the drug. Additionally, other compounds in the gut can bind to the drug and prevent its absorption by the small intestine. Absorption can be impaired if the patient’s gut does not work properly or has unusual anatomy. Because of all of these factors, the oral route of administration leads to decreased bioavailability, which is the fraction of drug that is distributed in the systemic circulation relative to the total amount of drug given. This is why IV and PO dosing of medications is usually very different. Some drugs are delivered directly to their sites of action. Local anesthetics are injected subcutaneously to anesthetize the area around the injection site (local infiltration). They can be injected around a large nerve (nerve block) or
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Chapter 4 • Pharmacokinetics
17
TABLE 4.1 ROUTES OF DRUG ADMINISTRATION, THEIR ABBREVIATIONS, AND
EXAMPLES OF COMMON ANESTHETIC MEDICATIONS GIVEN BY EACH ROUTE ROUTE
ABBREVIATION
EXAMPLES OF ANESTHESIA MEDICATIONS
Intravenous
IV
Propofol, esmolol, fentanyl
Oral
PO
Bicitra, gabapentin
Inhaled
Isoflurane, nitrous oxide, albuterol
Subcutaneous
SC/SQ
Lidocainea, insulin
Intramuscular
IM
Ketamine, methylprednisolone
Transdermal
Scopolamine, fentanyl, nitroglycerin
Sublingual
SL
Nitroglycerin
Intraosseous
IO
Epinephrine, atropine (emergency drugs)
Rectal
PR
Acetaminophen
Intrathecala
IT
Bupivicaine, fentanyl
Epidurala
Bupivicaine, fentanyl
Perineurala (nerve block)
Chloroprocaine, bupivicaine
a
Works at the site of delivery.
into the epidural space to anesthetize an entire limb or portion of the torso. They can be injected into the subarachnoid space (intrathecal space), where they will act directly on the nerves that make up the spinal cord. In these situations, the drug remains where it was injected in order to work. It is also important to know that some drugs have multiple uses and multiple sites of action. Lidocaine is a local anesthetic that can be injected for local infiltration or nerve blocks. It is also frequently given intravenously to anesthetize the vein and reduce the pain on injection of induction agents. It can also be given intravenously to treat cardiac arrhythmias or chronic pain. It is always important to know where the drug you are injecting is going. Most catheters, whether leading into a vein or epidural or intrathecal space, have the same Luer-lock mechanism to attach syringes. The vast majority of medications used in anesthesia are given intravenously, but some are intended only for other routes. Giving a drug by the wrong route can have devastating consequences (like seizures, paralysis, and death). Drugs intended for other routes but accidentally given into the central nervous system (either intrathecal or epidural) tend to have the most serious consequences. However, drugs that are given intravenously (when intended for other routes) can also be very harmful. Institutional
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policy will vary as to whether the administration of drugs is in the scope of practice for anesthesia technicians. However, if not directly administering drugs, most anesthesia technicians are at least assisting with the administration of drugs. Great care must be taken to ensure that the right drug as well as the right dose is administered through the right route, even in emergencies. Good communication is essential when more than one person is involved in the administration of a drug. Errors in drug administration are one of the most common preventable errors in health care.
■ DISTRIBUTION As stated earlier, most drugs are delivered to their target organs by the bloodstream. It is important to know what happens to the drug after it is given. For example, general anesthesia is induced with an IV bolus of propofol. As soon as propofol has been injected, it starts mixing with the blood and will go where the blood goes. Peripheral veins drain into larger veins and eventually back to the heart, then lungs, heart again, and then to the systemic circulation. The propofol will soon mix evenly throughout the entire blood volume (30-60 seconds) and will reach a concentration in the blood dependent upon the dose given and the patient’s blood volume. The diluted propofol will start to make its way out of the bloodstream (at the capillary beds) and into
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Section II • Anatomy, Physiology, and Pharmacology
the tissues of the body. This movement is driven by passive diffusion (force that drives molecules from compartments of high concentration to compartments of low concentration). As propofol moves from the bloodstream to the tissues, the concentration in each compartment (blood, fat, extracellular fluid) will gradually equilibrate. Within the systemic circulation, different organs get different fractions of the total blood flow (cardiac output). The organs that get the most blood flow are the brain, kidneys, liver, and heart, which are collectively known as the vesselrich group. Since the vessel-rich group gets most of the blood, it will get most of the propofol (initially). The tissue concentration of propofol in all the organs in the vessel-rich group will reach the concentration of propofol in the bloodstream rapidly. If the propofol concentration in the brain is high enough, it will render the patient unconscious.
■ REDISTRIBUTION The propofol concentrations rapidly equilibrate between the bloodstream (plasma concentration) and the vessel-rich group organs. It’s also equally important to know about the other organs in the body, those that get a smaller fraction of the blood flow. The muscle group gets the next largest fraction of blood flow, followed by the vesselpoor group (tendons, cartilage, and fascia). These tissues will continue to take up propofol as long as their propofol concentration is lower than the plasma level. As they absorb more propofol, the plasma level of propofol goes down, causing it to drop below the level in the vessel-rich group. The propofol in the vessel-rich group now diffuses down the concentration gradient back into the bloodstream, which takes it to the other tissues of the body. This is the concept of redistribution; a drug has an initial distribution to the vessel-rich group but then redistributes to other areas with lower blood flow. Redistribution is responsible for the offset of many short-acting drugs like propofol and thiopental. After an induction dose of propofol, a patient will lose consciousness because propofol above a minimum concentration interferes with the brain’s ability to maintain consciousness. The drug then redistributes, and its concentration in the brain drops below the minimum concentration and the patient will start to regain consciousness (8-10 minutes depending upon the dose of propofol).
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■ ELIMINATION As soon as a drug is given, physiologic processes involving several organ systems will start to remove it from the body through a process known as elimination. Even though the clinical effects of a drug may or may not have ended due to redistribution, the drug will still be present in the body until it has been completely eliminated, which can take hours to days. Some drugs must undergo several steps of chemical processing in order to be inactivated, while others are removed unchanged in the urine and feces. Biotransformation, the process by which drugs are chemically altered, either activates the parent compound (in prodrugs) or transforms active compounds into inactive substances that are excreted. Common locations for drug biotransformation include the liver and bloodstream. As previously discussed with first pass clearance, the liver is responsible for detoxifying the blood. Hepatic metabolism deactivates drugs and removes them from the bloodstream via numerous types of chemical reactions, most of which are categorized as Phase 1 or Phase 2 reactions. Phase 1 reactions alter the parent compound through oxidation/reduction (change in number of electrons), hydrolysis (breakdown by the addition of water), or the addition/removal of small functional groups (e.g., -OH, -COOH, and -NH2). In Phase 2 reactions, functional groups (e.g., glucuronic acid) are attached to the parent compound, thereby facilitating its excretion from the body. The family of enzymes that carries out the majority of hepatic metabolism is known as the cytochrome P450 (CYP) system. The functional level of these enzymes can vary greatly between patients and even within each individual. These differences can be due to genomic polymorphisms or acquired through the use of other medications or chronic exposure to toxins. A classic example is carbamazepine inducing the production of more CYP3A4 enzyme, causing increased metabolism of midazolam. Hepatic metabolism can also be significantly impaired in the setting of liver disease—hepatitis, alcoholic cirrhosis, liver cancer—or drugs or agents that interfere with the cytochrome P450 enzymes. Drugs can also be broken down by plasma cholinesterases (or pseudocholinesterases). Examples include some muscle relaxants (succinylcholine and mivacurium) and the opioid
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Chapter 4 • Pharmacokinetics
remifentanil. These compounds are all esters, which are cleaved at the ester linkage by plasma cholinesterases, rapidly inactivating them. The ubiquity of plasma cholinesterases accounts for the rapid breakdown of these drugs. There are very few acquired medical conditions, other than liver disease, that lead to reduced activity of these enzymes. Plasma cholinesterases are primarily produced in the liver, and alterations in liver function can decrease the amount of cholinesterases produced. In addition to liver disease, there are genetic defects that can cause either an atypical (poorly functioning) enzyme or a deficiency of the enzyme. Either situation may cause unexpectedly prolonged clinical activity of drugs that are metabolized by this class of enzyme. Many drugs and drug metabolites (breakdown products) are removed via renal clearance. The kidneys are constantly filtering the blood to control levels of water, electrolytes, pH, etc. within the body. As drugs are filtered by the kidneys, they end up in the urine and are soon eliminated. Some drugs are excreted unchanged in the urine, such as gabapentin, penicillins, and etomidate. However, this removal process does not work as well for drugs that are not easily filtered (those that are highly protein-bound or carry a strong electrical charge) or those that are reabsorbed by the kidney after filtering. Patients with impaired renal function will have a prolonged elimination phase for medications that are primarily excreted by the kidney, and their doses must be adjusted according to the degree of renal dysfunction.
■ VOLUME OF DISTRIBUTION Every drug has a unique set of chemical properties. They can carry a positive or negative charge or be electrochemically neutral. They can have regions with large polar functional groups, which make them dissolve easily in water (hydrophilic, “water loving”). They can have regions with large nonpolar groups, which make them repelled from water (hydrophobic, “water hating”) and more apt to dissolve in fat tissue (lipophilic). Some are bound up avidly by plasma proteins. These are the characteristics that determine how quickly a drug will start to work, how long it will work, and where the drug gets deposited until it is broken down and eliminated. Hydrophilic drugs tend to stay in the bloodstream, while hydrophobic drugs deposit themselves happily in fat tissue. Propofol is hydrophobic, which
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makes it able to cross membranes quickly (fast onset) and get deposited in fat tissue. The volume of distribution of a drug is the apparent volume into which a drug gets distributed. This is not an actual physical volume but rather one that is conceptual; it is calculated by the following equation: Vd = dose of drug given/initial drug plasma concentration Vd is the volume of distribution. This volume can be very small or several times the total volume of the patient (sufentanil’s is 195 L, while the total body volume of an adult male is about 70 L). For example, if a 1-mg dose of a drug were dissolved in a vat of blood, and the measured concentration of the drug was 0.5 mg/L, you could calculate that there must have been 2 L of blood in the vat. The 2 L is the volume of distribution. The experiment is repeated with the same vat of blood and a different drug; 1 mg of the new drug is mixed into the vat, and the concentration of this drug is measured. In this case, most of the drug sticks to the sides of the vat and very little is left in the blood. The measured concentration is 0.1 mg/L. The calculated volume of blood or volume of distribution would be 10 L (if 1 mg of drug were dissolved in 10 L, the concentration would be 0.1 mg/L). Of course, the vat does not contain 10 L of blood, only 2 L. The calculated volume of distribution is larger due to the sequestration of the drug on the walls of the vat. A similar phenomenon is what happens with sufentanil and many other lipophilic drugs. These drugs are highly sequestered into fat, leaving only a small amount in the bloodstream, which inflates the calculated volume of distribution.
■ HALF-LIFE The concentration of a drug in the body over a given time can be described through mathematical modeling. Most drugs follow first-order kinetics, which means that a constant fraction of drug is eliminated over a given time period (e.g., half of the drug is removed every 2 hours). Some drugs (e.g., ethanol, aspirin) follow zero-order kinetics, which means a constant amount of drug is eliminated over a given time period. So, stated another way, with first-order kinetics, the time that it takes the body to remove 50% of a drug is that drug’s half-life. For example, a patient is given 100 mg of a drug that has a 2-hour half-life.
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Section II • Anatomy, Physiology, and Pharmacology
After 2 hours, only 50 mg will remain. Over the next 2 hours, the body will remove another half of what remains (25 mg), so after 4 hours, there is still 25 mg in the patient. After another 2 hours (three half-lives total), the remaining level drops to 12.5 mg. Mathematical formulas can be used to predict the amount of drug present at any time point following a dose. From these, we can establish dosing schedules to reduce the risk of reaching toxic levels of drugs in those patients with decreased ability to eliminate drugs.
■ STEADY-STATE CONCENTRATION If anesthesia providers want to maintain a steady concentration of a drug within a patient, there are different ways to achieve this. One way is to give a loading dose (initial dose of drug), which will reach a certain concentration in the blood (based on the dose and volume of distribution). The drug concentration will drop from elimination and redistribution. Additional doses of the drug can be given periodically to maintain the concentration of the drug at therapeutic levels. If we know how much drug is eliminated (e.g., 50 mg over a period of 30 minutes), then we can maintain a steady-state concentration, or constant level of drug in the bloodstream, by giving an additional 50-mg dose of the drug every 30 minutes. These doses are known as maintenance doses because they maintain the level of a drug in a desired concentration range. By knowing the volume of distribution and the half-life of a drug, we can calculate a loading dose, maintenance dose(s), and frequency of redosing in order to achieve and maintain a drug in a specific concentration range. While this strategy of drug dosing is frequently used, such calculations are not typically performed in clinical practice; it is described here to demonstrate these concepts. Another way to achieve a steady drug concentration in the blood is to administer a drug as a constant infusion. Typically, drug effects are initially achieved with a loading dose given as a bolus, and then the drug effect is maintained with an infusion. For example, general anesthesia can be induced with a bolus dose of propofol, and it can be maintained with infusion of propofol at a constant rate of administration. The benefit of the infusion is that it avoids the peaks and troughs of drug concentrations that come with repeat bolus dosing; peak drug levels can lead to pronounced side effects and toxic reactions,
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while trough drug levels can lead to inadequate drug effects, like light anesthesia. Ideally, the drug is infused at a rate that is equal to the rate of elimination. Remember, though, that shortacting lipophilic drugs redistribute from the vessel-rich group to other tissues much faster than they are eliminated from the body. So, infusion of propofol to maintain a constant plasma concentration is really just adding drug at the rate at which it redistributes to other tissues. If we were to continue a propofol infusion for several hours at the same rate, we would start to saturate the peripheral tissues. As more drug is redistributed over a long period of time, the level of drug in peripheral tissues will continue to rise until it is equal to the level in the bloodstream, at which time redistribution no longer occurs. Now, any additional drug that is administered will remain in the bloodstream and vessel-rich group until it is eliminated from the body (which takes much longer than the process of redistribution). If the infusion rate is not adjusted, the concentration of propofol in the bloodstream would begin to rise. When the infusion is stopped, the kidneys and liver remove drug from the central compartment (bloodstream), but more drug will continue to seep out of the peripheral tissues into the central compartment. The plasma concentration (and brain concentration) decreases very slowly. This demonstrates the concept of context-sensitive half-life, which describes how the half-life of a drug is proportional to the duration over which the drug has been administered.
■ CLEARANCE Clearance refers to the amount of a substance removed from the circulation, either by metabolism or by excretion, over a certain period of time. Drugs can be excreted with their chemical structures intact. Drugs can be filtered by the kidney and excreted in the urine, or they can leave the body in other fluids: tears, sweat, breast milk, etc. This is how some medications can be transferred from breast-feeding mothers to their babies, sometimes with harmful effects. Some drugs, like inhaled anesthetics, are eliminated by exhalation, again having undergone very little chemical degradation. Other drugs undergo metabolism as discussed above. The metabolites can then be eliminated by the kidney. All of these mechanisms of elimination lead to clearance of the drug from the circulation.
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Chapter 4 • Pharmacokinetics
REVIEW QUESTIONS 1. How would drug onset and duration of action be affected in a patient with heart failure (low cardiac output)? A) Speed drug onset B) Increase metabolism of the drug C) Shorten the duration of action D) Slow the onset E) Both A and C Answer: D. A patient with a reduced cardiac output, as in heart failure, will circulate the blood more slowly to the target organs, resulting in a delay in onset of action. The duration of action is usually, but not always, prolonged due to reduced blood flow to the liver (reduced metabolism) and kidneys (reduced elimination).
2. What process is responsible for the offset of effects of a bolus of propofol? A) First pass effect B) Redistribution C) P450 enzyme reduction D) Increased renal blood flow E) None of the above Answer: B. Redistribution. The bolus of propofol is mixed and distributed rapidly to the central compartment and to the vessel-rich group. Subsequently, the plasma level falls as the propofol is redistributed to muscles and the vessel-poor group.
3. Dysfunction of what organ systems will increase the elimination half-life of many anesthetic drugs? A) Liver B) Kidney C) Heart D) All of the above E) None of the above Answer: D. All of the above. Many drugs are metabolized in the liver, while many others are excreted unchanged by the kidneys. Any condition that reduces blood flow to the liver or kidneys can reduce the amount of drug that is cleared, which will cause an increase in the half-life of the drug.
4. Which of the following statements is FALSE? A) Oral administration of drugs may be subject to the first pass effect. B) IV administration is the route with the fastest onset of drug effects. C) Inhaled drugs cannot be absorbed into the bloodstream. D) Certain drugs may only be administered by certain routes. E) Appropriate drug dose may differ depending upon the route of administration.
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Answer: C. Inhaled drugs cannot be absorbed into the bloodstream. This statement is false. Many drugs including the inhaled anesthetics, nitric oxide, and lidocaine are all taken up into the bloodstream after inhaled administration. Orally administered drugs are absorbed by the gut and taken up into the bloodstream. From there, the blood passes through the portal circulation in the liver before mixing with the systemic circulation. As the blood passes through the liver, it has the opportunity to metabolize the drug. Drugs given intravenously have the fastest onset because drugs are delivered to their target organs by the bloodstream, so the rate of onset is largely determined by how long it takes for a drug to get to the bloodstream. A critical safety concern is making sure the right drug in the right dose is given by the right route. Some drugs are toxic if given by one route but not another. Other drugs have 100-fold different doses depending upon the route of administration.
5. Half-life is defined as A) Half way to the expiration date for a drug B) The time it takes the body to eliminate 50% of a drug C) The dose of drug that is effective in 50% of patients D) One half the volume of distribution E) None of the above Answer: B. Drugs are gradually eliminated from the body. Some are eliminated at a constant rate (xxx amount of drug per hour— zero-order kinetics). With the vast majority of drugs, the amount of drug eliminated is dependent upon the concentration of the drug—a fixed percentage of the drug, not a fixed amount, is eliminated each hour—first-order kinetics. The half-life is the amount of time it takes for 50% of the drug to be eliminated.
REFERENCES Davis L, Britten JJ, Morgan M. Cholinesterase: its significance in anaesthetic practice. Anaesthesia. 1997;52:244-260. Egan TD, Lemmens HJ, Fiset P, et al. The pharmacokinetics of the new short-acting opioid remifentanil (GI87084B) in healthy adult male volunteers. Anesthesiology. 1993;79(5):881-892. Evers AS, Crowder CM, Balser JR. General anesthetics. In: Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 11th ed. [online] 2006. Jackson, WY: Teton Data Systems; 2010. Available from.Accessed April 6, 2011. http://accessmedicine.com/content.aspx?aid=16664636 Gonzalez FJ, Tukey RH. Drug metabolism. In: Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 11th ed. [online] 2006. Jackson, WY: Teton Data Systems; 2010. Available from. Accessed April 6, 2011. http://accessmedicine.com/content.aspx?aid=16659426 Zhang L, Reynolds KS, Zhao P, et al. Drug interactions evaluation: an integrated part of risk assessment of therapeutics. Toxicol Appl Pharmacol. 2010; 243(2):134-145
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CHAPTER
5
Pharmacodynamics Pamela Kirwin
P
harmacodynamics is the relationship between the plasma drug concentration and the pharmacologic effect of the drug on the body, or more simply put, pharmacodynamics is the study of what drugs do to the body. Pharmacodynamics can be divided into three general areas: • The transduction of biologic signals: how drugs act at a cellular level to affect what is happening within the cell. A major component in understanding transduction is understanding how cellular receptors work. • Molecular pharmacology: the molecular properties of drugs and how they interact with organisms at a molecular level. • Clinical pharmacology: the clinical effects drugs have on an organism or organ system.
■ TRANSDUCTION AND RECEPTORS Receptors are external components of cells (in the cell membrane) that interact with compounds such as drugs or biochemical signals to start an intracellular cascade of reactions. There are three main components of the receptor theory. These include the quantitative actions of drug binding and the resulting effect, the selectivity of drugs and their ability to activate the cell, and the pharmacologic activity of those drugs at the receptor. The ability of drugs to bind to receptors is critical to their action. The specific receptor is an important determinant of what intracellular cascade gets triggered. Drugs that have similar biochemical structures often adhere to the same receptor. When a drug interacts or binds to a receptor, there is a quantitative relationship between the dose of the drug and the resulting effect of the intracellular cascade it sets off. In addition to the quantity of drug binding to receptors, drugs may bind with variable strength to a receptor. The biologic activity of a drug that strongly binds may be different than the activity of a drug that weakly binds. Drugs are sometimes
developed to bind selectively to certain subsets of receptors in order to either enhance drug effect or avoid drug side effects. A drug that binds to a receptor to initiate a cellular process is called an “agonist.” It is important to be aware that not all drugs bind to receptors to activate a process. Some drugs bind to receptors in order to inhibit a process from happening within the cell. These drugs are called “antagonists.” A cornerstone to receptor theory emerged from the work of Paul Erhlich. Erhlich studied the activity of curare on parts of the central nervous system and developed the concept that “agents cannot act unless they are bound.” This is the foundation on which the receptor theory was built. Classical receptor theory is best described through the mathematical relationship shown in Figure 5.1. In this equation, L is the ligand (the agent binding to the receptor), R is the receptor, Kon is the speed at which the ligand binds to the receptor, Koff is the speed at which the ligand is released from the receptor. The speed at which drugs bind and are released from receptors greatly impacts their effect on the receptor and the cell. This equation can be rearranged to form an equation that describes the relationship between the speed at which binding and release from the receptor takes place. This is called “Kd,” the dissociation constant (Fig. 5.2). From the dissociation constant, you can extrapolate the activity of the molecule and how it binds to a receptor. A low Kd means that the speed at which the drug binds to the receptor is much greater than the speed at which it is released from the receptor; therefore, not many molecules of the drug are required to occupy the majority of the target receptors. A low Kd indicates the drug tightly binds to the receptor. A higher Kd means that more molecules of a drug are required to occupy the majority of the receptors. Therefore, the drug is weakly bound to the
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Chapter 5 • Pharmacodynamics
■ FIGURE 5.1 Equilibrium for a ligand L binding to a receptor R.
receptor and falls off quickly. To have an equivalent activity to a drug with a high Kd, a drug with a low Kd would require many more drug molecules to keep attempting to bind to the receptor to make up for the weak binding. A great deal can be learned about a drug by measuring the amount of drug necessary to produce an effect on a cellular process. For example, how much drug is necessary to add to a group of cells in a test tube to get them to produce a certain quantity of hormone? How is receptor binding measured in actual humans? This is often accomplished by measuring an indirect action (secondary endpoint) as a result of receptor binding. A secondary endpoint is used to derive information about the way molecules bind to receptors. For example, to measure how a blood pressure medicine binds to a receptor and then compare it to another blood pressure medicine, which targets the same receptor, you might measure the percent and duration of a change in blood pressure not the actual binding of the molecule to the receptor. Measurement of drug activity at a receptor in actual humans can be very complicated. It may be difficult to find or measure secondary endpoints, the drug may require metabolism or shifting into other compartments of the body in order to finally bind to its receptor, or there may be physiologic delay in the actual effect.
Receptor Agonists and Antagonists Drugs are agonists of receptors if they attach to a receptor and create an effect. The effect may be excitatory or inhibitory on a process within the cell. In other words, an agonist may cause an effect that is inhibitory and still be considered an
■ FIGURE 5.2 Calculation of the Kd dissociation constant.
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“agonist” of that effect. Agonists of receptors fall into two common categories: partial agonists and full agonists. A drug that is highly effective at activating a receptor is called a full agonist. Any drug that activates the same receptor but has a significantly less effect on activating the receptor is considered a partial agonist. Buprenorphine is a partial opioid agonist that only partially activates the euphoria associated with opioids. Some believe partial agonists do not bind strongly to the receptor and this may be why their effect is more weakly produced. In addition, the partial agonist may be incompletely bound to the receptor or is unable to maintain the receptor’s activated shape after it is bound. Even at increasingly higher doses, partial agonists cannot fully activate a receptor. Antagonists bind to a receptor and prevent the receptor from causing a process to occur. Some antagonists bind irreversibly to the receptor, and in some cases this can be for the life of the cell. Others bind and release from the receptor (see disassociation constants above) and are called competitive antagonists. Competitive antagonists inhibit either endogenous molecules or other drug molecules from binding to the target receptor. Because there is a competition between agonists and antagonists for binding to the receptor, the competitive antagonists can be overwhelmed by giving higher and higher doses of an agonist. Noncompetitive antagonists, those that bind irreversibly to the receptor, cannot be overwhelmed by increasing the amount of agonist. An example of a noncompetitive antagonist is aspirin, which fully antagonizes the blood clotting function of the platelets after it binds to the cyclooxygenase receptor. Once aspirin binds to the platelet cyclooxygenase receptor, it is irreversible. This is why aspirin is usually withheld for 5 to 7 days prior to surgery. The body needs 5 to 7 days to generate new platelets that have not been exposed to aspirin and can help the patient clot during surgery. The use of competitive antagonists can be found in the administration of anesthesia. One example is nondepolarizing muscle relaxants (e.g., rocuronium, cis-atracurium, and vecuronium). These drugs are frequently used in the operating room to create muscle paralysis. Muscle paralysis may be necessary to intubate a patient or to create relaxed muscles that will make it easier for the surgeon to perform surgery.
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Section II • Anatomy, Physiology, and Pharmacology
These muscle relaxants are competitive antagonists that compete with acetylcholine for the nicotinic receptor on muscle cells. This concept is more fully discussed in Chapter 16. αq/11 β GDP
αq/11
γ
Inactive state
Active state
A
Agonist (histamine)
αq/11 β GDP
Receptor States
GTP
Histamine
αq/11
γ
GTP
Inactive state
Active state
B H1-antihistamine Inverse agonist (H1-antihistamines)
αq/11 β GDP
Most receptors remain in the inactivated state and spontaneously cycle through to the activated conformation (shape); however, the receptor is only in the activated form for the minority of its time. Therefore, only a small percentage of a type of receptor is usually in its activated state. This percentage represents the receptors’ baseline state of activation. When a ligand binds to a receptor, the receptor is stabilized in the active state. In the activated state, receptors will interact with intermediate proteins within the cell wall and the cell, thus initiating the response cascade within the cell. Many classic antagonists are now considered to be inverse agonists. An inverse agonist is thought to bind to the receptor and stabilize the inactivated state of the receptor. This reduces the number of receptors in the activated state, which brings the activity of the receptor below its usual baseline (see Fig. 5.3).
αq/11
γ
Receptor Structure
GTP
Inactive state
Active state
C ■ FIGURE 5.3 Stabilization of a receptor in its inactivated state by an antagonist. (With permission: Figure 42-3: Adapted with permission from Leurs R, Church MK, Taglialatela M. H1-antihistamines: inverse agonism, antiinflammatory actions and cardiac effects. Clin Exp All. 2002;32:489–498, Figure 1.)
α
β
There are four types of receptor channels that are important in anesthesia. These include membrane receptor (G-protein coupled), ligand-gated ion channel, voltage-sensitive ion channel, and enzyme receptors (see Fig. 5.4). Membrane receptors on cell membranes are typically structured with a water-loving (hydrophilic) portion of the receptor, which is outside
γ
GDP
A
B
C
D
■ FIGURE 5.4 Four different types of drug receptors. (From Golan DE, Tashjian AH, Armstrong EJ. Principles of pharmacology. The Pathophysiologic Basis of Drug Therapy. 2nd ed. Baltimore, MD: Wolters Kluwer Health, 2008, with permission.)
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Chapter 5 • Pharmacodynamics
of the cell membrane. The external hydrophilic portion is able to bind water-soluble ligands. These ligands would otherwise be unable to cross into the cell that has a lipid interior. In the cell, just like in your kitchen, oil (lipid or hydrophobic molecules) and water (ionized or hydrophilic molecules) do not mix. Therefore, ligands that are water loving or hydrophilic cannot cross into the lipid portion of the cell membrane. To cross the membrane without any help, the molecule must be able to dissolve in fat (lipophilic). The receptor serves as the messenger system across the lipophilic cell membrane and allows the ligands to send its message without entering the cell itself. Some membrane receptors couple with G proteins to create their message within the cell. The most common version of the G-protein–coupled receptor is the cyclic adenosine 3’5’–monophosphate system “cAMP.” In this chain reaction, the ligand binds to a receptor that causes G proteins to activate the enzyme responsible for synthesizing cAMP. Many drugs are coupled to this enzyme system including betaagonists like epinephrine. The ligand-gated ion channel opens an ion channel when the ligand binds to the receptor. The opening of the channel will cause ions (molecules with a positive or negative charge) to flow into or out of the cell. The ions flowing into the cell can cause a process to occur within the cell or at the cell membrane. γ-Aminobutyric acid is a ligand-gated ion channel and it is the location of action of most hypnotic drugs such as benzodiazepines, barbiturates, propofol, and etomidate. Another method of cellular messaging is when a change in the electrical potential across a cell membrane changes and is propagated along the length of the cell. The electrical potential across a cell membrane is determined by the concentration of charged ions on either side of the membrane. When a ligand-gated channel opens, the concentration of ions across the cell membrane changes, which changes the membrane potential. This change in membrane potential can cause a change in conformation of a nearby voltagesensitive channel and allow the transit of molecules across the channel. In some cases, these are ions that can cause further membrane potential changes and so on. The end result is the membrane potential change (depolarization) is propagated along the cell membrane for the length of the cell. One example of this type of cellular
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messaging is a nerve cell. Eventually the cell must restore the ion concentrations across the cell membrane (repolarization) in order to reset the voltage-dependent channels, and be prepared to send another message. Local anesthetics target voltage-gated receptors. These agents often work by binding to a receptor on voltage-gated sodium channels. Once bound to the receptor, the conformation of the channel changes and allows sodium to pass through the channel. Because the conformational change is slow to reverse, the cell cannot reset and repolarization is slow to occur, thus inhibiting further cellular signal transmission. The ion pump is another type of receptor, one example of which is the adenosine triphosphatase (ATPase) ion pump. This pump serves as a motor, which pumps sodium out of the cell in exchange for potassium moving into the cell. This pump requires adenosine triphosphate (ATP) to bind to a receptor on the inside of the cell to activate the pump.
■ PHARMACODYNAMICS AND CLINICAL PHARMACOLOGY Pharmacodynamics also looks at what happens after a drug has attached to its receptor and created a conformational change and the ensuing cellular response. What is the final effect that we see on the human body?
Dose-response Curves A dose-response curve looks at the concentration of drug versus the response in the individual. This relationship is based on dose and concentration but does not take into account the time course of the response. This effect is described through the “Hill” equation (see Fig. 5.5).
Potency and Efficacy Potency describes the dose versus response relationship. This is typically described best as a concentration versus response relationship. Efficacy is a measure of the ability of the drug to produce a physiologic effect (see below). If two drugs create the magnitude effect, the drug that creates that effect at a lower dose is more potent. Effective Dose and Lethal Dose Effective dose or ED 50 is the dose of a drug required to produce a specific effect in 50% of patients to whom it is administered. The LD 50 is the dose of a drug that would be expected to be lethal in 50% of patients to whom that dose is
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drug binding to receptors. Receptors mediate the action between the drug (or ligand) and the cellular cascade of events within the cell that are ultimately responsible for the drugs action at a cellular level. Drug action at a receptor can be as an agonist or antagonist. The relationship between how quickly a drug binds and releases from a receptor can be described by the disassociation constant. The potency and efficacy of a drug can be described by the ED 50, LD 50, and the therapeutic index.
A Linear 1.0 Drug A Drug B E
EMAX
0.5
0 EC50(A) EC50(B)
[L]
B Semilogarithmic 1.0
REVIEW QUESTIONS
Drug A Drug B E
EMAX
0.5
0 EC50(A) EC50(B) [L]
■ FIGURE 5.5 Hill equation for describing a dose-response curve. (From Golan DE, Tashjian AH, Armstrong EJ. Principles of pharmacology. The Pathophysiologic Basis of Drug Therapy. 2nd ed. Baltimore, MD: Wolters Kluwer Health, 2008, with permission.)
administered. The therapeutic index is the ratio of the LD 50 to the ED 50. The larger the therapeutic index of a drug, the safer it is for administration. Opioid-tolerant patients have a small therapeutic index or therapeutic window of administration. In the post anesthesia care unit (PACU), opioid-tolerant patients require higher doses of opioids than other patients. The opioid-tolerant patient can be sedated and difficult to arouse in the PACU, and as a consequence, when woken from sleep, they will describe intense pain. If they receive more opioids to treat their pain, they may be dangerously sedated and still not achieve proper pain control. These patients have a small therapeutic index and the risk may exceed the benefit of the medication.
■ SUMMARY Pharmacodynamics is the study of what drugs do to the body. Central to the understanding of how drugs work in the body is to understand
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1. What is pharmacodynamics? A) The effect of the drug on the body B) Drugs acting on a cell C) Drugs acting on a molecular level D) Drugs effect on an organ system E) All of the above Answer: E. All of the above. Pharmacodynamics is the result of the drug’s effects on the body that include actions on systems, cells, and molecules. Pharmacokinetics describe what the body does to the drug.
2. Receptors site are _____ and cell membranes are _____? A) Hydrophilic and hydrophobic B) Hydrophilic and hydrophilic C) Hydrophobic and lipophilic D) Lipophilic and lipophilic Answer: A. Hydrophilic and hydrophobic. Cell membranes are made of lipid and are hydrophobic (repels charged molecules or water). They are also lipophilic (accommodate fat-soluble molecules, those that are not charged). Receptors can attach to ionized molecules and send a message through the cell membrane to effect change within the cell.
3. Aspirin is a _____ of platelet clotting function. A) Competitive agonist B) Competitive antagonist C) Noncompetitive agonist D) Noncompetitive antagonist Answer: D. Aspirin is a noncompetitive antagonist of platelet function. It attaches to platelets irreversibly; in other words, aspirin cannot be removed from its receptor on the platelet with another competitor ligand. Competitive antagonists compete for binding to the receptor with other molecules. The concentration of the molecules and the Kd of the molecules determine which competitor binds more receptors.
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Chapter 5 • Pharmacodynamics
REFERENCES 1. Booij LH. Neuromuscular transmission and its pharmacological blockade. Part 2. Pharm World Sci. 1997; 19(1):13–34. 2. Eger EI, Saidman LJ, Brandstater B. Minimum alveolar anesthetic concentration: a standard of anesthetic potency. Anesthesiology. 1965;26:756–763. 3. Ghanouni P, Steenhuls JJ, Farrens DL, et al. Agonistinduced conformational changes in the G-proteincoupling domain of the beta 2 adrenergic receptor. Proc Nal Acad Sci USA. 2001;98:5997–6002. 4. Hall, R. Mazer, DC. Antiplatelet drugs: A review of their pharmacology and management in the perioperative period. Anesth Analg. 2011;112(2):292–318. 5. Hudson R. Basic principles of clinical pharmacology. In: Barash PG, Cullen BF, Stoetling RK, eds. Clinical Anesthesia. Philadelphia, PA: Lippincott Williams & Wilkins; 1997:253–260. 6. Lai J, Hunter JC, Porreca F. The role of voltage-gated sodium channels in neuropathic pain. Curr Opin Neurobiol. 2003;13:291–297. 7. Pasternak GW. When it comes to opiates, just say NO. J Clinl Invest. 2007;117(11):3185–3187.
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8. Mason RP, Giles T, Sowers J. Evolving mechanisms of actions of beta blockers: focus on Nebivolol. J Cardiovasc Pharmacol. 2009;54(2):123–128. 9. Rolley E, Fudala P. Bruprenorphine: considerations for pain management. J Pain Symptom Manage. 2005;29(3): 297–326. 10. Sadean MR, Glass PSA. Pharmacokinetic– pharmacodynamic modeling in anesthesia, intensive care and pain medicine. Curr Opin Anaesthesiol. 2009; 22:463–468. 11. Shafer SL, Flood P, Schwinn D. Basic principles of pharmacology. In: Miller RD, et al., eds. Anesthesia. 6th ed. New York, NY: Churchill Livingstone; 2005: 495–507. 12. Skrabanja ATP, Bouman EAC, Dagnelie PC. Potential value of adenosine 5’-triphosphate (ATP) and adenosine in anesthesia and intensive care medicine. Br J Anaesth. 2005;94(5):556–562. 13. Swaminath G, Deupi X, Lee TW, et al. Probing the beta adrenoreceptor binding site with catechol reveals differences in binding and activation by agonist and partial agonists. J Biol Chem. 2005;280:22165–22171.
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CHAPTER
6
Efficacy, Toxicity, and Drug Interactions Amy Opilla and Kim Mauer ■ EFFICACY As introduced in the previous section, efficacy is the maximal effect produced by a drug. It is related to the ability of a drug to bind with the appropriate receptors to cause a desired effect. It is affected by the route of administration, volume of distribution, and clearance of the drug from the body. Therefore, efficacy of a particular drug can vary among patients depending on drug pharmacokinetics, pharmacodynamics, or both with respect to the individual patient. As the concentration of a drug increases, its effect also increases. However, there is a point when increased drug concentration does not produce any additional effect, which is defined as maximal efficacy. From this dose-response relationship, the value of ED 50 is derived (as stated in Chapter 5, this is the dose at which 50% of patients exhibit the desired effect of the drug). The dose-response relationship is also used to define the lethal dose of medications (again, as stated earlier, LD 50 is the dose that will cause mortality in 50% of the population). This is derived experimentally in rats or mice.
■ ADVERSE EFFECTS The desired effect of a drug is the effect that treats the patient’s symptoms or disease. In addition to the desired effects, drugs also can produce unwanted effects. When these unwanted effects are mild, they are called side effects and can include a myriad of symptoms such as dry mouth, headache, or nausea. However, these side effects also have the potential to be harmful or toxic and these are known as adverse effects. These adverse effects can be pharmacologic or dose related, meaning that giving an overdose of medication leads to toxic effects. Drugs with a narrow therapeutic index (ratio of LD 50 to
ED 50) are more likely to cause adverse effects due to overdose. For example, in anesthesiology, opioid medications (e.g., fentanyl and morphine) are commonly used to treat pain in the perioperative period. Opioids have a dose-related adverse effect of respiratory depression. Therefore, if too high a dose is given to a particular patient, the patient’s respiratory rate will decrease and he or she may stop breathing. Adverse effects are also related to lack of selectivity of drugs for the desired target. The target may be one organ or system, but the drug has the ability to interact with receptors all over the body, which may produce adverse effects in other organs. One example of this would be β antagonists, which is a drug commonly used in anesthesiology to treat tachycardia and hypertension. β receptors are located all over the body, and blocking all of these receptors may have adverse effects in other systems, such as triggering bronchospasm in patients with reactive airway disease. Adverse effects can also occur as a result of the metabolism of the drug. If drug breakdown produces a toxic metabolite, this can lead to adverse effects. In an acetaminophen overdose, enzymatic pathways are saturated, and a reactive toxic metabolite is formed, leading to liver injury. Allergic reactions to drugs are another form of adverse effect, the most severe being anaphylaxis, which is an immediate hypersensitivity reaction. In an anaphylactic reaction, the drug antigen activates the patient’s immune system, causing mast cells to release histamine via an IgE-mediated response. This leads to edema, vasodilation, hypotension, and shock. When the causes of adverse effects of a drug are not dose related or are unclear, they are called
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Chapter 6 • Efficacy, Toxicity, and Drug Interactions
idiosyncratic reactions and may be due to individual patient characteristics such as metabolism, receptor-drug interaction, immunologic factors, or a combination of multiple factors. Many common drugs in anesthesiology can lead to pathologic toxicity in different organ systems. Therefore, when administering a drug, the dose for each particular patient must be carefully calculated and the risk to benefit ratio must always be considered. In other words, does the benefit of the desired effect of this drug outweigh the risk of adverse effects for this particular patient?
■ DRUG INTERACTIONS The concept of drug interactions is very important in anesthesiology; a standard general anesthetic can include as many as 10 different drugs. Drug interactions can be due to a number of factors, such as pharmaceutical, pharmacokinetic, pharmacodynamic, or a combination thereof. Pharmaceutical drug interactions occur prior to the drug being administered or absorbed, such as the formation of a precipitate when mixing drugs in the same syringe. Pharmacokinetic factors of drug interactions include absorption, distribution, metabolism, and elimination. Absorption may be altered due to the effect of a drug on the body, such as in the gastrointestinal system, where certain drugs can alter the gastric pH or gastric motility, causing differences in absorption of other drugs administered by mouth. Another example of altered absorption is when anesthesiologists use local anesthetics combined with epinephrine. The epinephrine causes vasoconstriction, which helps to decrease absorption and prolong the effect of the local anesthetic. Distribution can be altered by competition at plasma protein binding sites or displacement from or alteration of tissue-binding sites. Metabolism of one drug can be altered by another drug administered concurrently. Drugs may induce or inhibit enzymes that break down drugs, such as cytochrome P450, causing an increase or decrease in efficacy. Pharmacodynamic factors of drug interactions include addition, synergism, or antagonism. Drugs that act on the same receptors are additive, whereas drugs that bind with different receptors but have the same effect are synergistic. Both of these types of drug interactions lead to an increase in the desired effect. Drugs that cause opposing effects are antagonists and may
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cause a reduced response of one drug or both when administered together. Anesthesiologists often utilize pharmacodynamic properties of drug interactions during administration of general anesthesia. For example, a volatile anesthetic, benzodiazepine, propofol, and an opioid can be combined to produce central nervous system (CNS) depression due to their additive and synergistic properties. Also, the reversal of neuromuscular blockade is an example of utilizing antagonistic drug interactions. Adverse effects of drugs can also be additive, such as both acetaminophen and alcohol can cause hepatoxicity, and this negative effect is greatly increased when both drugs are administered together. In addition to drug-drug interactions, herbal supplements can also interact with drugs to cause adverse effects. Herbal supplements, often identified as nutraceuticals, are consumed by a significant proportion of patients scheduled for surgical procedures. This is largely due to the use of herbal supplements in the United States, which has increased dramatically in recent years. The Food and Drug Administration (FDA) does not regulate these products with the same scrutiny as conventional drugs. This is concerning as some of these agents have the potential to cause serious drug interactions and hemodynamic instability during surgery. Thus, it is extremely important to identify patients self-administering these medications. Ginkgo, garlic, ginger, and ginseng increase the risk of bleeding when taken independently, and a provider should be aware of these substances before anesthetizing patients. Acetaminophen, when added to ginkgo, garlic, ginger and ginseng, further increases the risk of bleeding. The hepatotoxic herbs, echinacea and kava, become more hepatotoxic in combination with acetaminophen. Nephrotoxicity becomes a concern when acetaminophen is combined with herbs containing salicylate (willow and meadowsweet). The concomitant use of opioid analgesics with the sedative herbal supplements, valerian, kava, and chamomile, may lead to increased CNS depression. The analgesic effect of opioids may also be inhibited by ginseng. Aspirin interacts with the herbal supplements that are known to possess antiplatelet activity (ginkgo, garlic, ginger, bilberry, dong quai, feverfew, ginseng, turmeric, horse chestnut, fenugreek, and red clover) and with tamarind, enhancing the risk of bleeding.
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Herbals known to increase blood pressure include goldenseal, licorice, ephedra (Ma-Juang), and St. John’s wort. Kava kava may prolong the effect of certain anesthetics and increases the risk of suicide for people with certain types of depression.
■ SUMMARY The administration of anesthesia involves multiple drugs with multiple routes of administration. This chapter introduces the concepts of efficacy and toxicity, adverse reactions, and drug interactions. Anesthesia technicians will be more familiar with the perioperative environment if they have a basic understanding of the principals of pharmacology.
3. Which of the following is the correct definition of ED 50? A) The ratio of effective dose to lethal dose in 50% of the population B) The ratio of IV to oral medication that produces equivalent effect in 50% of the population C) The dose that causes mortality in 50% of the population D) The dose that produces the desired effect in 50% of the population E) The dose that produces adverse effect in 50% of the population Answer: D. This is the definition of ED 50.
SUGGESTED READINGS
REVIEW QUESTIONS 1. Which of the following can cause adverse drug reactions? A) Overdose B) Metabolites C) Allergy D) All of the above E) None of the above Answer: D. Adverse reactions can be dose related, and the more narrow the therapeutic window, the more likely that adverse reactions due to overdose will occur. Breakdown of drugs can form toxic metabolites, which may lead to adverse effects. Allergic reactions are a form of adverse reaction to a drug, the most severe being anaphylaxis.
2. Which of the following statements about drug interactions is TRUE? A) Drugs that act on the same receptors and cause the same response are antagonists. B) When two drugs mixed together form a precipitate, a pharmacokinetic reaction has occurred. C) Anesthesiologists commonly utilize drug interactions to their advantage in standard general anesthetics. D) Herbal supplements are natural and do not interact with drugs administered by anesthesiologists.
Gonzalez FJ, Coughtrie M, Tukey RH. Drug metabolism. In: Brunton LL, Chabner BA, Knollmann BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill; 2010. Gupta D, Henthorn T. Pharmacologic principles. In: Barash PG, Cullen BF, Stoelting RK, et al., eds. Clinical Anesthesia. 6th ed. Philadelphia: Lippincott, Williams & Wilkins; 2009:137–164. Munir Pirmohamed M, Breckenridge AM, Kitteringham NR, et al. Fortnightly review: adverse drug reactions. BMJ. 1998;316:1295–1298. Osterhoudt Kevin C, Penning Trevor M. Drug toxicity and poisoning. In: Brunton LL, Chabner BA, Knollmann BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill; 2010. Roscow RE, Levine WC. Drug interactions. In: Barash PG, Cullen BF, Stoelting RK, et al., eds. Clinical Anesthesia. 6th ed. Philadelphia: Lippincott, Williams & Wilkins; 2009:549–566. von Zastrow Mark, Bourne Henry R. Drug receptors & pharmacodynamics. In: Katzung BG, ed. Basic & Clinical Pharmacology.11th ed. Available from: http:// www.accessmedicine.com.liboff.ohsu.edu/content. aspx?aID=4509384.gff
Answer: C. Anesthesiologists commonly utilize drug interactions to their advantage in standard general anesthetics. This statement is true. For example, the drug interaction that occurs when intravenous (IV) and volatile anesthetics are combined is a form of synergism.
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CHAPTER
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Cardiovascular Anatomy and Physiology Glenn Woodworth, Asish Das, and Valerie Sera ■ INTRODUCTION Anesthesia and surgery is a delicate dance with the cardiovascular system. The majority of anesthetics interact with the cardiovascular system by depressing sympathetic outflow, dilating blood vessels, or directly interacting with the heart. Surgical stimuli, blood loss, and anesthetic procedures have the further ability to interact with the patient’s cardiovascular system. This chapter introduces the anesthesia technician to the fundamental anatomy and physiology of this important body system.
■ SURFACE ANATOMY OF THE HEART The heart is a set of hollow muscular pumps combined into a single organ. It is located in the middle of the chest (the mediastinum) between the lungs and their pleural coverings. It is shaped like an upside down pyramid that is tilted to the patient’s left. The base of the heart lies superiorly, and the apex lies inferiorly and leftward (Fig. 7.1). The heart itself is covered in a thick sac called the pericardium. The heart is divided into two sides, a right and a left, and consists of a total of four chambers. The upper two chambers comprise the right and left atria, while the lower chambers are termed the right and left ventricles. The inferior and superior vena cava are connected to the right atrium (RA), and the pulmonary artery is connected to the right ventricle (RV). On the left side of the heart, the pulmonary veins are connected to the left atrium, and the aorta is connected to the left ventricle (LV) (Fig. 7.2). The heart is rotated slightly to the left, and the apex is tilted slightly anteriorly. Thus, the RA is anterior to the left atrium (LA), and the RV forms most of the anterior aspect of the ventricular mass. The LV is positioned on the left side of the
heart, but because of the rotation and the tilting, it is also positioned slightly posterior and inferior to the RV. An understanding of the position of the heart is important to properly read the electrical signals that are generated by the heart and recorded on an electrocardiogram (ECG). The ECG is discussed in more detail later in this chapter.
■ FETAL DEVELOPMENT Major organ development occurs between the 4th and 8th week of fetal life. The heart is the first organ to complete its development during fetal growth. The heart begins as a primitive vascular tube that curves back on itself and bends anteriorly and rightward to form three distinct portions called the single-chambered primitive atrium, a ventricle, and the truncus. These develop further into a right heart and a left heart, atria and ventricles with intervening atrioventricular (AV) valves, and the aortic and pulmonary trunks. Errors in fetal development of the heart can result in significant malformations. For example, the heart may fail to form two ventricles, or the aorta and pulmonary trunks may be fused into a single trunk arising from both ventricles. An average adult heart is 12 cm from base to apex, 8–9 cm at its broadest transverse diameter, and 6 cm anteroposteriorly. Its weight varies with average 300 g in male and 250 g in females, with adult weight achieved between the ages of 17 and 20 years.
■ PERICARDIUM The heart is enclosed in a three-layered sac called the pericardium. The outer fibrous layer of the pericardium is attached to the great vessels, the sternum, and the diaphragm. It secures the heart to the sternum anteriorly and to the diaphragm inferiorly. The inner serous layer 31 tahir99-VRG & vip.persianss.ir
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■ MYOCARDIUM
■ FIGURE 7.1 Normal heart anatomy, anterior view.
consists of a visceral and parietal portion. The visceral pericardium, also known as the epicardium, covers the entire heart and great vessels. The parietal pericardium forms an inner lining to the fibrous pericardium. The space between the two layers of the serous pericardium is called the pericardial space. Normally, the pericardial space contains 30–50 mL of serous fluid that acts as a lubricant to decrease friction while the heart beats. The fibrous layer of the pericardium is noncompliant (not easily expandable) and helps to prevent dilation of the heart and restrict cardiac filling beyond the normal range. When there is an acute collection of fluid or blood in the pericardial space, a clinical condition called cardiac tamponade develops. Rapidly accumulating fluid in the pericardial space can put pressure on the heart chambers, severely restricting blood from entering the heart, and can result in circulatory collapse. Surgical intervention is often necessary to relieve cardiac tamponade.
The heart wall consists of three layers. The outermost layer of the heart is the epicardium, consisting of epithelial cells that form a serous membrane that covers the entire heart. The innermost layer of the heart is the endocardium. It lines the inner surface of the heart, its valves, the papillary muscles, and the fibrous cords that connect the valves and continues into the major cardiac veins and arteries. The middle layer of the heart is the muscular layer known as the myocardium. It is responsible for the contractile action of the atria and ventricles. The human body contains three types of muscle: cardiac muscle, smooth muscle (found in other hollow organs like the bowel or bronchi), and skeletal muscle. Cardiac muscle cells are specialized muscle cells with amazing resiliency and capabilities. At an average heart rate (HR) of 60 beats per minute, the heart beats 3 billion or more times without resting in one’s lifetime. To accomplish this incredible feat, myocardial cells function in a slightly different manner than do skeletal muscle cells. Myocardial cells are rich in mitochondria, the energy engine of the cell. The large number of mitochondria makes the cells resistant to fatigue. This allows myocardial cells to perform almost continuous work as long as they have a rich supply of oxygen and nutrients. Unlike skeletal muscle, myocardial cells rapidly become unable to function if their blood supply is interrupted. In addition to extra mitochondria, myocardial cells have other unique properties. For example, they have the intrinsic ability to contract in the absence of stimuli in a rhythmic manner and have the ability to conduct electrical impulses from one myocardial muscle cell to the next. Both of these functions play an important role in the cardiac conduction system described below.
■ CARDIAC CHAMBERS AND THE CIRCULATION OF BLOOD As described above, the heart has four chambers: the RA, the RV, the LA, and the LV. The purpose of the heart is to circulate blood throughout the body where it can deliver oxygen and other nutrients, as well as pick up waste products like carbon dioxide. The blood circulates through the body in two loops or systems: the pulmonary circulation and the systemic circulation (Fig. 7.3). Beginning with the terminal portion of the systemic circulation, blood is drained into the venous
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NORMAL HEART ANATOMY
Cross Section
Superior vena cava Aorta Pulmonary trunk Right atrium Left auricle Pulmonary valve
Mitral valve
Tricuspid valve
Left ventricle
Inferior vena cava
Right ventricle
■ FIGURE 7.2 A coronal cut through the heart demonstrating the four chambers of the heart and their vascular connections.
system from the various organs and extremities. Blood from the lower portion of the body eventually drains into a large vein, the inferior vena cava (IVC). Blood from the upper portion of the
body, including the upper extremities and the head and neck, drains into the superior vena cava (SVC). This venous blood has had much of its oxygen removed (deoxygenated) by the tissues
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Superior vena cava Aortic arch
Pulmonary arteries Pulmonary arteries
Pulmonary veins
Pulmonary veins
Left atrium Bicuspid (mitral) valve
Right atrium
Tricuspid valve
Left ventricle Right ventricle
Inferior vena cava
■ FIGURE 7.3 Blood circulates through the heart in two loops forming the pulmonary and systemic circulations.
and contains extra waste products like additional carbon dioxide (CO2). The systemic venous blood from both large veins drains into the RA. Contraction of the RA pushes the deoxygenated blood through the tricuspid valve into the RV. Contraction of the RV forces the blood forward past the pulmonic valve into the pulmonary artery, the beginning of the pulmonary circulation. The pulmonary arteries branch into ever smaller arteries and arterioles before turning into capillaries. Capillary blood flows close to the pulmonary alveoli. The blood can now add oxygen from the alveoli and discharge CO2 into the alveoli (see Chapter 11). Once the blood has been oxygenated and discharged some of its CO2, it begins to collect from the capillaries into venules and eventually into the large pulmonary veins. The four large pulmonary veins drain into the left side of
the heart and the LA. Contraction of the LA forces the oxygenated blood forward through the mitral valve and into the LV. The forceful contraction of the LV can generate high pressures, and the blood is ejected out of the LV through the aortic valve and into the aorta. From the aorta, the blood flows out to the systemic circulation, where it can perfuse the body. The blood can then return to the heart to complete the two loops. It is the continuous forward pumping action of the heart that keeps blood flowing through the body where it can deliver nutrients and pick up waste products.
Right Atrium The RA is a thin-walled muscular chamber. It receives deoxygenated venous blood from the SVC, the IVC, and the coronary sinus. The coronary sinus empties into the RA just above the
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tricuspid valve. In addition to the main chamber of the atrium, the RA has a small muscular pouch, the right atrial appendage. The RA is separated from the LA by the septum. The septal wall has an oval depression, the fossa ovalis. There are no true one-way valves in the venae cavae; thus, when the right atrial pressure rises, elevated pressure is reflected into the IVC and the SVC. Venous distention and systemic venous congestion are commonly seen when pressures are elevated in the heart as in congestive heart failure. Normal right atrial pressure ranges from 2 to 10 mm Hg.
Right Ventricle The RV extends from the tricuspid valve nearly to the apex of the heart. The tricuspid valve prevents flow of blood backward from the RV into the RA. At the base of the heart, the RV extends to the left to form the infundibulum. The pulmonary valve prevents the flow of blood from the pulmonary artery backward into the RV. In addition to the main muscular walls of the RV, the RV contains two major papillary muscles and a third smaller papillary muscle. The papillary muscles connect the chordae, fibrous collagenous cords, to the leaves (cusps) of the tricuspid valve. The RV receives blood from the RA through the tricuspid valve and ejects it through the pulmonic valve into the pulmonary artery where it can flow to the lungs. The resistance to flow in the pulmonary circulation is approximately 1/10th that of the systemic circulation. Therefore, the RV does not need to generate as much pressure to pump blood to the lungs as the LV needs to pump blood to the body. This also explains why the RV muscle is much thinner than the thick muscular wall of the LV. Systolic pressure in the RV ranges from 15 to 25 mm Hg with end-diastolic pressures from 0 to 8 mm Hg (the concepts of systolic and diastolic pressures are discussed in detail below).
Left Atrium The LA is the smaller of the two atria but has thicker walls. Its cavity and walls are mostly formed by the proximal part of the pulmonary veins, which are incorporated into the atria during fetal development. The left atrial aspect of the septum between the atria has a rough appearance and marks the site of the foramen ovale. In fetal life, the foramen remains open and is essential for fetal circulation. At birth, this foramen closes spontaneously, but in about 20%–30% of
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the normal population, the defect may persist without any symptoms. Although asymptomatic, a patent foramen ovale presents a potential passageway for gas bubbles or debris to pass from the right side of the heart to the left side without passing through the lungs. Under normal circumstances, most debris, like small blood clots or gas bubbles, will be stopped by the pulmonary microcirculation before they can reach the left side of the heart. Under abnormal circumstances (i.e., conditions in which the right atrial pressure is elevated), passage of gas or debris from the RA across the foramen ovale to the LA becomes a real possibility. This is important as any debris or bubbles in the left side of the heart could flow out of the heart and directly into the brain, causing a stroke. The LA receives oxygenated blood from the lungs through pulmonary veins. Normal filling pressure ranges from 4 to 12 mm Hg. Like the RA, the LA also has an appendage. The LA appendage forms a portion of the left heart border as seen on a chest x-ray. In atrial fibrillation (disorganized electrical activity of the heart), it can be a source of intracardiac blood clots. These clots can embolize systemically, causing a stroke or limb ischemia. When the atria fibrillates, it loses its contractile function and the left atrial appendage is less able to empty blood into the atrial main cavity. Blood pooling in the atrial appendage is prone to clotting.
Left Ventricle The LV wall is almost three times thicker than the RV wall. It is designed to be a powerful contractile chamber that can maintain flow in the high-pressured systemic arteries. The LV cavity extends from the AV groove to the cardiac apex. The mitral valve forms the inlet to the LV. The outlet region is formed by the aortic valve. The septum dividing the right and left ventricles is thick and is functionally more a part of the LV than the RV (Fig. 7.4). A ventricular septal defect is the most common congenital heart defect in children younger than 2 years of age. Most small defects close spontaneously. Only the larger defects need surgical correction. The normal thickness of the LV wall is between 0.8 mm and 1.1 cm. In hypertrophic cardiomyopathy, the septum may get disproportionately thickened. When the ventricle contracts, the hypertrophic septum can obstruct the outflow of blood from the ventricular cavity into the aorta (dynamic
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Cardiac Skeleton The heart’s fibrous skeleton, the “annulus fibrosus,” is a firm anchor to which most of the heart’s muscles and valves are attached. The annulus fibrosus gives structure to the heart and acts as an insulator. Because the annulus fibrosus is not made up of myocardial muscle cells it does not conduct electrical impulses from one region of the heart to another. This ensures that electrical impulses traveling from the atria myocardial cells to the ventricular myocardial cells must move through a specialized pathway, the AV node. This system helps the heart regulate electrical signaling to coordinate contraction of the atria and ventricles as well as to help prevent abnormal electrical heart rhythms (arrhythmias).
Cardiac Conduction System
■ FIGURE 7.4 Cross-section of the heart demonstrating right and left ventricles.
subaortic obstruction). This clinical condition may cause sudden death and requires medical treatment. The LV receives blood from the LA through the mitral valve and ejects blood through the aortic valve to the systemic circulation via the aorta. The mitral valve prevents the flow of blood backward into the LA during contraction of the LV. There are several fibrous chords attached to papillary muscles in the ventricle that support the mitral valve cusps. These chordae are essential for the proper functioning of the mitral valve. Pressure in the LV is high during muscular contraction (“systole”) and equals systemic blood pressures. When the ventricle relaxes (“diastole”), the pressure falls. Normal end-diastolic pressures in the LV range from 4 to 12 mm Hg. The smooth left ventricular outflow tract ends at the cusps of the aortic valve. The cusps of the aortic valve are attached in part to the aortic wall and in part to the supporting ventricular structures. The aortic valve in its closed position has three coronary sinuses (out pouching between the aortic wall and the cusp).
Myocardial muscle cells differ from skeletal muscle cells because of their inherent ability to spontaneously depolarize and repolarize in a rhythmic fashion (automaticity). Ventricular muscle cells spontaneously depolarize at a lower frequency (30–40 beats per minute) than atrial muscle cells, but in the intact heart, both are synchronized to a more rapid rhythm, generated by pacemaker cells in the RA. The pacemaker cells, called the sinoatrial (SA) node, and the specialized myocardial cells, which conduct the electrical signals to synchronize the contraction of all myocardial cells, make up what is known as the “cardiac conduction system” (Fig. 7.5). The SA node is located in the high RA near the junction of the SVC and the RA. These “pacemaker cells” spontaneously depolarize and initiate contraction of the myocardial cells in the atria. Because all myocardial cells can conduct the electrical impulse and cause adjacent myocardial cells to depolarize, the electrical depolarization and subsequent contraction of atrial cells spreads like a wave beginning at the SA node. Several other specialized myocardial conduction cells conduct the electrical impulse from the RA to the LA (Bachmann’s bundle). The depolarization must also be conducted from the atria to the ventricles and more importantly the timing of atrial and ventricular contractions synchronized (see “Cardiac Cycle” below). If the atria and ventricles contract simultaneously, blood would not flow from the atria into the ventricles. The speed of conduction of electrical impulses through normal atrial and ventricular cells is about 0.5 m/s. The speed of
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Sinoatrial node
Interatrial septum Atrioventricular node
Atrioventricular bundle (bundle of His)
Right and left bundle branches
Interventricular septum
■ FIGURE 7.5 The myocardial conduction system is made of specialized myocardial muscle cells forming the pacemaker region (the SA node), the AV node, the bundle of His, and the Purkinje fibers.
conduction of the electrical signal is much faster than the time it takes for muscular contraction; thus, the electrical signal from the SA node would reach the ventricle rapidly, long before the atrium has contracted. This would cause near simultaneous contraction of the atria and ventricles. In the normal functioning heart, this does not happen because the fibrous annular tissue that separates the atria from the ventricles does not conduct the electrical impulse. Instead the impulse must pass through a region of cells in the inferior posterior portion of the atrial septum called the AV node. This group of specialized myocardial cells conduct the impulse at 1/10th the speed of normal myocardial cells. This has the effect of slowing the electrical signal before reaching the ventricles. This gives the atria a chance to contract and eject blood into the relaxed ventricle before the ventricle begins its contraction. In order to efficiently eject blood and generate pressure within the ventricle, the septum and apex
of the ventricles must contract first, followed by the base of the heart. This coordination of contraction would not occur if the depolarization wave spread from the AV node through the ventricles from one cell to another. The heart utilizes additional specialized myocardial cells to rapidly conduct the electrical signals to the different portions of the ventricle to achieve effective contraction and blood ejection. These cells conduct the electrical signal 10 times faster than normal myocardial cells. After leaving the AV node, the electrical signal passes through the bundle of His to reach the base of the heart. It then passes on the endocardial side of the interventricular septum using specialized myocardical conduction cells (Purkinje fibers). It then moves along the endocardial side of each of the ventricles from apex to base using right and left branches of Purkinje fibers. The SA node, Bachman bundle, the AV node, the bundle of His, and the Purkinje fibers make up the myocardial conduction system.
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Wolff-Parkinson-White and other syndromes have abnormal electrical pathways in the heart that lead from the atria directly to the ventricles bypassing the AV node. These conditions can lead to very fast heartbeats (tachycardia) and even to life-threatening abnormal heart rhythms.
Coronary Arterial Supply The right and left coronary arteries arise from the ascending aorta just above the aortic valve. The coronary arteries supply the capillaries of the myocardium with oxygenated blood. One might think that the LV would not need any arteries because it could obtain oxygen directly from the oxygenated blood that flows through the ventricular cavities. However, the walls of the ventricles are too thick to obtain sufficient oxygen or eliminate waste products, like carbon dioxide, by diffusion. Arteries branching into arterioles and then capillaries must do the job. The blood is then collected into veins, which drain into the coronary sinus. The left coronary artery (LCA) has two main branches: the left anterior
descending (LAD) and the left circumflex (LCX) arteries (Fig. 7.6). The right coronary artery (RCA) and the LCX course around the heart in opposite directions in the AV groove. These two arteries throw off branches, with the terminal portions of the arteries meeting on the posterior aspect of the heart at an important landmark known as the crux of the heart. At this point, either the RCA or the LCX supplies the posterior descending artery (PDA), which descends in the interventricular groove toward the apex of the heart. This terminal branch supplies the posterior and inferior parts of the heart. Right or left coronary dominance is determined by which artery supplies the PDA. Seventy percent of people are RCA dominant, 10%–15% are LCA dominant, and 10%–15% have mixed right and left dominance. This is an important anatomical fact as the PDA supplies the crux and the posterior third of the ventricular septum. The AV node is located at the crux and is nourished by the PDA. Obstruction of the blood supply to the AV node can cause malfunction of the
Anterior view
Right coronary artery
Left coronary artery Circumflex artery
Branch to sinoatrial node Left marginal branch Right ventricular branch Diagonal branch Right atrial branch Posterior interventricular branch Anterior interventricular artery Right marginal branch
■ FIGURE 7.6 Coronary artery anatomy.
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node and prevent electrical impulses from traveling from the atrium to the ventricle properly (AV block). The RCA supplies the RA, RV, and inferior wall of the LV (if right coronary dominant). The LAD runs in the anterior interventricular groove and supplies the anterior wall of the LV. Along its course, it gives off diagonal arteries, which supply the lateral LV wall, and septal arteries, which supply the anterior two-thirds of the ventricular septum. The LCX artery supplies the LA and the lateral and posterior walls of the LV. The LAD, LCX, and RCA are considered major arteries because of their large area of distribution. Blockage in the proximal portion in any of these arteries can cause a large amount of myocardial cell death (myocardial infarction) and can significantly affect the heart’s ability to contract.
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Coronary Venous Circulation The venous system of the heart consists of the thebesian veins, the anterior cardiac veins, and the coronary sinus (Fig. 7.7). The coronary sinus is located in the posterior AV groove near the crux and collects about 85% of the blood from the LV. It opens into the RA at the coronary sinus ostium near the orifice of the IVC. During cardiac surgery, the coronary sinus must often be cannulated. Anomalies in coronary sinus anatomy can present significant challenges for both the anesthesiologist and the cardiac surgeon.
Innervation The heart is richly innervated by the autonomic nervous system to provide control of HR and the force of cardiac contractions (see Chapter 14).
Posterior view
Great cardiac vein Posterior vein of left ventricle
Anterior interventricular vein
Coronary sinus
Small cardiac vein
Middle cardiac vein
■ FIGURE 7.7 The coronary venous circulation.
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Autonomic influence on the heart can modify cardiac function appropriately to meet the changing supply and demand of the body for blood flow. All portions of the heart are richly innervated by sympathetic fibers. When active, these sympathetic nerves release norepinephrine to act on the myocardial cells. Norepinephrine binds to β1-adrenergic receptors on cardiac muscle cells to increase the HR (chronotropy), increase the conduction velocity of electrical signals (dromotropy), increase the force of contraction (inotropy), and increase the speed of contraction and relaxation (lusitropy). Cholinergic parasympathetic innervation to the heart arises from the right and left vagal nerves and innervates the SA node, the atria, and the AV node. When active, these parasympathetic nerves release acetylcholine to act on myocardial cells. Acetylcholine interacts with muscarinic receptors on these cells to decrease the HR (SA node) and decrease the velocity of electrical signals moving through the AV node. Parasympathetic nerves may also act to decrease the force of contraction of atrial (not ventricular) muscle cells. Overall, parasympathetic activation acts to decrease cardiac pumping.
■ CARDIAC PHYSIOLOGY Cardiac Action Potential Like skeletal muscle, myocardial cells are able to contract due to the interaction of cellular proteins, actin and myosin. This interaction and subsequent contraction is dependent upon calcium for it to occur. As discussed above, the initiation of normal myocardial contraction begins with an electrical signal from the SA node. The electrical signal travels through the myocardial conduction system before reaching the rest of the myocardium. Upon reaching the myocardial cells, the electrical signal depolarizes the cell membrane, which opens channels to allow extracellular sodium and calcium to flow into the cell (Fig. 7.8). The inward flow of calcium causes additional calcium stores within the cell to be released. The calcium causes the cell to contract by promoting a temporary binding between actin and myosin. The calcium must be actively sequestered back into storage units within the cell to allow the muscle cell to relax. In addition, the myocardial membrane must be repolarized to prepare for another electrical signal. This sequence of events is called the cardiac action potential.
■ FIGURE 7.8 The cardiac action potential demonstrates cell membrane potential changes over time caused by changing flows of ions into and out of the cell. A) standard action potential. B) action potential from a cell with automaticity-automatic depolarization. Note how phase 4 shows the cell slowly depolarizing until it reaches a threshold to initiate phase 0. (From Topol EJ, Califf RM, et al. Textbook of Cardiovascular Medicine. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.)
The relative ratios of ions (molecules with strong positive or negative charges) like sodium, potassium, and calcium, inside and outside of the myocardial cell membrane create small electrical potentials or voltages across the membrane. For example, if there are more net positive ions outside of the cell than inside the cell, the cell would have a negative potential (the cell is polarized). By custom, the “positive” or “negative” potential of a cell is determined by the charge of the interior of the cell compared to the outside. At rest, myocardial cells have a negative potential called the resting membrane potential. Because of the charge differential between the inside and outside of the cell, the resting myocardial cell is a minibattery. Ions are kept inside and outside of the cell because the cell membrane is not permeable to ions. If an appropriate cellular channel for that ion is open, ions will flow into or out of the cell, depending upon the charge and concentration gradients. Once a sufficient electrical signal reaches the myocardial cell, it triggers a sequence of actions that open and close ion channels. The flow of ions across the channels causes the cell membrane potential to change over time resulting in the cardiac action potential. The phases of the cardiac action potential are as follows (Fig. 7.8): • Phase 4: Resting membrane potential • Phase 0: An electrical signal has caused the cell to open sodium channels and sodium rushes into the cell, depolarizing the membrane.
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• Phase 1: Fast sodium channels close. Small movements of potassium and chloride cause a slight dip in the membrane potential. • Phase 2: The membrane is kept depolarized by the inward flow of calcium ions balanced by an outward flow of potassium. • Phase 3: Repolarization occurs as the calcium channels close, but potassium continues to flow out of the cell. The cell must reset the ion balance by actively pumping sodium out of the cell and potassium into the cell. The cell must also restore calcium gradients by actively pumping calcium into storage. The cardiac action potential is much longer than that of skeletal muscle, and during this phase, cells remain unresponsive to further excitation. This is the refractory period.
41
Supplemental right precordial leads
V5R
V4R V3R V2R V1R
Mid-clavicle Anterior axillary line Horizontal plane of V4–V6 RA
LA V1 V2 V3 V4 V5
Cardiac Electrophysiology During the phases of the cardiac action potential, ions move in and out of the cell, causing changes in membrane potential and causing small electrical currents. When the tiny electrical currents from multiple myocardial cells are added up, the currents can be measured with electrodes. A machine with lead wires and electrodes attached to the surface of the chest can measure these currents, amplify them, and record them on a graph, the ECG. The electrodes are small adhesive pads with electroconducting gel. They are attached to the ECG machine with lead wires. Each lead wire, with its attendant electrode, is attached to the body in a specific arrangement (Fig. 7.9). The specific location of the electrodes allows monitoring of signals from different directions and can be used to monitor different regions of the heart. Two or more electrodes are combined to form a “lead,” which should not be confused with a single lead wire. Each lead monitors the electrical signals from a specific direction. For example, the electrodes and lead wires from the right arm and the left arm are paired to create lead I. Electrical signals that travel along the axis from the right arm toward the left arm are measured and displayed as lead I. Signals traveling toward the designated electrode will be recorded as positive or upward deflections on the ECG. Therefore, electrical signals traveling toward the left arm electrode along the axis formed by the right arm and left arm electrodes will be recorded as upward deflections on the ECG. If the electrodes and lead wires for the right arm and the
WoodWorth_Chap07.indd 41
ECG strip
ECG machine RL
LL
■ FIGURE 7.9 Electrode placement in different positions to generate a 12-lead (ECG). (Adapted from Molle EA, Kronenberger J, West-Stack C et al. Lippincott Williams & Wilkins’s Pocketguide to Medical Assisting. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.)
left arm are placed properly, lead I will measure electrical forces in the heart that are traveling toward the left. In another example, the electrodes placed on the right arm, left arm, and left leg are combined into a single reference point in the center of the chest that is paired with the left leg electrode to form lead II. The axis from the reference point in the center to the left leg points leftward and inferiorly. Therefore, if the electrodes are properly placed, lead II will measure electrical forces in the heart that are traveling leftward and inferior. A standard ECG uses 10 electrodes (with 10 lead wires) in specific locations. The lead wires are used in various
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Section II • Anatomy, Physiology, and Pharmacology
Views reflected on a 12-lead ECG
Lead
View of the heart
Limb leads (bipolar) I
Lateral wall
II
Inferior wall
III
Inferior wall
aVL aVR
I
Augmented limb leads (unipolar)
III
aVR
No specific view
aVL
Lateral wall
aVF
Inferior wall
II aVF
Precordial, or chest, leads (unipolar) V1
Septal wall
V2
Septal wall
V6
V3
Anterior wall
V5
V4
Anterior wall
V5
Lateral wall
V6
Lateral wall
V4
V1 V2
V3
■ FIGURE 7.10 The spatial orientation of the 12 standard ECG leads. (From Springhouse. ECG Facts Made Incredibly Easy. 2nd ed. Ambler: Wolters Kluwer Health; 2010, with permission.)
combinations to produce 12 standard “leads.” Each lead measures the electrical forces from a specific direction. Figure 7.10 demonstrates the spatial orientation of the electrical forces measured by each of the standard 12 leads. Figure 7.11 shows a 12-lead ECG. Each small 1-mm box on the vertical axis of the ECG is 0.1 mV in a standard ECG (the sizing can be
WoodWorth_Chap07.indd 42
changed). By convention, most clinicians refer to the size of the waves in millimeters and not millivolts. The ECG waves are recorded over time, with the paper moving at 25 mm/s. At that paper speed, each large box (5 mm) represents 0.2 seconds; each small box (1 mm) represents 0.04 seconds. In this way, we can measure various features of waves on the ECG. If two events on the
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Chapter 7 • Cardiovascular Anatomy and Physiology
43
■ FIGURE 7.11 Standard 12-lead ECG.
ECG are separated by four small boxes, the time separating the events is 0.16 seconds. Just as the size can be changed from the standard 1 mm equal to 0.1 mV, the speed of the paper (or tracing on a monitor) can be changed. The clinician needs to be aware of the size and speed settings to properly interpret the ECG. Typical 12-lead ECGs measure and record from three leads simultaneously for about 2.5 seconds, before switching to three more leads, and so on until all 12 leads are recorded over about a 10-second period on a single sheet of specialized graph paper. The leads are displayed in a standardized pattern as illustrated in Figure 7.11. In addition to graphing the standard 12 leads, most ECGs graph 2 or 3 of the leads over the entire 10-second period. They are graphed at the bottom of the ECG printout. Although these recordings are a subset of the same leads, graphed above, they represent a continuous 10-second period. These long recordings are useful in the diagnosis of abnormal electrical rhythms (arrhythmias). ECG monitors in the perioperative setting usually use a 3, 4, or 5 lead wire system. Depending upon how many lead wires you are using, they can be combined to produce anywhere from 3 to 12 modified leads. These monitors can display one or more leads continuously on the screen, as well as print one or two leads on a “strip” that may be easier to analyze than by looking at the monitor.
WoodWorth_Chap07.indd 43
Basic ECG waveform The typical ECG wave for one cardiac cycle includes a “P” wave, a “QRS” complex, and a “T” wave (Fig. 7.12). The SA node initiates the cardiac cycle and causes the atria to depolarize followed by atrial contraction. Because the SA node is located in the high RA, the atrial depolarization wave spreads from superior to inferior and from right to left. If you imagine a clock face on a patient’s chest, lead II measures electrical forces heading toward 5 o’clock, inferior and
■ FIGURE 7.12 The ECG wave is formed by the P wave, the QRS complex, the ST segment, and the T wave. (From Weber J, Kelley J. Health Assessment in Nursing. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003, with permission.)
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Section II • Anatomy, Physiology, and Pharmacology
slightly leftward. Therefore, atrial depolarization creates a small positive wave in lead II (the “P” wave). This is why lead II is frequently monitored to determine if the SA node is driving the cardiac rhythm. It is an excellent lead to monitor atrial depolarization. As discussed earlier in the chapter, the myocardial conduction system funnels the electrical depolarization to the AV node where the signal is slowed to allow the atria to contract. The signal is then transmitted to the ventricles using the His-Purkinje bundles. The ventricular septum is the first to depolarize followed by the walls of the ventricles. The walls depolarize from the inside of the ventricular wall (endocardium) to the outside of the wall (epicardium). The depolarization of the septum from the left to right produces a short, small electrical signal that is directed anterior, rightward, and slightly superior due to the tilt of the heart in the chest. This electrical signal is moving away from lead II and produces a short, small downward deflection called a “Q” wave. The right and left ventricular depolarizations produce much larger waves due to their larger muscle mass compared to the atria. The RV depolarization is a rightward, anterior signal. The LV depolarization produces a large left, inferior, and slightly posterior signal. Because the LV is much more muscular than the RV, the electrical signal from the LV overwhelms the RV signal. Think of the electrical signals
being added together, except they are in opposite directions. Therefore, the RV signal slightly reduces or subtracts from the large LV signal. This combined signal produces a large upward deflection in lead II, which detects leftward and inferior signals. This upward deflection is the “R” wave. Following the R wave, there is often a small negative deflection called the “S” wave. Combined, these three deflections constitute the “QRS” complex. After a short delay, ventricular repolarization follows ventricular depolarization. This repolarization produces the “T” wave. The atria also repolarize; however, this occurs during ventricular depolarization and the small electrical signal of atrial repolarization is masked by the large ventricular depolarization signal. In addition to the P wave, QRS complex, and T wave, clinicians examine the intervals between the waves. The time from the beginning of the P wave to the beginning of the QRS complex is called the “PR interval.” The PR interval represents the time it takes for the electrical signal to travel from the SA node through the AV node and the rest of the myocardial conduction system before reaching the ventricles. The time from the end of the QRS complex to the beginning of the T wave is called the “ST segment.” These waves and intervals are used by clinicians to diagnose problems with the myocardial conduction system and heart muscle (Table 7.1).
TABLE 7.1 SEVERAL EXAMPLES OF DIAGNOSTIC INFORMATION DERIVED
FROM THE ECG ECG MEASUREMENT
DIAGNOSTIC INFORMATION
P wave
Large or broad P waves can indicate atrial hypertrophy. Abnormally shaped P waves can indicate an abnormal focus serving as the pacemaker for the heart instead of the SA node. The relationship between the P wave and the QRS complex can help determine the rhythm.
PR interval
A prolonged PR interval can indicate disease or medication-induced problems in the AV node. A short PR interval may indicate an abnormal connection between the atria and ventricles that bypasses the AV node.
QRS complex
Large amplitudes in the QRS complex can indicate ventricular hypertrophy. The changing shape of the QRS complex across leads can indicate a loss of electrical forces due to loss of active heart muscle from a heart attack. A prolonged duration of the QRS complex is common with abnormal function (blocks) of the Purkinje fibers (right and left bundles of the myocardial conduction system)
ST segment
ST-segment elevation or depression commonly occurs when myocardial cells have insufficient blood and oxygen (ischemia) or are injured (infarction). ST-segment abnormalities are also common with hypertrophied ventricles or bundle branch blocks
T wave
The shape of the T wave can be diagnostic for myocardial ischemia or infarction. It is also abnormal in bundle branch blocks or hypertrophied ventricles as well as electrolyte abnormalities.
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Chapter 7 • Cardiovascular Anatomy and Physiology
■ ABNORMAL HEART RHYTHMS Normal adult hearts beat between 60 and 85 beats per minute according to the rhythm set by the SA node. The HR can be accelerated or slowed by actions of the autonomic nervous system. For example, a vigorously exercising adult can have a HR of 140 beats per minute. HRs above 100 beats per minute are referred to as tachycardia. HRs below 60 beats per minute are referred to as bradycardia. Adults are rarely symptomatic until the HR decreases below 50 beats per minute. Some degree of bradycardia and tachycardia is normal in healthy populations (i.e., bradycardia during deep sleep and in a well-trained athlete; tachycardia following extreme emotion, excitement, after strenuous exercise, or with a fever). The SA node is the normal pacemaker for the heart. Several conditions are characterized by abnormalities with the origin of the pacemaker signal in the atria. One common condition is atrial fibrillation. In the normal heart, the SA node pacemaker initiates the signal, which then spreads like a wave across the atria. In this condition, the individual atrial myocardial cells are depolarizing and contracting completely independent of one another. The end result is that there is no coordination between the cells, a wave of depolarization is not produced, and the atria fail to contract. The independently depolarizing and contracting atrial muscle cells produce quivering atria. The disorganized atrial muscle cell depolarizations can be seen on the ECG as a fine wavy line (Fig. 7.13). Because the atria are not depolarized in a wave, the P wave is absent on the ECG. Besides lack of atrial contraction, another consequence of disorganized atrial depolarizations is that these electrical signals can be conducted through the AV node and produce irregular ventricular depolarizations and contractions. This might not seem like a bad thing; however, the atria can produce electrical signals at a rate of over
■ FIGURE 7.13 ECG demonstrating the lack of a P wave and an irregular heart rate characteristic of atrial fibrillation. (From Springhouse. ECG Facts Made Incredibly Easy. 2nd ed. Ambler, PA: Wolters Kluwer Health; 2010, with permission.)
WoodWorth_Chap07.indd 45
45
500 per minute. If these signals were conducted to the ventricles, the heart would beat too fast. At rates above 180–200 beats per minute, the ventricles do not have enough diastolic time to fill and forward flow begins to fall. The faster the rate, the more forward flow falls. The heart will rapidly reach the point where it cannot produce enough cardiac forward flow to perfuse the major organs. The heart attempts to protect itself from too many atrial signals reaching the ventricles by blocking them at the AV node. With very fast atrial signals, the AV node is unable to conduct every signal and begins “dropping” signals (beats) so that the ventricular rate is much slower than the atrial rate. In addition, the pattern of dropped or conducted signals can be variable, producing irregular ventricular contractions. Other atrial arrhythmias include atrial flutter and multifocal atrial tachycardia. Both of these rhythms have abnormal P waves. Because the atrial signal is conducted through the myocardial conduction system to the ventricles, the shape of the QRS complex will be relatively normal. These atrial arrhythmias usually produce fast HRs with normal (narrow) QRS complexes and are termed narrow complex tachycardias. Disease- or drug-induced reductions in conduction velocity through the AV node can cause serious problems. When conduction through the AV node slows to the point where the PR interval exceeds 0.2 seconds or the AV node fails to conduct normal atrial beats, it is referred to as heart block or AV block. When the AV node fails to conduct any atrial signals to the ventricle, the patient has “third degree” or “complete heart block.” Disease in the Purkinje bundles can cause abnormal transmission of the electrical signal to the ventricles (a “bundle branch block”). Often one or the other of the bundles is malfunctioning and failing to conduct the signal. In this condition, the normal bundle conducts the signal to its ventricle and then the signal must spread to the other ventricle through the heart muscle. Because the heart muscle conducts the signal 10 times slower than the myocardial conduction system, the ventricle supplied by the blocked bundle will depolarize later and more slowly than the other ventricle. This will result in a broad QRS complex, reflecting the slowed conduction, and an abnormally shaped QRS complex, reflecting the altered timing in depolarization of the ventricles.
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Section II • Anatomy, Physiology, and Pharmacology
■ FIGURE 7.14 ECG demonstrating wide QRS complexes at a fast rate characteristic of ventricular tachycardia. (From Springhouse. ECG Facts Made Incredibly Easy. 2nd ed. Ambler, PA: Wolters Kluwer Health; 2010, with permission.)
Arrhythmias can also originate in the ventricles. When an organized fast rhythm originates in the ventricle, it is called ventricular tachycardia (V tach) (Fig. 7.14). As mentioned above, fast ventricular rhythms can be associated with low cardiac output (CO) due to insufficient time to fill between contractions. In V tach, the ECG demonstrates a wide QRS complex tachycardia reflecting the slow conduction of the electrical signal through the heart muscle, even though the HR is fast. V tach is life threatening and requires immediate treatment. The most dangerous arrhythmia is ventricular fibrillation (V fib). This condition is physiologically similar to atrial fibrillation. The ventricular muscle cells depolarize and contract in a completely disorganized and independent fashion, producing a quivering ventricle that cannot generate any forward blood flow. The ECG demonstrates a completely disorganized electrical signal (Fig. 7.15). V fib produces no forward blood flow and is a life-threatening arrhythmia. Treatment for V fib requires application of an immediate electrical shock to the heart that causes all of the ventricular muscle cells to simultaneously depolarize. In many cases, after the shock (defibrillation) is delivered to the heart, the heart’s natural SA node pacemaker can take over and begin sending signals to coordinate the depolarization of the ventricles. One way to illustrate this concept is to think about a stadium filled with people. Each person represents an individual muscle cell. Beginning at one
■ FIGURE 7.15 ECG demonstrating a bizarre disorganized signal characteristic of ventricular fibrillation. (From Springhouse. ECG Facts Made Incredibly Easy. 2nd ed. Ambler, PA: Wolters Kluwer Health; 2010, with permission.)
WoodWorth_Chap07.indd 46
end of the stadium, the fans stand up and initiate the “wave.” As fans stand up and sit down raising their arms in order, the wave travels around the stadium pushing a beach ball in front of it. This is a coordinated contraction. Now imagine that every fan in the stadium is standing up and down randomly in a completely disorganized fashion. The stadium would appear to be quivering or fibrillating. A wave would not be produced, and the beach ball would not be pushed smoothly around the stadium. Now imagine someone got on the public address system and screamed, “SIT DOWN.” All the fans suddenly sit (depolarized by the shock), and the stadium is quiet. Then, the fans at one end of the stadium stand up and initiate the wave again (the SA node takes over as the pacemaker). The stadium has been successfully “defibrillated,” and we have the return of normal sinus rhythm. V fib is a life-threating event and if not treated promptly, the patient will die. Although many things can cause arrhythmias, some of the most common causes include the following: • Myocardial ischemia or infarction: Myocardial cells starved of oxygen do not function normally. They will not contract normally or conduct electrical impulses normally. The same is true for dead myocardial cells that have turned into a scar. These abnormal cells can be the origin of an arrhythmia or can alter conduction of a signal, causing an arrhythmia • pH or electrolyte imbalances: Normal pH and electrolyte levels are important for the myocardial cells to maintain their membrane potentials. Abnormalities in membrane potentials can cause abnormalities in the cardiac action potential and subsequent arrhythmias. • Overstretching of the heart due to valvular disease. Incompetent cardiac valves can cause blood to flow backward in the heart, stretching and overfilling chambers. These stretched and overfilled chambers are prone to abnormal heart rhythms.
■ CARDIAC CYCLE The cardiac cycle is defined as the period from the beginning of one heartbeat to the beginning of the next heartbeat. It includes systole
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Chapter 7 • Cardiovascular Anatomy and Physiology
the coronary arteries and then into the small arterioles and capillaries that feed the heart muscle itself. The capillaries are where the distance between the myocardial cells and blood flowing through the capillaries is short enough that gas and nutrient exchange can occur. During systole, ventricular pressures are high and essentially obstruct blood flow though the small arterioles and capillaries. This means that ventricular heart muscle is only supplied with oxygen and nutrients during diastole. Higher HRs can eventually lead to insufficient diastolic times to perfuse the heart muscle. To better understand the cardiac cycle, examine Figure 7.16. This figure depicts several simultaneous things happening during the course of two heartbeats. The top line represents the pressure in the aorta. The next line, the blue line, represents the pressure inside the LV, while
(i.e., contraction) and diastole (i.e., relaxation). The duration of each cycle is variable depending upon the HR. For example, with a HR of 72 beats/min, the cardiac cycle is 0.8 seconds (e.g., 60 Seconds per minute divided by 72 beats per minute = 0.8 seconds per beat). During this 0.8 seconds, the ventricles are in systole 0.3 seconds and in diastole 0.5 seconds. Although cardiac muscle contracts and relaxes faster at higher HRs, there is a limit. In general, as the HR increases, forward blood flow also increases. However, at HRs above 180–200 beats/min, the heart does not have enough time in diastole to fill before the next contraction begins. At HRs above this range, cardiac function progressively declines. Another important aspect of the HR is that the amount of time the heart spends in diastole affects myocardial perfusion. As mentioned earlier, blood flows from the aorta through Isometric contraction period Pressure (mm Hg)
47
Isometric relaxation period
120 Aortic valve closes
100 80
Aortic pressure 60 Aortic valve opens
40
Left ventricular pressure
20
Atrial pressure
100 Ventricular volume 80 (mL) 40 R
R
P
T
P
ECG Q 1st Heart sounds
Systole 0
Q 4th
2nd 3rd
0.2
Diastole 0.4
0.6
0.8
Time (sec) ■ FIGURE 7.16 The cardiac cycle depicted by measuring the pressures in the cardiac chambers during a heartbeat. (From Porth CM. Pathophysiology : Concepts of Altered Health States. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005, with permission.)
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Section II • Anatomy, Physiology, and Pharmacology
the gray line below it represents the pressure in the LA. The red line represents the volume of blood within the LV. Although similar things are happening with the RA and RV, in order to simplify the diagram, the figure depicts only the LA and LV pressures. The dark blue line represents the ECG tracing from a single lead. Finally, the last gray line shows the phonocardiogram and depicts the sounds of the heart during the cardiac cycle. The mitral and tricuspid valves are often referred to as the AV valves and they are labeled on the diagram as the AV valves.
Ventricular Systole The first section of the diagram in Figure 7.16 represents ventricular systole, which is divided into three phases: isometric contraction, rapid ejection, and slow ejection. • Isometric contraction phase: This phase represents the beginning of ventricular contraction. The increase in pressure within the ventricle causes the mitral valve to close, preventing the flow of blood backward into the LA. The beginning of ventricular contraction is seen on this ECG as the R wave, a large positive upstroke created by the depolarization of the muscular ventricle. The sound of the closure of the AV valves can be detected on the phonocardiogram or heard with a stethoscope. AV valve closure produces the first heart sound (S1). S1 is a low, slightly prolonged “lub” caused by the vibrations of the sudden closure of the AV valves. They can best be heard with a stethoscope over the apex of the heart. The isometric contraction phase is also called the isovolumetric contraction phase because all the valves are closed and there is no ejection of blood. The volume of blood in the ventricle does not change until the ejection phase. During the isometric contraction phase, the ventricular pressure rises. The pressure in the ventricle must rise above the aortic pressure to get the blood to flow into the aorta. The atrial pressure has also started to rise, not because of atrial contraction, but rather because the blood pouring in from the vena cava is filling up in the RA and the blood from the pulmonary veins is filling up the LA. • Rapid ejection phase: When left ventricular pressure exceeds aortic pressure and right ventricular pressure exceeds pulmonary artery
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pressure, the aortic and pulmonic valves open. Blood ejects out of the ventricles into the aorta and pulmonary arteries, respectively. The majority of the ventricles’ blood is emptied during the first third of the ejection period, rapid ejection. The aortic pressure curve peaks sharply because the rapid flow of blood flow out of the ventricle into the aorta soon and causes the pressure within the ventricle to fall. • Slow ejection phase: A small amount of additional blood is ejected during the latter twothirds of the ejection phase. This is referred to as the slow ejection phase. Even though the ventricles continue to contract during this phase, very little blood is ejected during this period. The total volume of blood ejected during the rapid and slow ejection phases is called the stroke volume (SV). During the slow ejection phase, a slow broad wave appears on the ECG, the T wave. The T wave is the detection of the electrical currents created by the repolarization of the ventricles. Once repolarization occurs, the ventricular muscle starts to relax.
Ventricular Diastole Ventricular diastole can be divided into four phases: isovolumetric relaxation, rapid ventricular filling, slow ventricular filling, and atrial systole. • Isometric relaxation phase: The isometric or isovolumetric relaxation phase is the beginning of diastole. The ventricular pressure has fallen due to left ventricular relaxation to a point where it is lower than that in the aorta (lower than that in the pulmonary artery for the RV). The aortic valve and the pulmonary valves snap shut due to the pressure gradient and prevent the backward flow of blood. This pressure reversal, and closure of the aortic and pulmonary valves, produce the second heart sound (S2) as shown on the phonocardiogram. S2 is a shorter, high-pitched “dup,” caused by the vibrations of the closing aortic and pulmonic valves just after the end of ventricular systole. They can be easily heard with a stethoscope at the left second intercostal space. During the isometric relaxation phase, the ventricular pressure curve falls close to 0 mm Hg. • Rapid ventricular filling phase: When ventricular pressure falls below atrial pressure, the AV valves open and blood enters rapidly from
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Chapter 7 • Cardiovascular Anatomy and Physiology
the atria into the ventricles. The rapid flow of blood out of the atria into the ventricles causes the pressure in the atria to fall. This is the downward slope of the V wave on the atrial pressure tracing. • Slow ventricular filling phase: The slow ventricular filling phase is also known as diastasis or the last part of diastole. During this phase, only a small amount of blood drains from the lungs and peripheral circulation into the atria and into the ventricle. The rising pressure in the ventricles reduces the pressure gradient from the atria to the ventricles, resulting in reduced flow. Toward the end of this phase, atrial depolarization occurs and is seen as a small upward deflection on this ECG (the P wave). • Atrial systole phase: Atrial contraction begins during the last phase of ventricular diastole and contributes 10%-25% of the total amount of blood that fills the ventricles in a normal individual. Atrial contraction begins about the time of the peak of the P wave. When individuals lose their regular atrial contraction (e.g., atrial fibrillation), they often underfill their ventricles, leading to a reduction in cardiac function. The “a” wave of the central venous tracing correlates to atrial contraction just before the closure of the AV valves.
■ CARDIAC VOLUMES AND CARDIAC OUTPUT The blood volume in the ventricles at the end of diastole is approximately 120 mL. This volume is called end-diastolic volume (EDV). Sixty percent of the total blood volume in the ventricles is ejected out during systole, and the residual volume after ventricular systole is approximately 50 mL. The difference between the EDV and the end-systolic volume (approximately 70 mL) is known as the SV and is equal to the amount of blood ejected after each ventricular contraction. To determine ejection fraction (EF), SV is divided by EDV. The normal adult EF is approximately 50%-70% depending upon hemodynamic and volume status. The EF is a good indicator of cardiac function because cardiac disorders (e.g., ischemic heart disease, cardiomyopathies, valvular heart disease, or congestive heart failure) can markedly reduce the EF. The volume of blood the heart pumps in liters per minute is called CO. It is equal to the SV multiplied by the HR. A person with a HR of
WoodWorth_Chap07.indd 49
49
72 beats/min and a SV of 70 mL has a CO of 5.0 L (CO = HR × SV). This value is within the normal range for a resting average-size adult; however, CO can vary significantly with exercise, fever, or metabolic conditions like hyperthyroidism or hyperthermia. During periods of strenuous exercise, a well-trained athlete’s CO can reach as high as 35 L/min. Decreases in CO can be produced by a variety of physiologic and pathologic conditions. For example, arrhythmias (abnormal heart rhythms), ischemic heart disease, or valvular heart disease can produce significant reductions in CO. CO can also vary based on the size of the individual. The cardiac index (CI) is a measurement used by clinicians to adjust for individual differences in body size (CI = CO/body surface area [BSA] or SV × HR/BSA) and is the CO per square meter of BSA. The CI is therefore expressed in liters per minute per meter squared. The CI gives a better representation of perfusion than CO alone. The normal CI is 2.5–4.0 L/min/m2 of BSA.
■ FACTORS AFFECTING CARDIAC OUTPUT There has been a great deal of research into the major physiologic factors that affect CO. These include the HR, the EDV of the ventricle (preload), the force with which the ventricle can contract (contractility), and the resistance against which the heart must eject blood (afterload). The description of how these factors affect cardiac function is the cornerstone of cardiac physiology.
Preload The total volume of circulating blood affects preload. The greater the venous return to the heart, the more the myocardial fibers will stretch to accommodate the load on the heart. According to the Frank-Starling law, the greater the initial myocardial fiber length the greater will be the force of contraction. This mechanism has been compared to the increased recoil of a rubber band when stretched. The increase in contractile force is related to an increase in sarcomere length (the contractile unit of a cardiac muscle cell). After a certain point, the sarcomere can become overstretched and the contractile force will decrease. In conditions where there is decreased filling of the heart (e.g., hypovolemia), the sarcomeres are short and the force of contraction is diminished. With increasing blood volume (increasing preload) the contractile force increases. When the
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Section II • Anatomy, Physiology, and Pharmacology
Normal
D A
E
C
HF with positive inotrope Untreated HF
Symptoms of high end-diastolic pressure
Normal
Cardiac output
Cardiac output
Symptoms of high end-diastolic pressure
F G
HF with ACE inhibitor Afterload reduction
C
Untreated HF
Preload reduction
B
Ventricular end-diastolic pressure
Ventricular end-diastolic pressure Symptoms of low cardiac output
Symptoms of low cardiac output
■ FIGURE 7.17 The physiologic relationship between the Starling Law of the heart and venous return pressure and volume. (With permission Figure 24-11: Adapted with permission from Harvey RA, Champe PC, eds. Lippincott’s Illustrated Reviews: Pharmacology. Philadelphia, PA: Lippincott Williams & Wilkins; 1992:157, Figure 16-6.)
blood volume is too high and there is excessive filling and stretching of the heart, the force of contraction begins to fall and is referred to as congestive heart failure. The ventricular function curve as depicted in Figure 7.17 shows the relationship between fiber length and the force of contraction. The left panel of the figure depicts ventricular end-diastolic pressure graphed against CO on the y axis. The upper “normal” curve demonstrates that increasing end-diastolic pressure (a measure of the preload volume in the ventricle) increases to a point. After that point, even with increasing end-diastolic pressure, the CO begins to fall as the ventricle becomes overstretched. Clinically, preload is estimated by measuring the pulmonary capillary wedge pressure. A catheter is placed in the pulmonary artery (pulmonary artery catheter or PAC) and a small balloon is inflated (see Chapter 34). The balloon wedges in a small pulmonary artery. The pressure from the LA is transmitted backward through the pulmonary circulation and is measured by the pulmonary artery capillary wedge pressure (PCWP). Higher PCWP can correspond to a higher preload. Another way to measure the volumes of the heart (preload) is to use echocardiography (see Chapter 9). Echo machines can use sound waves to image the heart and examine the size and contractile function of the cardiac chambers.
Afterload Afterload is an indication of the amount of wall tension that is produced by the ventricle.
WoodWorth_Chap07.indd 50
Clinically, afterload cannot be directly measured, and as a surrogate, clinicians think of afterload as the amount of pressure the ventricle must generate to eject blood. Anything that impedes the ability of the heart to eject is referred to as increasing afterload. For example, a constricted aortic valve or narrowed peripheral arteries would make it harder for the heart to eject blood, and thus increase afterload. The LV would compensate by working harder to generate higher pressures to overcome the increased resistance to ejection. Because increasing afterload increases the work of the heart, it also increases myocardial oxygen consumption. Conversely, decreasing afterload makes it easier for the heart to eject blood and decreases myocardial oxygen consumption. Afterload is an important concept. Many clinical conditions and drugs, including anesthetic agents, can increase or decrease afterload. Clinicians will often administer different medications in order to manipulate afterload. For example, a clinician may administer an arterial vasodilator to decrease afterload in a patient with a failing heart. The goal in this case is to ease the burden on the heart. Figure 7.17 demonstrates the effect of afterload reduction in the panel on the right. The failing heart is depicted in the bottom Frank-Starling curve. When the angiotensin-converting enzyme (ACE) inhibitor is given, the heart changes to the middle curve. Even with a lower end-diastolic pressure, the heart is able to produce a higher CO because of the afterload reduction.
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Chapter 7 • Cardiovascular Anatomy and Physiology
Contractility Myocardial contractility is the intrinsic ability of the heart to contract. We have already seen how preload and afterload can affect contractile function. Independent of these factors, the heart is able to produce a stronger or weaker contraction depending upon its contractility. In other words, if preload and afterload are kept constant, the “contractility” of the heart can affect the force of contraction. Many drugs change the intracellular amount of myocardial calcium and can increase contractility (e.g., epinephrine, norepinephrine, milrinone). Another word for contractility is “inotropy”; thus, drugs that increase contractility are referred to as positive inotropes. It is also important to understand that increasing contractility increases myocardial oxygen consumption. The left panel of Figure 7.17 demonstrates the effects of giving a positive inotrope to a patient with heart failure. Once the inotrope is given, the patient moves to the middle curve. Now for the same end-diastolic pressure the heart is able to produce a greater CO. Agents that reduce intracellular calcium decrease contractility. Examples of negative inotropes include calcium-channel blockers and beta-blockers. Acidosis and hypoxemia also negatively affect the contractility of the heart. One way to quantify contractility is through measurement of the EF with echocardiography. Under resting conditions, normal EF is between 50% and 70%. If afterload and preload are the same, a change in EF is a sensitive indicator of a change in contractility.
■ CARDIAC REFLEXES As discussed above, the heart is innervated by the autonomic nervous system. This innervation is responsible for several reflex changes in cardiovascular function. These reflexes are often feedback loops that help the body maintain normal HR and blood pressure. In the aortic reflex, a rise in blood pressure stimulates baroreceptors (pressure or stretch receptors) in the aortic arch and carotid sinuses. These baroreceptors stimulate the brainstem, causing a reflex parasympathetic outflow through the vagal nerve that slows the HR. Conversely, decreases in blood pressure cause decreases in baroreceptor output, resulting in decreased parasympathetic outflow and a resultant increase in HR in an attempt to restore blood pressure. The vagus nerve is responsible
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for the effector outflow to the heart. Any stimulus that leads to changes in vagal output can affect the heart. For example, carotid sinus massage (pressure in the neck over the carotid artery) can activate the carotid baroreceptors, resulting in increased vagal output and a slowing HR. In the past, this maneuver was used to intentionally increase vagal outflow to the AV node to attempt to disrupt certain kinds of tachyarrhythmias. The valsalva maneuver is another method to attempt to increase vagal output. A sustained increase in intrathoracic pressure causes an acute reduction in CO (reduced flow of blood into the heart). The sympathetic system is briefly activated to stimulate the heart and increase CO. When the intrathoracic pressure is released, blood flows rapidly back into the heart, increasing preload and blood pressure. The body responds with parasympathetic outflow, resulting in bradycardia. The sustained increase in intrathoracic pressure can be achieved by asking patients to “bear down” while holding their breath. In intubated patients, the anesthesia provider can deliver a large tidal volume and hold the inspiratory pressure for several extra seconds before releasing it. Other reflexes that result in increased parasympathetic flow include stimulation of ocular structures (pressure on the globe, cornea, eye muscles), stretch of hollow organs in the abdomen, traction on the attachments of the intestines to the abdomen, or even application of ice water to the face. One example of a reflex that decreases parasympathetic outflow and increases sympathetic outflow is the Bainbridge reflex. This reflex is triggered by high venous blood pressure that stimulates venous stretch receptors in the venae cavae and the RA.
■ MYOCARDIAL OXYGEN SUPPLY AND DEMAND When myocardial cells have insufficient blood supply and begin to dysfunction, it is referred to as myocardial ischemia. When the myocardial cells sustain irreversible damage and die, it is referred to as a myocardial infarction, more commonly known as a heart attack. The sudden onset of either of these conditions is referred to as acute coronary syndrome. Common symptoms include chest pain, shortness of breath, arm pain, and nausea. An ECG can be useful in making a diagnosis. Because the heart muscle is constantly
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Section II • Anatomy, Physiology, and Pharmacology
contracting, it requires a continuous supply of blood flow and oxygen to support its metabolic demands. The balance between myocardial oxygen supply and oxygen demand determines whether the oxygen delivered to the heart is sufficient for the work it is doing. This is an important concept in understanding and treating heart disease. The major determinants of myocardial oxygen supply are the blood flow to the heart cells and the oxygen content of the blood.
Blood Oxygen Content Ventilation and gas exchange in the lungs affect the amount of oxygen in the blood (see Chapter 11). Even with sufficient inspired oxygen concentration and a perfectly functioning respiratory system, very little oxygen dissolves in blood. The body overcomes this limitation with hemoglobin. Hemoglobin is a protein within red blood cells that has a very high affinity for oxygen. Therefore, the total amount of blood oxygen content comes from dissolved oxygen and oxygen bound to hemoglobin. With normal lung function and inspired oxygen, hemoglobin is fully saturated (carries as much oxygen as it can). With hypoxic inspired gas mixtures or abnormal lung function, hemoglobin may not be fully saturated with oxygen. Clinicians frequently monitor the percentage of oxygen saturation of blood with a pulse oximeter, with normal values ranging between 97% and 100%. At this level of saturation and a normal hemoglobin level (14–15 g/dL), there is 20 times as much oxygen bound to hemoglobin as there is dissolved oxygen. Even when fully saturated, if the hemoglobin level falls to less than 6 g/dL, there may be insufficient oxygen to supply the heart. If the oxygen saturation of the hemoglobin is less than 97%, values of higher than 6 g/dL may be required to supply the heart. To summarize, the oxygen content of blood is determined by the inspired oxygen level, the function of the lungs, and the amount of hemoglobin.
Myocardial Blood Flow Oxygen delivery to the myocardium is determined by the amount of oxygen in the blood and by how much blood flows to the myocardium. As described earlier in this chapter, the coronary arteries deliver blood to the myocardium. The major coronary arteries (RCA, LCA, LCX) branch like a tree to form multiple smaller arteries,
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arterioles, and eventually capillaries. If a blood vessel supplying the myocardium is obstructed, the myocardium supplied by that artery may become ischemic, or even infarcted. The amount of heart muscle affected is determined by how much myocardium is supplied by that vessel and the presence of any collateral circulation. The closer the obstruction occurs to the root of the tree (the origin of the major artery), the greater the amount of myocardium that will be affected. For example, an obstruction near the origin of the LCA will damage a very large portion of the heart and is often fatal. Even an obstruction in smaller arteries can be important, for example, if they supply a critical portion of the heart such as the myocardial conduction system. The heart has a backup system to protect against obstructions in arteries. This is accomplished by forming multiple cross-connections between arteries, collateral circulation. This way, if an obstruction occurs, it is possible that another artery is connected to the obstructed artery below the obstruction and can supply blood flow to that part of the heart. Even if coronary arteries are unobstructed, the amount of blood flowing through them will depend upon aortic pressure. Recall that the coronary arteries originate from the proximal aorta. Any condition causing low blood pressure (hypotension) reduces the driving pressure that causes blood to flow through the coronary arteries. It is important to remember that many drugs can affect the coronary circulation. Vasodilators such as nitrates, including nitroglycerin, can dilate coronary vessels and increase coronary blood flow. Other drugs that are commonly used to raise blood pressure can constrict coronary arteries and reduce coronary blood flow. These drugs are discussed in more detail in the section on cardiovascular pharmacology. Finally, recall the earlier discussion about diastole. The majority of myocardial perfusion occurs during diastole because of compression of arterioles within the myocardium during systole. Therefore, high HRs, which minimize overall diastolic time, can reduce myocardial perfusion.
Myocardial Oxygen Demand The other side of myocardial oxygen balance is demand. The amount of oxygen the heart consumes is related to the HR (doubling the HR doubles oxygen consumption), the amount of
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Chapter 7 • Cardiovascular Anatomy and Physiology
resistance the heart must pump against (afterload), the force and speed with which the heart generates pressure (contractility), and the size of the cardiac chambers. Atria or ventricles that are stretched utilize more oxygen in order to generate the same amount of pressure as normalsized chambers. Increases in any of these factors increase myocardial oxygen consumption.
Myocardial Infarction Maintaining the balance between myocardial oxygen demand and supply is crucial to normal cardiac function. One of the most common causes of cardiac dysfunction is an acute interruption of coronary blood flow to the heart. Either with aging or disease, lipid material (like cholesterol) can build up within the wall of an artery. The body’s response to the lipid forms what is knows as an atherosclerotic plaque. The buildup of plaque within the wall of a coronary vessel can gradually obstruct the vessel. This can gradually lead to ischemia of the region supplied by the vessel. A more dangerous condition occurs when the plaque “ruptures.” The narrowing of the vessel lumen by the plaque causes turbulent blood flow. This turbulence can disrupt the cells covering the plaque and expose material to the blood that initiates clotting of blood. Clot formation by platelets and clotting proteins can rapidly cause complete obstruction of the vessel, leading to ischemia or infarction of myocardial tissue. This often requires emergent treatment. If the region of ischemia or infarction is large enough, it can impair the heart’s ability to pump. In addition, even small regions of ischemic tissue can interfere with the electrical activity of the heart and produce a sudden, life-threatening arrhythmia. The treatment for myocardial ischemia is to attempt to restore the balance between myocardial oxygen supply and demand. Reducing demand starts with a resting patient and drugs to reduce the HR (e.g., beta-blockers), contractility (e.g., beta-blockers, calcium-channel blockers), and afterload (e.g., calcium-channel blockers, alpha-blockers, nitrates). Care must be taken in the administration of these drugs because they can also decrease blood pressure and cardiac filling. If oxygen saturation or hemoglobin levels are low, these need to be addressed as well. In many cases, these treatments may not be enough and an attempt will be made to improve coronary
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blood flow by relieving an obstruction with clotbusting drugs, a percutaneous intervention by a cardiologist, or surgery. Drugs like aspirin (interferes with platelets) or heparin (interferes with clotting proteins) can reduce further clot formation. Other drugs (thrombolytics) directly attack the clot itself. In many cases, testing is necessary to determine which arteries are obstructed. A cardiologist or radiologist can inject dye into the circulation, which can be viewed by fluoroscopy or a computed tomography (CT) scan. Cardiologists can then attempt to expand a narrowing in a coronary artery with a balloon (angioplasty) and then keep it open with an expandable mesh (stent). In other cases, surgery is required to place a graft from one coronary artery to below the obstruction to create an alternative blood supply to the affected area.
■ VALVULAR HEART DISEASE As described earlier, the valves of the heart perform the important function of preventing backward flow of blood within the heart. Dysfunction of heart valves can occur when they become narrowed (stenotic) or incompetent (allow backward flow of blood). Both conditions can severely impair cardiac function and represent important challenges to the anesthesiologist. In the following section, we briefly discuss some of the more important valvular conditions.
Aortic Stenosis Aortic stenosis (AS) is one of the most common valvular problems. Rheumatic heart disease or degeneration of congenitally malformed valve leaflets is often the cause of the stenosis. The narrowing of the aortic valve impedes the outflow of blood from the LV. The worse the stenosis, the more the LV must work to eject blood. Early on in the progression of this disease, the LV becomes thick (hypertrophied) and generates very large pressures to overcome the obstruction. The thick ventricle is also stiff and does not relax as well as a normal ventricle. This makes it more difficult to fill the ventricle. The heart becomes very dependent upon preload and, in turn, left atrial contraction to fill the stiff ventricle. Patients without AS can often tolerate loss of atrial contraction (e.g., atrial fibrillation), whereas patients with AS are acutely sensitive to changes in preload or atrial fibrillation. In addition, the hypertrophied heart working against
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high resistance consumes more oxygen and is susceptible to ischemia. As the stenosis becomes worse, the heart can no longer compensate with ventricular hypertrophy and the patients become more symptomatic. The LV begins to dilate and the increased end-diastolic pressure causes the LA to dilate and often fibrillate. In addition, the increased diastolic pressure within the atrium backs up into the lungs, causing congestion. This congestion and the significant decrease in CO is referred to as congestive heart failure. Ischemia is also common with moderate to severe stenosis. These patients can have difficulty with even minimal exertion. Patients reaching this stage require repair or replacement of the stenotic valve. Whether presenting for valve surgery or noncardiac surgery, anesthetic management of these patients is complex and the stress of surgery can often prove fatal. Anesthetic goals include maintenance of preload at the right level (not too much, not too little), avoidance of arrhythmias (may require urgent cardioversion), maintenance of contractility (must be able to generate enough pressure to overcome the obstruction), avoidance of tachycardia (need time for ventricular filling), and avoidance of peripheral vasodilation and hypotension (maintain sufficient aortic pressure to maintain coronary blood flow). These patients will often require invasive monitors (arterial line, central venous pressure) and in severe cases transesophageal echocardiography (TEE). One of the biggest concerns is the lack of reserve in these patients. They can rapidly go from maintaining CO to severe congestive heart failure.
by increasing the HR. This increases the CO and reduces the amount of time the heart spends in diastole, thus reducing the amount of regurgitation. Unlike AS, the heart can compensate for aortic regurgitation for some time. By the time symptoms appear, the disease is usually severe and the heart quite dilated. Anesthetic management includes the following: maintain adequate HR (reduces regurgitation and maintains CO), ensure adequate preload, avoid hypertension, and reduce afterload (reduces back pressure causing regurgitant flow). The anesthesia technician should consult with the anesthesia provider about the need for invasive monitoring (e.g., arterial line, central venous line) and vasoactive infusions (vasodilators, inotropes).
Mitral Stenosis The most common cause of a stenotic mitral valve is rheumatic heart disease. Much like AS, the LA must work harder against the obstruction to flow into the ventricle. The heart compensates with dilation of the LA and pressures within the LA rise. As the disease progresses, congestion in the lungs and atrial fibrillation are common. The good news about this disease is that left ventricular function is preserved. Anesthetic concerns surround avoiding or treating volume overload and tachyarrhythmias that reduce diastolic time. The heart requires adequate diastolic time to fill the LV when the mitral valve is obstructed. The anesthesia technician should be ready for invasive monitoring. Although venodilators to reduce preload may be required, vasoactive infusion is not needed as often as in other valvular conditions.
Aortic Regurgitation Rheumatic heart disease, trauma, aortic dissection, and congenital abnormalities are the most common causes of an aortic valve regurgitating blood backward into the LV. This regurgitation occurs during diastole when the aortic valve is supposed to be closed. The regurgitating blood overloads the LV and it dilates over time. The increased end-diastolic volumes and pressure can back up into the LA and the lungs. The heart must eject a much larger amount of blood (SV) because a significant portion can flow right back into the heart after ejection due to the incompetent valve. The amount of backflow depends on how leaky the valve has become. In addition to increased SV, the heart attempts to compensate
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Mitral Regurgitation Mitral regurgitation is common and can be caused by multiple factors. Similar to aortic regurgitation, the regurgitant flow from the LV back into the LA overloads the LA. Pressures within the LA are significantly increased, and the LA can be dramatically dilated. The increased LA pressures commonly cause congestion in the lungs. The reduction in forward flow from the LV to the aorta (much is lost due to the backward flow into the LA) reduces CO. As in aortic regurgitation, the heart requires an adequate preload and a normal atrial rhythm and contraction to fill. Afterload should be slightly reduced to promote forward blood flow. The anesthesia
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Chapter 7 • Cardiovascular Anatomy and Physiology
technician should be ready for invasive monitors and vasoactive infusions. TEE may be required in severe cases (see Chapter 39).
■ SUMMARY Anesthesiologists deal with patients who have cardiac disease on a regular basis. In addition, surgery and multiple drugs, including anesthetic agents, can severely affect cardiovascular function. Anesthesia technicians should have a working knowledge of cardiovascular anatomy and physiology to better understand the effects of surgery and drugs on the cardiovascular system. This knowledge will also help the technician understand why particular forms of cardiovascular monitoring are utilized. This chapter introduces the anesthesia technician to cardiac anatomy, the circulation of blood through the four cardiac chambers, the innervation of the heart, the myocardial conduction system and cardiac rhythms, the cardiac cycle and the pressures within the heart, the factors that affect cardiac function (preload, afterload, contractility), myocardial oxygen balance, and valvular dysfunction.
REVIEW QUESTIONS 1. Which of the following is TRUE about how blood flows through the heart? A) RA to RV to LV to LA to aorta B) RV to RA to pulmonary artery to LV to LA to aorta C) RA to RV to pulmonary artery to LA to LV to aorta D) RA to LA to pulmonary artery to RV to LV E) None of the above Answer: D. Blood flows from the RA into the RV where it is ejected into the pulmonary artery and lungs. Oxygenated blood returns from the lungs into the LA and then into the LV where it is ejected into the aorta.
2. Which of the following veins return blood DIRECTLY into the RA? A) SVC and IVC B) Pulmonary veins C) Femoral vein D) Subclavian vein E) Internal jugular vein Answer: A. The SVC collects blood from the upper extremity through the subclavian vein and from the head and neck from the internal jugular vein. The SVC then drains directly into the
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superior RA. The blood from the lower extremities drains into the femoral vein and eventually into the IVC. The IVC drains directly into the inferior portion of the RA.
3. Which of the following statements are TRUE about the ventricles? A) The ventricles have thicker walls than the atria. B) The LV has much thicker walls than the RV. C) The right and left ventricles are separated by the interventricular septum. D) The ventricles receive blood from the atria. E) All of the above are true. Answer: E. The ventricles receive blood from the atria after which they pump the blood into a major artery. This pumping action requires a larger pressure and thus the ventricles have thicker, more muscular walls than the thin-walled atria. The LV must pump blood into the aorta at very high pressures and is much more muscular than the RV, which pumps blood into the lower pressure pulmonary circulation.
4. Which of the following is TRUE regarding the myocardial conduction system? A) The system is composed of specialized nerve cells that conduct impulses. B) The conduction system conducts blood from the LA into the LV. C) The conduction system conducts electrical impulse from the autonomic nervous system to different portions of the heart. D) The conduction system is made up of specialized myocardial muscle cells. E) None of the above. Answer: D. The myocardial conduction system is made up of specialized myocardial muscle cells that are responsible for pacing the heart and conducting electrical impulses to synchronize and coordinate the contraction of the atria and ventricles.
5. Which of the following statements are TRUE regarding the coronary circulation? A) The RCA, the LAD coronary artery, and the LCX are the major “trunk” arteries that supply large areas of the heart. B) The right and left coronary arteries originate from the aorta. C) The heart protects itself with cross-connections between arteries (collateral circulation). D) The majority of myocardial blood flow occurs during diastole. E) All of the above are true. Answer: E. All of the above statements are true. The right and left coronary arteries originate from the proximal aorta. The LCA branches into the LAD and circumflex arteries. These are all major arteries, and an obstruction in one of these arteries will damage a very large portion of the heart,
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Section II • Anatomy, Physiology, and Pharmacology possibly resulting in death. The heart protects itself from obstructions in its blood supply by connections between arteries (the collateral circulation). The majority of blood flow through the myocardial arterioles and capillaries occurs during diastole, when the ventricular pressure is lower.
6. The cardiac action potential represents the changes in membrane potential in myocardial muscle cells from the flow of ions across the membrane. A) True B) False Answer: B. True. The myocardial cells maintain a resting membrane potential like a minibattery. When the membrane is depolarized from an electrical signal, ion channels open, allowing the flow of ions across the membrane further depolarizing the membrane. Eventually, the membrane is repolarized by changing which ion channels are open, allowing the flow of ions.
7. Which of the following statements are TRUE regarding the ECG? A) The ECG machine amplifies and measures tiny currents generated by the depolarization of myocardial cells. B) A “lead” is formed by two or more electrodes. C) Currents flowing toward a lead are displayed as positive deflections on the ECG. D) The spatial orientation of the leads can help monitor electrical currents generated by different portions of the heart. E) All of the above are true. Answer: E. All of the above are true. The ECG measures the tiny electrical currents produced by depolarizing myocardial cells. A lead is formed by at least two electrodes (more than one electrode can be combined to form a reference electrode). The electrical forces traveling toward a lead are displayed as upward deflections on the ECG; therefore, the spatial orientation of the leads is important. The leads are positioned so that each lead displays the electrical forces coming from a different region of the heart.
8. The ECG is useful for monitoring which of the following? A) The pressure in the central venous circulation B) Arrhythmias C) The PCWP D) Cardiac output E) None of the above Answer: B. The ECG is useful for monitoring the rhythm of the heart, the function of the myocardial conduction system, and myocardial ischemia (insufficient oxygen delivery to myocardial cells). The central venous pressure and the PCWP are measured with catheters placed in the central circulation and pulmonary artery, respectively. CO can be measured with a PAC or echocardiography.
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9. Which of the following statements is FALSE regarding the cardiac cycle? A) As blood flows from the atria into the ventricles, the ventricular pressure rises. B) After the atria contracts, the ventricles reach their EDV. C) When the LV contracts, the pressure rises in the ventricle until it overcomes the aortic pressure and it begins ejecting blood into the aorta. D) Systole is defined as when the ventricles begin to relax. E) None of the above. Answer: D. Systole is defined as when the ventricles are contracting. Diastole is when the ventricles are relaxing. Blood flows from the atria into the ventricle. As the volume increases in the ventricle, the pressure rises. Just before systole begins the atria contract to add more blood into the ventricles. The volume in the ventricles just before they contract is the EDV and determines the end-diastolic pressure.
10. Which of the following statements are TRUE about the cardiac cycle? A) Valves within the heart prevent the flow of blood backward. B) EF is defined as the amount of blood ejected from the heart during diastole. C) CO is equal to the EF times the HR. D) Diastole is when the heart is contracting. E) None of the above. Answer: A. The valves within the heart are very important as they prevent blood from flowing backward into the atria during ventricular contraction and backward into the ventricles from the pulmonary artery and aorta. The EF is the fraction of the end-diastolic ventricular blood that is ejected during systole. In normal resting patients, around 50% of the blood in the heart at end-diastole is ejected during systole. CO is equal to the SV (the amount of blood ejected with each heartbeat during systole) times the HR.
11. Which of the following factors DO NOT affect the force of contraction of the heart? A) The AV node B) Preload C) Contractility D) Drugs E) Afterload Answer: A. The AV node is a portion of the myocardial conduction system that regulates the speed of conduction from the atria to the ventricles. Preload, afterload, and contractility are the major determinants of the force of myocardial contraction and can be explained by using Frank-Starling curves. Drugs can both positively and negatively affect contractility as well as affect preload and afterload.
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Chapter 7 • Cardiovascular Anatomy and Physiology 12. Which of the following are potentially lethal cardiac arrhythmias? A) Ventricular fibrillation B) Ventricular tachycardia C) Sinus bradycardia D) A and B E) A and C Answer: D. Both ventricular fibrillation and ventricular tachycardia may not produce any forward blood flow. Unless the ventricular tachycardia is slow, the patient will die.
13. Which of the following is NOT a determinant of myocardial oxygen supply? A) Hemoglobin level B) Afterload C) Blood oxygen saturation D) Coronary blood flow E) Diastolic time
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SUGGESTED READINGS Agur AMR, Dalley AF. Grant’s Atlas of Anatomy. 11th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005: Chapter 1 Thorax. Guyton AC, Hall JE. Textbook of Medical Physiology. 11th ed. Philadelphia, PA: Saunders Elsevier; 2005. Kaplan J, Reich D, Lake C, Konstadt S. Cardiac Anesthesia. 5th ed. St. Louis, Missouri: Saunders Elsevier; 2006. Barrett K, Barman S, Boitano S, Brooks H. Section VI: Cardiovascular physiology. In: Ganong’s Review of Medical Physiology. 23rd ed. McGraw-Hill Companies; 2010. Warwick R, Williams P (Eds). The anatomical basis of clinical practice. In: Gray’s Anatomy. 35th ed. Toronto, Ontrario, Canada: Elsevier Churchill Livingstone; 2005: Chapter 60. Widaier EP, Raff H, Strang KT. Vander’s Human Physiology: The Mechanisms of Body Function. 12th ed. London: McGrawHill; 2011: Chapter 12. Cardiovascular Physiology.
Answer: B. Afterload is a determinant of myocardial oxygen demand (the harder the heart works, the more oxygen it uses). Oxygen is supplied to the blood by binding to hemoglobin in the blood. Low hemoglobin levels can result in insufficient oxygen for the heart. In normal humans, hemoglobin is 97%-100% saturated with blood. If insufficient oxygen is loaded onto hemoglobin in the lungs, the heart may not get enough oxygen. Finally, coronary blood flow during diastole is what brings the oxygen in the blood to the myocardial cells. High systolic pressures compress the coronary arterioles and prevent blood from flowing to the heart muscle during systole.
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CHAPTER
8
Cardiovascular Pharmacology Markus Kaiser and David C. Warltier ■ INTRODUCTION The cardiovascular system can be influenced by a variety of medications used in the operating room and intensive care units. Pharmacologic agents may change the contractility of the heart (inotropy), heart rate (chronotropy), conduction of electricity through the atrioventricular (AV) node (dromotropy), or relaxation of the heart in diastole (lusitropy). Vasoactive drugs may constrict (vasopressors) or widen (vasodilators) blood vessels either by influencing receptors of the autonomic nervous system (alpha1, beta1, and beta2 receptors) or by direct actions on the smooth muscle of the vascular wall. Maintaining a normal heart rate and rhythm is essential for optimal cardiac function. Antiarrhythmic agents are commonly used in the perioperative period to accomplish this. Drugs impacting the cardiovascular system are used to overcome the sequelae of cardiovascular disease, the effects of cardiovascular-depressant drugs (e.g., anesthetic agents), physiologic reflexes, and/or any combination of these. This chapter introduces the anesthesia technician to the mechanism of action and uses of positive inotropic agents, vasoactive drugs, and antiarrhythmic agents. The cardiovascular actions of anesthetic drugs are described elsewhere.
■ POSITIVE INOTROPIC AGENTS Drugs that increase the force of myocardial contraction are called positive inotropic agents and include catecholamines, phosphodiesterase (PDE) inhibitors, and myofilament calcium sensitizers. Catecholamines and PDE inhibitors increase calcium concentration in the cytoplasm of cardiac muscle cells by different mechanisms to help generate a greater force of contraction. Myofilament calcium sensitizers enhance the interaction between the contractile proteins within myocardial cells without increasing intracellular calcium.
Stimulation of beta1-adrenergic receptors that are coupled to G proteins activates the enzyme adenylyl cyclase, which, in turn, forms cyclic adenosine monophosphate (cAMP) from adenosine triphosphate (see Fig. 8.1). cAMP increases contractility (via increased intracellular calcium concentration) of cardiac muscle while also causing relaxation in smooth muscle (e.g., in blood vessels). It is metabolized by the enzyme PDE. PDE is targeted by a variety of drugs called PDE inhibitors that increase cAMP levels by inhibiting PDE and preventing breakdown of cAMP.
■ CATECHOLAMINES The naturally occurring catecholamines epinephrine, norepinephrine, and dopamine are produced in the medulla of the adrenal gland. Norepinephrine is also synthesized in adrenergic nerves and functions as a neurotransmitter in the sympathetic division of the autonomic nervous system (see Chapter 14). Epinephrine and norepinephrine are considered stress hormones when released into the bloodstream from the adrenal gland. The half-lives of endogenous as well as synthetic catecholamines, such as dobutamine and isoproterenol, are short (minutes), and these drugs are quickly deactivated primarily by reuptake into presynaptic neurons or metabolism by enzymes. The metabolites can be detected in the urine and are elevated in patients with catecholamine-producing tumors such as pheochromocytoma. The drugs stimulating alpha and beta adrenoceptors to produce their actions have proportionally different effects on heart, vasculature, and other smooth muscles dependent on their affinity for receptor types (see Table 8.1).
■ EPINEPHRINE Epinephrine is a naturally occurring catecholamine that is produced from its precursor, norepinephrine, exclusively in the adrenal medulla.
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59
stimulation of these receptors by low doses of epinephrine produces vasodilation. Epinephrine also influences metabolism by increasing glycogenolysis in the liver and lipolysis in adipose tissue. In anesthetic practice, epinephrine may be used intravenously in life-threatening situations including cardiac arrest, low cardiac output syndromes, anaphylaxis, or bronchospasm. Added to solutions of local anesthetics in a concentration of 1:200,000, it prolongs the action of the anesthetic by constricting surrounding blood vessels and decreasing systemic reabsorption. In cardiopulmonary resuscitation, epinephrine is administered intravenously in 1-mg (0.02 mg/kg) increments every 3 minutes per advanced cardiac life support (ACLS) guidelines in a dilution of 1:10,000 (0.1 mg/mL) (see Chapter 61). At this high dose, the arterial vasoconstrictor properties predominate causing increased diastolic pressures, which improve coronary artery perfusion. As a continuous infusion, epinephrine is usually administered between 0.03 μg/ kg/min and 0.15 μg/kg/min. At lower doses, the effects on beta1 and beta2 adrenoceptors (bronchodilation, inotropy, and chronotropy) usually predominate, while at high doses epinephrine can cause profound vasoconstriction through alpha1 activation. Epinephrine can produce cardiac arrhythmias, especially in the presence of the anesthetic halothane. Increases in heart rate in patients with coronary artery disease may cause myocardial ischemia. In general, the betaadrenergic stimulant properties of epinephrine
■ FIGURE 8.1 Function of catecholamines and phosphodiesterase inhibitors in the myocyte. Catecholamines increase cAMP through an energy-dependent pathway. In the presence of phosphodiesterase inhibitors, the breakdown of cAMP to AMP is slowed and the effect of catecholamines potentiated. (AMP, adenosine monophophate; ATP = adenosine triphosphate; β1, β1 adrenoreceptor; cAMP, cyclic adenosine monophosphate, Gs, Gs protein; PDE3, phosphodiesterase [isoenzyme 3]). (Adapted from Klabunde RE. Cardiovascular pharmacology concepts. Available from: www.cvpharmacology.com)
It has a wide range of physiologic effects including increasing heart rate, myocardial contractility, and conduction in the heart by stimulating primarily beta1-adrenergic receptors. Increased peripheral vascular tone (afterload) is mediated by the activation of alpha1-adrenergic receptors, while relaxing bronchial smooth muscle (bronchiodilation) is caused by the activation of beta2 receptors. Beta2 receptors are also located on vascular smooth muscle cell membranes, and
TABLE 8.1 PHARMACOLOGY OF ALPHA- AND BETA-ADRENERGIC AGONISTS RECEPTOR FUNCTION
PHYSIOLOGIC EFFECT
DOSING RANGE
DRUG
a1
b1
b2
SVR
MAP
CO
BOLUS (mg/kg)
Epinephrine
+
++
++
+/−
+
++
0.2 (1 mga)
0.03-0.15
+++
++
0
+++
+++
+/−
NR
0.03-0.15
++
++
+
+
+
++
NR
1-10
Norepinephrine Dopamine
INFUSION (mg/kg/min)
Isoproterenol
0
+++
+
++
+/−
+++
0.02-0.1
0.01-0.05
Dobutamine
(+)
+++
(+)
+/−
+/−
+++
NR
2-10
++
+
+
+
++
+
0.15-0.4
NR
+++
0
0
+++
+
−
0.5-0.2
0.5-2.0
Ephedrine Phenylephrine a
For cardiopulmonary resuscitation SVR, systemic vascular resistance; MAP, mean arterial pressure; CO, cardiac output; NR, not recommended. Modified from Stoelting K, Hillier S, eds. Pharmacology & Physiology in Anesthetic Practice. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.
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and other catecholamines will be diminished in patients taking beta-blocking drugs. There is a very high variability in the response between patients, and thus this drug should always be titrated carefully to the desired effect. Infusion through a central venous line is recommended for higher concentrations as extravasation can cause tissue necrosis. In general, solutions containing catecholamines for infusion should be prepared in 5% glucose to avoid deactivation in alkaline solutions.
■ NOREPINEPHRINE Norepinephrine is an endogenous hormone secreted from the adrenal medulla and is the neurotransmitter released from postganglionic adrenergic nerve endings following sympathetic nervous system stimulation. In addition, norepinephrine plays a role in the stress response and is secreted from noradrenergic neurons in the central nervous system. Norepinephrine must be infused intravenously (approximately 0.05-0.15 μg/kg/min) and has dose-dependent effects mediated via alpha1- and beta1-adrenergic receptors. In the lower dose range, increased heart rate and contractility through beta1 activation may result in a higher cardiac output. Unlike epinephrine, norepinephrine has little to no activity at beta2 receptors. Norepinephrine is a positive inotrope and is an excellent drug for the treatment of lowoutput, low vascular resistance heart failure. In higher doses, alpha1 activity predominates and norepinephrine causes a profound vasoconstriction in the vasculature of the kidney, liver, skeletal muscle, and skin. The resulting increase in systemic vascular resistance, reduced venous return, and increased arterial pressure can elicit reflex bradycardia (baroreceptor reflex), and cardiac output may actually decline. Norepinephrine is a drug of choice in shock states characterized by diminished peripheral vascular resistance such as severe septic shock. Like epinephrine, it reduces renal and splanchnic perfusion and may contribute to organ dysfunction particularly if the patient is hypovolemic. This can lead to renal failure and mesenteric infarction. In the pulmonary vasculature, norepinephrine increases vascular resistance by stimulation of alpha1 receptors that may contribute to pulmonary hypertension and right heart failure. Patients should be carefully monitored
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while receiving norepinephrine, and due to its very short half-life (approximately 2 minutes), a continuous infusion is recommended.
■ DOPAMINE Dopamine is an endogenous catecholamine and an important neurotransmitter in the central nervous system. It is the direct precursor in the biosynthesis of norepinephrine and has a highly dose-dependent effect on cardiac, vascular, and endocrine functions. In addition to beta1 and alpha1 activity, dopamine has specific effects on a group of dopaminergic receptors. Due to its fast metabolism, dopamine has to be given as a continuous intravenous (IV) infusion. In lower dose ranges of approximately 1-3 μg/kg/min, dopamine activates mainly dopamine-1 (D1) receptors that cause vasodilation and increased blood flow in the coronary, renal, and splanchnic vascular beds. Higher doses stimulate beta1 (3-10 μg/kg/min) and alpha1 adrenoceptors (>10 μg/kg/min). Dopamine at midrange doses will increase cardiac output by increasing stroke volume, but at higher doses, characterized by increased peripheral vasoconstriction, impedance to ejection may limit this action. Like other catecholamines, dopamine has arrhythmogenic properties at high doses. Because of the individual variability of effects of dopamine, the dose should always be titrated to effect.
■ SYNTHETIC CATECHOLAMINES AND PHOSPHODIESTERASE INHIBITORS Dobutamine Dobutamine is a selective beta1 agonist and must be given by continuous infusion due to its short half-life. This drug has predominantly beta1 activity. It is used to treat ventricular failure by increasing cardiac output by increasing myocardial contractility and heart rate. Doses between 2 and 10 μg/kg/min are commonly used. Lower doses have beta2 effects and can cause additional vasodilator actions, reducing systemic and pulmonary vascular resistance. Compared to dopamine, dobutamine is a coronary vasodilator improving blood flow to myocardium. Its use does not lead to significant increases in vascular resistance even at higher doses as does dopamine. Higher doses of dobutamine commonly cause tachyarrhythmias and ventricular ectopy, especially in the presence of myocardial ischemia. Similar to other catecholamines,
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dobutamine will increase oxygen demand of the heart and is often used in nonexercise cardiac stress testing. Dobutamine and other positive inotropic drugs can be combined with different pharmacologic agents such as vasodilators to enhance their actions to increase cardiac output.
Isoproterenol The clinical value of isoproterenol for improving contractility has diminished with the introduction of other inotropic drugs. It is the most potent agonist of beta1 and beta2 adrenoceptors and is primarily used to increase heart rate to overcome heart block. Due to its short halflife (5 minutes), it must be given by continuous infusion (1-5 μg/min) but may be injected intramuscularly or subcutaneously (0.2 mg). A low-dose infusion should be started and titration slowly increased to the desired ventricular rate. Isoproterenol increases heart rate and myocardial contractility while decreasing arterial pressure. These hemodynamic effects can cause large increases in myocardial oxygen demand and decreases in oxygen supply resulting in myocardial ischemia in patients with coronary artery disease.
Milrinone Milrinone is a PDE inhibitor indirectly leading to increased intracellular cAMP concentrations in cardiac and vascular smooth muscle. This subsequently increases contractility of the heart and causes vasodilation in arterial blood vessels resulting in afterload reduction. Milrinone is frequently used in cardiac surgery to improve ventricular pump function, particularly of the right heart, while simultaneously reducing pulmonary vascular resistance (and right ventricular afterload). In addition, this drug may have a positive effect on diastolic function. Milrinone is usually administered in a loading dose of 50 μg/kg followed by a maintenance infusion of 0.375-0.75 μg/kg/min. It is commonly used in combination with catecholamines. It will potentiate the effect of these agents by blocking the metabolism of cAMP, the concentration of which is increased by stimulation of beta adrenoceptors. Patients should be closely monitored during drug administration and the dose adjusted to hemodynamic or clinical endpoints, so as to avoid excessive hypotension and cardiac arrhythmias.
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■ MYOFILAMENT CALCIUM SENSITIZERS Levosimendan Levosimendan is member of a new group of inotropes termed myofilament calcium sensitizers. It increases the contractility of muscle cells by binding to a regulatory protein. This allows actin and myosin filaments to contract more quickly and with greater force without increasing the intracellular calcium concentration. Levosimendan also opens adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle and has PDE inhibition properties, which facilitate vasodilation of coronary, pulmonary, and systemic blood vessels, thereby reducing right and left ventricular afterload. This overall function leads to an increase in cardiac output while minimizing the risk of arrhythmias and with a more favorable balance of oxygen supply and demand as compared to catecholamines and PDE inhibitors. In clinical trials, this drug has been given as a loading dose of 6-12 μg/kg over 10 minutes followed by a continuous infusion of 0.05-0.2 μg/kg/min. Levosimendan is not yet FDA approved but has gained significant use in Europe and Asia.
■ VASOPRESSORS Vasopressin Vasopressin (arginine vasopressin [AVP]) is a hypothalamic peptide hormone released from the posterior pituitary gland in response to hyperosmolarity and hypovolemia. It regulates urine output in the kidney and is a very potent arterial vasopressor, which is mediated through receptors in blood vessel walls. Vasopressin is used clinically to counteract the profound vasodilation in septic shock or catecholamine-resistant, postcardiopulmonary bypass shock. Vasopressin demonstrates variability in arterial vasoconstriction with greater effects in the skeletal muscle and splanchnic vasculature and much less in coronary, cerebral, and pulmonary blood vessels. In cardiopulmonary resuscitation, vasopressin (40 U IV) is considered an alternative to the first or second dose of epinephrine in the treatment of pulseless cardiac arrest.
Phenylephrine Phenylephrine is an alpha1-adrenergic receptor agonist. Clinically, this drug has no positive inotropic activity in contrast to norepinephrine.
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It has similar actions to norepinephrine in the presence of blockade of beta receptors, only it is less potent and has a longer duration of action. It causes greater vasoconstriction in veins than in arteries and thus can increase cardiac output by increased venous return and stroke volume. Large increases in arterial pressure, however, can affect the increase in cardiac output by reflexively decreasing heart rate. All pure vasoconstrictors including phenylephrine when given in high doses can cause reduced blood flow to a variety of tissues resulting in ischemia. Vasoconstrictor agents are best used to reverse hypotension caused by reduced peripheral resistance.
Ephedrine Ephedrine is an indirect acting sympathomimetic agent and is commonly used by anesthesiologists to treat intraoperative hypotension secondary to general or regional anesthesia. It stimulates alpha and beta receptors directly and also increases norepinephrine concentrations at these receptors by releasing norepinephrine from adrenergic nerve terminals and therefore has actions very similar to those of norepinephrine. Bolus doses (5-10 mg IV) increase heart rate, blood pressure, and cardiac output similarly but of lesser magnitude as compared to epinephrine, and its duration of action is approximately 10-15 minutes.
■ ANTIHYPERTENSIVE MEDICATIONS Achieving hemodynamic stability of patients in the perioperative period can be challenging. Perioperative stress through anesthetic or surgical manipulation often contributes to high sympathetic nervous system activity with elevated arterial pressure and heart rate on the day of surgery. Large increases in blood pressures can cause significant morbidity and even mortality in conditions associated with cardiac and cerebrovascular events. Several classes of drugs have antihypertensive properties and can be used to manage blood pressure. These include direct vasodilators, beta-adrenergic blocking agents, and calcium antagonists.
■ VASODILATOR AGENTS Nitroprusside Nitroprusside is a direct vasodilator with a very rapid onset (1 minute) and very short duration of action (1-2 minutes) and should only be given by continuous infusion. Nitroprusside reduces pulmonary as well as systemic vascular resistance and
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is frequently used when fast and reliable reduction of blood pressure is needed. Although this agent is used to reduce afterload to enhance left ventricular ejection, nitroprusside also reduces preload. Reduction of arterial pressure in chronically hypertensive patients should be done with caution, as a rapid decrease in pressure may lead to ischemia in brain, kidney, or heart. Nitroprusside may cause vascular steal by diverting blood flow away from ischemic areas of myocardium. Doses from 0.1 to 2 μg/kg/min should be carefully titrated to the desired level of blood pressure and/or other hemodynamic parameter. Nitroprusside is deactivated by light, and thus the drug infusion reservoir must be adequately protected from light to prevent degradation and loss of potency. The nitroprusside molecule contains cyanide, and cyanide toxicity can develop from the breakdown of the drug, particularly after long-term or high-dose infusions. Cyanide toxicity leads to tissue hypoxia and acidosis despite high oxygen saturations by interrupting intracellular oxygen utilization.
Nitroglycerin Nitroglycerin directly relaxes vascular smooth muscle and has a greater effect on the venous versus arterial vasculature. This leads to pooling of blood in venous capacitance vessels and subsequent reduction in venous return to the heart with a decrease in right and left ventricular filling pressures. The latter results in a reduction in wall stress during systole and less energy consumption of the heart muscle. Nitroglycerin reduces pulmonary vascular resistance, increases coronary blood flow, and improves perfusion to ischemic regions of the heart. Stroke volume and cardiac output will decrease with lower preload in normal individuals, but in patients with myocardial ischemia improvement in coronary perfusion can result in increased cardiac output. All these effects make nitroglycerin a drug of choice in the management of chronic heart failure (CHF) and acute myocardial infarction. Higher doses of nitroglycerin can cause a decrease in blood pressure by reducing systemic vascular resistance, which may compromise coronary perfusion. Low doses of this drug in hypovolemic patients can also cause profound decreases in pressure. The onset of action is rapid, and the half-life of nitroglycerin ranges from 1 to 3 minutes. IV bolus doses of 20-100 μg can be used to titrate to
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effect, while continuous infusions range between 0.1 and 7.0 μg/kg/min and often provide more stable hemodynamic conditions. Nitroglycerin also dilates the cerebrovasculature, which may lead to increased intracranial pressures through increases in intracranial blood volume.
Hydralazine Hydralazine is a direct vasodilator and has a greater effect on arterial vessels than the venous system and is mainly used in acute hypertension. Blood vessels in muscle and skin are less affected than coronary, cerebral, and renal vessels. Hydralazine can trigger sympathetic nervous system stimulation by the baroreflex with an increase in heart rate and cardiac output. Compared to other direct vasodilators, the onset of action is relatively slow (5-15 minutes), which may make treatment of acute hypertension more difficult. In addition, hydralazine has a longer duration of action and therefore moment-to-moment control of arterial pressure as with nitroprusside is impossible. Finally, the efficacy of hydralazine is considerably less than that of other vasodilators.
Fenoldopam Fenoldopam is an agonist of D1 receptors (and to a lesser extent of alpha2-adrenergic receptors) and a rapidly acting vasodilator. It is approved for the management of severe hypertension when a rapid, easily reversible reduction in arterial pressure is warranted. It has strong vasodilator effects on the splanchnic and renal arterial vessels and increases renal perfusion, diuresis, and natriuresis. In the cerebral circulation, fenoldopam reduces global and regional blood flow. The half-life of fenoldopam is approximately 5 minutes, and infusion rates are commonly started at 0.05 μg/kg/min and subsequently titrated to the desired blood pressure response with doses up to 1.6 μg/kg/min. The diuretic effect is readily observed at lower doses. Compared to nitroprusside, fenoldopam does not carry as much risk of systemic toxicity especially at high doses.
■ CALCIUM CHANNEL BLOCKERS The ability of cardiomyocytes and vascular smooth muscle cells to contract is directly related to the intracellular concentration of calcium. Calcium enters the cardiomyocyte through special Ca2+ channels, which triggers an additional boost of Ca2+ release from stores in the sarcoplasmic reticulum. During systole, the Ca2+
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concentration increases and during diastole Ca2+ is pumped back into the sarcoplasmic reticulum enabling cardiac muscle to relax. Calcium channel blockers reduce the flow of Ca2+ into the cell and in turn cause a much smaller release of Ca2+ from the sarcoplasmic reticulum. All calcium channel blockers produce vasodilation and reduce arterial pressure, which leads to a reduction in left ventricular afterload. Calcium antagonists are used to reduce peripheral resistance in the management of hypertension and to treat cerebral vasospasm after subarachnoid hemorrhage. They also slow conduction and impulse formation in areas of the heart and can be used as antiarrhythmic agents. The various calcium channel blockers show differences in their affinity for vascular smooth muscle and cardiac muscle cells. Nifedipine and nicardipine are much more effective vasodilators than myocardial depressants, while verapamil is used for its ability to slow conduction through the heart and has little effect on vascular muscle tone. Diltiazem has vasodilator action as well as antiarrhythmic effects. In patients with acute heart failure, calcium channel blockers should be avoided due to their negative inotropic effects.
Nicardipine In clinical practice, nicardipine is a prototypical calcium channel blocker and is very effective in controlling perioperative hypertension, improving coronary perfusion in myocardial ischemia, or treating cerebral vasospasm after subarachnoid hemorrhage. It is associated with less rebound hypertension than other vasodilators, has a short half-life, and can be effectively titrated by continuous IV infusion (1-4 μg/kg/min).
■ BETA ADRENERGIC ANTAGONISTS (BETA BLOCKERS) Beta adrenergic blocking agents have a variety of effects on the cardiovascular system including reduction in heart rate, contractility, and myocardial oxygen consumption. Beta blockers play a role in the treatment of hypertension and have antiarrhythmic properties used mainly to treat atrial (supraventricular) arrhythmias. Due to their effect to slow conduction between atria and ventricles, these drugs can cause severe bradycardia and different severities of AV block (see Chapter 7). By antagonizing the effects of endogenous catecholamines on beta2 receptors,
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bronchospasm may be triggered in susceptible patients. The use of beta-blockers has been shown to reduce mortality in a variety of medical conditions, including hypertension, postmyocardial infarction, and CHF, and in high-risk vascular surgery patients. Beta-blockers differ in their affinity for betaadrenoceptor subtypes (e.g., beta1 selective), duration of action, coactivity on alpha-receptors (combined alpha- and beta-receptor antagonists), and intrinsic sympathominetic activity or the ability to both stimulate and block receptors (partial agonist properties). Beta-blockers are commonly used perioperatively to reduce and/or prevent excessive increases in heart rate.
Metoprolol Metoprolol is a cardioselective beta-blocker commonly used in the management of hypertension and coronary artery disease. Like most beta-blockers it undergoes extensive metabolism in the liver when given as an oral dose (first pass effect) reducing drug bioavailability. Effective oral doses are much higher (100-200 mg/d) compared to the IV dosing at 2.5-5 mg every 510 minutes. With its high affinity for beta1 receptors, this drug carries a smaller risk for bronchospasm in patients with asthma.
Labetalol Labetalol has nonselective competitive beta1-, beta2-, and selective competitive alpha1-adrenergic receptor blocking activity. Depending on oral or IV administration, the ratio of alpha to beta blockade is either 1:3 or 1:7, respectively, due to a profound first pass effect. Labetalol produces a dose-dependent reduction in blood pressure without reflex tachycardia. Doses of 0.25-0.5 mg/kg decrease arterial pressure within 5 minutes, and subsequent doses can be repeated in 5- to 10-minute intervals until the target blood pressure is reached. Cumulative doses of more than 3 mg/kg may be necessary in severe hypertensives. The duration of action of labetalol may be up to 18 hours.
Esmolol Esmolol is a cardioselective beta1 antagonist that has to be administered intravenously. Its popularity is due to a very rapid onset (25 mL), or if the aspirate contains particles such as chunks of food. A fiberoptic bronchoscope may be used to remove particulate matter.
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Bronchospasm occurs when the circumferential muscles lining the airways constrict and decrease airway diameters. This increases the resistance to airflow and makes both spontaneous and mechanical ventilation significantly more difficult. Bronchospasm can be accompanied by airway inflammation and edema, particularly with asthma or an infection. A foreign body in the airway can be a trigger for bronchospasm. In patients with reactive airway disease, the stimulation of an endotracheal tube in the airway can trigger bronchospasm. There are multiple other causes of bronchospasm. Treatment consists of inhaled and intravenous bronchodilators and anti-inflammatory medications (i.e., corticosteroids). Laryngospasm and stridor most commonly occur during induction or emergence from anesthesia. Laryngospasm is a spasmodic closing of the vocal cords spasmodically due to mechanical stimulation of the airway. The vocal cords are more sensitive to stimulation during emergence than they are at other times. The vocal cords may partially close, resulting in a high-pitched sound during inspiration called stridor. The vocal cords may close completely and prevent any gas movement. Treatment of laryngospasm includes positive pressure using a bag-mask system or muscle relaxation. Partial or complete upper airway obstruction may occur due to residual anesthesia or muscle relaxants. Methods of relieving upper airway obstruction include a jaw thrust maneuver to lift the tongue forward and create a patent passage for gas movement, or the insertion of a device into the airway (“oral airway”) that pushes the tongue forward to allow space for gas flow. A nasal airway that stents open the oropharynx can be used as well. Hypoventilation is common after anesthesia due to the effects of anesthetic agents and opioids used for pain relief. These medications decrease the drive to breathe by affecting areas of the brain that are responsible for regulating carbon dioxide levels. Patients may have a slow respiratory rate and/or small tidal volume, which results in hypoventilation. CO2 levels in the blood can rise significantly, and if the hypoventilation is severe, blood oxygen levels will fall. In some cases, oversedated patients can stop breathing (apnea).
Abnormalities in a patient’s upper airway anatomy can make either mask ventilation or endotracheal intubation difficult. The inability to ventilate a patient during the induction of anesthesia is a true emergency and if not corrected can lead to severe patient morbidity or even death. Airway management is covered in Chapter 18, and airway emergencies are covered in Chapter 60.
■ SUMMARY One of the roles of an anesthesia provider in the operating room is to ensure that patients maintain optimum respiratory function, despite the physiologic aberrations that result from sedation, analgesia, general anesthesia, or muscle relaxation. Understanding upper and lower respiratory anatomy, respiratory physiology, and perturbations caused by anesthesia, respiratory pharmacology, surgery, and patient comorbidities help the anesthesia provider formulate an effective anesthetic plan that decreases the risk of perioperative complications. The anesthesia plan will include the type of anesthetic, a plan for airway management, and a plan for managing ventilation. During the course of the anesthetic, the anesthesia provider will make use of multiple devices to monitor respiratory function.
REVIEW QUESTIONS 1. Which of the following are functions of the lung? A) Warm and humidify inspired gases B) Deliver oxygen to the blood C) Remove carbon dioxide from the blood D) Filter inspired air E) All of the above Answer: E. All of the above represent the main functions of the lung.
2. Which of the following are functions of the UPPER airway? A) Prevent alveoli from collapsing B) Deliver oxygen to the blood C) Remove carbon dioxide from the blood D) Filter inspired gases E) None of the above Answer: D. Both the nose and the mouth, parts of the upper airway, play a role in filtering inspired gases. Oxygenation of blood and removal of carbon dioxide occur in the alveoli that are part of the lower airway.
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Chapter 11 • The Respiratory System 3. Which of the following structure is NOT a part of the upper airway? A) Nose B) Mouth C) Trachea D) Pharynx E) Larynx Answer: C. The nose, mouth, pharynx, and larynx constitute the upper airway. The trachea is part of the lower airway.
4. What is the purpose of the conducting airways? A) Filter gases B) Heat gases C) Direct gases to the respiratory airways D) Participate in gas exchange E) None of the above Answer: C. The conducting airways do not participate in gas exchange and form part of the anatomical dead space of the lung. They are conduits to direct gases to the respiratory airways and alveoli where gas exchange occurs. Filtration and heating of gases occur primarily in the nose.
5. What is the main muscle of respiration? A) Diaphragm B) External intercostal muscle C) Internal intercostal muscle D) Sternocleidomastoid E) None of the above Answer: A. The diaphragm is the main muscle of respiration. Contraction of the diaphragm pushes the chest wall out and the abdominal contents down. These actions cause an increase in intrathoracic volume and a decrease in intrathoracic pressure. The intercostal muscles and the sternocleidomastoid muscle are accessory muscles of respiration. They are utilized to augment the diaphragm if a larger inspiration is necessary.
6. What determines the oxygen reserve available in the lungs after induction of general anesthesia? A) Total lung capacity B) Functional residual capacity (FRC) C) Tidal volume D) Inspiratory reserve volume E) All of the above Answer: B. The FRC is the volume of gas in the lungs at the end of a normal exhalation. If a patient were to become apneic, this volume of gas and its residual oxygen form a reserve of oxygen that can be taken up into the bloodstream. Once this oxygen reserve is exhausted, the blood oxygen will fall. Patient factors like morbid obesity that reduce the FRC increase the risk of desaturation during the induction of general anesthesia.
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7. What is the term for the volume of gas moved during quiet ventilation? A) Tidal volume B) Total lung capacity C) Expiratory reserve volume D) Residual volume E) Inspiratory reserve volume Answer: A. The tidal volume is the volume of gas moved during a normal inhalation and exhalation. The inspiratory reserve volume is the amount of extra gas that can be taken in from a maximal inspiration. The total lung capacity is the total volume in the lungs after a maximal inspiration. The residual volume is the volume left in the lungs after a maximal exhalation. The extra amount of gas that can be expired after a normal exhalation is the expiratory reserve volume.
8. What structures protect the trachea from aspiration of stomach contents? A) Tongue B) Alveoli C) Conducting airways D) Vocal cords E) Mainstem bronchus Answer: D. The epiglottis and the vocal cords work in concert to occlude the entrance to the trachea to prevent aspiration. The vocal cords close and the epiglottis covers the vocal cords.
9. Where in the lungs does gas exchange occur? A) Trachea B) Carina C) Conducting bronchioles D) Alveoli E) All of the above Answer: D. The trachea, the bronchi, and the conducting bronchioles all are conducting airways that direct the gas to the alveoli. Gas exchange occurs in the alveoli where the lung tissue is very thin and the capillaries come in close contact with the alveoli to allow gases to diffuse. The carina is the junction where the distal trachea divides into the two mainstem bronchi.
10. What is dead-space ventilation? A) Ventilation during basic life support B) Regions of the lung that receive ventilation but not perfusion C) Regions of the lung that receive perfusion but not ventilation D) The volume in the lungs after a maximal expiration E) The volume in the lungs after a maximal inspiration Answer: B. When alveoli are ventilated but not perfused, no gas exchange takes place and it is referred to as dead space. When alveoli are perfused but not ventilated, no gas exchange takes place and it is referred to as shunt. It is as if
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Section II • Anatomy, Physiology, and Pharmacology the blood was “shunted” by the lungs without participating in gas exchange. The volume in the lungs after a maximal expiration is the residual volume. The volume in the lungs after a maximal inspiration is the total lung capacity.
11. How does the respiratory system participate in maintaining a physiologic pH? A) Respiratory function maintains CO2 homeostasis. B) CO2 can form carbonic acid. C) The brainstem modulates respiratory function in response to pH changes. D) Hyperventilation can decrease CO2 levels in response to acidosis. E) All of the above. Answer: E. All of the above. The respiratory system plays a critical role in acid-base balance. Because CO2 can be converted to carbonic acid, CO2 levels affect the pH of the blood. The brainstem adjusts minute ventilation in response to pH changes in the blood. Changing minute ventilation, either up or down, will affect CO2 levels and can compensate for the pH change. Hyperventilation decreases CO2 levels and decreases carbonic acid in the blood.
12. Which monitor is NOT used to monitor ventilation? A) End-tidal carbon dioxide B) Esophageal stethoscope C) Pulse oximetry D) Arterial blood gas E) Central venous pressure Answer: E. The central venous pressure is used to monitor blood volume. The remaining monitors are all used to monitor ventilation.
SUGGESTED READINGS Barrett KE, Barman SM, Boitano S, et al. Pulmonary function. In: Barrett KE, Barman SM, Biotano S, et al., eds. Ganong’s Review of Medical Physiology. 23rd ed. New York, NY: McGraw-Hill Medical; 2010: Chapter 35. Boer F. Drug handling by the lungs. Br J Anaesth. 2003:91(1):50–60. Conti G, Dell’Utri D, Vilardi V, et al. Propofol induces bronchodilation in mechanically ventilated chronic obstructive pulmonary disease (COPD) patients. Acta Anaesthesiol Scand. 1993;37:105–110. Hashiba E, Hirota K, Suzuki K, et al. Effects of propofol on bronchoconstriction and bradycardia induced by vagal nerve stimulation. Acta Anaesthesiol Scand. 2003;47(9):1059–1063. Kabara S, Hirota K, Hashiba E, et al. Comparison of relaxant effects of propofol on methacholine-induced bronchoconstriction in dogs with and without vagotomy. Br J Anaesth. 2001;86(2):249–253. LeBlond RF, Brown DD, DeGowin RL. The chest: chest wall, pulmonary, and cardiovascular systems; the breasts. In: LeBlond RF, Brown DD, DeGowin RL, eds. DeGowin’s Diagnostic Examination. 9th ed. New York, NY: McGrawHill Medical; 2009:302–332. Levitsky MG. Pulmonary Physiology. 7th ed. New York, NY: McGraw-Hill Medical; 2007. Morgan GE Jr, Mikhail MS, Murray MJ, eds. Respiratory physiology: the effects of anesthesia. In: Clinical Anesthesiology. 4th ed. New York, NY: McGraw-Hill Medical; 2005: Chapter 22. Prendergast TJ, Ruoss SJ, Seeley EJ. Pulmonary disease. In: McPhee SJ, Hammer GD, eds. Pathophysiology of Disease. 6th ed. New York, NY: McGraw-Hill Medical; 2003.
13. Which medications cause bronchodilation? A) Beta agonists B) The volatile anesthetics sevoflurane and isoflurane C) Neostigmine D) A and B E) B and C Answer: D. Beta agonists (e.g., albuterol, epinephrine) are potent bronchodilators. Volatile anesthetics (e.g., sevoflurane and isoflurane) cause bronchodilation. Desflurane produces minimal bronchodilation and is a potent airway irritant (causes coughing and breath holding). Neostigmine blocks the breakdown of acetylcholine, which is a potent vasoconstrictor.
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Acid and Base Physiology Aaron Kirsch and Jeffrey Kirsch ■ INTRODUCTION There is a vast amount of water in the human body, distributed as the cytoplasm within cells (intracellular fluid) and the extracellular fluid, which includes plasma. Dissolved in all of this water are a wide variety of solutes. Among the most important solutes are acids and bases. Acids are compounds that, when dissolved in water, will donate a hydrogen ion (H+). Bases are compounds that, when dissolved in water, will accept an H+ from an acid. Examples of acids include hydrochloric acid (HCl) or carbonic acid (H2CO3); examples of common bases include ammonia (NH3) or sodium hydroxide (NaOH). We measure the concentration of acid in the body fluids using the pH scale. The pH of a solution is defined as follows: pH = − log ⎡⎣H + ⎤⎦ where [H+] is the concentration of H+. If there is an abundance of acid in the fluid, there will be a high [H+]. This corresponds to a low pH. Therefore, the lower the pH measurement, the more acidic is the fluid. If there is an abundance of base in the solution, there will be a relatively lower [H+], because bases will eagerly accept and incorporate free H+. This corresponds to a high pH. Therefore, the higher the pH measurement, the more alkaline (basic) is the fluid. In chemistry, a pH of 7 is considered neutral, a pH less than 7 is considered acidic, and a pH greater than 7 is considered alkaline. In human physiology, however, the optimal pH of arterial blood is 7.4 or slightly alkaline. Venous blood will have a lower pH, as it is carrying waste from the periphery for removal by the lungs, kidneys, liver, and bowel. The balance between acids and bases is crucial to proper body functioning. Even slight deviations from a pH of 7.4 can result in serious pathologic consequences. For example, reduction in
pH to less than 7.0 can be fatal. This is because the organs and tissues of the body depend on the functionality of their cells. The functional actors in cells are enzymes, special proteins that catalyze chemical reactions. Alterations to the body’s acid-base balance change the chemical structure of enzymes, rendering them dysfunctional. This may result in organ malfunction. When the pH of the plasma is less than 7.4, the plasma is acidotic. When the pH is greater than 7.4, it is alkalotic.
■ PHYSIOLOGIC CONSEQUENCES OF ACID-BASE DISTURBANCES In the operating room (OR), acidosis produces its most significant and obvious effects on the cardiovascular system. As pH drops to 7.2, there is a noticeable reduction in heart muscle contractility and at a pH of 7.1, the entire cardiovascular system becomes much less responsive to catecholamines, making it very difficult for the anesthesiologist to treat hypotension with commonly used agents (e.g., norepinephrine, phenylephrine, ephedrine). Acidosis also causes hypotension due to peripheral arteriolar dilatation and constriction of the pulmonary arteries. Importantly, acidosis results in shifting of potassium out of cells and into the general circulation, which then may result in additional cardiac dysfunction.
■ RESPIRATORY ACID-BASE DISTURBANCES The acids in the body come from a variety of sources. When proteins are metabolized, weak acids are released into the bloodstream. But the main contribution of acid comes from a gas. When cells metabolize fats and carbohydrates, carbon dioxide (CO2) gas is produced. Inside of cells, this CO2 dissolves in the cytoplasm, producing H2CO3. 101 tahir99-VRG & vip.persianss.ir
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The enzyme carbonic anhydrase (CA) rapidly converts this H2CO3 into H+ and HCO3− (bicarbonate), which can be illustrated as follows: CA CO2 ↔ H2CO3 ↔ H + + HCO3 − As illustrated above, CO2 production results in an increase in [H+]. This translates into a lower pH. Therefore, excess CO2 leads to acidosis. If CO2 were not removed from the body, acid would build up and pH would decrease dramatically. Fortunately, the CO2 produced in metabolism is transported in the bloodstream to the lungs. Here, it is removed from the blood in exchange for oxygen (O2) and is breathed off into the environment. CO2 travels in the blood in three forms. The majority of CO2 dissociates into H+ + HCO3−. The H+ binds to hemoglobin molecules (Hb⋅H+), while the HCO3− travels freely in the plasma. Once at the lungs, the H+ and HCO3− recombine to form CO2, where it is exhaled. A small amount of CO2 also travels as dissolved CO2, and a small amount binds directly to hemoglobin (Hb⋅CO2). When acidosis is caused by the lungs being unable to breathe off CO2, it is termed respiratory acidosis. When alkalosis is caused by the lungs breathing off too much CO2, it is termed respiratory alkalosis. Respiratory acidosis occurs when ventilation is impaired. For instance, the diaphragm or intercostal muscles may be paralyzed or too weak. A paralyzed diaphragm can be commonly observed following interscalene blockade, whereas intercostal muscles become weak in patients with a high spinal anesthetic. Patients who are administered opiate drugs will also have a predictably depressed breathing rate. Patients with respiratory acidosis may appear anxious or delirious, or even have myoclonic convulsions or seizures in extreme cases. The acidosis is best treated by increasing ventilation (breathing rate), by treating the underlying cause, or, if necessary, by mechanically ventilating the patient (oxygen treatment). Other common causes of respiratory acidosis include pulmonary disease that impairs gas exchange (e.g., chronic obstructive pulmonary disease). Respiratory acidosis also occurs when there is excess production of CO2, beyond the ability of the patient’s ventilatory ability. For example, in patients who are anesthetized and mechanically ventilated (i.e., have a fixed ventilation), excess CO2 production may occur
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from high fevers or malignant hyperthermia. Decreased ability to clear CO2 from the lungs may occur secondary to extremely compromised pulmonary function. Respiratory alkalosis occurs due to hyperventilation (breathing too fast). This happens in patients suffering anxiety attacks. It is also seen in patients with pulmonary embolisms (blood clots that typically travel from the legs to the lungs), liver failure, pregnancy, and an overdose of aspirin. Patients might present with arrhythmias (irregular heartbeats), muscle cramps, tingling sensations, or even seizures. Although correcting the underlying cause is essential, hyperventilation can be urgently treated with sedating drugs if necessary. Oxygen (O2) is another important gas in maintaining acid-base balance. It is inhaled from the environment and enters capillaries in the lungs in exchange for CO2. If breathing is impaired, O2 cannot enter the lungs to be exchanged with CO2. As shown above, the buildup of CO2 in the blood results in acidosis. Furthermore, O2 is essential for aerobic metabolism. When cells lack O2, they produce energy via anaerobic glycolysis. Prolonged glycolysis causes the accumulation of lactic acid. This results in further acidosis. Low O2 supply to the tissue may result from systemic hypoxia (e.g., high altitude, poor pulmonary gas exchange) or compromised circulation to an individual body region (local ischemia). Global ischemia may be caused by overall poor circulation (e.g., cardiac failure or severe hypotension), while local ischemia may be secondary to surgical intervention (e.g., aortic cross-clamp, limb tourniquet) or patient disease (arterial blood clot, peripheral vascular disease, trauma, etc.).
■ ARTERIAL BLOOD GASES Because O2 and CO2 are important factors in determining acid-base balance, being able to measure their partial pressures (concentrations) in the bloodstream can provide valuable insight into the physiologic condition of the patient. This is accomplished by arterial blood gas measurement (ABG). A sample of blood is drawn from an artery and is placed into a blood gas analyzer device (See Chapter 37). This device uses a variety of electrochemical probes to measure the pH and the partial pressures of O2 and CO2. It is important to understand that the [HCO3−] is
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calculated and not directly measured by most blood gas machines. Assessment of a patient’s acid-base status from a reading on the blood gas analyzer can depend on the temperature of the patient and the temperature setting on the machine performing the measurement. Two different approaches exist: “alpha-stat” and “pH stat.” In blood, the pH changes inversely with temperature. Thus, at temperatures below 37°C, a pH of 7.4 would be considered acidotic. With the pH-stat approach, the anesthesia technician will run the blood sample entering the patient’s temperature into the blood gas machine, while with the alpha-stat approach, all blood gases are run at 37°C. Since there is great controversy among anesthesiologists regarding the best approach (alpha or pH-stat), the anesthesia technician should ask anesthesiologists their preference before analyzing the sample blood on the blood gas machine. When obtaining a patient’s vital signs during an operation or at the bedside, oxygen saturation (“pulse ox”) is often measured by clipping a pulse oximeter probe to the fingertip (see Chapter 33). Both the red and infrared waves emitted by this probe allow for the measurement of the amount of hemoglobin in the blood that is bound to the oxygen (Hb⋅O2). This defines oxygen saturation (SaO2). Although this gives us a good estimate of oxygenation, it does not tell us anything about CO2 or acid-base balance. This is why we must examine the ABG. ABG is obtained in the following manner. First, you must evaluate the arteries of the patient. Because of ease of access and the presence of a redundant circulation to the hand via the ulnar artery, the radial artery is typically used. You can palpate the radial artery pulse by placing one or two fingers just proximal (above) to the hand on the anterior-lateral (front, thumb side) surface of the wrist. Next, some clinicians try to assess the collateral circulation of the hand. They argue that if the radial artery is damaged during the procedure, it is important to be assured that collateral circulation to the hand via the ulnar artery is intact. The test that is done is called the Allen test. Those who use this test will choose an alternate site (e.g., femoral artery) for drawing an ABG if the Allen test demonstrates poor collateral circulation in the hands. However, a number of authors have demonstrated that the Allen test has very limited predictive value, regardless
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of whether it demonstrates good or poor collateral circulation via the ulnar artery. Therefore, this test is not used very often in clinical practice. In order to perform the Allen test, 1. The patient should extend the hand at the wrist 2. The patient should make a fist 3. The clinician should compress both the radial and ulnar arteries at the patient’s wrist 4. Have the patient open and close a tight fist several times 5. The palm should appear white, as it is not receiving any blood flow 6. Release your hold on the ulnar artery, restoring ulnar blood flow If there is good ulnar circulation, the palm should become red within 5-10 seconds (maximum of 15 seconds) after restoring ulnar blood flow. A palm that remains white constitutes a failed Allen test, meaning that ulnar flow is too poor for an ABG to be measured in this hand. If your hospital has preassembled kits for ABG measurement, they should be used. A 23-gauge (or smaller) needle is used, along with a preheparinized syringe, containing 30-100 units of heparin per milliliter of blood to be obtained. A syringe with too much heparin risks diluting the sample. When preassembled kits for ABG measurement are not readily available, the inside of a regular syringe can be lightly coated or rinsed with heparin (usually 1,000 unit/mL strength), taking care to remove as much liquid heparin from the syringe as possible. Glass syringes are preferable to plastic. The ABG sample is obtained as follows: 1. Clean the wrist with chlorhexidine, alcohol, or betadyne. 2. Prepare the puncture site with sterile drapes (towels). 3. The clinician should be wearing sterile gloves and a face mask. 4. Extend the patient’s wrist 30-45 degrees. 5. Your nondominant hand should palpate the point of maximal pulsation over the radial artery. 6. Local anesthetic should be infiltrated at the site prior to arterial puncture. 7. With your dominant hand, position the needle at an angle of 45 degrees and enter the radial artery just distal to where your other hand is palpating.
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8. Blood will fill the syringe spontaneously in specialized ABG syringes but will need to be withdrawn in standard syringes. 9. Expel any air bubbles from the syringe. 10. Send the sample (be sure it is labeled correctly) immediately to the laboratory for analysis. 11. After removing the needle, have the patient apply direct pressure over the site for 5 minutes. In the OR many patients who require frequent analysis of an ABG will have an indwelling catheter in a peripheral (usually radial) artery. Some institutions use arterial monitoring sets that include a blood withdrawal chamber in a closed system that minimizes blood wastage and contamination. With these sets, blood is drawn back into the chamber and the arterial blood sample is withdrawn from a special sampling port. Withdrawal of the appropriate amount of blood into the chamber ensures that pure blood is at the sampling site and not blood that has been mixed with the arterial line flush solution. After obtaining the blood sample for ABG analysis, the blood in the chamber, which will be a mixture of blood and dead-space fluid from the catheters, is infused back toward the patient. Finally, the catheter is flushed using a pressurized fluid system (using a pressurizing compression bag) to prevent blood clotting in the tubing system. Some institutions do not utilize the closed system tubing configuration. In this situation, the clinician will attach a sterile syringe to the stopcock that is most proximal to the patient and withdraw at least three times the amount that is included as dead space in the tubing system. The withdrawn blood must then be discarded and additional blood drawn to fill the ABG syringe. Finally, flush the tubing system with saline (or heparinized saline) to prevent blood from clotting in the tubing. There are certain pitfalls in ABG measurement that should be avoided. First, there should be minimal delay in transporting the sample to the analyzer. Within the blood sample, there are cells whose metabolic activity will alter the partial pressures of CO2 and O2. If you anticipate a delay of more than 10 minutes, the sample should be cooled on ice for no more than 1 hour to slow this metabolic activity. In cases of delay, glass syringes are superior as gases may dissolve over
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a short period of time in plastic. Additionally, any small air bubbles should be expelled from the syringe, as they result in inaccurate analysis (gas from the bubble can diffuse into the blood or gas in the blood can diffuse into the bubble). Large air bubbles indicate an unusable sample that should be discarded. Complications for the patient include mistaken venous sampling, hematoma, excessive bleeding, occlusion of the artery, and infection. A venous blood sample will have higher pCO2 and lower pO2 than arterial blood, and the values may not correspond to the patient’s clinical condition.
■ ABG INTERPRETATION The first step when evaluating an ABG is to determine if the pH is in the normal range of 7.35–7.45. Thus, if the patient’s pH is below 7.35, the patient is acidotic, and if it is higher than 7.45, the patient is alkalotic. Next, review the pCO2. When deviations in pCO2 account for changes in the pH, the patient is said to have a respiratory acid-base disorder. If the pCO2 is above 45 in acidotic patients, the patient has respiratory acidosis; if the pCO2 is below 35 in alkalotic patients, the patient has respiratory alkalosis. Next, it is important to analyze the HCO3- (normal 22-26 mEq/L). When the direction of change in HCO3- matches that of the pH, the patient is said to have a metabolic acidbase disorder. If HCO3- is below 22 in acidotic patients, the patient has metabolic acidosis, and if HCO3- is above 26 in alkalotic patients, the patient has metabolic alkalosis. Finally, patients may have alterations in both CO2 and HCO3-. In some cases, this is due to disorders in different organ systems. In other cases, the patient’s body is attempting to compensate for an acid-base disorder and restore the pH to as close to normal as possible. In these patients, the primary cause of the disorder (respiratory or metabolic) tracks the change in pH. Thus, a patient who has a low pH, a high pCO2, and a high HCO3- is said to have a primary respiratory acidosis with a compensatory metabolic alkalosis. Similarly, a patient who has a low pH, a low HCO3-, and a low pCO2 is said to have a primary metabolic acidosis with compensatory respiratory alkalosis.
■ METABOLIC ACID-BASE DISTURBANCES Besides the H+ generated from CO2, other metabolic processes—such as protein breakdown—generate
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acids such as H2SO4 and H3PO4. It is the responsibility of the kidneys to excrete enough H+ in the urine to ensure that excess acid is not retained in the body. Furthermore, feces are rich in HCO3−, and so every bowel movement results in loss of HCO3−, a base. Again, it is the responsibility of the kidneys to reabsorb enough HCO3− to balance these losses. When the kidneys are unable to adequately excrete H+ or fail to reabsorb enough HCO3−, acidosis results. This sort of acidosis is termed metabolic acidosis. Added H+ is moderated to a limited extent by the body’s buffer system. Buffering is the process by which increases in H+ concentration are partially bound to other molecules to reduce the amount of free H+ and its attendant impact on pH. Buffers can also absorb HCO3−. Finally, molecular buffers can release H+ or HCO3− to counteract pH changes when the concentration of H+ or HCO3− is falling. Hemoglobin buffers pH by directly binding H+. Bone can buffer pH during extreme acidosis by releasing HCO3− into the circulation. But the most important buffer is plasma HCO3−. As acid accumulates in the bloodstream, H+ combines with HCO3−. H2CO3 forms almost immediately and becomes CO2, which can be exhaled. Yet, if the body is overloaded with acid, the HCO3− buffer is exhausted and ceases to be effective. It is then that metabolic acidosis seriously affects the pH. When attempting to find the cause of a metabolic acidosis, you will find valuable clues in the concentrations of electrolytes (ions) in the patient’s blood. Plasma is electrically neutral— all of its positively charged constituents (cations) are balanced by an equal number of negatively charged constituents (anions). The major cations are sodium (Na+), potassium (K+), calcium (Ca2+), and magnesium (Mg2+). The major anions are HCO3−, chloride (Cl−), and proteins. Out of all these ions, Na+, HCO3−, and Cl− are considered the major, “measured,” ions. And, the difference in concentration between the measured cations and the measured anions is called the anion gap. Anion gap = ⎡⎣Na + ⎤⎦ – ( ⎡⎣ HCO3 − ⎤⎦ + ⎡⎣Cl − ⎤⎦ ) Normally, the anion gap ranges from 8 to 12. This reflects the concentration of the so-called unmeasured anions, mainly proteins. In a patient with diarrhea, extensive amounts of base, HCO3−, are lost in the stool. This results
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in a metabolic acidosis. As HCO3− is lost from the bloodstream, Cl− shifts from within cells to the bloodstream, replacing the lost negative charges, thus preserving electrical neutrality. Because the rise in [Cl−] offsets the fall in [HCO3−], there is no change in the anion gap. This is termed normal anion gap metabolic acidosis. It is treated by replacing lost fluids and electrolytes and quieting the underlying gastrointestinal disturbance. In severe cases, NaHCO3 (a base) may be gradually infused to raise the pH. Normal anion gap metabolic acidosis also occurs when the kidneys fail to reabsorb HCO3− due to damage to kidney tubule cells, when the CA enzyme is inhibited by medications (e.g., acetazolamide), and when there are deficiencies in the hormone aldosterone. One of the most common causes of metabolic acidosis in the OR is excessive infusion of chloride-containing fluid. This usually results from the anesthesiologist administering intravenous (IV) fluid in the form of normal saline (0.9% sodium chloride). Increases in blood chloride concentration causes the kidneys to excrete HCO3−, and the patient can become acidotic. Unfortunately, this acidosis is often not recognized to be secondary to excess chloride administration, with clinicians confusing this acidosis as being secondary to poor perfusion. The clinician may administer “volume resuscitation” with normal saline, making the acidosis and patient’s condition worse. When acids are added to the plasma, the acid dissociates into its ionic components. H − A → H+ + A − The added H+ combines with plasma HCO3−, depleting it. But, since the acid’s dissociation produces an anion (A−), there is no need for Cl− to shift from the cells to the plasma, because the lost negative charges of HCO3− are balanced by the added A−. Since neither [Na+] nor [Cl−] changes, while [HCO3−] decreases, the anion gap becomes larger. Such a situation is labeled increased anion gap metabolic acidosis. Certain causes of increased anion gap metabolic acidosis are commonly encountered. In the perioperative setting, the most common cause is lactic acidosis from poor perfusion. In patients whose tissues are starved of oxygen (e.g., systemic hypoxia, decreased blood flow to organs, or rarely carbon monoxide poisoning), anaerobic
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glycolysis predominates. The end product of this process is lactic acid, which results in an increased anion gap metabolic acidosis. In the OR, lactic acidosis is most common during prolonged periods of hypotension or when a large percentage of the body is excluded from normal circulation (e.g., aortic cross-clamp during aortic artery surgery). Severe ischemia, hypoxia, or shock is likely to increase the blood concentration of lactic acid. In critically ill patients, a lactic acid concentration of less than 2 mmol/L can be considered normal. With lactic acid levels of 2-5 mmol/L, the body can usually compensate and the patient may not present as being acidotic. However, lactic acid levels of greater than 5 mmol/L are usually associated with systemic acidosis. Treatment includes improvement of circulation (e.g., pharmacologic treatment of hypotension or removal of cross-clamps) and IV fluid rehydration (for decreased blood flow to organs). In the case of systemic hypoxia (e.g., congestive heart failure or poor lung function), treatment includes administering 100% oxygen therapy by using mechanical ventilation with aggressive use of positive end-expiratory pressure. Other causes of increased anion gap acidosis occur when acids other than lactic acid accumulate in the body. Aspirin (aminosalicylic acid) overdose decreases the pH and fills the blood with salicylate anions. This is best treated by preventing further aspirin absorption (using activated charcoal) and by alkalinizing blood and urine to encourage salicylate elimination (administer NaHCO3 until the blood pH is higher than 7.45). Patients with kidney failure are unable to excrete H3PO4 or H2SO4, resulting in the accumulation of metabolic acids. This is remedied by hemodialysis. Patients with poorly controlled type-1 diabetes mellitus accumulate keto acids (e.g., acetoacetic acid) leading to the emergency situation of diabetic ketoacidosis. This is best treated with insulin and IV fluid rehydration. When the kidneys excrete too much H+, the result is alkalosis. This sort of alkalosis is termed metabolic alkalosis. When a person vomits, HCl is expelled from the stomach. Similarly, inserting a suctioning nasogastric (NG) tube into the stomach to relieve a patient’s gastrointestinal distress also removes HCl. This loss of acid causes metabolic alkalosis. In order to reclaim the fluid volume lost, the kidneys reabsorb more Na+ and water. The Na+ is reabsorbed in exchange for H+, which is excreted
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from the bloodstream into the urine, exacerbating the metabolic alkalosis. This latter sort of alkalosis is also caused by diuretic drugs (e.g., furosemide) that cause volume loss by increasing urination. Properly rehydrating the patient with IV fluids corrects all of these alkaloses. Certain tumors produce an excess of the hormone aldosterone. Increased aldosterone results in metabolic alkalosis by causing increased Na+ reabsorption in exchange for H+. Aldosterone’s actions can be blocked by medications (e.g., spironolactone) or by surgical removal of the tumor. Although there are many causes of pH disturbances, ABG results, analysis of electrolytes and the anion gap, and patient history can point you toward a diagnosis and direct subsequent treatment.
■ COMPENSATION Changes in pH disrupt healthy body functioning. Fortunately, the body has built-in mechanisms to correct disturbances to its acid-base balance. In patients who are not anesthetized and have metabolic acidosis or alkalosis, ventilation (breathing rate) rapidly adjusts. Breathing faster expels CO2 more rapidly with each exhalation. The removal of CO2 is equivalent to breathing off H+, which makes the pH less acidic. Breathing rate, though, cannot increase infinitely, and this limits the effectiveness of respiratory compensation. On the other hand, breathing more slowly causes less CO2 to be exhaled. Thus, more H+ is retained, and the pH becomes more acidic. Breathing rate can only decrease a certain amount to compensate for alkalosis. This is because a decrease in ventilation also causes a decrease in O2 intake. Consequently, decreased ventilation never lowers the pH quite to 7.4. The body acts as its own blood gas analyzer by using chemoreceptors. A chemoreceptor is an apparatus that detects concentrations of chemicals. It consists of a sensor that relays information to an integrator. This integrator then instructs an effector to respond accordingly. There are two groups of chemoreceptors in charge of ventilation: peripheral and central. The peripheral chemoreceptors are located in the aortic body (near the heart) and the carotid body (in the neck). They detect pO2, increasing ventilation when pO2 decreases. The central chemoreceptors are located in the medulla of the brainstem (between the cerebrum and the spinal cord). They detect pCO2 and strive to maintain it at 40 mm Hg.
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In metabolic acidosis, when H+ is increased, increased CO2 is present in the central nervous system. Central chemoreceptor sensors send a signal to the respiratory centers of the brainstem, which instruct the lungs to increase ventilation. This increase in ventilation, which occurs minutes after the pCO2 is increased, decreases the pCO2. In this way, pH change is minimized. When metabolic or respiratory acid-base balance is disturbed for a prolonged period of time, further compensation is provided by the kidneys. They are responsible for maintaining optimal concentrations of electrolytes in the blood. Although their function is very complex, they essentially act as intelligent filters. As blood passes through the kidneys, electrolytes are reabsorbed back into the bloodstream, or they may be expelled by the kidney into the urine. The kidney senses alterations in voltage and pH and adjusts its filtering accordingly. For instance, if the blood pH is too acidic, the kidney secretes excess H+ into the urine, while simultaneously reabsorbing HCO3− back into the bloodstream. Nevertheless, this compensation never brings the pH back to a normal 7.4. In other words, a chronic (prolonged) acidosis will be compensated to a pH less than 7.4, while a chronic alkalosis will be compensated to a pH greater than 7.4.
■ SUMMARY Acid-base balance is crucial for normal physiologic functioning. Alterations in ventilation cause changes in pCO2. This results in respiratory acidosis or respiratory alkalosis. The loss of HCO3− via bodily excretions, and the accumulation of acids from metabolism and ingestions, results in metabolic acidosis. The body has its own mechanisms to compensate for alterations in pH. Within minutes, ventilation adapts to compensate metabolic acid-base disturbances. After 1 day, the kidney begins to compensate for both metabolic and respiratory acid-base derangements. Unfortunately, the body’s compensatory mechanisms can be overwhelmed. It is essential to treat the underlying cause of the acid-base disturbance, as it may easily become life-threatening. Measurement and analysis of an ABG, electrolytes, lactate level, and anion gap, as well as patient history, will guide diagnosis and treatment.
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REVIEW QUESTIONS 1. Infusing pure HCl will have what effect on H+ and pH? A) Increase H+; increase pH B) Increase H+; decrease pH C) Decrease H+; decrease pH D) Decrease H+; increase pH E) Unchanged H+; unchanged pH Answer: B. HCl is an acid. It will donate its H+, so that the concentration of H+ will increase. An increase in H+ translates to a decrease in pH. If a base were infused instead, there would be a decrease in H+, which translates into an increase in pH (option D).
2. Before attempting an ABG measurement in the right radial artery, you notice the patient fails the Allen test. What should you do next? A) Obtain a sample from the left radial artery. B) Obtain an ABG sample from the right radial artery. C) Obtain a sample from the right brachial vein. D) Measure oxygen saturation. E) Perform the Allen test on the left hand. Answer: E. A failed Allen test means that the arterial supply of the hand is inadequate, and this wrist is not suitable to be used for ABG sampling. The next step involves performing the Allen test on the patient’s other hand to see if it is a suitable site for ABG sampling (E). Most clinicians would support performing an Allen test before obtaining the ABG sample (option A). It is not appropriate to sample from a vein (option C). The oxygen and carbon dioxide contents differ in arterial and venous blood. Measuring oxygen saturation is not part of the protocol for obtaining an ABG sample (option D).
3. You are asked to see an anxious patient who you suspect may have respiratory alkalosis. Which of the following studies best assesses the patient’s acidbase status? A) Arterial blood gas (ABG) B) Pulse oximetry (Pulse ox) C) Lactic acid level D) Central venous pressure (CVP) E) Electrocardiogram (EKG) Answer: A. The ABG sample is passed through an analyzer machine, providing us with the arterial pH, pCO2, and pO2. This is the most informative study for the patient’s acid-base status. Pulse oximetry only measures oxygen saturation (SaO2). Decreased SaO2 will result in decreased tissue oxygenation and increased lactic acid levels. It is not as informative as ABG. Lactic acid levels increase when tissues are not supplied with adequate oxygen but do not give a good picture of global acid-base status. CVP is a measurement of body blood volume. It is decreased in hemorrhage, but it does not directly inform us about acid-base status. EKG findings are nonspecific and not very informative about acid-base status.
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SUGGESTED READINGS Adrogué HJ, Rashad MN, Gorin AB, et al. Assessing acid-base disorders. Kidney Int. 2009;76:1239–1247. Adrogue Horacio J, Madias NE. Management of life-threatening acid-base disorders: first of two parts. New Engl J Med. 1998;338:26–34. American Association for Respiratory Care. AARC clinical practice guideline: sampling for arterial blood gas analysis. Respir Care. 1992;37:913–917. Barthwal MS. Analysis of arterial blood gases: a comprehensive approach. J Assoc Phys India. 2004;52:573–577. Brackett NC. An approach to clinical disorders of acid-base balance. South Med J. 1974;67:1084–1101. Breen PH. Arterial blood gas and pH analysis: clinical approach and interpretation. Anesthesiol Clin North Am. 2001;19:885–902.
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Gehlbach BK, Schmidt GA. Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit – the role of buffers. Crit Care. 2004;8:259–265. Gluck SL. Acid-base. Lancet. 1998;352:474–479. Kellum JA. Clinical review: reunification of acid-base physiology. Crit Care. 2005;9:500–507. Koeppen B. The kidney and acid-base regulation. Adv Physiol Educ. 2009;33:275–281. Lahiri S, Forster RE II. CO2/H+ sensing: peripheral and central chemoreception. Int J Biochem Cell Biol. 2003;35:1413–1435. Shapiro BA, Harrison RA, Walton JR, Guidelines for sampling and quality control. In: Clinical Application of Blood Gases. 2nd ed. Chicago, IL: Year Book Medical Publishers, Inc; 1977: Chapter 14. Williams AJ. Assessing and interpreting arterial blood gases and acid-base balance. BMJ. 1998;317:1213–1216.
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CHAPTER
13
Central Nervous System Josh Finkle and Jeffrey Kirsch ■ INTRODUCTION The majority of anesthetic procedures involve the central nervous system (CNS), from inducing unconsciousness to performing regional anesthesia. In order to understand anesthesia, the anesthesia technician will need a basic understanding of the anatomy and physiology of the CNS. This chapter introduces the anatomy of the brain and spinal cord, which make up the CNS. The chapter also covers the physiology of the CNS beginning with the main cells of the CNS, neurons.
■ ANATOMY OF THE BRAIN The central and peripheral nervous systems together make up a complex network of cells and fibers that extends throughout the body. This network uses electrical and chemical signals to gather, interpret, and react to information from the external environment and from within the body. The CNS processes and integrates signals received by the peripheral nervous system and sends instructions to the rest of the body. Signals going into and out of the CNS are carried by peripheral nerves, which interact directly with the environment. The CNS can be divided into two distinct anatomic structures: the brain and the spinal cord. The brain is a complex organ with many functions, including the processing of sensory input, the generation of movement, and higher functions such as cognition, language, and emotions. The brain is functionally divided, with specialized regions that are primarily responsible for unique sets of functions. The structures that collectively make up the brain are the cerebral hemispheres, the central cerebral structures, the brainstem, and the cerebellum (Fig. 13.1). The cerebral hemispheres are the most prominent of the brain’s structures and consist primarily of the cerebral cortex, and some underlying
white matter, which are axons that serve to connect cells between brain regions. The cortical tissue of the cerebral hemispheres contains many folds, called gyri, and grooves, called sulci. The cerebral hemispheres can be divided into four major areas, or lobes: frontal, temporal, parietal, and occipital lobes (Fig. 13.2). Each lobe of the cortex contains specialized areas that are responsible for unique functions and responses, leading to a predictable distribution of the functional areas of the cortex. The occipital lobe is primarily associated with the processing of visual information and the formation of a coherent interpretation of the visual world. The temporal lobe is the primary site of auditory perception and contains a structure called the hippocampus, which is responsible for storage and retrieval of memories. The parietal lobe is a locus for integration of multiple senses and is responsible for the understanding of symbolic language and spatial relationships. The frontal lobe is responsible for executive functions, such as attention, conscious motor movement, and behavioral control. Knowledge of the link between structure and function allows the clinician to predict the location of pathology based on clinical presentation. It also allows the surgeon to warn patients preoperatively regarding expected postoperative neurologic deficits following brain tissue resection during tumor and seizure surgery. During any brain surgery, surgeons and patients are challenged with balancing the opportunity for cure (e.g., complete resection of a tumor with surrounding tissue) with the devastation that resection may cause to an individual’s postoperative cognitive and functional outcomes. Internal to the cerebral cortex, there are a number of structures that serve to connect and modulate the signals of the rest of the CNS. The basal ganglia, a set of nuclei below the cortex, are responsible for modulation of complex 109
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Section II • Anatomy, Physiology, and Pharmacology Cerebrum Diencephalon Thalamus Hypothalamus Pineal gland
Infundibulum Pituitary gland Cerebellum Brainstem Midbrain
Spinal cord
Pons Medulla oblongata
■ FIGURE 13.1 The brain (in situ; sagittal section). Showing the location of the four principal parts: cerebrum, diencephalon, brainstem, and cerebellum. (From Stedman’s Medical Dictionary. 27th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2000, with permission.)
Frontal motor control, some aspects of personality
Parietal sensation, some aspects of language
Occipital vision
Temporal speech, hearing The brain is divided into two hemispheres. The right half controls the left side of the body and the left half controls the right side of the body. Each hemisphere is divided into four lobes. Within the lobes there are even smaller areas, each associated with specific functions. ■ FIGURE 13.2 Segments of the brain and their role in the body labeled.
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motor signals sent from the frontal cortex. The thalamus is a large central structure within the cerebral hemispheres, and acts as a sensory integration point, with regions corresponding to inputs from various sensory modalities (vision, audition, touch, pain) on their way to the cortex. The hypothalamus is a region just below the thalamus with many important functions, the most notable of which is to connect the CNS to the endocrine system. The hypothalamus has direct input to the principal endocrine organ, called the pituitary gland, which sits just below the hypothalamus and controls chemically mediated signaling functions such as growth, metabolism, blood pressure, and sexual development. The cerebellum is in the posterior aspect of the skull, below the occipital lobe of the cortex. The cerebellum has connections to other CNS structures, including the cerebral cortex, the basal ganglia, and the spinal cord. The cerebellum’s major function is to integrate tactile and proprioceptive sensory inputs with motor signals for the
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production of smooth motion and the maintenance of balance and posture. The brainstem is the most caudal structure in the brain, and it connects the higher areas of the brain to the spinal cord. The sensory and motor pathways from the body (carried by the spinal cord) and the sensory pathways from the head (the trigeminal system) pass through the brainstem and make important functional connections. The brainstem is divided both structurally and functionally into three areas—the midbrain, pons, and medulla (from rostral to caudal). The medulla controls vital and unconscious functions, including breathing, heart rate, blood-vessel tone, and vomiting. Throughout the brainstem are nuclei (collections of cell bodies) for the cranial nerves, a set of nerves that control various functions within the head and neck, such as taste, audition, and sensation, as well as eye movements, vocalization, and facial expression.
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Within the cranial cavity there are structures that offer support to the tissues of the brain, namely, the meninges and the vasculature. The meninges are a set of three layers of protective tissue that surround the structures of the CNS (Fig. 13.3). The outermost of the meninges, the dura mater, is a thick protective layer that directly contacts the skull. Just below the dura mater is the arachnoid mater, which surrounds a fluidfilled cavity called the subarachnoid space. The subarachnoid space contains cerebrospinal fluid (CSF) that acts as a cushion for the brain against traumatic insults. The pia mater is a thin layer that runs along the surface of the brain, following the sulci and gyri of the cerebral cortex. The blood supply to the brain comes from the vertebral arteries and the internal carotid arteries, which meet on the ventral surface of the brain to form an arterial network, referred to as the circle of Willis. Branching off the circle of Willis are the arteries that supply the regions of the brain,
Dura mater Subdural space Arachnoid Choroid plexus
Subarachnoid space Pia mater
Arachnoid Subarachnoid space Pia mater Spinal cord Dura mater Subdural space
■ FIGURE 13.3 Meninges and cerebrospinal fluid flow.
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including the cerebral arteries, cerebellar arteries, and their branches. Blood returning from the brain enters a network of cavities within the dura mater, called venous sinuses, which collectively drain into the internal jugular vein.
■ CLINICAL IMPLICATIONS OF ANATOMY The rigid structure of the skull and meninges in combination with an increase in the intracranial volume of any component within the intracranial vault (e.g., brain, CSF, blood, or foreign bodies) will result in an increase in intracranial pressure and secondary brain injury. The brain component can increase because of abnormal growth (e.g., tumor) or swelling (e.g., from trauma or surgery). The blood component can increase because of ruptured blood vessels (i.e., ruptured aneurysm, hemorrhagic stroke, or trauma). Unfortunately, all of the inhaled (gas) anesthetics cause dilation of the cerebral blood vessels and an increase in intracranial pressure. Therefore, a typical neuroanesthetic will include an intravenous anesthetic (e.g., propofol, opiates) at concentrations that minimize the doses of inhaled anesthetic required to maintain a reasonable plane of anesthesia. The CSF component can increase from overproduction or poor reabsorption. Although each of these pathologies results in increased intracranial pressure, the definitive treatment is usually left to the discretion of the surgeon. Pressure within the brain can be measured via a catheter placed in the central CSF-containing spaces (e.g., lateral ventricles), or a “bolt” can be placed through the skull and a fluid connection with the CSF space is established through the dura and arachnoid tissues. In both cases, the device is attached to a transducer (as one would use for measurement of invasive blood pressure or central venous pressure) that is zeroed and balanced at the level of the external auditory canal. Alternatively, a fiber-optic Camino device can be placed by the surgeons into the brain parenchyma. Although all techniques provide an accurate assessment of intracranial pressure, only the catheter in the lateral ventricle can be used therapeutically to lower intracranial pressure by withdrawing CSF. Other means of decreasing intracranial pressure that are under the control of the anesthesiologist include hyperventilation (low pCO2 causes cerebral vasoconstriction and decreases blood
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volume in the brain) and intravenous administration of osmotic diuretics (e.g., mannitol and hypertonic saline), which reduce the amount of edema fluid in the brain. Because of the use of hyperventilation by anesthesiologists to lower intracranial pressure in patients having intracranial surgery, the anesthesia technician is likely to observe low arterial pCO2 values and high pH values on blood gases taken during the procedure. In addition, the administration of osmotic diuretics to neurosurgery patients will often result in an increase in the osmolarity measurement by the anesthesia technician.
■ ANATOMY OF THE SPINAL CORD The spinal cord begins just below the base of the brainstem, and continues down, through the vertebral column. The vertebral column is divided into four segments based on anatomic location (Fig 13.4). The cervical region of the vertebral column spans the length of the neck and has seven segments. The thoracic region spans the upper part of the back and is divided into 12 segments. The lumbar region spans the lower back and is divided into five segments. The sacral region of the vertebral column extends into the pelvis and is composed of five bones fused to form a single structure. A single coccygeal bone (referred to as the tailbone) is found at the end of the spinal column. Found within the vertebral column is the spinal cord itself. Although in the adult the spinal cord ends in the thoracic region of the vertebral column, the spinal cord levels are divided into segments based on the spinal column level for exit of their paired sensory and motor spinal nerves. Each of the four regions of the spinal cord controls motor and sensory functions for a specific part of the body. For example, the cervical spinal cord controls motion and sensation from the neck and upper extremities. The thoracic spinal cord controls motion and sensation from the trunk. The lumbar and sacral regions of the spinal cord control motion and sensation in the lower extremity and the pelvic/genital region. Within the spinal cord, there is gray matter and white matter. The gray matter is composed primarily of neuronal cell bodies, and the white matter is composed of long bundles of nerve cell tissue for signal conduction. The meningeal layers continue inferiorly and surround the spinal cord throughout its length. At the level of the spinal cord, the three layers of the meninges lie
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Spinal cord 1 2 3 Cervical cord
C2
4 5
Cervical
6 7 8 1 Thoracic cord
Vertebra
T1
2 3 4 5 6 7
Thoracic
8 9 10 11 12 Lumbar cord
Sacral cord
L1 1 2 Lumbar 3
4
5
Sacral S1
1 2 3 4 5
Spinal nerves ■ FIGURE 13.4 Segmental organization of the spinal cord. The spinal cord is divided into cervical, thoracic, lumbar, and sacral divisions (left). The right side shows the spinal cord within the vertebral column. Spinal nerves are named for the level of the spinal cord from which they exit and are numbered in order from rostral to caudal. (From Bear MF, Connors BW, Parasido MA. Neuroscience—Exploring the Brain. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001, with permission.)
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within the vertebral column and external to the spinal cord itself. As with the intracranial CNS, the meninges and CSF serve an important role to protect the spinal cord from trauma. The meninges and ligaments of the bones of the spinal canal are also used strategically by anesthesiologists for placement of spinal or epidural anesthesia. In the case of a spinal anesthetic, the needle is placed between the vertebral bones with the goal of advancing the needle (and medication) into the CSF (subarachnoid) space. When placing an epidural, the anesthesiologist places the needle (usually along with a catheter) in the epidural space, which is a potential space found as the needle passes past ligamentum flavum (the innermost ligament of intervertebral space), without penetrating the dura. The blood supply to the spinal cord comes from the vertebral arteries and a set of segmental branches off of the aorta, called medullary arteries. These arteries join at the surface of the spinal cord to form a network of arteries that invest the tissue of the spinal cord. Prominent in this network are the larger anterior and posterior spinal arteries, which run the length of the spinal cord, giving off smaller arterial branches at each level. Because of the anatomy of the spinal cord blood supply, patients are at great risk experiencing a critical reduction of blood flow and injury to the spinal cord during surgery that requires crossclamping of the thoracic aorta.
■ PHYSIOLOGY The CNS principally functions as a means to transduce and manipulate electrical information. This information can be used to quickly encode and interpret information from the external world, or allow for manipulation of the environment through motor functions or other complex activities such as language and cognition. The major functional cell type in the CNS is called the neuron. In the peripheral nervous system, neurons interact directly with the environment, acting as sensors for pain, temperature, and tactile information and directly innervating skeletal muscle as well as other muscles and glands that regulate automatic body functions (see Chapters 14 and 15). In the CNS, neurons interact with one another and with peripheral nerves to create and regulate the complex actions of the nervous system. The structure of a neuron reveals important functional properties (Fig. 13.5). A unique
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characteristic of neurons when compared with other cell types is the existence of a long cellular projection, called an axon. In the CNS, each cell’s axon terminates on other neuronal cells, forming an elaborate network of interactions among the cells of the CNS. Depending on the function of a neuron, its axon may be short (like some locally acting neurons in the brain) or as long as a meter (such as upper motor neurons, which can span the length of the spinal cord). An axon can also branch into hundreds of thousands of discreet terminals, making connections with other neurons in a local or diffuse pattern. Another important neuronal cell structure is the dendrite. Each CNS neuron has many dendrites that act as connecting points for the axons of other neurons. The most common neuronal interaction within the CNS is the axon of one neuron terminating on a dendrite of another neuron. The axon and dendrites of each neuron are projections off of a central structure, called the cell body (soma), that contains the nucleus and other important cell organelles and acts to integrate and process the incoming signals from the dendrites. Neurons function by propagating a signal in the form of an electrical impulse. The functional connection between two neurons is called a synapse. The most common type of synapse found in the CNS is the axon terminal of one cell (the presynaptic cell) contacting a dendrite of another cell (the postsynaptic cell). It is also possible for an axon terminal to synapse on a cell body or another axon. When a nerve signal reaches the end of the presynaptic axon, it causes release of chemicals, called neurotransmitters, from the axon terminal into the synaptic cleft, a small space between the presynaptic axon and the postsynaptic cell. These neurotransmitters interact with specialized receptors on the surface of the postsynaptic cell and ultimately affect the activity of the postsynaptic cell (Fig. 13.5). In addition to neurons, there are a number of cells in the CNS that function as supportive structures; these cells are collectively referred to as glial cells. Their functions include support of neuronal growth and signaling, scavenging neurotransmitters and other debris, and providing immunologic protection within the CNS. An especially notable glial cell type in the CNS is the oligodendrocyte. These cells produce a substance called myelin, which wraps neuronal axons and allows for greater speed and efficiency of nerve signal
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Impulses to cell body Nucleus Dendrites
Cell body Axon
Myelin sheath Impulses away from cell body
Direction of nerve impulse
Synapses
Postsynaptic neuron Synaptic cleft
Mitochondrion
Vesicles of transmitter substance Receptors on postsynaptic membrane ■ FIGURE 13.5 Structure of a motor neuron. A neuron or nerve cell is composed of a cell body having a nucleus and two types of processes—dendrites and axons. Impulses pass to the cell body through the dendrites (upper black arrows), and the axon carries impulses away from the cell body (lower black arrows). A neuron influences other neurons at junctional points or synapses. The detailed structure of an axodendritic synapse is illustrated (inset); neurotransmitter substances diffuse across the narrow space (synaptic cleft) between the two cells and become bound to receptors. (From Moore KL, Dalley AF II. Clinical Oriented Anatomy. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999, with permission.)
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conduction. Myelin is rich in lipids and gives white matter (primarily composed of axons) its color. Functional anatomy of the CNS can be divided into sensory systems, motor systems, and complex functions such as language, emotions, and memory. All of the body’s sensory systems feed into the CNS, where the signals are processed to form an internal representation of the environment and the body’s position relative to the environment. Somatosensory processes include mechanosensory (touch), pain, and proprioception (sensation of bodily orientation) and involve both the spinal cord and the brain. These pathways begin with mechanical and chemical sensors throughout the body as part of the peripheral nervous system (see Chapter 15) and ascend to the brain via the spinal cord. As the tracts ascend through the brainstem, the fibers carrying the signals for touch, pressure, and proprioception cross sides at the level of the medulla, and so above this level, somatosensory information within the CNS pertains to the sensation of the contralateral body. All the sensory fibers then synapse in the thalamus and from there travel to the primary sensory cortex in the parietal lobe, where the conscious feeling of sensation occurs. The control of voluntary motor function within the CNS begins in the primary motor
cortex in the frontal lobe, with motor planning and guidance coming from other areas of the frontal lobe including the premotor and prefrontal cortex. The axonal fibers from the primary motor cortex descend through the brainstem, crossing to the contralateral side at the level of the medulla and continue to descend in the lateral column of the spinal cord. These axons terminate within the ventral portion of the spinal cord at the appropriate vertebral level and synapse with lower motor neurons that exit the spinal cord within the spinal nerve to innervate skeletal muscle. Modulation of the motor pathway comes from various locations within the CNS, including the cerebellum, which is mainly involved in smoothing and coordinating movements, and the basal ganglia, which helps generate complex motor patterns. Reflexes are simple sensorimotor circuits that involve only the spinal cord and not the brain. In a reflex pathway, the sensory neuron synapses directly on a lower motor neuron in the spinal cord or on an interneuron that then inhibits a lower motor neuron (Fig. 13.6). For example, in the patellar tendon reflex, the tendon stretch sensory neuron directly activates the nerves that signal the leg to extend while acting to inhibit those that would flex the leg. To brain
1 Stretching stimulates sensory receptor (muscle spindle) Tapping the tendon stretches muscle
5 Effector, (quadriceps) contracts to relieve stretching
Inhibitory interneuron
2 Sensory neuron excited Spinal nerve 4 Motor neuron excited
Antagonistic muscles relax
3
Within integrating center (spinal cord)
Motor neurons to antagonistic muscles (hamstrings) is inhibited
■ FIGURE 13.6 Reciprocal innervation. (From Premkumar K. The Massage Connection: Anatomy and Physiology. Baltimore, MD: Lippincott Williams & Wilkins; 2004, with permission.)
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The CNS is also involved with the set of “special senses,” which includes vision, hearing, smell, and the vestibular sense. Each of these systems involves a specialized type of sensory receptor that encodes information from the environment (in the form of light, sound waves, ingested chemicals) into neural signals that are sent toward the brain. Aside from olfaction (smell), the pathways of all the special senses involve nuclei in both the brainstem and the thalamus before arriving at the cerebral cortex. The central olfactory pathway is the simplest of all the sensory pathways as it does not involve processing within the brainstem or thalamus. Specialized chemical sensors on the surface of the nasal cavity respond to interactions with specific chemical compounds in the inhaled air. These sensory neurons project to the olfactory bulb, a nucleus located within the cranial cavity directly above the nasal cavity. Neurons of the olfactory bulb project their axons directly to the primary olfactory cortex within the temporal lobe. The complex functions carried out by the CNS include memory, emotions, and language and mainly involve specialized areas of the cerebral cortex. Because of the complexities of these systems, all the pathways and interactions are not
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fully understood, but some important features of each system can be explored. Language is an important tool for communication among people, and it involves the production and comprehension of complex vocal and verbal patterns. Within the cerebral cortex, the areas involved with language fall within the temporal and frontal lobes, predominantly on the left side. Because of the importance of language in daily functioning, the left side of the cortex is considered the dominant hemisphere. The right hemisphere plays a role in language, but it is mainly involved with the emotional content rather than the semantic processing of language. There are two specific regions of the cortex that have been identified as major centers for language within the brain. The first, called Broca’s area, is in the left frontal lobe, anterior to the primary motor cortex, and it is involved with the efficient production of language and speech. Broca’s area is important for the motor planning involved in speech and for fluid expression of language. The second important area involved with language is Wernicke’s area, a region of the cortex in the left posterior temporal lobe. Wernicke’s area is important in the understanding of language and is associated with auditory cortex (Fig. 13.7). Damage to these areas of the cortex causes a specific language deficit, called aphasia,
Motor strip Sensory strip Frontal lobe Motor control of voluntary muscles Personality Concentration, organization Problem-solving
Parietal lobe Sensory areas of touch, pain, temperature Understanding speech, language Express thoughts Wernicke’s center Interpreting speech
Broca’s center Motor control of speech
Occipital lobe Visual recognition Focus the eye
Temporal lobe Hearing Memory of hearing and vision
Brain stem Controls heart rate and rate of breathing
Cerebellum Balance Coordinating muscle movement
■ FIGURE 13.7 Topical anatomy of the brain.
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which can present as difficulty in language production (if Broca’s area is affected) or language comprehension (if Wernicke’s area is affected). Within the brain, emotional responses are dictated by a set of structures collectively referred to as the limbic system. The limbic system consists of deep areas of the cortex, like the cingulate gyrus and the hippocampus, as well as structures like the hypothalamus that affect the autonomic nervous system (see Chapter 14). When confronted with an emotionally charged stimulus, the limbic system activates and sends signals to various brain centers, including the prefrontal cortex, which is involved with decision making, the pituitary, which controls the endocrine system, and the brain’s pleasure centers. Emotion and memory within the brain are intimately connected with many structures contributing to both processes. An important brain structure involved with memory is the hippocampus, an area of the cortex found within the temporal lobe. The hippocampus is activated during the storage and retrieval of memory, and it is especially associated with memory for locations and events. The cerebellum is involved with procedural memory, also called muscle memory, which is important in learning motor-oriented skills like riding a bicycle or playing a musical instrument. Strong emotional states encourage memory encoding, and so emotionally charged events are remembered more accurately and with more detail.
■ PHARMACOLOGY There are many pharmacologic agents that have effects on the CNS. Psychomotor stimulants are drugs that increase the overall activity within the CNS. They do so by increasing neuronal firing rate or promoting neurotransmitter release. Examples include caffeine and d-amphetamine, a drug commonly used to treat attention deficit/ hyperactivity disorder (ADHD). Anticonvulsants are drugs that decrease the overall activity within the CNS. They are used to treat seizure disorders, which involve abnormally increased neuronal firing in the CNS. Examples include sedatives such as barbiturates and benzodiazepines, as well as many other drugs that have been designed to treat specific types of seizures. Usually, these drugs decrease neuronal firing frequency and enhance the effects of inhibitory neurotransmitters. The CNS has an inbuilt array of molecules and receptors involved with analgesia (pain
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reduction). Specifically, three families of peptides, called endorphins, enkephalins, and dynorphins, are collectively referred to as the endogenous opioids and act on opioid receptors within the CNS with analgesic effects. Opioid agonists are a class of drugs that themselves bind to and activate the brain’s opioid receptors and are used for analgesia. Morphine is the prototypical drug in this class and is a strong opioid agonist. General anesthetics are a class of drugs used during surgeries for sedation, analgesia, amnesia, and muscle relaxation. These drugs are administered either through injection (usually intravenous) or inhalation. The inhaled anesthetics include isoflurane, sevoflurane, and desflurane. The inhaled anesthetics presumably do not act through a receptor-mediated pathway but by their direct interactions with cell membranes within the CNS. Propofol is a fast-acting injected anesthetic that is quickly cleared from the circulation, and so continuous administration is needed to maintain anesthesia. In adult patients requiring surgery for intracranial pathology, general anesthesia is often induced with a quick-onset intravenous anesthetic (e.g., propofol) and a neuromuscular blocking agent (e.g., rocuronium or succinylcholine) to allow the anesthesiologist an opportunity to quickly control ventilation, avoiding the dangers of hypoventilation (which can result in an increase in intracranial pressure). Intravenous opiates are administered in order to blunt the hemodynamic response to noxious stimuli (e.g., intubation, placement of the patient’s head in pins, and surgical incision). Hemodynamic stability is important, as hypertension may result in brain swelling in areas of brain damage (e.g., in the region of a tumor or trauma) and hypotension may result in poor perfusion to important areas of the brain. During brain surgery, anesthesia is often maintained using a combination of intravenous agents (e.g., propofol infusion and/or an opiate) and inhaled agents (e.g., desflurane) in order to minimize the detrimental effects of the inhaled anesthetic agents administered in high concentrations on brain blood volume. As discussed above, an increase in brain blood volume may result in an increase in intracranial pressure and secondary brain injury. Patients also often receive neuromuscular blocking drugs so that they will not move while the surgeon is operating within the brain parenchyma.
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■ INHERENT TOXICITY OF ANESTHETIC AGENTS IN THE CNS Although our previous understanding of the anesthetic agents was to “protect” the brain from injury by their ability to put the brain in a quiescent state, more recent investigations have demonstrated that all of the inhaled anesthetic gases and several of the intravenous anesthetic agents cause direct neurotoxicity. The mechanism of this toxicity appears to be related to their effect on the release of specific brain chemicals (neurotransmitters) within brain tissues. Current research suggests that patients at the extremes of life (i.e., neonates and the elderly) are most susceptible to the direct damaging effects of anesthetic agents. Unfortunately, there is no current consensus on anesthetic agents that are free of neurotoxic effects on the brain. Ongoing research is trying to establish which, if any, of the anesthetic agents is truly safe and if there are clinically applicable management strategies that can be applied for care of patients in the most vulnerable periods for anesthetic-induced brain injury. The strategies may include administration of additional drugs to protect the brain from anesthetic-induced brain injury (e.g., lithium has been suggested) or development of new anesthetic agents (e.g., xenon has been suggested). In the meantime, the most reasonable approach is to minimize exposure of patients to anesthetic agents during their most vulnerable age periods (i.e., neonates and the very old).
■ ANATOMY, PHYSIOLOGY, AND PHARMACOLOGY OF NAUSEA AND VOMITING Emesis (vomiting) is a process in which the normal direction of digestive propulsion is reversed and the contents of the stomach are brought upward through the esophagus and out of the mouth. The process is often forceful and unpleasant and can be induced by a number of factors including gastrointestinal irritation, motion sickness, and drug reactions. Emesis is usually preceded by a process called retching that involves a rhythmic contraction of the diaphragm and abdominal muscles. These muscles then undergo prolonged intense contractions, as the stomach contents are expelled upward. The lower and upper esophageal sphincters are relaxed as the contents are forcefully ejected from the mouth. Often a feeling of relief follows this process.
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Within the medulla, there is a nucleus called the chemoreceptor trigger zone (CTZ) that, when activated, triggers the emesis response. The CTZ has receptors for a number of neurotransmitters, including dopamine, acetylcholine, histamine, serotonin, and opioids. Drugs that modulate the effects of these chemicals and their receptors may alter the emetic response. Drugs with proemetic effects are often those that increase the activity of neurotransmitters to which the CTZ is sensitive. Opioid drugs can also activate the CTZ through its opioid receptors, but the proemetic effect of these drugs is not apparent in all patients. Other ingested substances, such as syrup of ipecac, trigger emesis by irritating the gastric mucosa. There are a number of drug classes that antagonize emesis, mainly by inhibiting the neurotransmitters and receptors within the CTZ. Dopamine receptor blockers are used as antipsychotics (see CNS pharmacology section) and have antiemetic effects by blocking dopamine 2 (D2) receptors within the CTZ. Scopolamine is a drug that is used to combat motion sickness through its anticholinergic effects at the CTZ. Additionally, selective serotonin antagonists (e.g., ondansetron) are often given to inhibit the nausea that occurs as a side effect of anesthesia and chemotherapeutic treatments.
■ SUMMARY In summary, the CNS is a complicated organ system that requires an in-depth understanding by anesthesiology staff in order to establish the desired operating environment for the surgeon and outcomes for our patients. Effective communication between members of the anesthesiology team will facilitate creating an anesthesia plan that minimizes the opportunity of CNS damage by our anesthetic agents by maximizing dosedependent anesthetic beneficial effects, while minimizing the inherent toxicity of each agent.
REVIEW QUESTIONS 1. Which of the following areas of the cortex is most likely to be involved with language production? A) Left frontal lobe B) Left temporal lobe C) Right frontal lobe D) Right temporal lobe E) None of the above
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Answer: A. Broca’s area is in the left frontal lobe, anterior to the primary motor cortex, and is involved with the efficient production of language and speech. Wernicke’s area, a region of cortex in the posterior temporal lobe, is important in the understanding of language and is associated with auditory cortex. The right hemisphere plays a role in language, but it is mainly involved with the emotional content rather than the semantic processing of language.
2. Blocking which of the following neurotransmitter receptors in the CTZ will have an antiemetic effect? A) Serotonin B) Acetycholine C) Dopamine D) A and C only E) A, B, and C Answer: E. There are a number of drug classes that antagonize emesis, mainly by inhibiting the neurotransmitters and receptors within the CTZ. Dopamine receptor blockers are used as antipsychotics and have antiemetic effects by blocking D2 receptors within the CTZ. Scopolamine is a drug that is used to combat motion sickness through its anticholinergic effects at the CTZ. Additionally, selective serotonin antagonists (e.g., ondansetron) are often given to inhibit the nausea that occurs as a side effect of anesthesia and chemotherapeutic treatments.
3. Which of the following correctly describes the path of the electrochemical signal through a single neuron as it is received, then processed, then relayed down the length of the neuron? A) cell body → dendrite → axon B) dendrite → cell body → axon C) cell body → axon → dendrite D) axon → cell body → dendrite Answer: B. Neurons receive most of their input signals through receptors on their dendrites. These signals cause changes in the cell’s electrical gradient, first within the dendrites themselves and then in the cell body. If the cell is depolarized past threshold, it will then send an action potential down the length of its axon.
4. Which of the following answer choices correctly matches the region of the spinal column with the number of vertebrae in that region? A) Cervical—12 B) Coccygeal—5 C) Lumbar—7 D) Thoracic—12 E) Sacral—7 Answer: D. The cervical region of the vertebral column spans the length of the neck and has seven segments. The thoracic region spans the upper part of the back and is divided into 12 segments. The lumbar region spans the lower back and is divided into five segments. The sacral region of the vertebral column extends into the pelvis and is composed of five bones fused to
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form a single structure. A single coccygeal bone (referred to as the tailbone) is found at the end of the spinal column. Found within the vertebral column is the spinal cord itself.
5. An endogenous peptide is discovered to act on receptors within the CNS and cause pain relief as well as euphoria and sedation. Which of the following CNS drugs acts on the same receptor as this molecule? A) Isoflurane B) Succinylcholine C) Lithium D) Morphine E) Scopolamine Answer: D. The endogenous opioids are peptides that act on opioid receptors within the CNS with analgesic effects. Opioid agonists, such as morphine, bind to and activate the brain’s opioid receptors and are used for analgesia. The inhaled anesthetics (such as isoflurane) directly interact with cell membranes within the CNS to cause analgesia and sedation. Succinylcholine is a neuromuscular blocking agent that interferes with cholinergic signaling between motor nerve terminals and muscles. Lithium can be used as a mood stabilizer to treat bipolar and other mood disorders. Scopolamine is a drug that is used to combat motion sickness through its anticholinergic effects at the CTZ.
SUGGESTED READINGS Clarke RS. Nausea and vomiting. Br J Anaesth. 1984;56(1): 19–27. Hanes DE. Neuroanatomy: An Atlas of Structures, Sections, and Systems. Philadelphia, PA: Lippincott Williams & Wilkins; 2010. Hickok G. The functional neuroanatomy of language. Phys Life Rev. 2009;6(3):121–143. doi: 10.1016/j.plrev. 2009.06.001. Huffman JC, Alpert JE. An approach to the psychopharmacologic care of patients: antidepressants, antipsychotics, anxiolytics, mood stabilizers, and natural remedies. Med Clin North Am. 2010;94(6):1141–1160, x. doi: S00257125(10)00143-4 [pii]. 10.1016/j.mcna.2010.08.009 Ishizawa Y. Mechanisms of anesthetic actions and the brain. J Anesth. 2007;21(2):187–199. doi: 10.1007/s00540-0060482-x. Llinas RR. The intrinsic electrophysiological properties of mammalian neurons: insights into central nervous system function. Science. 1988; 242(4886):1654–1664. Mansour A, Khachaturian H, Lewis ME, et al. Anatomy of CNS opioid receptors. Trends Neurosci. 1988;11(7): 308–314. Phillips ML, Drevets WC, Rauch SL, et al. Neurobiology of emotion perception, I: the neural basis of normal emotion perception. Biol Psychiatry. 2003;54(5):504–514. doi: S0006322303001689 [pii]. Purves D. Neuroscience. 4th ed. Sunderland, MA: Sinauer Associates, Inc.; 2008.
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CHAPTER
14
Autonomic Nervous System Lori Nading and Ahmed Alshaarawi
T
he autonomic nervous system (ANS) is a subdivision of the peripheral nervous system, which acts autonomously, or involuntarily, to control the visceral (internal) functions of the body. In other words, its effects on the body happen automatically without conscious actions. The ANS is separated into two divisions: the sympathetic system and the parasympathetic system. The sympathetic nervous system works to prepare the body for stressful situations. Thus, the sympathetic nervous system is also referred to as the “fight-or-flight” system. The parasympathetic nervous system counteracts the sympathetic nervous system and works to return the body to normal after a stressful situation, helping to maintain homeostasis. It is sometimes referred to as the “rest-and-restore” system. The ANS differs from the somatic nervous system in several ways. A brief review of the somatic system reveals a one-motor neuron system with a synaptic cleft. Acetylcholine is the primary neurotransmitter that allows for propagation of an impulse across the synaptic cleft. The effector site for the somatic system is skeletal muscle. The ANS is a two-motor neuron system comprised of a preganglionic neuron and a postganglionic neuron. Located between the two neurons is a ganglion, and it is within this ganglion that the synapse occurs. The postganglionic neurotransmitters (at the effector site) used in the ANS consist of acetylcholine and norepinephrine. The effector sites of the ANS are smooth muscle, cardiac muscle, and secretory glands. Ganglia are a collection of neuronal cell bodies outside the central nervous system (CNS). Sympathetic ganglia are also called paravertebral ganglia. The sympathetic paravertebral ganglia branch off the spinal nerves anterior to the ventral roots. The paravertebral ganglia are connected vertically, forming a chain lateral to the
spinal cord. This chain is referred to as the sympathetic chain or trunk. In the sympathetic nervous system, the firstorder neurons of the ANS arise from the CNS. The preganglionic fibers deliver impulses to second-order neurons or the paravertebral ganglia. These ganglia contain the cell bodies of the postganglionic fibers responsible for delivering the impulse to the effector organs. The preganglionic fibers of the ANS are myelinated, and the postganglionic fibers of the ANS are nonmyelinated. Postganglionic fibers of the sympathetic division are long and are spread throughout the body. They produce a more generalized mass response. The postganglionic fibers of the parasympathetic division are short with their terminal ganglia near the effected organ. Their effect is more localized.
■ ANATOMY OF THE AUTONOMIC NERVOUS SYSTEM The sympathetic nervous system preganglionic fibers originate in the thoracic (T1-T12) segments and the first three lumbar (L1-L3) segments of the spinal cord (Figure 14.1). For this reason, it is sometimes referred to as the thoracolumbar division. The myelinated effector nerves leave the spinal cord and enter the ganglia. After reaching the ganglia, the impulse may travel in one of three ways: (1) directly across the ganglion to synapse with cell bodies of the postganglionic fibers, (2) cephalad or caudad to synapse with a higher or lower postganglionic neuron, or (3) through the sympathetic chain without synapsing. Some preganglionic fibers exit the sympathetic chain and synapse with outlying ganglia such as the celiac ganglia or the superior and inferior mesenteric ganglia. Synapses with these outlying ganglia, sometimes also referred to as collateral ganglia, innervate the visceral organs below the diaphragm. Innervation of the adrenal 121
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medulla is unique in that the secretory cells are considered modified postganglionic neurons. Therefore, preganglionic fibers do not synapse prior to reaching the adrenal gland. Because the preganglionic fibers are myelinated, the signal speed is quick, causing a rapid release of norepinephrine and epinephrine from cells within the adrenal medulla. The parasympathetic nervous system cell bodies stem from cranial nerves III, VII, IX, and X and the sacral segment of the spinal cord Figure 14.1. It is sometimes referred to as the craniosacral
division. The preganglionic fibers of the parasympathetic system differ from those of the sympathetic system in that they travel uninterrupted to their effector organ before synapsing with a short postganglionic fiber. Parasympathetic stimulation arising from the cranial nerves innervate viscera of the head, thorax, and abdomen. A large percentage of parasympathetic innervation to the thorax and abdomen stems from the vagus (X) nerve. This includes parasympathetic stimulation to the heart, lungs, stomach, small intestine, liver, gallbladder, and pancreas.
Ciliary ganglion
Lacrimal gland
Midbrain Pterygopalatine ganglion
III
Submandibular gland
Submandibular ganglion
Pons
Sublingual gland
VII Parotid gland
IX Otic ganglion
Spinal nerves Medulla X To neck
C1
Vagus nerve
C2
Superior cervical ganglion
C3 C4
Pulmonary nerves
C5
To upper limb
C6
Middle cervical ganglion
C7
Bronchus
Inferior cervical ganglion
C8
T1
Larynx Trachea
Heart
Lung Cervical cardiac nn.: Superior Middle Inferior
T2
T3
Thoracic Celiac cardiac nerves ganglia
T4
T5
Liver
Greater splanchnic nerve
T6
Gallbladder Bile duct
Spleen
To body wall
Red lines - Sympathetic
Pancreas
T8
Lesser and least splanchnic nerve
T9
T10
Aorticorenal ganglia
Solid lines - Preganglionic motor neuron
Adrenal gland cortex
Esophagus Stomach
Kidney
Superior mesenteric ganglion
T12
L1
Bladder
L2
IX - Glossopharyngeal nerve X - Vagus nerve
L4 L5
To perineum
C Colon: Ascending-A Transverse-B Descending-C
Prostate
A
Rectum
Urethra
S1 S2 S3
B
Lumbar splanchnic Inferior nerves mesenteric ganglion
L3
Dashed lines - Postganglionic motor neuron III - Oculomotor nerve VII - Facial nerve
T11
To lower limb
KEY Blue lines - Parasympathetic
T7
Sympathetic ganglion
Pelvic splanchnic nerve
S4 S5
Uterus Testis Spinal cord
■ FIGURE 14.1 Spinal cord with medulla pons and midbrain, connecting parasympathetic and sympathetic nerves to the ganglion to the affected organs, glands.
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The eye receives parasympathetic stimulation via the occulomotor (III) nerve, and the lacrimal and salivary glands are stimulated through fibers from the facial (VII) nerve. Additionally, salivary glands also receive parasympathetic stimulation through the glossopharyngeal (IX) nerve. Parasympathetic nervous system fibers arising from the sacral portion of the spinal cord innervate the large intestine, rectum, and bladder.
■ PHYSIOLOGY OF THE AUTONOMIC NERVOUS SYSTEM The primary neurotransmitters released in the ANS are acetylcholine and norepinephrine. The preganglionic fibers of the sympathetic division and the preganglionic and postganglionic fibers of the parasympathetic division all release acetylcholine. Most of the postganglionic fibers of the sympathetic division release norepinephrine. There are a few exceptions such as the postganglionic fibers of the sympathetic nervous system that stimulate the sweat glands. These fibers release acetylcholine. Acetylcholine exerts its effect on cholinergic receptors found in the ganglia or in the effector organs. There are two types of cholinergic receptors, nicotinic and muscarinic. Nicotinic receptors are almost always excitatory. Acetylcholine released from preganglionic fibers act on nicotinic receptors found in the ganglia on the postganglionic fibers in both the sympathetic and parasympathetic nervous systems. Acetylcholine that is released from postganglionic fibers in the parasympathetic nervous system exerts its systemic effects by acting on muscarinic receptors. Muscarinic receptors can exhibit excitatory or inhibitory properties. Muscarinic activation in the heart causes decreased heart rate and contractility. Muscarinic activation also causes bronchoconstriction (e.g., wheezing), increased secretion by salivary glands, and intestinal and bladder contraction with release of their sphincter tone (often resulting in urination and defecation). Within the sympathetic nervous system, norepinephrine released from postganglionic nerves acts on adrenergic receptors. The two major classes of adrenergic receptors are alpha (α) receptors and beta (β) receptors. These receptors are further subclassified as α1 and α2 and β1 and β2. In general, stimulation of α1 receptors that exist outside of the central nervous system
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(CNS) results in constriction of blood vessels (hypertension) and relaxation of bladder and bowel, while at the same time causing constriction of the sphincters of the bowel and bladder. Stimulation of α2 receptors results in decreased release of norepinephrine from nerve terminals. Stimulation of β1 receptors causes increased heart rate and increased cardiac contractility, whereas stimulation of β2 receptors causes dilation of blood vessels (hypotension), dilation of bronchioles (i.e., good treatment for bronchospasm/wheezing), and increased blood glucose (from glycogenolysis and gluconeogenesis).
■ EFFECTS OF AUTONOMIC NERVOUS SYSTEM STIMULATION Unlike innervation of skeletal muscle, which is all excitatory, visceral organs receive both excitatory and inhibitory innervation. The two divisions of the ANS are responsible for this antagonistic innervation. As noted previously, the sympathetic system is usually excitatory and the parasympathetic system inhibitory. Stimulation of the sympathetic division of the ANS produces a physiologic response characterized by increased heart rate, increased force of contraction of the heart, increased blood pressure through constriction of blood vessels (vasoconstriction), increased blood sugar through release of glucose from the liver, inhibition of digestion, dilation of respiratory passageways, increased blood flow to skeletal muscle, and dilation of pupils (Table 14.1). The individual receptors involved in this effect of the sympathetic nervous system are outlined above. These functions are the classic “fight-or-flight” response. Although the stimulation of these organ systems can be helpful to escape a bear attack, they can also be detrimental. For example, surgical stimulation produces a pronounced sympathetic response. The increases in heart rate could increase myocardial oxygen demand, and the patient could suffer a heart attack if there is limitation in oxygen supply (e.g., if the coronary arteries are partially occluded). Activation of the parasympathetic nervous system generally counterbalances the sympathetic system. When not being chased by a bear, it is time for the body to take care of other physiologic needs like eating and storing energy. Stimulation of the parasympathetic system decreases heart rate and increases blood flow to the digestive track, increasing peristalsis. The parasympathetic
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TABLE 14.1 CHARACTERISTICS OF THE AUTONOMIC NERVOUS SYSTEM STRUCTURE/SYSTEM
SYMPATHETIC EFFECTS
PARASYMPATHETIC EFFECTS
Cardiovascular system
Increased heart rate and contractility Vasodilation and vasoconstriction of blood vessels
Decreased heart rate and contractility
Respiratory system
Increased bronchiole dilation and increased respiratory rate
Decreased dilation and respiratory rate
Digestive system
Decreased activity Increased glycogen breakdown Glucose synthesis and release
Increased activity Glycogen synthesis
Skeletal muscle
Increased force of contraction Glycogen breakdown
Not innervated
Eye
Dilation of pupil Focusing for distance
Pupil constriction Focusing for close-up Secretion of tear glands
Urinary system
Decreased urine production Relaxation of bladder and constriction of sphincter
Increased urine production Increased bladder tone and relaxation of sphincter
Reproductive system
Increased glandular secretions
Erection of penis or clitoris
nervous system is also responsible for relaxation of sphincters, allowing for urination and defecation (Table 14.1).
■ ANESTHETICS AND THE AUTONOMIC NERVOUS SYSTEM Most of the medications that are administered during anesthesia affect the ANS. This is especially true during general and neuraxial anesthesia (spinal and epidural anesthesia). Anesthetic interventions can directly reduce autonomic signals from the CNS (including the spinal cord), act at the ganglia, or act on the end-organ receptors for the neurotransmitters of the ANS. For example, the induction of general anesthesia often results in a generalized reduction in sympathetic outflow from the CNS. This results in hemodynamic changes such as a decrease in blood pressure. In this section of the chapter, we describe effects on the ANS of the different classes of medications that are utilized during general or neuraxial anesthesia.
■ GENERAL ANESTHESIA Benzodiazepines These medications (e.g., midazolam, diazepam) are often utilized in the preoperative area and during sedation cases. At low doses, they produce minimal reductions in sympathetic nervous system output from the CNS. When they are combined with narcotic medications, the reduction
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in sympathetic outflow can be more pronounced and can result in a significant decrease in blood pressure. The calming effects of the benzodiazepines—termed anxiolysis—may cause the heart rate to decrease and the blood pressure to drop as a result of decreased catecholamine production.
Opiates Fentanyl, hydromorphone, and morphine are opiates and are some of the commonly administered perioperative medications. Most commonly, opiate analgesics will produce a reduction in the sympathetic nervous system activity. And as noted above, when opiates are administered together with benzodiazepines, they cause a more pronounced reduction in the sympathetic outflow and corresponding decrease in blood pressure.
■ HYPNOTICS/BARBITURATES/ SEDATIVES Propofol, methohexital, and etomidate are classified as hypnotics and sedatives. They are potent depressants of the CNS and are used in anesthesia in low doses to produce sedation and in higher doses to produce unconsciousness. With the exception of etomidate, hypnotics usually produce a profound reduction in central sympathetic outflow, which can result in significant decreases in blood pressure, even in healthy
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Chapter 14 • Autonomic Nervous System
patients. The reduction in sympathetic outflow reduces cardiac output and causes peripheral vasodilation. It is important to utilize these drugs judiciously, particularly in patients who may be more dependent on their sympathetic system to maintain blood pressure (e.g., a trauma patient) or in patients who may not be able to tolerate a significant decrease in blood pressure. Etomidate is the only hypnotic/sedative that does not result in significant attenuation of sympathetic outflow, and as a result, it is often chosen to induce anesthesia in hemodynamically precarious patients. Ketamine is a hypnotic anesthetic that is associated with sympathetic system stimulation, while at the same time causing direct myocardial depression. Thus, when given to normal patients, ketamine administration can be associated with hypertension and tachycardia. However, when administered to patients who have been in the intensive care unit for an extended period of time, ketamine causes direct myocardial depression and hypotension because these patients have often depleted their catecholamine stores.
■ INHALATION AGENTS Of all the currently utilized volatile inhalation agents, desflurane is the only agent that will produce an increase in the sympathetic outflow, causing tachycardia. However, this increase occurs only when there is a sudden elevated level of desflurane. Otherwise, all volatile inhalation agents will produce varying degrees of cardiovascular depression due to direct dilation of systemic blood vessels and reduced sympathetic nervous system activity. The result is often a drop in blood pressure that is antagonized with intravenous administration of a vasopressor drug (e.g., ephedrine or phenylephrine) or by release of endogenous catecholamines from painful stimuli such as surgical incision. Nitrous oxide is a nonvolatile inhalation anesthetic agent and is commonly associated with centrally propagated increase in sympathetic outflow, particularly when it is administered without other anesthetic agents. During noxious stimulation (e.g., tracheal intubation) patients who have nitrous oxide as part of their anesthetic have higher concentrations of blood catecholamines (particularly norepinephrine) due to direct effects of this drug on the sympathetic nervous system, but attenuated cardiovascular responses due to the anesthetic effect on the cardiovascular system.
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■ NEUROMUSCULAR JUNCTION BLOCKING AGENTS (MUSCLE RELAXANTS) In general, muscle relaxants do not exhibit significant effects on the ANS. That is especially true with rocuronium and vecuronium, two of the more commonly used muscle relaxants during anesthesia and surgery. Pancuronium is a long-acting muscle relaxant. Its administration is associated with tachycardia because of its effect to inhibit postganglionic muscarinic receptors on the heart. Succinylcholine, a depolarizing muscle relaxant, can produce dysrhythmias manifested as bradycardia, junctional rhythms, or ventricular dysrhythmias. As a depolarizing neuromuscular blocking agent, succinylcholine causes stimulation of both types of cholinergic receptors. Therefore, succinylcholine will activate both nicotinic ganglionic receptors and postsynaptic muscarinic receptors. The resulting stimulation of both sympathetic and parasympathetic nerves and muscarinic receptors in the sinus node of the heart the cardiovascular effects are unpredictable, but often result in bradycardia and cardiac arrhythmias.
■ MUSCLE-RELAXANT REVERSALS Neostigmine is one of the most commonly used medications in anesthesia to reverse the effects of the nondepolizer muscle relaxants (such as rocuronium, vecuronium, and pancuronium). This medication, which belongs to a class of drugs called anticholinestrases, has significant effects on the ANS, producing some of the most undesirable symptoms including salivation, bronchoconstriction, defecation, and bradycardia. These effects are counteracted by the concomitant administration of anticholinergic medications such as atropine and glycopyrrolate. The anticholinergics cause tachycardia and drying of secretions in order to oppose the effects of the anticholinesterases.
■ REGIONAL ANESTHESIA Epidural and spinal blocks involve injection of local anesthetics in close proximity to the CNS (spinal cord). These blocks are commonly used to inhibit sensory and motor transmission to various parts of the body. However, another important property of these procedures is the interruption of sympathetic (in the thoracic and lumbar region) and parasympathetic (in the
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TABLE 14.2 COMMON ANESTHESIA MEDICATIONS AND EFFECTS ON ANS ANESTHETIC-MEDICATIONS CLASS
EFFECTS ON THE AUTONOMIC NERVOUS SYSTEM
Benzodiazepines
Minimal reductions in sympathetic nervous system output from the central nervous system
Opiates
Reduction in the sympathetic nervous system activity
Hypnotics/barbiturates/sedatives
Profound reduction in central sympathetic outflow except for etomidate
Inhalation agents
Reduction in sympathetic nervous system outflow except desflurane (in sudden high concentrations) and nitrous oxide, both of which cause an increase in sympathetic nervous system outflow
Muscle relaxants
Negligible effects
Muscle relaxants reversals
Significant effects on the autonomic nervous system, causing profound dysrhythmias, gastrointestinal upset, and airway constriction
Epidural and spinal anesthesia
Chemical sympathectomy
sacral region) signals as well, as all transmission to or from the spinal cord can be blocked. When the level of anesthesia for a spinal or epidural anesthetic is allowed to ascend to the high thoracic region, the patient may experience a “chemical sympathectomy” because the spinal/ epidural anesthetic will inhibit all of the sympathetic outflow, since it originates in the thoracic and lumbar regions of the spinal cord. In this situation, the only part of the ANS that is functional is the parasympathetic system (cranial division), which in patients with a high spinal/epidural lacks the balance of the sympathetic nervous systems. Thus, during noxious stimulation above the level of spinal/epidural anesthesia (e.g., emergency tracheal intubation), the patient is more likely to exhibit bradycardia and hypotension from unopposed parasympathetic activity. On the contrary, paravertebral blocks may not inhibit sympathetic activity, as the sympathetic chain is anterior to the target for this block and there is much overlap of sympathetic innervation because of the sympathetic ganglia chain. Thus, even if the local anesthetic administered at a specific paravertebral level defuses anteriorly and anesthetizes the sympathetic ganglion at that specific level, the observed physiologic effect of that block will be minimal because sympathetic fibers will have likely reached the target via sympathetic ganglia more distant along the sympathetic chain. However, anesthetizing sympathetic ganglia outside of the sympathetic chain will have clear effects on target organs.
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For example, celiac ganglia, which provide sympathetic innervations to intraabdominal organs, are anesthetized to alleviate pain for patients who have cancer in these organs. It is important to recognize that, anatomically, celiac ganglia are also mixed with sensory nerves that originate in these organs. Table 14.2 in this chapter summarizes the commonly used medications in anesthesia and their effects on the ANS. In summary, the ANS is divided into two subdivisions. The sympathetic division arises from preganglionic fibers originating from the thoracic and lumbar segments of the spinal cord. The sympathetic division is activated during times of crises (“fight or flight”) and works to produce increased alertness, increased cardiovascular and respiratory function, and increased energy. The parasympathetic division arises from the preganglionic fibers originating in the cranial nerves of the brainstem and sacral segments of the spinal cord. Parasympathetic stimulation produces depression of cardiovascular function and promotes digestive function (“rest and restore”). These two divisions are antagonistic and work to counterbalance one another to regulate cardiovascular, respiratory, digestive, excretory, and reproductive functions. Most of the medications that are administered during anesthesia will affect the ANS. A general understanding of the ANS and the effects of medications will help the anesthesia technician participate in the anesthetic management of patients.
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Chapter 14 • Autonomic Nervous System
REVIEW QUESTIONS 1. The primary neurotransmitter released by the preganglionic fibers of the sympathetic nervous system and the preganglionic and postganglionic fibers of the parasympathetic nervous system is A) Epinephrine B) Acetylcholine C) Norepinephrine D) Dopamine E) None of the above Answer: B. Acetylcholine is the primary neurotransmitter for the preganglionic fibers of the sympathetic nervous system and the preganglionic and postganglionic fibers of the parasympathetic nervous system. Norepinephrine is released by most of the postganglionic fibers of the sympathetic nervous system. Epinephrine is released from the adrenal medulla after direct stimulation from preganglionic fibers.
2. Acetylcholine exerts its effect on which of the following receptors? A) Cholinergic B) Muscarinic C) Nicotinic D) Adrenergic E) A, B, and C Answer: E. Acetylcholine exerts its effect on cholinergic receptors of which there are two types: nicotinic and muscarinic. Nicotinic receptors are almost always excitatory. Muscarinic receptors exhibit both excitatory and inhibitory effects.
3. Which of the following effects is elicited by stimulation of the α1 receptors? A) Hypertension B) Hypotension C) Increased heart rate D) Dilation of bronchioles E) None of the above Answer: A. Hypertension and relaxation of bladder and bowel are effects caused by stimulation of the α1 receptor. Hypotension and dilation of the bronchioles is caused by stimulation of the β2 receptors. Increased heart rate is an effect of stimulating the β1 receptors.
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4. A patient with extremely poor cardiac function presents for surgery and requires a general anesthetic. Which of the following medications do you anticipate will likely be used during induction? A) Aspirin B) Etomidate C) Acetaminophen D) None of the above E) All of the above Answer: B. Etomidate is the only hypnotic/sedative that does not result in significant attenuation of sympathetic outflow, and as a result, it is often chosen to induce anesthesia in such patients. The other medications are not usually considered as anesthetic induction agents.
5. Which of the following inhalation anesthesia agents is considered to be the only inhalation agent that will produce an increase in the sympathetic outflow, causing tachycardia, when it is suddenly increased to high levels? A) Isoflurane B) Sevoflurane C) Desflurane D) Halothane E) None of the above Answer: C. Desflurane is the only agent that will produce an increase in the sympathetic outflow, causing tachycardia. Thus, it is not usually used as an induction agent.
SUGGESTED READINGS Boron WF, Boulpaep EL. Medical Physiology. Philadelphia, PA: Elsevier Science; 2003. Huether SE, McCance KL. Understanding Pathophysiology. 2nd ed. St. Louis, MO: Mosby; 2006. Martini FH, Bartholomew EF. Essentials of Anatomy & Physiology. 5th ed. San Francisco, CA: Benjamin Cummings; 2010. Morgan GE, Mikhail MS, Murray MJ. Clinical Anesthesiology. 4th ed. New York, NY: McGraw-Hill; 2006. Shier D, Lewis R, Butler J. Hole’s Human Anatomy & Physiology. 9th ed. New York, NY: McGraw-Hill; 2002. Stoelting RK, Hillier SC. Pharmacology & Physiology in Anesthetic Practice. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.
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CHAPTER
15
Peripheral Nervous System Eve Klein and Michelle Cameron
T
he nervous system transmits signals between different parts of the body and can be divided into the central nervous system (CNS), which includes nerves wholly contained in the brain and spinal cord, and the peripheral nervous system (PNS), which includes nerves outside of the CNS. The CNS and autonomic system are covered in Chapters 13 and 14, respectively, while this chapter focuses on the PNS, including anatomy, physiology, pathophysiology, and mechanisms of peripheral nerve blockade by local anesthetics.
■ PERIPHERAL NERVE ANATOMY Nerves of the PNS carry information to, or from, the CNS. The nerves that carry information to the CNS from the periphery are known as afferent nerves. Afferent nerves transmit a range of sensations, including touch, position, vibration, and pain. Sensory afferent nerves originate in the dorsal root ganglia just outside the spinal cord. The nerves that carry information from the CNS to the periphery are known as efferent nerves. Efferent nerves include both the somatic motor nerves that innervate skeletal muscles to make them contract voluntarily and the autonomic nerves that control involuntary muscles, such as smooth and cardiac muscle, and control glandular activity. Efferent somatic motor nerves originate in the anterior horn of the spinal cord.
■ NERVE CELLS Nerve cells, also known as neurons, are composed of a cell body, dendrites, an axon, and axon terminals (Fig. 15.1). The cell body contains the nucleus and various organelles (mitochondria, rough endoplasmic reticulum, ribosomes, and Golgi apparatus) needed to make proteins and process energy to maintain the nerve. The dendrites are branching and tapering extensions of the cell body that receive signals from other
neurons. The axon is a projection that carries signals from the cell body toward the axon terminals where signals are then transmitted to other nerves or to end organs such as muscles. Where the axon terminal of one neuron (the presynaptic neuron) meets an end organ or a dendritic ending or cell body of another neuron (the postsynaptic neuron) is known as a synapse, with the gap between the presynaptic neuron and the end organ or postsynaptic neuron referred to as the synaptic cleft. Neurotransmitters, proteins, and organelles are transported along axons using a system of microtubules and neurofibrils. Anterograde transport from the cell body of neurotransmitters and structures to replenish the plasmalemma is quick, whereas anterograde transport of proteins and organelles needed for axoplasm generation or replenishment (regenerating or mature neurons) is slow. Retrograde transport toward the cell body to return organelles to the cell body for disposal and to carry nerve growth factor toward the cell body also occurs slowly. Both anterograde and retrograde transport require an energy source that is compromised if the blood supply to the nerve is disrupted. A nerve is made up of multiple nerve cell axons. Each axon is surrounded by a delicate layer of loose connective tissue known as the endoneurium. Groups of axons are then arranged in bundles called fascicles, and each fascicle is surrounded by perineurium, which is composed of flattened cells, basement membrane, and collagen fibers. Groups of fascicles, with arteries and veins between them, are then held together by a layer of dense connective tissue known as the epineurium to form a nerve (Fig 15.2). It is important to know this anatomy when performing regional anesthesia, as inadvertent intraneural injection of local anesthetic—into the nerve itself—can cause mechanical or ischemic nerve injuries, which are discussed later in this
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Dendrites
Nucleus
Cell body
myelinated, the myelin wraps around the outside of the epineurium. Myelin is a lipoprotein that acts as an insulator for the axon. The myelin around peripheral nerves is made by Schwann cells. Each Schwann cell forms a segment of myelin about 1 mm long. There are small gaps of uncovered axon between each of these segments known as nodes of Ranvier. The segments of axon between the nodes are called internodes (Fig. 15.3). Myelin accelerates the transmission of signals along the axon because impulses can jump from one node to the next rather than having to traverse the entire length of the axon. This jumping is known as saltatory conduction. Unmyelinated nerve cell axons conduct nerve impulses much more slowly than myelinated nerve cell axons.
■ PERIPHERAL NERVE PHYSIOLOGY
Axon branch Axon covered with myelin sheath Myelin
Neuromuscular junction
Muscle ■ FIGURE 15.1 Components of the neuron: the cell body containing the nucleus and other organelles, dendrites to receive information, an axon to transmit information over a distance, and axon terminals to transmit a signal to an end organ. (From Cohen BJ. Medical Terminology. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003, with permission.)
chapter. Ultrasound is often used when performing regional anesthesia so that the anesthesia provider can visualize the location of the injection and thereby reduce the risk of intraneural or intrafascicular local anesthetic injection. Some peripheral nerve cell axons are wrapped in concentric layers of myelin. If a nerve is
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Two positively charged ions, potassium (K+) and sodium (Na+), are primarily responsible for the transmission of signals along nerves. At rest, when no signal is being transmitted, there is more sodium outside the neuron and more potassium inside the neuron. These concentrations are maintained by sodium-potassium adenosinetriphosphatase (ATPase) pumps on the cell membrane. These pumps use ATP as their energy source to pump three sodium ions out of the cell for every two potassium ions they pump into the cell. This results in the inside of the cell being less positively charged than the outside, which is considered a relative negative charge. This negative charge, of about −65 mV, is known as the resting membrane potential. When the nerve is sufficiently stimulated, sodium channels on the nerve membrane open allowing sodium ions to rapidly enter the neuron, causing the inside to become positively charged relative to the outside. More and more sodium channels open until all of the available channels are open. This causes a rapid rise in membrane potential, or depolarization, which is followed by sodium channel inactivation (closure). Once the sodium channels close, sodium ions no longer enter the neuron. Potassium channels then open, and potassium ions flow out of the nerve, causing the membrane potential to return to baseline. This sequential nerve depolarization and repolarization is known as an action potential (Fig. 15.4). To restore the membrane potential (repolarization), sodium is pumped
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Section II • Anatomy, Physiology, and Pharmacology Peripheral nerve
Epineurium Perineurium Fascicle Peripheral (myelinated) nerve fiber
Endoneurium
Blood vessels supplying nerve (vasa nervorum)
Myelin sheath (formed by neurolemma or Schwann cells) Axon ■ FIGURE 15.2 Arrangement and ensheathment of peripheral, myelinated nerve fibers. All but the smallest peripheral nerves are arranged in bundles (fascicles), and the entire nerve is surrounded by the epineurium, a connective tissue sheath. Each small bundle of nerve fibers is also enclosed by a sheath—the perineurium. Individual nerve fibers have a delicate connective tissue covering—the endoneurium. The myelin sheath is formed by neurolemma (Schwann) cells. (From Moore KL, Dalley AF II. Clinical Oriented Anatomy. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999, with permission.)
out of the cell and potassium is pumped into the cell. Action potentials can be initiated on the cell body or the axon, but they usually start at the axon hillock, the point where the axon leaves the cell body (see Fig 15.1) because this is the most readily excitable part of the nerve. Once an action potential occurs at any point on the axon, the resulting currents will trigger depolarization and an action potential on the neighboring stretch of membrane, with the signal then being propagated along the nerve in a domino-like fashion, until it reaches the end of the nerve. Since each action potential is generated anew along the next excitable stretch of axon, the signal does not decay in strength.
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Myelinated segments of axons are not excitable and do not produce action potentials. When an action potential reaches a myelinated segment, the current is quickly conducted, with some decay, to the next node of Ranvier where action potentials are generated to boost the signal. This saltatory conduction is much quicker than the sequential action potentials that occur along the entire length of unmyelinated nerves. When the action potential reaches the axon terminal it generally triggers release of a neurotransmitter from vesicles in the axon terminal into the synaptic cleft. The neurotransmitter binds to postsynaptic receptors, causing activation of the end organ or excitation or inhibition
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Chapter 15 • Peripheral Nervous System
Node of Ranvier
Schwann cell nucleus
Schwann cell nucleus
Layers of myelin
Axon
Layers of myelin Axon
■ FIGURE 15.3 The Schwann cell migrates down a larger axon to a bare region, settles down, and encloses the axon in a fold of its plasma membrane. It then rotates around and around, wrapping the axon in many layers of plasma membrane, with most of the Schwann cell cytoplasm squeezed out. The resultant thick, multiplelayered coating around the axon is called myelin.
of a postsynaptic nerve. A postsynaptic neuron or end organ may receive excitatory and inhibitory inputs from many other neurons. With a sufficient predominance of excitatory inputs, the end organ will be activated or an action potential will start in the postsynaptic neuron and propagate along the length of this nerve.
■ PERIPHERAL NERVE PATHOPHYSIOLOGY Damage to nerves of the PNS is known as peripheral neuropathy. Neuropathy is usually classified according to its distribution and its cause. The typical distributions of neuropathy are mononeuropathy, mononeuritis multiplex, polyneuropathy, and autonomic neuropathy. A mononeuropathy is a neuropathy that only affects one nerve. Mononeuropathies are usually caused by compression, for example, carpal tunnel syndrome at the wrist or peroneal nerve compression at the knee after prolonged compression during surgery. Mononeuritis multiplex is simultaneous or sequential involvement of multiple nerves that is asymmetric and evolves over time. Mononeuritis multiplex is associated with a range of medical conditions, including diabetes, HIV, and lupus. In contrast, in polyneuropathy, many nerve cells throughout the body,
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but not necessarily all neurons within a nerve, are affected. The most common form of polyneuropathy is a distal symmetric form in which the axons are affected in proportion to their length, with the longest axons being affected first. This type of polyneuropathy presents initially with symmetric distal symptoms and is most often caused by a disease process, most often diabetes. Autonomic neuropathy is a form of polyneuropathy that affects the autonomic nervous system. Autonomic neuropathy is usually seen in people with long-standing diabetes and usually develops after polyneuropathy affecting the sensory and motor nerves. Peripheral neuropathy can cause sensory, motor, and autonomic signs and symptoms. Sensory symptoms of peripheral neuropathy include those related to loss of function (negative symptoms) such as numbness or gait instability due to loss of proprioception (the sensation of where one’s body is in space) as well as those related to overactivity hypersensitivity of a nerve (positive symptoms) such as pain, itching, tingling, and skin hypersensitivity. Motor nerve involvement can also cause negative symptoms, including weakness and muscle fatigue, as well as positive symptoms, including cramps and fasciculations (small local muscle twitching). Autonomic nerve involvement can cause heart rate and blood pressure instability as well as constipation and urinary symptoms. The signs of peripheral neuropathy found during the neurologic examination typically include sensory loss, weakness, and reduced stretch reflexes (e.g., knee jerk and ankle jerk) in the area innervated by the involved nerve. There are many causes of peripheral neuropathy including metabolic diseases, genetically inherited disorders, toxins, inflammatory diseases, vitamin deficiencies, mechanical trauma, and a few others (Table 15.1). Diabetes mellitus is the most common cause of peripheral neuropathy. About 2% of the population and about 30% of people with diabetes have symptoms of peripheral neuropathy. Peripheral neuropathy is the most common complication of diabetes. Diabetes generally causes a symmetric length-dependent polyneuropathy that first affects sensation in the toes and feet, causing pain and numbness, and then gradually ascends up the legs. When the symptoms reach approximately to the midcalf they also start to
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Na+
Na+
Cl
Cl
Resting state (unstimulated state)
Excited state (stimulated state)
Action potential Depolarization Repolarization Resting potential Stimulus Na+
Hyperpolarization
Return to resting state
Nerve impulse Site of summation of multiple stimuli
All-or-none action potentials with transient reversal of polarity
■ FIGURE 15.4 Recording of electrical changes that occur at rest and on stimulation. (From Snell R. Clinical Neuroanatomy. Philadelphia, PA: Lippincott Williams & Wilkins; 2001, with permission.)
affect the fingers. This pattern of involvement is known as stocking-glove distribution. The progression of diabetic neuropathy can be controlled to some degree by good blood sugar control. With poor blood sugar control, the neuropathy associated with diabetes progresses to also affect the motor nerves, causing foot weakness, and
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the autonomic nerves, causing constipation and abnormal sweating and circulation. Charcot-Marie-Tooth (CMT) disease (also called hereditary motor and sensory neuropathy) is a group of inherited peripheral nerve disorders that can affect the sensory and/or motor nerves. It usually starts in the teens or twenties with distal
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TABLE 15.1 COMMON CAUSES OF NEUROPATHY AND EXAMPLES CAUSE OF NEUROPATHY
EXAMPLES
Metabolic diseases
Diabetes mellitus, hypothyroidism
Genetic disorders
Charcot-Marie-Tooth disease
Toxins
Alcohol, medications (e.g., certain chemotherapy agents), heavy metals, excess vitamin B6
Inflammatory diseases
Guillain-Barré syndrome, leprosy (Hansen’s disease)
Vitamin deficiencies
Vitamin B12, vitamin B1 (thiamine)
Mechanical trauma
Compression, traction, accidental injection, lacerations, ischemia
Other
Thermal injury, radiation, viral (varicella, HIV)
weakness and sensory loss and progresses gradually over the person’s lifetime. CMT is the most common inherited neurologic disorder in the United States, affecting approximately 1 in 2,500 (about 100,000) Americans today. Although CMT generally produces only mild weakness at onset, over a number of years some variants of this disease can progress to produce significant difficulties with walking and breathing. Alcoholic neuropathy presents with a gradual decrease in sensory and motor peripheral nerve function in patients who chronically consume excessive amounts of alcohol. About 10%-15% of chronic alcoholics have symptoms of neuropathy, and up to 75% show signs of neuropathy if they undergo sensitive sensory testing. Alcoholic neuropathy is more common in men than in women and increases in incidence with age and the amount of alcohol consumed. Patients present with symmetric distal sensory loss, weakness, and loss of reflexes, which progress in a stocking-glove distribution similarly to the neuropathy associated with diabetes. Guillain-Barré syndrome (GBS), also known as acute inflammatory demyelinating polyneuropathy (AIDP), is the most common cause of acquired acute and subacute areflexic paralysis in humans, with an annual incidence of 1-2 per 100,000. GBS is an autoimmune disease that generally causes demyelination, primarily of the motor nerves. The symptoms of GBS, primarily an ascending paralysis, come on over a few days and can progress to the point where the person cannot walk or breathe because of lower extremity muscle and diaphragm weakness. However, unlike the previously described types of neuropathy, after a few weeks, the signs and symptoms of GBS start to reverse, with full or almost full
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recovery occurring in most patients with GBS over weeks to months. Vitamin B12 and vitamin B1 deficiencies can both cause peripheral neuropathy. Vitamin B12 deficiency usually occurs in the elderly as a result of malabsorption and has a range of neurologic, psychiatric, and hematologic manifestations. Vitamin B12 deficiency can affect the peripheral nerves and the spinal cord and also cause anemia, mood changes, and psychosis. Vitamin B1 (thiamine) deficiency, also known as beriberi, usually occurs in alcoholics or in others with generally poor nutrition, and often occurs in conjunction with overall malnutrition. Thiamine deficiency can also cause the CNS disorders, Wernicke’s syndrome and Korsakoff’s syndrome, which are associated with confusion, ataxia, eye movement abnormalities, and memory loss. Mechanical trauma, usually from excessive compression or stretch, is a common cause of peripheral mononeuropathy. Most mechanically induced nerve injuries are also associated with inadequate blood supply to the nerve. Nerves may be injured by a single application of highforce compression or traction or by repeated or prolonged application of lower levels of compression or traction. Nerve compression may be caused by edema of surrounding soft tissue from acute or chronic inflammation, increased compartmental pressures, space-occupying lesions, contact against bones, entrapment within soft tissues, and iatrogenic causes such as tourniquets, blood pressure cuffs, or supports during surgery. The amount, distribution, and duration of compression force applied to a nerve affect the nature and degree of nerve damage. Ideally, the lowest effective pressure and the shortest necessary tourniquet times are recommended to reduce the risk
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of nerve injury. Use of a tourniquet for more than 2 hours and pressures of greater than 350 mm Hg in the lower extremity and more than 250 mm Hg in the upper extremity increases the risk of compression neuropathy. In patients with low baseline arterial blood pressure, lower cuff inflation pressures may be more appropriate. Classic teaching mandates that if a procedure requires that a tourniquet be applied for more than 2 hours, then it be deflated for 5 minutes each 30 minutes of inflation time. Some literature now suggests that tourniquets should not remain continuously inflated for longer than 60 minutes in the upper extremity or 90 minutes in the lower extremity. In addition, it is recommended that wide cuffs, or padding under the tourniquet, be used to distribute the pressure. Acute nerve stretching or traction injuries are associated with fractures, joint dislocation, extreme limb or body segment positioning, as can occur during positioning for surgical access, and pulling on a limb segment, as can occur in obstetrical brachial plexus injury. Traction that stretches the nerve a small amount may only impair circulation within the nerve. But a greater stretch can cause structural failure and complete conduction block and affect sensory and motor function. When a nerve is accidentally injected, it may be damaged by the physical trauma of the needle and by exposure to the drug or agent. Accidental injection injuries occur most often during medication delivery (intramuscular medications or regional anesthesia procedures), with the sciatic nerve being the nerve most frequently injured by injection. Needle-stick injuries to nerves during acupuncture are rare but have also been reported. Nerves can also be injured during vascular access procedures (e.g., starting peripheral intravenous [IV] lines, arterial lines). Injection of a substance into a nerve usually causes severe, radiating pain. Nerve lacerations can occur as a result of contact with a sharp object, such as a piece of glass, metal, knife, razor blade, or scalpel, or from contact with a blunt object, such as components of power tools or other machinery, and gunshot wounds. Sharp injuries may occur intraoperatively. Nerves may also be damaged by heat, either through direct exposure or by exposure to electrical current or radiation. Electrical currents
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tend to travel along neurovascular bundles, damaging the nerve directly by heating it and causing coagulation necrosis or by damaging the nerve cell membrane and increasing its permeability. Radiation injury to peripheral nerves can occur during cancer treatment, and when this occurs, the damage to irradiated nerves appears to be related to an increase in temperature and is generally permanent.
■ MECHANISM OF ACTION FOR PERIPHERAL NERVE BLOCKADE Local anesthetics may work either peripherally or centrally to block neural transmission. They do so by blocking sodium channels in neuronal cell membranes. When sodium ions cannot move freely in and out of cells, neuronal action potentials cannot form or propagate. When neuronal action potentials are blocked, nerve function is lost. Exactly how avidly a local anesthetic will block neuronal transmission depends on the size of the nerve fiber, the frequency of electrical stimulation of the nerve, and the particular local anesthetic. Local anesthetics may block nerves peripherally with local administration. Nerves may also be blocked in the spinal cord when medications are injected into the intrathecal or epidural space. When local anesthetics block the action of dorsal horn neurons in the spinal cord this results in blockade of nociceptive activity. When local anesthetics block activity in the ventral horn of the spinal cord, motor function is blocked. See Chapter 21 for an in-depth discussion of how local anesthetics are used in regional anesthesia.
■ PHARMACOLOGY OF LOCAL ANESTHETICS Pharmacodynamics Local anesthetics are weak bases. They may exist in either a neutral form, in which they are lipid soluble, or a charged form, in which they are hydrophilic. How much of the compound exists in each form depends on the pH of the environment and the dissociation constant specific to the local anesthetic in question. Generally, the charged form of the local anesthetic is the active form. However, local anesthetics in their lipid-soluble form more readily penetrate the nerve cell membrane to exert their blocking action on the intracellular side of
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the sodium channel. The more lipid soluble the local anesthetic, the more likely it is to become sequestered in the myelin sheath of the nerve fiber or in other lipid-soluble compartments. Therefore, increasing lipid solubility of local anesthetics generally slows their rate of onset of action. More lipid-soluble local anesthetics also tend to have a longer duration of action because their sequestration in lipid-soluble compartments creates a repository from which they are slowly released. Increased lipid-solubility also predicts increased potency of local anesthetics via increased affinity for sodium channel receptors. Local anesthetics also exist in protein-bound and unbound forms. It is the unbound form of the local anesthetic that is pharmacologically active. Local anesthetics that are more highly protein bound are generally longer acting. Although the mechanism is uncertain, epinephrine when added to local anesthetics is reported to increase the duration of action and intensity of the block while decreasing systemic absorption. Epinephrine causes vasoconstriction, which may reduce systemic absorption, allowing more of the anesthetic to remain available for local nerve blockade. In general, the vasodilation caused by most local anesthetics is associated with a shorter duration of action of the anesthetic, whereas the vasoconstriction caused by epinephrine serves to prolong the duration of anesthetic activity. The vasoconstrictive effects of epinephrine are thwarted in acidic environments. The common practice of alkalinizing solutions containing local anesthetics with epinephrine serves to promote vasoconstriction and the resultant beneficial effects of epinephrine previously discussed. Regardless of whether epinephrine is present in the local anesthetic solution, alkalinization of the local environment in and of itself serves to inhibit neuronal conduction. Although no confirmatory data are available in humans, animal studies have shown that there is an increased risk of peripheral nerve injury associated with local anesthetics when mixed with epinephrine as compared to local anesthetics administered without epinephrine. Therefore, the decision as to whether or not epinephrine should be added to the local anesthetic solution requires a complex analysis of the relative risks and benefits by the anesthesia provider.
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Pharmacokinetics Because local anesthetics can be toxic when absorbed systemically, it is important to understand the pharmacokinetics of local anesthetic administration. Blood levels of a local anesthetic depend on absorption, distribution, and elimination of the local anesthetic. The rate of absorption of a local anesthetic depends on its site of injection, dose, and physiochemical properties, including whether or not it has been mixed with epinephrine. When local anesthetics are injected into more vascular areas, they will be more avidly absorbed systemically than when they are injected into areas containing more fat. Higher total doses of local anesthetics also result in greater absorption and higher blood levels. Increased lipid solubility and increased protein binding both result in less systemic absorption of local anesthetics. Distribution of the local anesthetic depends on organ blood flow, the partition coefficient specific to the particular local anesthetic, and the affinity with which the local anesthetic binds to plasma proteins. Once absorbed into the circulation, local anesthetics will tend to distribute most rapidly to highly vascular regions such as the heart and brain. Local anesthetics can be categorized as either aminoesters or aminoamides. Aminoesters include chloroprocaine, procaine, and tetracaine. Aminoamides include bupivacaine, lidocaine, mepivacaine, and ropivacaine. The elimination of aminoesters depends on their clearance by serum cholinesterases. Aminoamides, by contrast, are cleared by the liver. Thus, the elimination of aminoamides depends on liver function and protein binding. Pharmacokinetics also varies between individuals. Children and the elderly may experience increased systemic absorption of local anesthetics as well as decreased elimination rates. Individuals with cardiac or hepatic dysfunction will have altered distribution or elimination of local anesthetics. Therefore, these groups should be treated cautiously using lower doses.
■ CLINICAL USES OF LOCAL ANESTHETICS There are many different clinical uses for local anesthetics. Local anesthetics may be used neuraxially in epidural or intrathecal injections or infusions. They may be used in peripheral nerve blocks either as a single injection or as
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a continuous infusion through a catheter. Local anesthetics can also be administered topically to the skin or mucous membranes. IV administration of lidocaine can be used to decrease airway sensitivity preceding endotracheal intubation. IV lidocaine infusions or oral administration of mexiletine and tocaininde may be used to treat chronic neuropathic and central pain conditions.
■ LOCAL ANESTHETIC TOXICITY Local anesthetics readily cross the blood-brain barrier. Therefore, systemic absorption of local anesthetics may result in CNS toxicity. In addition, local anesthetics can affect heart function and conduction of electrical impulses within the heart. In general, local anesthetics with decreased rates of protein binding and clearance carry more risk for toxicity, while those with decreased systemic absorption and increased rates of elimination carry less risk for toxicity. With local anesthetic administration, careful attention must be paid to the route of administration and potential toxic doses. By decreasing systemic absorption, the addition of epinephrine to local anesthetics decreases the likelihood of toxicity. In hyperdynamic states, as during a physiologic stress response, cerebral blood flow is increased while hepatic blood flow is reduced. Such conditions increase the likelihood of local anesthetic toxicity by increasing the concentration of local anesthetic in the CNS and reducing the rate of local anesthetic clearance. Another way in which local anesthetic toxicity may occur is via inadvertent intravascular injection. A dose that is perfectly safe to administer as a nerve block can be lethal if injected into an artery or a vein. For this reason, prior to injection of local anesthetic, it is critical to aspirate through the needle to confirm that the needle position is not intravascular. Another technique commonly employed for ruling out inadvertent intravascular exposure is the administration of an epinephrine test dose. Intravascular epinephrine produces elevations in heart rate or blood pressure with 80% sensitivity. Although the two large case series available offer inconclusive results regarding its reliability, ultrasound guidance is another commonly accepted technique for the prevention of inadvertent intravascular injection of local anesthetics. Signs of systemic toxicity from local anesthetics range from sedation, lightheadedness,
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tinnitus, metallic taste, and perioral paresthesias at low doses, to seizures, coma, and cardiopulmonary arrest at high doses. At the doses and concentrations typically used clinically, local anesthetics are safe for peripheral nerves; however, at significantly higher concentrations, local anesthetics can cause nerve injury. Local anesthetics may also cause concentration-dependent damage to the spinal cord and nerve roots. There have been multiple case reports in which spinal infusion of lidocaine was associated with damage to the cauda equina, resulting in long-term bladder and gait dysfunction. By virtue of their sodium channel blockade, local anesthetics also produce dose-dependent cardiac conduction block. The degree of cardiotoxicity varies between local anesthetics by their relative potencies, with bupivacaine being relatively more potent and cardiotoxic and lidocaine being less. Toxic systemic effects of local anesthetics are exacerbated in the setting of hypoxia, hypercapnea, and acidosis. Therefore, when systemic toxicity does occur, supportive measures such as oxygenation and ventilation are critical. If cardiovascular depression occurs, resuscitation with a 20% lipid emulsion may be life saving. Traditional advanced cardiac life support (ACLS) interventions may be ineffective, although cardioversion or defibrillation often become effective after administration of the lipid emulsion. Therefore, maintenance of oxygenation and ventilation, high-quality cardiopulmonary resuscitation (CPR), and the lipid emulsion are the cornerstones of treatment for local anesthetic toxicity. Although propofol contains lipid, it does not constitute an effective lipid emulsion and can worsen outcomes if given for cardiac arrest from local anesthetic administration. Single enantiomeric preparations of local anesthetics, such as ropivacaine and levo-bupivacaine, are associated with decreased systemic toxicity. Anaphylactic allergic reactions to local anesthetics are rare and generally involve ester rather than amide compounds. Certain preservatives that may be added to local anesthetics can also cause allergic responses. Local and regional anesthesia plays an important role in perioperative pain management. The safe and effective provision of local and regional anesthesia is a complex task that demands knowledge of the anatomy and physiology of
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the PNS, the mechanisms of action of local anesthetics, and the potential complications that can result from their use. Our understanding of these concepts is ever evolving as further data are published and newer, safer, and more effective local anesthetics are developed.
REVIEW QUESTIONS 1. Peripheral nerve myelin A) Is made by Schwann cells B) Has gaps known as nodes of Ranvier C) Speeds nerve conduction D) Slows nerve conduction E) A, B, and C Answer: A. Some, but not all, peripheral nerves are myelinated. Myelinated peripheral nerves are wrapped in concentric layers of myelin around the epineurium. The myelin is made by Schwann cells in about 1-mm long segments with gaps known as nodes of Ranvier between them. Myelin accelerates nerve conduction by allowing for saltatory (jumping) conduction of signals from one node of Ranvier to the next.
2. Which of the following statements are TRUE about nerve action potentials? A) A polarized nerve membrane is rapidly depolarized. B) Depolarization cannot be conducted from one stretch of nerve membrane to another. C) Phosphorus ions flowing into the cell cause depolarization. D) Phosphorus ions flowing out of the cell cause repolarization. E) None of the above. Answer: A. Nerves transmit signals from one area of the body to another with action potentials. At rest the nerve is polarized. During an action potential, sodium first rushes into the nerve to depolarize it and then potassium rushes out of the nerve to repolarize it. An action potential occurs in one place in the nerve and this then triggers depolarization and an action potential on the neighboring segment, propagating the signal along the nerve in a domino-like fashion.
3. All of the following paired definitions are correct EXCEPT A) Mononeuropathy: neuropathy affecting only one nerve B) Mononeuritis multiplex: simultaneous or sequential involvement of multiple nerves that is asymmetric and evolves over time
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C) Polyneuropathy: neuropathy affecting many nerve cells throughout the body, but not necessarily affecting all neurons within a nerve D) Autonomic neuropathy: a form of polyneuropathy that affects the autonomic nervous system E) Fasciculations: large involuntary muscle jerks or movements of an entire limb Answer: E. Fasciculations are small, involuntary muscle twitches that are not large enough to result in movement about a joint or movement of an entire limb. The other terms are correctly defined.
4. Signs of local anesthetic toxicity may include all of the following EXCEPT A) Tinnitus B) Burning smell C) Perioral numbness D) Respiratory arrest E) Metallic taste Answer: B. Auditory changes including tinnitus, perioral numbness, metallic taste, seizures, cardiac arrhythmia, coma, and respiratory arrest are all classically described signs of local anesthetic toxicity. A burning smell, which may precede a temporal lobe seizure, is a sign of a focal (starting in an isolated area of the brain) seizure rather than a generalized (whole-brain) seizure as would be expected due to local anesthetic systemic toxicity.
5. Which of these local anesthetics is associated with the highest risk of cardiotoxicity? A) Lidocaine B) Bupivacaine C) levo-bupivacaine D) Ropivacaine E) Mepivacaine Answer: B. In general, the cardiotoxicity of local anesthetics is proportional to their potency, with bupivacaine being more potent and more cardiotoxic than lidocaine or mepivacaine. The single enantiomeric local anesthetic preparations including ropivacaine and levo-bupivacaine are associated with decreased systemic toxicity.
SUGGESTED READINGS Barash P, Cullen B, Stoelting R. Clinical Anesthesia. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001. Henderson, CA. A Comprehensive Introduction to the Peripheral Nervous System. Medtutor.Com. 2010. Neal J, et al. ASRA Practice Advisory on Local Anesthetic Systemic Toxicity. Reg Anesth Pain Med. 2010;35(2): 152-161. O’Brien M. Aids to Examination of the Peripheral Nervous System. 5th ed. Elsevier; 2010.
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16
Neuromuscular Anatomy and Physiology Jodi H. Kirsch and Jeffrey Kirsch ■ INTRODUCTION One of the key activities in conducting a general anesthetic for surgery can be to provide muscle relaxation (paralysis) in order to facilitate placement of an endotracheal tube in the trachea or to provide optimum operating conditions for the surgeon with quiet, soft muscles. This is accomplished with medications that interfere with normal functioning of the junction between nerves and muscles. Knowledge of the anatomy and physiology of the neuromuscular system will help anesthesia technicians understand the mechanism of how drugs affect the neuromuscular junction (NMJ) and how nerve stimulators can be used to monitor the condition of the neuromuscular system.
■ ANATOMY OF THE NEUROMUSCULAR SYSTEM The neuromuscular system, as implied by the name, is composed of nerves and muscles. These nerves are considered peripheral nerves. They exit from the spinal cord and then act upon the muscles of the body. There are three different types of muscle: cardiac muscle in the heart, smooth muscle, and skeletal muscle. Although similar, each of the different types of muscles has slightly different properties. Whereas skeletal muscle can be controlled at the desire of an individual, both cardiac and smooth muscle contraction and relaxation occur independent of direct individual control. Smooth muscle is an involuntary type of muscle that is controlled by the autonomic nervous system (see Chapter 14). Examples of smooth muscle include the walls of blood vessels, lymphatic vessels, bronchioles in the lungs, urinary bladder, and the reproductive tract of males and females. Contraction or relaxation of these muscles occurs in response to
activity/need, rather than by direct control of the individual. Cardiac muscle is also a type of involuntary muscle. While our body is composed of smooth muscle, cardiac muscle, and skeletal muscle, the majority of the body is skeletal muscle. Skeletal muscle is a voluntarily controlled, striated (under the microscope)-appearing tissue that enables our body to move. Skeletal muscles attach to bones by way of tendons. Skeletal muscle is composed of many muscle fibers, which are held together by protein and fibrous tissue (Fig. 16.1). These muscle fibers in turn are composed of multiple myofibrils (the actual individual muscle cells). Within each myofibril are abundant mitochondria (the energy-producing organelle in all cells), smooth endoplasmic reticulum (the cell organelle that produces lipids, metabolizes carbohydrates, and regulates calcium levels in the cell), and most importantly multiple nuclei. Multiple nuclei are imperative for skeletal muscle function due to the high activity level required of these muscles. The main contractile unit in skeletal muscle cells is called the sarcomere. There are many sarcomeres within one myofibril. When a sarcomere is further examined under an electron microscope, one observes repeating sections of light and dark areas. The light areas are the thin filaments. Thin filaments are composed of the protein, actin. The dark areas of the sarcomere are the thick filaments and are composed of the protein myosin. During contraction the myosin on the thick filaments binds to actin on the thin filaments. The binding of actin to myosin is a process that requires calcium and energy. The energy for the reaction is supplied by adenosine triphosphate. Overall, this process results in shortening of the sarcomere, which is anatomically
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Tendon
A dense, fibrous connective tissue that is continuous with the periosteum and attaches muscle to the bone
Periosteum
A tough, fibrous connective tissue that covers the surface of bones, rich in sensory nerves, responsible for healing fractures
Belly
Epimysium
Thick contractile portion (or body) of the muscle
Fibrous tissue enveloping the entire muscle and continuous with the tendon
Perimysium
Fibrous tissue that extends inward from epimysium, surrounding bundles of muscle. Each bundle bound by perimysium is called a fascicle.
Fascicle
A group of fibers that have been bound by perimysium
Endomysium
A delicate connective tissue that surrounds each muscle fiber
Z-line
Boundary of two sarcomeres
H-zone
Consists of stacks of myosin filaments
Z-line
Sarcomere
Portion of muscle fibers found between two Z-lines
Muscle fibers
Long, cylindrical, multinucleated cells with striations
Myosin Actin
Thick and thin filaments active during muscle contraction
■ FIGURE 16.1 Muscle anatomy.
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recognized as muscle contraction. The molecular basis of muscle contraction is explained by the “sliding filament theory.” This theory states that in the presence of calcium and energy, actin and myosin slide past each other and the sarcomere shortens. The protein filaments overlap but do not shorten. The overlap is what causes the sarcomere to shorten.
■ THE NEUROMUSCULAR JUNCTION The NMJ is composed of the terminal portion of a motor neuron axon and the motor end plate of a muscle fiber. The function of the NMJ is to allow the muscle to contract based on messages originating in the brain. Once the motor cortex of the brain sends the message, the message is delivered by way of action potentials (electrical signals) along the axons of motor neurons. When the action potential is sent down the axon, it eventually reaches the NMJ (Fig. 16.2). The junction across which one nerve sends a signal to another nerve, muscle, or gland is called a synapse. The terminal portion of the nerve where the signal originated is the “presynaptic” nerve. Once the nerve action potential arrives at the terminal portion of the presynaptic nerve, it causes acetylcholine (ACh) to be released from the axon terminal into an area between the axon and the motor end plate, called the synaptic cleft. The ACh then travels across this area to attach to nicotinic ACh receptors on the motor end plate of the muscle (Fig.16.3). Binding of ACh to these receptors causes sodium and potassium channels to open in the muscle cell membrane. Sodium and potassium travel opposite each other; sodium travels into the cell, and potassium trickles outward. Because sodium rushes into the motor cell much more quickly than potassium leaves the cell, the cell becomes more positively charged and
Peripheral nerve Neuromuscular junction Anterior horn cell
Muscle fiber
Ventral root ■ FIGURE 16.2 A motor nerve axon terminating at the junction between the nerve and muscle.
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depolarizes (a change in the charge of the interior of the cell membrane compared to the outside). Depolarization of the muscle cell then causes the release of calcium from sarcoplasmic reticulum in the muscle cell. Excess calcium in the muscle cell binds to the thin filament in the sarcomere, triggering a cascade of events resulting in muscle contraction. But how does our brain send a message to the many muscles of the body to contract or relax? Let us use the example of an anesthesia technician carrying an arterial line setup to an operating room. When the anesthesia technician wants to lift his or her arm, the bicep muscle must contract. A message is sent from the brain to tell the biceps muscle that it must shorten to accommodate the weight of the arterial line setup. The message originates in upper motor neurons in the motor area of the brain. The upper motor neuron crosses to the opposite side at the level of the brainstem and then synapses with a lower motor neuron in the anterior portion of the spinal cord, just before exiting the spinal canal. Thus, movement of the right side of your body comes from a message that originates in the left side of your brain. Because the movement of the arm happens almost instantaneously, the signal must travel very quickly from the brain to the muscles. This is why motor neurons are myelinated nerve fibers, to speed conduction (see Chapter 15). Myelin is an insulating material that covers nerve axons to increase the speed of signal transmission.
■ DISEASES THAT ALTER NEUROMUSCULAR FUNCTION Normal function of the complex transmission of information from the brain to muscle through the NMJ is essential to each individual for normal movement. Unfortunately, there are several disease processes that interrupt this normal function with defects that affect each of the steps along the way. Most proximal to the NMJ would be a defect in the motor cortex. For example, a stroke (an obstruction in a blood vessel or a ruptured blood vessel) in the motor cortex can prevent movement in the extremity on the opposite side of the body. This type of injury would present with upper motor neuron signs and symptoms (see below). The motor signals that originate in the cortex of the brain are sent out to the body through motor neurons. Disease of
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Nerve impulse Cerebral cortex
Axon motor neuron
Spinal cord
Motor end plate Packets of acetylcholine Nerve impulse From cerebral cortex Upper motor neuron
Lower motor neuron
Muscle cell nucleus
A
Axon branches
Acetylcholine receptors
Bundle of myofibrils
Neuromuscular junction
Synaptic space
Muscle fibers
Myofibril
Muscle fiber Type 1 fibers Type 2 fibers
Capillary
Nucleus
B ■ FIGURE 16.3 The neuromuscular junction with release of presynaptic acetylcholine binding to postsynaptic nicotinic receptors.
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the upper motor neurons themselves can affect transmission of the signal. Two of the most common central nervous system diseases affecting motor neurons include multiple sclerosis and Parkinson’s disease. A spinal cord injury could also interfere with upper motor neurons as they pass through the spinal cord. Because the nerves have already crossed over to the opposite side of the body at the level of the brainstem, a spinal cord injury will cause upper motor neuron signs and symptoms on the same side as the injury. Upper motor nerve signs and symptoms evolve over time (weeks to months) and include increased intensity of reflexes (e.g., knee jerk reflex) and muscle spasticity. Disease or injury can also affect lower motor neurons. Diseases that directly affect lower motor neurons include Lou Gehrig’s disease, Charcot-Marie-Tooth disease, and Guillain-Barré syndrome. Trauma is another common source of injury to low motor neurons after they leave the spinal canal. This can even happen in the operating room. For example, poor positioning of a patient on the operating room table can cause prolonged compression of a nerve, resulting in permanent injury. Patients with lower motor neuron injuries exhibit decreased reflexes and muscle wasting. Disorders of either upper or lower motor neurons can cause proliferation of ACh receptors on the muscle membrane. Finally, disease can strike the NMJ itself. There are two main diseases of the NMJ: Lambert-Eaton syndrome and myasthenia gravis. In LambertEaton syndrome, patients have antibodies to the mechanism that causes release of calcium within the presynaptic nerve cell. Patients with LambertEaton syndrome often have concurrent lung cancer. Although there are medications that make the symptoms (weakness and fatigue) better, the best treatment for weakness in patients with LambertEaton syndrome is to address the underlying cancer. In myasthenia gravis, patients have antibodies to nicotinic receptors on the postsynaptic side of the NMJ (muscle motor end plate). Efforts to treat patients with myasthenia gravis focus on preventing antibody attack of the nicotinic receptors, which ultimately improves transmission of nerve signals from the brain and strength/ endurance. Patients with myasthenia gravis are also treated with drugs that limit the breakdown of ACh (e.g., acethylcholinesterase inhibitors) in the synaptic cleft, which allows for a higher
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concentration of ACh and an increased ability to bind to the undamaged nicotinic receptors.
■ PHARMACOLOGIC NMJ BLOCKADE Anesthesiologists use their understanding of the anatomy and physiology of neuromuscular transmission and the NMJ to achieve muscle relaxation. In the clinical setting, muscle relaxation is important to prevent patient movement, to relax muscles and improve operating conditions for the surgeons, and to paralyze the laryngeal muscles (facilitate intubation). The agents used to achieve paralysis are referred to as neuromuscular blocking agents. Anesthesia providers must determine the proper way to block neuromuscular transmission. Insufficient paralysis may make intubation difficult, if not impossible, or a patient may move at an inopportune time during surgery and sustain an unintended injury. If too much neuromuscular blocking agent is given, the patient may have weak breathing muscles and respiratory insufficiency after surgery. It is by a thorough knowledge of the NMJ physiology and pharmacology that anesthesia providers can properly utilize neuromuscular blockers. There are two basic ways to block neuromuscular transmission: presynaptic inhibition of ACh release or postsynaptic blocking of the ACh nicotinic receptors on the muscle end plate. Although not used clinically in the operating room, one example of a substance that causes presynaptic inhibition of ACh release is botulinum toxin. Botulinum toxin can be administered in small doses to weaken overactive muscles in various muscle diseases (dystonias). This potent exotoxin works by destroying the proteins required for vesicles in the presynaptic nerve to release ACh. Other more commonly used medications that can cause presynaptic NMJ blockade are aminoglycoside antibiotics (e.g., streptomyosin, gentamicin). Aminoglycosides interfere with the movement of calcium, which limits the release of ACh into the synaptic cleft. Although these drugs are occasionally administered to patients in the operating room, they do not cause significant neuromuscular blockade, unless administered in very high concentrations or impaired kidney function decreases their elimination. In extremely rare situations, neuromuscular blockade caused by aminoglycoside antibiotics can cause respiratory depression. In order to limit the unwanted neuromuscular blockade that
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Chapter 16 • Neuromuscular Anatomy and Physiology
occasionally occurs with the administration of aminoglycoside antibiotics, the anesthesiologist may administer intravenous calcium or cholinesterase inhibitors (drugs that decrease the breakdown of ACh in the synaptic cleft). In the operating room, anesthesiologists administer NMJ-blocking drugs that primarily work on the postsynaptic side of the NMJ (they may also have very small effects on presynaptic nerves). Postsynaptic NMJ blockade falls into two main categories, with each achieving blockade by a different mechanism, depolarizing NMJ blockers and nondepolarizing NMJ blockers. Depolarizing agents (e.g., succinylcholine) bind to the nicotinic ACh receptor, causing a depolarization of the motor end plate. This causes the muscle to quickly contract and then relax. Continued presence of succinylcholine in the synaptic cleft with binding to nicotinic receptors prevents further stimulation of the muscle, resulting in paralysis. Whereas ACh is metabolized quickly to allow the muscle to quickly recover, metabolism of succinylcholine is much slower, which results in more prolonged (5-10 minutes) depolarization of the affected muscle cell and transient paralysis. Because succinylcholine causes depolarization of a large amount of muscle cells and the associated leakage of potassium out of the cell, its administration is associated with a small (0.7-1.0 mEq/L) increase in serum potassium level. This increase is generally not clinically significant; however, there are several groups of patients who are at risk for much greater increases in serum potassium. Any condition that results in a greater density of nicotinic receptors on the postsynaptic membrane is at risk for much greater rises in serum potassium after succinylcholine administration. Examples of patient groups with higher densities of nicotinic receptors include those with upper or lower motor neuron injury, prolonged periods of bed rest, or burns. Therefore, administration of succinylcholine is contraindicated in patients in these groups, as serum potassium may increase to levels high enough to cause cardiac arrest. Today in anesthesia, nondepolarizing agents are most commonly used to achieve NMJ blockade. Nondepolarizing NMJ blockers are often also called competitive blockers due to their mechanism of action. Competitive NMJ blockers compete against ACh for the ACh nicotinic receptor sites on the postsynaptic membrane.
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Nondepolarizing agents prevent the binding of ACh with nicotinic receptors; thus, depolarization does not occur and the muscle will remain in the noncontracted state. Various medications fall into the nondepolarizing category, including rocuronium, vecuronium, pancuronium, and atracurium. Nondepolarizing agents are longer acting than depolarizing agents due to their slower metabolism. They also have a slower onset time unless given in extremely high doses. For example, succinylcholine has an onset time of 30 seconds and will last for 7-10 minutes, whereas rocuronium has an onset time of 2-3 minutes and will last from 30 to 60 minutes. Both the onset time and the duration of action of nondepolarizing drugs are affected by the dose of the drug; the higher the dose, the quicker the onset and also the longer the duration of action. In addition, the duration of action of nondepolarizing agents can be prolonged even further in patients with certain medical conditions including kidney disease, liver disease, respiratory acidosis, metabolic alkalosis, hypothermia, presence of calcium channel blockers in the blood, increased magnesium in the blood, and decreased potassium in the blood. Due to the longer duration of action of nondepolarizing agents, it is often necessary to antagonize (“reverse”) the agent’s action. In order for the action of the NMJ-blocking agent to be antagonized, the patient must be given two different types of medications: acetylcholinesterase inhibitors (e.g., neostigmine or physostigmine) and anticholinergic agents (e.g., atropine or glycopyrolate). The acetylcholinesterase inhibitor prevents the metabolism of ACh in the synaptic cleft, which increases the amount of ACh in the synapse. The large amounts of ACh are better able to compete with the NMJ-blocking drug for the nicotinic receptor and initiate muscular contraction. Unfortunately, acetylcholinesterase inhibitors also increase ACh concentration at many sites in the body, not just at the NMJ. Due to binding with ACh receptors throughout the body, when used alone acetylcholinesterase inhibitors are associated with severe reductions in heart rate and gastrointestinal cramping referred to as a cholinergic crisis (see Chapter 14 for locations of cholinergic receptors in the body). In fact, anticholinesterases are commonly used as poisons. To prevent a cholinergic crisis, anticholinergic drugs that preferentially block
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muscarinic receptors for ACh (e.g., glycopyrolate or atropine) are administered simultaneously with the administration of an acetylcholinesterase inhibitor.
■ MONITORING NEUROMUSCULAR BLOCKADE The amount of neuromuscular blockade may be monitored by observing clinical signs or by objective assessment with a nerve stimulator. The use of objective means of measurement helps the anesthesiologist determine if the proper amount of blockade has been reached or to ensure that the blockade has been sufficiently reversed. As discussed earlier, the assessment of the degree of neuromuscular blockade is clinically important to prevent complications from insufficient blockade or inadequate reversal at the end of a case. Clinical signs can be used to estimate neuromuscular recovery. These signs include a head lift greater than 5 seconds, leg lift greater than 5 seconds, the patient holding a tongue depressor to the roof of his mouth while the anesthesiologist tries to pull it out, and lastly, a maximum inspiratory pressure of greater or equal to 50 cm H2O. They are often used as a measure of adequate reversal of neuromuscular blockade. Unfortunately, these signs require a cooperative patient and cannot be used during a general anesthetic to monitor the depth of neuromuscular blockade. The use of a nerve stimulator overcomes this limitation. These devices help to assess the function of the NMJ by stimulating a peripheral nerve and monitoring the effect on muscle innervated by the nerve (e.g., stimulation of the ulnar nerve and observation of the effect on the adductor pollicis muscle). After placing the stimulating electrodes near the peripheral nerve, the anesthesiologist will apply a train of four stimulations to the nerve. These stimuli are four equal impulses administered 0.5 seconds apart. The reaction of the muscle is used to determine the intensity of the block. The response of the muscle depends upon whether the neuromuscular agent administered was a nondepolarizing or depolarizing drug. Nondepolarizing agents are characterized by a response called fade; the muscle response to the stimulation decreases with repetitive nerve stimulation. With a train of four stimulations, the strength of each muscular contraction will
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diminish if there is residual neuromuscular blockade. The mechanism by which this fading occurs is controversial and may involve effects that the NMJ blockers have on presynaptic mechanisms of ACh release. Another characteristic of nondepolarizing agents is called posttetanic potentiation. If a tetanic stimulation is applied to a muscle and a single stimulus is immediately applied right afterward, the muscle twitch response to the single stimulus is greater than the previous tetanic muscle response. This response occurs because of an increase in presynaptic ACh release in addition to more ACh being present at the motor end plate. Depolarizing agents do not exhibit posttetanic potentiation or fade in response to a train of four stimuli. With depolarizing agents, the muscle response to all four of the nerve stimuli will be exactly the same.
■ SUMMARY As an anesthesia technician, it is imperative to understand the physiologic events leading to muscle contraction, what would happen if the normal neuromuscular response was blocked, the agents used to create the neuromuscular blockade, and how to measure the blockade during surgery. By understanding the fundamental general principles involved in the neuromuscular system and how it relates to anesthesia, it will better prepare anesthesia technicians to foresee what will be asked of them during many surgical procedures.
REVIEW QUESTIONS 1. Which of the following is the CORRECT order of events for muscle contractions? A) The motor cortex of the brain sends a message → Action potential sent down the axon → ACh attaches to the nicotinic ACh receptors on the motor end plate. B) ACh from the axon terminal goes to the synaptic cleft → Action potential sent down the axon → muscle contraction. C) ACh attaches to the nicotinic ACh receptors on the motor end plate → Action potential sent down the axon → muscle contraction. D) The motor cortex of the brain sends a message → ACh attaches to the nicotinic ACh receptors on the motor end plate → Action potential reaches the presynaptic terminal. E) None of the above.
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Chapter 16 • Neuromuscular Anatomy and Physiology Answer: A. The correct order of events is as follows: The motor cortex of the brain sends a message → Action potential sent down the axon → Action potential reaches the presynaptic terminal → ACh attaches to the nicotinic ACh receptors on the motor end plate→ muscle contraction.
2. If a patient were to have a stroke on the right side of the motor cortex, which area of the body would be affected and what would be the resulting symptoms? A) Right side of the body, lower motor neuron signs B) Right side of the body, upper motor neuron signs C) Left side of the body, upper motor neuron signs D) Left side of the body, lower motor neuron signs E) None of the above Answer: C. Due to crossover of nerve fibers, the motor cortex of the brain affects the opposite (contralateral) side of the body. Therefore, a stroke in the right motor cortex will affect the left side of the body. Upper motor neurons are in the brain. Lower motor neurons are in the nerves that leave the spinal cord.
3. What are the two basic ways to block neuromuscular transmission at the neuromuscular junction? A) Presynaptically block receptor release; postsynaptically block ACh nicotinic receptors on the muscle end plate B) Presynaptically block ACh release; postsynaptically block ACh muscarinic receptors on the muscle end plate C) Presynaptically block ACh release; postsynaptically block ACh nicotinic receptors on the muscle end plate D) All of the above E) None of the above Answer: C. The presynaptic neuron releases ACh as the neurotransmitter, which then binds to nicotinic ACh receptors on the motor end plate of the muscle. Muscarinic ACh receptors are present in other parts of the body. Receptors are not released; they are present on cell membranes.
4. Which of the following statements are FALSE regarding nondepolarizing agents? A) Examples of nondepolarizing agents include rocuronium, vecuronium, pancuronium, and atracurium. B) Nondepolarizing NMJ blockers are also called competitive blockers and are most commonly used in the operating room. C) Nondepolarizing agents are shorter acting and have a faster onset than depolarizing agents.
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D) Nondepolarizing agents can be reversed with anticholinesterases. E) All of the above are TRUE. Answer: E. All of the above statements are true regarding nondepolarizing neuromuscular blockers. These agents are competitive antagonists for the ACh receptor on the motor end plate. To reverse the effects of these agents, the administration of an anticholinesterase will prevent the breakdown of ACh and allow it to outcompete the nondepolarizing agent for the ACh receptor. The agent with the fastest onset and shortest duration of action is succinylcholine, which is a depolarizing agent.
5. Which of the following statement is TRUE when monitoring neuromuscular blockade on a twitch monitor? A) Nondepolarizing agents are monitored by placing the twitch monitor on the facial nerve only, while depolarizing agents are monitored by placing the twitch monitor on the ulnar nerve only. B) Nondepolarizing agents demonstrate a response called “fade” where the twitch response decreases with repetitive nerve stimulation. C) Depolarizing agents always cause “fade.” D) Neuromuscular blockade caused by nondepolarizing agents cannot be monitored with a nerve stimulator E) None of the above. Answer: B. Nondepolarizing agents cause the muscle response (twitch) to a stimulus applied to a nerve innervating the muscle to “fade.” The twitch strength will decrease with repetitive stimuli. This is a major method of monitoring the intensity of neuromuscular blockade caused by nondepolarizing agents. The nerve stimulator may be placed over a variety of nerves including the ulnar and facial nerves. Depolarizing agents, in most cases, do not cause “fade.”
SUGGESTED READINGS Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009. Chandler JT, Brown LE. Conditioning for Strength and Human Performance. Philadelphia, PA: Lippincott Williams & Wilkins; 2007. Fuchs-Buder T. Neuromuscular Monitoring in Clinical Practice and Research. Heidelberg: Springer; 2010. Neal MJ. Medical Pharmacology at a Glance. 5th ed. West Sussex, UK: Wiley-Blackwell; 2005. Subramaniam R. A Primer of Anesthesia. New Delhi, India: Jaypee Brothers Publishers; 2008.
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SECTION
III
Principles of Anesthesia
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CHAPTER
17
Sedation Angela Kendrick and Dawn M. Larson ■ INTRODUCTION Intravenous (IV) anesthetics may be used for induction of general anesthesia, maintenance of general anesthesia, and sedation. Sedation typically involves an agent called a “sedative-hypnotic” and refers to a state of calm and relaxation, whereas hypnosis refers to sleep. A sedative is often combined with an analgesic, which is used to treat pain. The combination of the two agents can be very effective; however, it may also potentiate each medication more than if they were given independently. Sedation involves a continuum from minimal sedation leading to moderate and deep sedation and eventually to general anesthesia. The definition of these states of consciousness has been published by the American Society of Anesthesiologists (ASA). In addition, the ASA has published practice guidelines for those who may administer sedation and standard monitoring required during a sedation case. The term monitored anesthesia care (MAC) does not refer to the depth of anesthesia but rather a sedation or service that is provided by an anesthesiologist. The term is falling out of favor and is being replaced by the term depth of sedation, regardless of who provides the service. Sedation is useful in a variety of settings: the intensive care unit (ICU) sedation for mechanical ventilation, sedation for procedures or imaging, and as an adjunct to regional anesthesia in the operating room (OR).
■ DEFINITION OF THE DEPTH AND LEVELS OF SEDATION/ANALGESIA Minimal Sedation (Anxiolysis): Cognitive function may be impaired, but there is a normal response to verbal stimuli with unaffected airway, ventilation, or cardiovascular function. Moderate Sedation/Anesthesia (aka Conscious Sedation): Purposeful response to verbal or tactile stimuli with airway, ventilation, and
cardiovascular functions that are adequate and should require no intervention. Deep Sedation/Analgesia: Purposeful response only following repeated or painful stimulation where the airway and ventilation often need support and the cardiovascular function is usually maintained. Providers who perform deep sedation should be qualified to respond to a patient who enters a state of general anesthesia. General Anesthesia: Unresponsive even to painful stimuli where the airway and ventilation are generally inadequate without intervention and the cardiac function may need intervention (Table 17.1).
■ PREEVALUATION FOR SEDATION CASES A task force of the ASA on sedation guidelines recommends that the clinician performing the sedation performs an assessment of the patient prior to administration of sedation. This should include the patient’s medical history, vital signs, allergies, current medications, response to previous sedation, and history of substance abuse. Additionally, a focused physical examination including heart and lung auscultation and airway evaluation should be included. An explanation of the risks, benefits, and alternatives of the level of sedation required should be provided to patients or their legal guardian prior to the procedure. Patients undergoing sedation should be advised not to eat solids or drink liquids according to the ASA guidelines for perioperative fasting. In emergency situations, the risks and benefits of sedation on nonfasted individuals should be considered and discussed with the patient or guardian regarding the potential for pulmonary aspiration of gastric contents (Table 17.2).
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TABLE 17.1 AMERICAN SOCIETY OF ANESTHESIOLOGY DEPTH OF ANESTHESIA
DEFINITIONS MINIMAL SEDATION (ANXIOLYSIS)
MODERATE SEDATION/ ANALGESIA (CONSCIOUS SEDATION)
DEEP SEDATION/ ANALGESIA
GENERAL ANESTHESIA
Responsiveness
Normal response to verbal stimulation
Purposeful response to verbal or tactile stimulation
Purposeful response after repeated or painful stimulation
Unarousable, even with painful stimulus
Airway
Unaffected
No intervention required
Intervention may be required
Intervention often required
Spontaneous ventilation
Unaffected
Adequate
May be inadequate
Frequently inadequate
Cardiovascular function
Unaffected
Usually maintained
Usually maintained
May be impaired
Monitoring is recommended by the ASA according to the level of sedation. Data should be recorded prior to the start of sedation, during the procedure, and after completion (Table 17.3). The personnel performing the sedation should not be the person performing the procedure and should be present to administer medications and monitor the patient during the procedure. This person may help with minor tasks related to the procedure when the patient is stable; however, he or she may not perform these tasks during a deep sedation. Additionally, he or she should be knowledgeable of the pharmacology of both sedating and analgesic medications as well as the reversal agents for those medications. There should be a basic life support (BLS) certified health care provider in the room, with advanced cardiac life support (ACLS) personnel available within
5 minutes. The exception is the administration of deep sedation, which requires the presence of an ACLS certified provider in the room.
■ SEDATION SCALES Many sedation scales exist to help categorize the level of arousal during a procedure or within the ICU. They attempt to standardize the level of consciousness to facilitate communication between providers. Two of the more common scales are the Ramsay Scale, which was introduced over 30 years ago, and the Riker SedationAgitation Scale (SAS) (Tables 17.4 and 17.5).
■ SUPPORT EQUIPMENT Because sedation is a continuum and medications are used that can cause respiratory depression and hemodynamic compromise, rescue equipment should be readily available (Table 17.6).
■ SEDATION AGENTS Propofol TABLE 17.2 AMERICAN SOCIETY
OF ANESTHESIOLOGY FASTING GUIDELINES INTAKE
MINIMUM FASTING PERIOD
Clear liquids
2h
Breast milk
4h
Nonhuman milk
6h
a
Light meal
6h
Heavy meal
8h
a
Light meal typically consists of clears and non–fat-based snack.
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Propofol is in the class of akylphenols and produces a state of anesthesia without analgesic (pain-relieving) properties. The mechanism of action is primarily by activation of γ-aminobutyric acid (GABA) receptors. It is lipid soluble and is prepared in an emulsion that consists of soybean oil, purified egg phosphatide, glycerol, and an inhibitor of antibacterial growth. It has a white milky appearance, is stable at room temperature, and once opened should be discarded after 6 hours to avoid bacterial contamination. It is also a potent antiemetic, even when used at dosing levels commonly used in sedation
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TABLE 17.3 SEDATION MONITORING – Pulse oximetry – Blood pressure and heart rate at 5-minute intervals – Electrocardiograph (EKG) for patients with cardiovascular disease and for all deep sedation procedures – Response to verbal commands if applicable – Adequacy of pulmonary ventilation (observation, auscultation) – Exhaled carbon dioxide monitoring when patients are at a distance from the sedation provider and for all deep sedation procedures (via nasal canula port or an angiocath inserted into a face mask)
dosing. Propofol may cause respiratory depression at therapeutic doses and a dose-dependent decrease in arterial blood pressure. Sedation dosing at 25-75 μg/kg/min is typically sufficient, although there is variability among patients. Metabolism occurs via the liver; however, other sites in the body may play a role as well. Propofol has a rapid onset and a short elimination half-life of 2-8 minutes, which is a desirable feature for sedation procedures. Because of propofol’s alternative use as an induction agent and its ability to continue into the level of general anesthesia, its use should follow guidelines for deep sedation regardless of the actual level of sedation planned.
Barbiturates Barbiturates are among the oldest IV anesthetics. They are still in use today but have been often supplanted by newer anesthetics. Barbiturates are hypnotics and do not possess analgesic properties. Their mechanism of action is mediated primarily on the neurotransmitter GABA; however, it is likely there are other neurotransmitters involved. They exist as sodium salts and are reconstituted for IV usage in sterile water or 0.9% sodium chloride solutions. As a basic solution,
TABLE 17.4 RAMSAY SCALE SCALE
DESCRIPTION
1
Anxious or restless or both
2
Cooperative, orientated, and tranquil
3
Responding to commands
4
Brisk response to stimulus
5
Sluggish response to stimulus
6
No response to stimulus
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this will precipitate when used with lactated Ringer’s solution or acidic medications such as pancuronium, rocuronium, alfentanil, sufentanil, or midazolam. The two classes of barbiturates are oxybarbiturates and thiobarbiturates, with the most commonly used being methohexital and thiopental, respectively. Thiopental was introduced into clinical practice in 1934. A sedation dose of thiopental is 50-100 mg IV. The onset of both medications is quick at 10-30 seconds, with the elimination half-life of 4 hours for methohexital and 12 hours for thiopental. Methohexital is commonly used in electroconvulsive therapy treatment for depression. Side effects include dose-dependent respiratory depression and hypotension. Metabolism for both classes is via the liver.
Benzodiazepines In addition to properties of sedation and hypnosis, all benzodiazepines have anticonvulsant activity. The mechanism of action for this group is mediated through activation of the GABA receptor. Of the many types of benzodiazepines, there are several that are more frequently encountered for sedation. The most widely used benzodiazepine in anesthesia practice is midazolam (Versed), which can be administered intravenously or orally (per os [PO]). It has a slower onset and metabolism than propofol but faster than other benzodiazepines, which makes it a desirable sedation medication. A typical IV sedation dose is 0.015-0.03 mg/kg in increments to achieve desired sedation. Lorazepam (Ativan) is an oral or IV medication and may be used frequently when only minor anxiolysis is required from an oral medication. Diazepam (Valium) is infrequently used because of its long halflife. Side effects of all benzodiazepines include dose-dependent respiratory depression and,
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TABLE 17.5 RIKER SEDATION-AGITATION SCALE SCORE
TERM
DESCRIPTION
+4
Combative
Overtly combative or violent; immediate danger to staff
+3
Very agitated
Pulls on or removes tube(s) or catheter(s) or has aggressive behavior toward staff
+2
Agitated
Frequent nonpurposeful movement or patient-ventilator dyssynchrony
+1
Restless
Anxious or apprehensive but movements not aggressive or vigorous
0
Alert and calm
−1
Drowsy
Not fully alert, but has sustained (>10 s) awakening, with eye contact, to voice
−2
Light sedation
Briefly ( 30 degrees) may also stretch the nerve.
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6. Which is the most common cause of perioperative peroneal neuropathy in a patient who is positioned in a lithotomy position? A) Compression of the nerve by a leg holder as the nerve wraps around the fibular head B) Hyperextension of the knee and ankle simultaneously C) Prolonged dorsiflexion of the foot in a leg holder D) Excessive hip flexion when the lower extremity is placed in a leg holder Answer: A. Leg holders should be padded to avoid direct pressure on the upper lateral leg when the peroneal nerve wraps around the fibular head. Peroneal neuropathies typically result in significant motor dysfunction, resulting in foot drop and difficulty with walking or running.
7. Which is the primary reason to pad peripheral nerves when positioning patients? A) The pad improves blood flow. B) The pad limits stretch of the nerve. C) The pad increases strain on the nerve. D) The pad distributes point pressure. Answer: D. Padding typically is used to distribute and disperse point pressure from hard surfaces. This dispersion of pressure reduces the risk of compressive injury to peripheral nerves. There are no studies that indicate any specific type of padding (e.g., gel, form, or other padding materials) to be any better than the others. The key is to distribute point pressure broadly or avoid pressure on a peripheral nerve entirely.
SUGGESTED READINGS American Society of Anesthesiologists Task Force on the Prevention of Perioperative Neuropathies. Practice guidelines for the prevention of perioperative neuropathies. Anesthesiology. 2000;92:1168–1182. Contreras MG, Warner MA, Charboneau WJ, et al. Anatomy of the ulnar nerve at the elbow: potential relationship of acute ulnar neuropathy to gender differences. Clin Anat. 1998;11(6):372–378. Litwiller JP, Wells RE, Halliwill JR, et al. Effect of lithotomy positions on strain of the obturator and lateral femoral cutaneous nerves. Clin Anat. 2004;17:45–49. Staff NP, Engelstad J, Klein CJ, et al. Post-surgical inflammatory neuropathy. Brain. 2010;133:2866–2880. Warner MA. Patient positioning and related injuries. In: Barash PG, et al, eds. Clinical Anesthesia. 6th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2009:793–814. Warner MA, Warner DO, Matsumoto JY, et al. Ulnar neuropathy in surgical patients. Anesthesiology. 1999;90:54–59.
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CHAPTER
20
Overview of a General Anesthetic Dalia Elmofty and Thomas Cutter ■ EARLY HISTORY OF ANESTHESIA AGENTS An anesthetic involves the administration of various intravenous and inhalational agents to produce a state in which a patient may safely and comfortably undergo a procedure. While the medical specialty of anesthesiology may be regarded as modern and “cutting edge,” many of the current medications have existed for centuries. The first known narcotic, opium, was found in a poppy plant, called the “joy plant” by the Sumerians, as far back as 3400 BC. In 1300 BC, the ancient Egyptians wrote about opium’s painrelieving or analgesic properties. In 40 AD, the Greek physician Pedanius Dioscordes noted the effects of the plant Atropa mandragora, when it was used in combination with alcohol prior to surgery, and coined the term “anesthesia” to describe its effect. In 1803, Friedrich Wilhelm Serturner of Germany extracted the active ingredient from opium and named it morphine, after Morpheus, the Greek god of dreams. The first inhalational anesthetic was described in 1800 by Sir Humphrey Davy as he personally experimented with nitrous oxide (“laughing gas”); he described it as producing a feeling of “well-being.” In 1818, Michael Faraday discovered that the volatile inhalational anesthetic ether could cause unconsciousness. In 1842, Crawford W. Long demonstrated ether’s effects on his colleagues during medical gatherings known as “ether frolics.” A dentist, William T. G. Morton, is credited with the use of the first inhalational anesthetic in a public demonstration at the Boston Massachusetts General Hospital in 1846 during a tooth extraction. The concept quickly spread and surgery flourished with the use of the new agents that could alleviate the pain and suffering of a surgical procedure (Figs. 20.1 and 20.2).
In Europe, chloroform was the preferred inhalational anesthetic. It was first described by Sir James Young Simpson, a Scottish obstetrician who administered it for labor pain. Dr. John Snow was recognized as the first professional anesthesiologist in England, when he provided a chloroform anesthetic to Queen Victoria during the birth of her children in 1853 and 1857. Intravenous anesthesia using sedative/hypnotic medications was not possible until the syringe and hypodermic needle were invented by Alexander Wood of Edinburgh in 1855. Barbituric acid, the source of the barbiturate sodium pentothal, was discovered in 1864 by Adolph von Baeyer, but it was another six decades before the first short-acting intravenous barbiturate was used to induce unconsciousness by the German obstetrician Rudolph Bumm in 1927. Barbiturates have been largely replaced by propofol, which was introduced in the 1980s. Benzodiazepines, which at low doses relieve anxiety but at higher doses may cause unconsciousness, have been available since 1960. Midazolam, the most commonly used benzodiazepine in anesthetic medicine, has been available for over 20 years. Curare was the first documented muscle relaxant, when, in 1800, Alexander von Humboldt wrote about a toxin from native plants by the Orinoco River that caused paralysis. It was not until the 1940s that curare was introduced into anesthesia as a muscle relaxant for surgery. Succinylcholine was introduced later by Bovet in 1949. The local anesthetic cocaine is derived from the leaves of the coca plant and has been used by Peruvians for centuries as a stimulant. It was isolated in 1860 and first used as a local anesthetic by Carl Koller in 1884. 175
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■ FIGURE 20.1 Morton’s ether inhaler (1846) consisted of a glass bulb, an ether-soaked sponge, and a spout to be placed in patient’s mouth. (From Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. Philadelphia, PA: Lippincott Williams & Wilkins; 2009, with permission.)
Inhalational gases, narcotics, local anesthetics, sedative hypnotics, and muscle relaxants are among the most commonly administered medications during anesthesia.
■ FOUR GOALS OF AN ANESTHETIC The four goals of an anesthetic are to provide a lack of awareness or amnesia, pain relief, immobility, and patient safety. Ideally, medications should have a fast onset, a predictable duration of action, and no side effects. Because no single medication can accomplish these four goals, an anesthesiologist often administers a “balanced anesthetic” with a small amount of a number of different drugs, thereby maximizing
■ FIGURE 20.2 Southworth and Hawes (1846) “Early operation using ether anesthesia.” The first public demonstration of inhalational anesthesia used during a tooth extraction by William T. G. Morton at Boston Massachusetts General Hospital. (Reproduced with permission from The J. Paul Getty Museum.)
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a drug’s positive effects while minimizing its side effects. The safe use of any anesthetic medication requires a thorough understanding of the drug’s pharmacology. Pharmacology can be divided into two parts: pharmacokinetics and pharmacodynamics (see Chapter 5). Pharmacodynamics is what the drug does to the body through interactions with receptors, cell membranes, enzymes and other proteins, and ion channels. The drug may either increase activity (agonist) or inhibit activity (antagonist). Pharmacokinetics is what the body does to the drug and includes the medication’s release from its formulation (liberation), its entry into the blood circulation (absorption), its spread through the fluids and tissues (redistribution), its breakdown (metabolism), and its elimination from the body (excretion).
Lack of Awareness Lack of awareness is on a continuum, ranging from fully awake to moderate sedation to deep sedation to unconsciousness/general anesthesia (GA) (Fig. 20.3). The effects of various anesthetic agents on consciousness have been studied using the electroencephalogram (EEG), an instrument that measures electrical brain activity. Modified EEGs such as the BIS monitor are also occasionally used in the operating room to measure brain activity as an estimate of the depth of anesthesia. Total unconsciousness is associated with a marked decrease in EEG activity. Other techniques to measure brain activity include positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). By definition, a general anesthetic results in total unconsciousness, while other anesthetic techniques may result in only sedation or no reduction in consciousness at all. For example, a spinal anesthetic for a woman undergoing a cesarean section may not include any drugs to diminish awareness because of the concern for their effects on the baby. Medications that can cause unconsciousness include both inhalational gases and injectable medications. Inhalational Gases Nitrous oxide is a relatively weak inhalational anesthetic and does not typically produce total unconsciousness; thus, it is never used alone in a general anesthetic but instead supplements other medications. It works through both ion channel
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■ FIGURE 20.3 Excerpted from Continuum of Depth of Sedation: Definition of General Anesthesia and Levels of Sedation/ Analgesia (Approved by the ASA House of Delegates on October 27, 2004, and amended on October 21, 2009) of the American Society of Anesthesiologists. A copy of the full text can be obtained from ASA, 520 N. Northwest Highway, Park Ridge, IL 60068-2573.
and receptor activity and has a relatively benign side effect profile. Sevoflurane, desflurane, and isoflurane are common volatile inhalational agents and can be used as the sole agent for a general anesthetic. The exact mechanisms by which these volatile inhalational agents work are not entirely understood, but several theories have been proposed. On a molecular level, Meyer and Overton suggested that anesthetics work at the lipid portion of the nerve cell membrane. Later, Franks and
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Lieb determined that the site of action is at the protein layer of the cell membrane. The main receptor involved is the γ-aminobutyric acid (GABA) receptor, which is an inhibitory receptor. It is thought that certain anesthetic agents increase the inhibitory action of this receptor, thereby decreasing nerve cell activity and consciousness. Volatile inhalational anesthetics must be vaporized from the liquid state and are administered from agent-specific vaporizers. A carrier gas
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(e.g., oxygen) passes through the vaporizer and takes up the inhalational agent, just as a breeze will carry steam. The agent will then be carried to the patient through the breathing circuit to enter the lungs. Once in the lungs, it diffuses into the bloodstream where it is carried to the brain and elsewhere throughout the body. The inhalational agent’s speed of onset is inversely proportional to its solubility, which is indicated by the blood/ gas coefficient (Table 20.1). The minimum alveolar concentration (MAC) is the concentration of the inhalational agent in the lungs that prevents movement in 50% of patients undergoing a surgical stimulus (e.g., being cut by a scalpel). Inhaled anesthetics are mainly eliminated from the body by exhalation, although there is some metabolism in the liver and excretion in the urine and through the skin. As with all medications, gases have side effects. In the brain, they increase cerebral blood flow and intracranial pressure while decreasing cerebral metabolic oxygen consumption. Their effect on the ventilatory system (airway and lungs) is to depress respiration and bronchodilate. The pungent nature of desflurane can cause airway irritation. They also can decrease systemic vascular resistance and the heart’s contractility, thereby lowering blood pressure (hypotension). Isoflurane and desflurane can cause increased heart rate, which can cause ischemia (inadequate blood flow) in a patient with coronary artery disease. Injectable Medications Common intravenous sedative hypnotic agents that produce unconsciousness include propofol, etomidate, benzodiazepines (e.g., midazolam), and barbiturates (e.g., sodium pentothal) (Table 20.2). These work by depressing the
reticular activating system, an area in the brain responsible for regulating arousal/wakefulness, and by increasing GABA action, inducing a loss of consciousness. Ketamine is an N-methyl D-aspartate (NMDA) antagonist that induces a state known as “dissociative anesthesia.” All of these agents are typically injected intravenously, although some can be injected intramuscularly or absorbed through moist surfaces (mucosa) such as those found in the nasal passages, the rectum, and the mouth. Their high lipid solubility in the brain results in a rapid onset of action. In many cases, their duration of action is primarily determined by redistribution (dilution) throughout the body rather than by metabolism or excretion. Thus, they accumulate when large doses are given and are more often used to start (induce) a general anesthetic than to maintain it. Propofol’s side effects include pain at the site of injection, so it is often preceded by or administered along with the local anesthetic lidocaine. It also produces a dose-dependent hypotension as a result of decreasing the heart’s contractility and lowering the systemic vascular resistance and causes significant ventilatory depression (i.e., the patient can stop breathing). Sodium pentothal’s clinical profile is similar to propofol’s, but it does not hurt when injected and it does not lower the blood pressure quite as much. Its disadvantage is that its sedating effects persist longer than those of propofol. Etomidate causes less hypotension than either propofol or sodium pentothal, but it can suppress hormone (steroid) production and is relatively expensive. Midazolam is noted to have less adverse cardiovascular and ventilatory effects than any of the preceding drugs, but the doses required to cause unconsciousness require a long time to wear off. Ketamine also maintains hemodynamic and
TABLE 20.1 BLOOD/GAS COEFFICIENT, MAC, AND SIDE EFFECTS OF INHALATIONAL
AGENTS INHALATIONAL AGENT
BLOOD/GAS COEFFICIENT
MAC (%)
SIDE EFFECTS HEART RATE
BLOOD PRESSURE
Desflurane
0.42
6.6
0-↑
↓
Sevoflurane
0.65
1.8
0
↓
Isoflurane
1.46
1.17
↑
↓
MAC, minimal alveolar concentration; ↓, decrease; ↑, increase; 0, no change. Adapted from Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:420.
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TABLE 20.2 COMMONLY USED INTRAVENOUS ANESTHETIC AGENTS INTRAVENOUS ANESTHETIC AGENT
DOSE (mg/kg)
Propofol
1–2
ONSET (s)
DURATION (min)
SIDE EFFECTS HEART RATE
BLOOD PRESSURE
15–45
5–10
0-↓
↓
Thiopental
3–6
100 beats/min)
Markedly increased (>120 beats/min)
Mental status
Awake, alert
Lethargic
Obtunded
Mucous membranes
Dry
Very dry
Parched
Urinary output
Mildly decreased
Decreased
Markedly decreased
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There are several laboratory measurements that aid in determining a patient’s fluid status. These include the hematocrit, serum sodium, creatinine, and blood urea nitrogen (BUN) levels. Serial arterial blood gases provide information regarding how well tissues are being perfused by circulating oxygen in the blood (as measured by the arterial pH, the arterial oxygen pressure [PaO2], and the base deficit). The urine can also be examined by assessing the urinary-specific gravity, urine sodium, and urine chloride concentrations. Visual inspection of the urine can also help the anesthesiologist determine how “dry” the patient is, with a low volume and dark color suggesting highly concentrated urine and a dehydrated patient. Invasive hemodynamic monitoring via a central venous pressure (CVP) catheter or a pulmonary arterial catheter may also assist in assessing intravascular volume status, but both entail the risks associated with cannulation. A central venous catheter is often placed into a large vein in the neck (internal jugular vein), chest (subclavian vein), or groin (femoral vein) when rapid infusion of fluid or blood is required, vasoactive or irritating medications are infused, or if invasive hemodynamic monitoring is indicated. CVP is measured from the tip of a central venous catheter that is properly placed at the junction of the superior vena cava and the right atrium. Theoretically, CVP measurements provide information regarding the volume of blood entering the heart. CVP monitoring must be assessed in conjunction with clinical signs. Normal values range from 5 to 12 mm Hg, but trends may be more useful than single measurements. A pulmonary arterial pressure catheter can be placed through central venous access, into the pulmonary artery, to assess volume status when the patient has right-heart dysfunction or to better assess pulmonary arterial pressures. Clinical correlation between data from pulmonary arterial catheterization and other diagnostic data is critical. Recently, transthoracic echocardiography and transesophageal echocardiography (TEE) have become useful tools in evaluating volume
status. A skilled clinician can assess the filling, emptying, and contractile function of the heart, in real time, with the use of these devices. During surgery, ongoing losses of fluid and blood must be monitored. The anesthesiologist must estimate the blood loss in the surgical field, even in cases in which little blood loss is anticipated. One can measure the blood that has collected in the surgical suction container (taking into account the amount of irrigating solution that has been added to the field by the surgeons), assess the number of laparotomy pads and sponges, along with the blood accumulated on them, and visually inspect the field regularly to detect bleeding into the wound or under the surgical drapes. Following serial hemoglobin and hematocrit levels is also helpful. The clinical signs mentioned previously (increased heart rate, decreased blood pressure, decreased urine output, etc.) are late signs of hypovolemia. By closely monitoring the blood loss throughout the procedure, one is able to continually replace the lost fluid, rather than “get behind” and expose a patient to the risks of insufficient fluid administration.
■ SUMMARY Surgical patients require intravenous access so that drugs can be administered promptly and necessary fluids can be infused. Fluid infusion should be regarded with the same seriousness as drug administration. Inadequate or excessive fluid administration is associated with complications, some of which are life threatening. During surgery, most anesthesiologists use crystalloid solutions, supplemented as necessary by colloids, which are more effective at maintaining plasma volume. Ongoing research is rapidly defining appropriate targets regarding fluid administration for specific types of surgery. Ultimately, fluid therapy can be personalized based on the characteristics of a patient and the type of surgery. Although considerable information is available to assist in monitoring the need of an individual patient for fluids, no single piece of information is sufficient—vigilance and close monitoring are always required.
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Chapter 22 • Fluid Therapy
REVIEW QUESTIONS 1. A 90-kg-male is scheduled for an inguinal hernia repair at 7 a.m. He has not had any food or water since dinner the night before (7 p.m.). What is his water deficit? A) 1,560 mL B) 850 mL C) 1,750 mL D) 550 mL E) 2,750 mL Answer: A. Using the 4:2:1 rule, this patient would have a deficit of 40 mL/hr for the first 10 kg, 20 mL/hr for the next 10 kg, and 70 mL/hr for the next 70 kg. This would total to 130 mL/hr multiplied by 12 hours, which equals 1,560 mL.
2. Which of the following physical exam findings suggests dehydration? A) Excessive sweating B) Clammy, moist hands C) Heart rate of 65 beats/min D) Blood pressure of 135/85 mm Hg E) Heart rate of 125 beats/min Answer: E. Tachycardia (fast heart rate) is a sign of dehydration as well as low blood pressure. In addition, patients who are dehydrated do not produce sweat.
3. If administering a citrated blood product, it is best to use lactated Ringer’s solution as a carrier. A) True B) False Answer: B. Lactated Ringer’s solution contains calcium, which can combine with the anticoagulant citrate used in blood products. This may cause the blood products to form clots.
4. Which of the following is NOT a means to assess ongoing blood loss intraoperatively? A) Monitoring suction canisters B) Periodically weighing the patient C) Counting soiled laparotomy pads D) Checking the hematocrit level E) All of the above Answer: B. It would be impractical to weigh the patient during surgery. In addition, changes in patient weight would be affected by fluid losses as well as blood losses (e.g., evaporative losses). Monitoring suction canisters and blood-soaked laparotomy pads is important to follow blood loss during surgery. Serial hematocrits are also useful to monitor blood loss.
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5. Which of the following statements are TRUE? A) Colloid solutions contain large-molecular-weight proteins or sugars. B) Lactated Ringer’s solution contains potassium. C) CVP can be used to monitor fluid status. D) Urine output can be used to monitor fluid status. E) All of the above. Answer: E. All of the above statements are true. The largemolecular-weight proteins and sugars in colloid solutions cause them to stay in the intravascular space longer than crystalloids. Lactated Ringer’s solution contains sodium, potassium, chloride, calcium, and lactate. Both CVP and urine output are commonly used to assess the volume status of a patient. Dehydrated patients do not make as much urine as they would normally.
SUGGESTED READINGS Boldt J, Mengistu A. Balanced hydroxyethyl starch preparations: are they all the same? In-vitro thrombelastometry and whole blood aggregometry. Eur J Anaesthesiol. 2009;26:1020–1025. Brandstrup B, Tonnesen H, Beier-Holgersen R, et al. Effects of intravenous fluid restriction on postoperative complications: comparison of two perioperative fluid regimens— a randomized assessor-blinded multicenter trial. Ann Surg. 2003;238:641–648. Finfer S, Bellomo R, Boyce N, et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004;350:2247–2256. Holte K, Klarskov B, Christensen DS, et al. Liberal versus restrictive fluid administration to improve recovery after laparoscopic cholecystectomy: a randomized, doubleblind study. Ann Surg. 2004;240:892–899. Magner JJ, McCaul C, Carton E, et al. Effect of intraoperative intravenous crystalloid infusion on postoperative nausea and vomiting after gynaecological laparoscopy: comparison of 30 and 10 ml kg−1. Br J Anaesth. 2004;93:381–385. Maharaj CH, Kallam SR, Malik A, et al. Preoperative intravenous fluid therapy decreases postoperative nausea and pain in high risk patients. Anesth Analg. 2005;100: 675–682. Nisanevich V, Felsenstein I, Almogy G, et al. Effect of intraoperative fluid management on outcome after intraabdominal surgery. Anesthesiology. 2005;103:25–32. O’Malley CM, Frumento RJ, Hardy MA, et al. A randomized, double-blind comparison of lactated Ringer’s solution and 0.9% NaCl during renal transplantation. Anesth Analg. 2005;100:1518–1524, table. Yogendran S, Asokumar B, Cheng DC, et al. A prospective randomized double-blinded study of the effect of intravenous fluid therapy on adverse outcomes on outpatient surgery. Anesth Analg. 1995;80:682–686.
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CHAPTER
23
Transfusion Medicine Curtis Bergquist and Kamila Vagnerova ■ INTRODUCTION Transfusion of blood products is a common occurrence during surgery. Anesthesia technicians may be called upon to retrieve blood products, help check them in, and help administer them. Transfusion of incompatible blood products to a patient can cause serious patient injury, and anesthesia technicians should be familiar with basic transfusion medicine. This chapter provides an introduction to the different types of blood products, what makes them compatible or incompatible with a patient, how they should be administered, and the potential complications or adverse reactions from the transfusion of blood products.
■ BLOOD TYPES The different blood types (blood groups) and their relationship to the immune system is the basis of transfusion science. Blood types are inherited and represent contributions from both parents. A total of 30 human blood group systems are now recognized by the International Society of Blood Transfusion (ISBT). A blood type is a classification of blood based on the presence or absence of inherited antigenic substances on the surface of red blood cells (RBCs). Antigens, which may be proteins, carbohydrates, glycoproteins, or glycolipids, are present on the cellular membrane of RBCs and are also secreted to plasma and body fluids. Antigens determine the blood group type. In 1900, Karl Landsteiner discovered the ABO blood groups for which he received the 1930 Nobel Prize in Medicine and Physiology. The ABO antigen system is the most important determinant of blood type grouping in transfusion medicine. The two major RBC antigens are known as A and B. The blood groups are A, B, AB, and O, where O is when the RBCs lack both A and B antigens. People with AB blood type have RBCs that have both antigens. People
with RBCs that only have the A or B antigen are blood type A and B, respectively. ABO compatibility remains the major safety consideration of blood product transfusions (Table 23.1). Compatibility means that the recipient does not recognize the blood transfusion as foreign. Immune systems of virtually all individuals produce antibodies directed against antigens they do not have (anti-B antibodies in type A individuals, anti-A antibodies in type B individuals, and anti-A and anti-B antibodies in type O individuals). The process whereby foreign antigens from blood groups cause production of antibodies directed against them in the recipient is called alloimmunization. This concept is extremely important to the understanding of transfusion medicine. If a patient receives blood (recipient) that has antigens that are foreign to the recipient, the recipient can mount a massive immune reaction (allergic reaction) against the foreign blood. These reactions are particularly severe if the recipient has preformed antibodies (a primed immune system) against the foreign antigen. This type of reaction is akin to an anaphylactic reaction except that the foreign antigen is the transfused blood. Humans form antibodies to A or B antigens in the first years of life if they do not have them on their own RBCs. This is thought to be from exposure to environmental antigens (food, bacteria, virus, etc.). Thus, humans are usually “primed” against ABO-incompatible blood. A reaction to ABO-incompatible blood is called an acute hemolytic transfusion reaction and is fatal in about 10% of cases. The recipient may not only manifest symptoms of an anaphylactic reaction (low blood pressure, fever, bronchospasm) from the immune mediators released but also suffer because his or her immune system attacks the foreign blood cells, causing them to hemolyze (rupture) and release free hemoglobin into the
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Chapter 23 • Transfusion Medicine TABLE 23.1. ABO COMPATIBILITY
CHART ABO COMPATIBILITY
Recipient
DONOR A
B
O
AB
A
Yes
No
Yes
No
B
No
Yes
Yes
No
O
No
No
Yes
No
AB
Yes
Yes
Yes
Yes
bloodstream. Free hemoglobin is a large protein and is very toxic to the kidney. It is not surprising that many of the first recipients of blood transfusions, before there was an understanding of blood group antigens, died from a severe transfusion reaction. Other types of transfusion reactions will be discussed below. The primary cause of transfusing ABO-incompatible units (incorrect blood type) is clerical errors in patient identification or errors in sample labeling. The second most important blood group system is the Rhesus (Rh) system. Rh positivity is indicated by the presence of D antigen in the membrane of the RBC; D antigen is absent in Rh (D)-negative individuals. About 15% of people are Rh (D)-negative. Unlike anti-A or anti-B antibodies, Rh (D)-negative individuals do not produce anti-Rh (D) antibodies until they are exposed to Rh (D)-positive blood. When an Rh (D)-negative individual is exposed to Rh (D)-positive cells, sensitization occurs and the immune system can produce anti-D alloantibody. Any subsequent exposure to Rh (D)-positive blood can result in a severe adverse reaction. Sensitization can occur by transfusion or during pregnancy. If an Rh (D)-negative mother is pregnant with an Rh (D)-positive baby (the baby inherited the Rh (D) antigen from the father), the mother will become sensitized to the Rh (D) antigen. This happens because there can be some mixing of the baby’s blood with the mother’s blood at delivery. Once a mother is sensitized to the Rh (D) antigen, she can form antibodies that can attack the blood of a subsequent fetus if the fetus is Rh (D)-positive. Even in emergencies, Rh (D)-positive blood should not be given to Rh (D)-negative patients to avoid sensitization. Typically, type-O Rh (D)-negative blood (O neg) is stored by hospitals for emergency transfusion
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because of its near-universal safety for patients with untyped blood due to its lack of AB or Rh (D) antigens. Several other blood group systems exist in addition to the ABO and Rh (D) systems: Lewis, I system, P system, MNSsU system, Kell Protein, and the Duffy and Kidd antigens. These antigens can be present on RBCs and result in incompatibility, but these are not necessarily tested for in every patient because they are either extremely rare, extremely common, or compatibility can be ensured by providing warmed blood (above 30°C). Patients who have received multiple transfusions over the course of their life are at higher risk of developing antibodies, and it may be more difficult to find a compatible unit. Procuring a compatible unit can take extra time and may result in a surgical delay.
■ COMPATIBILITY TESTING Before any RBC unit is given to a patient, it undergoes several different tests to ensure that it is compatible with the recipient. The tests are separate from the testing done for diseases such as hepatitis and human immunodeficiency virus (HIV). Screening of potential donors and rigorous testing of donated units have largely eliminated the risk of units containing HIV, hepatitis, and other infections. The first test, known as the type and screen, is done on donated blood before releasing the unit. This test determines the blood type—A, B, AB, O, and Rh (D)-positive/negative. This testing is also done on the patients to determine their blood type as well as screen for the presence of antibodies to A or B and antibodies against other antigens known to cause hemolytic reactions. The test is performed by mixing the sample blood (the patient’s blood or the donated blood) with a solution containing antibodies against the antigen being screened. For example, if one wants to determine if a patient has A antigen on his or her RBCs (he or she is blood type A or AB), a blood sample from him or her is mixed with a solution containing anti-A antibodies. If the resulting mixture agglutinates (clumps), it is because the antibodies have bound to cells with the A antigen. A second phase of the test involves mixing the patient’s plasma with commercially available O-negative RBCs that have approximately 20 different antigens that can cause a hemolytic reaction. If the patient’s plasma does not agglutinate these cells, the screen is negative.
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If the patient’s plasma does react to the cells, the patient possesses at least one antibody to a significant antigen and the screen is positive. If the screen is positive, further testing must be done to identify the antibody and to locate blood units that lack the antigen. The second test, the crossmatch, checks the patient’s blood against a specific donor unit for errors in ABO type. If the screen portion of the type and screen test was negative, the crossmatch consists of matching the patient with compatible donor blood. No real “test” is performed. The crossmatch involves matching the paperwork for the donor unit and the recipient. This step can even be performed by automated vending style machines that scan barcodes from the patient ID and the donor unit. If the patient’s screen was positive, a serologic crossmatch test is performed. This test is conducted by mixing the patient’s serum with a specific donor unit that has been selected because it lacks the antigens that the patient has antibodies against identified during the screen. A crossmatch is only necessary when the patient receives RBCs, as opposed to plasma or other blood derivatives. Compatibility of plasma is different from that of whole blood or RBCs. Plasma from an AB blood type donor can be transfused to a recipient of any blood group. This is because the AB donor plasma lacks A or B antibodies and will not react with the recipient’s RBCs even if he or she has the A or B antigen. Type O recipients already have A and B antibodies and can receive plasma from any blood type. The only problem is plasma from a type O donor. This donor has A and B antibodies in the plasma, and it cannot be given to a type A, B, or AB recipient. In emergency situations when RBC transfusion is immediately needed, abbreviated testing methods are necessary. Type-specific blood is always essential (unless the donor unit is O), but there are abridged versions of the crossmatch: Partial crossmatch checks for the most severe errors (ABO-Rh (D) blood type) and takes less than 10 minutes; uncrossmatched blood is less risky in previously untransfused patients and those who have not born children. The risk of complication from uncrossmatched blood varies between 1 in 1,000 to 1 in 100 patients depending on the history of previous exposure to donated blood. Trauma centers may also keep type O, Rh (D)-negative (“universal donor”) blood on hand for immediate use. Ideally, it should be
completely compatible, but it is always possible that there are anti-A or anti-B antibodies in the donor unit that could cause a reaction.
■ INDICATIONS FOR TRANSFUSION According to the list of guidelines provided by the American Society of Anesthesiologists in 2006, transfusion is rarely indicated when the hemoglobin concentration is greater than 10 g/dL and is almost always indicated when it is less than 6 g/dL, especially when the anemia is acute. However, the hemoglobin level should not be the sole consideration, as there are other patientrelated and surgical factors that help determine the “trigger” for transfusion. Patients can either receive his or her own previously donated blood (autologous blood) or someone else’s donated blood (allogenic, homologous blood). Autologous blood, which needs to be donated ahead of time, is considered safer than allogenic blood mainly due to lower risk of infection and is preferred over allogenic transfusion. However, there are complications related to autologous transfusion like anemia from the donation itself, the need for more frequent transfusions, and even febrile and allergic reactions. Autologous units are typed and crossmatched just as all allogenic units are.
■ COMPLICATIONS AND ADVERSE REACTIONS There are a variety of adverse reactions that come from a few basic sources: contaminated or infected blood (e.g., HIV or hepatitis), incompatible blood, and problems related to the infusion of RBCs (e.g., transfusion-related lung injury, volume overload, electrolyte disturbances, and coagulopathy). Table 23.2 summarizes some of the possible complications of transfusions. As soon as an acute adverse reaction to a transfusion is suspected, the first step is to stop the transfusion and call the blood bank. The three most common causes of transfusion-related deaths are hemolytic transfusion reactions, septic transfusions, and transfusion-related lung injury. Acute hemolytic transfusion reaction is caused by type incompatible blood, typically due to human error at some point between issuing the unit and transfusion. The body mounts an immune response to the offending blood, which can lead to severe coagulation issues, kidney failure, and even death.
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Chapter 23 • Transfusion Medicine
213
TABLE 23.2. OTHER ADVERSE REACTIONS Immune-mediated reactions Delayed hemolytic transfusion reaction Febrile nonhemolytic transfusion reaction Allergic reaction Anaphylactic reaction Alloimmunization—sensitization to antigens present in transfusion Posttransfusion purpura—caused by platelets’ transfusion Transfusion-associated graft versus host disease—immunocompromised at greatest risk Transfusion-related acute lung injury—causes pulmonary edema Nonimmunologic reactions Hypothermia, fluid overload, electrolyte toxicity, iron overload, and others Infections Transfusion-associated viral infections: HIV type 1; Hepatitis B, C, and G virus; cytomegalovirus (CMV) and other viral and bacterial infections
Other complications are more common during a massive transfusion (loss of at least one times the patient’s blood volume): • Hypocalcemia: The citrate used to preserve blood can bind calcium in the patient, leading to hypocalcemia. This is more common when the units are transfused quickly (>1 unit in 5 minutes), it is a massive transfusion, or the patient has liver dysfunction and has difficulty in metabolizing citrate. Monitoring of blood calcium levels will guide treatment with calcium. • Coagulopathy: Packed RBC units contain minimal platelets or plasma clotting factors. Patients who receive large transfusions will require replacement of platelets and clotting factors to avoid a dilutional coagulopathy. • Hyperkalemia: Typical blood units contain less potassium than normal blood; as the blood is stored, the RBCs release potassium. Rapid or large transfusions of RBC units, particularly older units, can lead to a significant potassium increase in the recipient.
■ HANDLING, VERIFICATION, AND STORAGE Retaining the oxygen-carrying capacity of blood throughout its shelf life is one of the primary problems of blood storage. Over time red cells lose their capacity to carry the same amount of oxygen as they could when fresh. It is hard to standardize the capacity of each unit because each starts from a different level and degrades at different rates. Different products are added
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to each unit to prolong the shelf life. One of the most common is citrate-phosphate-dextroseadenine (CPDA-1): Citrate is an anticoagulant, phosphate is added as a buffer, dextrose provides an energy source for the red cells, and adenine allows the cells to make adenosine triphosphate (ATP), a common cellular energy source. AS-1 (Adsol), AS-3 (Nutricel), and AS-5 (Optisol) are similar to CPDA-1 with slight variations. Storing the units between 1°C and 6°C slows down the metabolic processes of the red cells, but glycolysis (RBCs do not use the citric acid cycle because they lack mitochondria) still converts glucose to lactate. This accumulation of lactate lowers the pH of the unit and alters the intraand intercellular concentrations of sodium and potassium. The lower pH also contributes to the decreased oxygen-carrying capacity of the RBCs. If several units of plasma or packed red cells are needed in the operating room, they are often kept in a cooler or bucket with ice; the ice and blood product should be separated by a towel or other barrier to prevent the blood from freezing. The formation of ice crystals damages the RBCs. Another important reason to keep the blood cold for possible transfusion in the operating room is if the blood is kept cold, it can be returned to the blood bank if it is not used.
■ ADMINISTRATION Each unit must be checked at the bedside check before transfusing. The check consists of double checking the information on the unit and
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the paperwork that came with it. This procedure will vary from institution to institution, but typically requires two people, and often one of them must be licensed (e.g., a physician or a nurse). Commonly, the unit number, expiration date, blood type, and some type of patient identifier are used (Fig. 23.1). Blood products are typically administered through special blood administration tubing (Fig. 23.2). The vast majority of blood administration sets have an in-line filter to remove cellular debris and coagulated proteins. Most filters are designed for transfusion of two to four RBC units before they should be changed. Refer to the product information for specific guidelines. Some practitioners prefer to attach a separate blood filter to the spike. After multiple units have been transfused, the filter can be replaced without having to replace the entire tubing setup. Again, refer to the product information for the number of RBC units that can be transfused before filter replacement is recommended, as some filters allow up to 10 units. The tubing
■ Figure 23.1. Transfusion unit of red blood cells (RBCs). 1. Blood type: A Rh (D)-positive. 2. RBCs transfusion unit—leukoreduced. 3. Unit number. 4. Expiration date.
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■ Figure 23.2. Blood administration tubing. 1. Y connector. 2. Filter—holds debris and particles. 3. Chamber— blood can be pumped by squeezing the chamber to speed delivery. 4. Warmer—blood is warmed by passing through the hot-line system.
used in operating rooms usually has a Y connector with two separate “spikes” so that a unit or fluid can be prepared on one spike while the other is being actively used for transfusion or fluid administration. Typical blood administration sets used in the operating room also include a squeezable chamber that allows pumping the fluid or blood products to speed administration. Pediatric blood sets can come equipped with a chamber (buretrol) in which the provider can measure out a specific amount of blood product or fluid. This allows more precise administration of fluids or blood products, which can be critical in pediatric patients. Blood products are typically warmed before being given to a patient. This is often achieved with in-line heated tubing. The majority of these units utilize heated water, which is circulated outside an inner set of tubing through which the blood product or fluid is administered. As mentioned earlier, heating units above 30°C can reduce the risk of some complications. Additionally, blood is typically stored at 4°C and transfusing cold units to a patient could rapidly lower his or her body temperature. Platelets are the exception and are stored at room temperature. This is further discussed in the section on different blood products. There are many other transfusion devices that are mainly used during emergency situations, such as the Level One, Belmont, and pressure bags. These devices are covered in more detail in Chapter 34, but in essence, they provide heating, filtration, and the ability to rapidly administer blood products and fluid. It is routine practice to draw blood samples for laboratory testing of the patient’s blood before and after transfusion.
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Chapter 23 • Transfusion Medicine
Testing includes hematocrit and other values like electrolytes, glucose level, coagulation studies, etc., and it is often the anesthesia technician’s responsibility to run these samples if the operating room suites have their own blood gas analyzer machine.
■ DIFFERENT BLOOD PRODUCTS While blood donations typically consist of whole blood, or blood containing all of its normal components (red blood cells, plasma, etc.), they are routinely processed into several different products for clinical use. Today, whole blood is not readily available for transfusion and instead serves as the basis for further processing. Because the different components in blood differ in density, blood banks use centrifugation to separate the different parts, resulting in different blood products (see Table 23.3). • Packed red blood cells (PRBCs): PRBCs provide additional oxygen-carrying capacity because of the hemoglobin they contain. Transfusion of white blood cells (leukocytes) increases the risk of infection because they suppress the immune system of the recipient. Transfusion of leukocytes can also sensitize the recipient to leukocyte antigens. For these reasons, most PRBC units have the vast majority of leukocytes removed by filtration (leukoreduction). The hematocrit value of a PRBC is 70%. When RBCs are separated from whole blood, plasma and other blood components are retained for other use.
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• Fresh frozen plasma (FFP): FFP contains plasma proteins including factors V and VIII, which are needed for effective blood clotting. FFP replaces the coagulation factors lost with bleeding and can also be used as a reversal agent for anticoagulation drugs likewarfarin, in treatment of immunodeficiencies, in antithrombin III deficiency, in massive blood transfusion, and in other coagulation system deficiencies. FFP does increase the circulating volume but should never be used as primary volume expander. FFP is stored frozen and after thawing it must be used between 24 hours and 5 days, which will be indicated on the expiration date printed on the bag. Because of the time it takes to thaw stored FFP, there can be a delay in receiving FFP after it has been requested. As mentioned above, FFP must be compatible with the recipient’s ABO Rh (D) type. • Platelets: Platelets play a vital role in how the body forms blood clots. Platelets can be collected either from whole blood donations or from separately from platelet-specific donations. Because they are stored at room temperature (never place them in the refrigerator with other blood products), they present a higher risk of bacterial contamination. Indications for platelet transfusion vary but are guided by the patient’s platelet count (provided by the laboratory) and the extent of the surgical bleeding. It is not necessary to provide ABO-compatible platelets.
TABLE 23.3. DIFFERENT BLOOD PRODUCTS PRODUCT
STORAGE TEMPERATURE (°C)
VOLUME (ml)
SUPPLIES
HEMATOCRIT
Whole blood
4°C
500ml
Oxygen capacity, blood volume
40
PRBC Packed Red Blood Cells
4°C
300ml
Oxygen capacity, increases hematocrit 3%
70
Fresh frozen plasma
4°C
200ml
Factors V and VIII deficiency
—
Cryoprecipitate
4°C
10ml
Factor VIII and fibrinogen
—
Platelets
Room temperature
50–200ml
Increases platelet count 5,000–10,000/uL
—
Prothrombin complex
4°C
—
Factor IX
—
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• Cryoprecipitate: Cryoprecipitate contains high concentrations of clotting factor VIII and fibrinogen and is used to treat clotting factor deficiencies including hemophilia A. Cryoprecipitate also contains other clotting factors and plasma proteins. Cryoprecipitate should be filtered when administered, and it must be used within 6 hours of thawing. Cryoprecipitate is usually administered as ABO compatible, but it is not too important since the concentration of antibodies in cryoprecipitate is extremely low. • Prothrombin complex: Prothrombin complex is a mixture of clotting factors II, VII, IX, and X. It is used to treat factor IX deficiency, hemophilia B, and other bleeding disorders.
■ SUMMARY Blood cells are intimately related to the immune system and carry multiple antigens. Because of the presence of these antigens, the transfusion of foreign blood products may activate the immune system of the host, resulting in severe reactions, even death. Both patients and blood products prepared by the blood bank undergo extensive testing to ensure compatibility between the donor and the patient receiving the transfusion. This chapter introduced the basic concepts of transfusion medicine including blood types, compatibility testing, indications for transfusion, and potential adverse reactions to transfusions. Familiarity of these concepts is essential for all operating room personnel, including anesthesia technicians, who are involved with the transfusion process.
REVIEW QUESTIONS 1. What is an antigen? A) A unique cellular marker on cell surfaces B) A molecule made up from amino acids C) A part of the cell’s nucleus D) The oxygen-carrying part of a red cell Answer: A. Antigens are markers that are used by the body to identify different cells.
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2. Why is compatibility testing important? A) To avoid losing blood units at the blood bank B) To avoid adverse reactions, even death, from transfusion C) To screen for HIV-1 D) To prolong unit shelf life Answer: B. Compatibility testing ensures that patients will not receive incompatible transfusions, for this could cause death.
3. What are the primary causes of noncompatible transfusions? A) Bacterial contamination B) Excessively clumped platelets C) Clerical errors D) Expired crossmatch test tubes Answer: C. Compatibility testing is very sophisticated, but clerical errors can cause an incompatible transfusion.
4. What is FFP used for? A) Raising hematocrit B) Expanding blood volume C) Replacing clotting factors D) Lowering patient temperature Answer: C. FFP contains factors V and VIII, which aid clotting.
5. Why are O-negative patients considered universal donors? A) They have a lower hematocrit. B) They lack Rh (D) antigen. C) They lack antigens on their cell surfaces. D) They provide extra factor VII. Answer: C. Type O blood does not contain antigens that the recipient could recognize as foreign.
6. How is the shelf life of stored blood extended? A) The addition of nutrient supplements B) Repeated freezing and thawing C) Inverted storage freezers D) Constant centrifugation Answer: A. Nutrients help keep red cells alive while they are outside of the body.
7. What is the Rhesus blood group? A) The markers of the Kell blood group system B) What makes AB patients universal recipients C) The determinant of cryoprecipitate effectiveness D) Blood group with D antigens in cell membranes Answer: D. The Rhesus blood group is identified by the D antigen.
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Chapter 23 • Transfusion Medicine
SUGGESTED READINGS Dzieczkowski JS, Anderson KC. Transfusion biology and therapy. In: Fauci AS, Longo DL, eds. Harrison’s Principles of Internal Medicine. 17th ed. New York, NY: The McGrawHill Companies; 2008:707–712. Hess JR. Conventional blood banking and blood component storage regulation: opportunities for improvement. Blood Transf. 2010;8(suppl 3):s9–s15.
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Miller RD, ed. Transfusion therapy. In: Miller RD, Erikson LI, eds. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2009:1739–1766. Welsbay IJ, Bredehoeft SJ. Blood and blood component therapy. In: Longnecker DE, ed. Anesthesiology. China: The McGraw-Hill Companies; 2008:1892–1911.
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SECTION
IV
Equipment Setup, Operation, and Maintenance
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CHAPTER
24
Infectious Disease Brett Miller ■ INTRODUCTION Microorganisms are all around us. They are in the air, on our hands, on items we touch, and even in the food we eat. Many microorganisms are helpful (i.e., gut bacteria that aid in digestion); however, some microorganisms known as pathogens are capable of causing disease within humans. In health care settings, pathogens are very common and appropriate measures must be taken to protect our patients, our coworkers, and ourselves. The goal of this chapter is to • Identify the various types of pathogens that lead to infectious disease. • Describe the methods and precautions used to minimize the spread of infections in the health care setting. • Describe how to minimize transmission even after exposure.
■ PATHOGENS There are several types of organisms capable of producing disease (also known as pathogens): bacteria, virus, fungus, parasite, and prion. Bacteria are very small, single-celled organisms that lack a nucleus. They are extremely diverse and often very specialized. They are capable of utilizing many different energy sources such as oxygen, sunlight, and even geothermal heat. A single bacterium may trade DNA with another bacterium and confer traits to the recipient. A particularly important example of this capability is when one bacterium confers resistance to an antibiotic to another bacterium. Bacteria cause disease by producing toxins that interfere with cells, eliciting an inflammatory response, or invading host cells. Examples of bacteria include Staphylococcus aureus (methicillin-resistant Staphylococcus aureus [MRSA] is a common form of antibiotic-resistant bacteria found in health care settings), Streptococcus pneumoniae
(the most common cause of bacterial pneumonia), Clostridium difficile (common cause of diarrhea), and Mycobacterium tuberculosis (the cause of tuberculosis). Bacterial illness is generally treated with antibiotic medications (e.g., penicillin, vancomycin, azithromycin, and ciprofloxacin) that work by attacking specific bacterial cell targets that are not found in humans. A virus is even smaller than a bacterium and much simpler (Fig. 24.1). It is composed of RNA or DNA (genetic material) surrounded by a protein shell and a lipid envelope. Unlike other organisms, a virus does not contain the cellular machinery to produce energy, manufacture proteins, or even reproduce. In order to perform these functions, it must take over a host cell. A virus “infects” a cell by attaching to the host cell membrane and becoming incorporated into the cell. Once inside, the virus can use host enzymes and proteins to replicate its own genetic material and produce viral proteins. The virus eventually kills the host cell and is released. It is capable of infecting all kinds of living cells, including bacteria, plants, and animals. Examples of viruses that infect humans are influenza (cause of the flu), herpes virus (a viral class that may cause cold sores, chicken pox, genital herpes, and even a form of cancer), human immunodeficiency virus (the cause of acquired immunodeficiency syndrome or AIDS), and hepatitis viruses (cause liver inflammation and eventually cirrhosis). Antiviral medications (e.g., acyclovir, highly active antiretroviral therapy (HAART) are available to treat many illnesses caused by viruses. A fungus is a cellular organism containing a nucleus that shares many features of animals (i.e., they lack chlorophyll and require organic compounds as energy sources) and plants (i.e., presence of a cell wall and ability to reproduce sexually and asexually). It exists in many forms, including molds, yeast, and mushrooms. Only a
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prion can occur by grafting infected tissue (i.e., cornea transplant, dural grafts) or ingestion. Prions are extremely resistant to standard medical sterilization protocols. Presently, treatments for prion disease are only experimental.
■ PREVENTION OF HEALTH CARE– ASSOCIATED INFECTIONS
■ FIGURE 24.1 The HIV virus.
very small percentage actually causes disease in humans. Examples of fungal infections are tinea pedis (causes athlete’s foot), apergillosis (causes lung infections), and candidiasis (causes skin and mucous membrane infections). Antifungal drugs are available and include amphotericin, fluconazole, and caspofungin. Parasitic infections are often caused by organisms from the Protozoa kingdom. Protozoans are single-celled organisms with a nucleus that resemble yeast. Examples of Protozoan infections include malaria (an infection of red blood cells caused by Plasmodium) and amoebic dysentery (caused by Entamoeba histolytica). Other parasitic infections are caused by multicellular worms including hookworms (intestinal worm that can cause severe diarrhea, intestinal obstruction, and anemia) and tapeworms (intestinal worms usually from eating undercooked meat that can invade into tissues of the body such as muscles and brain). A variety of antiparasitic medications exist including quinine (for malaria infection) and mebendazole (for worm infections). Prions are the most recently discovered class of pathogens. They are proteins that have been folded into an abnormal shape. Once a prion has infected a cell, it induces host proteins to become misfolded, thereby producing disease. Creutzfeldt-Jakob disease is an example of a prion infection that causes progressive brain degeneration. In fact, all known prions affect brain and neural tissue. More importantly, prion infections are universally fatal. Transmission of a
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A health care–associated infection (HAI) is an infection that occurs during hospital admission with no evidence that the infection was present at the time of admission. In 2002, there were 1.7 million HAIs in the United States that led to 99,000 deaths. The most common types of HAIs are urinary tract infection (34%), surgical site infection (17%), pneumonia (13%), and bloodstream infection (14%). Remarkably, many of these infections are preventable. The United States Department of Health and Human Service and other international health care organizations have launched major initiatives to reduce or eliminate HAIs. One of the most common sources of HAIs are bloodstream infections caused by indwelling venous catheters, particularly central venous catheters. A bloodstream infection (also known as septicemia) is a life-threatening infection in which a pathogen can spread throughout the body by way of a patient’s blood. This can lead to severe sepsis, multiple organ dysfunction, and death. Central venous catheters (or central lines) place patients at increased risk for bloodstream infections because the catheter provides a direct route for pathogens to enter the bloodstream. Infections have been demonstrated to occur from organisms found on the hands of individuals placing central lines or injecting medications through ports on a central line, infected medications, or bloodstream infections that attach and grow on the central line. An important risk factor for the development of a catheter-related bloodstream infection (CRBSI) is the site of the catheter. Central lines placed in a femoral vein are associated with the highest risk of infection, whereas subclavian central lines are associated with the lowest risk. The Centers for Disease Control and Prevention (CDC) has recommended several techniques that have been proven to reduce the risk of CRBSI including hand hygiene before catheter insertion, maximal sterile barrier precautions (cap, mask, sterile gown, sterile gloves, and large
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sterile drape), and appropriate prep (chlorhexidine for patients >2 months old and povidone iodine, alcohol, or chlorhexidine for infants 0. The absorbent material can become dried out or desiccated if it is exposed to prolonged periods of fresh gas flow. Unfortunately, detection of desiccation is difficult. Some, but not all, absorbents change color with desiccation. Desiccation is also associated with heat formation. If either of these signs is noted after a prolonged period of machine inactivity, the absorbent should be replaced. The hazards associated with the use of a desiccated absorbent include carbon monoxide formation, compound A formation with sevoflurane, and fire within the canister. Compound A is a decomposition product of sevoflurane that is known to cause kidney injury in rats. Clinical vigilance is important, as desiccation is difficult to detect. This vigilance includes turning off the fresh gas flowmeters at the end of a case and replacing the absorbent when prolonged fresh gas flow may have occurred. The absorbent should also be replaced if the absorbent
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temperature is felt to be high or checked with a temperature probe and found to be greater than 50°C. A classic example of desiccation occurs with an anesthesia machine that is not used for surgery but accidentally left on with high gas flows over the weekend. If inspection of a machine indicates that this may have occurred, the absorbent should be replaced.
■ COMMON GAS OUTLET The common or fresh gas outlet receives the gas output from the anesthesia machine for delivery to the anesthesia circuit. When the outlet is in an external location, it may have a 15-mm female slip-joint fitting with a coaxial 22-mm male connector. As the common gas outlet contains the output of the vaporizers and various flowmeters, it should not be used to provide supplemental oxygen. This may lead to the unintentional administration of nitrous oxide or volatile anesthetic. A safer source of supplemental oxygen is the auxiliary oxygen connection or connection to an oxygen tank or wall source.
■ OXYGEN FLUSH VALVE The oxygen flush valve delivers high-pressure high-flow oxygen to the common gas outlet from either the tank or pipeline (see Fig. 26.6). Barotrauma of the patient’s lungs can occur if the oxygen flush valve is depressed during inhalation with a spontaneously ventilating patient. Barotrauma of the lungs is injury to the lung tissue caused by high pressure. The increased pressure can lead to a pneumothorax or hole in the lung. This can also occur if the valve is depressed when the ventilator is delivering a breath with some anesthesia machines.
■ BREATHING CIRCUIT The breathing circuit is the critical connection between the anesthesia machine and the patient and is discussed in more detail in Chapter 29. The most commonly used breathing circuit in the operating room is the circle system (Fig. 26.7). The basic circle system contains a Y-piece, inspiratory/expiratory tubes, unidirectional valves, fresh gas inlet, adjustable pressurelimiting (APL) valve, pressure gauge, reservoir bag, ventilator, bag/ventilator switch, airway gas monitor, airway pressure monitor, respirometer, and CO2 absorber. The design of the circle
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■ FIGURE 26.6 The oxygen flush valve introduces highpressure oxygen into the breathing circuit when depressed.
system allows for the conservation of heat, moisture, and volatile anesthetic because of the CO2 absorber and humidification devices. The APL valve, reservoir, and airway pressure monitor allow for the monitored delivery of positivepressure ventilation. The patient can be switched from spontaneous/manual ventilation to the ventilator with the bag/ventilator switch within the system. The other commonly used breathing circuits include Mapleson circuits. A common type of Mapleson circuit used in the perioperative setting is the Mapleson F or Jackson-Rees circuit. They are frequently used for transporting patients. The advantages of the Mapleson systems are that they are simple, lightweight, portable, and robust. The disadvantages include that they require high fresh gas flow, scavenging of gas is difficult, and rebreathing of gas can occur without high gas flows.
■ VENTILATOR A critical aspect of the practice of anesthesiology is the ability to ventilate patients. Anesthesia machines integrate the ventilator and its various
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controls and alarms. If the patient is unable to breathe adequately on his or her own, the ventilator can provide support and enhance the underlying pattern of breathing. If the patient is paralyzed or unable to adequately breathe for other reasons, the ventilator can serve the critical role of ventilation and subsequent oxygen delivery and carbon dioxide removal. The ventilator also serves to deliver and remove anesthetic gases. See Chapter 30 for a further discussion of anesthesia machine ventilators and ventilation modes. A simple distinction between the various ventilation modes is those with which the patient generates a breath versus those generated by the ventilator. The two basic modes of ventilation in which the anesthesia machine generates the ventilation are pressure control (a set pressure is delivered) and volume control (a set tidal volume is delivered). Another major type of ventilation mode involves augmenting a patient-initiated breath with a small amount of positive pressure (pressure support ventilation). This type of ventilation is sometimes combined with backup ventilator-generated breaths. Depending on the type of surgery, the patient, the patient’s comorbidities, and the anesthetic plan, the anesthesia provider will decide which type of ventilation is appropriate for the patient during the surgery.
■ SCAVENGING Scavenging systems remove the waste anesthetic gases from the operating room. This helps reduce exposure to nitrous oxide and halogenated anesthetic agents, which are potentially hazardous gases. These systems can be broken down into five basic components: 1. Gas Collection Assembly The gas collection assembly gathers the excess gas from the ventilator via the ventilator relief valve and from the manual side via the APL valve. Failure of these valves could lead to a buildup of pressure within the breathing circuit. 2. Transfer Tubing The transfer tubing carries the gas to the scavenging interface. It is of a specific size and rigidity to prevent easy kinking. If these tubes are blocked or kinked, there can also be a buildup of pressure in the breathing circuit. There is also tubing carrying gas from the gas analyzer to the scavenging interface.
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Chapter 26 • Overview of Anesthesia Machines
237
■ FIGURE 26.7 The circle breathing system is the breathing system used during most general anesthetics. (From Dorsch JA, Dorsch SE, eds. Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:239, with permission.)
3. Scavenging Interface The scavenging interface is either an open or a closed system. It protects the breathing circuit from excessive positive or negative pressure. An open interface is open to the atmosphere and has no valves. These are used with active disposal systems. A closed interface has valves to connect to the atmosphere. With passive disposal systems, there is a positive-pressure relief valve. With active disposal systems, there are both a positiveand a negative-pressure relief valve. The positive-pressure relief valve prevents the buildup of pressure within the scavenging system and back into the breathing circuit. The negative-pressure relief valve prevents the vacuum from emptying out the breathing circuit.
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4. Gas Disposal Assembly Tubing This tubing carries the gases from the scavenging interface to the gas disposal assembly. It is noncollapsible to prevent blockages. 5. Gas Disposal Assembly The gas disposal assembly is either an active or a passive system, which is the last step in removing the gas from the operating room. An active system uses a vacuum to induce flow and remove the gas. This can be through the regular suction outlets and couplings or through a waste anesthesia gas (WAG) line with its specific couplings and purple tubing. Typically two suction lines are needed for an anesthesia machine. One is used for patient suctioning equipment and the second for the waste gases. Some older machines only have one suction line, and the
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negative-pressure has to be balanced between the two uses. In active systems, there is an adjustable flowmeter showing the amount of negativepressure present, which should be checked to verify the presence of the vacuum. The gases are usually vented outside the building. A passive system does not use a vacuum to induce flow. The gases are pushed out through ventilation ducts as more gas flows from the anesthesia machine.
■ MONITORS Monitors form a critical connection between the patient, the anesthesia machine, and the anesthesia provider. They provide vital information needed to ensure safe care of patients. Monitors are discussed in depth in several chapters of this book. Chapter 32 discusses the gas analyzers used to monitor O2, CO2, N2O, and volatile anesthetic concentrations. Chapter 33 describes the basic monitors typically used during an operation. These monitors include electrocardiogram, which monitors the electrical activity of the heart, the arterial pulse oximeter, which monitors the oxygen saturation of arterial blood, the noninvasive blood pressure, capnography, which monitors the inspiratory and expiratory concentration of carbon dioxide, and temperature. Chapter 9 discusses more advanced invasive monitoring including arterial blood pressure and central venous pressure. Another important type of monitor incorporated in the anesthesia machine is an LCD, which contains information about the ventilation parameters and error messages from the machine. This functions as a monitor of the anesthesia machine and its various parts including the ventilator. In fact, there may be significant overlap between this monitor and patient-specific information displayed on a different monitor with the basic and invasive patient monitors. An example of the overlap is the anesthesia machine’s oxygen analyzer, which is displayed on the anesthesia machine’s LCD, and inspired oxygen concentration from the gas analyzer, which is usually displayed on the monitor with the patient’s vital signs. The anesthesia machine ventilator will also have a display for pressures and volumes monitored in the anesthesia circuit (see Chapter 30). In modern anesthesia machines with an LCD, the process of checking out the anesthesia machine usually includes a review of information displayed
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on this monitor. An understanding of the various machine-related error messages that are displayed is critical for proper machine operation and patient care. Chapter 31 discusses machine maintenance and troubleshooting and reviews common error messages and potential remedies.
■ SUMMARY The anesthesia machine is a critical component of the anesthesia work environment. These devices have grown in complexity and now often include not only the components necessary to deliver gas flows and anesthetic agents, but come bundled with sophisticated ventilators and monitoring equipment. Anesthesia technicians are intimately involved with working with anesthesia machines performing machine checkouts, routine maintenance, and troubleshooting. This chapter provides an overview of the basic machine components tracing them from the gas supply through the flowmeters, the vaporizers, the ventilator, and the breathing circuit to the patient and out through the waste gas scavenging.
REVIEW QUESTIONS 1. You are scheduled to work at your hospital’s ambulatory surgery center on Monday morning. As you start setting up equipment for the first case, you notice that the anesthesia machine is on and the oxygen is flowing at 10 L/min. You note that the operating room had not been in use since the previous Thursday when the surgery center was last open. What should you do? A) Turn off the oxygen. Finish setting out equipment for this room and then continue setting up the rest of the rooms for the day. B) Turn off the machine and the oxygen. Finish setting out equipment for this room and then continue setting up the rest of the rooms for the day. C) Do not touch the machine. Finish setting out equipment for this room and then continue setting up the rest of the rooms for the day. D) If the CO2 canister has not changed colors, do not replace it. Finish setting out equipment for this room and then continue setting up the rest of the rooms for the day. E) Replace the CO2 canister. Finish setting out equipment for this room and then continue setting up the rest of the rooms for the day. Answer: E. Prolonged fresh gas flows can lead to desiccation or dehydration of the carbon dioxide absorbent. If desiccation
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Chapter 26 • Overview of Anesthesia Machines is suspected, the absorbent should be changed. Desiccation can sometimes but not always lead to a change in the color of the absorbent. The hazards associated with the use of desiccated absorbent include carbon monoxide formation, compound A formation with sevoflurane, and fire within the canister.
2. At the end of a long operation, a new anesthetist calls you into the operating room. The anesthetist tells you that he is trying to switch volatile anesthetic agents from isoflurane to desflurane but is unable to turn the dial on the desflurane vaporizer to turn it on. He currently has the isoflurane vaporizer on. Both vaporizers are noted to be full of medication. The anesthetist wants to know if he needs a new vaporizer. What should you tell the anesthetist? A) Yes, the anesthetist needs a new vaporizer. You should be able to turn on both vaporizers at the same time to switch medications. B) Yes, the anesthetist needs a new vaporizer. There must be a leak in the vaporizer as the anesthesia machine has a safety mechanism that prevents the vaporizer from turning on if there is a leak. C) No, the vaporizer does not need to be replaced. You explain that there is a safety feature on the anesthesia machine that will not let him or her switch volatile anesthetics during an operation. D) No, the vaporizer does not need to be replaced. You explain that there is a safety feature on the anesthesia machine that will not let more than one vaporizer from being open at a time. E) No, the vaporizer does not need to be replaced. You tell the anesthetist that if he wants to switch medications, he should just add some desflurane to the sevoflurane vaporizer rather than use a different vaporizer. Answer: D. The vaporizers are properly functioning. When there is more than one vaporizer present on the anesthesia machine, there is a mechanical link called an Interlink that prevents more than one vaporizer from being opened at a time. This prevents the patient from receiving a simultaneous administration of two volatile anesthetics from the anesthesia machine.
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3. The Pin Index Safety System is designed for which purpose? A) To prevent the gas hose from one gas to be connected to another B) To prevent the backflow of gas from one cylinder to another C) To prevent the placement of gas tanks onto the wrong yoke D) To allow the quick release/connection of gas hoses to the machine E) To allow any gas tank to be connected to any yoke on the machine Answer: C. The Pin Index Safety System ensures that each gas tank can only be attached to the specific gas yoke for which it was designed. The Diameter Index Safety System prevents one gas hose from being connected to another. They can only be attached to the specific gas line they are made for. The backcheck valves prevent the flow of gas from one tank or gas line into another tank.
4. There are many parts to a scavenging system. Which part listed below is part of an active gas disposal system but not part of a passive system? A) Ventilator relief valve B) Rigid transfer tubing C) Adjustable pressure relief valve (APL) D) Vacuum system E) Positive-pressure relief valve Answer: D. The vacuum system is required for the active scavenging system and provides suction to draw the gases out of the building. The ventilator relief and APL valves allow the excess gas to flow from the breathing circuit to the scavenging interface. The rigid transfer tubing is part of all scavenging systems. The positive-pressure relief valve is part of a closed systems design in both active and passive systems.
SUGGESTED READINGS Baresh PG, Cullen BF, Stoelting RK, eds. Clinical Anesthesia. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006. Dorsch JA, Dorsch SE, eds. Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.
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CHAPTER
27
Anesthesia Machine Checkout Ramon Larios and Esther Sung ■ INTRODUCTION The delivery of a safe anesthetic in modern-day practice begins with a checkout of the anesthesia machine. Improper or lack of inspection of anesthetic equipment prior to use has been associated with several significant incidents. Failure to check equipment clearly results in an increased risk of operative morbidity and mortality. With the large variety of anesthetic delivery systems available today, it is critical to understand the basic components of the system so that malfunctions can be detected prior to use or when failure occurs during use. Moreover, regular testing may lead to improved preventive maintenance and enhanced familiarity with the equipment. This chapter focuses on the fundamental components of the anesthesia machine checkout. Specific issues related to unique anesthesia delivery systems should be resolved by referring to the appropriate manufacturers’ operator manuals.
■ HISTORY OF MACHINE CHECKOUT RECOMMENDATIONS In 1993, a joint effort between the American Society of Anesthesiologists (ASA) and the U.S. Food and Drug Administration (FDA) resulted in the 1993 FDA Anesthesia Apparatus Checkout Recommendations. This simplified the initial 1986 preuse checkout and made it more userfriendly. At the time, the 1993 checklist focused on components that were immediately dangerous for patients and mechanisms that failed more regularly. This checklist was applicable to most commonly available anesthesia machines. Nevertheless, despite the recognized importance of an anesthesia machine checkout, available evidence suggests that the 1993 recommendations were neither well understood nor reliably used by anesthesia providers.
Moreover, because of recent and ongoing fundamental changes to the various anesthesia machine designs, the 1993 FDA preuse checklist may no longer be universally applicable to all anesthesia delivery systems. As more machines incorporate electronic checkouts, the user must determine which portions are automatically checked and which portions require manual checks. In such cases, the anesthesia care provider must be aware that the electronic machine check may not be a comprehensive preanesthesia checkout, and the user should follow the original equipment manufacturers’ recommended preuse checklist. As a result, in 2005, the ASA’s Committee on Equipment and Facilities, in conjunction with the American Association of Nurse Anesthetists (AANA) and the American Society of Anesthesia Technologists and Technicians (ASATT), began to develop a revised preuse checklist that was designed to be more workstation specific. These recommendations were published in 2008 and were intended to eventually replace the 1993 FDA Anesthesia Apparatus Checkout Recommendations. Rather than a checklist with specific instructions on how to perform each test, these new guidelines elaborate on specific systems and subsystems that must be evaluated. It is ultimately up to the user, along with the anesthesia machine manufacturer, to determine the actual mechanisms and/or specific checks that should be used to accomplish these subsystem evaluations. Appropriate personalized checkout procedures may need to be developed for individual machines and practices. The 1993 Anesthesia Apparatus Checkout Recommendations placed all of the responsibility for the preuse checkout on the anesthesia provider. The new 2008 recommendations identify certain aspects of the preanesthesia checkout that may be performed by a qualified anesthesia
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technician or a biomedical technician (http:// www.apsf.org/newsletters/html/2008/spring/ 05_new_guidelines.htm). Redundancy in the critical aspects of the checkout process makes it more likely that problems will be identified prior to use for a patient. Nevertheless, regardless of the additional support of technicians, the anesthesia care provider is ultimately responsible for the proper function of all equipment used to deliver anesthesia care.
■ ANESTHESIA MACHINE CHECKOUT PROCEDURE As stated earlier, the goal of the preanesthesia checkout is to allow for the safe delivery of anesthesia care. Requirements for safe delivery of anesthetic care include the following: • Reliable delivery of oxygen at any appropriate concentration up to 100% • Reliable means of positive pressure ventilation • Availability of functional backup ventilation equipment • Controlled release of positive pressure from the breathing circuit • Anesthesia vapor delivery (if intended as part of the anesthetic plan) • Adequate suction • Means to conform to standards for patient monitoring The new guidelines for the preanesthesia checkout procedures consist of 15 items. These items must be performed as part of a complete preanesthesia checkout on a daily basis. (Items that must be completed prior to each procedure are in bold). The 15 items are as follows: 1. Verify auxiliary oxygen cylinder and selfinflating manual ventilation device are available and functioning. Anesthesia ventilator failure resulting in the inability to provide patient ventilation is rare but can occur at anytime. For those situations where the problem cannot be immediately identified or corrected, a manual ventilation device (e.g., bag valve mask) may be necessary to provide positive pressure ventilation until the problem is resolved. As a result, a self-inflating manual ventilation device and an auxiliary oxygen cylinder should be available and checked for proper function at each anesthesia setting.
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In addition, the oxygen cylinder should have a regulator and a device to open the cylinder valve should be present. A full E cylinder of oxygen has a pressure of about 2,000 pound-force per square inch gauge (psig), which is equivalent to around 625 L of oxygen. After checking the oxygen cylinder pressure to ensure adequate supply, the cylinder should be stored with the valve closed in order to prevent unintended leakage or drainage of oxygen. 2. Verify patient suction is adequate to clear the airway. The immediate ability to clear airway secretions or gastric contents is essential for safe anesthetic care. Inability to visualize the glottic opening and therefore delay in timely acquisition of a secure airway can be dangerous and possibly fatal. Aspiration of gastric contents can cause prolonged intubation and airway complications. Adequate strength of the suction can be tested by occluding the suction tubing orifice with the underside of a thumb and determining if the weight of the suction tubing can be supported at waist height. Prior to anesthesia, adequate suction should be checked and a rigid suction catheter (e.g., Yankauer) should be available on the machine. 3. Turn on the anesthesia delivery system and confirm that AC power is available. AC power and the availability of backup battery power should be confirmed prior to the delivery of anesthesia. Visual indicators of the power systems exist on most anesthesia delivery systems. These should be confirmed as should appropriate connection of the power cord to a working AC power source. If the AC power is not confirmed, complete system shutdown is at risk when battery power is unknowingly depleted. Desflurane vaporizers, if used, should be checked for adequate electrical power source as well. 4. Verify availability of required monitors and check alarms. The patient’s oxygenation, ventilation, circulation, and temperature should be continually evaluated according to the ASA’s Standards for Basic Anesthetic Monitoring. Verification of the availability and proper function of the appropriate monitoring supplies should be performed prior to each anesthetic. Examples of necessary equipment include, but are not
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limited to, blood pressure cuffs, pulse oximetry probes, electrocardiogram (ECG) leads, and capnography. Moreover, the appropriate audible or visual alarms that would indicate problems with, or disruption of, patient oxygenation, ventilation, circulation, and temperature should be intact. It is prudent for the anesthesiology technician to turn off the monitors and then turn them back on between cases to be sure that alarms are reset to default values as designed by each individual institution. 5. Verify that pressure is adequate on the spare oxygen cylinder mounted on the anesthesia machine. Spare oxygen cylinders are mounted on anesthesia machines in the event that central oxygen supply is lost. Anesthesia machines require oxygen not only to provide oxygen to the patient but often to power pneumatically driven ventilators. The pressure of the oxygen cylinders should be checked to ensure an acceptable amount of backup oxygen is available. The oxygen cylinder valves should be closed after verification in order to prevent unrecognized depletion of the cylinder due to pressure fluctuations in the machine during mechanical ventilation or in the event of actual pipeline supply failure. Rarely, the cylinder is intended to be the primary oxygen source. In these cases, if the ventilator is pneumatically driven, then the oxygen cylinder supply may be depleted quickly. As a result, manual or spontaneous ventilation may be more appropriate in order to maximize the duration of oxygen supply. On the other hand, the duration of oxygen supply for electrically powered or piston-driven ventilators depends only on total fresh oxygen gas flow. 6. Verify that the piped gas pressures are ≥50 psig. Since there are many scenarios that may cause disruption of gas delivery from a central source, pressure in the piped gas supply should be checked at minimum once per day in order to ensure that adequate pressure is available for proper function of the anesthesia machine. If the pipeline hoses have been disconnected in order to move the anesthesia machine at any point during the day, the hoses should be reconnected to the central pipeline supply, and the fittings
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should be examined for firm connections without audible leaks. The pipeline pressure should be 50–55 psig. 7. Verify that vaporizers are adequately filled and, if applicable, that the filler ports are tightly closed. (Provider completes prior to each procedure; technician can complete daily.) Adequate supply of volatile anesthetics is requisite for vapor-based anesthetics in order to reduce the likelihood of inadequate anesthesia and recall under anesthesia. In addition, many vaporizers do not have low-agent alarms, so checking prior to usage is important. After filling the vaporizers, filler ports should be adequately tightened to prevent unrecognized leakage, especially for older vaporizers that do not have systems that automatically close after completion of refilling. Vaporizers should also be secured so that they cannot tilt or be lifted from their mounts. 8. Verify that there are no leaks in the gas supply lines between the flowmeters and the common gas outlet. (If the vaporizer has been changed, this should be rechecked prior to use.) The low-pressure component of the anesthesia machine circuit is located between the flow control valves to the common gas outlet. The leak test checks the integrity of the anesthesia machine in this part of the circuit. The components located within this area are subject to breaking and developing leaks. Leaks in the low-pressure circuit can cause leakage of oxygen from the inspired gas and delivery of a hypoxic gas mixture. Likewise, leakage of inhaled anesthetic can result in the patient receiving much less gas anesthetic than is indicated on the machine vaporizer, which places the patient at risk for awareness under anesthesia. In addition, each individual vaporizer must be turned on in order to check for leaks within each vaporizer or at the mount, and it is especially important to recheck this test whenever a vaporizer is changed. Several different methods have been used to check the low-pressure circuit for leaks. One reason for the large number of methods is that the internal design of various machines differs considerably. The clearest example is the difference between most GE Healthcare/Datex-Ohmeda and Dräger
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Medical workstations. Most GE Healthcare/ Datex-Ohmeda workstations have a check valve near the common gas outlet, whereas Dräger Medical workstations do not. The presence or absence of this check valve may determine which preoperative leak test is indicated. The check valve is located downstream from the vaporizers and upstream from the oxygen flush valve, and it is open in the absence of back pressure. Gas flow from the manifold moves a rubber flapper valve off its seat, thereby allowing the gas to proceed freely to the common outlet. The valve closes when back pressure is exerted on it, preventing the flow of gas back into the machine and through a leak. Examples of back pressure that can cause the check valve to close are oxygen flushing, peak breathing circuit pressures generated during positive-pressure ventilation, and the use of a positive-pressure leak test. Typically, the low-pressure circuit of anesthesia workstations without an outlet check valve can be tested with a positivepressure leak test (e.g., with Dräger Medical machine). When performing a positivepressure leak test, the operator generates positive pressure in the low-pressure circuit by using flow from the anesthesia machine or from a positive-pressure bulb to detect a leak. One common test is the retrograde fill test, which is performed by closing the adjustable pressure-limiting (APL) valve and occluding the patient port. Oxygen flow or flush is used to fill and distend the reservoir bag, and flow is adjusted so that a pressure of 30 cm H2O on the manometer is maintained in the breathing system. No more than 350 mL/min flow should be necessary to maintain a steady pressure. When complete, the pressure should be relieved by opening the APL valve, not by opening the patient port. Relieving the pressure by opening the patient port could cause CO2 absorbent dust to enter the system. Notably, the retrograde fill test checks both the lowpressure part of the machine and the breathing circuit and does not isolate the source of the leak. In addition, it is not very sensitive to small leaks. Machines with check valves must be tested with a negative-pressure leak test (e.g.,
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GE Healthcare/Datex-Ohmeda machine). When performing a negative-pressure leak test, the operator creates negative pressure in the low-pressure circuit by using a suction bulb to detect leaks. In order to do this, the machine’s master switch, flow control valves, and vaporizers should all be initially turned off. The suction bulb is attached by tubing and an adapter to the common fresh gas outlet, and the bulb is squeezed repeatedly until it is fully collapsed. This creates a vacuum in the low-pressure system. If the bulb stays collapsed for at least 10 seconds, the system is free of leaks, but if the bulb reinflates during this period, a leak is present. The test is repeated with each vaporizer individually turned to the “on” position because leaks inside the vaporizer can be detected only when the vaporizer is turned on. The negative-pressure leak test is the most sensitive leak test, as it can detect leaks as small as 30 mL/min. This test used to be considered the universal leak test since it works for machines with or without a check valve, but unfortunately, some new machines do not have accessible common gas outlets. For specific instructions, the appropriate anesthesia machine manual should be referenced, as there are many machines that have automated checks and/or variations to these procedures. 9. Test scavenging system function. To prevent room contamination by anesthetic gases, a functional scavenging system is necessary. The connections between the anesthetic machine and the scavenging system must be checked daily to ensure integrity of the scavenging system. The anesthesia technician should be particularly careful to remember to attach the scavenging system to the evacuation system when moving anesthesia machines to out-of-operating room (OR) locations of care. There are various scavenging system designs that may require that an adequate vacuum level be present. On active systems (e.g., full vacuum), vacuum pressure can be modulated by the screw valve. Most modern scavenging systems have positive and negative pressure relief valves. The positive relief valve allows exhaled gases to be released into the OR in the event of
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inadequate vacuum (usually occurs in an active system when someone inadvertently closes the screw valve). The negative relief valve prevents suction in an active vacuum system from affecting airway pressure in the breathing circuit for the patients. As these valves are important to protect the patient from pressure fluctuations coming from the scavenging system, they must be checked daily. The checks on these valves can be quite complex; therefore, the anesthesia technician should receive specific troubleshooting training from the hospital biomedical engineers and refer more complicated problems to them directly. 10. Calibrate or verify calibration of the oxygen monitor and check the low oxygen alarm. Calibration of the oxygen sensor is critical for safe patient care. Continuous monitoring of the inspired oxygen concentration helps prevent the delivery of a hypoxic gas concentration to patients. The oxygen monitor is crucial to detect any changes in the oxygen supply. Oxygen sensor calibration should occur at least once per day. Some anesthesia machines are self-calibrating. For these machines, they should be verified to read 21% when sampling room air. The oxygen sensor calibration can be performed by an anesthesia provider or anesthesia technician. If more than one oxygen monitor is present, the primary sensor that will be relied upon for oxygen monitoring during patient care should be the one checked. The low oxygen concentration alarm should also be checked at this time. This is done by setting the low oxygen alarm above the measured oxygen concentration and confirming that an audible alarm is generated. Detailed oxygen sensor calibration instructions can be found in the specific anesthesia machine’s operator manual. 11. Verify carbon dioxide absorbent is not exhausted. A circle breathing system relies on the removal of carbon dioxide to prevent rebreathing of carbon dioxide by the patient. There is a characteristic color change in the carbon dioxide absorbent, depending on the particular absorbent being used, that indicates depletion of the absorbent. When this color
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change occurs, it is a visual reminder that the absorbent must be replaced. Some newer absorbents change color when they become desiccated. If the carbon dioxide absorbent is exhausted or desiccated, it should be changed. It is possible that the carbon dioxide absorbent loses its ability to remove carbon dioxide without producing a color change. For example, an exhausted desiccated absorbent may return to its original color after a period of rest. Capnography, which must be used in every anesthetic, can be helpful in indicating the need to replace the absorbent. When the inspired carbon dioxide concentration is detected to be greater than 0, this indicates that the patient is rebreathing carbon dioxide and that the absorbent may be used up, and therefore, needs to be replaced. When replacing carbon dioxide absorbent canisters, it is important to install them correctly. Incorrectly installed carbon dioxide absorbent canisters are a common source of leaks within the anesthesia machine. 12. Breathing system pressure and leak testing. The breathing system leak test must be performed on the components that will be used during a particular anesthetic. If any portion of the circuit is changed after completing the leak test, the leak test must be performed again to ensure the integrity of the breathing system. The purpose of this test is to ensure that adequate pressure can be generated and maintained in the breathing system during assisted ventilation. Adequate pressure is usually considered to be greater than or equal to 30 cm H2O. This test also checks the ability to relieve pressure in the breathing circuit with the APL valve during manual ventilation. To manually check the breathing system for leaks, the APL valve is closed and the patient port is occluded at the Y-piece. The oxygen flush valve is used to instill 30 cm H2O pressure into the breathing circuit. If the circle system is free of leaks, the value on the pressure gauge should not decrease. Of note, newer machines may have automated testing that can be used to detect leaks. Additionally, they can also determine the compliance of the breathing system. Once adequate pressure is obtained in the circle
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system, it can be released by completely opening the APL valve. This step can test for proper functioning of the APL valve, ensuring that it entirely relieves the pressure in the circle system. 13. Verify that gas flows properly through the breathing circuit during both inspiration and exhalation. Although checking the breathing system for pressure and leaks is important, this test does not assess the function of the unidirectional inspiratory and expiratory valves. The presence of the valves can be assessed visually. To test for proper function of the unidirectional inspiratory and expiratory valves, first remove the Y-piece from the circle system. Next, breathe through the two corrugated hoses separately. The valves should be present, and they should move appropriately. The person performing the test should be able to inhale but not exhale through the inspiratory limb and able to exhale but not inhale through the expiratory limb. At the completion of this test, the breathing circuit should be changed to a fresh circuit prior to attaching the anesthesia machine to the patient. This flow test can also be performed by attaching a breathing bag to the Y-piece and using the ventilator. In addition, capnography can also be useful to detect an incompetent valve. For example, an incompetent inspiratory valve should be considered in situations of high (greater than zero) inspired carbon dioxide concentration. 14. Document completion of the checkout procedures. A printed copy of the preanesthesia checkout procedures should be retained near or in the anesthesia machine since an organized and systematic list may result in improved fault detection over memory alone. Moreover, a pictorial checklist may be helpful as it can be simpler to follow than a typewritten list. Documentation of checkout procedure completion should be performed and may be important in the case of an adverse incident, as omission of the checkout can by cited as evidence of substandard care. Dates and times of certain checkout procedures may be recorded automatically by some computerized checkout
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systems, but those that are not automatically recorded should be manually documented by the individual who performs the checkout procedure. Record keeping is important to provide supporting evidence that equipment is being appropriately maintained. Should service be necessary, this record may also be helpful for service representatives who come to repair the equipment, for providing a reminder to check on the repair that was done, and for referencing at a later date what was repaired and who performed the repair. A log of malfunctions may also help to determine if a particular piece of equipment warrants replacement. This record should be retained, should an adverse outcome lead to litigation. 15. Confirm ventilator settings and evaluate readiness to deliver anesthesia care. (Anesthesia provider should perform.) Prior to starting each anesthetic, the completion of the preanesthesia checkout procedures should be verified as well as the availability of essential equipment. Ventilator settings should be confirmed and pressure limit settings used as a secondary backup to prevent barotrauma once positive pressure ventilation is used. Specifically, the presence and functionality of appropriate monitors, the capnogram, and oxygen saturation by pulse oximetry should be checked. Proper flowmeter and ventilator settings, placement of the ventilator switch to manual, and adequate filling of the vaporizers should also be ensured before initiation of an anesthetic. The delivery of safe anesthetic care in modern practice begins with a thorough evaluation of the anesthetic delivery system being used. Anesthesia providers, along with trained anesthesia technicians and biomedical technicians, must have a thorough understanding of the fundamental components of the anesthesia machine. Thus, malfunctioning components can be repaired or replaced to decrease the potential for patient injury. These preanesthesia machine checks should be documented not only for maintenance records but also for medical-legal reasons. With the great variation in anesthesia machine design, it
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is important to always refer to the specific anesthesia machine manufacturer’s instruction manual for more detailed information and instruction.
■ SUMMARY The anesthesia machine is a critical component of the OR. Failures in the anesthesia machine have the potential to cause significant patient injuries. Proper maintenance and a thorough checkout procedure can identify many machine problems before they have a chance to cause problems in the OR. Multiple organizations and the anesthesia machine manufacturers have been instrumental in devising detailed anesthesia machine checkout procedures. Each machine will have a unique checkout procedure detailed by the manufacturer. This chapter presents an overview of the machine checkout procedure that should be customized for each anesthesia machine according to the manufacturer.
REVIEW QUESTIONS 1. Which organization(s) was involved in developing the 1993 Anesthesia Apparatus Checkout Recommendations? A) FDA B) American Medical Association (AMA) C) ASA D) A and C E) All of the above
Answer: D. It is important to check for adequate pipeline supply pressure for all gases connected to the anesthesia machine. Although failure of pipeline pressure is rare, it can affect the delivery of gases to the patient and function of the ventilator.
4. Who is qualified to perform portions of the anesthesia machine check? A) Anesthesia care provider B) Anesthesia technician C) Biomedical technician D) A and B E) All of the above Answer: E.
5. How often should the breathing system pressure and leak testing be performed? A) Once per day B) Prior to the start of each case C) Only at the end of the day D) A and B Answer: D.
6. Vaporizers should A) Be checked for adequate agent prior to each case B) Have filler ports tightened after filling to prevent leakage C) Never be tipped D) A and B only E) All of the above Answer: E. Not only should the vaporizers be checked for adequate agent prior to each case, but after filling, the filler ports should be tightened. Vaporizers should NEVER be tipped, as tipping may cause the internal wick to become saturated and the delivery concentration could become inaccurate.
Answer: D.
2. All anesthesia machines have a check valve in the low-pressure system. A) True B) False Answer: B. A check valve in the low-pressure system will negate a positive-pressure leak test. A negative-pressure leak test will be necessary to perform an adequate anesthesia machine checkout. Anesthesia technicians should consult the manufacturer’s operator manual for the presence of a low-pressure system check valve and the proper procedure for testing for leaks in this system.
3. Piped gas pressure should be A) 20–25 psig B) 30–35 psig C) 40–45 psig D) 50–55 psig E) Greater than 55 psig
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SUGGESTED READINGS Brockwell RC, et al., for American Society of Anesthesiologists. Recommendations for Pre-Anesthesia Checkout Procedures. 2008. Available at: http://www.asahq. org/For-Members/Clinical-Information/∼/media/ For%20Members/Standards%20and%20Guidelines/ FINALCheckoutDesignguidelines.ashx; 2008. Dorsch JA, Dorsch SE. Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008. Edward MG, Mikhail MS, Murray MJ. Clinical Anesthesiology. 3rd ed. New York, NY: McGraw-Hill; 2003. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2009. Standards for Basic Anesthetic Monitoring, Committee of Origin: Standards and Practice Parameters (Approved by the ASA House of Delegates on October 21, 1986, and last amended on October 20, 2010, with an effective date of July 1, 2011).
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Vaporizers Roy Esaki and Alex Macario ■ INTRODUCTION
Vapor and Vapor Pressure
Inhalational agents are drugs with anesthetic properties administered in the form of a gas. For a drug injected intravenously, the dosing relates to the mass the patient receives (e.g., in grams), in the form of a specific volume at a specific concentration. Inhalational agents, however, are delivered as a concentration in a volume of gas. The “volume” is being continuously delivered with each breath the patient receives. As these agents normally exist as liquids at room temperature and atmospheric pressure, a vaporizer is used to turn the liquid into a gas that the patient can inhale. In the middle of the 19th century, the first available “vaporizers” were merely devices that allowed the patient to breathe evaporated liquid agents. The device used by William Morton in the first public demonstration of ether anesthesia in 1846 was a container that contained a sponge soaked with ether (Fig. 28.1). The patient breathed in the agent as it evaporated off the sponge. Later, chloroform was administered by dropping the liquid agent using special dropper bottles (Fig. 28.2) over a cloth that was placed either directly over the patient’s mouth or draped over a wire mask. Although such devices allowed the liquid to evaporate into a gaseous form, the concentrations of the agent could not be controlled. Modern vaporizers were thus developed to deliver a precise and constant concentration of the agent.
A vaporizer turns the liquid anesthetic agent from a liquid form to a gas, or vapor. All substances can exist in liquid, solid, or gas forms, depending on the pressure and temperature of the substance. As a gas is compressed under increasing pressure, the particles are pushed closer together until the gas turns into a liquid. For example, when nitrogen gas is compressed enough, it turns into liquid nitrogen. For some gases, there is a critical temperature above which a gas cannot exist as a liquid, no matter how much pressure is applied. A vapor is a substance in the gaseous phase at a temperature below its critical point. That is, it is a gas that has the potential to become a liquid when compressed, or subjected to a higher pressure. When a volatile liquid is placed in a closed container, a certain percentage of the liquid molecules evaporate to become vapor. This vapor creates a pressure, called the vapor pressure. As more heat is applied, more molecules enter the gaseous phase, resulting in a greater pressure. As such, the vapor pressure of any substance increases with temperature. The concentration of an agent delivered by a vaporizer depends on the vapor pressure of the agent. Because different agents have different vapor pressures, each modern vaporizer is calibrated for use with a specific agent. Of note, desflurane has a much higher vapor pressure at room temperature than other agents, and thus requires a vaporizer with unique features (see below).
■ PHYSICAL CHEMISTRY
Gas Concentration: Partial Pressure and Volume Percent
To understand the basic principles of how modern vaporizers work, we need to review some principles of physical chemistry: the concepts of vapor, vapor pressure, and gas concentrations.
The concentration of a vapor can be expressed as either a partial pressure or a volume percent. In a mixture of gases, each gas independently
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body, concentrations delivered by a vaporizer are commonly expressed as a volume percent for practical convenience. Volume percent is the fraction of the total pressure attributable to the gas of interest expressed as a percent (partial pressure of gas/total ambient pressure × 100). This term may be a slight misnomer as the gas molecules are mixed together in a shared volume. Nonetheless, because the volume of a gas is proportional to the number of particles, given a constant pressure and temperature, the volume percent of an agent can be thought of as a percentage of the total number of gas molecules delivered to the patient.
■ PRINCIPLES OF MODERN VAPORIZERS ■ FIGURE 28.1 Early vaporizer. A replica of the inhaler used by Dr. William Morton to demonstrate the use of ether anesthesia in 1846. An ether-soaked sponge was placed inside, and the patient breathed in the evaporated vapor. (Photo courtesy of the Wood Library-Museum of Anesthesiology, Park Ridge, IL [http://www.woodlibrarymuseum.org/museum_view.php?id=2].)
contributes part of the total pressure, which is the sum of the partial pressures of all gases present. The portion of the total pressure created by any given vapor is called the partial pressure of that gas. Although the partial pressure of the gas is what actually corresponds to the clinical effect of an anesthetic gas in the
■ FIGURE 28.2 Chloroform dropper. From left to right: a chloroform drop flask, a drop bottle with a control valve, and an alembic flask. Such devices allowed careful titration of the liquid agent. (Photo courtesy of the Wood Library-Museum of Anesthesiology, Park Ridge, IL [http://www.woodlibrarymuseum.org/museum_view. php?id=25].)
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Vaporizers vary greatly in their design and construction. Figure 28.3 shows one common type of modern vaporizer. All modern (concentrationcalibrated vaporizers) are placed out of circuit— that is, between the flowmeter and the common gas outlet, rather than within the breathing system or between the common gas outlet and the breathing system. The intent of this chapter is not to go over the specifics of the operation of any specific vaporizer model but to provide an overview of the principles underlying the operation of modern vaporizers.
■ VARIABLE BYPASS VAPORIZERS As mentioned previously, the basic purpose of a vaporizer is to deliver a set concentration of anesthetic gas in a volume of inert gas, such as oxygen. Figure 28.4 shows the general schematic
■ FIGURE 28.3 The Drager Vapor 2000 series; from left to right, a desflurane, a sevoflurane (turned on), and an isoflurane vaporizer.
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the vaporization chamber and for the flow that would skip the chamber had to be manually adjusted to achieve a desired output gas concentration. Modern variable bypass vaporizers do this automatically when the concentration dial is set to a desired concentration. Although the input fresh gas flow rate theoretically can increase the output gas concentration, this effect is minimal with most modern vaporizers. The input gas composition (i.e., if nitrous oxide is used in addition to oxygen) can also affect the concentration. To account for these effects, many electronic vaporizers have a feedback system that adjusts its internal settings based on the actual gas output. In other types of vaporizers, such as the Tec 6 used for desflurane, there are two separate input circuits, rather than a single fresh gas flow that is split.
■ VAPORIZATION METHOD ■ FIGURE 28.4 Schematic of a variable bypass vaporizer. Simple schematic of modern vaporizer: Fresh gas flow enters the vaporizer inlet (top left) and is directed either down into the vaporizing chamber to become saturated with vapor or into a bypass chamber across the top. By varying the ratio of the split, the output vaporizer concentration (top right) can be changed. (Figure courtesy Dr. Guy Watney [http://www.asevet.com/resources/ vaporizer/index.htm].)
of a vaporizer. In this schematic, fresh gas flow enters from the top left, corresponding to the vaporizer inlet. The inert gas can then flow across the top bypass chamber, without being exposed to any volatile agent. Alternatively, some of the fresh gas flow can be diverted down into the vaporizing chamber, where it becomes saturated with a certain concentration of the volatile agent, as determined by the partial pressure of the agent. The concentration dial can vary the percentage of gas, called the splitting ratio that bypasses the vaporizing chamber; this construction is thus called the variable bypass vaporizer. The end result is that the partial pressure of the volatile agent in the vaporizing chamber is diluted by the fresh gas flow through the bypass to obtain the desired concentration of anesthetic. The gas with the desired vapor concentration exits through the outlet of the vaporizer, shown at the top right of the schematic. In an older type of vaporizer, called the copper kettle, the gas flows for both the flow directed to
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Older vaporizers such as the copper kettle bubbled the carrier gas up through the liquid anesthetic to saturate the carrier gas with the anesthetic. Most modern vaporizers have the carrier gas flow over the liquid agent where it takes up the anesthetic. Increasing the surface with internal wicks and baffles makes the vaporization and uptake of the anesthetic more efficient. To accommodate the higher vapor pressure of desflurane, the Tec 6 vaporizer uniquely uses a gas/vapor blender in which the desflurane is heated to a constant temperature to produce a vapor that is then injected into the gas flow in a regulated fashion (Fig. 28.5).
■ FIGURE 28.5 Schematic of Tec 6 desflurane vaporizer. The liquid desflurane (liquid) is heated (H) to a vapor form (gas), which is then mixed with the carrier gas to produce a vaporizer output of the desired concentration. (Figure courtesy Dr. Guy Watney [http://www.asevet. com/resources/vaporizer/index.htm].)
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TABLE 28.1 PROPERTIES OF VARIOUS VAPORIZERS VAPORIZER MODELS MOST MODERN VAPORIZERS*
COPPER KETTLE, VERNITROL
TEC 6 (DESFLURANE)
Carrier gas flow
Variable-bypass
Measured-flow (operator determines carrier gas split)
Dual-circuit (carrier gas is not split)
Method of vaporization
Flow-over
Bubble-through
Gas/vapor blender
Temperature compensation
Automatic temperature compensation
Manual (i.e., by changes in carrier gas flow)
Heated to a constant temperature
Calibration
Calibrated, agent-specific
None; multiple agent
Calibrated, agentspecific
Position
Out of circuit
Out of circuit
Out of circuit
*Tec 4, 5, 7, SevoTec, Aladin (ADU); Vapor 19, Vapor 2000. Table adapted with permission courtesy Dr. Michael Dosch (http://www.udmercy.edu/crna/agm/05.htm).
■ TEMPERATURE COMPENSATION Since vapor pressure depends on the temperature of the gas, the output vapor concentration of older vaporizers was often dependent on temperature. Modern vaporizers have an automatic mechanism built in that regulates the variable bypass to compensate for changes in temperature, keeping the gas concentration roughly constant over standard operating temperatures. The degree of temperature compensation depends on the specific vaporizer; some vaporizers have gas outputs that slightly increase as ambient temperature increases (Table 28.1).
vaporizer are potential causes of a vaporizer leak. Before mounting or detaching a vaporizer, it and all adjacent vaporizers should be turned off. The “travel” setting on the vaporizer should be used, if present, to prevent the agent from filling the bypass chamber (Fig. 28.6). Even with the travel setting in use, care should be taken to
■ OPERATION OF VAPORIZERS Anesthesia technicians know how to install and remove, transport, fill, operate, and drain vaporizers. It is important to be familiar with safety features and potential problems associated with each process.
Installation of Vaporizer Vaporizer mounting systems can be permanent or detachable. Permanent mounting systems have the advantage of less risk of physical damage and leaks, but the disadvantage is that vaporizers cannot be swapped out if a different agent is needed, or if a vaporizer malfunctions. Most modern anesthesia machines have detachable mounting systems, in which vaporizers can be mounted or removed without tools. In general, each vaporizer position has an input and output port valve, each with O-rings to prevent an air leak between the mounting system and the vaporizer. Missing or broken O-rings or improper mounting of the
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■ FIGURE 28.6 The concentration dial must be in the Travel (T) position of the Vapor 2000 vaporizer before the vaporizer can be unlocked from the machine. This isolates the vaporizer chamber to prevent liquid from entering the bypass chamber.
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transport all vaporizers in an upright position to prevent liquid agent from entering inappropriate compartments.
Filling the Vaporizer As vaporizers are calibrated for use with specific agents with given partial pressures, an incorrect gas concentration will be delivered to the patient if an incorrect agent is used to fill the vaporizer. Because of this, the filling systems of modern vaporizers are designed to allow a vaporizer to be filled with only a specific agent. In a bottlekeyed system, each agent comes in a specifically designed bottle that may itself be used to fill the vaporizer or that uses an attachment (filler) that uniquely connects to the bottle of the agent and the filling port of the corresponding vaporizer. A common bottle-keyed system (Easy-fill system) uses a bottle collar that is color coded according to the anesthetic agent. The filling attachment of the same color as the bottle collar is designed in such a way that it can only screw onto the appropriate bottle (Figs. 28.7 and 28.8). There may be a metal block in some vaporizers that must be removed prior to attachment of the filling device. After the bottle-filler assembly is inserted into the vaporizer, some vaporizers have a latch that
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must be opened, after which the bottle is rotated up to fill the vaporizer as shown in Figure 28.9. Funnel-fill systems are less frequently used but exist in some older vaporizers; a screw-in plug is removed to expose the opening of the funnel, into which the liquid agent is poured. A screw-in adaptor can be attached to the funnel, for use with the bottle-keyed system. Desflurane vaporizers often use a Quick-Fill System in which the grooved filling attachment is permanently attached to the bottle. This is an extra measure to prevent desflurane from being poured into the wrong vaporizer (Fig. 28.10). The level of liquid agent remaining in the vaporizer may be displayed electronically on the anesthesia machine, or more commonly by a liquid fill indicator. The level of anesthetic agent remaining should be checked prior to the start of every case. Each type of vaporizer will have a different rate of consumption based on its efficiency, but a rough estimate of how long the liquid anesthetic should last is given by the following formula: 3 × Fresh gas flow (L/min) × volume% = milliliters of liquid used per hour Thus, a case using sevoflurane at 1.8% at 2 L/min fresh gas flow yields an hourly consumption
■ FIGURE 28.7 As an example of the bottle-keyed system, the collar of the sevoflurane bottle (left) has a color and spacing of protrusions that match an agent-specific filling attachment (right) with appropriately spaced indentations.
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block must be replaced snugly. This is a very common oversight that can create a leak in the system, resulting in anesthetic gas leaking out to the atmosphere when the vaporizer is turned on. Most modern vaporizers have a system to prevent the vaporizer from being overfilled, but care should nonetheless be taken to not fill the vaporizer above the fill line.
Delivery of Anesthetic ■ FIGURE 28.8 Filling attachment for use with a keyed filling system. The color-coded base attaches uniquely to the collared bottle, and the rectangular filling block is grooved to uniquely fit into a specific vaporizer.
of 10.8 mL. The capacities of vaporizers vary greatly from roughly 100 to 400 mL, but based on the equation above, a vaporizer filled to 200 mL would last about 18.5 hours. Gloves should always be used when filling the vaporizer, as the liquid agents can be caustic to skin. Whichever system is used, the cap on the vaporizer filling receptacle or the metal
■ FIGURE 28.9 After insertion of the filling attachment with the bottle upright, a latch is pulled to secure the attachment, and the bottle is rotated 180 degrees to an inverted position to fill the vaporizer.
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Modern vaporizers generally have a dial calibrated in terms of volume percent; a counterclockwise rotation of the concentration dial universally increases the concentration. Some vaporizers have a button on the dial that needs to be depressed while the gas is turned on as an additional safety feature. All vaporizers have a vapor exclusion, or interlock, system that mechanically prevents more than one vaporizer from being turned on at the same time. As mentioned earlier, there may be a discrepancy between the concentration dial setting and the actual vaporizer output as the vaporizer function may be affected by the fresh gas flow, the temperature of the gas, and the vaporizer itself. The gas composition (whether nitrous
■ FIGURE 28.10 A desflurane bottle with a permanently attached filling attachment that uniquely fits into a desflurane vaporizer.
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oxide is present in the fresh gas flow) may also slightly affect the vaporizer output.
Removal of Anesthetic The method of draining an agent from a vaporizer varies according to the vaporizer model. In general, there is a drain valve or nozzle that may simply require removal of a plug or insertion of a drain attachment (as with the desflurane QuickFill system). The removed agent can theoretically be set to evaporate in an area that people will not be exposed to the vapor. Alternatively, the agent could be poured into a container connected to the vacuum system, which will remove the vapor as the agent evaporates.
■ TROUBLESHOOTING An anesthesia technician will be called upon to help troubleshoot vaporizers when they malfunction. In diagnosing an issue, it is helpful to categorize the problem as one in which the vaporizer is delivering higher than expected vapor output or lower than expected output. These abnormalities can be detected when an agent monitor is utilized and the detected agent appears to be higher or abnormally lower than the concentration selected on the vaporizer dial.
Higher than Expected Vapor Output If the vaporizer is overfilled, or if the vaporizer is tipped, the liquid agent can spill into the bypass chamber. When this happens, the normally agent-free diluent (fresh) gas that “bypasses” the agent is now exposed to the anesthetic and picks up some vaporized agent. The result is that the vaporizer output contains more vapor than the vaporizer dial has been set for. As mentioned above, the “travel” setting on some vaporizers seals the vaporizing chamber during transport to prevent liquid from entering the bypass chamber. A failure of the vaporizer interlock system may also result in more than one vaporizer being turned on at the same time. This problem can be detected by an agent monitor (see Chapter 32). The monitor will display an error message or the presence of multiple volatile agents. Although a properly mounted vaporizer should not have this problem, the reversal of flow (i.e., fresh gas flow entering through the exit port) through a vaporizer can in some vaporizers cause excessive vapor pressure. Another cause of higher than expected agent readings occurs when an agent
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■ FIGURE 28.11 The yellow sevoflurane keyed filling device is incorrectly screwed onto an isoflurane bottle and a purple isoflurane keyed filling device is incorrectly screwed onto a sevoflurane bottle. (From Keresztury MF, et al. A surprising twist: an unusual failure of a keyed filling device specific for a volatile inhaled anesthetic. Anesth Analg. 2006;103(1):124–125.)
is used incorrectly in a vaporizer meant for use with an agent with a lower vapor pressure. In this case, the output gas concentration will be higher than expected. The keyed filling systems meant to prevent this problem can be circumvented (Fig. 28.11). This practice must be strictly avoided. The clinical effect of the increased concentration will depend on the relative potencies of the two agents, which is reflected by the minimum alveolar concentration (MAC) values.
Lower than Expected Vapor Output A simple and common cause of decreased vapor output is absent or low anesthetic agent levels in the vaporizer. Checking the agent level is a quick first step in troubleshooting decreased vapor output. Many modern vaporizers will sound an alarm when the agent level is low. Another cause of lower than expected output is if a vaporizer leak is present. The most common cause of a leak is a missing or loose cap on the filling port. Other sources of leaks
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are vaporizer misalignment (i.e., resulting from a foreign object wedged under the vaporizer), a damaged or missing O-ring in the vaporizer, or internal mechanical failure (e.g., from physical damage). A leak in the downstream circuit may also result in a lower agent level being detected by the agent monitor. If a leak is suspected, the gas sampling line can be used to “sniff” around the vaporizer and circuits to detect the source of the leak.
Other Problems A physically damaged vaporizer or particulate contaminants in the vaporizer may cause a multitude of nonspecific problems, and the vaporizer should be immediately set aside and sent out for appropriate repair. Regular maintenance should be performed according to the manufacturer’s guidelines and institutional protocols; in general, semiannual preventative maintenance with annual servicing would be appropriate.
■ SUMMARY Anesthetic agent vaporizers are a critical component of anesthesia machines. The laws of physics govern how liquid agents vaporize and this determines how liquid anesthetic agents function within a vaporizer. Modern vaporizers add anesthetic vapor to the fresh gas flow to deliver a desired concentration of anesthetic gas. A thorough knowledge of the inner workings of vaporizers will help an anesthesia technician troubleshoot vaporizer problems.
REVIEW QUESTIONS 1. Which of the following statements about filling an isoflurane vaporizer with sevoflurane are TRUE? A) Agent monitors cannot detect different anesthetic agents. B) The output of the vaporizer would be unchanged. C) The output of the vaporizer would change. D) The vaporizer would not output any vapor. E) None of the above. Answer: C. Sevoflurane has a much lower vapor pressure than isoflurane. Each vaporizer is calibrated for the specific vapor pressure of the agent intended for the vaporizer. If the vaporizer is filled with an agent of a different vapor pressure, the output will differ from what is set on the dial. Agent monitors are specifically designed to detect the amount of agent in the
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circuit and are the best way to determine if there is a discrepancy between the dial setting and the vaporizer output.
2. The majority of modern vaporizers have the following characteristics EXCEPT A) Agent-specific B) Variable bypass C) Temperature compensated D) In-circuit E) Flow-over Answer: D. Modern vaporizers are placed such that the agent is introduced into the system prior to the common gas outlet. Very old vaporizers injected agent directly into the breathing circuit (in-circuit design). All of the answers describe features of modern vaporizes.
3. Which of the following would be least likely to cause an overdose of anesthetic agent? A) Damaged O-ring on the vaporizer-mounting bracket B) Filled vaporizer that has been tipped over C) Vaporizer usage in an especially hot environment D) Failed interlock system E) All of the above. Answer: A. Damaged O-rings typically cause a leak with some of the gas containing anesthetic escaping (not added to the fresh gas). This will result in lower than expected vaporizer output. Vaporizers that have been tipped over can introduce the agent into the bypass circuit, causing the bypass gas to pick up the agent, resulting in a higher than expected vaporizer output. As temperature increases, the vapor pressure of liquids increases, which could increase the amount of agent added to the fresh gas. Most modern vaporizers compensate for temperature variations within a set range. A failed interlock system may allow multiple vaporizers to contribute agents to the fresh gas flow, potentially resulting in an overdose.
SUGGESTED READINGS Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Williams; 2009. Dosch M. The anesthesia gas machine. Available at: http:// www.udmercy.edu/crna/agm/05.htm. Accessed May 1, 2011. Ehrenwerth J, Eisenkraft J. Anesthesia Equipment: Principles and Applications. St Louis, MO: Mosby; 2007. Keresztury MF, et al. A surprising twist: an unusual failure of a keyed filling device specific for a volatile inhaled anesthetic. Anesth Analg. 2006;103(1):124–125. Rosch J, Dosrch S. Vaporizers in Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Wolters Kluwer/ Lippincott Williams & Williams; 2008.
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CHAPTER
29
Anesthesia Breathing Systems Charles A. Vacanti ■ INTRODUCTION It is exceedingly important for anesthesia personnel to understand and become proficient at using a variety of breathing systems. Fortunately, anesthesia breathing systems represent very simple and logical devices and are consequently quite easy to learn. For the purpose of this chapter, anesthesia breathing apparatuses are defined as devices that enhance the ability to breathe a desired gas or vapor (including air or oxygen). The reader should note that this discussion does not include a detailed discussion of the anesthesia machine itself, but only the breathing circuit. Ventilators that assist breathing and masks and other aids for breathing (such as masks and nasal prongs) are discussed in Chapter 30 and Chapter 35, respectively. This chapter focuses on the development of anesthesia breathing systems from a functional perspective.
■ BREATHING DEVICE REQUIREMENTS One of the most straightforward breathing systems was demonstrated in an early Tarzan film when the “ape man” cut a long reed through which he was able to breathe while submerged in a pond, to elude the natives pursuing him. The reed functioned in a manner similar to a modernday snorkel. Thus, the simplest form of a breathing system may still be one of the most commonly employed, the snorkel. Today’s “standard” snorkel is about 50 cm in length, with an internal diameter of 2 cm, resulting in a capacity, or dead space, of about 150 mL. At a length of 7.5 ft and an internal diameter of 1 cm, Tarzan’s reed would have contained the same volume. He could have easily disappeared from view in a murky pond while submerged at over 7 ft. Although it helped Tarzan hide, snorkel-type breathing tubes suffer from two limitations: (1) as you further decrease the diameter of the breathing tube, there will be
significantly increased resistance to breathing (try breathing through a standard soda straw for any length of time) and (2) as you increase the volume of the breathing tube by increasing either the internal diameter or the length of the breathing tube, it increases the dead space in the breathing system. Most of us intuitively understand the concept of dead space. Imagine trying to breathe through a very long garden hose. How long would you be able to survive? Dead space in a breathing circuit is defined as the volume from the patient end to the point at which exhaled gas can be flushed out of the system and exchanged for fresh gas. Imagine that Tarzan is breathing with a tidal volume of 500 mL (volume of each breath). As Tarzan exhales through his 150-mL reed, it fills with his exhaled breath until it is flushed out at the end. Just before Tarzan inhales his next breath, the 150 mL volume of the reed (dead space) is filled with his last exhaled breath. When he begins to inhale, the first 150 mL he breathes in will be his previously exhaled breath, depleted of oxygen and containing carbon dioxide (CO2). The next 350 mL of his inhalation will come from the fresh jungle air. This 350 mL is plenty of air for Tarzan. Now imagine that Tarzan is hiding on the bottom of a lake and is using a reed that is 30 ft long and 1 cm in diameter. The dead space volume of the reed is now 600 mL. If Tarzan were to exhale a 500-mL tidal breath, it would fill the reed. When Tarzan inhaled, he would breathe back in his exhaled breath from the dead space in the reed and never get any fresh air! A large dead space would have prevented Tarzan from breathing fresh air. The exhaled gas in the dead space contains residual oxygen and large amounts of CO2. Rebreathing this gas would rapidly prevent Tarzan from eliminating CO2 from his lungs. For a short period of time he could utilize the residual oxygen that he 255
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exhales and reinhales. Therefore, if Tarzan were breathing through a system with a large dead space, he would rapidly become hypercarbic and soon become hypoxic. Fortunately, Tarzan learned that he could breathe quite comfortably through a reed that was very long, and thus contained a tremendous dead space, by inhaling though his mouth and then exhaling through his nose. In this way, the reed always contained fresh air. As illustrated in our Tarzan example, rebreathing of exhaled gases can be prevented by inhaling through the mouth and exhaling through the nose. The same thing can be accomplished mechanically, by adding a one-way valve to a snorkel that converts an open breathing system to a semiclosed system. This is also what is done when you change from breathing air from the atmosphere through a snorkel to breathing air from a tank, using a self-contained underwater breathing apparatus (SCUBA). The valve allows inspired air to flow into the lungs, and then diverts exhaled air into the water. These examples allow us to understand the critical elements of an effective anesthesia breathing system. The device must have the following: 1.
2.
3.
A reservoir: A sufficiently large reservoir of inhaled gas (air, when snorkeling) is needed to expand the lungs with minimum effort. This means that the reservoir of gas or air must be within a very compliant system, allowing it to be easily drawn into the lungs. When using a snorkel, there is a virtually unlimited supply of air above the water. The atmosphere serves as an extremely compliant reservoir of air, which is pulled directly into the breathing tube. Low resistance to breathing: A conduit of sufficient diameter to conduct the gas being breathed, without creating significant resistance. In Tarzan’s example, the reed diameter was a major determinant of resistance in the system. Low dead space or a mechanism to effectively prevent rebreathing of exhaled gases: This prevents rebreathing any unwanted exhaled gases (CO2 or possibly anesthetic agents) and provides fresh gas replenished with oxygen. A snorkel contains a dead space < 150 mL (much less than a normal adult tidal volume). Alternatively, adding a one-way valve will prevent rebreathing of CO2 by diverting
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the exhaled gas from reentering the breathing tube. This modification converts an open breathing system into a semiclosed breathing system. The advantage is that it virtually eliminates dead space in the breathing system. The only disadvantage of a one-way valve is that the valve will add some resistance to breathing, and being an active mechanical modification, it may malfunction; that is, it could stick open or stick closed.
■ BREATHING CIRCUITS To design an effective anesthesia breathing system, one must identify the ideal goals, evaluate the theoretical limitations of the device or modifications being proposed, and make appropriate accommodations to meet the need. This is indeed what occurred historically in the development of breathing devices used in anesthesia. So, why in reality were these devices not originally based on the simple breathing tube described above? As stated previously, specific breathing devices were designed to meet specific needs. In Tarzan’s case, the need was to use the breathing system to breathe air from the atmosphere while submerged in a shallow pond. For the purpose of delivering anesthetic agents, the goal is to deliver known mixtures of gases and vapors (e.g., oxygen and anesthetic agents), delivered not from the atmosphere, but usually from a pressurized source of gas and an anesthesia machine. Now let’s design a breathing system to anesthetize Tarzan rather than enable him to breathe underwater, by modifying a simple snorkel. Rather than inserting the tube into his mouth, we will place the breathing apparatus over his mouth and nose using a mask. We can now examine the most effective way to connect this simple breathing apparatus to the gas source. The simplest way to connect the gas source to the breathing tube is to run the gas outlet hose from the gas source (from the anesthesia machine) and connect it to the breathing tube (Fig. 29.1). This type of breathing system would be classified as a Mapleson E system. This system can be extremely effective depending on how close to the mask the fresh gas source is connected. If the fresh gas is connected to the breathing tube far away from the mask, the patient will breathe in exhaled air mixed with room air and very little fresh gas from the gas source hose. If the fresh gas is connected
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Chapter 29 • Anesthesia Breathing Systems
■ FIGURE 29.1 Mapleson classification of breathing systems. FG represents the fresh gas flow. P represents the patient and mask. The round ball represents a squeezable “bag.”
to the breathing tube close to the mask, the fresh gas will flush the exhaled gas out of the end of the breathing tube. The patient will then inhale mostly fresh gas. This design improves the delivery of fresh gas, and if the flow is sufficient, helps remove exhaled CO2 by blowing it out of the breathing tube. The dead space in the system, where rebreathing occurs, is the volume distal to the end of the gas source hose (includes the mask). When the flow of fresh gas is at least 1.5–2 times the minute ventilation, exhaled CO2 is effectively washed out of the breathing tube, preventing rebreathing. In a slight modification of this system, the fresh gas hose is directed through the breathing tube before it connects close to the mask. This system is referred to as a Bain circuit. The Bain circuit is one of the simplest and most effective “open circuit” breathing systems still used in anesthesiology. In the Mapleson E circuit described above, the patient breathes spontaneously through the corrugated breathing tube. Positive pressure ventilation cannot be provided. Consequently, the system can be again modified, by adding a breathing reservoir bag on the end of the breathing tube with a pop-off valve on the base of the bag (see Fig. 29.1—Mapleson F). This system is classified as a Mapleson F or the Jackson-Rees circuit. By partially closing the valve on the end of the bag, ventilation can be assisted. Other modifications have been made to the circuit with changes in the length to the exhalation tubing or the addition of a “pop-off” pressure relief valve at various
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positions (see Fig. 29.1—Mapleson D circuit). In one modification, the exhalation tube is very short and a pressure relief valve was added near the face mask (see Fig. 29.1—Mapleson C). This is the design of the popular Ambu bag-valvemask system. While these above circuits are effective and efficient, a high gas flow (1.5–2 times the minute ventilation) is necessary to prevent hypercarbia. Although high gas flows are not impractical in small children, fresh gas flows of 10–20 L/min would be required in adults. To maintain such high flows is expensive and inefficient and produces large amounts of waste gases to be scavenged. One way to reduce both rebreathing and gas flow is to add a reservoir bag to the end of the tube. Although this is helpful, it is only moderately effective. Other simple solutions to reduce gas flows and prevent CO2 buildup are to add a CO2 absorber, and/or one-way valves, to any of the aforementioned open circuit systems.
■ CO2 ABSORBERS
Adding a CO2 absorber results in what is called a “to-fro” system. The first to-fro canister was developed by Waters to deliver cyclopropane. The system is quite effective but results in less than optimal mixing of fresh and expired gases when low flows are used. In to-fro systems, the fresh gas inlet may be connected either proximal or distal to the CO2 absorber. An effective way to reduce the dead space in this system is to direct the expiratory gases back to the inspiratory limb of the system, after being channeled through the CO2 absorber by means of the one-way valves. These changes effectively create what is referred to as a “circle system,” which is described in the following section.
■ CIRCLE SYSTEM In 1926, Brian Sword developed a unidirectional rebreathing system referred to as a circle system (Fig. 29.2). The circle system consists of a fresh gas inflow directed to an inspiratory limb and unidirectional valve, an expiratory limb and unidirectional valve, a CO2 absorber, an expiratory pop-off valve, and a reservoir bag. Circle systems may be classified as semiopen, semiclosed, or closed, depending on the amount of fresh gas inflow. During inspiration, the fresh gas, along with the gas in the reservoir bag, flows through the
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■ FIGURE 29.2 Circle system. “V” represents the ventilator. “B” represents the reservoir bag.
inspiratory limb and its associated unidirectional valve to the patient. During expiration, the inspiratory unidirectional valve closes and the expired gas flows through the expiratory limb and through a unidirectional valve to the CO2 absorber and to the reservoir bag. The CO2 is absorbed in the canister. The fresh gas flow from the machine continues to fill the reservoir bag. When the reservoir is full, a relief valve opens and the excess gas is vented into the atmosphere or a scavenging system. This system has the advantages of requiring only very low fresh gas flows (as low as 250–500 mL of oxygen), less consumption of anesthetic agents, reduction in atmospheric pollution, and conservation of heat and humidity. Disadvantages of circle systems include a complex design with increased opportunity for malfunction, incorrect arrangement, slow changes in the inspired anesthetic concentration with low flows, and increased resistance to breathing due to the CO2 canister and valves in the system.
■ CO2 ABSORBERS
The CO2 absorber itself introduces potential problems including inhalation of soda lime dust and potential generation of other toxic compounds from interaction with anesthetic agents. Circle absorber systems have been used extensively in North America for more than 30 years. They were developed to reduce rebreathing of CO2, reduce the cost and use of expensive gases and inhalational anesthetic agents as well as reduce the amount of gas required to be
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scavenged, and ultimately reduce the extent of environmental pollution. Two types of absorbers are widely used: soda lime and baralyme. Both react with CO2 and contain 80% calcium hydroxide and some potassium hydroxide. Baralyme is more commonly used in the United States. In addition to 80% calcium hydroxide, soda lime contains water and sodium hydroxide (15% water, 4% sodium hydroxide, and 1% potassium hydroxide). Small amounts of silicate are also added to provide strength and prevent powdering as soda lime pellets are fragile. Conversely, in addition to the 80% calcium hydroxide, Baralyme contains 20% barium hydroxide and may contain some potassium hydroxide. The addition of silica to Baralyme granules is not necessary to ensure integrity of the granules. It is also not necessary to add water to Baralyme because it is liberated by a direct reaction of barium hydroxide and CO2. The reaction of CO2 with absorbers at first seems to be complex, but the basic reactions are actually straightforward and quite similar in the two systems. Both involve reactions of CO2 and water to form carbonic acid (CO2 + H2O− > H2CO3). In each system, carbonic acid in the granules reacts with both calcium hydroxide and potassium hydroxide (present in each mixture) to form calcium carbonate, potassium carbonate, water, and heat. In addition, the carbonic acid also reacts very quickly with either the sodium hydroxide of soda lime or the barium hydroxide of Baralyme to form the carbonate salt, that is, sodium carbonate or barium carbonate. In the case of Baralyme, this concludes the reaction. For soda lime, the sodium carbonate then reacts with a calcium hydroxide mixture (as does the potassium bicarbonate) to form calcium carbonate as well as to re-form the sodium hydroxide and potassium hydroxide found in the original mixture. To be effective, the granules in the absorbing canisters must be properly configured to minimize resistance to airflow and to maximize the mixing of gases with the absorbent. A larger cross-sectional diameter allows less turbulence, with reduced resistance and less dust. Baffles in the canisters reduce gas tracking down the walls and passing through the canister without encountering the absorbent. To prevent rebreathing, the intergranular space should be greater than the patient’s tidal volume.
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■ INDICATION OF ABSORBENT EXHAUSTION Soda lime absorbs up to 26 L of CO2 per 100 g; however, both absorbents become exhausted when sufficient CO2 has reacted with the original chemicals. If CO2 continued to pass through the absorbent canister, it would pass through unchanged. How does the anesthesia provider know that the absorbent is exhausted? When the canister can no longer absorb any more CO2, the CO2 will build up in the circle system and the patient will inspire it. This can be detected with a CO2 agent monitor in the circle system that graphs both inspired and expired CO2 (capnography—see Chapter 32). The majority of gas analyzer’s alarms will alert you to indicate the presence of inspired CO2. High fresh gas flows in the circle system will help flush the CO2 into the scavenging system; however, most anesthesia providers are using low flows. With low flows, the patient can inspire CO2 and eventually the expired CO2 levels will rise significantly as well due to the accumulation of CO2 in the patient. Clinical signs of hypercapnia, such as tachycardia, hypertension, cardiac arrhythmias, and sweating, appear after substantial rises in body CO2. Another method of detecting that the absorbent is exhausted is the condition of the absorbent granules. Soft and crushable granules are converted to hard ones (calcium hydroxide changes to calcium carbonate—limestone), indicating exhausted soda lime. This would be difficult to discern with visual inspection alone. To solve this problem, different manufacturers add different indicator dyes to the absorber. Some change from pink when fresh to white when exhausted. Others changed from white when fresh to purple when exhausted. The indicators are an acid or base whose color depends on pH. Interaction of CO2 with the absorbent changes the pH of the water in the canister. Color change may be misleading in certain circumstances. As indicated above, multiple chemical reactions are taking place in the canister. Many of these affect the pH. It is not uncommon for the absorbent to turn color, indicating exhaustion, only to turn back to the “fresh” color after a rest period. Additional chemical reactions have taken place to further change the pH. When the absorbent is truly exhausted, the color change will be sustained.
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Another method of detection of exhausted absorbent is a temperature rise in the canister. Because CO2 neutralization is an exothermic reaction (heat producing), changes in the absorbent temperature occur earlier than color changes. Studies have suggested that when the temperature of the downstream canister is higher than that of the upstream one, the absorbent should be changed in both canisters.
■ ABSORBENT REACTION WITH ANESTHETIC AGENTS It is important to reiterate that the absorbents will interact with inhaled anesthetics to some extent. In some circumstances, interaction of sevoflurane with the strong bases present in soda lime or Baralyme results in the formation of a chemical called “Compound A,” which has been shown to cause nephrotoxicity in animals. The circumstances where this occurs include (1) low total gas flow rate (below 1 L/min), (2) higher concentration of sevoflurane, (3) the use of Baralyme rather than soda lime, (4) higher absorbent temperatures, and (5) desiccated CO2 absorbent. Exposure of desflurane and isoflurane to soda lime and Baralyme results in formation of carbon monoxide. The factors predisposing to carbon monoxide production include (1) higher anesthetic concentration, (2) higher temperature, (3) dry absorbent, (4) the use of Baralyme rather than soda lime, and (5) the specific anesthetic agent. The magnitude of carbon monoxide production from greatest to least is as follows: desflurane > enflurane > isoflurane > halothane = sevoflurane. Other CO2 absorbers (e.g., Amsorb; Armstrong Medical, Londonderry, Northern Ireland) have come on the market during the past several years. They consist of calcium hydroxide with a compatible humectant (a hygroscopic substance with the affinity to form hydrogen bonds with molecules of water), namely calcium chloride. The absorbent mixture does not contain strong bases such as sodium and potassium hydroxide. They were designed to be effective CO2 absorbents while being chemically nonreactive with anesthetic gases.
■ SUMMARY In conclusion, by understanding a few relatively simple principles, one should be able to
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understand and quickly become proficient with breathing systems that he or she encounters. With such an understanding, you should be able to evaluate the advantages and disadvantages of any breathing system, and to effectively troubleshoot problems. I strongly recommend that those interested in pursuing the principles of breathing systems in more depth refer to http://www. capnography.com/. Despite the Web address that might lead you to think that this Web site is focused on capnography, the overall focus of the site is on anesthesia breathing systems.
REVIEW QUESTIONS 1. To be an effective anesthesia breathing system, a device must have A) A large reservoir B) Low resistance C) Low dead space D) All of the above E) None of the above Answer: D. A large reservoir, low resistance to airflow, and low dead space are all key design features of an effective anesthesia circuit.
2. Which of the following are FALSE regarding dead space in a circuit? A) A large amount of dead space contributes to rebreathing. B) The location of unidirectional flow valves does not affect dead space. C) The location of the fresh gas flow can affect dead space. D) High fresh gas flow rates can minimize rebreathing. E) All of the above are true.
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Answer: B. Unidirectional valves, as in a circle system, can direct exhaled gases in one direction and minimize rebreathing (reduces dead space). Locating the fresh gas flow near the breathing tube helps flush fresh gas near the breathing tube and minimize rebreathing as does high fresh gas flow rates.
3. Which item is NOT an indication of exhausted CO2 absorbent? A) Change in color of granules B) Increase in temperature of absorber C) Moisture in the circuit D) Increased inspired CO2 E) None of the above Answer: C. Moisture is not an indication of exhausted absorbent and is a natural byproduct of the chemical reactions of most absorbents. All other indicators are regularly used to judge exhaustion.
4. CO2 absorbent does not react with anesthetic agents. A) True B) False Answer: B. The most common reaction of anesthetic gases with CO2 absorbent is the production of carbon monoxide. All anesthetic gases currently on the market have some carbon monoxide production when CO2 absorbent is used.
SUGGESTED READING Shankar R, Kodali B. Anesthesia breathing system. Available at: h t t p : / / w w w. c a p n o g r a p h y. c o m / n e w / i n d e x . p h p ? option=com_content&view=article&id=288:maplesona-system&catid=79:-anesthesia-breathing-systems. Accessed on November 3, 2008.
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CHAPTER
30
Anesthesia Machine Ventilators Eric Schnell and Valdez Bravo ■ INTRODUCTION A mechanical ventilator is a fundamental component of modern anesthetic practice. The ventilator performs two critical functions for an anesthetized patient: oxygenation and ventilation. Oxygenation supplies the lungs (and hence, the rest of the body) with oxygen. Ventilation delivers oxygen to the lungs and removes waste gases such as carbon dioxide from the lungs, allowing the body to maintain a physiologic acidbase balance. Additionally, ventilation can be used to administer and remove inhaled anesthetics. While awake, patients maintain spontaneous ventilation (breathing) by generating negative intrathoracic pressures with contractions of the diaphragm, causing air to flow into the lungs (see Chapter 16). After induction of general anesthesia, respirations are often depressed or absent, depending on the choice of anesthetics and muscle relaxants (i.e., neuromuscular junction–blocking agents). At this point, the airway is usually secured with an endotracheal tube (see Chapter 18). Ventilation and oxygenation are then accomplished by administering positive pressure to the patient’s airway, leading to the flow of oxygen and anesthetic gases into and out of the lungs. When the mechanical ventilator is not engaged, positive pressure can be manually delivered to the breathing circuit by squeezing the breathing reservoir bag with the adjustable pressure-limiting (APL or “pop-off”) valve partially closed (see Chapter 29). Alternatively, the breathing circuit can be placed in continuity with the ventilator, which delivers positive pressure breaths with a desired waveform and frequency. When the positive pressure is released, the patient passively exhales gases, including waste carbon dioxide, back into the breathing circuit.
Although both manual and mechanical ventilation are capable of providing oxygen, delivering anesthetic gases, and removing carbon dioxide, mechanical ventilation has several distinct advantages. First, it frees the anesthesia provider from having to perform continuous manual ventilation throughout the case. Second, it allows the anesthesia provider to set specific pressures and/or volumes for each breath, allowing for more precise control of ventilation than is possible manually. This fine control is critical when small changes in ventilatory parameters are required to optimize a complex patient’s respiratory function. Third, modern ventilators can deliver positive pressure waveforms that are difficult to achieve with manual ventilation, such as pressure control ventilation or end-inspiratory pauses (“holds”). Fourth, modern ventilators are linked to pressure monitoring systems that give important information about lung compliance. Thus, they are able to instantly release positive pressure if a threshold (maximum) pressure is reached, providing an additional measure of safety (for instance, when a patient coughs or strains against the ventilator). Finally, in certain modes, mechanical ventilators can even assist a patient’s spontaneous breathing by detecting a patient’s respiratory efforts and synchronously delivering positive pressure at the appropriate times.
■ VENTILATOR MODES Modern ventilators operate in specific modes that define the overall pattern of positive pressure delivery. The anesthesia provider independently programs parameters specific to each patient/procedure. Basic ventilator modes are distinguished based on two important characteristics: whether the ventilator delivers a fixed tidal 261
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volume or a specific inspiratory pressure and whether the ventilator is triggered by an internal timer or by the patient’s own respiratory efforts. Volume control ventilation delivers a set volume (also referred to as the tidal volume) with each positive pressure breath. These breaths are delivered at a provider-determined frequency, and thus provide a predictable minute ventilation (Minute Ventilation = Ventilator Rate × Tidal Volume). One major advantage of the volume control mode is the consistency of minute ventilation over prolonged periods of time, even during changes in lung expandability (known as lung compliance—see Chapter 11). For example, if a patient suddenly bears down and stiffens the chest muscles (making the lungs less compliant), the ventilator needs more pressure to expand the lungs than when the patient was completely relaxed. The ventilator will increase the pressure accordingly, and still deliver the same tidal volume as long as the inspiratory pressure limit
(Pmax, often set to 40 cm H2O in adults) is not reached. However, once the pressure limit is reached, the ventilator will stop delivering positive pressure and an alarm will sound, warning the anesthesia provider of the high airway pressure. One disadvantage of this mode is that it often requires slightly higher absolute peak pressures than other modes to achieve the same minute ventilation (Fig. 30.1A). Also, the lungs spend less time at larger lung volumes compared to pressure control ventilation, which may decrease the time available for gas exchange in some portions of the lung. Pressure control ventilation delivers a set plateau level of positive pressure with each inspiration (Fig. 30.1B). The actual tidal volume delivered depends on the patient’s lung compliance: A more compliant set of lungs will expand more easily and thus receive a higher tidal volume at the same pressure control settings than a less compliant (stiffer) set of lungs. One advantage
A Volume Control
B Pressure
Pressure Control
C Pressure Support
D SIMV
Time ■ FIGURE 30.1 Pressure-time waveforms of different ventilation modes. A: In volume control ventilation, pressure steadily increases during inspiration, as gas (typically at a constant flow rate) fills the lungs. During expiration, pressure drops quickly as the chest and diaphragm passively recoil. Breaths are delivered at regular time intervals. B: In pressure control ventilation, the ventilator quickly reaches the plateau (control) pressure and maintains this throughout the breath. This requires an increased respiratory flow at the outset of the breath and a small delay for the ventilator to reach the target pressure. Expiratory flows are passive and follow the same waveform as in volume control. C: In pressure support ventilation, the patient initiates each pressure-controlled breath by generating negative pressure (note the downward deflections prior to the pressure support), and thus inspiratory timing is dependent on patient effort. D: In SIMV, a volume-controlled breath is delivered with each inspiratory effort. If the patient fails to initiate a breath after a set interval, the ventilator will deliver a volume-controlled breath regardless.
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Chapter 30 • Anesthesia Machine Ventilators
of this mode is that for any given peak pressure, the patient will spend a larger amount of time at larger lung volumes, and have a larger tidal volume, than that reached during volume control ventilation. It may be particularly useful in patients with very stiff lungs, or those in whom it is otherwise difficult to sustain adequate ventilation without resorting to very high inspiratory pressures. A disadvantage of this ventilator mode is that minute ventilation can change substantially if the patient’s pulmonary compliance changes. However, this can be easily countered by programming the alarms on the ventilator to notify the provider when tidal volumes or minute ventilation fall outside of a predetermined range. Both of the aforementioned ventilator modes are designed to deliver a set number of breaths per minute (the respiratory rate) on a regularly timed basis. This is absolutely necessary when an anesthetized patient is paralyzed and unable to breathe spontaneously. However, many anesthetics do not require complete muscle paralysis, and these patients may continue to make respiratory efforts while fully anesthetized. Modern ventilators are able to assist these efforts by synchronizing positive pressure delivery with a patient’s own respiratory rate. This assistance helps to counter the respiratory depressant effects of many anesthetics and the increased work of breathing through the resistance of an endotracheal tube. In pressure support ventilation (sometimes referred to as PSV-Pro ventilation), the ventilator senses a patient’s inspiratory effort as a drop in breathing circuit pressure and delivers a set level of positive pressure to augment the patient’s tidal volume (see Fig. 30.1C). In this mode, the patient is less likely to breathe in opposition to the ventilator, and thus less likely to cough or strain. As this mode depends on the patient’s effort to initiate an inspiratory cycle, if the patient stops making ventilatory efforts (or these efforts are too weak to trigger the ventilator), he or she receives no ventilation. For this reason, pressure support modes often have a backup mode that automatically begins timed positive pressure ventilation after a specified interval if no breaths are detected (often 30 seconds). One last commonly employed ventilator mode, synchronized intermittent mandatory ventilation (SIMV), delivers a specified volume synchronously with a patient’s respiratory efforts (Fig. 30.1D). However, it is also programmed to
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deliver the same volume after a specified time even if the patient has not made any inspiratory breaths during this interval. More advanced modern ventilators function using combinations of several of the above characteristics. Additionally, more detailed settings such as the ratio of time the ventilator spends in inspiration versus expiration during each respiratory cycle (the I:E ratio) can be changed, which may be useful in managing clinical situations such as bronchospasm. One commonly used, and clinically important, ventilator function is the ability to maintain positive pressure between breaths, called positive end expiratory pressure (PEEP). Without PEEP, the patient exhales gas back into the circuit until the airway pressure reaches atmospheric pressure. With PEEP engaged, expiratory flow is mechanically stopped when the desired expiratory pressure is reached, and thus positive pressure is maintained until the next inspiratory cycle. PEEP prevents lung alveoli from collapsing between breaths and can be of extreme utility in patients with pulmonary edema or obesity. In addition, it is critical in the management of ventilation during many thoracic surgery procedures. However, if the respiratory rate is set so high that the patient does not have time to exhale completely between breaths, the pressure may never fall back to the PEEP or atmospheric pressure, causing a phenomenon known as breath stacking and a gradual increase in pressures throughout the respiratory cycle.
■ VENTILATOR OPERATION Most mechanical ventilators used in operating room (OR) environments today can be categorized by the reservoir compressing the gas for each breath: bellows or piston. In each of these designs, the gas reservoir is in continuity with the breathing circuit and delivers whatever gas mix is in the circuit to the patient. During inspiration, external force compresses the reservoir, pushing the gas into the patient. At the beginning of expiration, the force is released, depressurizing the circuit. As the circuit pressure falls, gas moves out of the patient, driven by the patient’s elastic chest recoil. The ventilator’s gas reservoir refills with a combination of fresh gas from the anesthesia machine and expired gas returning from the patient (after having passed through the carbon dioxide absorption canister). Depending
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on the mode of ventilation, an inspiratory cycle may be based upon achieving a certain desired pressure or delivering a particular volume over a specified amount of time. Each ventilator model employs different designs to accomplish similar goals. However, all modern anesthesia machine ventilators share certain characteristics:
pressure measurement as well. A flow sensor is incorporated into the expiratory limb of the circuit and can be used by the anesthesia machine to calculate tidal volumes. • Pressure alarms and release valves to alert the provider of changes in lung compliance and to prevent pressure-related lung damage (barotrauma).
• A manual/mechanical control switch, which converts between manual and mechanical ventilation. This can be either a manual toggle or a digitally controlled servo. Thus, either the ventilator or the reservoir bag is able to ventilate the patient, but not both simultaneously. When the mechanical ventilator is engaged, the APL valve is bypassed, and compression of the bag does not cause gas to flow into the patient. • Check valves integrated into the inspiratory and expiratory limbs of the patient breathing circuit (see Chapter 29) to ensure unidirectional gas flow in all spontaneous, manual, and mechanical ventilatory modes. Although not part of the mechanical ventilator per se, properly functioning valves are critical to the function of anesthesia ventilators. • Excess gas scavenging. Fresh gas from the anesthesia machine is often supplied in excess of what is required for ventilation, so ventilators must have a mechanism to shunt excess gas (particularly at high gas flows) from the ventilatory circuit into the scavenging system (see Chapter 26). Additionally, ventilators must contain a valve that isolates the positive ventilator pressures from the scavenging system during inspiration, in order to allow the ventilator to deliver the positive pressure to the patient. • A PEEP valve, which is either a manual (rotary) valve or a digitally controlled expiratory valve that is able to stop gas return from the patient when a particular circuit pressure has been reached. In some older machines, PEEP is accomplished by attaching a mechanical ball valve to the expiratory limb of the circuit. • Flow and pressure sensors that measure circuit pressure and expiratory flow. At the very least, circuit pressure can be measured by the analog pressure gauge in line with the circuit, but newer machines often display a digital
A bellows-type ventilator uses pressurized gas to compress the bellows and thus deliver anesthetic gases to the patient. As mentioned above, bellows are simply a collapsible reservoir in which to store the mixed anesthesia gas. Older bellows ventilators do not require electricity but use manual controls to regulate the flow of pressurized gas into a sealed chamber surrounding the bellows. As the pressure in this chamber increases, the bellows are compressed and anesthetic gas inside the bellows flows into the breathing circuit. At the end of the inspiratory cycle, the pressure in the chamber is released, allowing the bellows to refill with gases from the patient and from the anesthesia machine. This functional bellows design has been in practice for many decades as a mechanical/pneumatic system and has since been enhanced through the addition of electromagnetic valves, which increase precision in gas flow delivery and pressure control. A diagram of a bellows-type ventilator is presented in Figure 30.2. Note that bellows-type ventilators necessitate an exhaust valve to separate the breathing circuit from the scavenging/ overflow system during inspiration. A typical bellows ventilator uses the increased drive gas pressure in the bellows chamber to close the exhaust valve, thus directly uncoupling the ventilator from the scavenging system during inspiration. In the event of a power failure, they do not require power to generate ventilator pressure. However, because they require pressurized oxygen, they will fail in the absence of pressurized gas and cause a backup tank to run out more quickly in the event of wall oxygen supply failure. Newer bellows ventilators are computer controlled, and thus require electrical power in addition to pressurized gas for operation (from wall outlets or a machine’s internal backup battery system). Piston ventilators use a motorized drive to compress a piston chamber, thus compressing the gas in the circuit. Newer piston-driven
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Chapter 30 • Anesthesia Machine Ventilators 1 4
30 cm H2O
Open Closed
2
3
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Inspiratory Phase 5 3 cm H 2O Closed 3 cm H2O
6
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■ FIGURE 30.2 Bellows ventilator function: Inspiration and expiration. A: 1. During inspiration, bellows ventilators inject pressurized gas into the bellows’ housing chamber. 2. The bellows are compressed, forcing anesthetic gases inside the bellows into the breathing circuit, through the CO2 absorber, and into the patient. 3. Simultaneously, the ventilator drive pressure closes the overflow valve to the scavenging system, preventing gas from leaving the circuit. 4. Thus, during inspiration, all gas, including fresh gas from the machine, enters the patient. B: 5,6. During expiration, ventilator drive pressure is released, allowing gas to return and refill the bellows reservoir. 7. Release of bellows driving pressure also opens the scavenging valve, such that any additional anesthetic gases can exit the system once the ventilator bellows has filled.
ventilators provide more precise volume delivery, as the linear displacement of the piston allows the actual volume delivered to the circuit to be exactly determined. Additionally, piston ventilators are typically able to deliver higher peak pressures than many bellows ventilators, which may be of value in patients with lung disease but which also increase the potential for lung damage from the higher pressures. These ventilators do not need a gas source to power the ventilator but absolutely require electricity to run, from either a wall source or a battery backup. A typical piston ventilator design is detailed in Figure 30.3, which also shows how computer-controlled valves isolate the ventilator from the scavenging circuit as well as maintain PEEP.
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Other ventilator designs, for example, those employing turbines to deliver positive pressure, are not currently integrated into modern anesthesia machines. They are increasingly common in intensive care and transport ventilators, and thus might be used in the OR in rare circumstances, but are not be discussed here. Many modern ventilators have additional features that improve ease of use, safety, and accuracy. Commonly available features include the following: • Digital display/controls: Most modern ventilators incorporate a computerized control interface, which allows digital control of ventilator modes, pressures, volumes, PEEP, and alarm settings (see Fig. 30.4). Despite the fact that the most modern ventilators include digital readouts of tidal volumes and pressures, the bellows and pistons can be seen moving through a clear window, which serves as an important visual cue to confirm ventilator function. • Compliance compensation: Because the disposable breathing circuit tubing expands during inspiration, some of the measured tidal volume stays in the expanded tubing and never reaches the patient. Newer ventilators are able to measure circuit compliance (during machine checkout) and compensate for the volume lost in expanding the circuit by increasing the delivered tidal volume. • Fresh gas decoupling excludes fresh gas from the breathing circuit during inspiration. In older ventilator designs, fresh gas entering the circuit during inspiration was added to gas being delivered from the bellows, significantly (and potentially dangerously) increasing tidal volume when respiratory rates were slow or flow rates were high (Fig. 30.2). • Feedback compensation: Newer ventilators are able to dynamically regulate the delivered tidal volume in order to compensate for leaks in the circuit or the airway. These ventilators compare the tidal volumes returned from the patient with the programmed values and increase the volumes delivered in order to maintain the provider-specified volumes.
■ VENTILATOR MAINTENANCE The maintenance for both types of ventilators is the same: periodic replacement of parts on a maintenance schedule prescribed by the original
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A
1
3
2
B
5
4 6
■ FIGURE 30.3 Piston ventilator circuit example. A: 1. In this example of a piston-driven ventilator (Dräger Fabius GS), piston movement compresses circuit gases during the inspiratory phase of the cycle. 2. A computer-controlled valve (PEEP/PMAX control) closes during this phase, allowing pressure to increase in the circuit and expand the patient’s lungs. 3. A separate one-way (fresh gas decoupling) valve isolates the inspiratory flows to the patient from the fresh gas arriving from the anesthesia machine. B: 4. At the end of inspiration, the PEEP/PMAX valve opens, allowing expiration. 5. Gas returning from the patient passes through the CO2 absorber and returns to the piston reservoir. 6. In this particular model, the breathing bag actually stores anesthetic gases that can be used to refill the piston chamber during expiration, while in bellows design, the breathing bag is entirely removed from the circuit when the mechanical ventilator is engaged. 7. If PEEP is desired, the PEEP/Pmax valve closes when the circuit pressure reaches the desired PEEP pressure, thus maintaining this pressure until the next inspiratory cycle.
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■ FIGURE 30.4 A typical ventilator control screen. This image demonstrates features found on many computer-controlled ventilator interface screens. These include displays of the actual measured tidal volume, respiratory rate, and minute ventilation, and buttons (left to right on bottom) to set the peak inspiratory pressure limit (PMAX), tidal volume, rate, I:E ratio, an inspiratory pause, and PEEP. Also shown is a continuously charted graph of airway pressure versus time, with numerical readouts of the peak, plateau, and PEEP pressures. This ventilator is functioning in a volume control mode. The oxygen concentration measured from the oxygen sensor is displayed in the upper right corner.
equipment manufacturer (OEM). However, this level of maintenance will be performed by inhouse biomedical equipment specialists, support specialists, or vendor field service engineers. Obviously, any ventilator malfunction should be thoroughly diagnosed and repaired prior to administering an anesthetic if at all possible. In the event of an intraoperative ventilator failure, a patient can be manually ventilated with the breathing bag (or a separate Ambu-Bag or Jackson-Rees circuit) while troubleshooting the ventilator and perhaps arranging for an intraoperative machine switch. In the absence of malfunction, ventilators, either piston driven or a regular bellows, should have the rubber components of the gas reservoirs replaced regularly, often every 6 months. There may also be some O-rings/seals that are replaced in conjunction with the bellows. The discs that serve as the inspiratory and expiratory check valves are replaced on a periodic basis, although often less frequently than the bellows.
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Frequent problems with ventilators include holes in the rubber material, collapsed bellows that fail to compress gas, bellows that catch/hang on one side, thus preventing accurate gas delivery, or pistons that lose their calibration. Pistondriven vents typically have an electronic eye that looks for a sensor to be in a certain light path when in the start position. If this finely tuned measurement is compromised, the piston-driven ventilator will not know what location it is in and will display errors on the display screen. If any lubrication of piston rubber O-rings/seals/ hoses is needed, it should be done by trained service professionals. They have special instruments for the job and will use lubricants that are manufacturer approved for the oxygen-rich environment.
■ SUMMARY Mechanical ventilation is an essential component of anesthetic practice. Anesthesia technicians play a key role in assisting patient care by
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understanding the modes in which mechanical ventilation is delivered and how different ventilator designs accomplish this task. Although different ventilator models will vary slightly from the designs shown in this chapter, an understanding of the functional components of a standard ventilator will make it straightforward to contextualize these differences. With any particular model, a review of technical and functional specifications particular to that ventilator (provided by the manufacturer) will allow you to inspect, maintain, and ensure the safe and proper functioning of each machine.
REVIEW QUESTIONS 1. Which of the following ventilator modes requires patients to initiate a respiratory cycle? A) Volume control B) Pressure support C) Pressure control D) PEEP mode E) None of the above Answer: B. With pressure support ventilation, the ventilator senses a drop in circuit pressure initiated by a patient’s breath and then delivers the set pressure to augment the patient’s breath. This mode is often used to synchronize the ventilator with the patient’s respiratory efforts. Volume control delivers a fixed volume breath at a given rate regardless of patient effort. Pressure control delivers a fixed pressure breath at a given rate regardless of patient effort. PEEP is not really a ventilator “mode” but rather a setting for the ventilator to deliver a small amount of fixed pressure during expiration.
2. Which of the following is TRUE regarding pistondriven ventilators? A) Pressurized gas drives movement of the piston. B) They are unable to work in pressure-support mode. C) They require wall outlet electricity to be functional at all times. D) They require a servo-controlled valve that prevents the circuit pressure from exiting to the scavenging system during inspiration. E) None of the above. Answer: D. Piston control ventilators use a motorized drive to move the piston and deliver the breath. Bellows control ventilators, not piston control, use pressurized gas to collapse the bellows and deliver a breath. Piston control ventilators require electricity to drive the piston and will not work if there is a power failure. All anesthesia machine ventilators must have a mechanism to prevent a breath from escaping into the
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scavenging system instead of being delivered to the patient. Piston control ventilators have a servo-controlled valve that is triggered at the same time the piston is triggered. The valve shuts off flow to the scavenging system.
3. Why is fresh gas decoupling important? A) It prevents wall oxygen from mixing with the anesthesia gases. B) It allows patients to breathe spontaneously while the ventilator is active. C) It allows delivered tidal volumes to be independent of gas flow rate through the machine. D) It allows fresh volatile anesthetics to be separated from those exhaled from the patient. E) It allows ventilators to deliver positive pressure during both expiration and inspiration. Answer: C. In many older ventilators, the fresh gas flow continues to flow into the circuit while the ventilator is delivering a breath. This means that the fresh gas flow during inspiration will be added to the breath. At high fresh gas flows, this can significantly increase a delivered tidal volume if the ventilator is set to volume control. Fresh gas decoupling excludes fresh gas from flowing into the circuit during an inspiration from the ventilator.
4. What is the function of PEEP? A) It can improve patient oxygenation by preventing alveolar collapse. B) It prevents backward flow of ventilator gases through the vaporizer. C) It pushes breathing circuit gases through the CO2 absorber. D) High PEEP allows more comfortable breathing for lightly anesthetized patients. E) It accelerates the flow of gases at the beginning of the next inspiratory cycle. Answer: A. With PEEP, the breathing circuit is pressurized with a small amount of positive pressure (5–10 cm H2O controlled by the PEEP setting). When a patient exhales, the lungs deflate. Maintaining a small amount of pressure during exhalation prevents the lungs and alveoli from completely deflating. This can improve oxygenation in some patients.
5. Which of the following is NOT an advantage of mechanical ventilation? A) It allows precise control of tidal volumes. B) It allows precise control of minute ventilation. C) It allows the anesthesia provider to perform other tasks without manually ventilating. D) It prevents patients from trying to initiate spontaneous breathing. E) It allows fine adjustment of inspiratory and expiratory pressures. Answer: D.
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Chapter 30 • Anesthesia Machine Ventilators Mechanical ventilation can allow the anesthesia provider to control tidal volumes, respiratory rate, minute ventilation (rate × tidal volume), inspiratory pressure, and expiratory pressure. It also does not require the anesthesia provider to squeeze the bag and can free him or her up to perform other tasks. However, just because a patient is on a mechanical ventilator does not mean that the patient cannot attempt to breathe on his or her own. Patients can “fight” or “overbreathe” the ventilator as they attempt to take breaths. The clinician may need to paralyze the patient, or alter the ventilator settings or mode to achieve smooth ventilation, for example, changing to pressure support ventilation to augment the patient’s breathing efforts.
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SUGGESTED READINGS Barash PG, Cullen BF, Stoelting RK, et al. The anesthesia workstation and delivery systems. In: Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:Chapter 26. Dorsch JA, Dorsch SE. Anesthesia ventilators. In: Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:Chapter 12. Miller RD, Eriksson LI, Fleisher LA, et al. Respiratory care. In: Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2010:Chapter 93.
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CHAPTER
31
Anesthesia Machine Operation, Maintenance, and Troubleshooting Andrew Oken and Scott Richins ■ INTRODUCTION The anesthesia machine began quite humbly as a basic device to deliver anesthetic gases. It has evolved to a sophisticated integrated computerassisted physiologic monitoring system and anesthesia delivery system. Fundamentally, it continues to serve principally to facilitate gas exchange in the anesthetized patient; however, a number of functions have been integrated to improve the machine’s safety profile. Some of these improvements include agent-specific vaporizers, oxygen proportioning systems, oxygen analyzers, oxygen failure safety valves, breathing circuit pressure monitors, and the pin index safety system. The anesthesia machine consists of various components managing gas delivery and elimination, including a ventilator, gas inflows from a variety of sources, anesthetic vaporizers, scavenging system, breathing circuit, and CO2 absorption system. All these systems have appropriate check mechanisms and associated alarms or notifications to alert the medical providers to potential problems. While there are a number of machines available on the market, they principally share some very similar fundamental components and functionalities. It is therefore critical to have a basic understanding of the principles of the workings of the machine. Such a core base of knowledge is absolutely necessary to safe medical practice and the maintenance and evaluation/troubleshooting of anesthesia machines. Despite the similarities between anesthesia machines, it is important to recognize that machines have distinct differences. Anesthesia technicians should be thoroughly familiar with the unique properties of machines in use at their institutions.
The American Society of Anesthesiologists (ASA) and the Food and Drug Administration (FDA) have collaborated to develop recommendations for checking out an anesthesia machine prior to administering an anesthetic (see Chapter 27). Each manufacturer provides maintenance schedules, troubleshooting instructions, and guidelines for checkout of its specific machines. Internal machine designs vary and hence the need for specific manufacturer recommendations. In addition to testing machine components, the checkout will test associated alerts/ alarms. Anesthesia technicians should have detailed knowledge of the anesthesia machine checkout procedures as this can be the first indication that there is a problem with a machine. Anesthesia technicians will also be asked to troubleshoot machine problems between cases or even during a case. This chapter assists the anesthesia technician with the operation, maintenance, and troubleshooting of anesthesia machines.
■ BRIEF OVERVIEW OF THE ANESTHESIA MACHINE Although anesthesia machines can include several functions, the main function will always be to provide a controlled supply of oxygen and other anesthetic gases to the patient during surgery. The details of gas supply to the machine have been discussed previously; however, a short review is presented here to facilitate a troubleshooting discussion (see Fig. 31.1). The machine circuit can be broken down into high- and low-pressure circuits. The highpressure circuit starts where the gas enters the machine and ends at the flow control valves.
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N2O Cylinder Supply Check Valve
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Check Valve (or Internal to Vaporizer)
O2 Second Stage O2 Pressure Regulator
O2
Oxygen Flush Valve
O2 Cylinder Supply O2 Pipeline Supply
Machine Outlet (Common Gas Outlet)
■ FIGURE 31.1 Diagram of a generic gas anesthesia machine. (With permission from Barash P G, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.)
Gas enters the machine at a pressure near 50 psi from the pipeline. Gas can also be supplied from E cylinders, which supply a pressure of 2,200 psi for oxygen and 745 psi for nitrous oxide when tanks are full. This pressure is then further regulated to 45 psi downstream. Traveling toward the patient the next device is the fail-safe valve, which is downstream from the nitrous oxide source and serves to decrease the supply of nitrous oxide if the oxygen pressure drops. Most Datex-Ohmeda machines also have an oxygen supply alarm that sounds when the pressure drops below a safe level. Both these devices serve to decrease the potential for delivering a hypoxic mixture of gas. Gas then enters the flow control valves. The oxygen and nitrous oxide valves are coupled together to limit the percent of nitrous oxide that can be given as another
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means to reduce the risk of giving the patient a hypoxic mixture of gas. The low-pressure system of the anesthesia machine begins downstream of the flow valves. Gas travels through the flowmeters into a common manifold and then into one of the calibrated vaporizers. Between the vaporizers and the common gas outlet, which connects to the patient circuit, there is a check valve that prevents gas from flowing backward through the vaporizers. Exhaled gas passes through the carbon dioxide (CO2)-absorbing canister and rejoins the fresh gas here as well. The combined gas fills the ventilator or the bag depending on which manual ventilation or the ventilator is selected. If excess gas is present at this juncture, it overflows to the scavenging system past the adjustable popoff lever (APL), or through the ventilator relief
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⫹30 cm H2O Open Closed Closed
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B
Expiratory Phase Late
■ Figure 31.2 Picture of circle system with ventilator. (From Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.)
valve. Gas then flows out through the inspiratory flow device past the oxygen analyzer to the patient through the inspiratory limb of the circuit. Expired gas is recycled as it flows back though the expiratory limb of the circuit, through the flow sensor, and then through the CO2-absorbing canister to ultimately rejoin the fresh gas from the common gas outlet prior to entering the ventilator or bag (see Fig. 31.2).
■ GENERAL AND DAILY MAINTENANCE Regular service should be performed by a machine representative according to the manufacturer’s recommendations. Daily maintenance
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by an anesthesia technician is crucial for proper function. Previous chapters have described sterilization techniques and daily machine checkout. These will not be covered in this chapter, but we will refer to the checkout process frequently because many of the problems that require troubleshooting can be prevented or later identified by the simple tests performed in a daily machine checkout. At the end of the day, further routine maintenance should be done. This includes removing the flow transducer to dry unwanted moisture, exchanging the CO2 absorber if it is exhausted, ensuring the gas flowmeters are off, and powering down the machine.
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■ TROUBLESHOOTING COMMON PROBLEMS Low Pressure If low pressure in the anesthesia machine is detected, the following items should be examined: • Check for low pressure leak. • Check for a circuit disconnect starting with the patient and working back to the machine. • Inspect bellows. • Inspect CO2 canister. • Check lids/coupling of vaporizers. • Inspect the flow sensor. • Check oxygen pressure from pipeline/cylinder. • Check for incompetent ventilator relief valve. The most common cause for a low-pressure alarm is a leak in the low-pressure circuit, and the most common cause of a leak is a disconnection or partial disconnection in the patient circuit. This is evaluated quickly starting at the patient and moving back to the machine evaluating the placement of the endotracheal tube (ETT), the ETT cuff pressure, the connection between the ETT and the circuit, the gas sample line port, and the connection of the inspiratory and expiratory tubing distal and proximal to the machine. If the leak is not resolved, continue to move upstream. Ensure the flow sensor is installed properly and tightly engaged. Check that the oxygen sensor is properly installed and all fittings are tight. Another common place for a leak is in the canister holding the CO2 absorber (see Fig. 31.3). Check to see that the latch is tight and there are no granules in the way of the seal with the gasket. Also, look and listen for cracks in the canister and ensure the condensation drain is closed. When the ventilator is turned off, if the pressure in the circuit returns to normal with hand ventilation, the leak can be isolated to the ventilator. The housing can be removed to look for cracks. This, along with poor seating of the plastic housing, can result in inappropriately low tidal volumes delivered to the patient because the driving gas is leaking into the room rather than compressing the bellows. Next, inspect the vaporizer lids to ensure they are on tight and inserted into the coupling system correctly. With the use of electronic flowmeters in newer machines there are no fluted tubes that can crack, but this is another place a leak can occur and should be examined when mechanical flowmeters exist.
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■ FIGURE 31.3 Carbon dioxide absorption canister in open/unlocked position (see space between plastic housing and blue plastic gasket); also condensation drain open at bottom.
It is uncommon for a low-pressure alarm to be due to problems in the high-pressure circuit, but they can occur. Pressure can be lost from inadvertent disconnects from the main supply, loss of the main supply pressure, or unrecognized depletion of a cylinder. Other less common causes may include a malfunctioning scavenging system or the vacuum is set too high such that the negative pressure from the scavenging system is able to lower the pressure in the circuit. Occasionally, high negative pressure in the scavenging system can also cause high pressure in the breathing circuit. In some machines, high negative pressure from the scavenging system can close the ventilator relief valve blocking excess gas from exiting the circuit, leading to increased airway pressures. Lastly, an incompetent ventilator relief valve can lead to hypoventilation because gas is delivered to the scavenging system instead of to the patient when the bellows collapse.
Hypoxic Gas Mixture • Turn on 100% oxygen and check for proper reading from the oxygen sensor. • Recalibrate the O2 sensor.
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• Replace O2 electrode if it does not appropriately recalibrate. • Check for main pipeline crossover. A common cause for a hypoxic gas mixture alarm is improper calibration of the oxygen sensor at the time of machine checkout. If the alarm sounds while a patient is connected to the circuit, the patient should be put on 100% oxygen (the patient may need to be ventilated with an alternative oxygen source during troubleshooting, e.g., bag-mask or replacement anesthesia machine). If the sensor does not read 100% after stabilizing for several minutes, the sensor should be recalibrated. If it will not recalibrate to the proper setting, the oxygen cell should be replaced. If there is a hypoxic reading, the highpressure circuit should be evaluated. If a central pipeline crossover is suspected, the oxygen tank should be opened and the pipeline supply disconnected. If oxygen levels are restored by this change, it is critical to alert the appropriate hospital staff to avoid further serious adverse events.
Flowmeter Problems • Check for a leak. • Check for a stuck bobbin. Flowmeter problems can often be detected during machine checkout. If the flowmeters are set to specific values and the oxygen or gas sensors are not reading the correct percentages of gas, either the sensors are malfunctioning or there is a problem with the circuit or flowmeters. Newer models of anesthesia machines are equipped with electronic flowmeters rather than the standard fluted glass tubes with a floating bobbin. Troubleshooting of electronic flowmeters should be done by the machine representative. The most common problem with fluted tube flowmeters is a float that is stuck from debris, leading to inaccurate readings. The quick fix is to gently flick the flow tube in an attempt to free the float from the debris. Ultimately, this should be brought to the attention of the machine representative for definitive cleaning and repair. The presence of a crack in the glass flow tube can cause a leak and thus a faulty reading. This can usually be detected during machine checkout when the low-pressure leak test is performed. Cracks that cause only a very small leak may be hard to detect. In some machines, a check valve, located between the
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common gas outlet and the flowmeters, prevents gas from flowing back through the vaporizer and into the flow tubes. In these machines, a positive-pressure leak test of the low-pressure circuit will not detect a leak in the flowmeters. A negative-pressure leak test should be performed on machines with a check valve in this location.
■ VENTILATORS For a full description of anesthesia machine ventilators, see Chapter 30. A brief review is provided in order to discuss how to troubleshoot common ventilator problems. The ventilator is typically pneumatically or mechanically driven. Mechanically driven ventilators use a pistondriven system to deliver a set volume or airway pressure to the circuit. Many current ventilators use an ascending pneumatically controlled bellow as part of a semiclosed circle system (Fig. 31.2). The pressure inside the clear plastic hood surrounding the bellows is regulated by a pneumatic circuit. During inspiration, gas enters the hood and the increase in pressure (1) closes the ventilator relief valve, blocking gas from going to the scavenging system, and (2) drives the bellows down, pushing anesthetic gas to the patient (older ventilators may have hanging bellows instead of standing bellows). During expiration, the pressure in the hood decreases, which allows fresh gas and scrubbed (i.e., CO2 removed) exhaled gas to fill up the bellows. The drop in pressure also opens the ventilator relief valve and when there is back pressure inside the bellows (inside the breathing circuit); excess gas overflows into the scavenging system. The ventilator system also incorporates airway volume and pressure monitors. Volume monitors often sense exhaled tidal volume and minute ventilation but can also sense inspiratory volumes. Pressure monitors sense expiratory and inspiratory peak and plateau airway pressures. Default alarm settings are programmed into the machine to sound when certain volumes and pressures exceed or fail to meet specified limits. The volume sensor is often in the expiratory limb of the circuit and is susceptible to errors when too much moisture is in the system.
Ventilator Maintenance Regular maintenance includes that performed by the manufacturer representative along with frequent visual inspections and functional testing,
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in addition to allowing the flow transducer and flow valves to dry at the end of the day.
Troubleshooting Common Ventilator Problems Ventilator will not fill: The most common cause is a leak in the system. Perform the same steps as above to investigate a low-pressure alarm. In addition, check for an incompetent ventilator relief valve. • Check for low-pressure leak. • Check for a circuit disconnect starting with the patient and working back to the machine. • Inspect bellows. • Inspect CO2 canister. • Check lids/coupling of vaporizers. • Inspect the flow sensor. • Check oxygen pressure from pipeline/cylinder. • Check for an incompetent ventilator relief valve. Ventilator will not deliver a breath • Look for inspiratory reverse flow/negative inspiratory flow alarm. • Check for high airway pressures. • Check for an incompetent expiratory valve. Sometimes, the ventilator is unable to deliver a breath even though it is able to fill. A common cause of this problem may be with the flow transducer or flow valves. Alarms such as “inspiratory reverse flow” or “negative inspiratory flow” can be displayed on the screen. In each case, too much moisture in the circuit can affect the flow transducer’s capacity to measure flow. This can be resolved easily by exchanging the flow sensor for a dry one. High airway pressures can also limit the ventilator from delivering a proper breath, particularly when using pressure control ventilation. This will be addressed further below. If the expiratory flow valve is incompetent, the ventilator will be able to deliver a breath, but it will be much smaller than programmed, as there will be volume lost into the expiratory limb. High airway pressures with mechanical ventilation • Check the breathing circuit from the machine to the patient for kinking or any type of obstruction. • Check the ETT for obstruction (kinking, secretions, mainstem intubation, etc.).
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• Consider patient pathophysiology (bronchospasm, tension pneumothorax, stone chest, etc.). • Check pop-off valve. • Check positive end expiratory pressure (PEEP) settings. • Check ventilator parameters. There are many common causes for ventilator alarms to sound. Low airway pressure was addressed previously under the gas delivery section and is most commonly due to a disconnection or leak in the system. High-pressure alarms can sound because of a number of patient-related processes, including bronchospasm and pneumothorax. These should be addressed by the anesthesia provider and are beyond the scope of this chapter (but cannot be disregarded). There are several equipment malfunctions that can trigger a high-pressure alarm. The most common is due to an occlusion in the breathing circuit. Commonly, this is due to a kinked or obstructed ETT or a kinked hose on the inspiratory or expiratory limb. Once this has been addressed, ensure the pop-off valve and PEEP are set appropriately. If a volume-controlled mode of ventilation is in use, ensure the tidal volume is correct. Other possible contributors include problems with the scavenging system, which will be addressed below. Lastly, the parameters of the preset alarms should be evaluated and reset as necessary for the clinical situation.
■ GAS ANALYZER Historically, operating room (OR) gas analyzers were separate devices from the anesthesia machine. Newer models have gas analysis incorporated into the main machine. These monitor the concentrations of CO2, oxygen, and inhaled anesthetics (see Chapter 32). A small gas sample line from the analyzer is connected to the end of the breathing circuit and samples are taken regularly from the inhaled and exhaled gas. The percent of gas is shown on the monitor. The continuous monitoring of CO2 levels is called capnography, and a tracing correlating to these levels is displayed on the monitor.
Maintenance of Gas Analyzers The gas analyzer should be serviced by a machine representative. The water trap and sample tubing should be replaced regularly, especially if condensation can be seen.
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Troubleshooting Common Problems with Gas Analyzers No CO2 tracing • Check that the gas analyzer has been turned on and has completed its warm-up cycle. • Check that the gas analyzer is not performing a temporary self-test. • Check for sample line disconnect or obstruction. • Anesthesia provider should confirm ETT placement. • Check for a circuit disconnect. Ensuring a proper CO2 tracing is part of the machine checkout and most, if not all, problems should be identified early and easily rectified. If no tracing appears, there are two very common causes. First, ensure the machine is on and has had time to calibrate. Next, examine the sample line to look for kinks, disconnects, or fractures in the tubing (Fig. 31.4). Other problems that can be quickly fixed include checking to see if the moisture trap is inserted properly and not full of water. If the CO2 tracing “stops working” (i.e., is not registering a positive number) during the time of patient care, it is critical to first confirm that it is not a lack of patient ventilation before checking for a machine problem. Inaccurate gas analyzer readings • Check water trap for condensation. • Check sample line for disconnect, obstruction, or condensation. • Check for recent aerosolized medication administration. • Check vaporizers (properly installed and not empty).
■ FIGURE 31.4 Gas sample line has been broken at the connection from surgeon leaning on line during case.
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A common cause for inaccurate readings from the gas analyzer is condensation in the sample line and/or an incomplete connection to the machine. Kinked, fractured, or poorly connected sample lines can also cause faulty readings (Fig. 31.4). If aerosolized medication is given through the ETT, the gas analyzer can often have trouble identifying the various gases. For example, aerosolized albuterol may give an endtidal reading of halothane, despite the complete absence of halothane. Less commonly, end-tidal and inspiratory gas readings may not correlate with the vaporizer dial. If desflurane is the gas, ensure the electronic vaporizer is plugged in. Alarms should sound from a battery if it is unplugged, but if the battery is depleted, no alarm will sound. Another cause related to the vaporizer is spilling of volatile agent when the machine is tipped. This can be rectified by flushing the system for 20 minutes at high flows with the vaporizer set at a low concentration.
■ CO2 ABSORBER
Exhaled gas from the patient travels back to the machine through the expiratory limb of the circuit and flows through the CO2 absorbent to be “scrubbed” of CO2. Most current anesthesia machines contain a clear cylinder into which prepackaged or loose CO2 absorbent can be placed. After flowing through the absorbent, the exhaled gas reenters the circle system and combines with the fresh gas to return to the bag or ventilator. The two absorbents used most commonly include soda lime and calcium hydroxide lime. The agent Baralyme was previously used; however, because of problems with adverse reactions with anesthetic agents it has been removed from the market. Other problems with CO2 absorbents are due in part to oxygen that had been left flowing for a long period of time after the completion of a case, causing the absorbent to dry out. It is very important that gas flow be turned off when a patient is not connected to the machine. The absorption of CO2 from exhaled gas occurs through several chemical reactions eventually forming sodium carbonate, or potassium carbonate and water. A chemical indicator ethyl violet is added to the absorbent and changes from white to purple as the absorbent becomes exhausted, signaling that it is time to be replaced (see Fig. 31.5).
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■ FIGURE 31.5 Partially exhausted granules; the exhausted granules will have purple tint in contrast to the white fresh granules.
Maintenance of CO2 Absorbers
The CO2 “scrubber” should be evaluated at least on a daily basis and should be part of the checkout between patients. When using low flows of fresh gas, a significant amount of absorber can become exhausted quickly. When replacing the canisters, ensure the plastic canister is closed (Fig. 31.3) and that there are no granules between the gasket and the plastic housing. If a drain is present in the bottom of the cylinder, water should be emptied daily.
Troubleshooting Common Problems with CO2 Elevated CO2 on capnography
• Replace the CO2 absorber. • Examine inspiratory and expiratory flow valves. If an exhausted CO2 absorber is not recognized and replaced during the machine checkout, it will often be recognized intraoperatively. The patient’s capnogram tracing will not fall to zero during inhalation. Although there are several other serious clinical scenarios that can cause this, commonly high inspired CO2 is due to exhausted absorber. Although not related specifically to the CO2 “scrubbing” system, another cause of elevated end-tidal CO2 is a faulty inspiratory or expiratory flow valve. The valves can become incompetent if they are damaged, dried out, cracked, or get stuck in an open position from too much moisture (Fig. 31.6).
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■ FIGURE 31.6 Moisture in inspiratory and expiratory valves causing incompetent valve.
Moisture in the CO2 canister • Drain the moisture or replace the canister. Because water is a by-product of the CO2 reaction with the absorbent, and the patient’s expired gas is humidified, condensation can accumulate below the CO2 canister. This can lead to higher airway pressures and sporadic PEEP pressures. A drain is often located at the bottom of the canister and can be opened to drain excess fluid that inhibits gas flow.
■ SCAVENGING SYSTEM There are three places exhaled gases can go when they leave the patient. Gas can escape into the room from a leak around a face mask or past a deflated ETT cuff. Gas can go back through the circuit into the bag and if the APL valve is open it will accumulate in the collecting assembly of the scavenging system. If the ventilator is engaged, the gas can fill the ventilator and then spill over to the collecting assembly through the ventilator relief valve. The scavenged gas then moves through the tubing into the scavenging interface or reservoir. Once in the reservoir, it is removed through a conduit to the disposal assembly, which is most often a central vacuum that pumps gas to the outside of the building. One of the safety features of the scavenging system exists in the interface. If the rate of flow is greater than the removal, a positive-pressure relief valve opens and gas spills out into the room, preventing an increase in the pressure in the patient circuit.
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Scavenging System Maintenance Maintenance is performed by service representative at regular intervals. The dial controlling the suction in the disposal conduit should be checked daily and set appropriately.
Troubleshooting Common Problems with Scavenging Systems Overwhelmed scavenging system • Turn down fresh gas flow if >10 L/min. • Check the vacuum control valve for proper adjustment (may need to increase the vacuum). • Check that the gas disposal conduit is working. An overwhelmed evacuation system most often presents with opening of the positive-pressure relief valve and the sound of escaping air into the room heard on expiration. The most common cause for an overwhelmed scavenging system is having high fresh gas flows with high minute ventilation. This can be checked by turning down the fresh gas flows and seeing if the evacuation system is capable of keeping the scavenging reservoir bag
■ FIGURE 31.7 Distended scavenging reservoir due to inadequate level of vacuum suction or impaired pop-off valve.
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from becoming overdistended. If not resolved, the next step would be to ensure that the vacuum control valve is adjusted correctly. If the control valve is set too low, it is unable to keep up with the regular gas flows and the amount of vacuum should be increased (Fig. 31.7). If the reservoir is still distended after increasing the vacuum flow, check that the gas disposal conduit is working properly. Assess for any kinks in the line that could limit the elimination of scavenged gas (Fig. 31.8). If the vacuum is weak even after maximal adjustment of the valve, a problem exists in the central gas disposal system and should be addressed quickly to avoid gas contamination of multiple ORs. Increased circuit pressures • Check the transfer means for kinks. • Check the vacuum control valve for proper adjustment. • Check the positive-pressure release valve for proper functioning. The most common cause for increased circuit pressures is typically not related to issues with the scavenging system. However, occasionally the scavenging system circuit may become
■ FIGURE 31.8 Kinked gas disposal tubing of scavenging system.
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occluded in a location proximal to the pressure relief valve of the scavenger and cause high circuit pressures. Alternatively, high pressures in the scavenging system may result from a malfunctioning pressure relief valve, thus allowing the high pressure in the scavenging system reservoir bag to translate to increased circuit pressure. In both these situations, increased airway pressures and barotrauma may result for the patient. The patient must be disconnected from the breathing circuit and ventilated by alternate means while the problem with the scavenging system is being corrected. If the problem cannot be immediately corrected, a new anesthesia machine will need to be brought into the room. Decreased circuit pressures • Check that the vacuum control valve is adjusted properly. • Check the ventilator relief valve. The most common cause for decreased circuit pressures is typically not due to problems with the scavenging system. But again, if the vacuum control valve is maladjusted, negative pressures may transfer to the main breathing circuit if the scavenger system has an incompetent check valve. This can be managed temporarily by adjusting the vacuum control valve so that the bag is not completely deflated with low circuit flows. An incompetent ventilator relief valve may also lead to lower pressures as gas is delivered to the scavenging system instead of the patient. As with the situation of an incompetent scavenger check valve resulting in high circuit pressures, when the incompetent valve results in low pressure the anesthesia provider should consider changing the anesthetic to intravenous agents and then ventilating the patient with an intensive care unit (ICU) ventilator or Ambu bag, until a new anesthesia machine can be brought into the room or the current machine fixed.
■ SUMMARY While equipment failure certainly does occur, many machine-related issues may be prevented through regular maintenance, a complete anesthesia machine checkout, and thorough understanding of the operation and design of anesthesia machines. The methodical completion of a thoughtfully tailored and specific checkout for your institution’s machines
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will help enormously to avoid many of the commonly encountered machine issues and complications. When such events occur, you will also be better prepared to address the circumstance at hand. A regular maintenance program, in tandem with vigilance from the anesthesia providers, will help to identify many issues before they become system-threatening failures, leading to potential patient injury. The collaborative team approach between the anesthesia technician and the anesthesia provider is clearly demonstrated in this particular arena with significant overlap of responsibilities. Prompt cooperation and collaboration of all parties will help remedy the situation in a timely fashion and thereby minimize and/or avoid clinical complications.
REVIEW QUESTIONS 1. Which of the following would correctly identify a leak in an oxygen flow tube? A) Positive-pressure leak check B) Oxygen analyzer C) Negative-pressure leak test D) All of the above E) None of the above Answer: C. Because most machines have a check valve between the patient circuit and the common gas inlet, a positive-pressure leak test will not identify a leak upstream. If a small leak was present, the oxygen analyzer would be unable to identify that 1 L of 100% oxygen instead of 5 L of oxygen was flowing through the circuit. Only a negative-pressure leak test will identify this.
2. The most common cause of improper delivery of oxygen to the patient is A) Improper gas cylinder connected to the machine B) Crack in oxygen flow tube C) Crossing of gas supply from the wall D) Disconnection of circuit from the patient E) Incompetent inspiratory flow valve Answer: D. Failure to properly deliver oxygen to the patient is most commonly caused by a disconnection in the patient circuit. Although A, B, and C can cause problems with delivery of oxygen, these are much less common causes. An incompetent inspiratory valve can lead to elevated baseline levels of carbon dioxide, but it should not cause poor oxygenation.
3. You are called into a room where the anesthesia staff complains that the airway pressure continues to rise in a relaxed patient with regular breath
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sounds. Which of the following problems with the machine could be causing this? A) A kink in the scavenging transfer means B) A faulty positive-pressure release valve in the scavenging system C) An incompetent pressure relief valve in the ventilator D) A and B E) All of the above Answer: D. If the scavenging transfer means is kinked, excess gas cannot be vented from the circle system to the scavenging system and barotraumas can occur from elevated airway pressures. This can also occur if flows are high in the system and the positive-pressure release valve does not function properly to vent the excess gas. An incompetent pressure relief valve in the ventilator will allow gas that is compressed by the ventilator to escape into the scavenging systems and would cause lower airway pressures and a leak in the circuit.
4. You are called into a room because of problems with the end-tidal carbon dioxide tracing not going back to a baseline of “0.” Which of the following could cause this? A) Incompetent expiratory valve B) Incompetent inspiratory valve C) Exhausted soda lime granules D) A and C E) All of the above Answer: E. The most common cause for elevated end-tidal carbon dioxide levels is exhausted absorbent, but improperly functioning inspiratory and expiratory valves can also cause this. Expired gas escapes down the inspiratory limb, and the patient is ventilated with this gas again. Inspired gas can also push a small amount of expired air back down the expiratory limb if the valve is incompetent. If this were to occur, the tracing would never reach “0” because small amounts of expired air would pass by the sampling port during inspiration.
5. The following steps should all be performed if a problem with the central gas supply is suspected in a room, EXCEPT A) Open the oxygen cylinder on the back of the machine B) Alert the OR front desk C) Disconnect the wall supply from the machine D) Ventilate the patient with a separate circuit E) All should be performed Answer: D. If a central pipeline crossover is suspected, the oxygen tank should be opened and the pipeline supply disconnected. If the pipeline supply is not disconnected, gas from the tank won’t be used. If oxygen levels are restored by this change, it is critical to alert the appropriate hospital staff to avoid
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further serious adverse events. There is no need to change to a separate circuit once a proper oxygen source is connected to the machine.
6. The safety and reliability of oxygen and anesthetic gas delivery are principal concerns and of critical importance to safe medical practice. Which machine improvements have been key components in helping to achieve this goal? A) Agent-specific vaporizers B) Oxygen proportioning systems C) Oxygen analyzers D) Oxygen failure safety valves E) All of the above Answer: E. There are many key safety developments that have been integrated into the modern anesthetic machine and importantly include the components noted above in addition to circuit pressure monitors, pin indexing systems, and central display and consolidation of assorted patient physiologic data points/trending.
7. Anesthesia machines have progressed in sophistication and complexity and routinely include a number of important components to manage gas delivery including A) Anesthetic vaporizers B) Ventilators C) Scavenging systems D) CO2 absorption E) All of the above Answer: E. While there are a number of anesthetic machines available and in use today worldwide, they principally share many similar fundamental components and functionalities. It is critical that one has a solid basic understanding of the principals of the workings of the anesthetic machine and its fundamental components.
SUGGESTED READINGS Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005;644–694. Dorsch JA, Dorsch SE. Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007. GE Health Care Aestiva/5. Anesthesia Delivery System Owner’s Handbook. Datex-Ohmeda, Inc; Madison WI, 2003. Miller DR, Eriksson LI, Fleisher LA, et al. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2009:Chapter 25. Morgan G, Mikhail M, Murray M. Clinical Anesthesiology. 3rd ed. New York, NY: McGraw-Hill; 2002:Chapters 1–4.
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CHAPTER
32
Gas Analyzers Wesley Simpson II
T
he primary difference between a device labeled an “analyzer” and one labeled a “monitor” is that a monitor includes adjustable low, or low and high alarm settings. In other words, a gas analyzer will measure whatever substances it is designed for but will not alert you if the values measured fall outside an acceptable range. Although the terms analyzer and monitor are frequently used interchangeably, a true analyzer should only be used in situations where continuous, uninterrupted observation is possible. Because the addition of alarm settings can contribute to vigilance, a monitor should always be used with patients undergoing an anesthetic. Gas monitors can measure either a single gas or multiple gases and are grouped into two general classifications: mainstream and sidestream. Although anesthesia providers can use mainstream monitors, the vast majority of monitors in current use are sidestream. Sidestream monitors divert gas mixtures from the breathing circuit by means of a continuous pump. The sample gas (normally 50–250 mL/min) is either returned to the breathing circuit or sent into the gas scavenger system. The exhaust from a sidestream monitor must be connected to one of these outflow sources. With the exception of a true emergency, it should never be allowed to empty into the room air. Mainstream monitors measure the gas of interest directly in the breathing circuit, usually consisting of a disposable cuvette and a reusable sensor cell. The primary limitations are that mainstream monitors are only capable of measuring one gas and there is a potential for interference caused by moisture collecting in the cuvette. The simplest form of gas analyzer/monitor, and the one that was used first by anesthesia providers, is the fractional inspired oxygen (FIO2) monitor. As its name implies, the FIO2 monitor
measures the fraction (displayed as a percentage) of oxygen present in the inspiratory limb of a breathing system. Human error or anesthesia machine malfunction could cause a gas mixture with insufficient oxygen to be delivered into the breathing system; therefore, inspired oxygen monitoring is essential to prevent hypoxia in an anesthetized patient. It is also a key component of both the American Society of Anesthesiologists (ASA) Standards for Basic Monitoring and Recommendations for Pre-Anesthesia Checkout. Anesthesia technicians have a responsibility to ensure that FIO2 monitors are properly calibrated prior to anesthesia machine use. At minimum, calibration to room air (21% oxygen) should be performed at least every 24 hours and prior to use on the first patient. Some monitors have the capability of performing a 100% oxygen calibration as well. This should be performed in addition to room air calibration and should not be performed in place of it. Be sure to follow the manufacturers’ recommendations when performing either a room air or 100% oxygen calibration. Keep the following key points in mind with all brands of FIO2 monitors you are working with or the type of sensor it uses: 1.
2.
3.
If you can access the sensor, remove it from the circuit and expose it to room air for several minutes prior to performing a 21% calibration. This allows time for the sensor to equilibrate and any trace gases to diffuse. Perform the room air calibration. This may be as simple as pushing a button with some monitors, or it may require a manual adjustment to obtain a reading of 21%. Whether or not the monitor provides for a 100% calibration, expose the calibrated sensor to pure oxygen. A final reading of 95%–100% is considered acceptable by most manufacturers. A sensor that has been calibrated to room air and then tested with 281
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100% oxygen and does not achieve a final reading of 95%–100% should be either serviced or replaced. If the FIO2 monitor is battery operated, check the battery level as part of the calibration procedure.
There are three primary types of sensor (measurement) cells used in oxygen monitors: polarographic, galvanic, and paramagnetic. Each type of sensor has strengths and drawbacks as well as specific concerns for the anesthesia technologist. Polarographic cells, sometimes referred to as Clark cells, use an anode and a cathode that are suspended in an electrolyte solution containing potassium chloride. The solution is separated from the inspiratory gases by a semipermeable membrane, usually made of Teflon or polypropylene. The strength of the current generated between the anode and the cathode is proportional to the concentration of oxygen in the gas mixture being analyzed. These sensors are highly accurate but can be slow to respond to rapid changes in gas composition. Polarographic cells are sold as either reusable or disposable. Cells that have reached the end of useful life can be placed in regular trash. Reusable sensors should be serviced whenever they fail to calibrate properly. Emptying the used electrolyte gel and using a soft cotton swab to clean the electrodes, membrane, and inner surface of the sensor capsule normally accomplish this. Fill the capsule with fresh electrolyte gel and replace the electrodes, being careful not to entrap any air bubbles. Galvanic or fuel cell sensors also use an anode and a cathode suspended in an electrolyte solution such as potassium hydroxide. The principle of operation is similar to that of the polarographic cell, and currents generated in the cell are in proportion to the concentration of oxygen molecules in the gas being sampled. Single-cell sensors can be slow to respond to changes in gas composition and are more prone to calibration drift. Newer dual-cell designs offer increased accuracy, faster response times, and greater stability. Galvanic cells are similar in composition to your car battery. The correct method of disposal will vary with state and local laws, but they should never be placed in regular trash, sharps, biohazardous, or pharmaceutical containers. Paramagnetic sensors expose the gas sample to an uneven magnetic field. Oxygen has a
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relatively high magnetic susceptibility as compared to nitrogen, carbon dioxide, nitrous oxide, and inhaled anesthetic agents. As the gas sample is sent through the sensor, oxygen molecules are attracted to the stronger of the magnetic fields. The resultant shifts measured in the sensor are proportional to the percentage of oxygen in the sample. Paramagnetic sensors react rapidly to changes in gas composition and have a long life span but are motion sensitive. As a result, they are not utilized within a breathing system because of the potential for movement of the breathing circuit during ventilation but are built into multiple gas monitors. They are not calibrated separately, but with other gases the monitor is designed to detect. This may be accomplished through an internal calibration standard or by using an external calibration gas. Since paramagnetic sensors are not used in discrete FIO2 monitors, they are an exception to the 24-hour calibration standard. The frequency for calibration will vary with the manufacturers’ recommendations and/ or department policies. In addition to monitoring FIO2, it is desirable for anesthesia providers to monitor other gases including carbon dioxide and a variety of anesthetic gases. The gas monitor can be as simple as a device that only monitors carbon dioxide (CO2) or as complex as a monitor capable of measuring multiple gases simultaneously. Monitoring of CO2 in the circuit is important because it provides information about the adequacy of ventilation for the patient and can detect conditions like apnea, underventilation, bronchospasm, or even circuit disconnects (see Chapter 33). Continual monitoring of end-tidal carbon dioxide (ETCO2) is a part of the ASA Monitoring Standards. Although the ASA guidelines are silent on the need to monitor other airway gases, in many instances it has become a “community standard of care” to do so. Monitoring of anesthesia gases can detect insufficient anesthetic gas delivery (i.e., the vaporizer is empty) or dangerously high anesthetic gas levels (i.e., vaporizer set inappropriately high or a machine malfunction). Carbon dioxide, as well as other common airway gases, can be measured by a variety of methods. The most common of these used in anesthesia is infrared monitoring. Infrared monitors employ the concept that most gases absorb infrared light, and the amount of light absorbed is in direct proportion to the concentration of
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that gas (Beer-Lambert Law). Infrared monitors are capable of analyzing carbon dioxide, nitrous oxide, inhaled anesthetic agents, and alcohol vapors. Because oxygen does not absorb light in the infrared spectrum, a galvanic or paramagnetic cell must be used in an infrared multiple gas monitor. Other means of measuring multiple gases include Raman spectroscopy, which sends a laser beam through the gas sample; photoacoustic spectroscopy, which uses microphones to “listen” to the frequencies generated by gas molecule; and mass spectrometry in which differences in the molecular weight of gas molecules being monitored are separated. Regardless of the technology used, correct calibration of the monitor is the only way to ensure that accurate measurements are obtained. Manufacturer instructions must be followed exactly in order for an accurate calibration to be ensured. Although the details may vary from brand to brand, the following general principles should always be observed: 1.
2.
3.
4.
The sensor cell must “warm up” and obtain a stable temperature in order for calibration to be accurate. In some types of monitors, this interval can be as little as 5 minutes or as long as 45 minutes. If a calibration gas is used, it must be specific to the monitor being calibrated. Although most formulations (blends) of calibration gas can be used to “spot check” the accuracy of an analyzer, the only blends used for calibration must match manufacturer specifications. Calibration should be performed, at minimum, at the intervals specified by the manufacturer. Any monitor that fails manufacturer calibration standards should be removed from service immediately, or as soon as reasonably possible.
Taking time to make sure that gas monitors are properly calibrated and functional prior to use will minimize potential problems during an anesthetic. There will be times, however, when you will be asked to troubleshoot and repair a monitor while it is in use. Several of those requests are due to readings on the monitor that do not match the expected range for a particular patient, or if there has been a sudden change in
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the readings. In other words, what clinicians are seeing on the monitor does not correspond with what they think they should be seeing. Keep in mind that when troubleshooting, it is not always a monitor problem. There will be occasions when the abnormal reading truly reflects what is going on with the patient. When asked to evaluate a gas monitor problem, the following steps are suggested as a means of doing so quickly and efficiently: 1.
2.
3.
4.
5.
6.
7.
Be prepared and take everything you may reasonably need with you. For example: If a problem occurs with an FIO2 monitor, bring a fresh sensor cell, batteries, etc. For a sidestream monitor, you may need to replace the sample “T,” sample line, or water trap. When you arrive, take a moment to make your own assessment of the problem. The most important tools you bring to the situation are a fresh set of ears and eyes. The clinician may be involved with multiple tasks or problems and may not have been able to do a thorough analysis of the monitor problem. If there are multiple faults or alarm conditions, you will need to prioritize. If the patient is being adequately ventilated by a clinical evaluation, gas monitor alarms may be annoying, but may not be the highest priority. Use a standard approach to troubleshooting so that you do not miss any steps. For example: Check connections at the monitor first and then work your way one connection at a time until you reach the final connection to the breathing system. Alternatively, start with the connection to the breathing circuit and work your way back to the machine. When you remove the sample line or the water trap, cap off the sample port on the breathing circuit so that the resulting leak does not set off volume or pressure alarms. Have a backup plan in mind. If you cannot make an immediate repair, be prepared to give the anesthesia provider an accurate time estimate for replacement. Know where spare monitors are and how long it would take to get them ready for use. If you do remove a monitor from service, follow your facility’s defective equipment policy to facilitate repairs and minimize downtime.
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Most gas monitor alarms fall into one of three categories; the reading is lower than expected, higher than expected, or there is no reading. The following are common problems you may encounter in each category: If all or most of the readings are lower than expected: • Cracked sample line: This most commonly occurs where the sample line connects to the port on the breathing circuit. Even if you cannot see the crack, tightening the connection will not solve the problem and may actually make it worse. The crack or leak may also occur where the sample line connects to the monitor. • Leaking water trap or filter: This is easy to check, even if you cannot see the defect. Remove the sample line and cover the inlet of the trap/filter with your finger. If this does not create an occlusion alarm, replace the trap/ filter. • If you cannot find a leak, have the clinician check the cuff balloon on the endotracheal tube or supraglottic airway. • The monitor may not be properly calibrated, or the calibration may have failed. If only one gas is reading low: • Suspect that the monitor is not properly calibrated, or the calibration may have failed. If only the inhaled anesthetic is reading low, the vaporizer may be leaking or empty. Check the “sight glass” on the vaporizer. If the vaporizer is not empty, make sure it is securely mounted, listen for an audible leak, and smell for the presence of gas vapors. If all or most of the readings are higher than expected: • Check the exhaust port or line to make sure it is not occluded. An exhaust occlusion changes the flow of gas through the monitoring chamber and can result in false high readings. • Suspect that the monitor is not properly calibrated, or the calibration may have failed. • If only the inhaled anesthetic is reading high, the vaporizer may have failed. If the vaporizer is easily removed, replace it with another vaporizer and see if the readings become normal.
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If there is no reading: • There may be an occlusion. In some models of monitors, there is no occlusion alarm. Check for an occlusion at the sample port, in the sample line, and at the water trap/filter inlet. • The patient may have become unintentionally extubated (although this condition should also cause volume and pressure alarms on the anesthesia machine to respond). • The monitor’s calibration may have failed. • The internal pump may have stopped working. You can check this by occluding the inlet port with your finger to see if you can feel negative pressure. • The sample cell of a mainstream monitor may have failed or become disconnected. Disconnections can occur at either the breathing system connection or at the monitor.
REVIEW QUESTIONS 1. A sidestream gas analyzer A) Can measure only one gas B) Uses a continuous pump C) Should never be allowed to empty into room air D) B and C only E) All of the above Answer: D. Mainstream analyzers are limited to one gas. Sidestream monitors are able to monitor multiple gases.
2. When called into a room, you are told the O2 readings are lower than expected. Which of the following could be a likely cause? A) Failed vaporizer B) Occlusion C) Cracked sample line D) Patient extubation E) Exhaust port occluded Answer: C. With a cracked sample line, O2 could be leaking from the system, resulting in lower than expected O2 readings. A failed vaporizer may affect gas readings but not O2 readings. A patient or exhaust port occlusion may result in higher than expected O2 readings or no reading. A patient extubation should result in the absence of a reading altogether.
3. FIO2 monitors A) Should be calibrated to room air (21% O2) B) Should be calibrated at least every 24 hours C) Should be calibrated prior to use on the first patient D) A and C only E) All of the above
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Chapter 32 • Gas Analyzers Answer: E. All of the above is the standard recommendation from all manufacturers of FIO2 monitors.
4. The use of ETCO2 monitoring A) Is part of ASA monitoring standards B) Can detect conditions such as apnea, underventilation, bronchospasm, and circuit disconnect C) Can detect dangerously high anesthesia gas levels D) A and B only E) All of the above Answer: D. ETCO2 monitors do not detect agent. An agent analyzer may be incorporated into the ETCO2 monitor as a added system, but it is the ETCO2 portion that is an ASA standard and is able to detect noted conditions.
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SUGGESTED READINGS American Society of Anesthesiologists. ASA Recommendations for Pre-Anesthesia Checkout. 2008. Available at: https:// www.asahq.org/For-Members/Clinical-Information/2008ASA-Recommendations-for-PreAnesthesia-Checkout.asp. Accessed September 5, 2011. American Society of Anesthesiologists. Standards for Basic Anesthesia Monitoring 2011. Available at: http://www. asahq.org/For-Members/Clinical-Information/StandardsGuidelines-and-Statements.aspx. Accessed September 5, 2011. Simpson W. Need for FIO2 monitor strongly defended [letter to the editor]. APSF Newslett. 1993;8:1. Available at: http://apsf.org/newsletters/html/1993/spring/#art3. Accessed September 5, 2011.
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CHAPTER
33
Basic Monitoring Wesley Simpson II
This chapter is focused on basic monitors required for patient safety during the conduct of an anesthetic, as defined by the American Society of Anesthesiologists (ASA) Standards for Basic Monitoring and the role of the anesthesia technician in complying with these standards. The ASA standards were first approved in October 1986. The most recent update was completed in October 2010, and became effective July 1, 2011. Each of the five standards is discussed here. Standard I is a general statement, with standards II through V being specific to the monitoring techniques that should be used to assess a patient’s oxygenation, ventilation, circulation, and body temperature. These monitors are discussed in roughly the same order as the standards they fulfill.
■ ASA STANDARD I “Qualified anesthesia personnel shall be present in the room throughout the conduct of all general anesthetics, regional anesthetics and monitored anesthesia care.”
■ PULSE OXIMETRY (ASA STANDARDS II AND IV) Pulse oximetry is a noninvasive method used to determine oxygen levels in arterial blood. Similar to some gas analysis techniques, pulse oximetry is based on the principal that hemoglobin (Hgb) absorbs a specific wavelength of light differently whether it is saturated or desaturated with oxygen. Hgb is a protein contained in red blood cells (RBCs). Each Hgb molecule is capable of binding four oxygen molecules. Although oxygen dissolves in blood, binding oxygen to Hgb found in RBCs allows the blood to carry 70 times as much oxygen. In arterial blood, about 98.5% of the oxygen is bound to Hgb and only 1.5% is dissolved within the blood. Hgb that has bound
oxygen is termed oxyhemoglobin, and Hgb that does not have oxygen bound to it is termed deoxyhemoglobin. A standard pulse oximeter contains a light source and a sensor. The light is passed through a portion of the patient’s body that is small enough that some of the light can pass through the body part to be detected by the sensor on the other side. A pulse oximeter uses two bandwidths of light: infrared (660 nm) to measure oxyhemoglobin and nearinfrared (940 nm) to measure deoxyhemoglobin. The amount of light that is absorbed and the amount of light that passes through the body part are dependent upon the amount of oxygen bound to the Hgb within the RBCs. Sensor readings of the light absorbed for both wavelengths are processed through an algorithm that compares the ratio of absorption for the two wavelengths. The pulse oximeter can then calculate and display a value that represents the percentage of arterial blood oxygenation. Normal values for humans range from 95% to 100%. There are two types of pulse oximeter probes, transmission and reflection. Transmission probes were the first to be developed and remain the most common. Transmission probes have the light source on one side, with the detector directly opposite. Light from the source is transmitted through the tissues of interest to the detector, and the amount of light that reaches the detector is used for calculations. Transmission sensors can be placed anywhere near the light source, and the detector can be positioned on opposite sides of a pulsatile blood flow. Care must be taken when placing sensors, as both accuracy and stability depend on the transmitter and detector being directly opposite to each other. This is especially true for the newer cooximetry probes. Common sensor sites include fingertip, toe, nose, and earlobe for children and
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adults and foot and forearm for neonates. Less common sites include the cheek for adults and the penis for neonates. Reflection probes have both a light source and a detector placed near one another. The amount of light reflected to the sensor is used for calculations. The forehead is the most common site for reflectance sensors. Pulse oximeter probes can be either disposable or reusable (Fig. 33.1). Reusable probes are classified as “noncritical” items for disinfection purposes, and low-level disinfection between patients is suitable as long as the probe is placed over intact skin or does not become soiled with blood or body fluids. Any reusable probe that does become soiled should be treated with highlevel disinfection or sterilization. Regardless of the treatment used, make sure the probe has
■ FIGURE 33.1 Reusable and disposable pulse oximetry probes.
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dried completely before using it on the next patient.
■ LIMITATIONS OF PULSE OXIMETRY Although pulse oximetry information is extremely useful and has contributed to the safety of modern anesthesia, its limitations must be understood. A patient can have a reading in the normal range (95%–100%) and still have insufficient oxygen in the blood. What a pulse oximeter reading of 100% means is that of the Hgb that is available to transport oxygen in the arterial blood, 100% is occupied with oxygen. What it does not tell you is what percentage of Hgb is available to carry oxygen or what the total Hgb is. For example, if a patient’s Hgb is 16 g/dL and all of the available Hgb is carrying oxygen, the saturation reading would be 100%. If that same patient’s Hgb drops to 8 g/dL, the saturation reading can still be 100%, even though the total amount of oxygen carried in the arterial system has been reduced by half. Another important factor to consider is the effect of other substances and the ability of Hgb to bind oxygen and their simultaneous effect on pulse oximetry readings. Carbon monoxide binds to Hgb 20 times more strongly than oxygen. The presence of carbon monoxide effectively lowers the oxygen-carrying capacity of blood (available amount of Hgb to carry oxygen). In addition, carbon monoxide bound to Hgb (carboxyhemoglobin) absorbs one of the wavelengths of light used by the pulse oximeter and interferes with the calculation of oxygen saturation. Therefore, patients with high carboxyhemoglobin levels may not have enough oxyhemoglobin, yet still have high pulse oximetry readings (e.g., patients with carboxyhemoglobin concentrations of 70%—more than two-thirds of the Hgb is not available to carry oxygen—have had pulse oximetry readings of 90%.) Other forms of Hgb including methemoglobin and sulfhemoglobin also interfere with both the ability of oxygen to bind to Hgb and pulse oximetry readings. Patients with methemoglobinemia typically have pulse oximetry readings of 85% despite severe reductions in oxygen-carrying capacity. In most cases, a co-oximeter can be used to overcome the limitations of standard pulse oximeters mentioned above. Co-oximeters use multiple wavelengths of light (as many as eight) and can not only measure oxyhemoglobin but also
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provide values for other states of Hgb, such as carbhemoglobin, carboxyhemoglobin, methemoglobin, and sulfhemoglobin, as well as the total amount of Hgb. Co-oximeters are commonly available with blood gas machines; however, pulse co-oximeters are available for bedside use as well. Pulse oximeters also measure the volume of the sample body part and rely on the principle that during an arterial pulsation (increase in volume), the blood is fully oxygenated and this is when the reading should be taken. This is why most pulse oximeters provide a value for the heart rate and many display a waveform as they measure the rhythmic change in volume of the sample body. This property also leads to a limitation in pulse oximetry readings. When the pulse oximeter cannot detect regular, rhythmic changes in volume, it cannot give an oximetry reading. This can occur with peripheral vasoconstriction (peripheral vascular disease, vasospasm, cold body part, etc.), low blood flow (hypotension, reduced cardiac output), or arrhythmias that are irregular (atrial fibrillation, multifocal atrial tachycardia, etc.). There are several sources of interference that can affect the accuracy and usability of a pulse oximeter. Although all pulse oximeters can experience problems, newer models include features and software to help minimize them. The most common of these are light, motion, nail polish (some blues, reds, and browns), hypoperfusion, and intravenous dyes. Problems and possible solutions are presented below: • Light: Ambient light normally affects both the saturation reading and the pulse rate. Shield the sensor with a surgical towel, drapes, etc. or change the sensor site. • Motion: Motion of the probe interferes with readings. This can occur when the probe is jostled (e.g., surgical personnel leaning against the probe) or by medical devices that can cause patient movement (e.g., neuromuscular monitors or muscle-evoked responses). Use a disposable probe, secure the moving limb, or change the sensor site. • Nail polish: Nail polish, particularly dark red colors, can absorb the light emitted by the pulse oximeter. Change the sensor site or remove the nail polish. • Hypoperfusion: It can be caused by hypovolemia, hypothermia, vasoconstriction, or
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vascular blockage. If the patient is normothermic, but the sensor site is cool to the touch, cover the limb with warm blankets or a warm air blanket or change sensor sites. Other common problems encountered with pulse oximeters: • No light at sensor or light at sensor but the oximeter does not produce a reading or waveform—Check the cable connections at the sensor and monitor. If connections are not the problem, consider replacing the sensor, then the cable, then the monitor. • Erratic or suspected incorrect readings—Is the sensor placed correctly? Is it too tight? Is it on the same limb as the blood pressure cuff? Is the patient cold? Is the patient vasoconstricted? Modify the sensor placement or consider using a sensor on the earlobe, nose, or forehead.
■ CAPNOGRAPHY (ASA STANDARD III) Capnography is the measurement of carbon dioxide gas in the breathing system, with the measurements displayed in both numerical and graphic forms. The basic technology and related troubleshooting has been discussed in Chapter 32. In this chapter, we focus on the practical application of that technology in anesthesia. The role of capnography within the ASA standards is to help ensure a patient is adequately ventilated during all anesthetics. Continuous readings of exhaled carbon dioxide (CO2) can instantly communicate changes in the status of the patient and the anesthesia machine. Although the numerical readings from a capnometer will satisfy the basic requirements, a capnograph with a continuous waveform is preferred. The shape of the waveform can yield additional diagnostic information about how a patient is being ventilated. The “normal” capnogram is a waveform that represents the varying CO2 level throughout the breath cycle over time (Fig. 33.2A-E). Measured exhaled CO2 is a function of CO2 production by the body, delivery of the CO2containing blood to the lungs, gas exchange in the alveoli, and ventilation of the lungs to pick up CO2 from the alveoli and eliminate it to the outside. One of the most important functions of CO2 monitoring is to confirm the placement
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■ FIGURE 33.2 A-E: Normal capnogram. A,B: Baseline represents continued inhalation (value should be zero) or lack of gas movement. B,C: Expiratory upstroke (sharp rise from baseline represents the beginning of exhalation and consists of a mixture of air and alveolar gas. C,D: Expiratory plateau (continued exhalation of alveolar gas, should be straight or nearly straight). D: Endtidal concentration (value at the end of exhalation); D,E: Inspiration begins (sharp downstroke as fresh gas is inspired). (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
■ FIGURE 33.4 Rising ETCO2 levels as detected on a capnogram. (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
of an endotracheal tube into the trachea. If the tube is placed in the trachea and the patient is ventilated, and there is sufficient cardiac output to deliver CO2 to the lungs and there is sufficient gas exchange between the blood and the alveoli, the CO2 monitor will register CO2. If the endotracheal tube is placed in the esophagus, the CO2 monitor will not register sustained CO2 (Fig. 33.3). Although there may be some carbon dioxide in the esophagus and stomach, the concentration is normally low and will rapidly be depleted with ventilation of the stomach. Below is a discussion of the differential diagnosis of changes in measured CO2 values or waveforms. Increased CO2: An increase in the level of EndTidal Carbon dioxide (ETCO2) from previous levels can result from either an increase in the patient’s production of CO2 or a decrease in ventilation (Fig. 33.4):
• •
• Increased metabolic rate (rising body temperature from blankets or external warming
■ FIGURE 33.3 ETCO2 levels rapidly diminish or are not present with an esophageal intubation. (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
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• •
•
devices, thyrotoxicosis, malignant hyperthermia, etc.) Increased cardiac output Chemicals or metabolic products that have been administered to the patient that are converted to CO2 (bicarbonate, lactate, CO2 gas embolus, etc.) Decreased respiratory rate or tidal volume Decreased gas exchange with eventual rising CO2 blood levels (pulmonary failure, chronic obstructive pulmonary disease [COPD], bronchospasm, etc.) Machine problems leading to decreased ventilation (leaks, obstructions, depleted CO2 absorber, etc.)
Decreased CO2: A decrease in the level of ETCO2 from previous levels can result from a change in the body’s production of CO2 (rare), the delivery of CO2 to the lungs, or an increase in ventilation (Fig. 33.5): • Decreased metabolic rate or decreased core body temperature • Decreased cardiac output • Decreased pulmonary blood flow (pulmonary embolus) • Increased tidal volume or respiratory rate • Partial disconnect of CO2-monitoring tubing
■ FIGURE 33.5 Diminishing ETCO2 levels as detected on a capnogram. (Adapted from Capnography SelfStudy Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
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No CO2: A numerical reading of 0 or a flat waveform at 0 can indicate that CO2 is not being delivered to the monitor or a monitor malfunction. CO2 may not be delivered to the monitor/ sensor under the following critical conditions: • • • •
Circuit disconnect or sample line disconnect Apnea Cardiac arrest Total obstruction of the endotracheal tube, airway, or breathing circuit • Total obstruction of gas sampling (sample port, sample line, water trap) • Monitor malfunction Abnormal baseline CO2: Mechanical or anesthesia machine problems can often be a source of abnormal baseline CO2 readings (Fig. 33.6). Elevation of the baseline indicates rebreathing of CO2, which may also result in an increase in ETCO2. Possible causes include • Faulty expiratory valve on ventilator or anesthesia machine • Inadequate inspiratory flow • Exhausted CO2 absorbent • Partial rebreathing • Insufficient expiratory time Changes in the shape of the CO2 waveform: An obstruction to expiratory gas flow or differential emptying of obstructed small airways can present as a change in the slope of the expiratory upstroke of the capnogram (Fig. 33.7). The obstruction can be so severe that the CO2 wave never reaches a flat plateau before inhalation begins. Diagnoses to consider include • Obstruction in the expiratory limb of the breathing circuit • Presence of a foreign body in the upper airway
■ FIGURE 33.6 Elevated baseline CO2 levels as detected on a capnogram typical of rebreathing. (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
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■ FIGURE 33.7 ETCO2 waveform does not reach a plateau typical of bronchospasm or small airway obstruction. Electrocardiogram. lead color codes. (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
• Partially kinked or occluded endotracheal tube or supraglottic airway • Bronchospasm The “curare cleft” is seen in the plateau portion of the waveform. It is an indication that muscle relaxants are wearing off and the patient is returning to spontaneous ventilation (Fig. 33.8).
■ ELECTROCARDIOGRAM (ASA STANDARD IV—CIRCULATION) The electrocardiogram (ECG or EKG) is a record of the electrical activity of the heart over time. Although a “12-lead” ECG is traditionally used for diagnostic purposes, most anesthesia and critical care monitoring is accomplished using either a three-wire harness or a five-wire harness. The term ECG lead can mean different things to different people, often with confusing results. When people mention an ECG lead, it could mean the specific tracing, a specific wire on the ECG harness, or the adhesive electrode that attaches to the skin. To avoid confusion, we use the term leads to mean the specific tracings, lead wires to refer to the harness that connects from the monitor to the adhesive pads, and electrodes to refer to the adhesive pads that attach the lead wires to the skin. ECG lead wires are placed on patients
■ FIGURE 33.8 A “cleft” in the ETCO2 plateau. (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
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Chapter 33 • Basic Monitoring
in standard patterns. There are two primary color coding systems used throughout the world, American Hospital Association/Association for the Advancement of Medical Instrumentation (AHA/ AAMI) and the International Electrotechnical Commission (IEC). The AHA/AAMI colors are used in North America, while IEC colors are used throughout Europe. Other countries around the world vary in which standard they follow. Standard nomenclature is as follows: RA for right arm, RL for right leg, LA for left arm, LL for left leg, and V for any of the six cardiac lead positions. The standards are compared in Table 33.1. A three-wire harness is the most basic of ECG monitoring systems. The ECG display is limited to leads I, II, and III. Although ST-segment monitoring for cardiac ischemia can be done, the most sensitive leads (V1–V6) cannot be monitored. The standard three-lead harness consists of RA, LA, and LL, although some monitors may use RA, LA, and RL. A five-wire harness provides significant improvement in monitoring and diagnostic capabilities (Fig. 33.9). The addition of a ground lead (RL) and the cardiac leads (V1–V6) allow most modern monitors to display and print up to eight leads simultaneously. ST-segment and arrhythmia analysis is also improved with the additional leads. When placing the V lead wire on a patient, it can be in any one of six positions, V1–V6. • V1—Fourth intercostal space, right sternal border • V2—Fourth intercostal space, left sternal border • V3—Midway between V2 and V4 • V4—Fifth intercostal space, left midclavicular line • V5—Level with V4, left anterior axillary line • V6—Level with V4, left mid axillary line
TABLE 33.1 ECG LEAD WIRE COLOR
CODES LEAD
AHA/AAMI
IEC (EUROPE)
Right arm (RA)
White
Red
Right leg (RL)
Green
Black
Left arm (LA)
Black
Yellow
Left leg (LL)
Red
Green
Cardiac (V)
Brown
White
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■ FIGURE 33.9 Five-lead wire system with harness and electrodes.
The most common V lead wire positions used in critical care units are V1 and V2. The most common V lead wire positions used by anesthesia are V5 and V6, primarily due to the need for a clear surgical field and protection of the electrodes from surgical skin prep solutions. No matter which ECG monitoring harness is used, it is critical to place the lead wires in the proper position. Remember that the position of the lead wires is used to measure electrical forces from particular regions in the heart. Improper positioning of the leads can lead to abnormal ECG signals and errors in interpretation. Interference in the ECG signal usually stems from three primary sources: motion artifact, inadequate preparation and placement of the electrodes, and electronic interference. Movement of the lead wires can cause faulty electronic signals. Care should be taken that the lead wires are not being moved or in contact with moving or vibrating equipment. Even the respiratory movements of the chest can
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affect the ECG signal. Electronic interference is usually either 60 cycle (from faulty wiring) or excessive radio frequency (from electrocautery units). Options for minimizing electrical interference include changing the circuit the monitor is plugged into or adjusting the ECG filter on the monitor (although this can reduce diagnostic quality). Make sure cables and lead wires do not have breaks in insulating materials. Extreme instances may require use of a power conditioner. Correct skin preparation and lead placement are the key to obtaining quality ECG tracings. The signals received through the electrodes are relatively weak and can easily be obscured by impulses from other sources. In order to enhance the ECG signal quality and reduce artifact • Make sure the electrode gel has not dried out. • Shave or clip any excess hair. • Gently abrade the skin where the electrode will be placed (many electrodes have an abrasive area on the cover). • Wipe the area with an alcohol pad to remove skin oils.
■ NONINVASIVE BLOOD PRESSURE (ASA STANDARD IV) The arterial walls are muscular and elastic in the absence of vascular disease. Blood flows through the arteries in a pulsatile fashion as a result of pressure differences between the systolic and diastolic phases of the cardiac cycle (see Chapter 7). This flow pattern causes the arteries to alternately expand and contract, resulting in the pulse that we can feel with our fingertips. Blood pressure is not constant throughout the arterial system. In general, systolic pressure increases and diastolic pressure decreases the further blood moves from the heart. This is due to increasing resistance (friction) that blood encounters as it is forced through progressively narrower arteries. Changes in peripheral vascular resistance (vasoconstriction or vasodilation) can further alter these pressures. Mean arterial pressure (MAP) is not affected to the same degree, with a normal variation of only 1–2 mm Hg. Several noninvasive technologies have been developed to measure these pulsations and translate them into the blood pressure readings we are familiar with. The five most commonly
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used methods are pulse detection, auscultation, oscillation, applanation tonometry, and the volume clamp (photoplethysmographic or Penaz technique). Pulse detection, made practical by Dr. RivaRocci in 1896, was among the first techniques used for measuring blood pressure noninvasively. In this technique, a blood pressure cuff connected to a manometer is placed around a limb and a distal artery is palpated. The cuff is inflated about 20 mm Hg above the point where the pulse becomes absent. As the cuff is slowly deflated, the manometer reading at the point of pulse return is noted as the systolic pressure. Alternatively, the first “tick” in needle movement on an aneroid manometer or the point at which an SPO2 waveform returns can be noted as the systolic pressure. If a cuff or manometer is available, systolic pressure can be estimated by the body location at which a pulse can be palpated, as shown in Table 33.2. For example, if you can only obtain a carotid pulse, then the systolic pressure is at least 60 mm Hg. Similarly, a radial pulse is usually unobtainable below a systolic pressure of 80 mm Hg. Whenever you are palpating a pulse, make sure to use only the tips of your index and middle fingers. Never use your thumb to palpate a pulse. The artery in your thumb is large enough that you can mistake your own pulse for that of the patient. Unfortunately, palpation of pulses to estimate blood pressure is unreliable even when performed by health care providers. Auscultation, a refinement of the arterial occlusion technique, is the most frequently used method for noninvasive blood pressure monitoring. Auscultation, or “listening,” adds a stethoscope to the cuff and manometer. Dr. Nikolai Korotkoff developed this technique and described five distinct sounds that can be heard as a cuff is
TABLE 33.2 SYSTOLIC PRESSURE ESTIMATES ARTERY PALPATED
MINIMUM SYSTOLIC PRESSURE (MM HG)
Carotid
60
Femoral
70
Radial
80
Dorsalis pedis
90
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deflated over an occluded artery. These sounds result from the turbulent return of blood flow in the artery. The first sound is described as a clear snapping or tapping sound, and the manometer reading is noted as the systolic pressure. The second is a murmur that is heard for most of cuff deflation. The third marks a return of a clear, tapping sound. The second and third sounds have no known clinical significance. The fourth sound is referred to as thumping or muted and occurs within 10 mm Hg above the diastolic pressure. The fifth sound is silence as cuff pressure drops below diastolic pressure. This disappearance of sound is recorded as the diastolic pressure. The limitation of this method is dependence on proper technique and the differences in audio and visual acuity among clinicians. Despite these limitations, a cuff, manometer, and stethoscope should be readily available as a backup for automated systems. The oscillatory technique is used by the majority of anesthesia and critical care automatic blood presssure monitors. Although oscillometers still rely on the turbulent flow resulting from partial cuff compression, the form of energy measured (pressure vs. sound) differs from auscultation. Arterial pulsations create pressure variations (oscillations) that are transferred from the cuff to pressure transducers inside the
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monitor. These pressure fluctuations, along with their amplitude, are used to calculate displayed values. Although there is variation among manufacturers, systolic pressures are normally derived from the first significant oscillation detected, while diastolic pressures are calculated from the last. MAP is measured at the peak amplitude measured. Unlike auscultation techniques, oscillometers may have difficulty providing accurate readings in patients with arrhythmias or pulsus paradoxus. Most automatic oscillometers include a rapid determination, or STAT mode. These modes cycle the monitor continuously to provide frequent readings but sacrifice accuracy in the process. Despite manufacturers’ claims, when in STAT mode, you should only accept MAP readings (as a trend rather than as an absolute figure) after the first few minutes, as vascular congestion caused by continual, repeated cuff inflation makes systolic and diastolic readings less reliable. STAT modes should be reserved for emergent situations and used for the shortest possible amount of time. The difference between auscultation and oscillation measurements is demonstrated in Figure 33.10. Applanation tonometry provides a continuous noninvasive blood pressure (CNIBP) reading.
■ FIGURE 33.10 Simultaneous display of blood pressure cuff oscillations and auscultated blood pressure sounds.
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Although it can be used on most patients, it is especially useful for obese patients, patients where you have difficulty placing a cuff, and as an alternative for an invasive pressure line when deliberate hypotension is desired. In this technique, the radial artery is partially compressed against the styloid process of the radius. Physical location of the sensor is slightly distal to standard placement for a radial arterial line. In order to be accurate, tonometry requires entry of standard body mass index (BMI) information and relative position of the sensor in relation to the atria of the heart. MAP is directly measured. Systolic and diastolic values are calculated by processing BMI data through a nomogram. The volume clamp, also known as the photoplethysmographic or Penaz technique, can also be used to measure blood pressure. Like tonometry, it is designed to be used as a CNIBP device. Blood pressure is measured at the fingers using the principle of the “unloaded artery.” A small cuff containing a plethesmograph (similar to a pulse oximeter, but using only near-infrared light) is partially inflated around the finger(s) and maintained at a constant pressure. Pressure variations, along with changes in transmitted light, are used to determine MAP, which is calibrated against a standard cuff placed on the same limb. Comparisons between oscillations in the finger cuff and the arm cuff are used to estimate systolic and diastolic pressures. Although there have been improvements in recent years, estimates of systolic and diastolic pressures can be over- or underestimated. With the exception of tonometry, these technologies all rely on the use of a blood pressure cuff. A blood pressure cuff is basically an inflatable bladder encased in a sleeve that is wrapped circumferentially around an arm or leg. The accuracy of readings obtained is dependent on the selection of the correct cuff size. Although there is no industry standard for cuff sizes, most manufacturers follow the American Heart Association (AHA) guidelines, summarized in Table 33.3. It is critical to note that cuff sizes are designated based on the size of the internal bladder, not the external sleeve. A cuff that is labeled “long” is not the same as one labeled “large.” A long cuff has extra sleeve material to wrap around the limb, but the bladder dimensions
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TABLE 33.3 AHA BLOOD PRESSURE CUFF SIZE RECOMMENDATIONS EXTREMITY CIRCUMFERENCE (CM)
CUFF NAME
5–7.5
Newborn
7.5–13
Infant
13–20
Child
17–25
Small adult
24–32
Adult
32–42
Wide/large adult
42–50
Thigh
remain the same as a regular cuff of the same size. Using the correct cuff size is essential for accurate readings. A cuff that is too small will result in false high readings and one that is too large will result in false low readings. Using too small a cuff can also be very painful for an awake or lightly sedated patient. Most manufacturers include a printed index range on the sleeve as a visual confirmation of cuff size, making it easier to avoid size errors. If there is no index range, make sure that the end of the blood pressure cuff falls within the middle 75% of the bladder when it is applied. Proper cuff placement is also critical for accurate readings. In general, proper placement is approximately 1″ above the elbow for an arm cuff, 5″ below the elbow when using the forearm, and just below the groin fold for a thigh cuff. Most manufacturers include an “artery” marker in the center of the bladder. Placing this marker directly over the artery to be occluded results in even compression of the artery and helps limit artifact. Blood pressure cuffs can be either disposable or reusable. Reusable cuffs are classified as “noncritical” items for disinfection purposes, and low-level disinfection between patients is suitable as long as the cuff is placed over intact skin or does not become soiled with blood or body fluids. Any reusable cuff that does become soiled should be treated with high-level disinfection or sterilization. Regardless of the treatment used, make sure the cuff has dried completely before using it on the next patient. With the exception of tonometry, potential problems and related troubleshooting are similar
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regardless of which technique is used. Problems will usually present as an inability to obtain a reading. The basic troubleshooting questions to answer are as follows: • • • •
Is the cuff the correct size? Is the cuff placed correctly? Are all connections tight? Is a member of the surgical team leaning against the cuff? • Does the patient have excess muscle movement? If this sequence does not solve the problem, consider replacing the blood pressure cuff first. If replacing the cuff does not solve the problem, replace the tubing that connects the cuff to the monitor. If you are still unable to obtain a pressure, the problem may be internal to the monitor or related to the physical status of the patient. Consider a different cuff location, monitor, or technique.
■ TEMPERATURE (ASA STANDARD V) Temperature monitoring is key to the concept of temperature management. Consequences of unintended hypothermia can include increased oxygen demand, myocardial ischemia, platelet dysfunction, impaired renal function, delayed wound healing, and increased infection and mortality rates. Unintended hyperthermia can result in multiorgan failure. Temperature is normally expressed in degrees Celsius (C) rather than Fahrenheit (F) in anesthesia and critical care settings. Most monitors allow temperature to be displayed in either format, but the following formulas can be used to covert from one format to another: C = F − 32 × 5/9 and F = C × 9/5 + 32. Like arterial blood pressure, temperature is not constant throughout the body. For example, a core temperature of 36°C can result in temperature site readings of oral, 35.8°C; rectal, 36.5°C; axillary, 34.5°C; and skin surface, 33°C. Because of this, monitors should be labeled with temperature site whenever possible. Common monitoring sites for anesthesia include nasopharyngeal, esophageal, rectal, bladder, tympanic membrane, pulmonary artery (PA) catheter, and skin. Less common are oral, axillary, and vaginal. The most reliable site for monitoring core temperature is via the PA catheter.
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Most temperature monitoring is achieved using electronic and liquid crystal technologies. Electronic methods rely on either a thermistor “400 Series” probe or a thermocouple “700 Series” probe. Thermocouple probes are more accurate, but more expensive, so they are usually purchased when a reusable probe is used. Thermistor probes are less accurate, but significantly less expensive, and are normally purchased when disposable probes are used. Although most modern patient monitors are designed to work with either 400 Series or 700 Series probes, you may encounter some that only work with one or the other. Monitors that work with either series will have a soft key or physical switch that is used to select the correct type. Liquid crystal technology is used for disposable skin sensors. These are normally used on very short cases or as an adjunct to regional anesthesia. Interference with temperature monitoring is rare and primarily limited to heat sources affecting skin surface sensors. Temperature probes can be either disposable or reusable. Reusable probes are classified as “semicritical” items for disinfection purposes, and high-level disinfection between patients is suitable as long as the probe does not become soiled with blood or body fluids. Any reusable probe that does become soiled should be treated with high-level disinfection or sterilization. Regardless of the treatment used, make sure the probe has dried completely before using it on the next patient. Troubleshooting for temperature monitors is usually straightforward. If you have either no reading or an erratic reading, check the following to solve the problem: • Is the monitor correctly set for the series of probe being used? (check the 400/700 switch or soft key.) • Are all connections tight? • Is there an electronic short or frayed wiring? If checking these does not solve the problem, replace the probe/sensor. If replacing the sensor does not resolve the issue, replace the cable that connects the probe to the monitor. If that does not resolve the problem, consider an internal fault in the monitor. A spare module or standalone temperature monitor should be readily available for these needs.
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REVIEW QUESTIONS 1. You are called into the operating room (OR) and told that the pulse oximeter is broken. You look at the monitor and see that the reading is lower than expected with little, if any, waveform present. The likely cause(s) could be A) Cold body part B) Vasospasm C) Reduced cardiac output D) Patient disconnect E) A, B, and C only Answer: E. A patient disconnect would result in no reading and absence of waveform. All others could be likely causes of the scenario.
2. An elevation in the baseline of a CO2 monitor can be due to A) A faulty expiration valve on the ventilator B) Inadequate inspiratory flow C) Exhausted CO2 absorbent D) Insufficient expiratory time E) All of the above Answer: E. All of the above can cause an elevation in the CO2 baseline.
5. The most reliable site for monitoring core temperature is A) Esophageal B) Skin C) Oral D) PA E) Nasopharyngeal Answer: D. When measuring core temperature, the most reliable site is via the PA catheter.
SUGGESTED READINGS American Society of Anesthesiologists. Standards for Basic Anesthesia Monitoring 2011. Available at: http://www.asahq.org/For-Members/ClinicalInformation/Standards-Guidelines-and-Statements.aspx. Centers for Disease Control and Prevention. Guideline for Disinfection and Sterilization in Healthcare Facilities. 2008. Dorch JA, Dorsch SE. Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:776–795. Geddes LA. Cardiovascular Devices and Their Applications. New York, NY: John Wiley; 1984.
3. A three-lead EKG harness commonly consists of A) RA (white), LA (black), V (brown) B) RA (white), RL (green), LL (red) C) RA (white), LA (black), LL (red) D) RA (white), RL (green), V (brown) E) None of the above Answer: C. The RA, LA, and LL make up the common three-lead harness. The RL and V lead are added to make up the common fivelead harness.
4. Using a blood pressure cuff that is too small for the patient can result in false high readings. A) True B) False Answer: A. Conversely, a blood pressure cuff that is too large for the patient can result in false low readings.
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CHAPTER
34
Vascular Access Equipment and Setup MicHael Moore and Izumi Harukuni ■ INTRODUCTION Anesthesia can be administered in multiple ways; however, regardless of the type of anesthesia, it is imperative to obtain vascular access to provide anesthesia care. The purposes of obtaining vascular access during anesthesia are (1) administration of fluid, (2) administration of medications, (3) administration of blood products, (4) blood sampling for laboratory testing, and (5) monitoring of hemodynamic parameters. Different types of vascular access may be required for each of these different activities. This chapter discusses the preparation, technique, and complications of different types of venous and arterial access. In addition, the associated equipment, setup, and troubleshooting for each technique are discussed as well.
■ PERIPHERAL INTRAVENOUS CATHETER Definition and Indications Peripheral intravenous (PIV) catheters are short, thin tubes (catheters) that are inserted into a peripheral vein (intravenous [IV]). Peripheral veins are those veins that are on, or near, the surface of the arms, hands, legs, and feet. The major deep vein in the leg and groin region is the femoral vein (FV), and it is considered part of the central venous system. PIV catheters are commonly used as they are usually easy to insert and associated with minimal complications. About 95% of hospitalized patients have PIV catheters. PIV catheters are usually placed in peripheral and superficial veins in the upper extremities. In some patients, they need to be placed in the lower extremities due to limitations or difficulty in obtaining access in the upper extremities (e.g., bilateral arm surgery may prevent extremity access; all the peripheral veins in the arms have been damaged).
PIV catheters vary in length. According to Poiseuille’s law, the rate of fluid flow that can be delivered through a tube is related to the diameter and the length of the tube, the pressure gradient (from one end of the tube to the other), and the viscosity of the fluid moving through the tube. The effect of the diameter of the tube on fluid rate is exponential to the fourth power. This means that a doubling in the diameter of a tube would result in a 16-fold increase in fluid rate (24 = 16). Therefore, small changes in the diameter of a PIV catheter will result in large changes in how fast fluid can flow through the catheter. The flow rate in a tube is inversely proportional to the length of the tubing. For example, doubling the length of the tubing cuts the flow rate by half. Taken together, fluid runs faster through a larger diameter and shorter length catheter. By convention, most catheters and needles in health care are sized according to the “Stubs iron wire gauge system,” which was first used to quantify the thickness of metal wire. In this inverse system, the smaller the “gauge,” the larger the diameter. When labeling catheters, the gauge is shortened to G. For example, a 14-gauge (14G) catheter is larger than a 20G catheter (Fig. 34.1). This can be confusing because there is a difference if you are referring to the actual gauge of a catheter or the Stubs gauge of a catheter. The actual gauge of a 14G catheter is approximately 2 mm. The actual gauge of a 20G catheter is 1 mm. When someone asks you for a larger gauge catheter, which should you get, the 14G or the 20G? By convention, when health care providers refer to smaller or larger “gauge,” they are referring to the actual size of the needle or the catheter. When they specify a number with gauge (e.g., 14G), they are referring to the Stubs gauge. Depending on the situation and purpose, 297
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■ FIGURE 34.1 Peripheral intravenous catheters. BectonDickinson Insyte Autogurad catheter in different sizes. The yellow catheter is 24G, the blue is 22G, the pink is 20G, the green is 18 G, the gray is 16G, and the orange is 14G.
the practitioner will decide on the size of the PIV catheter depending upon the desired potential flow rates required and the viscosity of the fluid to be used. Blood is much more viscous than saline and would run more slowly through the same tubing. If blood products or large volumes of fluids may need to be administered in a case, the anesthesia provider would opt for larger bore (smaller G) catheters. The indication for the placement of PIV catheters include • • • •
Administration of fluids Administration of medications Blood transfusion Blood sampling for laboratory testing
Contraindications for PIV catheters depend upon the site where the IV line will be placed. Common contraindications include • Massive edema • Burns or injury • Insertion site distal to the potential vascular injury (i.e., access in lower extremities when the patient sustained abdominal or thoracic trauma) • Local infection • Existing arteriovenous fistula • Previous radical axillary dissection
PIV Catheter Equipment All of the necessary materials and equipment should be available, prepared, and assembled at
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■ FIGURE 34.2 Setup for peripheral intravenous catheter placement.
the bedside prior to placement (Fig. 34.2). Basic equipment includes the following: • Appropriate size IV catheters (14–24G), at least two or three in each size. The full range of catheters should be available in the anesthesia cart; however, in most circumstances, it is not necessary to bring the full range of sizes to the bedside during a catheter insertion. The providers will have chosen a particular size they would like to insert. That size, and a couple of smaller catheters, should be ready at the bedside. The smaller catheters are ready in case the provider cannot locate a vein that can accommodate the desired size catheter. Two or three sizes of each of the appropriate catheters should be available in case more than one attempt at cannulation is necessary or a catheter is defective or inadvertently becomes unsterile. • Nonlatex tourniquet • Alcohol or chlorhexidine swab • Sterile or nonsterile gauze • Transparent dressing • Adhesive tape • IV fluid bag with IV infusion set (flushed with fluid) or saline lock (short tubing flushed with saline and saline syringe). Note that there are different types of IV sets that are used for different purposes. See Associated Equipment section below for additional information. • 3-mL syringe with a small needle (25G or 30G) and 1% lidocaine if local anesthesia at the insertion site is desired. • In rare cases, an ultrasound or other device may be necessary to assist in peripheral vein location.
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To prepare the IV infusion set, first, remove the protective cap on the IV fluid bag. Close the flowregulating clamp on the infusion set and insert the uncapped “spike” into the receptacle on the fluid bag. When “spiking” the bag, care should be taken that the spike on the infusion set remains sterile and does not touch anything other than the inner portion of the receptacle on the fluid bag. Once spiked, hold the fluid bag and drip chamber in an upright position and fill the drip chamber with fluid up to half of the chamber by squeezing the drip chamber a few times. Then, hang the bag on an IV pole and slowly open the regulating clamp to flush the entire tubing with fluid. While flushing, tap the tubing, stopcocks, and ports to remove small air bubbles trapped in these places. It is imperative to de-air the tubing when preparing the IV set for pediatric patients or adults with an intracardiac shunt (i.e., patent foramen ovale, atrial or ventricular septal defect) as even a small amount of air entering systemic circulation may cause an air embolism to vital organs.
Technique for Placing PIV Catheters Choosing the site and appropriate superficial vein is the first and most important step in placing PIV catheters. Superficial veins in upper extremities are the first choice unless there are contraindications. Generally, the most distal peripheral sites are chosen as the first attempt. This allows the practitioner to move to a more proximal site if the initial attempt fails (cannulating a vein distal to a recent prior attempt that drains the same vein can lead to fluid and medications leaking out of the prior cannulation site). In situations requiring large-bore IV access, such as trauma or cases in which the provider is anticipating significant blood loss, the median cubital vein is often preferred. These veins are usually large and stable. Unfortunately, infiltration (fluid or medications leaking out of the vein) can be harder to detect. In the circumstances where the veins of the upper extremities are not accessible, the saphenous vein of the lower leg or the veins of the lower leg and feet are the next choices. In difficult cases with poor peripheral venous access, the use of transillumination or an ultrasound-guided technique may be necessary. As with any other invasive procedures, universal precautions should be applied in placing PIV catheters (see Chapter 24). Because
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infection rates from PIV catheters are very low, full sterile technique is not necessary; however, the site is still prepped with alcohol and care is taken to maintain the sterility of the catheter and needle. Nonsterile gloves must be worn, and eye/ face protection is recommended. A gown should be considered in special circumstances.
PIV Catheter Procedure • Tightly apply a tourniquet to the extremity above the site (Fig. 34.3). • Identify the vein by visualization and/or palpation. • Cleanse the site with alcohol or chlorhexidine using an expanding circular motion. • In awake patients, consider infiltrating local anesthesia (i.e., 1% lidocaine with a 27 or 30 gauge needle) in the subcutaneous tissue at the insertion site, being careful not to enter the vein. • Unpack the needle catheter and inspect for any defect. • Insert the catheter (you will observe blood in the flow back in the needle hub chamber) and then advance the needle catheter a short distance into the vein (2–3 mm). Slide the catheter off the needle into the vein. • Release the tourniquet and retract the stylet needle (any sharp material should be discarded in the appropriate sharp container, including safety needles). Blood in catheter hub should be observed (Fig. 34.4). • Connect the IV set tubing or saline flush and ensure the correct placement of the IV catheter (observe free drip of fluid in the drip
■ FIGURE 34.3 Peripheral intravenous catheter placement: Preparation. The tourniquet is placed proximal to the venipuncture site.
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■ FIGURE 34.4 Peripheral intravenous catheter placement: Completing insertion. Once the catheter is in the vein, release the tourniquet. The blood in the hub of the catheter confirms that the catheter is in the correct position.
■ FIGURE 34.5 Peripheral intravenous catheter placement: Saline flush. The catheter is secure with Tegaderm and the tubing is attached. The blood is now flushed with saline.
chamber or flush without resistance or signs of infiltration). • Secure the catheter with a clear adhesive dressing (e.g., Tegaderm). The clear dressing allows for future inspection of the insertion site (Fig. 34.5) (some practitioners prefer to place a piece of tape over the catheter hub before applying the adhesive dressing). • Secure the IV tubing with tape over the skin. After applying the tape, check the security of the tubing, the connection to the catheter hub, and if fluid is infusing properly. • Adjust the flow rate with a regulating clamp.
• Local infection at the insertion site • Phlebitis/thrombophlebitis: inflammation or clotting (thrombosis) of the vein. Infiltration: leakage of fluid or medication into the subcutaneous tissue. Depending on the pH and other properties of the fluid or medication that has infiltrated into the subcutaneous tissue, infiltration may cause inflammation or even tissue necrosis. If a large volume of fluid infiltrates, it may result in compartment syndrome (severe swelling in the extremity, causing compression of blood vessels and potentially cutting off the blood supply to the extremity or tissues).
Removing PIV Catheters When a PIV catheter is no longer required, it is malfunctioning (infiltrating or occluding), or any complication is identified, the catheter should be removed. • Stop fluid infusion by occluding the regulating clamp. • Remove the tape and Tegaderm. • Place gauze over the IV site and remove the catheter while applying gentle pressure to the insertion site to stop any bleeding. You may need to apply pressure for 3–5 minutes until bleeding stops. Then, secure the gauze over the site with tape.
Complications of PIV Catheters Complications related to PIV catheters include the following: • Bleeding from the vein may result in bruises or a hematoma.
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Troubleshooting PIV Catheters Regardless by whom and where PIV catheters are placed, monitoring for proper functioning and any signs of complications should be performed on a regular basis. • Patient response: If the patient does not respond as expected to a medication administered through a PIV catheter, this may be the first sign that the IV is obstructed/kinked or has become disconnected or dislodged or is infiltrating (the medication is going into the subcutaneous tissue and not the vein). • Inspect the IV bag to make sure that it is not empty. • Inspect the insertion site for signs of infection or infiltration. • Inspect the fluid flow rate by observing the drip chamber (flow rates are frequently adjusted during cases and the provider may
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forget to return the flow rate to a desired level after making an adjustment). Also, checking that the IV fluid is flowing normally is reassuring that the IV line has not become disconnected or infiltrated. • Check the drip chamber to make sure it is half full and air cannot get into the infusion tubing. • It is also wise to keep IV lines labeled and untangled to prevent the injection of medications or infusions into the wrong IV. Administration ports should be readily accessible.
■ CENTRAL VENOUS CATHETER Definition and Indications “Central lines” or central venous catheters (CVCs) are invasive catheters placed directly into the patient’s central venous circulation. There are a variety of locations, methods of placement, and types of catheters available for use depending on the clinical circumstance. The choice of location and type of line can have a dramatic impact on proper patient care. Prior to setup, confirm the desired line type and location with the placing provider. Ideal placement of a central line leaves the catheter tip at a location in the superior vena cava, approximately 3–5 cm above the right atrium (RA), or the cavoatrial junction. This is always confirmed by chest x-ray some time after insertion. This location allows administration of medications with negligible circulation times so as to speed their onset. Based on their presence in the central circulation, central lines are a convenient location for blood sampling (discussed elsewhere in this chapter). With all blood returning to the heart via the inferior and superior vena cavae, the unique location of central lines also allows sampling of mixed venous blood for determination of SCVO2, or central venous oxygen saturation. While the uses of this laboratory value are beyond the scope of this chapter, it is important to be aware of this if assisting in blood sampling (see Chapter 9). The most common site for placement of a central line remains the internal jugular vein (IJV) in the neck. From the right side of the neck, the cavoatrial junction lies at a depth of approximately 16–18 cm from the right and 19–21 cm from the left side of the neck of adults. This difference is important to note as certain catheters may not have sufficient length for proper placement in the vein if using the left rather than
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the right side. Importantly, subclavian insertion locations affect the length of the catheter insertion similarly. Using a subclavian central line approach, the cavoatrial junction lies at a depth of approximately 13 cm from the right and approximately 16 cm from the left side of the chest wall (see below for proper placement location on the chest). A nice trick to estimate proper depth can be done by placing a catheter or a piece of string on the patient’s chest from the insertion site to approximately 2–3 cm below the sternomandibular junction and then measuring the length. While it is possible to place these catheters using physical landmarks, current recommendations are that internal jugular lines be placed using ultrasound guidance. The use of ultrasound in the placement of the central lines has been found to decrease catheter-related complications and time of insertion in some studies.
Central Venous Anatomy There are multiple locations for central line placement. This chapter provides brief anatomic descriptions of the three most common approaches. Internal Jugular Anatomy The IJV is the primary draining vein from the head and leaves the skull at the level of the jugular foramen. It follows into the neck, entering the carotid sheath along with the common carotid artery, vagus nerve, and deep cervical lymphatics (Fig. 34.6). The vein traverses below and medial to the sternocleidomastoid (SCM) muscle, to enter the anatomic triangle bound by the two muscle bodies of the SCM and the clavicle (an important fact for placing central lines). The IJV then joins with the subclavian vein (SCV) to form the innominate vein near the medial edge of the anterior scalene muscle. The innominate vein then follows into the superior vena cava entering the heart. Subclavian Vein Anatomy Primarily draining the upper extremities, the SCV is a continuation of the axillary vein. Importantly, it is attached by fibrous tissue to the posterior aspect of the clavicle for approximately 3–4 cm. These attachments do not allow the vein to collapse even in severely hypovolemic patients, making this technique beneficial in such situations. After passing medial to the clavicle, the SCV joins the IJV to form the innominate
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Digastric muscle (anterior belly)
Mandible Mylohyoid muscle Stylohyoid muscle Hyoid bone
External carotid artery Internal carotid artery
External jugular vein Thyroid cartilage
Superior thyroid vein
Sternocleidomastoid
Common carotid Left vagus nerve
Cricoid cartilage
Internal jugular vein
Sternothyroid muscle
Deep cervical lymph node
Brachial plexus
Middle thyroid vein
Trapezius muscle
Brachial plexus Thoracic duct
External jugular vein
Subclavian vein
Omohyoid muscle (inferior belly)
Thyroid gland
Trachea
Recurrent laryngeal nerve L. brachiocephalic vein
Inferior thyroid vein Anterior view
■ FIGURE 34.6 Internal jugular vein anatomy. (With permission from Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999.)
vein at the level of the sternoclavicular junction, then passing into the heart as the superior vena cava (Fig. 34.7). It is important to note that the subclavian artery, brachial plexus, phrenic nerve, and internal mammary artery lie just posterior to different regions of the SCV and are separated by the anterior scalene muscle, making damage to these structures a potential complication. Just inferior to the SCV lie the pulmonary apex and pleura, creating a higher potential for pneumothorax with this technique. Femoral Anatomy The FV anatomy is quite simple, which makes accessing this vein easier than many others. As a continuation of the popliteal vein from the lower extremity, the FV enters the femoral sheath in the thigh and continues to the level of the inguinal ligament (Fig. 34.8). Passing underneath this ligament, the FV becomes the external iliac vein, which then travels along the psoas muscle to join with the contralateral external iliac vein, forming the inferior vena cava. The femoral approach takes place in the inguinal region at the level of the femoral sheath. It is important to note that the femoral artery and nerve lie just lateral to the
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FV in this region, allowing for potential damage to these structures with a femoral access technique. The term NAVeL is a useful mnemonic for remembering the relative femoral anatomy. From lateral to medial —Nerve, Artery, Vein, empty, Lymphatics (Fig. 34.8).
CVC Types Triple-Lumen Catheter (Fig. 34.9) Size:
Length: Benefits:
Negatives:
7-French catheter with three lumens (proximal white and blue 18G, distal brown 16G) 15, 20, and 30 cm Provides ability to infuse multiple medications simultaneously and monitor the central venous pressure (CVP) Provides access to ports for blood sampling Does not allow rapid infusion of IV fluids
CVC Introducer (Fig. 34.10) Size: 8–10
Length: Benefits:
French single-lumen catheter typically used as a sheath for hands-free triplelumen or pulmonary artery catheter (PAC) insertion. It has an infusion side port. 10 cm Provides ability to rapidly infuse large amounts of IV fluids or blood products
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Sternocleidomastoid muscle (clavicular head) Sternocleidomastoid muscle (sternal head)
Anterior scalene muscle Clavicle
Index finger in jugular notch of manubrium
Right axillary vein
Superior vena cava
Right axillary artery Right subclavian artery and vein
■ FIGURE 34.7 Subclavian vein anatomy. (With permission from Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999.)
Negatives:
through the infusion side port. The main valved channel can be used to insert a PAC or hands-free catheter. Larger dilator with increased risk of injury to the cannulated vessel, especially if inadvertent intraarterial cannulation. By itself, it only provides one port for infusion. Insertion of a secondary catheter (hands-free triple-lumen or PAC) into the main introducer lumen decreases the flow rates that can be delivered through the infusion port.
Hands-Free CVC (Fig. 34.11) Single- or multilumen catheters are inserted through a CVC introducer and locked in place. Size: Length: Benefits:
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Vary, typically a 7 French double or triple lumen is used. 15–30 cm Allows addition of a multilumen catheter to an introducer without additional skin and vessel puncture.
Negatives:
Can be removed, while leaving the introducer in place (reduces the risk of CVC rupture). When inserted into a CVC introducer lumen, it decreases the flow rates that can be delivered through the infusion port. The lock is not tight enough and has a tendency to be pulled out with tension.
Peripherally Inserted Central Catheters These are longer, thin catheters typically placed by IV therapy teams in the hospital when longterm IV access is required or the patient has difficult venous access. As the name implies, they are placed peripherally, typically in the antecubital, basilic, or cephalic veins. Size: Length: Benefits:
2–6 French (adult and pediatrics) Vary by individual (typically 35–45 cm) Provides long-term venous access
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Anterior superior iliac spine
Inguinal ligament
Iliacus fascia and iliacus Deep circumflex iliac artery
Lateral cutaneous nerve of thigh
Femoral ring Lacunar ligament
Superficial circumflex iliac artery
Femoral
Pectineus and pectineal fascia
Nerve Artery Vein
Pubic tubercle
Deep artery of thigh
Obturator nerve, anterior division 1st perforating artery
Sartorius
Adductor longus
Rectus femoris
Gracilis Great saphenous vein
Iliotibial tract
Anterior femoral cutaneous nerves
■ FIGURE 34.8 Deep femoral vein anatomy. (With permission from Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999.)
Negatives:
without additional punctures Provides access to central circulation without risks of CVC placement Length and size limit flow rates (cannot be used for rapid infusion). Catheters are prone to clots and kinking.
Tunneled CVC Ports These are surgically placed, most often for infusion of chemotherapy and other caustic
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medications for long-term use. The infusion port is usually placed under the skin on the chest wall and can be accessed by placing a needle through the skin.
CVC Indications • • • •
Delivery of vasoactive medications Monitoring of intravascular volume Access for frequent blood draws Access for PAC
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■ FIGURE 34.9 Triple-lumen central venous catheter.
■ FIGURE 34.11 Hands-Off double-lumen central venous catheter.
• Inability to obtain peripheral venous access • Access for special CVC for potential aspiration of a venous gas embolus • Access for insertion of cardiac pacemaker wires or catheters • Access for long-term chemotherapy or parenteral nutrition • Access for dialysis or plasmapheresis • Infusion of medications that are irritating to peripheral veins
• CVC or CVC introducer
• 0.032″ diameter threading wire (straight of J-tip), usually contained within a special sheath • 7-French dilator • Scalpel • 18G thin-walled needle • 22G “finder” needle • 16G or 18G catheter-over needle • 10- to12-mL syringe (may be a special syringe that allows placement of the wire through the plunger) • Suture (possibly straight or curved) • Needle driver • Caps for infusion port • Gauze and sterile dressing material • Manometry tubing (may or may not be included in kit) • Large sterile drapes (may or may not be included in kit) • Prep sticks and solution (may or may not be included in kit)
■ FIGURE 34.10 Sheath introducer.
■ FIGURE 34.12 Central venous catheter insertion kit.
CVC Equipment Much of the equipment required for central venous access is contained in specialized kits. Contents of CVC kits vary slightly according to the type of catheter included in the kit. In addition, many manufacturers allow institutions to customize the contents of the kits. A description of a generic kit is included below. Generic CVC Kit (Fig. 34.12)
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• Local anesthetic (1% lidocaine), 25G needle, and a 5-mL syringe (equipment for local anesthetic infiltration may or may not be included in the kit) Additional equipment for CVC insertion that is usually not included in the kit: • Linear-array ultrasound with nonsterile ultrasound gel (nonsterile gel may be used for a “prescan” performed prior to the actual procedure). Sterile ultrasound gel is required for the actual procedure. • Sterile gown, mask, gloves • Sterile towels and sterile gauze pads • Pressure transducer setup (if needed) • Mobile table for setup of equipment • Sterile saline flushes • Sterile sleeve for the ultrasound probe • Sterile ultrasound gel • Additional sterile caps
Technique for CVC Insertion
•
•
The first steps are to assemble and prepare the necessary equipment for CVC placement. These steps are described below:
•
• Position the patient in 15 degrees of Trendelenberg for SVC or IJV placement (increases the size of the veins). Confirm with the provider if the Trendelenberg position is desired. • Turn on the ultrasound machine and place in position for easy viewing by provider. • Place a mobile table on the side of the provider’s dominant hand for ease of access. • In sterile fashion, open a central line kit, making sure not to touch the contents. Often, the providers will organize the contents of the kit how they prefer once it is opened. In other institutions, the anesthesia technician will don sterile gloves and organize the kit contents. • Place two sterile saline flushes and sterile ultrasound sleeve and gel onto the sterile field. • Some providers prefer to “prescan” the anatomy with the ultrasound before prepping the patient. If so, turn on the ultrasound, place a small strip of gel on the probe and hand to provider. • Once the “prescan” is finished, wipe gel off area and ensure the region is clean and clear of any debris. • If placing in the IJV, turn the patient’s head slightly to the contralateral side. It may also
•
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be necessary to remove the patient’s pillow if it is tilting the patient’s head too far forward or is in the way of the neck. If the patient is intubated, the circuit tubing should be moved so that it is out of the way and secure. In all of these steps, care should be taken to avoid dislodging the endotracheal tube. Using sterile technique, prep the region for at least 30 seconds. For IJV: prep from bottom of the ear to the clavicle and from the trachea to as far lateral as possible (Fig. 34.13). For SCV: prep from 1 to 2 inches above the clavicle to just above the nipple and from the anterior shoulder to the sternum. For FV: prep from just below the hip to approximately 6 inches below the inguinal crease and from medial groin to the lateral thigh. Assist the provider with gowning and gloving. Tie the gown in the back. Do not touch the provider’s arms, hands, or chest. Make sure the provider is wearing a mask and loose ties are not hanging down. Assist with draping, ensuring to only touch the underside of the drape when it is passed to you. Gently pull the drape until completely opened and the body covered (Fig. 34.14). When the provider is ready, place a small strip of nonsterile ultrasound gel on the probe. The provider will place his or her hand into the sterile sleeve and will grab the probe from you. As he or she passes the end of the sleeve to you, grab the very end and pull along the length of the cable, making sure no uncovered portion of the cable touches the sterile
■ FIGURE 34.13 Preparation of internal jugular vein: The skin is prepped with tinted chlorhexidine swab from just below the right ear and chin to the right nipple crossing the midline.
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■ FIGURE 34.14 Full-body drape. Patient’s entire body should be covered with a drape.
field (Fig. 34.15). Refer to Chapter 38 for the details on the operation of the ultrasound machine and transducer. The provider may ask for color Doppler during the procedure to confirm the location of vascular structures. • See below regarding the specifics of cannulating the vein and placing the catheter. • Once the vein has been entered and the guide wire is in place, the provider may ask you to take a picture with the ultrasound machine,
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■ FIGURE 34.16 This photograph is the still shot of the ultrasound machine screen that demonstrated the presence of the wire in the internal jugular vein. The photograph is taken and placed in patient’s chart for the documentation. This is required for the billing of ultrasound-guided central venous catheterization.
showing the wire inside the vessel (Fig. 34.16). In many institutions, the picture is printed and placed in the patient’s chart. Ask the provider if a picture will be required and what to do with the print. In some institutions, the provider will want a personal copy of the print for anesthesia billing. • During insertion, the providers’ attention may be focused on the line placement itself. Periodically, review the patient’s status on the monitors and notify the provider of any significant changes in blood pressure, oxygen saturation, machine alarms, heart rhythms, etc. Be prepared to assist with drug administration (vasopressors or anesthetics) or adjustment of anesthetic agents if the provider requires it. • After the procedure is completed, carefully remove the drapes, making sure not to pull the line out and to avoid extubating the patient. • Connect the CVP transducer tubing to one of the flushed ports on the central line (preferably one of the 18G lumens), open all stopcocks, and zero the CVP transducer. Review the waveform and pressure reading (Fig. 34.17).
Provider Technique for Placing a CVC
■ FIGURE 34.15 Ultrasound transducer is covered in sterile sheath for use in the sterile field.
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The details of the placement of the central line are intended to give the anesthesia technician a basic understanding of the procedure. This information will help you to be able to assist the provider as needed, particularly if in your institution, the anesthesia technician gowns and
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CVP a
v
■ FIGURE 34.17 Central venous pressure normal waveform. (With permission from Springhouse. Lippincott’s Visual Encyclopedia of Clinical Skills. Philadelphia, PA: Wolters Kluwer Health; 2009.) CVP, central venous pressure; ECG, electrocardiogram.
gloves and actively hands in sterile equipment to the provider. After the setup above is completed and all ports of the CVC are flushed with saline, the provider will identify the vein with the sterile ultrasound probe in one hand and a needle/syringe in the other hand. Details change depending upon slight variations in technique. Here we describe the Seldinger technique (the catheter-over needle technique) using an 18G catheter and needle (if the kit does not contain an 18G catheter over a needle, a regular 2-inch 18G PIV catheter may be opened using sterile technique and placed on the provider’s tray). The needle is advanced with constant negative pressure in the syringe by slightly pulling on the plunger. The provider will monitor the advancement of the needle on the ultrasound monitor. Once a flash of blood is noted in the syringe, the angle of the needle is to be changed to a more shallow angle and the catheter is threaded into the vessel (if the provider is using only the thinwall needle without the catheter, this step will be skipped and the provider will proceed directly to passing the guide wire into the vein through the needle). The needle is removed, covering the end of the catheter with a finger (patients who are breathing spontaneously create negative intrathoracic pressure during inspiration and can entrain air into the circulation through an open catheter or needle). If using manometry, the tubing is connected to the catheter hub and lowered below the head to fill with blood. This tubing is then raised above the head, to confirm
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that the blood column falls slowly and that the pressure in the tubing is consistent with venous pressure (if the artery is accidentally cannulated, the pressure in the tubing will be much higher). Some providers ask to have the manometry tubing connected to a transducer to measure the pressure. The manometry tubing is removed and the wire is advanced into the catheter (and vein) to approximately 15–20 cm, and the catheter is removed over the wire. A small skin nick is made with the scalpel to make room for the CVC. The dilator is advanced over the wire to open a path for the CVC through the skin and deeper tissues. The dilator is removed over the wire. The CVC is fed over the wire until it almost reaches the skin. In most cases, the wire will need to be pulled back and fed back into the CVC until it emerges from the brown 16G port. Holding the far end of the wire (to avoid losing a wire into the central circulation), the central line is then advanced all the way over the wire and into the vein. The wire is then removed. Each port is flushed with sterile saline once ability to draw back blood is confirmed (many institutions preflush the catheter ports before the catheter is inserted). The ports are capped, the line is sutured in place, and the site is covered with a clear sterile dressing.
Complications Potential complications of CVC insertion include the following: • • • • • •
• • • • •
Hemorrhage Infection Damage to pleura, pneumothorax Arterial damage or arterial cannulation Thrombosis Arrhythmias: The wire can be advanced into the heart and cause an arrhythmia, particularly if it is advanced into the ventricle. A few premature ventricular beats are not uncommon. The wire should be withdrawn until the abnormal beats subside. On occasion, medications or further treatment will be necessary if the arrhythmia is serious (e.g., ventricular tachycardia). Nerve damage Vascular erosion with bleeding into the chest Cardiac tamponade and wall rupture Phlebitis Infection: local site infection or bloodstream infection
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Troubleshooting Most common problems encountered with central lines will be managed by the provider; however, a few common problems and possible solutions are shown in Table 34.1.
■ PULMONARY ARTERY CATHETER Definition and Indications The PAC, also known as the Swan-Ganz catheter named after its inventor, was introduced in 1970 and now is widely used as a diagnostic and monitoring tool in the management of critically ill patients. The PAC is a balloon flotation catheter. It has a small balloon on its tip that is inflated after insertion and floats the catheter along with the blood flow through the vena cava into the right heart. The PAC is then further advanced into the pulmonary artery (PA). If balloon flotation is unsuccessful, it can be placed with fluoroscopy or ultrasound at the bedside. Basic features of PACs are illustrated in Figure 34.18. The length of the catheter is 110 cm and the diameter is 7–8 French depending on the number of lumens and additional features. The basic catheter has at least three lumens, a distal port near the tip, a proximal port 30 cm from the tip, and a port for inflating the balloon. Inflation of more than 3 mL of air into the balloon port can rupture the balloon. It is important not to confuse the ports and inadvertently attempt to inject
■ FIGURE 34.18 Pulmonary artery catheter. This photograph shows Hospira Opticath thermodilution pulmonary artery catheter. The blue port is the proxymal port, the yellow is the distal port, and the clear is the infusion port. The red tube has a locking system for inflating/ deflating the balloon. This catheter is equipped with a fiberoptic cable to measure mixed venousoxygen saturation (black) and a thermistor (white) for measuring cardiac output by thermodilation technique.
medications or fluids through the balloon port. In addition to the ports, there is a thermistor (transducer that senses the temperature) 4 cm from the tip of the catheter. The newer catheters are equipped with more features such as an extra lumen for infusion or passing temporary pacemaker leads into the right ventricle (RV) (opens at 14 cm from the tip) and a fiberoptic system that allows continuous monitoring of mixed venous oxygen saturation.
TABLE 34.1 TROUBLESHOOTING FOR CENTRAL VENOUS CATHETERS ISSUE
PROBLEM
POSSIBLE SOLUTION
Wire will not thread.
Catheter/needle may not be in vein.
Check for continued flow of blood with syringe again.
Thrombosis in vessel
Repeat needle puncture if needed or change site.
Pulsatile flow in manometry tubing
Accidental arterial puncture
Immediately remove needle or catheter and hold pressure.
One or more lumens will not draw blood back.
Catheter may not be in vein. Clot/kink on catheter. Faulty catheter
Try gentle flush to clear clot and then draw back. Pull back catheter small distance. Replace catheter or change site.
CVP will not zero.
Air bubbles in line Closed stopcocks Kink in tubing. Faulty equipment.
Detach tubing and flush tubing. Open all stopcocks. Straighten tubing. Change CVP cable or transducer.
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PAC functions include the following: • Direct measurement of right atrial pressure (CVP), right ventricular pressure, and pulmonary arterial pressure • Indirect assessment of left atrial pressure via the pulmonary artery occlusion pressure (PAOP) (wedge pressure). This measurement is obtained by properly positioning the catheter in a branch of the PA and temporarily inflating the balloon while the measurement is taken. • Measurement of cardiac output by thermodilution and hemodynamic calculation • Mixed venous blood sampling Because of the potential complications associated with PACs (see below) and the introduction of transesophageal echo to monitor heart function, the indications for placement of PACs have diminished. Commonly accepted indications include • Management of complicated acute myocardial infarction with cardiogenic shock • Management of acute decompensation in severe heart failure • Management of noncardiogenic shock • Diagnosis of pulmonary hypertension Contraindications include • Mechanical prosthesis in tricuspid or pulmonary valve • Tricuspid or pulmonary endocarditis • Presence of right heart mass
■ FIGURE 34.19 Triple-pressure transducer. Each transducer is color coded. The most left is for arterial line (red), the middle is for central venous pressure (blue), and the most right is for pulmonary artery pressure (yellow).
Technique for PAC Insertion 1.
Determine the insertion site: The PAC is inserted most commonly in the IJV or the SCV as the course of venous return to the RA is more straightforward from these insertion
PAC Equipment Although placing the PAC is not complicated and easily done at the bedside, appropriate training and equipment are required. • All equipment needed for CVC insertion as previously described • Two pressure transducers so that pressure can be monitored in both the proximal and distal port (Fig. 34.19) • Introducer kit (8.5–9 French) (Fig. 34.20) • PAC • Thermodilution set (a bag of saline, injector, tubing) and cardiac output cable • Resuscitation equipment and external pacing device (in the event of vascular complications, or life-threatening arrhythmias during insertion (see complications below)
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■ FIGURE 34.20 Sheath introducer kit. The kit contains a 9-French sheath introducer, a dilator, a stopcock and caps, a manometry tubing, syringes, needles, a guide wire, a suture kit, a blade, gauze, dressing, 1% lidocaine (5-mL ampoule), a sterile cover, and a hub cap. Some kits also contain chlorhexidine preps and a full-body drape.
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2.
3.
sites. In the cardiac catheterization lab, the FV is often accessed for right heart catheterization. In addition, fluoroscopic guidance is used in the cardiology suite. Position the patient properly and obtain central venous access with an 8.5-French or a 9-French introducer as described above (Central Venous Access section). Once access is obtained, the operator will remain sterile and an assistant will perform nonsterile tasks. Just prior to the insertion, prepare the PAC. If it is equipped with a fiberoptic system for continuous mixed venous O2 saturation, connect the cable to the module and perform preinsertion calibration. Remove the PAC from the plastic packet and connect the thermodilution cable to the thermistor port. Check for the temperature to display on the monitor screen (should be room temperature before PAC insertion). Place the sterile cover over the catheter and lock it at 100 cm. Connect the pressure tubing from the transducers to each port on the PAC and flush with saline (the distal port for PA pressure, the proximal port is for CVP). If the PAC has an infusion port, connect a stopcock and a 3-mL syringe to the port and flush with saline. Lastly, inflate the balloon with 1.5 mL of air using the syringe provided in the kit (the syringe is equipped with a lock system to prevent overinflation of the balloon) (Fig. 34.21A). Check to see that the balloon has inflated evenly. Deflate the balloon by releasing the syringe plunger.
4.
5.
6.
7.
311
Do not aspirate on the plunger to deflate the balloon. Most PACs have a mechanism to lock the balloon port to keep the balloon inflated (Fig. 34.21B). The operator is now ready to insert the catheter. Place the patient back to flat or in slight reverse Trendelenberg position. Slightly tilt the table to the right. This position assists the operator in floating the PAC into the PA. The operator inserts the catheter thorough the introducer up to 20 cm. Inflate the balloon slowly with 1.5 mL of air and lock the syringe. You should not feel resistance. If you do, stop inflating and notify the provider. Check the monitor for a venous waveform. As the catheter is advanced into the RV, the pressure waveform will change as shown in Figure 34.22. After advancing the PAC 30–35 cm in a normal-size adult, the catheter tip will enter the RV through the tricuspid valve. A pulsatile RV systolic pressure appears. The diastolic pressure is still equal to the RA pressure. Record the RV systolic and diastolic pressures. When the catheter is advanced across the pulmonic valve into the PA, the diastolic pressure rises whereas the systolic pressure remains unchanged. This occurs at around 45–50 cm in normal-size adults. Record the PA systolic and diastolic pressures. The catheter is then slowly advanced in the PA until the waveform changes again where the systolic pressure disappears and the waveform resembles the RA pressure waveform.
■ Figure 34.21 A: Inflating the balloon. The balloon at the tip of the catheter is fully inflated with 1.5 mL of air. Note that the syringe is locked. B: Deflating the balloon. The balloon is deflated when the syringe is unlocked and 1.5 mL of air is back in the syringe.
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■ FIGURE 34.22 Change in the pressure waveform correlates with the position of the tip of the pulmonary artery catheter.
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8.
This pressure is known as the pulmonary artery capillary wedge pressure (PACWP) or the PAOP. At this point, the operator will stop advancing the catheter. Record the pressure and then deflate the balloon by unlocking the syringe. Make sure that the same amount of air (1.5 mL) returns to the syringe without aspiration. If the air does not return, it can be a sign that the balloon has ruptured. The balloon should be deflated at all times while the PAC is left in place in the PA (prolonged inflation can cause PA rupture). Balloon inflation should be reserved for the measurement of PACWP. Inflate the balloon slowly until a wedge pressure tracing appears on the monitor screen. This can occur before the balloon is fully inflated. The catheter can migrate distally into a smaller portion of the artery. Overinflation can cause rupture of a PA. After the PACWP is recorded, the balloon should be deflated. Stretch the sterile cover toward the hub of the introducer and lock it over the hub. Lock the catheter by twisting the locking system on the cover to secure the catheter position.
■ FIGURE 34.23 Applying a sterile dressing over the pulmonary artery catheter insertion site.
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9.
Apply the sterile transparent dressing at the insertion site (Fig. 34.23). 10. The catheter has multiple ports with multiple tubes and cables connected. The weight of these devices can pull on the catheter and dislodge it. To prevent this, secure the proximal end of the PAC with a securing device or clamp (use caution so that you do not clamp the catheter). 11. As noted above, the balloon should be deflated at all times while the PAC is left in place in the PA. The balloon inflation should be reserved for measurement of PACWP. After the PACWP is recorded, the balloon should be deflated.
Cardiac Output Measurement (by Thermodilution Technique) 1.
After the PAC is inserted, connect the thermodilution kit to the injection port (the proximal port) at the stopcock (Fig. 34.24), making sure that there is no air in the fluid bag and the tubing (de-airing the bag and tubing should be done prior to connecting). Stop the fluid infusion from the side port of the introducer to avoid a temperature
■ FIGURE 34.24 The thermodilution kit connected to a pulmonary artery catheter.
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3.
4.
5.
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change. Infusion of cold fluid through the infusion port will interfere with cardiac output measurements. Activate the Cardiac Output window on the monitor screen. Draw the fluid in the syringe (normally 5 or 10 mL, depending on the setup). Press the “Start” button on the monitor. After the beep and the prompt on the monitor screen (“Inject now!”), inject the entire amount of fluid in the syringe quickly but at a steady rate. You will see the curve of the temperature change on the screen. Wait for the monitor to come back to “Ready” before performing the next measurement. Perform three cardiac output measurements and record the average value.
PAC Complications The complications related to PAC placement include the complications related to CVC access as described above. PAC-specific complications are listed below: • Arrhythmias: Atrial or ventricular arrhythmias are the most common complications while placing or removing the catheter. The catheter can touch the endocardium and irritate it. Arrhythmias are normally transient and do not need intervention; however, in some cases, the arrhythmias can be serious (i.e., complete heart block or ventricular tachycardia/fibrillation) and require urgent treatment. • PA rupture: This is very rare but a catastrophic complication that carries a mortality rate of 50%-70%. Risk factors include pulmonary hypertension, hypothermia, and overinflation of the balloon. To minimize the risk, avoid overinflating the balloon and minimize PACWP measurements. • Pulmonary infarction: Overwedging of the catheter (prolonged balloon inflation) or overinflation of the balloon can cause pulmonary infarction. Prolonged inflation of the balloon usually occurs when a PACWP measurement was taken and deflation of the balloon was forgotten. • Catheter knotting: During insertion of the catheter, coiling of the catheter occasionally occurs in the cardiac chambers. This can lead to knot formation. If the catheter does not advance to the next chamber at the expected
length, it should be pulled back with the balloon deflated. Risk factors for knotting include a large RV, multiple attempts at passing the catheter into the PA, and a warm, flexible catheter.
PAC Troubleshooting • Cannot see the venous waveform: Make sure that the pressure transducers are connected to the correct ports and all transducers are zeroed. When any questions arise, withdraw the catheter and recheck by flushing each port. • On the inflation of the balloon, there is excessive resistance and very high pressure appears on the monitor: This could be caused by inflating the balloon in the sheath. Let the balloon deflate and advance the catheter to 20 cm. If it happens at 20 cm, the tip might be against the vessel wall. Deflate the balloon and reposition the catheter by rotating. • The catheter will not advance into the RV or the PA: Position the patient in reverse Trendelenberg position and slightly tilted to the right. Perform a Valsalva maneuver followed by release. This promotes the forward flow of blood in the right heart and can help float the catheter through the right side of the heart. Alternatively, temporarily increasing ventricular contractility by administering an inotropic agent may help advance the catheter into the PA. If still unsuccessful, transesophageal echocardiography may be helpful in guiding the catheter. In rare circumstances, fluoroscopy is necessary. • Unable to obtain a wedge pressure: In some patients, a typical PACWP waveform does not appear even at the maximum depth (60 cm in normal-size adult). The observed waveform could be a prominent v wave from significant mitral regurgitation or simply caused by nonuniform inflation of balloon, but the true cause is unknown in many cases.
■ INTRAOSSEOUS VENOUS ACCESS Definition and Indications The intraosseous route is one of the quickest ways to establish access for fluid infusion, administration of medications, or blood transfusions in an emergency situation, such as pediatric resuscitation. The bone marrow cavity is in continuity with the venous circulation; therefore, it can be used to administer medication, fluid, and blood. tahir99-VRG & vip.persianss.ir
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Intraosseous access can be obtained in the proximal tibia, the distal tibia, the proximal humerus, the femur, the iliac crest, or even the sternum. Intraosseous access sites can be used for blood samples for laboratory tests and cross match. Intraosseous access is indicated when emergent vascular access is required but peripheral or central access cannot be obtained or cannot be obtained in a timely fashion (i.e., life-threatening situation, pediatric emergency). It is not the first choice for access but after attempts to obtain vascular access fail, and time is limited, it can be a life-saving and efficient alternative. Intraosseous access takes less than 2 minutes to obtain. Contraindications include fractured bones, bones with osteomyelitis, and proximal bone fracture (i.e., do not use tibia if ipsilateral femur fracture is present).
Intraosseous Access Equipment • • • • •
Alcohol or chlorhexidine swab Local anesthetics (1% lidocaine) 5-mL syringe 50-mL syringe Intraosseous infusion needle (There are different needle sizes: 14G, 16G, and 18G. Smaller sizes are used for infants (Fig. 34.25). • Specialized intraosseous access tools (e.g., FAST1 and EZ-IO) (Figs. 34.26 and 34.27) are available, which may include special devices or handheld battery-operated drills to drive the needle system through the bone and into the intraosseous space.
■ FIGURE 34.25 Intraosseous infusion needle with Dieckmann modification and standard hub design (Cook Medical). (With permission from Tobias JD, Ross AK. Intraosseous infusions: a review for the anesthesiologist with a focus on pediatric use. Anesth Analg. 2010;110(2):391–401.)
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■ FIGURE 34.26 First Access for Shock and Trauma (FAST1) device (PYNG Medical). (With permission from Tobias JD, Ross AK. Intraosseous infusions: a review for the anesthesiologist with a focus on pediatric use. Anesth Analg. 2010;110(2):391–401.)
Technique 1.
2.
Determine the site. The anteromedial aspect of the tibia is most commonly used as it lies just under the skin and can be easily identified. Palpate the tibial tuberosity. The anteromedial tibial insertion site will be 1–3 cm below and 2 cm medial to the tuberosity.
■ FIGURE 34.27 EZ-IO device (Vidacare). (With permission from Tobias JD, Ross AK. Intraosseous infusions: a review for the anesthesiologist with a focus on pediatric use. Anesth Analg. 2010;110(2):391–401.)
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Wear sterile gloves and clean and then prep the skin by using an outward circular motion. In awake patients, inject local anesthetic in the skin and continue to infiltrate until the periostium (hard surface) is encountered. Position the lower extremity as flexing the knee and placing a pillow or sandbag behind the knee for support. If not available, have an assistant stabilize the lower leg by holding the knee and ankle from the other side. Hold the limb just above the insertion site and insert the intraosseous needle perpendicular to the skin and slightly caudal (toward toes) to avoid injury to the epiphyseal growth plate. Advance the needle with a drilling motion (or with the drill) until loss of resistance is felt when the needle penetrates the cortex of the bone and enters the marrow cavity. This may not be obvious in younger children. Remove the stylet and connect the 5-mL syringe. Confirm the correct position by aspirating blood. Inject 10 mL of saline to check for any signs of infiltration (swelling of limb or increase in resistance). In awake patients, inject 3–5 mL of preservative-free 1% lidocaine into the intraosseous space. The injection should be performed slowly to avoid patient discomfort. If not successful, remove the needle and try another site. Secure the needle in place with a clear dressing, sterile gauze, and tape.
Intraosseous Complications This is a relatively simple procedure, but there is the possibility of serious complications including • • • • •
Tibial fracture Compartment syndrome Osteomyelitis Skin necrosis Microscopic pulmonary fat and marrow embolism (not clinically significant)
The intraosseous needle should be removed as soon as peripheral or central vascular access is obtained, or within 24 hours, to minimize the risk of complications.
■ ARTERIAL LINE (A-LINE OR ART LINE) Definition and Indications An arterial line is an invasive catheter inserted into a peripheral artery that allows the provider to
directly monitor continuous real-time blood pressure changes. This provides beat-to-beat analysis of arterial blood pressure and allows continuous access to blood samples throughout surgery and afterward. The most common site chosen for placement of an arterial line, by far, is the radial artery given its superficial location and ease of access. Other potential sites include the brachial and axillary arteries in the upper extremities and the femoral, dorsalis pedis, and posterior tibial arteries in the lower extremities (see Table 34.2 for risks and benefits of each location). Umbilical and temporal arteries can be used in neonatal patients. Arterial lines are one of the most frequently placed invasive catheters and, as such, anesthesia technicians require a thorough understanding of why and how they are placed. The following indications for placement, general setup, technique for placement, and troubleshooting tips are general recommendations from our institution. Specific protocols may vary by hospital. The anesthesia technician should be familiar with local protocols for arterial line placement and management.
Indications for Arterial Line Placement There are multiple indications for the placement of an A-line including, but not limited to • Expected frequent or abrupt changes in blood pressure or hemodynamic instability • Expected large blood loss during surgery • Frequent need for blood draws (this prevents multiple arterial or venous sticks during surgery) • The need for titration of vasoactive medications to support blood pressure • Assessment of a patient’s intravascular volume status (“Systolic Pressure Variation”) • The need for blood gas monitoring
Contraindications to Arterial Line Placement • Infection or severe scarring at the site of expected placement • Coagulopathy or administration of tissue plasminogen activator • Substantial trauma in the same extremity • Arteriovenous fistula in the same extremity
Arterial Line Equipment (Fig. 34.28) • 20G Angiocath or Arrow kit (extra catheters and kits should be immediately available tahir99-VRG & vip.persianss.ir
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TABLE 34.2 RISKS AND BENEFITS FOR CHOSEN ARTERIAL LINE SITES SITE
BENEFITS
RISKS
Radial
Easiest to access and palpate
Bleeding, infection, thrombosis, embolism, vasospasm.
Good collateral flow
Short catheter can be inaccurate with high-dose vasopressors.
Accurate Brachial
Similar benefits to radial but can be harder to palpate
Often needs ultrasound for placement. Longer catheter needed.
Axillary
Larger diameter
Bleeding, infection, thrombosis, embolism, vasospasm.
Not many benefits
Difficult to place. Higher infection risk. Easy to dislodge.
Often a last-ditch effort
Can damage nearby nerves. Bleeding, infection, thrombosis, embolism, vasospasm.
Femoral
Often used if other sites are inaccessible
Higher risk of infection. Often needs ultrasound for placement. Patient must lie flat.
Dorsalis pedis/ posterior tibial
Can use if there are problems with upper extremity circulation
Bleeding, infection, thrombosis, embolism, vasospasm.
Ease of access and superficial
May not accurately represent systemic pressure.
Good if the provider will not have access to upper extremities during surgery
Easy to dislodge. Bleeding, infection, thrombosis, embolism, vasospasm.
as multiple attempts at cannulation are not uncommon). In addition, smaller catheters may be necessary, particularly in small patients, severe vascular disease, or pediatric patients. For femoral artery cannulation, most institutions have special femoral artery kits that contain a longer catheter, longer access needles, and other supplies. • Pressure transducer (compatible cable, IV pole attachment) • Threadable wire (64 mm) • Rigid pressure tubing with three-way stopcock. Many institutions utilize closed, needle-free, in-line reservoir tubing systems to avoid wasting of patient blood during blood sampling and to decrease the risk of accidental needle puncture. Examples include Safeset
•
• • • • • • •
and VAMP. Confirm with your institution on availability (see “Blood Sampling” section for further explanation). 500-mL bag of 0.9% NaCl. Some institutions utilize heparinized saline (heparin 2 units per milliliter), but it is not standard practice due to increased risk of heparin-induced thrombocytopenia (HIT). Check with your facility. Sterile prep (1% chlorhexidine) Sterile towels, gauze Sterile gloves (sterile gown is optional in most institutions) Mask, eye protection, and cap Arm board attached to operating room (OR) table Wrist immobilizer, tape to secure Pressure bag (capable of at least 300 mm Hg) tahir99-VRG & vip.persianss.ir
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■ FIGURE 34.28 Arterial line setup: The materials needed for arterial line placement are set up on the mobile cart for ease.
• Mobile table for easy access to supplies • Clear sterile dressing (e.g., Tegaderm or Opsite). • Tape • 2-0 silk sutures and needle driver, scissors • 1% lidocaine, 3-mL syringe, 25G or 30G needle • Ultrasound machine, sterile sleeve for the probe (ultrasound is used routinely by some providers and only for special circumstances with others). Ultrasound is almost always used for femoral artery cannulations.
Arterial Line Technique • Prepare transducer and monitoring line. For description of the proper setup of pressure transducers, please refer to “Pressure Transducers” section below. • Wash your hands and use gloves before handling or setting up any invasive device. • Identify the patient using hospital armband and, if able, the patient confirming his or her identity. • Confirm with the provider which artery on which extremity will be used. • Using tape, position patient’s arm on prepared arm board at an abducted position of less than 90 degrees on the OR bed (Fig. 34.29). In some cases, the femoral artery will be used. If so, slightly abduct the leg. • Clean the wrist of any obvious contamination; then, using sterile prep and sterile technique, clean arm for at least 30 seconds to 1 minute with enlarging outward circles. Include the area from the patient’s palm up
■ FIGURE 34.29 Preparation for radial arterial line placement. Patient’s upper extremity is secured on the arm board with tape proximally and distally with a roll under the wrist for extension. Supinate the lower arm so that the palm side of the wrist is in horizontal position. Tape the thumb to add more supination if necessary.
to approximately halfway up the forearm. Be sure to clean both medial and lateral aspects of hand and arm. If using the femoral artery, prep the groin area from 5 cm above the ilioinguinal ligament to the midthigh. • Using sterile gloves and towels, drape patient’s arm exposing only the desired field as shown in Figure 34.30. • Using sterile technique, open Angiocath or Arrow kit as well as sterile gauze. Have wire nearby as well. • Once the provider has successfully cannulated the artery and inserted the arterial catheter, remove the cap from the end of the rigid tubing and hand the provider the tubing without touching the end (Fig. 34.31).
■ FIGURE 34.30 Draping for radial arterial placement.
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■ FIGURE 34.31 Connecting the tubing to the radial arterial catheter.
• Confirm presence of a waveform on the monitor screen. • If desired by the provider, open and hand in the sterile needle driver and sutures. • Zero the arterial line. (See “Pressure Transducer” section.)
Placement of Arterial Line Once the proper setup is complete, the provider will place the arterial line by first palpating the chosen artery. After locating optimal pulse, the provider will insert the intended catheter or Arrow kit at a 30–45-degree angle until a flash of bright red blood is noted in the catheter. Using the Seldinger technique, leave the catheter in the vessel and withdraw the needle. Once pulsatile flow is noted from the catheter, a wire is threaded into the vessel and the catheter is advanced over this until securely inside the vessel. At this point, the wire is removed and pressure is placed just past the arterial catheter to avoid outflow of blood. The tubing is then connected to the catheter. Some providers attempt to advance the catheter needle assembly into the artery (specialized arterial line catheters have a self-contained wire that can be advanced at this point). The catheter is then advanced over the needle and into the artery in much the same way as PIV catheters are placed. If the catheter cannot be advanced off the needle into the artery, the catheter/needle setup is advanced, with the assumption that the operator has passed through the back wall off the artery. The needle is removed and the catheter is withdrawn as described above. When pulsatile flow is obtained, a wire is passed into the artery and then the catheter can be advanced over the wire
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into the artery. The wire can then be removed. Pulsatile flow should still be present. Securely attach the monitoring tubing to the catheter hub and check the monitor for an arterial waveform. For femoral arterial lines, the same basic technique is often utilized, with the exception that it is more common to use ultrasound to locate the artery. Prepare the ultrasound machine and probe as described in the section on central venous access. Prep and drape the patient as described above. The operator will attach a syringe to a needle and advance the needle under ultrasound guidance or by palpation into the artery. The syringe will be removed and pulsatile flow confirmed. A wire is passed into the artery and the needle removed. The specialized long arterial catheter can then be advanced over the wire and into the artery. The wire is removed and pulsatile flow is confirmed. The remaining steps are the same as those described for cannulation of the radial or brachial artery in the arm.
Arterial Waveform Basics The exact morphology of an arterial waveform can explain much about the arterial line setup, patient pathology, and hemodynamics. See Figure 34.32 for an example of a normal arterial waveform. The normal initial upslope indicates early systole with the opening of the aortic valve and left ventricular contraction. The peak indicates runoff after ventricular contraction and occurs during midsystole. The typical notch seen on the downward slope (dicrotic notch) indicates the closure of the aortic valve and indicates the beginning of diastole. The final downward slope indicates further diastole. Common variations in waveforms include both under- and overdampening. In a very simplistic sense, overdampening
■ FIGURE 34.32 Arterial pressure waveform.
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occurs when the transducer cannot sense the pulsation clearly. The waveform tracing will be flattened with a much smaller difference between systolic pressure and diastolic pressure. This can be due to kinked tubing or a kinked catheter, closed or partially closed stopcocks, flexed wrist, air bubbles or clots in the tubing, overdistensible tubing, underpressurized IV bag, vasodilation, or the catheter being up against the wall of the artery. This results in underestimation of blood pressure. Similarly, underdampening is an exaggerated peaked waveform that can overestimate blood pressure. This can be due to excessive tubing length, overly rigid tubing, vasoconstriction, kinked tubing, or partially closed stopcocks. Further explanation of waveform variation can be helpful but is beyond the scope of this chapter.
Arterial Line Complications Commonly cited complications can include bleeding, hematoma, and infection. It is critical to secure the tubing to the catheter as patients can lose blood upward of 500 mL/min if an arterial line becomes disconnected. Potential, but
less common, complications include damage to nearby structures (veins, nerves, tendons, etc.), decreased hand perfusion, air embolism, thromboembolism, and even compartment syndrome with hidden bleeding.
Arterial Line Troubleshooting Common conditions and troubleshooting tips are included in Table 34.3. Other items to consider include the following: • If the patient is awake, always introduce yourself and explain what you are doing and why. • The choice of artery remains up to the provider placing the line. In the vast majority of cases, the radial artery is chosen for convenience and safety. Other options include the ulnar, brachial, and axillary arteries in the upper extremities and the femoral, dorsalis pedis, and posterior tibial arteries in the lower extremities. • The site chosen for the catheter can be influenced by the surgical procedure, ease of access, and, in some cases, patient safety. Confirm the site with the provider prior to setup.
TABLE 34.3 TROUBLESHOOTING FOR ARTERIAL LINE PROBLEM
LIKELY ISSUE
SOLUTION
Inability to aspirate blood
Kink in tubing Closed stopcock No arterial placement Clot in catheter Faulty equipment
Flush tubing Straighten tubing Replace catheter/transducer Small traction on catheter Open all stopcocks
No waveform present
Kink in tubing Closed stopcock No arterial placement Clot in catheter Faulty equipment Disconnected tubing
Flush tubing Straighten tubing Open stopcocks Replace catheter/transducer Check all equipment
Unable to zero or reach baseline
Closed stopcock Air bubbles in line Not zeroed Faulty equipment
Open all stopcocks Disconnect and flush line Rezero line Replace catheter/transducer
Underdampened
Excess tubing Catheter movement Vasoconstriction
Remove extra tubing segments if able Secure catheter more Inform provider
Overdampened
Kink in tubing Air bubbles in line Closed stopcocks Vasodilation Clot in catheter Empty IV bag IV bag not pressurized
Straighten tubing Open stopcocks Flush line Repressurize bag (300 mm Hg) Replace IV bag Inform provider
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• Examine the arm for evidence of infection, trauma, existing vascular access, and arteriovenous fistulas prior to preparing the region. Miscommunications between the provider and the anesthesia technician can occur. If you observe a potential contraindication for placement of the arterial line in the location you are preparing, discuss the issue with the provider. • If the patient is alert and oriented, it can be helpful to ask about his or her handedness (which hand he or she brushes his or her hair or teeth with, etc.). It is more comfortable for the patient in the postoperative period if the catheter is placed in the nondominant arm. • Do not hyperextend the wrist if the radial artery is chosen as this can induce radial nerve injury. • Check for capillary refill in region distal to the catheter after insertion to ensure continued perfusion. • Arterial line transducers need to be changed out every 96 hours. • Change catheter to 22G in pediatric patients and 24G in the neonatal population.
■ ASSOCIATED EQUIPMENT Basic IV sets A basic IV setup consists of a bag of IV fluid; an IV infusion set that has a spike, a drip chamber, a tube, a regulating clamp, and injection ports; one or two three-way stopcocks; and an extension tube. Some of the sets are preassembled (Fig. 34.33); however, be sure to tighten and secure
■ FIGURE 34.33 Regular intravenous set. This shows a preassembled regular IV set with a macrodrip chamber, a clamp, double stopcocks, and an extension tubing.
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■ FIGURE 34.34 Macrodrip (right) and microdrip (left) IV sets.
all connections before clinical use. Additional IV setups include the following: • Microdrip (Fig. 34.34): The regular IV set (macrodrip) has a drip chamber that delivers 10, 12, or 15 drops equal to 1 mL. The microdrip IV set has a drip chamber that delivers 60 drops equal to 1 mL. Microdrip IV sets are used when small amounts and more exact fluid or drug administration are required (e.g., pediatrics or critical care settings). Because 1 hour is 60 minutes, the number of drops in 1 minute represents the milliliters delivered in 1 hour (100 drops in 1 minute is equal to 100 mL/hr). • Buretrol (Fig. 34.35): It is an in-line receptacle between the IV set and the IV fluid bag that has a maximum volume of 150 mL. It is a safety mechanism to avoid the overadministration of fluid to small patients (less than 15 kg). A defined amount of fluid is filled in
■ FIGURE 34.35 A preassembled intravenous set with a buretrol.
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■ FIGURE 34.36 Y-tubing blood transfusion set.
■ FIGURE 34.37 Infusion pump set.
the buretrol from the IV bag and then connecting tube to the bag is clamped off. Even with an IV pump malfunction, only the amount in the buretrol would be administered to the patient. • Basic blood tubing: The infusion set for blood transfusion is equipped with a 200-μm filter in the drip chamber. Some blood transfusion sets used intraoperatively also have a manual pressure pump for rapid infusion. • Y tubing (Fig. 34.36): It is used as the IV line when blood transfusion is anticipated. One side of Y tubing is spiked to normal saline and used to flush the tubing. When blood transfusion is needed, spike the blood bag with the other side of Y tubing to start blood transfusion. • Setups for infusions pumps (Fig. 34.37): Infusion pumps require specific tubing that fit certain pumps. Generally, it consists of a drip chamber, a regular tubing, a clamp, and the elastic tubing that lies inside of the pump.
■ FLUID WARMER
All IV sets should be primed prior to use to avoid injecting air into the patient. To flush the entire set with fluid, close the regulating clamp first and then spike the IV bag. Fill the drip chamber up to half of the capacity by squeezing and releasing the chamber. Then, open the clamp to flush the tubing until all air and bubbles have been removed from the tubing. The stopcocks and injection ports tend to trap the air. Tap these places with a finger or a surgical clamp to release bubbles. Once all air has been removed, close the clamp. Label the set with the date and the time as it should be used within 24 hours. Do not write on the fluid bags directly with markers.
Patients undergoing general anesthesia for operative procedures become hypothermic due to multiple reasons (i.e., lack of muscle activity, vasodilatation, hypothalamic depression, radiation, conduction, evaporation, convection of body heat). Administration of continuously warmed fluid has been shown to decrease the incidence of intraoperative hypothermia. Different types of fluid/blood warmers are available on the current market; however, they share several common characteristics. Most consist of a warming device and a disposal tubing component (e.g., HOTLINE, Level1) (Fig. 34.38). The IV tubing is connected to the proximal connector of the disposable warming tubing. The distal end of the warming tubing is connected to IV tubing, which is connected to the patient. They function by circulating warm sterile water through the outer lumen of the warming tubing, which surrounds an inner lumen through which the IV fluid flows. The Bair Hugger warming system uses a special coil of tubing that can be attached to the hose of the forced-air warming units. Another system is the Ranger fluid warming system that uses a proprietary cassette and highly conductive heating plates. All of these systems require special disposable components and wall socket power. Thermal Angel is a disposable, inline, battery-powered warming device. Its major advantage is that it can be used during transport of critically ill patients. Although it is very rare, there is a case report of a superficial burn caused by Hotline tubing touching the patient’s skin over a long period of time. Caution must be taken to prevent this type
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■ FIGURE 34.38 Hotline.
of complication. Setting up and troubleshooting vary in different brands and require in-service training by the manufacturer or distributor and referring to the manufacturer-specific manuals. However, the basic setup is very simple. After installing a prefilled tubing, coil, or cassette in the warming unit, simply turn the device on.
■ RAPID INFUSION SYSTEMS Rapid infusion systems are commonly used intraoperatively to transfuse massive amounts of fluids and of blood components rapidly. Some of the devices use pressure (e.g., Level1) (Fig. 34.39), and others use rotary pumps (e.g., Belmont) (Fig. 34.40). Both systems are equipped with filters, line pressure monitors, air detectors, and a warming device with temperature monitors. In addition, the Belmont system has a reservoir and a computer system to regulate flow rate. Both systems should not be used to transfuse platelets,
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■ FIGURE 34.39 Level1.
cryoprecipitates, or granulocyte suspensions. They should not be used where rapid infusion is medically contraindicated. Administration of blood (red cells) under pressure may cause hemolysis, resulting in hyperkalemia and hemoglobinemia. Continuous supervision by trained personnel is required in the use of these devices. General setting up is described below; however, it is essential to follow the manufacturer’s instruction for setup, operation, and troubleshooting. 1. 2. 3. 4. 5.
Inspect the system. Install the disposable set (including a reservoir for Belmont). Turn the power on. Spike the saline bag and prime the tubing (and fill the reservoir in Belmont). Connect extension tubing to the patient’s IV access and start infusing.
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■ FIGURE 34.41 Autotransfusion system (Cell Saver).
■ FIGURE 34.40 Belmont rapid infuser system.
■ CELL SAVER (AUTOTRANSFUSION SYSTEM) As a part of the effort to decrease the need for allogenic blood transfusion, autologous blood transfusion (autotransfusion) has been employed in surgeries since the early 19th century. A cell saver device consists of suction for the surgical field to collect the blood, a collection reservoir, a filter, a centrifuge, and a collection bag (Fig. 34.41). An anticoagulant (usually heparin) is added to the shed blood as it is collected. The blood is mixed with a washing solution to remove undesirable components such as debris from the surgical field, cytokines, free hemoglobin, and lipid microparticles. The mixture is then centrifuged to separate out the red blood cells. The red blood cells are transferred to a collection bag for transfusion. The end product will have very high hematocrit (60%-70%); however, it will lack platelets and clotting factors. The final concentration of red blood cells is dependent upon the amount of blood in the collection reservoir before the wash cycle is begun (the
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less blood in the reservoir, the lower the final hematocrit). The use of a cell saver is indicated for procedures in which anticipated blood loss is 20% or more of patient’s estimated blood volume (more than 1 L in adults). The type of procedure should be individualized by the institution and by surgeons. Contraindications include infection, topical anticoagulants (Avitene, Hemopad, Instat, etc.), liquid or soft bone cement (okay to use if the cement is hard) conditions that result in extensive hemolysis, topical antibiotics (can get concentrated to the point of nephrotoxicity), or where the suctioned blood is contaminated by sterile water, hydrogen peroxide, or alcohol. Relative contraindications include shed blood from obstetrics or malignancy. In all cases, if the washing process is not adequate, administration of cell saver blood could result in serious complications, such as hemoglobinemia, renal insufficiency, hyperkalemia, dilutional anemia, microembolism, and inadvertent anticoagulation. It is imperative that the cell saver be operated and monitored by trained personnel. Setup and operation vary in different brands; however, general operation is described as follows:
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1. 2. 3. 4. 5. 6. 7. 8.
Turn the power on. Open the centrifuge lid. Install the disposable set (reinfusion bag, waste bag, washing chamber, pump adapter). Close the lid. Spike the saline bag. Start the priming procedure. Set up the blood collection reservoir and connect it to the disposable set. After sufficient blood is collected, start the wash program.
■ PRESSURE TRANSDUCERS A pressure transducer is a device containing a fluid-air interface that converts fluctuations in pressure to electronic data, which is then displayed on the patient monitor. The transducer contains a diaphragm with a silicon chip that continuously translates the pressure against the diaphragm from the column of fluid between the transducer and the patient’s circulation. The continuity of the fluid column is essential to proper functioning of the transducer, and, as such, any air bubbles, clots, or kinks in the tubing will cause inaccurate reporting of pressure changes. Also key to obtaining accurate information is properly “zeroing” the device. Gravity and the weight of the fluid in the column pressing against the diaphragm (if the fluid column is above the transducer) or pulling away from the diaphragm (if the fluid column is below the transducer) can affect pressure readings. To control for this effect, the transducer should be placed at the same height as the point in the body that will serve as the reference pressure, a point called the phlebostatic axis. For operations with the patient in the supine position, the phlebostatic axis is the point at which the fourth intercostal space intersects with the midaxillary line in order to use the RA as a reference point (zero level). It is important to maintain this relationship between the patient and the reference point. When the height of the operating table is changed, the transducer height will have to be changed as well. Small variations in the height of the transducer compared to the reference point will create inaccurate values in the measured pressure. Transducers can be used in the hospital to monitor a variety of pressures, including central venous blood pressure, arterial pressure, PA pressure, tissue compartment pressure, and even intracranial pressure.
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Setting up a Pressure Transducer • Connect the rigid tubing to the patient end (top) of the pressure transducer; also insert a three-way stopcock near the patient end of the tubing for blood sampling. If using VAMP, Safeset, or other in-line reservoir, ensure that the in-line reservoir is connected to the patient end of the pressure transducer (Fig. 34.42). • Connect the flexible tubing with the bag spike to the appropriate connection on the pressure transducer (bottom). • Spike normal saline or heparinized saline bag. Insert the fluid bag into the pressure bag and pressurize it to 200 to 250 mm Hg. Fill the drip chamber up to two-thirds of the capacity by squeezing the chamber a couple of times (Fig. 34.43). • Prime the entire tubing length with fluid by gently pulling on the red rubber tag on the pressure transducer (flush valve). If unable to prime, ensure all stopcocks and valves are open to the tubing. • VAMP and Safeset systems often come preassembled and you simply need to spike the IV bag and prime the tubing as above. • It is crucial to thoroughly flush the entire tubing and ensure there is NO AIR in the tubing as this can lead to severe patient complications. Periodically flick tubing and stopcocks with finger to release and remove any extra air bubbles. • Ensure arterial line transducer is attached to an IV pole at a point level with the phlebostatic axis.
■ FIGURE 34.42 Arterial line transducer and tubing (Safeset).
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2.
3.
ferent reference point than the RA—ask the provider if you are unsure). With the transducer patient tubing connected to the catheter, open the pressure transducer stopcock to the air. Then, press the “Zero” button on the monitor setup. Press the button appropriate for the line for which you are performing the zero. For example, for arterial lines, press “Zero ABP” button. At this point, the waveform should be flat. The numeric value on the monitor should read “0,” and most monitors provide an audible alert to indicate that the zeroing process is complete. Close the stopcock, positioned so that the transducer is open to the patient side. The waveform will reappear and give a digital display of the pressure
■ BLOOD SAMPLING
■ FIGURE 34.43 Fluid-filled drip chamber for pressure transducer to 250 mm Hg (green line).
• Certain arterial line tubing sets come with stopcock caps with holes in them that, when placed on the pressure transducer stopcock, allow for zeroing of the transducer without removal of the cap. It is important to ensure that these caps are only on the pressure transducer stopcock and not on the blood sampling stopcock near the patient end. If so, please replace with a yellow occlusive cap. • If asked to set up multiple invasive lines/ monitors, you will need a holder for multiple pressure transducers, as well as a single pressurized saline bag with the properly spiked flexible tubing (i.e., use 2:1 split tubing for an arterial line and CVP and 3:1 split for adding a PAC). Make sure to label each pressure transducer with the corresponding line it represents. Ensure that all lines and tubing are again properly flushed and contain NO AIR.
One of the benefits to placing an arterial line is that it allows repeated sampling of blood for arterial blood gases and other laboratory tests. With the proper technique, the patient risk associated with blood sampling will be minimized. Blood samples need to be drawn into tubes containing heparin or other anticoagulants to prevent hemolysis, unless otherwise specified for that particular test. For arterial blood gas samples, syringes that are preheparinized can be used or a small amount of heparin can be drawn up into a 1- to 3-mL syringe, coating the inside of the tube, and then squirted out. Of note, sterile procedure and universal precautions should be followed for all blood sampling. Withdrawing the blood sample in an open sampling set: 1. 2. 3. 4.
Zeroing the Pressure Transducer 1.
Set the transducer to the desired height in relation to the reference point (in some cases, the provider may want to use a dif-
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5.
Remove sterile cap from stopcock and wipe port with alcohol swab for 30 seconds. Attach 5- or 10-mL regular syringe to the port. Turn the stopcock off to the flush/transducer. Withdraw 5–10 mL of patient blood into syringe and then close the stopcock at 45-degree angle to prevent flush from flowing to patient (to avoid dilution of the sample, withdraw at least two times the dead space volume). Discard the waste syringe (the sample is diluted with flush solution) and attach an
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6. 7.
8.
9.
appropriately sized syringe to the stopcock (blood gas samples must be drawn into heparinized syringes). Again turn the stopcock off to the flush and withdraw 1–3 mL of blood for the sample. Close the stopcock to the port and cap the sample syringe. Replace the sterile cap on the port. Pull the red rubber pigtail to flush the tubing until it is clear. Make sure to pull the red pigtail for only 2–3 seconds at a time, and repeat after a couple of seconds as needed to clear the line. Flushing the line for more than 3 seconds can push fluid back into the proximal arterial circulation as far as the aorta (or cerebral circulation in pediatric patients). Proper flushing of the tubing should require no more than one or two short pulls on the pigtail. If this is not clearing the tubing, ensure the saline bag is properly pressurized. Confirm the presence of a waveform.
Withdrawing blood in a closed sampling set: 1.
2.
3.
4.
When utilizing an in-line sampling set such as the Safeset, a blunt tip needle is necessary for the heparinized syringe. The Safeset system comes with an in-line syringe that collects the “discarded blood” into a 10-mL syringe. Five to ten mL of patient blood (at least two times the dead space volume) is slowly withdrawn into the syringe, and the stopcock at the end of the syringe is closed. After cleansing the closest Safeset port to the patient with alcohol, the blunt needle is inserted into the port and blood is removed for the sample. The syringe stopcock is then opened and the prior “discarded blood” is injected back into the patient, and the red rubber pigtail is pulled to flush the line until clear. Again confirm the presence of an appropriate waveform.
Withdrawing a sample from a PIV catheter: After placing a PIV catheter, venous blood sample can be obtained from the catheter before releasing the tourniquet and the infusion set is connected. After an infusion is started, a blood sample can also be obtained from a PIV catheter
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or central access catheter by the following procedure; however, small veins can collapse and blood sampling may not be possible in those circumstances. 1.
2.
3.
4.
5. 6. 7.
Stop all infusion at least 1 minute before sampling to avoid dilution. Make sure that the clamp flow through the IV is closed. Apply a tourniquet proximal to the IV insertion site if the sampling site is from a PIV catheter. If the blood pressure cuff is applied on the extremity that has the PIV catheter, the “Venipuncture mode” of the automated noninvasive blood pressure machine can be used. Attach a 10- to 20-mL syringe to the closest (to the catheter) stopcock or injection port and slowly withdraw at least four times the dead space volume. Discard the waste syringe and attach the sampling syringe (5–10 mL). Take caution not to apply excessive negative pressure as this will cause hemolysis of the sample. Collect the blood sample needed for the test. Release the tourniquet and turn off the “Venipuncture mode.” Open the regulating clamp and flush the blood in the tubing with IV fluid.
■ SUMMARY Obtaining vascular access, inserting CVCs, and starting arterial lines are extremely common procedures in anesthesia. In addition, the anesthesia provider may request a fluid warmer, rapid transfuser, or cell saver. The anesthesia technician will be frequently called upon to assist the anesthesia provider in obtaining and setting up equipment for these procedures, and the technician should be thoroughly familiar with the equipment. In addition, the technician should be familiar with sterile technique, different infusion sets, pressure transducers, and monitor operation for setting up, zeroing, and monitoring pressures. The anesthesia technician should also be prepared to troubleshoot a wide variety of equipment utilized for these procedures. Errors during equipment preparation or operation can have disastrous consequences, including air emboli in the arterial circulation, thrombosed or infiltrated catheters, or central bloodstream infections.
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REVIEW QUESTIONS 1. The rate of fluid flow in a catheter INCREASES with A) The fourth power of the increased radius of the catheter lumen B) Higher pressure applied to the fluid line (e.g., a pressurized IV bag) C) Increasing length of the catheter D) A and B E) All of the above Answer: D. The radius of the catheter is a critical determinant of fluid flow rates and is related to the fourth power of the radius. Increasing the catheter length would decrease the fluid flow rates.
2. In French sizes, the larger the number is, the larger the diameter is. A) True B) False Answer: A. In French sizes, the larger the number, the larger the catheter. This is in contrast to the Stubbs wire gauge system in which the larger the gauge, the smaller the catheter.
3. Which of the following are potential complications from the placement or use of a PAC? A) Carotid puncture B) PA rupture from balloon inflation C) Ventricular tachycardia D) Pulmonary infarction E) All of the above Answer: E. All of the above are potential complications.
4. Rapid infuser system is NOT equipped with A) Filter B) Heat exchanger C) Roller pump D) Reservoir E) Centrifuge Answer: E. The rapid infuser system is equipped with filters, line pressure monitors, air detectors, and a warming device with temperature monitors. In addition, the Belmont system has a reservoir and a computer system to regulate flow rate. The centrifuge is one of the features of an autotransfusion system (cell saver).
5. Which of the following is TRUE regarding setting up or using a transducer for an arterial line? A) Bubbles in the line can cause a venous embolus. B) The drip chamber should always be in the upright position. C) Damping of the signal will cause an overestimation of blood pressure. D) When flushing the line into the patient, hold the pressurized flush open for at least 6 seconds.
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E) The femoral artery should never be used for an arterial line. Answer: B. The drip chamber of the pressurized flush should be kept in the upright position to prevent air from entering the line to the patient. Bubbles in the line could cause an embolus in the artery and not the vein. In addition, bubbles in the line could dampen the signal (flatten the waveform), leading to an underestimation of the blood pressure. When flushing the line with pressurized fluid, the flush should not be applied for more than 3 seconds to prevent flush from reaching the central arterial circulation. The femoral artery is not uncommonly accessed for arterial pressures.
6. Which infusion set should be used to maintain strict control over the volume of fluid or medication delivered? A) Buretrol B) Microdrip C) Infusion pump tubing with an infusion pump D) Y-type blood administration tubing E) A, B, and C Answer: E. A buretrol is a 150-mL chamber that can be used to control medication or volume delivery, particularly in pediatric patients. A microdrip set has smaller drops (approximately 60 drops per milliliter) and can be used to deliver lower infusion rates. An infusion pump can be set to control infusion amounts and rates. A Y-type blood administration set would be used to deliver higher volumes of fluid or blood.
7. Which of the following statements are FALSE in regard to zeroing a transducer? A) The transducer should be opened to air to perform the zero. B) It is necessary to press a button on the monitor to initiate zeroing. C) Zeroing is not necessary the first time you set up and use a pressure transducer. D) The monitor should read “0” when the transducer is open to air. E) All of the above are FALSE. Answer: C. Every time you set up a transducer it must be zeroed. In addition, when the transducer cable is disconnected, the transducer may have to be rezeroed. To perform a zero, the transducer is opened to air and the monitor button for that particular line is pressed to initiate the zero. The monitor should give an audible beep when the zero process is complete and the monitor should read “0.”
8. Which of the following statements are TRUE with regard to central venous access? A) The internal jugular, subclavian, and femoral veins can be used for peripheral venous access. B) It is not necessary to gown when inserting a CVC.
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Chapter 34 • Vascular Access Equipment and Setup C) Manometry is used to verify the CVC is not in the lung. D) A cordis introducer CVC should be used if you do not expect large amounts of blood loss. E) All of the above are TRUE. Answer: B. It is necessary to use a sterile gown and gloves and use a mask when inserting a CVC to reduce the incidence of bloodstream infections. The internal jugular, subclavian, and femoral veins are used for central venous access. Once a CVC has been inserted, measuring the pressure in the line can help determine that the line was placed in a vein (low pressure) and not inadvertently in an artery (high pressure). A cordis introducer has a very large infusion channel (if nothing else is put into it, e.g., hands-free catheter or PAC) and can be used for high flow infusions.
9. Which of the following should be available to place a CVC? A) Ultrasound machine B) CVC kit C) Infusion setup D) IV fluids E) All of the above Answer: E. All of the above should be available for CVC insertion. Ultrasound is extremely common to identify the relevant anatomy and guide needle insertion into the vein.
10. Which of the following statements are TRUE with regard to peripheral venous access? A) A tourniquet should never be used. B) A transducer should be set up. C) Ultrasound can be used to identify the vein. D) The FV can be used. E) All of the above are TRUE. Answer: C. In rare circumstances, a peripheral vein can be difficult to see or palpate. In these cases, ultrasound can be utilized to identify a vein. A tourniquet is almost always used to enlarge the vein so that it can be more easily palpated and cannulated. A transducer is used to monitor CVPs and is not used for peripheral venous lines. The FV is part of the central circulation and is not considered a peripheral vein.
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SUGGESTED READINGS Atalay H, Erbay H, Tomatir E, et al. The use of transillumination for peripheral venous access in paediatric anaesthesia. Euro J Anaesthesiol. 2005;22:312–323. Celinski S, Seneff M. Procedures, Techniques, and Minimally Invasive Monitoring in Intensive Care in Intensive Care Medicine: Arterial Line Placement and Care. Philadelphia, PA: Lippincott; 2008. Chaney JC, Derdak S. Minimally invasive hemodynamic monitoring for the intensivist: current and emerging technology. Crit Care Med. 2002;30:2338–2345. Chatterjee K. The Swan-Ganz catheters: past, present, and future: a viewpoint. Circulation. 2009;119:147–152. Evans DC, Doraiswamy VA, Prosciak MP, et al. Complications associated with pulmonary artery catheters: a comprehensive clinical review. Scand J Surg. 2009;98(4):199–208. Goldstein JR. Ultrasound-guided peripheral venous access. Israeli J Emerg Med. 2006;6(4):46–52. Greenberg S, Murphy G, Venderm J. Standard monitoring techniques. In: Barash PG, Cullen BF, Stoelting RK, et al., eds. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott; 2009. Hasselberg D, Ivarsson B, Anderson R, et al. The handling of peripheral venous catheters—from non-compliance to evidence-based needs. J Clin Nurs. 2010;19:3358–3361. Hignett R, Stephens R. Radial arterial lines: practical procedures. Br J Hosp Med. 2006;67(5):M86–M88. Hocking G. Central venous access and monitoring. World Anaesth Online, 12:1–6, 2000. Available at: http://www. nda.ox.ac.uk/wfsa/html/u12/u1213_01.htm. Josephson DL. Intravenous Infusion Therapy for Nurses: Principle & Practice. 2nd ed. Clifton Park, NY: Delmar Learning; 2004. SAFESET Blood Sampling System. Critical Care Systems, San Clemente, CA: ICU Medical Inc.; 2005. Available at: http://www.icumed.com/criticalcare/safeset.asp. Silva A. Anesthestic monitoring. In: Basics of Anesthesia. 5th ed. Philadelphia, PA: Churchill Livingstone; 2007. Stoker M. Principles of pressure transducers, resonance, damping and frequency response. Anesth Intens Care Med. 2004;5(11):371–375. Tobias JD, Ross AK. Intraosseous infusions: a review for the anesthesiologist with a focus on pediatric use. Anesth Analg. 2010;110(2):391–401. Tokarczyk A, Sandberg W. Monitoring. In: Clinical Anesthesia Procedures of the Massachusetts General Hospital. 7th ed. Philadelphia, PA: Lippincott; 2007.
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CHAPTER
35
Airway Equipment Setup, Operation, and Maintenance Norman E. Torres, Anita Stoltenberg, and Glenn Woodworth ■ INTRODUCTION The management of the airway is one of the most important tasks of the anesthesia provider (see Chapter 18). Because of the complexity of airway management, manufacturers continue to produce an endless array of tools and equipment to aid in the management of the airway. This chapter introduces the most common types of airway equipment currently available as well as describes any special setup that might be required, how the equipment is generally used, and tips on maintenance and troubleshooting.
■ OROPHARYNGEAL AIRWAY In anesthetized or unconscious patients, the soft tissues of the oropharynx, especially the tongue, can obstruct the passageway between the mouth and the glottis. Oropharyngeal airways (OPAs) are used to stent open the oropharynx to allow passage of air/oxygen through the oropharynx. The majority of OPAs are made of curved hard plastic to conform to the oropharynx. They usually have an interior channel that allows the passage of gas or suction devices from the mouth opening through the channel into the posterior pharynx (Fig. 35.1). OPAs are used in anesthetized or unconscious patients who cannot be easily ventilated by bag/ mask ventilation or who are spontaneously breathing but have airway obstruction. They are usually not tolerated by awake patients and can cause gagging and even vomiting when used in a conscious or semiconscious patient. When inserting an oral airway, the anesthesia provider may use a tongue depressor to keep the oral airway from pushing the tongue back into the pharynx. Oral airways should be kept immediately available (easy to grab) in all settings in which airways are managed (e.g., operating room,
recovery area, emergency room, rapid response, or code carts). OPAs come in a variety of sizes from newborns to extra large adults and are often color coded to indicate the size of the airway. They are usually marked with the actual size in millimeters (50–100 mm) or with a number (5–10) that corresponds to the size in centimeters, with 8–10 the typical size range used in adults. OPAs generally cost between $0.30 and $3.00 each. The vast majority are disposable and latex free. Many institutions have single-use prepackaged disposable oral airways (Fig. 35.2). When removing the airway from the package, care must be taken to ensure that none of the packaging material remains attached to the airway prior to insertion in a patient. Plastic remnants from the packaging can be swallowed or aspirated into the patient’s lungs. Types of OPAs • Guedel airways have a single central channel with a reinforced bite block (Fig. 35.3). • Berman OPAs have dual-side channels (Fig. 35.4). Although many of these airways can be boiled or gas/cold sterilized, the majority OPAs are meant for single use only.
■ NASOPHARYNGEAL AIRWAYS Much like OPAs, nasopharyngeal airways (NPAs) are designed to be used in patients with airway obstruction. These airways are inserted through the nose and into the posterior pharynx where they can prevent the tongue from collapsing against the posterior wall of the oropharynx. NPAs are usually better tolerated than OPAs in awake or semiconscious patients with an intact gag reflex. NPAs are soft and flexible and have
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■ FIGURE 35.3 Guedel oropharyngeal airway. ■ FIGURE 35.1 Three different sizes of oropharyngeal airways.
an interior channel to permit the flow of gas, a beveled edge to ease passage through the nose, and a flared end to prevent the NPA from passing completely into the nose. Because of the flared end, many refer to them as a “nasal trumpet” (Fig. 35.5). Because NPAs can cause trauma to the nasal passages, a decongestant (e.g., phenylephrine nose drops) to shrink the nasal mucosa and lubricating jelly (e.g., “Surgilube” or 2% xylocaine jelly) can be used to facilitate passage of the NPA through the nose. NPAs come in a variety of sizes. They are often sized using the “French” scale, with sizes ranging from 12 to 36 French. Dividing the French number by 3 gives the diameter of the NPA in millimeters. The majority of modern NPAs are latex free and single use only. Older NPAs were made of rubber. Do not assume an NPA is latex free unless the packaging clearly states that it is. NPAs come individually packaged or can be purchased in bulk. Prices range from $3.00 to
■ FIGURE 35.2 Prepackaged disposable oral airway.
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$7.00 each. Some packages include a lubricant. As with many other medical products, the vast majority of NPAs are designed for single use and should not be cleaned and used in another patient.
■ FACE MASKS AND NASAL CANNULA Face masks and nasal cannula are used to deliver supplemental oxygen to the patient. One concept that is universal to all types of oxygen delivery systems is to make sure oxygen is flowing from the source. If a portable oxygen delivery source is to be used (oxygen tank), make sure it has sufficient oxygen for the trip. A full e-cylinder of oxygen at 1,900 psi contains about 660 L of oxygen. The amount of oxygen left in the tank is directly proportional to the amount of pressure left in the tank. If the tank reads about 950 psi, it is half full and contains about 330 L of oxygen. At 10 L/min flow through a simple face mask, this tank would have 33 minutes of oxygen left. If using wall-mounted oxygen, make sure the flowmeter is on and oxygen is flowing.
■ FIGURE 35.4 Berman oropharyngeal airway.
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■ FIGURE 35.5 Argyle nasopharyngeal.
■ PASSIVE OXYGEN DELIVERY— NASAL CANNULA Nasal cannulas are designed to supplement the flow of oxygen to the patient. In general, one end of the tubing is connected to a metered oxygen source and the nasal portion is secured to the patient’s head with the tips (“prongs”) of the nasal cannula resting a short way inside the patient’s nostrils (Fig. 35.6). The oxygen flow is adjusted between 2 and 6 L of oxygen per minute and delivers approximately 24%-44% oxygen to the patient. If the patient requires a higher concentration of oxygen, an oxygen face mask must be used. Delivering higher than 6 L of oxygen per minute through nasal cannula is irritating to the patient and can dry out the nasal mucosa, resulting in nosebleeds. This can happen even if the cannula is attached to a humidification system. Nasal cannulas are generally very similar in design and are usually made of a soft plastic material. They are intended for single patient use and prices range from $0.50 to $2.00 each. One of the major features of the cannula to consider
■ FIGURE 35.6 Nasal cannula. One end connects to the oxygen source, while the tips are secured in the entrance to the nostrils.
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is the length of the oxygen tubing, which can range from 7 to 100 ft. During patient transport, if the oxygen source is at the foot of the bed, the 7-ft length of oxygen tubing may be insufficient for the cannula to reach the patient’s head. Some anesthesia providers stretch the tubing to slightly increase its length. Other features to consider when using a nasal cannula include attaching the tubing to a breathing circuit or sampling exhaled carbon dioxide through the nasal cannula while it is delivering oxygen. Some nasal cannulas come with an adaptor to attach the oxygen source end of the tubing to the breathing circuit (Fig. 35.7). This will allow the anesthesia provider to control the upper limit of the percentage of oxygen delivered through the cannula. For example, the anesthesia provider may wish to control the percentage of oxygen to reduce the risk of fire during a head and neck procedure performed on an awake patient. Unfortunately, the control over the oxygen concentration is not very precise. During inhalation the entrainment of room air affects the delivered oxygen concentration. If the cannula does not come with an adaptor, tape can be wound around the oxygen source end of the tubing to increase its diameter to the point where it can be snuggly fit into the breathing circuit. Some nasal cannulas come with a gas sampling line built into the tubing. The sampling port is near the nostrils, and a separate connection port is near the oxygen source end of the cannula, which can be attached to a CO2 gas analyzer (Fig. 35.8). The sampling tubing can often be separated from the oxygen delivery tubing to facilitate attachment to the gas analyzer. These cannulas are extremely useful during procedures performed under sedation. The sampling line is connected to a CO2 gas analyzer and the anesthesia provider can monitor the respiratory rate,
■ FIGURE 35.7 Adaptor to connect oxygen tubing to the anesthesia breathing circuit.
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■ FIGURE 35.10 Venturi mask.
■ FIGURE 35.8 Nasal cannula with a CO2 sampling port.
• Simple face masks: These masks should be connected to an oxygen source delivering between 6 and 12 L of oxygen per minute. This corresponds roughly to an inspired oxygen concentration of 28%-50% (Fig. 35.9). • Venturi masks: These masks have a mechanism to adjust the inspired oxygen concentration (Fig. 35.10).
• Partial non-rebreathing masks: These masks have an attached reservoir of oxygen. When a patient inspires the oxygen from the face mask, the reservoir provides the majority of the gas flow. This limits the entrainment of air from around the mask. Any entrainment of air around the mask would dilute the oxygen delivered to the patient (this happens in a simple face mask). Non-rebreathing masks can deliver oxygen concentrations of up to 70% (Fig. 35.11). • Aerosol masks: Simple face masks and partial non-rebreathing masks can come with a device to deliver aerosolized medications including bronchodilators (or lidocaine in preparation for awake fiberoptic bronchoscopy) (Fig. 35.12). • Tracheostomy mask: This is a specialized mask that fits around a patient’s neck and is designed to cover a tracheostomy or stoma site. In normal breathing, the nose provides humidification to inspired gases. Because tracheostomy patients bypass the nose, the tracheostomy mask should be attached to a humidified oxygen source (Fig. 35.13).
■ FIGURE 35.9 Simple face mask.
■ FIGURE 35.11 Partial non-rebreathing mask.
a reasonable estimate of end-tidal CO2, and can detect airway obstruction.
■ PASSIVE OXYGEN DELIVERY— FACE MASKS Face masks come in two general types: those used for the passive delivery of oxygen and those used for assisted ventilation. Face masks designed for the passive delivery of oxygen consist of plastic tubing for attachment to an oxygen source (or humidified oxygen source) and the delivery end, which may cover the patient’s entire face, the nose and mouth, a tracheal stoma, or just the nose.
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■ FIGURE 35.12 Aerosol mask.
• Nose mask: For those patients who cannot tolerate nasal prongs or a face mask, masks are available that fit only over the nose. Features to consider when selecting or purchasing face masks include the length of oxygen tubing, the type of mask, and the concentration of oxygen that needs to be delivered. The majority of the face masks on the market are for single patient use only and should not be used on other patients.
■ MASKS FOR POSITIVE PRESSURE VENTILATION In order to deliver positive pressure ventilation via a mask, the mask must be able to form a tight seal around the patient’s mouth and nose. These masks tend to be of a more durable design than passive oxygen masks and also have an inflatable cuff around the edge of the mask to help form a seal with the patient’s skin (Fig. 35.14). The mask also has a port that accommodates a standard 15-mm inside/22-mm outside connector that fits into standard breathing circuits. Finally, many masks have four “prongs” around the connector opening. These prongs are used to attach
■ FIGURE 35.13 Tracheostomy mask.
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■ FIGURE 35.14 Plastic masks with four prongs for strap attachments.
a head strap to secure the mask to the patient’s face. Older mask designs were made of black rubber and were sterilized after use, so they could be used on another patient. The disadvantage of these types of masks include the cost of sterilization, the risk of disease transmission, the masks are not latex free, the inflatable cuffs would decay and lose their ability to stay inflated, and the masks may prevent the anesthesia practitioner from seeing vomit come out of the patient’s mouth and into the mask. Despite these drawbacks, many are still in use today. These masks cost in the range of $20-$40. When using one of these masks, take care to ensure that the cuff is inflated properly and can hold pressure. Follow the manufacturer’s recommendations for sterilization. Newer mask designs are made of plastic and are intended for single use only. They are typically used in the operating room with anesthesia breathing circuits or with bag-valve-mask ventilation systems. Before purchasing a new mask type, consult your anesthesia providers. Some of the masks are more difficult to hold with one hand because of the dome shape on the mask. When using a disposable mask, always check the cuff as it can lose cuff pressure when stored. The cuff can be easily inflated by attaching a syringe to the cuff port. If the cuff will still not hold pressure, the cuff may have a leak. Commonly, the valve used to inflate the mask has become incompetent and is allowing gas to escape from the cuff through the valve. These masks generally cost between $2.00 and $4.00 each. Some breathing circuits come packaged with a disposable anesthesia mask. When removing a mask from individual plastic packaging, it is critical to
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make sure that plastic remnants are not present on the mask. If not completely removed, these remnants could be aspirated into the patient’s lungs when the mask is used.
■ SPECIAL FACE MASKS Some specialized anesthesia masks (e.g., the endoscopy mask) have a port with a membrane for entry of a fiberoptic bronchoscope and a port to ventilate the patient without removing the mask from the patient’s face and without losing the ability to provide positive pressure ventilation (Figs. 35.15 and 35.16). Other face masks are designed to deliver continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BIPAP). BIPAP and CPAP are used to treat obstructive sleep apnea as well as respiratory failure in the intensive care unit (ICU). Both require a tight-fitting mask with a head strap to create a good seal to deliver positive pressure. These masks can cover just the nose or mouth. (Fig. 35.17).
■ LARYNGEAL AIRWAYS Intubating the trachea is considered the gold standard for securing the airway and minimizing the risk of aspiration once the airway is established. Many consider intubating the trachea to be “invasive” and not without risk. Glottic structures like the vocal cords or arytenoid cartilages can be damaged while attempting to pass a tube through the trachea. In addition, tracheal intubation is quite stimulating to the patient and can lead to catecholamine release and large swings in heart rate and blood pressure, which can be detrimental to many patients. Since the 1960s, inventors have been experimenting with a variety of methods to establish an airway that minimizes obstruction caused by oropharyngeal structures without inserting a tube through the vocal cords
■ FIGURE 35.15 Endoscopy mask.
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■ FIGURE 35.16 Endoscopy mask with a special port to admit a fiberoptic bronchoscope.
into the trachea. Because these devices are positioned above the vocal cords (glottic region), they are termed laryngeal or supraglottic airways. The term laryngeal airways would only include those devices that are positioned in the pharynx just outside the larynx and does not include devices like OPAs. There are many types of laryngeal airways. The basic design features that are present in many of these airways include the following: • Blind insertion technique: The glottis does not need to be visualized during insertion. The devices are inserted “blind” with visual markings and tactile feedback to indicate proper
■ FIGURE 35.17 CPAP and BIPAP mask.
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positioning. Proper positioning must be confirmed by listening to breath sounds and the presence of persistent end-tidal CO2. The ease of insertion of many of these devices has allowed them to be used effectively by nonanesthesia providers in emergency settings (emergency room, field airway management by paramedics or emergency medical technicians). Insertion of laryngeal airways does not require the use of paralytic agents to paralyze the vocal cords. Inflatable pharyngeal cuff: These devices include a “cuff” or balloon that is inflated after proper positioning of the device in the pharynx. Inflation of the cuff holds the device in position just outside the larynx and creates a seal to divert gas flow into the trachea and not into the esophagus. Because the device can also be taped in position, it frees up the medical provider to use both hands for other tasks once the airway has been established. At least one laryngeal airway has replaced the inflatable cuff with a proprietary gel material that conforms to the laryngeal inlet. Ventilation channel: All of the devices have a channel or tube through which ventilations or spontaneous ventilation can occur. The tube has a standard 15-mm/22-mm breathing circuit connector on the end. Esophageal suction channel: Many contain a separate tube or channel that will admit a suction device into the esophagus and from there into the stomach. This will allow partial removal of stomach contents and reduce the risk of subsequent aspiration. Intended for use in semiconscious, unconscious, or anesthetized patients: These devices are not tolerated by awake patients unless extensive topical anesthesia to the oropharynx has been applied. Positive pressure ventilation: These devices allow positive pressure ventilation with the caveat that, in general, only low airway pressures can be utilized. Modifications of these devices over the years have increased the amount of airway pressure that can be used to provide ventilation but not overcome the pharyngeal seal and begin pushing gas into the stomach. Intubation aid: During difficult intubations a laryngeal airway may be placed to establish ventilation. Once in place, many laryngeal airways can be used to facilitate insertion of
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an endotracheal tube. Because the laryngeal airway is placed close to the laryngeal inlet, an endotracheal tube or tube exchanger can sometimes be passed blindly through the ventilation channel into the trachea. In other circumstances, a flexible fiberoptic scope can be passed through the ventilation channel into the trachea and an endotracheal tube passed over the scope (see Chapter 18). Not all laryngeal airways have an opening near the laryngeal inlet that is large enough to permit passage of an adult-sized endotracheal tube. • Sizing: Laryngeal airways come in a variety of sizes and can be used in neonates to adults. Sizing nomenclatures are manufacturer specific. • Single use or multiuse: The early airways tended to be multiuse; however, many sites have switched to single-use airways to minimize sterilization costs and the potential for disease transmission. Follow the manufacturer’s instructions regarding single use or multiuse. If the device is multiuse, follow the manufacturer’s instructions for sterilization and the number of acceptable uses/sterilizations. Typical recommendations are between 30 and 50 uses. If the device is reused, care must be taken to clean the ventilation channel with a brush-type cleaner. • Troubleshooting: The most common fault observed with laryngeal airways is failure of the balloon or cuff to hold inflation. This can be due to a leak in the cuff or balloon; however, more commonly, the pilot valve used to inflate the cuff or balloon can become incompetent and leak. These problems occur more frequently with multiple reuses of the device.
■ LARYNGEAL MASK This device was introduced in the late 1980s and has become one of the most popular laryngeal airways worldwide, almost eliminating the use of prolonged mask ventilation. The laryngeal mask (LM) consists of a plastic, silicone, or rubber tube connected to an inflatable silicon “mask” that forms a seal around the laryngeal inlet (Fig. 35.18). A pilot tube with an inflation valve is connected to the cuff. The device is easy to insert and highly effective. Single-use disposable models are generally made of polyvinylchloride (PVC) and range in price from $5.00 to $10.00. Multiuse models generally have a silicone cuff and range in price from $100 to $250.
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■ FIGURE 35.18 LMA™.
Numerous manufacturers produce Several examples are provided below:
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■ FIGURE 35.19 LMA™ Fastrach.
LMs.
• Cuff design has been improved to allow higher positive pressures.
• Ambu: Full line of LM products • Merlyn Medical: ° Endomask Elite: silicone reusable, no laryngeal bars ° Endomask Essential: single-use PVC • Flexicare: Laryseal • Smiths Medical: Portex Soft Seal LM • Intersurgical: I-GEL • Intersurgical: Solus—full line of LMs • LMA™ North America/LMA™ International ° LMA™ Classic—multiuse, does not allow fiberoptic intubation ° LMA™ Unique—single use, latex free ° LMA™ Classic Excel—multiuse (up to 60), permits fiberoptic intubation ° LMA™ Supreme—single use, bit block, precurved, suction/gastric drain tube ° LMA™ ProSeal—multiuse, 30 cm H2O seal pressure for positive pressure ventilation, gastric drain tube ° LMA™ Fastrach
An additional modification has been made to the design of the LM to facilitate intubation (LMA™ Fastrach) (Fig. 35.19). Although blind or fiberoptic intubation can be accomplished with several current LM models, the “intubating” LM is specifically designed for this purpose. The intubating LM illustrated in Figure 35.19 has three components: the LM, a flexible endotracheal tube with removable airway adaptor, and an obturator. The device is first inserted into the oropharynx blindly and the cuff inflated to obtain a seal. The patient may be ventilated at this point with the anesthesia circuit or alternate breathing system. Once chest rise, maintenance of oxygen saturation with a pulse oximeter, and/or positive end-tidal CO2 measurement confirm adequate ventilation, the device can be used to blindly guide a flexible wire spiral endotracheal tube through the LM and into the larynx. Alternatively, a bronchoscope can be placed through the endotracheal tube to assist in guiding the tube into position. The intubating laryngeal mask device may be removed by first removing the endotracheal adaptor and pushing the endotracheal tube through and out of the LMA™ device with the obturator. The laryngeal mask portion of the device must be removed over the obturator while holding the endotracheal tube in position. Operators unfamiliar with this device can easily extubate the patient while attempting to remove the LM portion of the device over the endotracheal tube. After removal of the LM portion of the device, the endotracheal tube adaptor is attached to the endotracheal tube and ventilation is resumed. Breath sounds and end-tidal CO2 should be used to reconfirm tube placement.
• Cookgas: AirQ—disposable and reusable, precurved, bite block, permits bronchoscope • Winice Company • Ningbo TianHou Medical Supplies, Inc. • Teleflex Medical • Encore Several modifications have been made to the original design of LMs including the following: • The tubing can be reinforced with wire to prevent kinking. • The valve assembly can be made without metal to allow use in MRI suites. • The inflatable cuff has been replaced with a form-fitting gel material. • A gastric suction channel has been added.
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■ ESOPHAGEAL TRACHEAL COMBITUBE These devices were first described in the late 1960s. Their primary role has been to establish an airway in cases where a patient could not be intubated. Esophageal tracheal combitubes (ETCs) consist of a double-lumen tube with two inflatable balloons (Fig. 35.20). The “tracheal” lumen opens at the distal end of the ETC. The pharyngeal lumen opens in the lower pharynx via a series of side holes above the distal balloon. The ETC is inserted blindly into the oropharynx and should be advanced until the markings on the tube are at the teeth. The ETC may have been positioned in one of two locations: the esophagus (95% of the time) or the trachea. The large pharyngeal balloon is inflated (some ETCs require 70–100 mL of air to inflate the pharyngeal balloon) to seal the pharynx. The “tracheal” balloon is inflated with 7–10 mL of air. If positioned in the esophagus, the pharyngeal balloon seals the pharynx and ventilation can be accomplished with the pharyngeal lumen. Because the ETC is blindly placed into the esophagus 95% of the time, attempts to ventilate should be first made through the pharyngeal lumen. If breath sounds and end-tidal CO2 cannot confirm adequate ventilation via the pharyngeal lumen, the ETC may have gone into the trachea. In this case, the tracheal balloon would prevent gas from the pharyngeal lumen from entering the trachea. The user would then switch to attempt ventilation via the tracheal lumen. If the ETC is in the trachea, the tracheal lumen will function like a normal endotracheal tube. Note: the lumens are color coded and labeled. Because these devices are only used in emergencies, the operator may not be familiar with their use. The two lumens can confuse a
■ FIGURE 35.20 Esophageal tracheal Combitube.
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novice operator. These devices are single use, come in several sizes (adult only), are produced by several manufacturers (Mallinckrodt, Puritan Bennett, Kendall), and are generally priced between $70 and $100 each.
■ LARYNGEAL TUBE The laryngeal tube is made up of a single ventilation lumen surrounded by a proximal pharyngeal cuff and a distal esophageal cuff (Fig. 35.21). The ventilation tube is occluded at the distal end and like an ETC has a port above the distal cuff and below the pharyngeal cuff that is positioned in front of the laryngeal inlet. The major design advantage over the ETC is that the shape of the laryngeal tube causes it to pass into the esophagus almost 100% of the time. In addition, a single inflation tube will inflate both cuffs simultaneously. The tubes are generally color coded for size, and pediatric sizes are available. Some laryngeal tubes have an additional gastric suction port. Laryngeal tubes are commonly used to establish an emergency airway and have been found suitable for short periods of positive pressure ventilation. Some are advocating their use as a replacement for the LM and that they can be used for routine surgical cases in which a laryngeal airway is not contraindicated. It is important to note that many laryngeal tubes will not permit the passage of an endotracheal tube. In addition, although passage of a tube exchanger through the laryngeal tube into the trachea has been described, it can be very difficult. Laryngeal tubes are manufactured by several different companies including King Systems, VBM Medizintechnik, and Claflin Medical Equipment. They are intended for single use or multiuse, are latex free, and are generally priced between $40 and $75 each.
■ FIGURE 35.21 King laryngeal tube.
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Other laryngeal type tubes: Similar designs to the laryngeal tube include the Pharyngeal Airway Express (Vitals Signs Inc.), the Streamlined Pharynx Airway Liner (SLIPA), and the Glottic Aperture Seal Airway (Arizant Healthcare, Inc., formerly Augustine Medical, Inc.). As of press time, these airways have yet to gain significant popularity.
■ ENDOTRACHEAL TUBES A variety of endotracheal tubes are used in the practice of anesthesia and critical care medicine. This section will discuss the different types of endotracheal tubes available, their features, indication for use, setup, and their care. Endotracheal tubes are flexible, long, and hollow tubes made of PVC. They are usually equipped with an inflatable cuff, a pilot balloon, and an airway connector (Fig. 35.22). Inflation of the cuff will require a syringe. Common endotracheal tubes used in the operating rooms are described as High Low tubes. This means that the cuff may take high volumes of air (6–8 mL) to seal the trachea and protect the airway; however, cuff inflation generates low pressures on the trachea to minimize trauma to the airway. Placement may require the use of a stylet for guidance. Once the endotracheal tube is placed, correct tracheal positioning should be confirmed with positive bilateral breath sounds, positive end-tidal CO2 with a gas analyzer or colorimetric devices, or with bronchoscopy. The endotracheal tube needs to be secured with adhesive tape, a tube tie, or commercially available devices designed for securing endotracheal tubes. These endotracheal tubes come individually packaged, are disposable, and are meant for single use only. Cuffed endotracheal tubes come in a variety of sizes based on their internal diameter. Sizes
■ FIGURE 35.22 Single-lumen cuffed endotracheal tube.
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TABLE 35.1 THE AGE AND WEIGHT
OF PATIENTS CAN BE USED TO ESTIMATE THE APPROPRIATE SIZE OF ENDOTRACHEAL TUBE AGE
WEIGHT (KG)
ET TUBE INTERNAL DIAMETER (MM)
Newborn
2.0–3.0
3.0 uncuffed
Newborn
3.5
3.5 uncuffed
0–3 mo
6
3.5 uncuffed
1y
10
4.0 uncuffed
2–3 y
12–14
4.5 uncuffed
4y
16
5 uncuffed
6y
20
5.5
8y
24
6.0
10 y
30
6.5
Adult
40
7
Adult
50–60
7.5
Adult
60–70
8
Adult
>70
8.5–10
range from 4.5 to 10.5 mm. The size is labeled on the proximal end of the endotracheal tube. Table 35.1 presents the typical endotracheal tube sizes based on the approximate age and weight of the patient.
Parker Endotracheal Tubes Parker endotracheal tubes have an added feature of a downward curved, soft, midline, flexible tip that is designed to minimize trauma to glottic structures upon insertion (Fig. 35.23). These FlexTip tubes have been used when intubating over an intubating introducer or over a bronchoscope.
■ FIGURE 35.23 Parker Flex-Tip tube.
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Uncuffed Endotracheal Tubes Uncuffed endotracheal tubes are typically used in patients younger than 8 years of age to minimize airway trauma. The cricoid ring is located just below the larynx and is the narrowest portion of a child’s airway. Trauma to this portion of the airway can cause inflammation and narrowing of the trachea. These uncuffed tubes lack a cuff and pilot balloon (Fig. 35.24). With the endotracheal tube inserted into the trachea, a leak test is performed to check the seal on the airway. This is done by pressurizing the airway of the intubated pediatric patient and checking on the manometer at what pressure a small leak is detected. A leak at about 20–30 cm of water is considered acceptable. If the leak is not within this range, the clinician will need to repeat the intubation with a different size endotracheal tube until the appropriate fit occurs. Too much leak at low pressures will require a larger tube, while insufficient leak at appropriate pressure will require a smaller tube. In preparing for intubation in a pediatric case, several tube sizes should be available. A stylet should also be readily available to facilitate intubation. The size of the uncuffed endotracheal tube required will depend on the age and size of the child (Table 35.1). The endotracheal tube size for children older than 2 years of age may also be determined by the Cole equation: size = 4 + age/4. Some clinicians choose to use a cuffed endotracheal tube that is half or 0.5 tube size smaller than the estimated uncuffed endotracheal tube. This prevents the need for repeated intubations of a child and also may minimize trauma to the airway. The cuff will be used to provide a seal to the airway.
■ FIGURE 35.24 Uncuffed endotracheal tubes.
■ FIGURE 35.25 Right angle endotracheal (RAE) tube. Oral RAE tube pictured on the right. Nasal RAE tube pictured on the left.
Right Angle Endotracheal Tubes RAE tubes are cuffed endotracheal tubes with an over 90-degree bend near the connector (Fig. 35.25). These tubes are typically used in head and neck surgical cases where the right angle diverts the endotracheal tube away from the surgical field. RAE tubes may be inserted through the mouth or nose into the trachea. Oral RAE tubes direct the tube from the oropharynx toward the foot of the patient. Placement of an oral RAE tube may require the use of a stylet to shape the tube and facilitate intubation. Nasal RAE tubes direct the tube from the nares toward the top of the head. If a nasal route is chosen, the clinicians will require nasal spray phenylephrine, viscous lidocaine, and laryngoscope. In many cases, they may also require Magill forceps to facilitate endotracheal tube placement (Fig. 35.26). The forceps are used to grasp the distal end of
■ FIGURE 35.26 Magill forceps used to facilitate endotracheal tube placement.
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the endotracheal tube under direct vision with a laryngoscope. The tube can then be directed to enter the trachea. RAE tubes are meant for single use only and are disposable.
the wire spiral endotracheal tube will need to be replaced immediately. It is highly recommended to place an oral bite block in a patient intubated with a wire spiral endotracheal tube.
Evac Tubes
Double-lumen Endotracheal Tubes
Special endotracheal tubes may be used in the ICU setting. The Mallinckrodt TaperGuard and TaperGuard Evac endotracheal tubes are endotracheal tubes with a large elliptically shaped opening on the back side of the endotracheal tube just above the cuff where secretions can pool in a supine patient. This opening is a drainage port through which secretions above the cuff may be suctioned through the evacuation lumen. This may reduce the number of ventilator-associated pneumonias in the ICU. This endotracheal tube may require a stylet to aid in placement and is disposable.
Double-lumen endotracheal tubes are used for clinical cases that require lung isolation and one-lung ventilation, or differential ventilation of the two lungs (Fig. 35.28). The doublelumen endotracheal tube may serve to protect one lung from the other with unilateral infection, abscess cavity, massive hemorrhage, or a large cyst or bulla that could rupture. Other indications for the use of these special endotracheal tubes are to provide ventilation if there is an opening in the conducting airways of the lung to the pleural cavity or outside of the body (e.g., bronchopleural fistula or bronchocutaneous fistula). These can occur from surgery or trauma. Double-lumen tubes are also used during surgery to facilitate surgical exposure by allowing one of the lungs to deflate while the other is ventilated so that the surgeon can visualize intrathoracic structures. Surgeries requiring double-lumen tubes include robotic cardiac surgery, thoracoabdominal aneurysm repairs, video-assisted thoracoscopic procedures, thoracotomies, and pneumonectomies. Double-lumen tubes come in a range of sizes; however, the 35 French size is commonly used in an average-size female and the 37 French size in an average-size male. The tubes come with a leftward-facing tip or a rightward-facing tip. The angle of the tip is designed to facilitate placement in either the right or left mainstem bronchus, depending upon the clinical situation. The tube will have both a tracheal cuff and a bronchial cuff. Each cuff is inflated separately. The double-lumen endotracheal tube has a special
Armored Endotracheal Tubes Armored endotracheal tubes have a spiral wire incorporated into the PVC tubing that reinforces the tube wall (Fig. 35.27). They are flexible and resistant to kinking. These may be either cuffed or uncuffed. They are used for flexible fiberoptic intubation or in airways that may have a tendency to collapse due to tracheal wall weakness or endobronchial tumors. They are also used in head and neck or oral surgery to prevent kinking with tube manipulation. Wire spiral endotracheal tubes may require either a fiberoptic bronchoscope or a semirigid stylet to facilitate placement. Most wire spiral tubes are single use only. Some may be sterilized and reused. One note of caution, if the patient actively bites down on the wire spiral endotracheal tube or the tube is kinked, the tube can remain kinked and the lumen can be significantly obstructed. In this clinical situation,
■ FIGURE 35.27 Wire-reinforced endotracheal tube.
■ FIGURE 35.28 Double-lumen endotracheal tube.
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while oscillatory ventilation could be applied to the other. In review, the following equipment may be necessary to facilitate the use of double-lumen endotracheal tubes:
■ FIGURE 35.29 Double-lumen endotracheal tube adaptor.
adaptor that allows for clamping of the airway and one-lung ventilation (Fig. 35.29). Double-lumen tubes may be placed with direct laryngoscopy or with the aid of a fiberoptic bronchoscope. Generally, the tube is placed through the glottis with the distal angle facing anteriorly. Once in the trachea, the tube is rotated so that the distal end enters the desired bronchus. A fiberoptic bronchoscope is used by the clinician to confirm the position of the tube. The tube is correctly positioned when the distal end of the tube is in the desired bronchus, the distal cuff is placed in the proximal bronchus just below the carina, and the bronchial cuff is not obstructing any distal bronchial openings. Many clinicians prefer to inflate the bronchial cuff while watching with the fiberoptic scope. The fiberoptic scope can be used to reposition the tube if necessary. Once properly positioned, the tube should be secured. Because these tubes may become slightly displaced during surgical manipulation or positioning of the patient, the fiberoptic bronchoscope should always be available in the operating room for the entire case. Once the adaptor is attached to the tube, both lungs can be ventilated. When one-lung ventilation is required, a clamp is placed over the tube leading to the lung that will not be ventilated. The cap over the lumen is opened to allow the desired lung to deflate. In some cases, one-lung ventilation is insufficient to maintain adequate oxygenation of the patient. The clinician may apply CPAP with oxygen to the “down” lung to slightly expand it with oxygen. In other special cases, each lung may be attached to a ventilator and differential ventilation applied to each lung. For example, standard ventilation could be applied to one lung,
• Appropriate size double-lumen tube • A right- or left-sided tube (check with provider which is desired) • Double-lumen tube endotracheal tube adaptor (comes with the tube) • Fiberoptic bronchoscope and all associated equipment (e.g., defogger) • Clamp • Lubricant to facilitate passage of the tube through the glottic opening • 10-mL syringe to inflate the tracheal cuff; 3- or 5-mL syringe for the bronchial cuff • CPAP device with a supplemental oxygen source • Tube exchanger (double-lumen tubes are frequently changed for single-lumen tubes at the end of the case)
■ ENDOTRACHEAL TUBE ADAPTORS Endotracheal adaptors connect the endotracheal tube to the airway circuit of the anesthesia machine or the mechanical ventilator. Most anesthesia circuits include an elbow connector. Other endotracheal adaptors serve specific purposes in the management of the airway. • A bronchoscope endotracheal adaptor allows the clinician to perform bronchoscopy on a patient airway while providing a sealed circuit to ventilate the patient (Fig. 35.30).
■ FIGURE 35.30 Bronchoscope adaptor.
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■ FIGURE 35.31 Endotracheal extender adaptor.
■ FIGURE 35.33 Heat and moisture exchanger.
• An endotracheal extender adaptor provides extra length from the endotracheal tube to the airway circuit (Fig. 35.31). • At times, special foam padding is used on the face of a prone patient. An extension adaptor may be used to connect an endotracheal tube in a prone patient through the padding to the airway circuit (Fig. 35.32). • Heat and moisture exchange (HME) adaptors are placed between the elbow connector of the endotracheal tube and the airway circuit of the anesthesia machine or the mechanical ventilator (Fig. 35.33). This allows the retention of warmth and humidity for the patient during ventilation. • Medication adaptors allow for the delivery of inhaled medications (e.g., bronchodilators) (Fig. 35.34). This adaptor is placed inline with the airway circuit just beyond the elbow connector. The drug is dispensed during the inspiratory cycle of ventilation.
■ STANDARD LARYNGOSCOPES
■ FIGURE 35.32 Endotracheal extender adaptor passing through padding for prone positioning.
■ FIGURE 35.34 Medication adaptor for the administration of inhaled medications.
The laryngoscope is an essential piece of equipment in the operating rooms and ICUs for airway management. The laryngoscope allows the clinician to directly visualize the glottic opening during intubations. A laryngoscope consists of a blade, light source, handle, and batteries. There are two basic rigid laryngoscope systems. The handle allows the clinician to manipulate the blade during intubation attempts. In addition, the handle serves as a power source for a bulb located at the blade tip (Fig. 35.35). The bulb is an incandescent tungsten filament surrounded by a halogen gas. The bulbs are either frosted or clear. In the other major laryngoscope system known as bulb-on-handle system, the laryngoscope handle not only serves as a power source but also provides a light source by using a light-emitting diode (LED). This light is then
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■ FIGURE 35.35 Laryngoscope handle for a regular blade.
transmitted to the tip of a special laryngoscope blade that has fiberoptic cables (Fig. 35.36). The special blades are referred to as fiberoptic blades. The LED light systems tend to last longer than the incandescent filament bulb, generate less heat, and use less energy. Both types of handles have either rechargeable or replaceable C- or D-size batteries. The rechargeable handles come with a recharging base (Fig. 35.37). After each use, the handles are wiped down with an antimicrobial wipe. Through the years, a variety of laryngoscope blades have been developed with minor variations in their designs. These include the Cranwall, Jackson, Janeway, Flange, Macintosh, Magill, Miller, etc. Despite the variations, blades come in two basic shapes: either straight (Fig. 35.38) or curved (Fig. 35.39). Both straight and curved blades come in a range of sizes: 0 (infants) through 4 (large adults). After each use,
■ FIGURE 35.36 Lighted handle for fiberoptic blade.
■ FIGURE 35.37 Rechargeable base for laryngoscope handle.
the laryngoscope blades are rinsed in an antimicrobial solution and dried. In preparation for every intubation, the laryngoscope must be inspected for proper working condition. If the laryngoscope fails to light up, several steps may be used to evaluate and remedy the situation: • Change the batteries in the handle (or recharge the handle). • Replace the handle.
■ FIGURE 35.38 Straight laryngoscopy blades sizes 1–3. tahir99-VRG & vip.persianss.ir
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■ FIGURE 35.39 Curved laryngoscopy blades sizes 2–4.
• • • •
Change laryngoscope blade. Change laryngoscope handle. Tighten the bulb on the blade. Change the bulb on the blade or the handle (bulb-on-handle system).
■ VIDEO LARYNGOSCOPES Rigid video laryngoscopes (RVLs) are transoral devices that can be used by the clinician to indirectly visualize the larynx during intubation with an endotracheal tube. Direct laryngoscopy with a standard laryngoscope allows the clinician to have a direct view of the vocal cords and the upper airway. Video laryngoscopes are composed of a light source, camera, video connector, video monitor, and electrical power source. The video monitor provides a real-time image useful in inspecting the upper airway and facilitating intubation. A flexible or rigid stylet (thick metal wire) placed inside the endotracheal tube is used to aid in the guidance of the endotracheal tube into the trachea. The RVLs that are currently available for clinical use include McGrath (LMA™ North America, Inc.), GlideScope (Verathon, Bothell, Washington), Storz DCI (Karl Storz GmbH & Co. KG, Tuttilngen, Germany), Airtraq (Prodol Meditech S.A., Vizcay, Spain), and PentaxAWS (Airway Scope; Pentax, Tokyo, Japan) (Figs. 35.40 and 35.41). RVLs cost between $10,000 and $20,000. The handling and maintenance of these devices are important. When provided separately, RVL blades and handles cost vary widely in price.
■ FIGURE 35.40 McGrath RVL.
Indications for the use of RVLs include the following: • Anticipated difficult airway (awake or asleep) ° Limited neck extension ° Upper airway (pharyngeal and laryngeal) partial obstruction Craniofacial abnormalities °
■ FIGURE 35.41 GlideScope.
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• As a rescue device for an unanticipated difficult airway Relative contraindications for the use of RVLs (mainly due to occlusion of the lens) include the following: • Massive upper airway bleeding • Upper airway (pharyngeal and laryngeal) total obstruction • Upper airway disruption from trauma • Need for emergent surgical airway All the videoscope systems require a brief warmup period prior to use. This prevents the clear plastic components from fogging during the intubation. If the user experiences difficulty with the image, check and clean all contacts and check the power source.
■ FIBEROPTIC SCOPES Indirect visualization of the glottic opening may also be done with fiberoptic scopes. Fiberoptic cables transmit light from a light source on the proximal portion to the distal portion of the scope. A different set of fiberoptic cables send an image from the distal portion of the scope to the eyepiece or camera and monitor. There are two varieties of fiberoptic scopes used in anesthesia: rigid and flexible. The Bullard scope is a rigid fiberoptic laryngoscope that is used for indirect visualization of the tracheal opening (Figs. 35.42 and 35.43). Figure 35.42 illustrates the three components that make up a complete Bullard blade: the power source (a regular rigid laryngoscope handle with two C-size batteries); the endotracheal tube stylet and guide; and the fiberoptic blade, handle,
■ FIGURE 35.42 Bullard scope components: handle, stylet, and fiberoptic laryngoscope.
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■ FIGURE 35.43 Bullard scope assembled.
and eyepiece. Figure 35.43 depicts a fully assembled Bullard scope with an endotracheal tube in position for intubation. This is a reusable device that requires germicidal cleaning of the blade, handle, and stylet sections of the Bullard blade in between use. The Wu scope is another rigid fiberoptic scope (Fig. 35.44). The Wu scope uses a short fiberoptic system that contains an eyepiece, a power source, and a light source. The eyepiece may be used directly, or a camera and monitor
■ FIGURE 35.44 Wu scope.
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system can be attached to the eyepiece. The flexible fiberoptic scope is placed into a rigid laryngoscope blade to provide the indirect image of the tracheal opening. This rigid blade contains another groove through which an endotracheal tube is passed into the airway. The component will also require germicidal cleaning in between uses.
■ FLEXIBLE FIBEROPTIC BRONCHOSCOPE The flexible fiberoptic bronchoscope has been the traditional gold standard in the management of a difficult airway either anticipated or nonanticipated (Figs. 35.45 and 35.46). The endotracheal tube may be placed into the trachea via an oral or nasal route with the guidance of the flexible fiberoptic scope. This scope is a steerable device that flexes and extends the tip by using a thumb control near the eyepiece. Rotation of the flexible fiberoptic scope clockwise or counterclockwise further refines the guidance of the scope. The light source may be an external device attached to the bronchoscope through a cable or directly attached with a small power source. The light is carried down to the distal tip of the bronchoscope by fiberoptic bundles. A different set of fiberoptic bundles carry the image to the eyepiece or camera at the proximal end of the scope. Care in handling of the fiberoptic bronchoscope is important since the fiberoptic bundles may break if bent too far. A separate channel is available to instill local anesthetic or oxygen to the distal tip and to serve as a suction port to clear secretions. The approximate cost of these scopes range from $10,000 to $15,000. Flexible fiberoptic scopes are useful for awake or asleep intubations. During an awake
■ FIGURE 35.46 Flexible portable bronchoscope disassembled.
intubation via the oral approach, the clinician will topicalize the airway with local anesthetics and place a bite block to prevent the patient from biting down on the scope or hand of the operator. The clinician may provide intravenous (IV) sedation to the patient if not contraindicated. An assistant may be necessary to displace the patient’s tongue forward with the use of clean gauze, laryngoscope blade, and/or Magill forceps. The technique for awake fiberoptic intubation is further discussed in Chapter 18. When performing a nasal fiberoptic intubation, various sized nasal airways, nasal vasoconstrictors (e.g., phenylephrine to shrink nasal tissues), and topical local anesthetics (e.g., cocaine-soaked Q-tips or 4% viscous lidocaine) are used to numb the airway and to facilitate intubation. After its use, the bronchoscope suction port should be cleared by holding the suctioning button and dipping the distal end of the scope into a container of water. The bronchoscope suction port should be cleaned to remove particulate matter with a long thin brush. This will prevent the solidification of material in the suction channel. Then, the entire scope, with the light source removed, is soaked in a bactericidal solution for several minutes, rinsed in clean water, suctioned with the use of a suction attachment, and then hand dried. A tray may be used to store, transport, and protect the bronchoscope in between uses.
■ OTHER AIRWAY ADJUNCTS Lighted Stylets ■ FIGURE 35.45 Flexible portable bronchoscope.
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There are several lighted stylets available for clinical use (Fig. 35.47). These include Trachlight (Laedral), Vital Light (Vital Signs),
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■ FIGURE 35.47 Trachlight.
■ FIGURE 35.48 Intubating bougie.
Trachlight (Rusch), and Surch-Lite (Aaron Medical Industries, Inc.). An endotracheal tube is placed on the flexible stylet but not over the lighted end. The lighted stylet is given a slight bend at the tip prior to insertion. The lighted stylets are blindly inserted devices through the mouth that use a bright light to transilluminate the anterior neck and to guide tracheal placement of an endotracheal tube. The ambient light in the room may need to be reduced when lighted stylets are used. Because the trachea is close to the surface of the skin, a small well-circumscribed glow in the anterior neck will occur when the stylet tip is located in the trachea. The tube can then be advanced into the trachea. If a dull diffuse light or no light is seen, then the tip of the lighted stylet is most likely within the esophagus.
need to be exchanged for different reasons (e.g., a different size tube, a broken pilot balloon, rupture endotracheal cuff, or exchange from a double-lumen tube to a single-lumen tube). In many cases, the original intubation was difficult, or subsequent swelling of airway structures may make laryngoscopy difficult while attempting to exchange an endotracheal tube. In these cases, a tube exchanger can be placed into the trachea via the original endotracheal tube. The endotracheal tube can be removed, and a lubricated endotracheal tube can be guided over the tube exchanger into the trachea. Tube exchangers have length measurements on the outer surface to estimate the depth of insertion. Tube exchangers come in a range of sizes and have either a luer lock or an airway attachment fitting that can be used for jet ventilation or insufflation of oxygen.
Intubating Bougie During direct laryngoscopy the clinician may have difficulty visualizing the glottis or passing an endotracheal tube. An intubating bougie is a long thin device with a slight bend at the distal tip that helps placement through the vocal cords (Fig. 35.48). In many cases, a bougie can be placed under direct visualization through the glottic opening even though the endotracheal tube could not. Once the bougie is in the trachea, an endotracheal tube can be placed over the bougie and into the trachea.
Tube Exchangers Tube exchangers are semirigid tubes that are used to exchange an existing endotracheal tube in a patient for another without the use of a laryngoscopy (Fig. 35.49). Endotracheal tubes
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■ FIGURE 35.49 Tube exchanger. (Courtesy of the Mayo Foundation.)
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■ CRICOTHYROTOMY
Direct Cricothyrotomy
The clinician is rarely confronted with a patient who cannot be intubated and cannot be ventilated despite the use of multiple different airway devices. This is an emergent situation that requires intervention to establish an airway within minutes or the patient may suffer irreversible brain damage or death (see Chapter 60). In this scenario, placing a large IV catheter (14G or larger), retrograde wire, or a cricothyrotomy tube through the cricothyroid membrane may be considered in attempting to establish an airway. The cricothyroid ligament is located between the thyroid cartilage and the cricoid ring in the upper airway (see Chapter 11).
An emergency cricothyrotomy kit consists of a catheter over a needle, stylet, syringe, guide wire, dilator, scalpel, soft neck strap, and a cricothyrotomy tube that attaches to an anesthesia circuit or a bag ventilation system (Fig. 35.50). The cricothyroid ligament is entered in a manner described above. The needle is angled toward the feet of the patient and a wire passed over the needle into the trachea. The scalpel is used to create a large opening into the trachea around the wire. The dilator is loaded inside the cricothyrotomy tube, and the entire unit is passed over the wire into the trachea. The dilator and wire are removed, and the breathing circuit is attached to the cricothyrotomy tube.
Cricothyrotomy and Jet Ventilation
Jet Ventilation Systems
An angiocatheter size 14G or larger may be placed in a sterile fashion through the cricothyroid ligament into the airway with the use of a fluid-filled syringe. The needle is angled toward the feet of the patient. As the needle enters the airway, bubbles will appear in the syringe, confirming proper entry. The angiocatheter is held in place by hand, and a lure locking jet ventilator is hooked to the catheter (see Jet ventilation below). This is only a temporary airway until a more definitive airway is established either surgically or via other techniques described in this chapter.
Jet ventilation systems are used to ventilate and oxygenate patients in both emergent airway situations and during surgeries in which traditional ventilation cannot be used. During emergencies jet ventilation via a catheter placed through the cricothyroid ligament can be life saving. Jet ventilators have a high-pressure hose that attaches to a wall cylinder (E or H size) oxygen source, a pressure regulator/gauge, an on/off valve, and a small-bore tubing assembly with a luer lock fit (Fig. 35.51). Once this device is hooked up to the catheter in the trachea, the on/off valve is pushed and the regulator is adjusted to the lowest pressure that allows for the patients’ chest to rise. The gas flow is delivered for about 1 second and released for 3 seconds to allow for passive exhalation through the mouth and nose. The catheter only allows flow into the patient. Expiration does not occur through the catheter, but rather through the patient’s nose and mouth. Another method of providing jet ventilation is the use of the oxygen flush valve of the
Retrograde Wire Cricothryotomy Another technique that is utilized if more time is available is to place a wire into the cricothyroid membrane. There are kits available that contain the necessary equipment. For the retrograde wire technique, the cricothyroid membrane is entered in a similar fashion described above except that the angle of the needle is toward the top of the head. Once the catheter is in the airway, a long flexible wire is passed into the oropharynx. When the wire is visualized in the oropharynx, Magill forceps are used to grasp the wire and deliver it out of the mouth. The endotracheal tube is then guided over the wire and into the trachea. In a modification of the retrograde wire-guided technique with the use of a fiberoptic scope, the wire is identified in the oropharynx. The wire is guided into the suction channel of the fiberoptic scope and the scope is advanced over the wire and into the trachea. The tube is then advanced into the trachea over the scope.
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■ FIGURE 35.50 Emergency cricothyrotomy kit.
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■ FIGURE 35.51 Jet ventilation system.
anesthesia machine. Here an adaptor must be fashioned to hook up the catheter luer lock to the anesthesia circuit. A 3-mL luer lock syringe with the plunger removed can be attached to the luer catheter. The endotracheal adapter for a size 7 French endotracheal tube is placed in the open end of the syringe to achieve a tight fit (Fig. 35.52). The adaptor is attached to the anesthesia circuit. Once properly attached to the
■ FIGURE 35.52 Jet ventilation adaptor using 3-mL syringe and size 7 endotracheal tube adaptor.
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circuit, the oxygen flush is held on for 1 second and released for 3 seconds to deliver high-pressure oxygen. Jet ventilation may also be accomplished with the use of an endotracheal tube exchanger passed through the vocal cords into the trachea. Some tube exchangers have a ventilating lumen and luer lock connector. The jet ventilator can be attached to the luer lock connector. Some neck and thoracic surgical cases are ventilated with this technique. A word of caution about the use of jet ventilation with a transcricothyroid ligament membrane catheter needs to be emphasized. If the catheter is not within the trachea, insufflation of oxygen in subcutaneous tissue, esophagus, blood vessels, and other solid structures may lead to damage to surrounding tissue and will not ventilate the patient. Furthermore, insufflation of gas into subcutaneous tissues can make further attempts establishing an airway even more difficult.
■ ROUTINE AIRWAY SETUP A routine airway checklist can be used prior to intubating a patient to ensure a safe intubation attempt. The checklist will cover the medications, equipment, and personnel that are important to have available during intubations. Setup for a routine intubation should include the following: • Functioning IV (checked that it runs well and is not infiltrated) • Anesthesia machine checked (if using) • Working suction with adequate tubing length and suction tip (e.g., Yankauer suction tip) • Bag-valve-mask as the primary or backup source of ventilation. Make sure the mask cuff is properly inflated. Mask cuffs can deflate over time. • Oxygen and a method to preoxygenate the patient (face mask, anesthesia mask, bagvalve-mask, etc.) • Appropriately sized oral airway or NPA • Appropriately sized endotracheal tube, cuff checked that it does not have a leak. If it is a cuffed endotracheal tube, a syringe to inflate the cuff should be ready (usually a 10-mL syringe). A backup endotracheal tube should be readily available. • Appropriate stylet for the endotracheal tube • Laryngoscope with appropriate blade. Light source and bulb have been checked. • Tape or other commercial device to secure the tube to the patient
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• CO2 monitor or colorometric CO2 detector to confirm tracheal intubation by the presence of CO2 • Stethoscope to evaluate breath sounds • Backup airway device available but not opened (e.g., laryngeal airway) • Intubation drugs: Succinylcholine immediately available for every intubation, other muscle relaxants as requested by the anesthesia provider, hypnotic (e.g., propofol or etomidate)
■ PLANNED DIFFICULT AIRWAY SETUP Once a patient has been identified as a difficult airway, patient positioning items, medications, adjunctive devices, videoscopes, flexible fiberoptic scopes, and alternative airway devices need to be available for the intubation attempt. The following should be available for a planned difficult airway: • Functioning IV (checked that it runs well and is not infiltrated) • Anesthesia machine checked (if using) • Working suction with adequate tubing length and suction tip (e.g., Yankauer suction tip) • Bag-valve-mask as the primary or backup source of ventilation. Make sure the mask cuff is properly inflated. Mask cuffs can deflate over time. • Oxygen and a method to preoxygenate the patient (face mask, anesthesia mask, bagvalve-mask) • Appropriately sized oral airway or NPA • Appropriately sized endotracheal tube, cuff checked that it does not have a leak. If it is a cuffed endotracheal tube, a syringe to inflate the cuff should be ready (usually a 10-mL syringe). A backup endotracheal tube should be readily available. The backup tube should be a smaller size and loaded with a stylet. • Appropriate stylet for the endotracheal tube • Laryngoscope with appropriate blade. Light has been checked. Difficult airways may require a variety of blades to be immediately available (different sizes or types from the primary blade). • Tape or other commercial device to secure the tube to the patient • CO2 monitor or colorometric CO2 detector to confirm tracheal intubation by the presence of CO2 • Stethoscope to evaluate breath sounds • Backup airway device available opened (e.g., laryngeal airway)
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■ FIGURE 35.53 Emergency airway cart with GlideScope.
• Intubating bougie/stylet available • Intubation drugs: Succinylcholine immediately available for every intubation, other muscle relaxants as requested by the anesthesia provider, hypnotic (e.g., propofol or etomidate) • Patient positioning devices (towels, blankets, specialized ramps) • Specialized laryngoscopes (videoscope and/or fiberoptic scope) • Airway adjuncts (lightwand, etc.) • Backup airway devices (laryngeal tubes, intubating laryngeal airway, emergency cricothyrotomy equipment) In most institutions, the majority of these items are assembled on a “difficult airway” cart that can be rapidly deployed to a location with a difficult airway (Fig. 35.53).
■ PLANNED FIBEROPTIC BRONCHOSCOPIC INTUBATION SETUP The planned fiberoptic bronchoscopic intubation may be done on either an awake or an asleep patient. If an awake intubation is planned, the difficult airway cart, if one is available, should be
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brought to the room. The most common method of awake intubation involves the use of the flexible fiberoptic bronchoscope. The following items should be set up to prepare for an awake intubation: • Functioning IV (checked that it runs well and is not infiltrated) • Anesthesia machine checked (if using) • Working suction with adequate tubing length and suction tip (e.g., Yankauer suction tip) • Bag-valve-mask as the primary or backup source of ventilation. Make sure the mask cuff is properly inflated. Mask cuffs can deflate over time. • Oxygen and a method to preoxygenate the patient (face mask, nasal cannula, anesthesia mask, bag-valve-mask). It is often desirable to be able to deliver oxygen to the patient while the awake intubation is being performed. The oxygen mask or nasal cannula should be fashioned to permit delivery of oxygen while the fiberoptic bronchoscope is being inserted into the patient’s mouth or nose. Some specialized masks are available to achieve this goal. They have a port to allow entry of the scope but still have the ability to maintain a tight mask fit around the patient’s mouth and nose. • Specialized equipment to assist in fiberoptic intubation ° Equipment to anesthetize the oropharynx: Topical anesthetic (2%-4% lidocaine solution, 2% lidocaine jelly) and a device to deliver the anesthetic (atomizer, nebulizer, cup for gargle and swallow, gauze and Magill forceps for possible glossopharyngeal nerve block, needle/syringe/catheter for possible transtracheal local administration, needle and syringe for possible laryngeal nerve block, etc). Tongue blade and gauze to open the mouth ° and possibly control the tongue ° Fiberoptic bronchoscope Light/power source has been checked. Video screen checked (if using) Test optics and focus of bronchoscope by using the scope to look at an object White balance the bronchoscope Specialized endotracheal tube (e.g., Parker endotracheal tube) to facilitate passage of endotracheal tube through the
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vocal cords. A regular endotracheal tube can be used as well. Scope has been lubricated to facilitate advancement of the endotracheal tube off the scope into the airway. Distal end of the scope has been treated with a defogger. Endotracheal tube is loaded onto the fiberoptic bronchoscope. The endotracheal tube should be secured to the handle of the bronchoscope to allow entry of the tip of the bronchoscope into the airway and prevent the endotracheal tube from slipping off the scope handle (Fig. 35.54). The cuff of the endotracheal tube checked and lubricated. Specialized oral airway to prevent the patient from biting on the bronchoscope as well as to guide the scope through the middle of the oropharynx (Ovassapian Airway, Williams Airway Intubator, Patil-Syracuse Oral Airway, Rapid Oral Tracheal Intubation Guidance System) (Fig. 35.55). These airway adjuncts allow for the forward displacement of the tongue along with a guide for the fiberoptic bronchoscope. These airways may be left in for a short duration of a surgical case or slipped out of the mouth over the endotracheal tube after the endotracheal tube adaptor is removed. Some clinicians will use a rigid laryngoscope blade (either Mac or Miller blade) to displace the tongue forward during fiberoptic intubation.
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■ ■
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■ FIGURE 35.54 Fiberoptic scope with endotracheal tube secured onto handle. (Courtesy of the Mayo Foundation.)
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•
■ FIGURE 35.55 Ovassapian airway. (Courtesy of the Mayo Foundation.)
10-mL syringe for possible injection of local anesthetic through the working or suction channel of the bronchoscope At the time of fiberoptic bronchoscopy, local anesthetic can be injected down the injection/suction port of the bronchoscope once the vocal cords or trachea have been visualized. About 1–2 mL of local anesthetic along with a few milliliters of air is placed into a 6- or 12-mL syringe. The air helps the local anesthetic to clear the injection port and to numb the area visualized by the operator of the bronchoscope. Some clinicians will pass an epidural catheter down the injection port and inject the local anesthetic through the epidural catheter, which is positioned just distal to the tip of the bronchoscope. Oxygen tubing and connector to allow possible oxygen administration through a port in the bronchoscope Suction and tubing that can be attached to the suction channel of the bronchoscope Stackable step stools to allow bronchoscopist to stand above patient Nasal fiberoptic intubation equipment ° Decongestant nasal spray (e.g., neosynephrine, 1% phenylephrine) to vasoconstrict the nasal passages and reduce bleeding Agents for anesthetizing the nasal passages (e.g., cocaine-soaked Q tips or ■
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viscous lidocaine applied with a nasal airway) Backup airway equipment ° Appropriately sized oral airway or NPA ° Appropriately sized endotracheal tube, cuff checked that it does not have a leak. The tube should be loaded with a stylet. Laryngoscope with appropriate blade. Light ° has been checked. Difficult airways may require a variety of blades to be immediately available (different sizes or types from the primary blade). Backup airway device available and opened ° (e.g., laryngeal airway, intubating laryngeal airway) Intubating bougie/stylet available ° Specialized laryngoscopes (videoscope and/ ° or fiberoptic scope) ° Airway adjuncts (lightwand, etc.) Tape or other commercial device to secure the tube to the patient CO2 monitor or colorometric CO2 detector to confirm tracheal intubation by the presence of CO2 Stethoscope to evaluate breath sounds Intubation drugs (succinylcholine immediately available for every intubation, other muscle relaxants as requested by the anesthesia provider) Sedatives (e.g., narcotic, propofol, etomidate, midazolam, dexmedetomidine) Drying agents to reduce oropharyngeal secretions (e.g., glycopyrolate) Infusion pump for delivery of medications
■ SUMMARY This chapter has outlined the airway equipment commonly used during the management of an airway including mask ventilation, laryngeal airways, and intubation of the trachea. The chapter covers equipment for routine, difficult, and emergent airways. It also includes checklists to aid the anesthesia technician in the setup, operation, and maintenance of airway equipment. It is intended to be a broad overview; however, due to the rapid introduction of new airway devices into the market, it cannot include all available airway devices.
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REVIEW QUESTIONS 1. Which of the following is NOT a feature of ALL common laryngeal airways? A) Inserted with a blind insertion technique B) Allows passage of an endotracheal tube through the ventilation channel C) Has a pharyngeal cuff or balloon to seal the pharynx D) Intended for semiconscious, unconscious, or anesthetized patients E) None of the above Answer: B. Some laryngeal airways have “ribs” or other design features that do not allow the passage of an endotracheal tube through the ventilation channel into the trachea. They all are inserted blindly (do not require a laryngoscope) and have a pharyngeal cuff or balloon to seal the pharynx. They are usually not well tolerated by awake patients unless the pharynx has been anesthetized.
2. SOME laryngeal airways have the following features: A) A channel for suctioning gastric contents B) A gel-based cuff that is not inflated with air for sealing the pharynx C) Allow positive pressure ventilation D) Are MRI compatible E) All of the above Answer: E. A few, but not all, laryngeal airways have a suction channel for gastric contents or a gel-based cuff. Many laryngeal airways are not MRI compatible. The pilot tube assembly may contain metal. Be sure to check the packaging on the airway before using it in the MRI suite. Almost all laryngeal airways allow some degree of positive pressure ventilation. Some are specifically designed with a pharyngeal seal to allow higher pressures during positive pressure ventilation.
3. Which of the following is NOT used as an emergency airway if initial attempts at intubation or ventilation fail? A) Laryngeal airway B) Esophageal combitube C) Laryngeal tube D) Venturi mask E) LM Answer: D. A venturi mask is a modification of a simple mask to deliver passive oxygen at specific oxygen concentrations. Use of the venturi mask requires a spontaneously ventilating patient. LMs and laryngeal tubes are two different kinds of laryngeal airways. Both are used to attempt to establish an airway if initial attempts at ventilation and intubation fail. An esophageal combitube is also used in emergencies. It can be placed blindly into the esophagus (95% of the time) or the trachea and can be used to attempt to establish an airway.
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4. Which of the following statements are TRUE about endotracheal tubes? A) All endotracheal tubes have a cuff that can be inflated to create a seal. B) All endotracheal tubes have a suction port above the cuff to prevent secretions from contaminating the airway. C) Parker endotracheal tubes have three lumens. D) RAE tubes are often used in oral and head/neck surgery. E) All of the above are TRUE. Answer: D. RAE tubes redirect the tube away from the surgical field and are often used in oral and head/neck surgery. Only a very few types of endotracheal tubes have special ports for aspirating secretions above the cuff. They are used in the ICU to reduce the risk of pneumonia. Parker tubes are similar to standard single-lumen endotracheal tubes except that they have a tapered tip to facilitate passage between the vocal cords.
5. Which of the following statements are FALSE with regard to double-lumen endotracheal tubes? A) Allow only one lung to be ventilated B) Can be used to ventilate both lungs C) Are positioned with a fiberoptic bronchoscope D) Allow each lung to be ventilated differently E) The distal tip is positioned in the trachea. Answer: E. The distal tip of a double-lumen tube is positioned in the right or left mainstem bronchus with the aid of a fiberoptic bronchoscope. Both lungs can be ventilated using a common anesthesia circuit, or each lung can be ventilated separately with a different kind of ventilator. The most common use of a double-lumen tube is to allow one lung to collapse during surgery (not be ventilated) to improve surgical visualization of intrathoracic structures.
6. Administration of inhaled medications through the anesthesia breathing circuit is best accomplished with a special adapter. A) True B) False Answer: A. True. Special adapters allow direct attachment of the inhaled medication delivery system to the breathing circuit near the endotracheal tube. In addition, they direct the flow of medication toward the endotracheal tube.
7. Which of the following statements are FALSE regarding RVLs? A) Often used for anticipated difficult intubations B) May be difficult to use with trauma or large amounts of oropharyngeal bleeding C) Have a flexible tip that can be manipulated D) Are used through the mouth, similar to other laryngoscopes E) None of the above
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Chapter 35 • Airway Equipment Setup, Operation, and Maintenance Answer: C. RVLs do not have a tip that can be manipulated. This is a feature of flexible fiberoptic scopes. RVLs are inserted into the mouth and provide a direct view of the larynx from the tip of the scope and can help the provider view the glottic structures. They are useful during difficult intubations. On occasion, blood can obscure the videoscope lens, making it difficult to see.
8. Which of the following airway adjuncts would NOT be useful during a difficult intubation? A) Heat and moisture exchanger B) RVL C) Flexible fiberoptic scope D) Intubating bougie E) Lighted stylet
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SUGGESTED READINGS Brown D, et al. Atlas of Regional Anesthesia. 2nd ed. Philadelphia, PA: Saunders; 1999. Cattano D, et al. The Cormak-Lehane Scale revisited. Br J Anaesth. 2010;105(5):698–699. Miller CG, et al. Management of the difficult intubation in closed malpractice claims. ASA Newslett. 2000;64(6):13–16, 19. Stone D, et al. Airway management. In: Miller RJ, ed. Anesthesia. 5th ed. Philadelphia, PA: Churchill Livingstone; 2000:1419.
Answer: A. An HME is a device that can be inserted into the breathing circuit to retain heat and moisture in the gas in the anesthesia circuit. This prevents some heat loss from the patient and prevents the respiratory mucosa from drying out. All of the other devices can be useful during a difficult intubation.
9. Which the following is part of an emergency cricothyrotomy kit? A) Scalpel B) Needle with syringe C) Wire D) Dilator E) All of the above Answer: E. A complete emergency cricothyrotomy kit includes a needle and syringe to puncture the cricothyroid membrane. The wire is inserted into the trachea. The scalpel is used to expand the hole in the tissues around the wire. The dilator tube assembly is passed over the wire and into the trachea. The wire and dilator are removed and the breathing circuit is attached to the tube.
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CHAPTER
36
Infusion Pumps Victoria Reyes ■ INTRODUCTION Medication errors account for almost 20% of all medical injuries. Administration is the stage of the medication process most vulnerable to error, and the intravenous (IV) route of drug administration often results in the most serious patient injuries. IV infusion errors, which involve highrisk medications delivered directly into a patient’s bloodstream with an infusion pump, have been identified as having the greatest potential for patient harm. An understanding of the function, components, and use of medication pumps is essential for the anesthesia technician. Medication pumps are commonly used in the operating room (OR), obstetric suite (OB), and postanesthesia care unit (PACU). Infused medications include vasopressors, vasodilators, inotropes, antibiotics, chemotherapy medications, local anesthetics, sedatives, hypnotics, opioids, and muscle relaxants. Advances in the technology of medication pumps have introduced many new features. Today’s “smart pumps” have computer processors to provide decision support and fail-safe functions to improve patient safety. The anesthesia technician will be called upon to deliver pumps to the OR suite or off-site location and should be able to properly set up each device used in the facility. While the infusion pump is in use, the technician may need to troubleshoot alarms and nonfunctioning devices and be able to determine if the device needs replacement or service. Because the majority of anesthesia technicians will be involved in pump setup and troubleshooting, they should attend available opportunities for in-service training, particularly when new pumps are introduced into the department. The individual vendors are a great source of information and instruction on the use and maintenance
of the medication pumps used at your facility. In addition, anesthesia technicians will be involved in the maintenance of pump units stored in the department. The anesthesia technician must ensure that “smart pumps” are updated on a predetermined basis by the pharmacy and that they meet all standards set by governing entities. The technician should be sure that after pumps are used, they are returned to the workroom and cleaned according to the protocol at the facility.
■ MEDICATION PUMP SAFETY A major goal in the campaign to improve medication safety is to develop safer systems for the monitoring and delivery of drugs. IV medications administered through a pump must be delivered with precision due to the nature of the medications and the IV route of administration. IV administration results in a more rapid onset of drug effect; therefore, harmful side effects or the effects of drug toxicity may be more severe than when the same medication is administered orally. In addition, medication pumps deliver continuous infusions of medications. Thus, any error in dosing or formulation can be compounded over time. These issues effectively reduce the safety margin when medications are administered by IV infusion. The Joint Commission has noted that infusion pumps were frequently involved in medication errors that lead to serious patient injury. Experts reviewing these incidents have identified several human and mechanical errors. One of the most common problems was the use of pumps that do not provide protection from the free flow of IV fluid/medication into the patient. In addition, problems can occur when the wrong drug or concentration is administered, or the wrong rate is set. To address these issues, manufacturers of medication pumps have developed
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a number of innovations. For example, medication “smart pumps” were introduced in 2002 by Alaris Medical Systems, Inc. These computerized pumps for volume infusion and medication delivery utilize traditional infusion pump technology, while adding control over medication delivery based on predetermined clinical guidelines. Smart pump design improves medication safety by making it harder for the clinician to inadvertently enter the wrong information when programming the pump. This class of pumps utilizes drug libraries that include dosage parameters and alerts, requiring the clinician to intercede if the medication to be delivered is outside the dose recommended by the pharmacy and clinical advisory teams. Prior to smart pumps, most hospitals did not have drug dosing limits built into medication pumps, and drug information on high and low limits for IV medications was not available at the point of care. Other safety features of newer generation medication pumps include dosing alerts, continuously updated drug libraries, and treatment unit–specific programming. Requiring the provider to actively override alerts improves patient safety while allowing for flexibility in treating unique patient situations. For example, the pump may alert the provider that the programmed medication should be administered through a central venous line. The physician can override the alert based on clinical circumstances. Linking the smart pump to a computer network can allow drug library information to be automatically uploaded to the device as changes in practice, medication libraries, alert or dosing limits, or use of medications and practice guidelines occur. Medication pumps can be configured to fit the needs of the patients according to the unit in which they are receiving care, such as the OR, PACU, and the adult, pediatric, and neonatal ICUs. Alert limits and drug libraries can be tailored for each specific treatment unit. When a patient is transferred to a different treatment unit, care must be taken to exchange the pump for one that is appropriate to the new treatment unit, or, if possible, reset the pump for the new treatment unit. For example, when a patient is transferred to the OR from the floor, any medication pumps may need to be reset to OR settings to allow the anesthesia provider to access drug libraries and utilize alarm parameters that are appropriate to the OR and delivery of medications by
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anesthesia personnel. New technologies incorporate systems that will allow a single pump to follow the patients throughout their hospital stay by entering the hospital department into the “smart pump” via the data screen. The pump will change the drug library and parameters particular to that department’s protocols. An additional safety feature of modern medication pumps is the ability to continuously record similar to an airplane “black box.” The pump software allows the data to be retrieved for quality improvement purposes. This information can be used to review programming errors or identify treatment processes that could be improved and was unavailable prior to the introduction of smart pumps. One critical error that cannot be detected by the pump is the attachment of the wrong medication or concentration to the pump. For example, a provider wants to administer a normal saline and an epinephrine infusion. The pump is properly programmed to deliver a normal saline infusion at 100 mL/hr and epinephrine at 0.15 μg/kg/min; however, the bag of epinephrine is inadvertently attached to the tubing going to the pump for the normal saline and the normal saline is attached to the pump for the epinephrine. This situation would lead to a severe reaction in the patient due to an overdose of epinephrine.
■ TYPES OF MEDICATION PUMPS Manufacturers produce medication pumps that meet the needs of a broad range of settings including those that deliver medications in IV bags and/or syringes. This section will give examples of several different types of medication pumps and emphasize the features that are common to that class of pump; however, a comprehensive list of all currently available medication pumps is beyond the scope of this text.
Analog Pumps Analog pumps have a simple user interface controlled by dials (Fig. 36.1). For the majority of these pumps, the only allowable control is to adjust the flow rate. Some allow entry of patient weight and the dose of drug to be delivered per minute. Most bag infusion systems no longer use this technology; however, some analog syringe pumps are still in use (e.g., Baxter Bard Infus O.R. Syringe pump). These devices are mechanical
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■ FIGURE 36.2 Microcomputer-controlled pump with multiple channels.
■ FIGURE 36.1 Simple analog syringe pump.
doses, or rates outside of preset parameters in the library. The majority of modern infusion pumps for bags or syringes are microcomputercontrolled pumps. In addition to inpatient use, sophisticated microcomputer-controlled pumps are available for temporary home use or for implantation in the body (e.g., insulin pumps).
Patient-controlled Pumps and do not have the ability to make calculations regarding drug concentration.
Microcomputer Pumps Microcomputer-controlled pumps contain a limited microprocessor that controls pump function and can perform calculations. They can be syringe pumps or pumps designed for medication bags. Examples include the Baxter AS50 syringe pump and the Alaris PC point-of-care system (Fig. 36.2). The vast majority have a liquid crystal display (LCD) and keypad. The user interface usually allows entry of drug concentration, patient weight, dose of drug to be infused or rate, and total volume to be infused. The microprocessor can perform calculations, which gives the user some flexibility in entering data to achieve a desired infusion or dose. Most of these devices allow the user to program an optional loading dose (an initial rate or amount of drug delivery) followed by a continuous infusion (maintenance dose). In addition to the above features, these devices usually have an internal memory device for storing drug libraries and data. The user can select medications from the drug library and then confirm concentration and dosing information. The unit will alert the user to concentrations,
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Patient-controlled pumps use a syringe or medication bag for the source of medication and include a device to enable the patient to control the infusion or give boluses of medication (Fig. 36.3). These devices are generally used for postoperative and labor pain. Key features of these devices include the ability for the provider to set parameters that control basal infusion rates and the maximum amount and timing of bolus administrations triggered by the patient. They also include a “lock out” device to prevent tampering with the medication by unauthorized personnel.
Continuous Infusion Pumps The desire to send patients home with a temporary continuous infusion of medication led to the development of a variety of simple, lowcost pumps. Many of the early “home” pumps were simple devices with an elastic chamber that could be filled with a medication solution. These “elastomeric” pumps could then deliver a constant infusion that would last until the device was removed or the chamber was empty. Subsequent designs allowed adjustment of the basal flow rate and an on-demand bolus with a timed lockout (e.g., On-Q with Select-A-Flow) (Fig. 36.4). These pumps are frequently used to
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■ FIGURE 36.3 Patient-controlled pump.
deliver a continuous infusion of local anesthetics, with or without narcotics, for postoperative pain control. The infusion catheter can be placed directly in a wound or joint space, or in proximity to peripheral nerves that supply the painful region.
■ GENERAL OPERATING PRINCIPLES FOR INPATIENT MICROCOMPUTER PUMPS Before using a pump, the anesthesia technician will first verify that it has been charged. Since
■ FIGURE 36.4 Elastomeric pump.
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these pumps all have a battery backup system, they should be stored in an area where they can remain plugged in and ready for use. There should be a battery or charge light indicator on the front of the pump. If the pump has not been plugged in, turn on the device and determine battery life, before taking it into the OR. In addition to the pump, operation of the pump may require special syringes (20, 30, or 60 mL), infusion tubing (pump tubing or microbore tubing), or smaller IV bags to which medication can be added (50 or 100 mL normal saline or D5W). Some medications require special nonabsorbent infusion tubing (e.g., nitroglycerin). If multiple medications are to be administered, a stopcock or manifold assembly may be helpful. This equipment should be brought to the OR along with the pump. In the OR, the technician should ensure that the pump is attached to a designated IV pole, taking care that the IV pole is balanced and will not easily tip over. The pump should be plugged into a wall outlet or a hospital-grade multiport outlet extension. Take care to position power cords out of the way so that OR personnel do not trip on the cords. In addition, position the pump or IV pole on the side of the patient where the anesthesia provider will attach the infusion. Depending on the facility, the anesthesia technician may assist the anesthesia provider in setting up the pump. Consult with the provider to determine which drug(s) or fluids will be administered. The operator can enter the patient information required by the specific pump (e.g., patient’s name or initials, patient weight, medical record number). Most pumps will have a front panel with hard or soft keys to navigate through menus. In addition, a keypad can be used to enter numerical data (Fig. 36.5). For fluid administration, the operator will be required to enter an infusion rate and a volume to be infused. For drug administration, the operator can select the drug from the drug library. If a drug is commonly administered in different concentrations, most drug libraries include choices for selecting the concentration for the drug. Once a drug and a concentration are selected, the operator can select the infusion rate in milliliters per hour or the dosage (e.g., mcg/kg/min). The medication infusion tubing should be flushed (primed) and clamped off. The infusion tubing can then be inserted into the pump. In most pumps, the insertion of the
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■ FIGURE 36.5 Infusion pump front panel for data entry.
special manufacturer-specific infusion tubing is accomplished by either opening a door through which the tubing is threaded or by installation of a “cassette” (Fig. 36.6). Syringe pumps require attaching the syringe and the plunger into a cradle (Fig. 36.7). Some manufacturers require that tubing be flushed completely before starting the pump. Many will have an alarm if bubbles are detected as they pass through the pump. Other pumps have a priming function that will allow the operator to flush the tubing after it is inserted into the pump but before it is connected to the patient. Be sure to open the roller clamp or other device that is occluding the tubing before flushing or beginning an infusion. Many pumps will detect an occlusion (high pressure) in the line and sound an alarm (e.g., clamp closed, kink in the line, closed stopcock). Once the infusion tubing has been inserted into the pump and the line primed, the anesthesia technician must verify that all settings are correct. In addition, if
■ FIGURE 36.6 Infusion pump channel with the door open for insertion of infusion tubing.
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■ FIGURE 36.7 Syringe in pump cradle.
multiple pumps are in use, the technician should ensure that the correct medication is attached to the correct pump. The tubing can then be connected to the patient. Medication infusions should be attached to a port in the IV tubing as close to the patient is possible. This will allow changes in medication dose to reach the patient quickly. It is good practice to verify that the IV line into which the infusion tubing is attached is not infiltrated and runs well. Many medication infusions will require a “carrier” infusion to be flowing at a minimum rate, usually at least 75 mL/hr. This is because the medication infusion itself may only run at a few milliliters per hour. The carrier infusion will flush (carry) the medication through the IV tubing to the patient quickly. It is important to make sure that all medications that are infused through the same IV line are compatible with each other and the carrier fluid. If the pump has been correctly set up and verified by the provider, the technician will place the pump in standby mode. If the medication is needed immediately, the provider will press start to begin the infusion. Before starting the infusion, make sure all clamps or other devices are not obstructing flow to the patient. A common safety practice is to leave the infusion line
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clamped when not in use. This is because if the tubing is attached to the patient when the tubing is removed from the pump, it may be possible for an infusion to be “wide open” and administer a dangerous amount of medication into the patient. Most modern pumps occlude the infusion tubing with a special device when the tubing is removed from the pump to prevent this occurrence. The flow restriction must be opened manually to allow free flow of fluid through the infusion tubing.
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the wrong medication or the wrong dose is administered by IV infusion, anesthesia technicians should be thoroughly familiar with pump operation and troubleshooting. Anesthesia technicians should take advantage of opportunities to attend in-services offered by the vendors and facility educators to remain current with changes in pump technology and the operation of new devices.
■ TROUBLESHOOTING
REVIEW QUESTIONS
Most pumps have alarms for different conditions and will display an error message on the screen. Common problems that can cause alarms during use include the following:
1. Medications NOT commonly used in drug pumps include A) Vasopressors B) Heparin C) Sodium pentothal D) Muscle relaxants E) All of the above
• Air in the tubing (air detection alarm). Make sure the medication bag is not empty. Make sure the drip chamber is appropriately filled (fill to the appropriate level if necessary). Make sure no air or bubbles are in the line. If air or bubbles are found, a clamp should be applied to prevent flow into the patient, the infusion tubing removed from the pump, and the air or bubbles removed from the tubing by aspirating from a distal port. It may even be necessary to detach the infusion tubing from the patient and reflush the tubing. • High pressure in the line. Check for valves, clamps, or stopcocks that are closed, kinked tubing, infiltrated IV, or improperly installed infusion tubing in the pump. • Medication dosing outside of usual parameters—verify the settings with the anesthesia provider. Most pumps allow the provider to override the warning and continue the infusion. • Low battery. Make sure the pump is plugged in.
■ SUMMARY Medication infusion pumps are commonplace in hospitals and outpatient centers alike. The anesthesia technician plays an important role in the setup, operation, troubleshooting, and maintenance of these devices. Anesthesia technicians will also be responsible for making sure device maintenance meets regulatory requirements. Due to the complexity of these devices and the potential for severe complications when
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Answer: C. Sodium pentothal is not a common drug to be used in an infusion pump. All the others are common.
2. Medication pumps are configured generically to fit the average needs of the patient in any area of the hospital. A) True B) False Answer: A. Most pumps are configured with pharmacy-recommended dosages and concentrations based on generic populations.
3. If a pump sounds an alarm, the technician should check all of the following EXCEPT A) The data screen for message alerts. B) The medication is appropriate for this patient. C) Air in the tubing D) A clamp on the IV tubing has not been opened. E) The tubing is properly installed. Answer: B. The anesthesia technician may check any of the possible reasons for alarm other than if the medication is appropriate for the patient. The anesthesia provider is responsible for making sure that is the case.
4. Using the keypad, the following data may NOT be entered into the drug pump. A) Patient’s weight B) Volume to be infused C) Patient’s gender D) Desired dosage Answer: C. The patient’s gender is not needed in order to utilize any drug pumps.
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5. The leading cause of patient harm is medication errors. A) True B) False Answer: A. It has been reported that approximately 20% of medical errors are caused by medication errors, making it the single leading cause of harm to patients.
SUGGESTED READINGS Bates DW, Cullen DJ, Laird N, et al. Incidence of adverse drug events and potential adverse drug events: implications for prevention. JAMA. 1995;274:29–34. Eskew JA, Jacobi J, Buss W, et al. Using innovative technologies to set new safety standards for the infusion of intravenous medications. Hosp Pharm. 2002;37:1179–1189. General hospital devices and supplies/infusion pumps. Available at: www.fda.gov.
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Hatcher I, Sullivan M, Hutchinson J, et al. An intravenous medication safety system: preventing high-risk medication errors at the point of care. J Nurs Admin. 2004;34:437–439. Hicks RW, Cousins DD, Williams RL. Summary of Information Submitted to MEDMARX in the Year 2002. The Quest for Quality. Rockville, MD: USP Center for the Advancement of Patient Safety; 2003. Joint Commission. National patient safety goals. Available at: www.jointcommission.org. Leape LL, Brennan TA, Laird N, et al. The nature of adverse events in hospitalized patients: results of the Harvard Medical Practice Study II. N Engl J Med. 1991;324: 377–384. Williams C, Maddox RR. Implementation of an IV medication safety system. Am J Health Syst Pharm. 2005;62: 530–536. Wilson K, Sullivan M. Preventing medication errors with smart infusion technology. Am J Health Syst Pharm. 2004;61:177–183.
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37
Blood Gas Analyzers and Point-of-Care Testing David Wilson and Guy Buckman ■ INTRODUCTION Point-of-care testing (POCT) is defined as tests designed to be used at or near the site where the patient is located; they do not require permanent dedicated space, and they are performed outside the physical facilities of the clinical laboratories. POCT has grown in popularity as advancements in computer chip technology made POC devices more affordable, portable, and easy to use. Examples include circulating blood glucose monitors (glucometer), blood gas analyzers, activated clotting time (ACT) monitors, and heparin concentration monitors (Hepcon). There are a myriad of other POCTs that are used outside of the operating room but are not discussed in this chapter. Some examples of these POCT devices include those for testing hemoglobin A1c (Hb A1c), mircoalbumin, cardiac enzyme markers, cholesterol, infectious disease, etc. POCT can be found almost anywhere patients need quick and cost-effective testing such as a physician’s office, ICU, emergency rooms, hospital wards, and even in a patient’s home. However, this chapter gives a brief overview on POCT equipment that is commonly found in or around the operating room. The main emphasis of this chapter is on the organization of POCT from initial start-up to daily operations. The operating room is a unique environment in which a life-threatening situation needs to be identified and treated immediately. For example, hypoglycemia can lead to poor neurologic outcomes, cardiovascular collapse, and death if not identified and treated promptly. The clinician cannot wait for the long turnaround time required for tests sent to a central laboratory. Even STAT labs have a much longer turnaround time than POCT. A handheld glucometer allows
the clinician to quickly detect the patient’s circulating blood glucose and perform the appropriate intervention. The most efficient use of POCT occurs when an abnormality is quickly detected and an intervention is performed before any harm or escalation of patient care has occurred. POCT is composed of five essentials: equipment, personnel (not trained as certified laboratory personnel), procedure, quality control, and records and reports. It is governed by the College of American Pathologist (CAP) and Clinical Laboratory Improvement Amendments (CLIA). CLIA issues the certificate that allows the laboratory to function, and CAP is the regulatory body that governs daily operations. The POCT laboratory allows no disruption of patient care, samples never leave the immediate patient care area, and the results are immediate; however, clinicians must guard against interpreting POCT as the same accuracy as the main laboratory. When there is a question of the results, the best rule of thumb is to draw another sample and perform a test on the POCT machine and send a sample to the central laboratory for comparison.
■ BLOOD GAS MACHINE A blood gas machine is a portable system that analyzes whole blood for pH, partial pressure of CO2 and O2, bicarbonate levels (HCO3−), electrolytes, lactate, and hematocrit. There are a multitude of clinical scenarios in which an anesthesiologist may need to interpret the blood gas. A blood gas sample may be obtained from an artery or a vein depending on the clinical situation as the blood gas values will differ and will yield different information for the clinician. Arterial blood gases are more common and most often obtained from the radial artery as it is easily accessible. 363
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The blood sample is drawn into a heparinized syringe to prevent the blood from clotting. The blood sample is then taken to the blood gas analyzer where the sample is drawn into the machine for analysis. Blood gas analyzers today are fast and accurate. Most instruments are fully self-contained, consisting of the machine and disposable cartridges containing reagents, sensors, waste containers, and quality control (QC) pack. Usual systems are fully automated with self-calibration and self-quality control. Although today’s blood gas analyzers are accurate, there are many preanalytic errors that can occur, which can give erroneous results: 1. Make sure the correct patient’s blood is being sampled. Often, anesthesia technicians in a busy service area must multitask and perform multiple blood gas samples at one time. Reporting the results for the wrong patient could have serious consequences. 2. Excess anticoagulant. The heparin used to prevent the blood from clotting can cause erroneous low CO2, low bicarbonate levels, and low base excess. Excess heparin can also bind to cations, yielding a lower value. 3. Inadequate removal of flush solution during the blood draw can cause dilution of the sample, resulting in erroneously low values. 4. Air bubbles in the sample syringe normally cause an erroneous increase in PaO2 levels. 5. A delay of more than 10 minutes before running the sample can yield a PaO2 level difference of more than 10 mm Hg to the actual PaO2 level in plastic syringes. Malfunctions such as calibration errors, failed quality control, and bad sensors are usually identified during machine-initiated calibrations or quality controls. These problems are corrected by most current blood gas machines with a “lock-out” feature that will not allow further sampling. In some cases, the machine will allow a sample, but without the faulty “locked-out” analyte. High and low settings are set internally during the machine setup prior to initial use. The high/low settings are agreed upon with the main laboratory, and in the case of hematocrit and glucose, a reading outside those settings will require a sample to be drawn and double checked with the main laboratory. Note: High and low settings are set by the main laboratory and reflect the range of normal values.
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While the patient is in the operating room, it is not unusual for PCO2, PO2, hematocrit, and other values to be out of the “normal” range due to a variety of circumstances encountered during surgery.
■ ACTIVATED CLOTTING TIME The ACT detects clot formation. Patients who are having certain invasive procedures, such as cardiac bypass, require anticoagulation with heparin to prevent catastrophic thrombosis formation while on bypass. The heparin required to achieve a specific target level varies with individual patients and must be closely monitored. Clot formation is detected with an optical electromechanism located in an actuator block of the instrument. Single-use disposable cartridges contain the activator kaolin. The actuator mixes the kaolin with the blood sample and starts the timer. When blood is exposed to a foreign surface, the clotting process is triggered and fibrin forms. The optical system detects this change and displays the clotting time in seconds. As with many POCTs, there are some instances that can cause false values: 1. The ACT monitor is not warmed to 37°C. A monitor that is inadequately warmed will give an erroneously high ACT. 2. Inadequate removal of flush during the blood draw will give falsely elevated ACT. It should also be noted that there are two major manufacturers of ACT monitors. The ACT is not a standardized measurement, so an ACT of 300 seconds from one manufacturer does not correlate with an ACT of 300 seconds from another manufacturer.
■ HEPCON The heparin concentration (Hepcon) monitor is a device that measures the actual concentration of heparin in the patient’s blood. Hepcon is another POCT equipment that is used to gauge the adequacy of anticoagulation for certain procedures such as cardiopulmonary bypass. Hepcon is an integrated system consisting of a component for tracking clot detection and computing results, a component for sample delivery, and the single-use test cartridges for actual performance of the tests. The cartridge instructs the system, through an optical code, as to the type of test being performed, the calculations and the format
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required for results, and the volume of sample needed for each channel. The detection process uses the plunger assembly within the cartridge. This assembly is lifted and dropped through the sample/reagent mixture by a lifting mechanism actuator. As the sample clots, a fibrin web forms around the daisy located on the bottom of the plunger assembly and impedes the rate of descent of the assembly. This change in fall rate is detected by a photooptical system located in the actuator assembly of the instrument. The end point of the test is the time at which clot formation is detected; from these clotting times, derived results are calculated for all tests. The causes of faulty Hepcon readings are basically the same as those that occur with the ACT machine.
■ THROMBOELASTOGRAPHY Thromboelastography (TEG) is a device that allows the clinician to evaluate the patient’s ability to maintain hemostasis. In order for a patient to form a fibrin clot that is sufficient in strength to maintain hemostasis, the body depends on the interaction of enzymatic proteins (clotting factors) and platelets. Laboratory tests such as international normalized ratio (INR), partial thromboplastin time (PTT), ACT, and Hepcon measure the integrity of the clotting factors, whereas the TEG evaluates the entire coagulation process including platelet function. The TEG is generally used to monitor defects in the coagulation process and help guide the clinician to the appropriate treatment for those defects. Less commonly, the TEG can be used to monitor the adequacy of anticoagulation for patients undergoing procedures such as cardiac bypass. The TEG evaluates the ability to form clots by measuring the tensile strength of the fibrinplatelet complex. A sample of blood is placed into a cuvette with a metal pin in the center. The cuvette is slowly rotated at approximately 6 cycles/min. An activator is added to the sample and clot begins to adhere to the side of the cuvette and the metal pin. This creates resistance to rotation, which is then measured and plotted on a graph. The shape of the graph and time to when clot is formed gives the clinician information on the integrity of hemostasis and the presence of specific deficiencies. There are several preanalytical errors that can cause erroneous values for the TEG:
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2.
3.
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Patient identification. As with all lab tests, care should be taken to make sure the sample and results are performed on the correct patient. Inadequate removal of flush solution during the blood draw can cause dilution of the sample, which will inhibit the sample from forming clots. Agitation, such as pneumatic tube transport of the sample, can cause the blood to prematurely start forming clots.
Appropriate blood samples for the TEG include whole blood, citrated blood, or heparinized blood. Each sample type is used in different clinical situations. Care should be taken to ensure the proper anticoagulant is used in the sample.
■ INTERNATIONAL NORMALIZED RATIO The INR is a test that measures the adequacy of anticoagulation for patients taking warfarin. Many patients presenting for surgery are taking warfarin for the treatment or prevention of thrombosis. Patients having invasive procedures or surgery normally stop taking warfarin 5–7 days prior to surgery. These patients need to have their INR checked the day of surgery as the effect of warfarin is highly variable from patient to patient. The INR is often sent to a central lab that may take hours to run the sample; POCT can give an accurate measurement of INR within minutes. This can decrease the time and complexity for patients who need to coordinate the timing of lab draws and the time of surgery. The INR is analyzed on a portable coagulometer much the same way that a patient’s circulating blood glucose is analyzed. A sample of blood is placed on a test strip after a finger stick is obtained. The test strip is then placed in the coagulometer at which time the sample is mixed with a thromboplastin reagent, causing a clot to form. There are several coagulometers available, and each has its own operating principles. However, all devices are accurate and can give results in under 3 minutes.
■ BLOOD GLUCOSE MACHINE (GLUCOMETER) Glucometer is a medical device for determining the approximate concentration of glucose in the blood. It is a key element of hospital and home blood glucose monitoring by people with
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diabetes mellitus or hypoglycemia. Glucometers are very accurate; however, a glucose reading from the main laboratory is always considered the gold standard. Clean the skin with an alcohol swab and allow the site to completely dry. Skin with alcohol may cause a faulty reading. A small drop of blood, obtained by pricking the skin with a lancet, is placed on a disposable test strip that is read by the meter and used to calculate the blood glucose level. The meter then displays the level in milligrams per deciliter or millimol per liter. With a hospital glucometer, daily quality controls are required prior to use and most meters have a lock-out system until the quality controls are complete. Quality control fluids are good for 90 days after opening unless the expiration date is before.
■ NEW EQUIPMENT Device Selection The key element to a successful program is a liaison between the main laboratory director, the POCT coordinator, and the anesthesia providers. POCT is a partnership between the main laboratory and anesthesia providers; however, inspectors hold the site performing the test and CLIA director responsible for noncompliance. This marriage of need is compelled from the moment the desire for a POCT site is recognized until the POCT site is decommissioned. Initial meetings between the main laboratory director, his or her POCT coordinator, and the anesthesia providers will establish a listing of acceptable analytic equipment. (1)(POC.06300) This analytic equipment must meet the standards of the laboratory and the needs of the anesthesia providers. Equipment standardization between the laboratory and POCT will minimize the number of different devices and be helpful when acceptance correlation verifications are required. With standardization, one policy can be shared among sites as well as a central data management system, operating procedures, clinical limitations, and reference intervals (normal values). Standardization will simplify training and competency for staff. When deciding on analytic devices, pay close attention to what extent they require operator interactions for calibration, quality control, temperature monitoring of the machine, quality controls that require monitoring of the expiration
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dates and materials that have opened dating, and special refrigeration or storage needs. Questions to ask when selecting a device are as follows: 1. 2. 3. 4.
5.
6.
7.
8.
9.
10.
11.
Can the product be trialed? What disposables are needed and their cost? What is the projected cost per test? Does the device self-prompt the operator and does the machine have automatic lockouts? These lockouts should include a lockout of anyone not qualified to operate the device and lockout a specific analytic if it fails quality control. Does the device perform automatic quality control or do personnel have to run daily shift quality controls? The automatic quality control mode with lockout would be the preferred since it eliminates human error and releases the staff to other work. What are the manufacturer’s requirements for calibration, quality control, and preventive maintenance? Will special power and/or computer hookup be required? An uninterrupted power supply system is highly recommended. Is there a secure data management system to capture quality controls and test results? Is there special software and licensing required? How much training will be provided to the operators? Who will perform this training? Will the manufacturer provide start-up assistance for the initial days? Contact the BioMedical repair department and ask BioMedical personnel to check medical device alerts for any product selected and establish any required training needed to maintain the device. Typically, BioMedical personnel check the device against the Emergency Care Research Institute (ECRI) database, which includes product repair information nationwide. Where will the quality control material be stored and what special handling will be required?
Once the device is selected, you should begin to write clear procedures and competencies and verify the procedure with the main laboratory POCT coordinator prior to going active, thereby reducing any problems that may arise. Define the quality control requirements and schedule,
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calibration cycle, and preventive maintenance schedule. The main laboratory may have a policy/procedure that can be tailored to the POCT area. At the very least, it will have a template for new lab policies and procedures that can be used as a starting point. The time spent in this initial phase will save the POCT director or his or her designee hours of time in the future. Once a good foundation is set, the program will run smoothly if you stay current with practices and perform internal audits. It may be helpful to establish a centralized POCT repository with all of the tools necessary to manage POCT.
Arrival of New Equipment Once newly purchased devices arrive, acceptance testing between the POCT device and the main laboratory device must be performed. Acceptance testing requires correlation verification between the POCT device and a main laboratory device. A minimum amount of acceptance testing is required and is set by the main laboratory or the manufacturer’s recommendations. In performing the test, a sample is drawn and run on the POCT device(s) and then the same sample is run on the corresponding main laboratory device. Results are documented between the POCT device(s) and the main laboratory device. Results must be within a set parameter established by the main laboratory or the manufacturer’s recommendations. These documented results are retained for the life of the device. Review the operating manuals to validate manufacturer’s requirements for calibration, quality control, and preventive maintenance. BioMedical repair personnel should be consulted for preventive maintenance (POC.06400). Identify the equipment using hospital-accepted identifying numbers for future preventive maintenance. Training for the operator prior to use must be accomplished and documented. A competency form for initial and ongoing training must be completed and retained for 3 years. The main laboratory POCT coordinator will initiate external proficiency testing (POC.03200). Review your policies/procedures prior to the activation date for the device.
■ PERSONNEL Operators need initial and ongoing training and certification. Identify only those operators who
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are required to perform the test to be authorized users (POC.06800). Large numbers of operators increase the amount of work to manage documentation and associated regulatory requirements. The job of training and proficiency testing will fall on the POCT director who is a physician or a doctoral scientist (POC.06600). The director or his or her designee will be responsible for developing initial training requirements, initial and ongoing competency, and the related documentation for both (POC.06700, .06850). This training must be accomplished prior to the initial use of any POCT device. Operators must document that they have read the policies and procedures for the facility, the main laboratory, and the new POCT. Each individual’s performance must be evaluated by an authorized user. This includes, but is not limited to, patient identification and preparation, specimen collection, handling, processing, and testing. Each individual must be monitored recording and reporting of test results. The POCT director ensures each operator conducts external proficiency testing and conducts ongoing monitoring of each operator performing tests, reporting results, and documenting results. This proficiency monitoring must be documented. A current list of POCT personnel that delineates the specific tests, levels, and methods that each individual is authorized to perform must be documented (authorized user list) and a copy sent to the main laboratory director (POC.06800). The competency of each person to perform the duties assigned must be assessed following training before the person performs patient testing (POC.06900). Semiannual competency during the first year of an individual’s duties is required. After an individual has performed duties for 1 year, competency must be assessed at least annually. Ongoing supervisory review is an acceptable method of assessing competency for certain elements. Competency assessment may be documented in a variety of ways, including a checklist completed by a supervisor.
■ QUALITY MANAGEMENT The quality management (QM) program for POCT must be clearly defined and documented. The program ensures quality throughout all phases of testing and should cover patient identification, specimen collection, identification
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and processing, as well as how to report results. The QM program must be capable of detecting problems and opportunities for system improvement. The POCT program must be able to develop plans of corrective/preventive action based on data from its QM system (POC.03500). Documentation should be maintained for all identified problems, corrective actions taken, and the outcome of those corrective actions. There must be a system in place that detects and corrects clerical errors and analytical errors in a timely manner (POC.03700). The usually accepted manner is to employ automatic quality controls with a lock-out feature that will not allow a specific analyte to be tested if an error is detected. Each device will also have internal high and low limits set for each analyte. The quality assurance test will indicate if an analyte is higher or lower than acceptable limits.
■ MANUFACTURER’S PROCEDURE MANUAL (USER MANUAL) A copy of the user manual should be located at the laboratory workbench for quick reference when there are questions or problems. A copy of the policies/procedures should be located with the user manual and reviewed annually by all authorized users. A copy of the annual review signature sheet should be retained with the user manual (POC.04100). When changes are made to the base policies/procedures, a review by the main laboratory director and the POCT director should document that the changes are acceptable (POC.04150).
■ SPECIMEN HANDLING A step-by-step procedure for specimen collections should be documented within the procedure and reference needle safety, how to identify the patient, how the test is requested, how the specimens are handled and identified, and how the results are reported (POC.04300).
■ RESULTS REPORTING Reference ranges specific for age, sex-specific normal values, and interpretive ranges (normal ranges) must be reported with patient test results; however, it is not necessary to include reference ranges when test results are reported as part of a treatment protocol that includes clinical actions (such as a surgical procedure), which are based on the test result. The test results must be recorded (POC.04500).
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After careful evaluation, the POCT site should set formal reference ranges and retain documentation of this evaluation. These reference ranges are set with the cooperation of the main laboratory (POC.04525). Critical limits must be established for appropriate tests, so immediate notification of a physician or other clinical personnel responsible for patient care occurs. These must be documented in the policies/procedures and within the procedures, a clear indication of how notification of a critical element is done and documented (POC.04550). The users must be familiar with critical limits for procedures that they perform (POC.04600). Personnel performing the test must be identified. This is usually accomplished with the assignment of a unique user code to access the test device (POC.04700).
■ QUALITY CONTROL Daily staff performing external controls must be run as follows (POC.07300): 1. For quantitative tests, two controls at two different concentrations must be run daily, except for coagulation tests (two controls required every 8 hours). 2. For qualitative tests, a positive and negative control must be run daily. Daily controls may be limited to electronic/procedural/built-in (e.g., internal, including built-in liquid) controls for tests meeting the following criteria: 1. For quantitative tests, the test system includes two levels of electronic/procedural/ built-in internal controls that are run daily. 2. For qualitative tests, the test system includes an electronic built-in internal control run daily. 3. The system is Food and Drug Administration (FDA)-cleared or approved and not modified by the laboratory. 4. The system is not classified as highly complex under CLIA. 5. The laboratory has performed and documented studies to validate the adequacy of limiting daily QC to the electronic builtin controls. Initial validation studies must include comparison of external and builtin controls for at least 25 samples. For validation of multiple identical devices, the 25-sample minimum applies to the initial
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device; the laboratory director is responsible for determining the sample size for the other devices. The laboratory director is responsible for determining criteria for acceptability and other details of the validation. 6. External controls are run for each new lot number or shipment of test materials and after major system maintenance and after software upgrades. Regarding the positive external control for qualitative tests, best practice is to run a weak positive control, to maximize detection of problems with the test system. 7. External controls are run at a frequency recommended by the test manufacturer or every 30 days, whichever is more frequent. Quality control data must be reviewed daily by testing personnel or supervisory technical staff to detect problems, trends, etc. The laboratory director or his or her designee must review QC data at least monthly (POC.07428). If the laboratory/POCT program uses more than one instrument to test for a given analyte, the instruments are checked against each other at least twice a year for correlation of results (POC.07568). This requirement applies to tests performed on the same or different instrument makes/models. This comparison must include all nonwaived instruments. The laboratory director must establish a protocol for this check. Quality control data may be used for this comparison for tests performed on the same instrument platform, with control materials of the same manufacturer and lot number. The use of fresh human samples (whole blood), rather than stabilized commercial controls, is preferred to avoid potential matrix effects. In cases when availability or preanalytical stability of patient/ client specimens is a limiting factor, alternative protocols based on QC or reference materials may be necessary but the materials used should be validated to have the same response as fresh human samples for the instruments/methods involved. Records of the correlations are required at least twice a year (POC.07568).
■ CALIBRATION A written procedure defining the use of appropriate calibration/calibration verification materials is needed. Criteria typically include the following:
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1. Changing of reagent lots unless the user can demonstrate that the use of different lots does not affect the accuracy of patient test results and the range used to report patient test data, or the control value. 2. When indicated by quality control data 3. After major maintenance or service 4. At least every 6 months 5. As recommended by the manufacturer
■ QUALITY IMPROVEMENT A successful quality improvement (QI) plan includes the monitoring of outcomes, events, problems, and utilization (benchmarks) with trends over time. Other aspects include the following: 1. QC documentation 2. Number of errors where wrong QC was analyzed 3. Percentage of QCs that fail 4. QC outliers with comment 5. Failed QCs with appropriate action (patients not tested) 6. Utilization (number of tests/site or device) 7. Tests billed versus tests purchased 8. Single lots of test and QCs in use at any time 9. Compliance 10. Untrained operators 11. Clerical errors or data entry errors 12. Medical record entry with reference ranges 13. Expired reagents and QC/reagents dated appropriately 14. Refrigerator temperature monitored 15. Proficiency testing successful Some or all of the QI information may be obtained from the computer systems (laboratory information system or LIS) when the POCT device is integrated into the hospital system.
■ REPORTS AND RECORDS Daily 1. Inspect the lab. 2. Review laboratory work. 3. Inspect blood gas machine and activated clotting machine. 4. Morning quality controls for each machine 5. Eight-hour quality controls 6. Refrigerator temperature checks for those that contain laboratory quality control products or test material.
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7. LIS (RALs) a. Data management b. Edit logs c. Flagged results d. Operators 8. Certification.
Weekly 1. Download glucometer results to laboratory information system or LIS.
Monthly 1. Activated clotting machine temperature checks 2. Activated clotting machine liquid quality control 3. Download stored laboratory test results into the LIS. 4. Records review 5. Review laboratory log sheets. 6. Laboratory results verification audit 7. Review competencies to ensure they are current. 8. Quality and performance report to main lab director. 9. Review refrigerator logs. 10. Operator reports 11. Cal reports 12. Levey-Jenning 13. QI reports
Quarterly 1. POCT director’s records review
Semiannual 1. 2. 3. 4.
Correlations Linearity studies Internal CAP audit of POCT Update authorized user list.
2. Initial validation records—5-year inspections 3. Response to inspection 4. Exception responses taken and follow-up RECORDS TO BE MAINTAINED
RETENTION (YEARS)
Policies and procedure
5
Current job descriptions of personnel and diplomas
5
Competencies
5
Personnel training and qualification
5
Signature, initials, and identification codes
10
Authorized user list
5
Equipment qualification/validation
5
Reviews and revisions of policies/procedures
5
■ SUMMARY POCT provides faster test results with the potential for improved patient outcome, but the quality of results is a concern. An organized POCT program is required to manage the quality of results supervised by laboratory staff (not dictated by the laboratory). This program should manage the validation of devices, training of operators, and day-to-day activities required for POCT to meet medical needs. POCT errors can occur in similar ways to laboratory errors. Training and QI programs should monitor the frequency of errors and act to improve detection and prevention of errors. Strategies to make POCT a part of routine patient activities have greater success at regulatory compliance and improved quality outcomes.
Annual 1. Competencies for operators, staff, and perfusionist for activated clotting, blood gas, and glucometer 2. Main laboratory audit of POCT 3. Records retention review 4. Policy/procedure review and signature
■ SAFETY Personnel Records 1. Competency records and what to include 2. Authorized user list
Records Retention 1. Equipment quality control, calibration, and preventive maintenance—include actions taken and follow-up
REVIEW QUESTIONS 1. All of the following can cause an erroneous value on a blood gas analyzer EXCEPT A) Excess anticoagulant in the sample tube B) Inadequate removal of flush solution during blood draw C) Excessive blood drawn into the sample tube D) Delay of more than 10 minutes before running blood gas sample E) None of the above Answer: C. Excess blood in the sample tube will not cause any problems. Flush solution can dilute the actual sample. A delay of more than 10 minutes can allow continued metabolism in the red blood cells and alter values.
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Chapter 37 • Blood Gas Analyzers and Point-of-Care Testing 2. Which of the following statement is TRUE regarding the ACT analyzer? A) The ACT measures the time to clot formation in seconds. B) The ACT analyzer should be cooled to 32°C prior to running the sample. C) Dilution of the blood sample has minimal effect on the results of the ACT. D) All ACT analyzers are standardized, so values from one manufacturer can be compared to values from another manufacturer. E) None of the above. Answer: A. The ACT is measured in seconds. The ACT analyzer should be warmed up prior to use. Failure to do so can produce faulty values. Similar to blood gas analysis, dilution of the sample can cause erroneous values. Two different ACT manufacturers have different methodologies to measure the ACT and the values cannot be compared.
3. Which of the following statements are TRUE in regard to the TEG? A) The TEG measures time to clot formation in seconds. B) The main advantage of the TEG compared to ACT is that heparin or citrated blood does not affect the results. C) The TEG does not evaluate the integrity of platelets on the clotting process. D) Excessive agitation of the blood sample can cause premature clot formation. E) All of the above. Answer: D. Agitation of the sample can cause premature clot formation and is a common source of errors with TEG measurements. The TEG results are plotted on a graph and not reported as a time. One of the advantages of the TEG is that it measures platelet function.
4. When there is a question about the validity of a test result, the best rule of thumb is A) Assume the values are true because today’s POCT machines are highly accurate and never give false values. B) Recalibrate the POCT machine in question.
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C) Draw two samples, reanalyze one on the POCT and send one to the central lab for comparison. D) Check to make sure the calibration reagents are not out of date. E) None of the above. Answer: C. If there is any doubt about the accuracy of a POCT device result, the best course of action is to perform another sample and compare the result to a result obtained from the central lab.
5. Which statement is TRUE regarding the INR? A) It is measured by a TEG. B) It evaluates the body’s ability to form clot as a whole dynamic process. C) It measures the adequacy of anticoagulation for patients taking warfarin. D) The blood sample must be drawn from an artery. E) None of the above. Answer: C. The INR is a measurement of a portion of the clotting cascade that is affected by warfarin. Thus, the INR is a common test for evaluating warfarin anticoagulation. The INR does not test the entire clotting process (e.g., another limb of the clotting cascade or platelet function). Blood samples for INR testing can be drawn from an artery or a vein.
SUGGESTED READINGS College of American Pathologist. Point-of-Care-Testing Checklist. Northfield, IL: College of American Pathologist; 2010. Hutchson AS, Ralston SH, DryBurgh FJ, et al. Too much heparin: possible source of error in blood gas analysis. British Med J. 1983;287:1131–1132. Mueller RG, Lang GE, Beam JM. Bubbles in samples for blood gas determinations—a potential source of error. Am J Clin Pathol. 1976;65(2):242–249. Picandet V, Jeanneret S, Lavoie JP. Effects of syringe type and storage temperature on results of blood gas analysis in arterial blood of horses. J Vet Intern Med. 2007;21(3): 476–481. Wallin O, Soderberg J, Grankvist K, et al. Preanalytical effects of pneumatic tube transport on routine haematology, coagulation parameters, platelet function and global coagulation. Clin Chem Lab Med. 2008;46(10):1443–1449.
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CHAPTER
38
Ultrasound Matthew Abrahams and Jorge Pineda ■ INTRODUCTION Anesthesiologists have recently started using ultrasound (US) for a variety of purposes. US can be used to evaluate a patient (diagnostic) or during procedures (interventional). US is a powerful tool that allows anesthesiologists to see structures beneath the skin, is noninvasive, and does not produce harmful radiation. Compared to other types of imaging, US is relatively portable and inexpensive. In addition, US images are generated nearly instantly, providing real-time information at the bedside. US equipment may appear complex at first, but by understanding a few basic principles and becoming familiar with your US machine’s basic controls, you can quickly become comfortable using it. Anesthesiologists may use US to determine the status of a patient’s medical condition. For example, US can be used to perform a detailed examination of the heart (echocardiography) either externally (transthoracic) or by placing a special transducer in the patient’s esophagus (transesophageal). US can also be used to evaluate the patient’s blood vessels for narrowing or blockage or to determine the patient’s volume status (do they have sufficient intravascular volume). It can be used to examine the patient’s internal organs or to look for fluid collections in the patient’s skin, muscle, or body cavities. US is also commonly used during procedures such as vascular access or nerve blocks. Specific uses of US are discussed in more detail in other chapters. This chapter focuses on the basic principles of US: the physics of US image formation, US machine controls, basic US terminology, storage of US images, tips for optimizing conditions during US exams and procedures, and proper use and maintenance of US equipment. In order to illustrate the concepts we discuss, we have included pictures showing various US machine
controls and sample US images. We made them using equipment available at our institution. This is not intended to be a comprehensive user’s manual for every US machine currently available. Different models of US machines have different types of controls, and the images may have a different “look.” It is important to become familiar with the machine(s) you will be using and apply the concepts in this chapter to understand how to use them.
■ BASIC US PHYSICS/MACHINE CONTROLS The basic underlying principle of US physics is that sound waves are emitted and received by the US transducer. A piezoelectric element (vibrates when an electrical current is applied) in the transducer emits sound waves that are reflected by the patient’s tissues. The reflected waves are received by the transducer, which measures the timing and strength of the reflected waves. The waves are emitted and received in a very thin beam, which is a flat plane about as thick as a piece of paper. The US machine then processes this information to produce the image on the US screen. The image produced is based on how fast the US waves move through various tissues and how much of the US energy the tissues reflect. US waves are above the range of normal human hearing (higher frequency) and so are not audible. The US transducer spends the majority of time receiving reflected US waves and is only emitting US energy about 0.1% (1/1000th) of the time. There are no known harmful effects to live tissue from exposure to US waves in frequencies used clinically.
Frequency of US Waves The behavior of US waves is governed by the simple equation: l = v/f. This describes the relationship between the frequency of US waves (f)
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and their wavelength (l). The velocity of US waves through tissue (v) is relatively constant at approximately 1600 m/s, though this varies slightly depending on the water content of the tissue. From this equation, you can see that the frequency and wavelength are inversely proportional, meaning that as the frequency increases, the wavelength becomes shorter. Conversely, as the frequency decreases, the wavelength gets longer. US waves’ ability to travel through tissue and the resolution (sharpness) of the US image also depend somewhat on the frequency and wavelength (Fig. 38.1). The resolution of the US image is approximately two wavelengths, so a shorter wavelength (higher frequency) will improve the resolution of the US image. The usual range of US waves emitted/received by US transducers commonly used by anesthesiologists is 2–15 megahertz (mHz) or 2– 15 million cycles per second. Unfortunately, higher-frequency US waves do not penetrate tissue well and are not capable of imaging deeper structures (Fig. 38.1). So it may be helpful to use a lower frequency to image these deeper structures, but the image will not be as sharp (lower resolution).
Gain The brightness of the US image can be adjusted using the gain controls on the US machine (Fig. 38.2). The gain is the amplitude of the US waves. Adjusting the overall gain control is similar to turning up the volume on a stereo. This makes the entire image brighter, but this may not improve the quality of the image, just as turning up the volume on a stereo may make the music louder but not improve the quality of the song. Fine gain controls such as time-gain compensation (TGC) or lateral gain compensation (LGC) can be used to brighten or darken specific areas of the image (Fig. 38.2). This is similar to adjusting equalizer settings on a stereo. To compensate for the effect of depth on signal strength, the TGC sliders are often arranged in a diagonal pattern to increase the brightness lower in the image (deeper). The most important point about TGC and LGC controls is that they should be checked to prevent overadjusting the image as this can produce significant artifacts and make US image interpretation more challenging. When in doubt, it is probably best to leave the sliders in a neutral position. Slight adjustments can then be made to “fine-tune” the US image as necessary.
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Depth The depth of the US image can be adjusted on nearly every US machine (Fig. 38.3). It is important to adjust the depth properly so that the structure(s) of interest is on the screen. Too much depth is not helpful as it makes the target structure(s) smaller in the US image, while deeper structures may not be relevant to the procedure being performed. In general, it is usually ideal to have the entire target structure(s) in the US image and adjust the depth so that the target(s) is roughly centered in the image. This allows the anesthesiologist to see other structures in the area that he or she may wish to avoid puncturing unintentionally, and to help visualize the needle if it is directed deeper than intended (Fig. 38.3).
Doppler/Color Another useful feature of most US machines commonly used by anesthesiologists is known as Doppler (or color) imaging. This uses a physical phenomenon known as the Doppler shift to measure movement. The Doppler shift describes the effect of an object’s direction and velocity on the sound emitted by the object as detected by the receiver. For example, as a train moves toward you, the sounds it makes have a higher pitch, while the sounds it makes have a lower pitch as it moves away from you. The faster the object is moving, the greater the change in pitch. The US transducer acts as the receiver. Objects moving toward the transducer reflect US waves at a higher pitch than emitted and those moving away at a lower pitch than emitted (Fig. 38.4). This phenomenon can be used to measure flow through blood vessels. The Doppler effect is displayed on the US screen as color, and the color scale can be used to show how fast blood (or any other substance) is moving toward or away from the US transducer. If the direction of flow is perpendicular to the transducer, flow is neither toward nor away from the transducer, and there may not be color on the US screen even though there is blood flowing through the vessels. Tilting the US transducer (discussed later) toward or away from the direction of flow may improve the color signal.
Focus The US waves emitted from the transducer are shaped like an hourglass (Fig. 38.5). The
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■ FIGURE 38.1 A: Schematic showing the relationship between frequency of US waves and tissue penetration. Red dots represent tissues/structures reflecting US waves (arrows). This shows that high-frequency waves are more likely to be reflected, preventing them from penetrating deeper. This is known as tissue attenuation. B: Controls for adjusting frequency on Sonosite (left) and Philips (middle, right) US machines. The Sonosite does not specify the actual frequency (in MHz) but uses a “Gen, Res, Pen” system. “Gen” is a midrange (general) frequency, “Pen” is a lower (penetrating) range, and “Res” is a high-frequency (resolution) range. The Philips machine also uses the “P,R,G” nomenclature on the US screen. C: US images of the same superficial area using high (left) and low (right) frequencies. The image on the left has better resolution.
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■ FIGURE 38.1 (Continued) D: US images of the same deep area using high (left) and low (right) frequencies. The image on the right shows the nerve better though the resolution is lower.
■ FIGURE 38.2 A: Pictures of gain controls for Sonosite (left) and Philips (middle, right) US machines. The Sonosite allows adjustment of overall gain and separate adjustment of gain in the near and far areas of the US image. The Philips unit allows for adjustment of overall gain as well as at different levels of the US image (time-gain compensation or TGC, top sliders, move side –to side) as well as on the edges of the US image (lateral-gain compensation or LGC, lower sliders, move up or down). The TGC and LGC sliders are arranged haphazardly in the middle, and more conventionally in the image on the right. B: Same US image with gain adjusted. On the left, the gain is too low, making the image dark and hard to interpret. On the right, the gain is too high, making the image too bright and again hard to interpret.
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■ FIGURE 38.2 (Continued) C: Same US image with TGC and LGC adjusted. The image on the left shows how improper use of the TGC controls can give the US image a “striped” appearance, making interpretation difficult. The image on the right shows how improper adjustment of the LGC controls can make one side of the US image too bright or too dark, again making interpretation difficult.
■ FIGURE 38.3 A: Depth controls for the Sonosite (left) and Philips (right) US machines. B: US images of the median nerve showing too little (left) and too much (right) depth. The nerve is not seen in the image on the left as the field of view is too shallow. The nerve appears very small in the image on the right as the field of view is too deep.
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■ FIGURE 38.4 A: Schematic showing the effect of movement of an object on the frequency of sound waves emitted or reflected by an object. The object (dot) is moving in the direction of the arrow (left) effectively compressing the sound waves moving in the same direction as the object (higher frequency) and dilating the sound waves moving in the opposite direction (lower frequency). This is known as the Doppler effect. B: Color imaging controls for the Sonosite (left) and Philips (right) US machines. C: Still image showing use of color imaging. The color denotes flow through blood vessels. In this image, the vein is blue and the artery is orange/red. This is due to the color scale seen in the upper right area of the US image. Veins may not always appear blue and arteries may not always appear orange/red depending on the color scale selected and the orientation of the US transducer relative to the vessels in the US image.
narrowest portion of the beam is known as the “focal zone.” In this area, there is the least interference among US waves and the US image is clearest. In general, the focus depth should be adjusted so that it is centered over the target structure(s). If multiple US beams are being used simultaneously (see below), the number of focal zones can be adjusted as well. If multiple beams
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are used, the focal zone can be made wider or narrower to include more or less of the US image.
Multibeam Many newer US transducers are capable of emitting multiple US beams simultaneously (Fig. 38.6). These may be oriented in slightly different directions or use frequencies that are
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■ FIGURE 38.5 A: The US beam has an “hourglass” shape that is focused where the beam is narrowest (the focal zone). The distance from the transducer at which the beam is focused (focal depth) as well as the number of beams that can be focused (number of focal zones) can be adjusted. If multiple focal zones are used, these can be tightly or widely spaced depending on the size of the area of interest. B: Focal zone controls for the Philips US machine. The focus depth controls are shown on the left, and the number of focal zones control is shown on the right.
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■ FIGURE 38.5 (Continued) C: Identical US images showing inappropriate (left) and appropriate focus depth (right). The nerve in the image on the right appears clearer. D: Identical US images using two (left) and four (right) focal zones. The number of focal zones is displayed on the right side of the US image (highlighted).
slightly different (harmonic imaging). This may reduce artifacts in the US image and may give the US image a “smoother” appearance. This also requires more processing of the image, and so the frame acquisition rate (number of times per second the US image is changed) may decrease. This can make movement within the image appear choppy. Multibeam imaging can usually be turned on or off easily, and there is usually a marker (varies depending on manufacturer) on the image to show if this feature is being used or not.
Compression Some US machines may allow for adjusting the compression or grayscale of the US image. A narrower grayscale (more compression) will
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make the image appear more homogeneous, while decreasing the compression (wider grayscale) will provide more contrast. Some types of US machines have different scales that can be selected from a menu, or filters that color the image differently (e.g., sepia or violet tone).
Presets Many US machines come equipped with “preset” combinations of the above settings to optimize the US image for specific types of procedures (Fig. 38.7). These have been created by the manufacturers to optimize imaging for specific types of exams or procedures without having to manually adjust all of the machine’s settings. Depending on patient-specific factors (such as size), the preset may or may not actually provide
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■ FIGURE 38.6 A: Schematic of multibeam imaging. The different colored areas below the US transducer represent distinct US beams, each oriented a slightly different direction. The US transducer receives reflections from each beam, and the machine combines the signals to reduce artifact and produce a “smoother” US image. Some anesthesiologists prefer not to use multibeam imaging, however. B: Multibeam controls for the Sonosite (left) and Philips (right) US machines. C: Identical US images with multibeam imaging turned on (left) and off (right). The appearance of the focus depth indicators (highlighted) is different if multibeam imaging is off or on.
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■ FIGURE 38.7 A: Presets button on the Philips US machine (highlighted). B: Screenshot showing presets menu on the Philips US machine. The appropriate preset can be selected for the procedure being performed.
optimal settings. Often the preset is a good way to start imaging, and fine adjustments (depth, frequency, gain, focus, etc.) can then be made to improve the image quality.
■ TYPES OF US TRANSDUCERS Different types of US transducers (probes) may be helpful for specific procedures (Fig. 38.8). Most US machines can be used with a variety of transducers. These may be all attached to the US machine at the same time or may need to be attached to the US machine separately. If multiple transducers are connected to the US machine, the transducer can be selected using a control on the machine. If only one transducer can be attached at a time, the transducer that is attached is obviously going to be the one being used. The interface between transducers and machines varies by manufacturer (Fig. 38.8). In general, manually changing transducers does not require any special tools and can be done in seconds. In general, US transducers can be divided into two main categories: linear array or curved array. Linear-array transducers emit and receive US waves directed perpendicular to the surface of the transducer (Fig. 38.8). This produces a squareor rectangular-shaped image on the US screen. Curved-array transducers emit and receive US waves directed radially from the surface of the transducer. This produces a wedge-shaped or semicircular image on the US screen. Lineararray transducers are most commonly used by anesthesiologists as they do not distort the image and allow straightforward needle guidance
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during procedures. Curved-array transducers may provide a wider field of view, which can be helpful in many circumstances. In addition, the curved-array transducer can be “rocked” from one side to the other to further widen the field of view. Due to distortion of the US image (especially near the edges), it may be more difficult to determine the correct angle for needle insertion/ advancement. Often the needle needs to be oriented more steeply than anticipated. Each transducer emits and receives US waves within a range of frequencies. Some transducers use low frequencies and are best suited for deeper exams and procedures. Others use higher frequencies and are best suited for more superficial procedures. The range of frequencies emitted/received by the transducer is usually written on the transducer and/or displayed on the US screen. Another feature of transducers relevant to their use by anesthesiologists is the size of the transducer. This is referred to as the transducer’s “footprint.” Wider transducers may provide a wider field of view but may be difficult to position in tight spaces such as between ribs. Most anesthesiologists will be able to do the majority of exams or procedures with a single transducer. As transducers are expensive (each one costs $3,000-$10,000), most practices will not use many transducers unless they use US very frequently. However, as more anesthesiologists use US and the applications for use of US continue to grow, more practices are likely to purchase and use a variety of transducers.
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■ FIGURE 38.8 A: Attachments for different transducers on the Sonosite (left) and Philips (right) US machines (both highlighted). B: Curved-array US transducers (left) and an US image obtained using a curved-array transducer (right). C: Lineararray US transducers (left) and an US image obtained using a linear-array US transducer (right). Both the curved- and linear-array transducers come in a variety of widths (see rulers in images). This is referred to as the “footprint.”
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■ US TERMINOLOGY Knowing the terminology used by anesthesiologists can help you communicate during US exams or procedures. Key terminology relates to the way structures are imaged, ways in which the US transducer can be moved during exams and procedures, and the orientation of needles relative to the US transducer during interventional procedures. Structures are usually imaged using a “shortaxis” or “long-axis” view (Fig. 38.9). The shortaxis view generally refers to a cross-sectional image. Advantages of the short-axis view are that it is often easier to recognize structures as well as the arrangement of adjacent structures in this view. In addition, the probe can be moved longitudinally along the patient’s surface to “follow”
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structures proximally or distally. This can help confirm the identity of a structure or plan a safe needle trajectory at a location where the target is close to a large blood vessel or other vital structure. The long-axis view involves rotating the transducer 90 degrees (see below) relative to its orientation during short-axis imaging to image a long section of a structure (Fig. 38.9). This may be especially useful for looking at blood vessels, as abnormalities (such as clots) may not be well seen using short-axis imaging. It may be difficult to keep structures in view, however, as slight tilting of the transducer (see below) may move the plane of the US beam so much that the structure of interest may no longer lie in the plane and so not appear on the US image.
■ FIGURE 38.9 A: Long-axis imaging of the median nerve in the forearm. The US transducer is oriented parallel to the nerve (left), producing an image of a section of the nerve that appears as a “stripe” on the US screen (right). B: Short-axis imaging of the median nerve in the forearm. The US transducer is oriented perpendicular to the nerve (left), producing a cross-sectional image of the nerve (right).
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The US transducer can be moved relative to the patient to optimize the US image. The basic moves that can be made are easily remembered using the “PART” mnemonic. The “P” refers to the amount of pressure used to make contact between the transducer and the patient (Fig. 38.10). Too little pressure can result in poor contact and lead to “shadowing” on the US image. This is an artifact cased by the inability of US
waves to travel through air. Too much pressure may be uncomfortable for the patient and can compress fluid-filled structures such as blood vessels (especially veins, which have thinner walls than arteries). The “A” refers to the alignment of the transducer relative to the target structure(s) (Fig. 38.10). The transducer can be moved from side to side and along the patient to fully evaluate the
■ FIGURE 38.10 The “PART” maneuvers. A: The amount of pressure applied to the US transducer can be adjusted. B: The alignment of the US transducer can be adjusted laterally or longitudinally.
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■ FIGURE 38.10 (Continued) C: The transducer can be rotated. D: The transducer can be tilted to either side.
anatomy of the area(s) of interest and to place the target(s) in an optimal position within the image on the screen of the US machine. The “R” refers to the rotation of the transducer relative to the target structure(s) (Fig. 38.10). Anatomic structures may be easiest to recognize in cross-section, so the transducer may need to be rotated relative to the patient’s surface in order to identify them. Once structures are identified, rotating the transducer 90 degrees will allow for evaluation of the structures using the long-axis view, which may provide additional
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information. Also, once the structure(s) of interest has been identified, the transducer can be rotated to produce an “oblique” image if this allows for a more advantageous needle trajectory during procedures. The “T” refers to tilting the transducer relative to the patient’s surface (Fig. 38.10). Again, as anatomic structures are often most easily recognized in cross-section, the transducer may need to be tilted if the structure is not parallel to the patient’s surface (moving deep to superficial or superficial to deep). Often structures can appear
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or vanish from the US image depending on the way in which the transducer is tilted. Another important area of terminology relates to the orientation of the needle relative to the US transducer during interventional procedures (Fig. 38.11). The “in-plane” technique involves inserting the needle in the center of the short side of the transducer and advancing the needle
so that its tip and the entire shaft (ideally) can be visualized within the plane of the US beam. The “out-of-plane” technique involves inserting the needle along the long edge of the US transducer so that it is oriented perpendicularly to the plane of the US beam. Each technique has advantages and disadvantages, and some anesthesiologists may prefer one technique over the
■ FIGURE 38.11 A: In-plane needle technique. The needle is inserted along the lateral edge of the transducer and directed parallel to the long axis of the transducer in order to place the needle’s shaft in the plane of the US beam (left). A US image showing the shaft of the needle approaching a nerve (right). The needle appears as a white stripe coming from the upper right portion of the screen toward the nerve in the center of the image. B: Out-of-plane needle technique. The needle is inserted along the long edge of the US transducer and directed perpendicular to the long axis of the transducer (left). This may not show the needle well as only a cross-section of the needle will be in the plane of the US beam. An US image of the out-of-plane technique (right) shows only a shadow where the needle’s shaft crosses the US beam, just to the right of the nerve in the center of the US image.
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other for specific procedures. In general, the inplane technique is most commonly used during nerve block procedures, and the out-of-plane technique is most commonly used during vascular access procedures. It is also important to be familiar with terminology used to describe the appearance of tissues or structures in the US image. The echogenicity of a tissue or structure refers to how strongly it reflects US waves. Hyperechoic structures reflect a large percentage of US waves that contact them, and as such they appear bright on the US screen. Conversely, structures that do not strongly reflect US waves appear dark on the US image and are described as hypoechoic. Different tissues or structures can be recognized as different parts may be hyper- or hypoechoic. For example, bones have a hyperechoic surface on the US screen but are hypoechoic below the surface as US waves bounce off the surface and do not penetrate deeper. In fact, US waves are not able to image past the surface of bone, producing a dark area below. This is known as acoustic shadowing, as it resembles a shadow formed as an object blocks light. Another important property of tissues and structures relevant to US is the ability of structures to be compressed or not. Fluid-filled structures usually are compressible, while solid structures usually are not. This can be helpful to distinguish nerves from blood vessels or muscles from fluid collections. Structures can be simply described as “compressible” or “not compressible.”
■ STORAGE OF US IMAGES Most machines have the capability of printing an image of interest. This is important for documentation and billing. It is easy for a provider to become engrossed in the procedure at hand to forget to ask for a print. It may be helpful to give a friendly reminder to the provider to print an image when appropriate. For central line placement, this image is typically an image of the guide wire or actual line in the vessel. For peripheral nerve blocks, this image is typically a picture of the needle near the nerve or with local anesthetic surrounding that nerve. Most modern machines are equipped with video capability. This is helpful for teaching and learning from the procedure. Not all machines are created equally, however. Some record
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antegrade (record images a preset limited amount of time after the record button is pushed), while others record retrograde (records a preset limited amount of time backward from the time the record button was pushed). The anesthesia technicians should be familiar with how the US machines in their facility record images and how long the preset recording times are. Be ready to push the record button frequently depending on the preset recording times.
■ TIPS FOR OPTIMIZING CONDITIONS FOR US EXAMS AND PROCEDURES Optimizing the US Image The first step is to select or attach the appropriate transducer. If a preset is available for the type of exam or procedure being performed, select it from the preset menu. The depth of the image should be then adjusted so that the entire target structure is seen in the US image. The frequency can be adjusted depending on the depth of the target structure. The frequency can be increased for more superficial structures and decreased for deeper structures. The focal zone(s) should be positioned over the target, and the gain and compression can then be adjusted to help distinguish structures from one another. A quick look with color imaging can help identify vessels that may not be easily seen. The anesthesiologist can then use the PART maneuvers to optimize image quality.
Ergonomics Proper placement of the machine in the room is essential. Ask the practitioner where they prefer to place it. Typically, this will be in a position near the patient and in the line of sight of the practitioner placing the line or block (Fig. 38.12). This avoids excessive turning of the head of the practitioner, which not only is uncomfortable and impractical but also draws attention away from the patient. Always position yourself near the US machine during the procedure should the need arise to make any adjustments or make use of other features on the machine.
■ PROPER USE AND MAINTENANCE OF US EQUIPMENT Preparation for Use To prepare the US machine, turn the power on (do this early as on some machines it takes a few minutes for the software to boot up), enter the
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acceptable. Affix a patient label on the form to ensure the image is charted and billed appropriately. The machine and transducers used should be wiped down between patients as explained in the following section. Time between patients is a good opportunity to restock supplies specific to the procedure. Specifically, in regard to the US machine, make sure the US gel (sterile and unsterile), sterile sheaths, or other means of probe cover are available for the next procedure. In order to improve efficiency, if the next patient name is known, this is a good time to enter demographic data, choose a preset, position the machine, and set up for the next procedure.
Maintenance ■ FIGURE 38.12 A block being performed using an advantageous ergonomic arrangement of operator, patient, and US machine. The picture is taken over the anesthesiologist’s shoulder to show how he is able to see the US image without turning his head. If necessary, he can check the position of his hands, the needle, or US transducer relative to each other or the patient with a quick glance down while still maintaining a view of the US image.
appropriate patient data for billing and study retrieval purposes, and ensure the appropriate US probes are available, functional, and clean. Make sure that adequate US gel (both sterile and unsterile) and sterile probe covers are available. Ask the provider what kind of procedure the US machine will be used for and on what location, including the side, if appropriate, of the patient it will be performed. If possible, position the machine on the correct side and select the proper probe and presets. Set the TGC sliders to the neutral position. Depending upon the type of procedure, assemble any other necessary equipment (e.g., block kits, vascular access kits, gloves, and gowns).
Following Use Once the exam or procedure is complete, ensure the images will be stored under the correct patient name. Prior to use, locate the save study button on the machine. This is typically easy to find and one push of the button will store all images and videos recorded for the patient. Make sure any pictures taken and saved have been printed, if necessary. Secure the printed picture to the appropriate institution-specific form. If one is not available, a progress note form is
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It is important to maintain the US machine in optimal condition and prevent potential damage as much as possible. The probes should be properly stored and protected when not in use. They are expensive and can be easily damaged. This is essential to providing safe, efficient patient care. Become familiar with any potential maintenance agreements your department has with the manufacturers of the machine. They often will provide a loaner machine for use while your department’s machine is either repaired or maintained. Some manufacturers recommend preventative machine maintenance and cleaning by a service representative on a quarterly basis. Contact information is frequently placed somewhere on the machine by the sales representative. Inspect the US machine daily. It may be easiest to do this at the beginning of the day. Ensure all connections such as probes and printers are plugged in properly. Evaluate the integrity of connection cables, wires, and transducers. Check the printer and make sure an adequate amount of printer paper remains. The machine and transducers should be wiped down, preferably with a nonalcohol-based solution. Alcoholbased solutions are effective but may decrease the life span of the transducers. Make sure to wear gloves when cleaning the US machine and transducers with hospital-grade cleaning wipes or cleaning solution. These wipes and solutions contain chemicals that can be caustic and irritating to the skin if direct contact occurs. Before each procedure, make sure to have some form of sterile covering available for the transducer, whether in the form of a sterile sheath or large clear adhesive. A brief inspection and thorough
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cleaning should occur between each patient and at the end of the day. Transesophageal echocardiogram probes should be sterilized between patients as per your institution’s protocol. Any problems encountered with the machine should be documented, and any significant issues should be reported to the sales representative as soon as possible. They can be helpful in organizing smooth and timely service to your machine and quick return for use. Some facilities choose not to obtain a maintenance agreement with the manufacturer of the machine, and instead choose an internal engineering department to handle all maintenance issues. US technology continues to evolve and many of today’s machines contain software that can be upgraded periodically. It is helpful to contact the sales representative to determine how often these upgrades should occur. Staying vigilant is the key to preventing or catching a problem with your machine early. Knowing the proper channels of communication will ensure timely service of your machine in order to avoid affecting appropriate patient care because a machine or probe is unavailable.
■ SUMMARY US is a powerful tool that can be used by anesthesiologists during a wide variety of procedures. US equipment may appear complicated, but a basic understanding of the physics of US image formation, machine controls, and terminology will allow you to properly use the equipment and assist during US exams and procedures. Proper use and maintenance of equipment will help provide safe and effective patient care.
REVIEW QUESTIONS 1. To adjust the brightness of the US image, which of the following controls on the US machine should be adjusted? A) Frequency B) Focus depth C) Depth D) Gain E) Focal zones Answer: D. Adjusting gain affects the brightness of the image. Gain may be adjusted overall or in specific areas of the image (near/far, TGC, or LGC). The other choices can all be adjusted on most
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US machines and are useful to optimize image quality, but they do not directly affect the brightness of the US image.
2. When using US to visualize deeper structures, which of the following adjustments are most likely to improve image quality? A) Decreasing depth, increasing frequency, decreasing focus depth B) Increasing depth, decreasing frequency, increasing focus depth C) Increasing gain, increasing frequency, decreasing focus depth D) Decreasing gain, increasing frequency, increasing focus depth E) Decreasing gain, decreasing frequency, decreasing focus depth Answer: B. To image deeper structures, there must be sufficient depth to the image to include the structure(s) of interest. Lower frequency US waves travel better through tissues and though they have by definition lower resolution than do higher frequency US waves, they can reach deeper structures better as they are less subject to tissue attenuation. Increasing the focus depth so that the US beams are focused at the depth of the structure(s) of interest will improve the quality of the image at that depth. Increasing or decreasing gain settings may or may not improve the ability to see deeper structures, depending on the specific sonographic properties of the particular structure.
3. Which of the following measures can help improve patient safety for US-guided procedures? A) Use of probe covers or other barriers, as well as cleaning the transducer between procedures to prevent cross-contamination B) Regular inspection and calibration of US equipment by the manufacturer or institutional biomedical engineering department to ensure proper function C) Presence of a practitioner experienced in USguided procedures to ensure adequate image acquisition and interpretation D) Archiving of images for possible future review as part of a teaching file of Continuing Quality Improvement mechanism E) All of the above Answer: E. All of these options are important safety measures associated with the use of US. Prevention of cross-contamination between patients will help reduce the risk of infectious complications. Ensuring proper function of US equipment will help to reduce the risk of error due to malfunctioning equipment and prevent risks of electrical shocks or other injuries. Knowledge of US imaging and US guidance techniques is essential for the safe use of US during patient care. Storage of images for periodic review can be helpful to determine potential causes of ineffective procedures or complications.
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4. With regard to probe manipulation during USguided procedures, the mnemonic “PART” stands for A) Polarity, activity, response, timing B) Power, arc, resonance, tension C) Pressure, alignment, rotation, tilting D) Positioning, access, reference, tone E) Point, aim, reflection, target Answer: C. The “PART” mnemonic stands for pressure, alignment, rotation, and tilting. The other choices are random words starting with the same letters.
5. US image formation at its most fundamental level involves a visual representation of the A) Direct measurement of the natural resonant frequencies of varying tissue compositions averaged over time B) Indirect measurement of electromagnetic waves emitted by movement of ions across cellular membranes C) Generation of sound waves by a piezoelectric element, the reflections of which are measured by the element and processed by a computer D) Direct measurement of microscopic oscillations of molecules, filtered through a white noise generator E) Generation of low-intensity ionizing radiation that penetrates tissues of varying density in a characteristic pattern
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Answer: C. The US image is a graphical representation of US waves that have been emitted from and received by the US transducer. The waves are generated by a piezoelectric element that vibrates when exposed to an electrical current. Waves are emitted for only a small percentage of the time, and the transducer is in the “receive” mode the majority of the time. The other choices are nonsense except for “E,” which describes the physics underlying roentgenograms (also known as x-rays).
SUGGESTED READINGS Guillory RK, Gunter OL. Ultrasound in the surgical intensive care unit. Curr Opin Crit Care. 2008;14(4):415–422. Neal JM, Brull R, Chan VW, et al. The ASRA evidence-based medicine assessment of ultrasound-guided regional anesthesia and pain medicine: executive summary. Reg Anesth Pain Med. 2010;35(2, suppl):S1–S9. Sites BD, Brull R, Chan VW, et al. Artifacts and pitfall errors associated with ultrasound-guided regional anesthesia, Part I: understanding the basic principles of ultrasound physics and machine operations. Reg Anesth Pain Med. 2007;32(5):412–418. Sites BD, Brull R, Chan VW, et al. Artifacts and pitfall errors associated with ultrasound-guided regional anesthesia, Part II: a pictorial approach to understanding and avoidance. Reg Anesth Pain Med. 2007;32(5):419–433.
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Transesophageal Echo Edward A. Kahl and Lisa Chan ■ INTRODUCTION There are several different vendors and models of transesophageal echocardiography (TEE) technology. This chapter provides a generalized overview of the basics of TEE, equipment setup, and handling. Equipment and protocols for handling TEE hardware and storing images vary from institution to institution, and it is recommended that the anesthesia technicians be familiar with these policies and practices at their institution.
■ BASIC PRINCIPLES OF ULTRASOUND AND TEE Energy is all around us in different forms. Heat from a fire and light from the sun are the most familiar examples; however, sound too is a form of energy. This form of energy is used frequently in nature by creatures like whales and dolphins. They emit sound waves underwater to detect objects in their surroundings. Submarines and ships have adopted a similar idea by emitting “pings” and gauging the distance to another object by the amount of time it takes for the “ping” to return. Closer objects will send the “ping” back sooner, whereas farther objects will cause the “ping” to return much later. This is because it takes the sound waves more time to travel to the farther object and then return back to the submarine. Somewhat similar to the submarine or the ship, the transesophageal probe (TEE) houses a crystal near the tip that generates several thousand “pings” per second and displays an image based on the time it takes for their return. The TEE probe is placed into the esophagus, and the crystal near the tip emits lots of tiny “pings” that travel through the wall of the esophagus and to the heart. When the “pings” bounce off the parts of the heart and return to the probe, the probe converts the “pings” to the image on the screen.
■ TYPES OF TEE: TWO-DIMENSIONAL AND THREE-DIMENSIONAL Two-dimensional (2D) TEE has been the imaging modality used most commonly for TEE procedures. More recently, three-dimensional (3D) TEE has made its way into mainstream cardiac operating rooms. 3D TEE is typically used in conjunction with 2D TEE to attempt to answer questions about structures of the heart that are not obvious with 2D images alone. TEE in general is helpful in evaluation of heart valves, heart function, cardiac masses, and even in evaluation of placing cannulae in the heart. If your institution has a limited number of 3D-capable TEE machines and probes, the 3D TEE machines should be reserved for valve surgeries or more complex procedures. However, one should always check with the anesthesia provider to inquire about whether 3D imaging will be necessary for a particular case. In cases that do not involve a valve, such as coronary artery bypass grafting (CABG), a 3D probe may not be necessary. For emergency cases that require TEE, the first TEE probe and machine available should be used, unless instructed otherwise. To obtain a 3D image, a 3D probe and an ultrasound machine that contains 3D software are required. If a 3D probe is placed in a patient and the ultrasound machine is not capable of 3D imaging, the probe may be disconnected from the machine (but kept in the patient) and reconnected to a machine that has 3D capability. However, if a 2D capable probe is inserted into a patient that requires 3D imaging, the probe will have to be replaced with a 3D probe connected to a 3D-capable machine for 3D imaging.
■ TEE PARTS The ultrasound machine is a computer processing unit. Some of the important components 391
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include a screen or monitor, keyboard, knobboard, pin ports for insertion of probe transducers (whether for TEE or other types of ultrasound probes), and outlets for transfer of information for digital storage. It is housed on wheels with a braking and locking system located at the bottom front of the machine. These machines can cost up to $250,000. The TEE transducer is a long, flexible probe that collects the picture information to be processed and viewed on the ultrasound machine. At one end of the probe is the housing unit that fits into the insertion port of the ultrasound machine. The locking mechanism on this housing unit should be set to “open” and once it fits snugly into the insertion port, the locking mechanism is turned 90 degrees to lock the connector into place. Different brands of TEE machines may have different mechanisms to engage the TEE probe onto the TEE machine. Further down the probe is the handle of the TEE. The handle consists of two rotating knobs and two rubber buttons. The rotating knobs control the movement of the tip of the probe anteriorly, posteriorly, left, and right. The larger knob moves the tip up (anterior) and down (posterior), whereas the smaller knob moves the tip left and right (Fig. 39.1). These knobs are also sometimes useful for distinguishing between 2D and 3D probes. For example, some vendors assign 2D probes black knobs and 3D probes gray knobs (Fig. 39.2). There is a locking lever located right next to the movement-control knobs that secures the probe tip in its current orientation. The lever should be released or “unlocked” and checked for resistance prior to placement of the probe in a patient. The probe should never be manipulated inside the patient with the tip in the locked position (Fig 39.3). In a fixed or locked position, the probe tip can damage the oropharynx, esophagus, or stomach. If the control knobs become incompetent, the probe loses its ability to be maneuvered and should not be placed in a patient. The two rubber buttons on the side of the probe control the plane of the sound beam emitted from the tip of the probe. The black cord between the handle and the tip contains electrical wires, which may become exposed after teeth repeatedly rub against the cord covering. Damage to the electrical cords may also occur if a patient bites
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■ FIGURE 39.1 TEE probe.
down with enough force. Therefore, in patients with teeth, it is prudent to place a bite guard to protect the cord from the patient. The tip of the probe houses the key elements that send out and receive the ultrasound waves. If the tip is broken, the probe requires repair. TEE probes themselves can cost up to $50,000.
■ FIGURE 39.2 3D TEE probe: Different-colored knob controls distinguish 3D from 2D probes. For this vendor, 3D probes have gray knobs and 2D probes have black knobs.
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Relative contraindications include: recent surgery in the throat, fragile veins in the esophagus (esophageal varices seen in liver disease), problems swallowing or pain on swallowing, neck arthritis, outpouchings in the esophagus or stomach, history of radiation to the chest or neck, or problems with bleeding.
■ COMPLICATIONS FROM TEE
■ FIGURE 39.3 Lever that locks the knob controls and hence locks the TEE probe tip in a fixed position. NOTE: TEE probe should NEVER be placed, removed, or manipulated inside the patient with the lever in the locked position.
■ INDICATIONS AND CONTRAINDICATIONS TEE is most commonly used in cardiac surgeries, liver and lung transplants, and major vascular surgeries. Specific guidelines for use can be found at the American Society of Anesthesia/Society of Cardiovascular Anesthesia/American Society of Echocardiography Web sites. Caution should be exercised in placement of the probe in conditions where the patient has had any neck, mouth, esophageal, stomach, or bleeding problems. Major complications include creating trauma or bleeding anywhere in the body where the probe comes into contact with. The question that must be always asked is: does the benefit of this procedure outweigh the risks? Some situations such as life-threatening emergencies may warrant the risk. Other options may be considered if a TEE cannot be placed safely, but information about the heart is needed. In these situations, transthoracic echocardiography (TTE) can be performed before surgery and/or an epiaortic exam (ultrasound of the heart and aorta in the surgical field) can be done once the chest is open. These technologies require different probes but can use the same ultrasound machine to process the signals and display an image. Absolute contraindications include: patient refusal, esophageal problems (esophageal stricture, tracheoesophageal fistula, postesophageal surgery, esophageal trauma, hole, rings/webs, tumor), unstable cervical spine, and previous esophagectomy or esophagogastrectomy.
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Fortunately, serious complications from TEE are rare. The following are the reported complications from TEE use: esophageal perforation, esophageal bleeding, problems swallowing (dysphagia), pain on swallowing (odynophagia), thermal burn injury to the esophagus or stomach from the probe tip heating up, lip trauma, dental damage, and rarely vocal cord damage from inadvertent endotracheal intubation.
■ TEE SETUP The TEE should be positioned in the room at or near where it will be located during the surgical procedure, especially if the machine is large and bulky. The initial step includes plugging the machine into a protected and grounded power outlet. The area around the TEE should be checked to ensure it is free of cords that would interfere with freely moving the TEE machine during the case. The next step is to ensure all network and/or media devices have been plugged in properly. Once this is accomplished, the TEE machine can be powered on. The startup time of the TEE from pressing the power button to entering patient data or being able to acquire images may take several minutes. Therefore, the technician should anticipate this delay in the emergent situation where TEE may be needed to make a fast therapeutic decision (i.e., used to diagnose the cause of hemodynamic instability). If TEE is needed in this situation, ensure that it is plugged in and powered on early, so there is no delay in waiting for it to power up. The next step after powering on the machine and ensuring its place in the operating room is to enter patient-identifying data. This information is required to associate the TEE images to the correct patient and to ensure they can be easily accessed in the future. The data elements collected vary from institution to institution. Therefore, it is up to the anesthesia technicians to be familiar with this process at their institution.
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If a TEE server/network is available at your institution, the proper network setup should be established. This includes ensuring that the network cable is connected to the TEE machine (usually in the back of the machine) as well as to the appropriate network jack in the operating room. The appropriate TEE jack in the operating room should be properly labeled to avoid confusion with other network jacks. Additionally, if a TEE network is not available at your institution, the proper media device should be available for saving the images if so required by your institution. These include DVDs, USB drives, and rarely VHS tapes or other media. Finally, connect the TEE probe to the machine as described above and ensure that the probe is recognized by the TEE machine. This step varies for different manufacturers. Once the probe is properly connected to the TEE machine, the integrity of the probe knobs should be checked for functionality. This means the locking lever should be in the unlocked position. Then, the large wheel and small wheels should be moved in both directions while inspecting the tip to ensure it moves appropriately. If the probe tip does not move properly, it should be sent for repair and should not be placed in a patient. Additionally, the locking lever should be in the unlocked position during placement to minimize trauma to the patient. Finally, the checked and ready TEE probe should be placed in a location where it is safe from damage. Probe covers are available to protect the crystal near the probe tip from inadvertent damage.
■ PREINSERTION CHECKLIST • Check that the TEE machine is the proper machine for the provider’s needs (i.e., does the provider require 3D capability?). • Check to ensure the proper TEE probe is available (i.e., 3D probe or 2D probe, epiaortic probe). • Be sure ultrasound gel is present near the TEE machine. • Have bite blocks or other probe protectors present. • Have an orogastric tube with lubricating jelly present (usually placed by anesthesia provider prior to TEE insertion to empty stomach contents). • Connect the power cord to the appropriate outlet and power up the machine.
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• Enter the required patient identification information as per your institution’s guidelines. • Ensure proper network setup and all necessary cables are connected; or check that proper media devices are available (DVDs, CDs, USB drives depending on institution). • Attach the ECG source (either ECG leads to be placed on the patient or connection to the anesthesia monitor ECG).
■ HELPING THE ANESTHESIOLOGIST PLACE THE PROBE AND ACQUIRE IMAGES The patient should be adequately anesthetized for this procedure. The jaw should be slack and easy to manipulate. The anesthesia technician should hold up the probe handle while the anesthesia provider inserts the TEE probe into the esophagus. Holding the handle up will prevent the tip from inadvertently being manipulated left, right, up, or down. This will also minimize the risk of the probe falling or twisting. Usually, the anesthesia provider will pull forward on the jaw to open up the back of the mouth during probe insertion. Other maneuvers that help placement are flexing the head so that there is a more gentle turn for the probe to make through the oropharynx. If these maneuvers fail, final attempts usually involve using a laryngoscope to find the esophageal opening. However, if there continues to be strong resistance to probe insertion, the procedure should stop. The probe should never be advanced forcefully. Additionally, the anesthesia technician can help the anesthesia provider acquire images by pressing the acquire image button on the TEE machine or adjusting the imaging depth. Also, the technician may help by turning on, off, or resizing the color flow windows or making caliper measurements of structures. The anesthesia providers should teach the anesthesia technicians how to perform these maneuvers as they differ from machine to machine. Some anesthesia providers may prefer to control these functions themselves.
■ END OF THE CASE Probe Removal Extreme care should be taken during TEE probe removal to protect both the patient and the TEE probe. During removal, the TEE probe is at risk of being damaged from the patient’s teeth and
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extra care should be taken during this process especially if a tooth guard has not been used. Even if it is common practice at your institution for anesthesia technicians to remove TEE probes from patients, still consult with the anesthesia provider before doing so. The locking lever should be checked to ensure it is in the unlocked position; and both knobs should be in the neutral position. The TEE probe should be removed slowly. Any amount of resistance should prompt the anesthesia technician to notify the anesthesia provider. After removal, the TEE probe should be examined for any signs of trauma to the probe and the patient. This includes looking for the presence of blood on the TEE probe. The “dirty” probe should be taken directly to central processing where it can be cleaned, unless there is a system in place that allows identification of dirty probes from clean ones. Leaving a dirty TEE probe lying around puts it at risk of being damaged or being inadvertently placed in another patient. Prior to removing the TEE probe or shortly afterward, the TEE exam should be ended. The images should be sent to the echo server/network if one exists, or the images should be saved onto a media device with a patient label placed on the media. It is important to save all images prior to powering down the ultrasound machine; otherwise, the images could be lost.
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contaminants. As such, it too should be cleaned in between patient use. Care should be taken to avoid using dirty gloves to handle the TEE probe or machine controls.
Probe Storage and Identification Once cleaned, the TEE probe should be stored in a clean place that is easily accessible and protects the probe from damage. A system should be in place to discern clean, postprocessed probes from dirty probes. This identification process is of utmost importance to avoid using a dirty probe in another patient.
■ SAFETY Safe handling of TEE equipment can save your institution tens of thousands of dollars or more. General rules, if followed, can ensure that the TEE probes and machines last at least their expected life span. These include the following: 1. Always keep the TEE machine and probe clear and safe from other equipment in the operating room (Fig. 39.4). 2. Never leave the TEE probe hanging loosely from IV poles or elsewhere without a tip protector because the probe tip (and the crystal inside it) can be damaged from contact with other objects.
Probe Processing TEE probe cleaning varies from institution to institution and from manufacturer to manufacturer. However, there are some general principles that should be followed: 1. Do NOT use bleach on any TEE transducer. 2. Do NOT use strong solvents such as acetone, freon, or other industrial cleaners on transducers. 3. Do NOT soak transducers for extended periods of time such as overnight. 4. Do NOT immerse or rinse the connector or cable portions near the connector. 5. Do NOT immerse or rinse the steering mechanisms. 6. Do NOT allow alcohol cleaning solutions or isopropyl alcohol to air-dry on the transducer. Additionally, the TEE machine itself may occasionally get soiled with blood or other
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■ FIGURE 39.4 TEE probe storage: The probe should be stored in a secure manner to avoid damage to the probe.
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3. Never leave the TEE probe lying on a tabletop where it could potentially be damaged by falling on the floor. 4. Always check the TEE probe controls and knobs prior to placing the probe into the patient. 5. Use caution when removing the TEE probe from patients with teeth, to avoid both dental injury to patients or damage to the TEE probe. 6. Never forcefully remove the TEE probe from a patient. It should come out with very little resistance. 7. Never insert, remove, or manipulate a TEE probe while in a patient if the lever that controls the knobs and the tip is in the locked position.
■ TEE IN EMERGENCIES TEE is sometimes needed emergently to diagnose hemodynamic instability either in the operating room or in the ICU. In these situations, keep in mind that the TEE machine may take several minutes to power up, so it should be promptly plugged in and powered on. Additionally, use caution to ensure the proper patient name is attached to the emergent study.
■ SUMMARY TEE is an established technology to evaluate the heart. The probe is inserted into the esophagus. Reflected sound waves are processed by the ultrasound machine and displayed on the monitor. The anesthesia technician should be familiar with the setup of the ultrasound machine, how to attach the probe to the machine, and how to operate the movement controls. TEE probes can be easily damaged. Anesthesia technicians should be familiar with how to properly handle, process, and store the probes. This chapter provides an overview of these topics.
REVIEW QUESTIONS 1. Which of the following should be available for a cardiac valve replacement procedure? A) Ultrasound gel B) Bite block C) Network connection or available media (DVD, USB drive)
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D) 2D or 3D TEE probe E) All of the above Answer: E. For a valvular procedure, a 3D machine and 3D probe are recommended if available but 2D is also acceptable. The rest of the options are part of the preinsertion checklist.
2. In which of these situations is it okay to continue placement of the probe? A) Strong resistance to probe insertion despite maneuvers B) On checking the knobs, the tip of the probe does not move. C) The probe insertion pins do not match up with the TEE machine insertion ports. D) The patient has consented for TEE and all necessary TEE equipment is available. E) The patient has a cervical spine injury. Answer: D. In Option A, when the probe is difficult to insert despite helpful maneuvers, do not force probe insertion. Option B is an example of a broken probe and should not be inserted into the patient. In Option C, the probe type and machine likely do not match one another or require an adapter. Option E is incorrect because TEE is contraindicated in cervical spine injury. Option D is true and correct as stated.
3. Why is it important to take extra care to ensure TEE equipment is clean and protected? A) There is a crystal in the TIP of the TEE probe that is expensive and can be easily damaged. B) Replacing broken TEE equipment can be very expensive. C) Ensuring probes are cleaned will avoid the complication of using a dirty probe on a patient. D) TEE is vulnerable to damage from surrounding operating room equipment. E) All of the above. Answer: E. All of the above are true.
4. Which of the following statements is FALSE? A) Purchase and maintenance of TEE machines and probes can cost hundreds of thousands of dollars. B) It is okay to insert a TEE probe into the patient with the tip in the locked position. C) Ultrasound gel should be available for TEE probe placement. D) An anesthesia technician can help the anesthesiologist with TEE probe placement by holding the handle of the TEE probe up while the anesthesiologist places the TEE probe into the patient. E) The TEE machine should be plugged into a grounded and protected outlet.
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Chapter 39 • Transesophageal Echo Answer: B. One should NEVER manipulate a TEE probe in the patient while the tip is in the locked position. All other lettered options are correct.
5. Which of the following statements is FALSE? A) TEE can be used to look at the heart’s valves and function. B) TEE is sometimes used in major vascular surgery. C) It is safe to leave the TEE probe hanging freely from an IV pole. D) 3D TEE is sometimes used to answer questions about the heart that 2D TEE is unable to. E) TEE is contraindicated in patients with recent stomach surgery. Answer: C. One should not leave the TEE hanging from an IV pole without a protective tip cover, as the tip can be damaged by surrounding operating room equipment. All other choices are true.
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SUGGESTED READINGS Practice Guidelines for Perioperative Transesophageal Echocardiography. An Updated Report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Copyright 2010, the American Society of Anesthesiologists, Inc. Philadelphia, PA: Lippincott Williams & Wilkins. Savage R. Organization of an intraoperative echocardiographic service. In: Savage R, ed. Comprehensive Textbook of Perioperative Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:3–41, 106–132. Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA guidelines for performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: recommendations of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography. J Am Soc Echocardiogr. 1999;12(10):884–900.
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40
Neuromuscular Blockade Assessment Ryan Goldsmith ■ INTRODUCTION Chapter 16 discussed the anatomy and physiology of the neuromuscular junction. In addition, Chapter 16 covered the clinical utility of neuromuscular blockade to induce patient paralysis, the medications used for this purpose, and the importance of monitoring the degree of neuromuscular blockade. This chapter focuses on how to use peripheral nerve stimulators to monitor neuromuscular blockade.
■ PERIPHERAL NERVE STIMULATORS There are multiple peripheral nerve stimulators on the market today; however, they share many common features. Peripheral nerve stimulators work by delivering a small electric current through the skin to a peripheral nerve. This electric current stimulates a muscle innervated by that nerve to contract. Various controls on the stimulator allow delivery of different types of electrical stimuli to the muscles in order to assess the degree of blockade between the neuron and the muscle. The different types of stimuli include single twitch, tetanus, and automatic train of four. Each type will be discussed below. Other controls on the nerve stimulator include power on/off and a control to adjust the intensity of the electrical current. These functions are easily selected on the face of most nerve stimulators by touching the membrane buttons or operating dials. The control to adjust the current usually allows the operator to adjust the output current from between 0 milliamps (mA) and 7.0 mA. The amount of current (in mA) that is delivered to the patient is often displayed on a digital LCD screen (less sophisticated nerve stimulators only indicate the mA on a dial and do not have a display). In addition, many nerve stimulators have an LED
light that flashes whenever a stimulus is sent. Others sound an audible beep each time a stimulus current is delivered (some systems do both). The loudness of the beep is often adjustable. All stimulators have a pair of lead wires that need to be attached to the stimulator and to the patient. The polarity of the electrodes is found on the stimulator box. The black polarity slot represents the negative lead, while red represents the positive lead. The lead wires can be attached and detached from the stimulator unit at the polarity connectors (Fig. 40.1). The lead wires attach to the electrodes using alligator clips or standard snap-on connectors. Some stimulators have an attachment that allows direct application of metal ball electrodes to the patient and do not require lead wires or electrode pads. Peripheral nerve stimulators can be purchased through most medical supply companies. To illustrate nerve stimulator functionality, we describe two popular nerve stimulators here: the MicroStim III and MicroStim Plus (Fig. 40.2). MicroStim III and MicroStim Plus have similar functionality. MicroStim Plus is smaller than MicroStim III and is easy to carry in a pocket. In addition, MicroStim Plus has metal probes that can be applied directly to the skin without the use of electrodes. The metallic probes attach to the nerve stimulator box at the polarity slots. The current is delivered through the probes. The current output is adjustable in 0.1-mA increments from 0 to 6.0 mA. The standby switch maintains power to the nerve stimulator without delivering a current. The twitch function delivers a pulse at 1 Hz (1 pulse per second) or 2 Hz (2 pulses per second). The tetanus function delivers 50 Hz (50 pulses per second) or 100 Hz (100 pulses per second). The twitch function
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■ NERVE STIMULATOR SETUP
delivers one pulse at a time, whereas the tetanus function delivers a sustained or constant stimulus. The train of four function key delivers four pulses every 2 seconds and then repeats every 10 seconds.
Electrodes are applied to the skin of the patient over a target nerve (nerve targets will be discussed below). The electrodes have an adhesive to attach to the skin. The center of the electrode that touches the patient has a conductive jelly to improve the conduction of the stimuli to the patient. The conducting gel area is small, approximately 7–11 mm in diameter. The other side of the electrode has a metallic nipple to allow the attachment of the lead wires (ECG electrodes can be used). The skin should be cleansed properly by rubbing it with an abrasive or alcohol swab and then dried before applying the electrodes. The nerve stimulator lead wires are then attached to the metallic nipples on the electrodes using the alligator clip (or snap-on connectors) on the lead wire (Figs. 40.3 and 40.4). The resistance to current at the skin ranges from 0 to 2.5 KΩ; however, with the body at cooler temperatures, the resistance can get as high as 5 KΩ. This can lead to misinterpretation of the response to a stimulus. Because of the resistance increase a stimulus may not elicit twitches that may be present at warmer skin temperatures. Some nerve stimulators have a display that shows the current delivered and alerts the user when the current selected is not being delivered due to an increase in resistance.
■ FIGURE 40.2 MicroStim Plus nerve stimulator.
■ FIGURE 40.3 Lead wires attached to electrodes over the facial nerve.
■ FIGURE 40.1 MicroStim III nerve stimulator.
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Black
Red
PULSE
DBS
TWITCH
TETANUS TOF
Path of ulnar nerve On-Off and intensity dial switch
■ FIGURE 40.4 Nerve stimulator box attached to the patient with lead wires over the ulnar nerve.
Once a nerve target is chosen, the negative (black) lead should be placed as close to the location of the nerve as possible. The positive (red) lead should be placed 3–6 cm proximal to the negative lead. The polarity is important. Nerve stimulators work better if the negative lead is placed over the nerve. Once the electrodes and leads have been attached, the unit can be turned on. Be sure the batteries are operational and the unit has power (the LED screen turns on or the power light turns on). The desired current output should be selected. A stimulus can then be applied by choosing a stimulus mode, and muscle twitches in response to stimuli can be observed.
■ SPECIFIC TARGET NERVES Several different nerves can be used to elicit a stimulated response from a muscle to evaluate neuromuscular function. The facial nerve, due to its accessibility during surgery, is one of the more common sites to stimulate and evaluate for muscle blockade. The temporal branch of the facial nerve can be found where the nerve emerges from the skull, approximately at the lower level of the ear. The nerve travels under the skin on the side of the face between the eye and ear. It supplies the muscles of the eyes, muscles around the ear, and the muscles on the side of the forehead. The negative electrode should be placed over the
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temporal branch of the facial nerve as close as possible to where it emerges on the face. A good landmark is the zygomatic arch (a bone just in front of the ear). The positive electrode can be placed on the forehead (Fig. 40.3). The location of the negative electrode is important. The intent is to stimulate the temporal branch of the facial nerve, which will then send the signal to the muscles around the eye, causing them to contract. If the neuromuscular junction is blocked, muscle contraction will be impaired. However, muscles can be stimulated directly by an electrical current (bypassing the motor nerve and any blockade at the neuromuscular junction), if the negative lead is placed close enough to the muscle. If placed too close to the muscle, a stimulus could be delivered and the muscle would contract, even though there was still neuromuscular blockade. This could lead a clinician to believe that a patient had recovered from a neuromuscular blocker, when in fact he or she had not. Another popular nerve to stimulate is the ulnar nerve (Fig. 40.4). With the arm placed in anatomical position, the ulnar nerve can be found as it runs along the medial and anterior side of the arm. The ulnar nerve supplies several muscles including muscles that flex the medial wrist, flex the 4th and 5th fingers, and adduct the thumb (pulls the thumb toward the 5th finger). For stimulation of this nerve, the electrodes are applied to the volar side (medial and anterior side) of the wrist over the ulnar nerve. The distal lead (negative/black) should be placed about 1 cm proximal to the point at which the wrist flexes (up the arm). Stimulation in this region may cause the wrist to flex due to direct stimulation of muscles in the forearm, particularly if the leads are placed too far proximally (up the forearm). Stimulation of the ulnar nerve at the wrist will cause the thumb to pull toward the little finger (adduction). The adductor muscles, which are responsible for this movement, are in the hand at the base of the thumb, far from leads placed on the wrist. Thus, assessment of the strength of thumb adduction is a good test of the neuromuscular junction between the ulnar nerve and the adductor muscles of the thumb.
■ NEUROMUSCULAR MONITORING After the administration of a nondepolarizing drug (e.g., rocuronium, cisatracurium), the muscle may experience different levels of paralysis
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including intense blockade, deep blockade, moderate blockade, and recovery. The nerve stimulator helps the anesthesiologist determine the level of neuromuscular blockade. If a sufficient initial dose of nondepolarizing neuromuscular blocker is administered, the muscle becomes flaccid or completely paralyzed. At this stage of intense blockade, the muscles will not respond (twitch) to a stimuli sent by a nerve stimulator. As the neuromuscular blockade begins to wear off, the muscle will begin to respond to a stimulus, but the twitch will be less than full strength. Additional stimuli administered immediately after the first twitch will either elicit progressively weaker twitches or fail to produce a muscle response at all (deep blockade). For example, most nerve stimulators produce four successive twitches, 0.5 seconds apart (2 Hz). During initial recovery, the four stimuli may only produce one or two weak twitches. After additional time has passed and the muscle has made further recovery (moderate blockade), all four stimuli may produce a twitch; however, each successive twitch will be progressively weaker. This is referred to as fade. The fade response is commonly used to assess the degree of neuromuscular blockade. Evaluation is accomplished by delivering four successive stimuli 0.5 seconds apart (referred to as the train of four [TOF]) to the target nerve and measuring the strength of any elicited muscle twitch. The strength of the muscle contraction can be measured by a special monitor, by feel, or by observation. An unblocked neuromuscular junction will produce muscle contractions with the greatest amplitude (strength of contraction), and subsequent contractions in the TOF stimulus will be just as strong (no fade). A common calculated measure is to divide the amplitude (strength) of the fourth muscle contraction in the TOF by the amplitude of the first muscle contraction (TOF ratio). One criterion for adequate recovery from neuromuscular blockade is that the TOF ratio is at least 0.7. For continuous monitoring of neuromuscular blockade, a TOF stimulus can be delivered automatically by the nerve stimulator every 10 seconds. Alternatively, the anesthesia provider may choose to monitor the TOF intermittently. Another useful nerve stimulator function is to deliver a tetanic stimulus, a 100-Hz or 50-Hz pulse to the nerve that will cause a normal muscle to spasm without relaxing (tetanus). Response
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to the tetanic stimulus, like the TOF function, is used to evaluate the level of neuromuscular blockade. Under an intense blockade, the muscle does not respond to either TOF or tetanus stimulus. Following intense blockade, the drug is metabolized over time and the ability for the muscle to respond to a nerve stimulus begins to recover. At this stage, the muscle will respond to a tetanus stimuli; however, the muscle will not be able to sustain the tetanic contraction. The ability to sustain a tetanic contraction is another criteria used to determine that a patient has sufficiently recovered from neuromuscular blockade.
■ MAINTENANCE FOR NERVE STIMULATORS Peripheral nerve stimulators should be stored in an organized storage box or shelf in order to decrease the damage to the stimulators, thus increasing the life of the stimulator. The leads should be coiled up and free from tangle in order to maintain their shelf life. Wires break frequently, and extra wires should be on hand. They can be purchased through medical supply companies. The power supply for most stimulators is a 9-V alkaline battery, and extras should also be available.
■ TROUBLESHOOTING If a stimulator does not appear to be working, check the following: • Check the batteries and replace if necessary. • Check all lead connections (stimulator to leads, leads to electrodes). • Check the lead wires. Try replacing the wires. • Check and replace electrodes if necessary (the conductive gel can become dried out and not transmit enough stimulus to the patient).
■ SUMMARY Neuromuscular blocking drugs are commonly used in anesthesia practice. Inadequate reversal or recovery from neuromuscular blockade can have severe clinical consequences. Peripheral nerve stimulators are an essential tool for anesthesia providers to monitor neuromuscular blockade, thus preventing clinical complications. A stimulus is applied to a nerve and the response of the muscle is an important indicator of the depth of blockade. Proper placement of the leads and electrodes is essential for proper interpretation of muscle responses.
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REVIEW QUESTIONS 1. Which of the following statements is TRUE regarding stimulation of the facial nerve to monitor neuromuscular blockade? A) The electrode should be placed directly over the muscle being monitored. B) The facial nerve is the ONLY appropriate nerve to stimulate. C) The facial nerve is a poor choice to monitor neuromuscular blockade. D) Both tetanus and TOF stimuli can be applied to the facial nerve. E) None of the above. Answer: D. Either TOF or tetanus can be applied to any nerve. The electrodes should not be placed directly over the muscle being monitored to avoid direct stimulation of the muscle (bypassing the neuromuscular junction). The facial nerve is a common location for monitoring because of its accessibility; however, many other nerves can be used.
2. Which of the following muscle responses indicate residual neuromuscular blockade? A) Fade to TOF B) Inability to sustain a tetanic contraction C) Twitch response is absent to a single stimulus D) Three out of four twitches are present after a TOF stimulus E) All of the above Answer: E. No muscle response to a stimulus indicates deep neuromuscular blockade. As the blockade begins to wear off, muscle
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twitches in response to stimuli will begin to appear; however, fewer than four twitches to a TOF stimulus still indicate a moderate blockade. A sustained muscle contraction without fade to a tetanic stimulus or four complete muscle twitches of equal and strong amplitude after a TOF stimulus indicate recovery from neuromuscular blockade.
3. A muscle does not respond to an apparent stimuli. Which of the following should NOT be performed? A) First, try a different nerve. B) Check that the power is on and the battery is functioning. C) Check that the stimulator box is delivering a stimulus (flashing indicator with each stimulus). D) Check the current setting. E) Check that the lead wires are properly attached to the box and to the patient. Answer: A. All of the other items should be checked first to ensure proper functioning of the nerve stimulator. If it appears to be functioning properly, check the position of the lead placement.
SUGGESTED READINGS Snell RS. Clinical Anatomy for Medical Students. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000: 668 pp. Viby-Mogensen J. Neuromuscular monitoring. In: Miller RD, Eriksson LI, et al., eds. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingston; 2009: Chapter 47.
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CHAPTER
41
Neurophysiologic Monitoring Judith A. Freeman ■ INTRODUCTION Surgery often involves operating in close proximity to peripheral nerves, the spinal cord, and the brain, or their blood supply. These structures can be damaged unintentionally from scalpels, retractors, electrocautery devices, or other surgical instruments. Neurophysiologic monitoring can be used during surgery to assess the status of peripheral nerves, the spinal cord, and the brain. It can serve as an early warning system to alert the surgeon that something is wrong while there is still time for corrections to be made before permanent injury occurs. The basic technique is to apply a stimulus in the central or peripheral nervous system and to measure the response. The health of the system is determined from the nature of the measured response. Neurophysiologic monitoring may also be used to monitor intracranial pressure (ICP) during neurosurgery or when the brain is injured. Finally, neurophysiologic monitoring can be used to assess the depth of general anesthesia to reduce the risk of intraoperative awareness. This chapter provides an introduction to the major neurophysiologic monitoring techniques and their implications for anesthesia.
■ NEUROPHYSIOLOGIC STIMULUS AND RESPONSE Neurophysiologic monitoring involves the measurement of electrical signals generated along the entire length of motor or sensory neural pathways from peripheral nerves to the brain. Needle or surface electrodes may be used to both initiate the stimulus and measure the response. There are two basic methods of performing this type of monitoring. First, an electrical stimulus is applied to a peripheral sensory organ or nerve and the response signal is measured as it travels to the brain. In the second method, the stimulus is applied to the scalp over a particular
brain region and the response is measured as it travels along the nerve pathways to the periphery. Measurements are averaged with a computer, and the results are displayed on a screen as continuously changing waveforms (older systems recorded the signals on graph paper). Both the amplitude (the strength) and the latency (the time it takes to travel) of the signal yield important information about the health of the pathways (Fig. 41.1). Amplitude and latency are continuously measured during the surgery, and changes in either of these may indicate damage in the neuronal pathway. This type of monitoring will help to detect impending nerve damage along any part of the pathway produced by surgical manipulation of the brain, the spinal cord, peripheral nerves, or the blood supply to these structures. It provides an early warning system of altered nervous tissue function, thus allowing the surgeon to take steps to avoid permanent postoperative neurologic damage. Some examples of surgeries where neurophysiologic monitoring is utilized include carotid artery surgery (interrupts blood flow to the brain), spine surgery (the operation is in close proximity to nerves), and operations directly involving nerves, the spinal cord, or the brain. Although nerve damage causes changes in monitored waveforms, they are also affected by changes in the physiologic milieu. Hypoxia, hypotension, hypothermia, and anesthetic drugs (see below) all can alter signal latency and amplitude. These variables must be controlled as much as possible during surgery to avoid affecting neurophysiologic monitoring. Any changes in signal latency or amplitude must be interpreted by taking into account any changes in physiologic parameters or the administration of anesthetic agents. In most institutions, neurophysiologic monitoring is carried out by certified neurophysiology 403
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Motor Evoked Potentials Electrical stimulation of the scalp overlying the motor cortex of the brain produces a response passing through the spinal cord to the peripheral nerve and finally to the muscle. The response can be detected at any point in this pathway. Of particular importance to anesthesia providers is that stimulation of the motor cortex in the brain intending to stimulate nerves to the legs often stimulates the facial nerve as well. This may lead to jaw clenching during stimulation. A soft bite block should be placed, so that the tongue does not get bitten. ■ FIGURE 41.1 An example of the mixed peripheral nerve somatosensory evoked potential on stimulation of the posterior tibial nerve. The amplitude or strength of the response is represented by the height of the wave. The latency of the response is represented by the time in milliseconds that it takes for the response to be detected. (From Frymoyer JW, Wiesel SM, et al. The Adult and Pediatric Spine. Philadelphia, PA: Lippincott Williams & Wilkins; 2004, with permission.)
technicians under the guidance of an expert neurophysiologist and ultimately overseen by a physician. Arrangements are usually made between the surgeon, the anesthesiologist, and the neurophysiologist regarding the appropriate monitoring for the specific case. The following sections will briefly describe the major neurophysiologic monitoring techniques.
■ TYPE OF STIMULUS RESPONSE NEUROPHYSIOLOGIC MONITORING Somatosensory Evoked Potentials Repeated electrical stimuli are delivered to a peripheral nerve and the signal is recorded as it passes up the spinal cord into the cerebral cortex. For example, the stimulus could be applied to the posterior tibial nerve near the ankle because the surgeon is working on the spine near the spinal nerve roots. The roots may be difficult to see, and they contribute to the makeup of the tibial nerve. Somatosensory evoked potential (SSEP) waveform changes would alert the surgeon to potential injury to the nerve roots. In another example, the blood flow to the carotid artery must be interrupted during surgery. SSEP waveform changes could indicate that the brain is not receiving enough blood flow.
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Brainstem Auditory Evoked Potentials or Responses Repeated clicking sounds are delivered via an earpiece placed in the auditory canal, and the responses are picked up by electrodes on the scalp. This technique monitors the condition of the ear, the cochlear nerve, and the pathway to the auditory cortex through the brainstem. It is most useful during resection of acoustic neuromas (tumor on a nerve leading from the ear to the brain), brain surgery close to the junction of the brainstem and the cerebellum, and during decompression of certain cranial nerves.
Visual Evoked Potentials Lights are repeatedly flashed in front of the eyes, and the pathway to the visual cortex in the brain is recorded. Visual evoked potentials (VEPs) may be useful information in patients who have tumors involving the optic pathway (the optic nerve and the pituitary gland).
Electromyography The sensing electrodes are placed in the muscles innervated by the nerve at risk for damage. When the surgeon touches the nerve, an electrical signal will be generated in the muscle. This method is used in spine surgery, surgery where the facial nerve is at risk of damage, and more recently in thyroid surgery with the introduction of the NIM electromyography (EMG) endotracheal tube. The NIM endotracheal tube has two sensing electrodes just proximal to the cuff. When the tube is placed into the trachea with the cuff just past the vocal cords, the sensors will detect signals from the vocal cords. If the surgeon irritates the recurrent laryngeal nerve, the electrodes will sense vocal cord signals. EMG is a test involving
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motor nerves; therefore, muscle relaxants should not be used during the anesthetic.
■ IMPLICATION FOR ANESTHESIA PERSONNEL Anesthetic agents affect the evoked potential signals in varying degrees. Inhaled anesthetic gases have the greatest effect by depressing signal amplitude and prolonging latency. Low-dose intravenous (IV) agents have less effect on waveforms, but at higher doses, they can significantly decrease amplitude. Some IV agents (e.g., ketamine and etomidate) will even augment the signals. Not all evoked potential signals are equally susceptible to anesthetic agents. For most cases in which neurophysiologic monitoring will be utilized, anesthesia will consist of a small amount of inhaled anesthetic gas, supplemented by IV infusions, primarily propofol (some institutions require total IV anesthesia when monitoring MEPs). Opioids are frequently used to supplement the anesthetic. Muscle relaxants should be avoided in all cases where the motor response of a nerve will be monitored visually or by EMG or MEP. Because propofol infusions often cause hypotension, it is important to maintain perfusion of the brain and the spinal cord. A phenylephrine infusion may be required. Cases involving neurophysiologic monitoring are often complex and carried out for many hours; therefore, large amounts of propofol may be administered. At the end of the procedure, it may not be possible for the patient to rapidly emerge from anesthesia and undergo extubation of the trachea. Transport of an intubated patient to either the postanesthesia care unit or the intensive care unit (ICU) is always a possibility, and a transport monitor and an Ambu bag should always be available. Anesthesia technicians should prepare for these cases with the following: • A multichannel infusion pump with appropriate tubing • 100-mL propofol vials for infusion • Possible phenylephrine infusion • Soft bite block • Transport equipment for an intubate patient
■ OTHER BRAIN MONITORS Electroencephalography Electroencephalography (EEG) measures brain activity through an array of 20 electrodes placed
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at specific locations on the scalp. It may also be measured directly during a craniotomy by electrodes placed on the brain (electrocorticography). The standard recording has 16 channels and requires special training and experience to interpret. The signal may be processed to produce a single number, which may be more easily interpreted and indicates in which general direction the EEG is going. The bispectral index (BIS) monitor is a form of processed EEG. Hypoxia, hypotension, temperature changes, carbon dioxide tension, and all anesthetic drugs may affect the EEG. EEGs may be used during neurosurgical ablation of a seizure focus, awake craniotomy for resection of a tumor or vascular malformation, or carotid surgery.
Bispectral Index (BIS Monitor) Although anesthesia has been delivered safely for many years, there is no specific monitor for determining whether a patient is actually unconscious. Adequacy of anesthesia is based on a combination of knowledge of drug doses and monitoring of changes in heart rate and blood pressure. Many have argued that these are not reliable indicators of the depth of anesthesia. Multiple studies involving thousands of patients have estimated an incidence of awareness under anesthesia of between 1 in 1,000 and 1 in 10,000 patients anesthetized. Awareness mainly consists of remembering conversations and an inability to move or breathe while experiencing pain (this can happen if the patient is paralyzed with neuromuscular blocking agents). Subsequent significant long-term psychological sequelae including posttraumatic stress disorder may ensue in about 33% of these patients. The causes for awareness under anesthesia have been attributed to the following situations: • It was unsafe to administer deep anesthesia to the patient (e.g., very sick patients, severely injured trauma patients, emergency obstetric surgery where it is important to minimize drugs to the fetus). • Anesthesia machine malfunction (e.g., the vaporizer is not delivering the set amount of agent, problems with gas flows diluting a volatile agent) • Anesthetic has run out (e.g., an empty vaporizer or infusion pump that goes unrecognized). • Total IV anesthesia
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• Sedated patients where the patient experiences awareness. They sometimes do not understand that awareness is normal and common when a patient is sedated and not under general anesthesia (e.g., sedation only or sedation with regional anesthesia). • Partial awareness during emergence that is interpreted by the patient as intraoperative awareness • Patients using chronic opioids, alcohol, or other substances of abuse (these patients may be tolerant to the usual doses of anesthetic medications) The BIS was developed and introduced in 1994 as a more objective tool to monitor patients’ levels of consciousness and to decrease the level of awareness under anesthesia. In addition, the BIS monitor has been reported to assist anesthesia providers in optimizing anesthetic doses for individual patients, resulting in faster wake-up times and cost savings from decreased drug dosages. BIS has also been used to guide the management of sedation in critically ill patients in ICUs, especially during mechanical ventilation both with and without neuromuscular blockade and management of drug-induced coma. Another use of BIS monitoring is during anesthesia for neurosurgical procedures and in which it is necessary to induce pharmacologic EEG silence or burst suppression on the EEG (electrical silence with intermittent short bursts of EEG activity). Patients with increased ICP or sustained seizures fall into this category. This may be achieved by using BIS monitoring instead of the more complex full EEG monitoring. In recent years, awareness under anesthesia has received a great deal of media attention. In 2004, the Joint Commission deemed awareness under anesthesia a sentinel event and described and promoted a heightened attentiveness to this issue but did not mandate the use of brainmonitoring devices. The American Society of Anesthesiologists issued a practice advisory regarding BIS monitoring stating that it should be used at the discretion of the anesthesiologist. They also added a caveat that maintaining low brain function monitor values in an attempt to prevent intraoperative awareness may conflict with other anesthesia goals, for example, preserving vital functions. Many studies have now been carried out with conflicting results on the value of BIS monitoring
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in preventing awareness under general anesthesia and its usefulness in both decreasing levels of awareness and cost and time saving. In addition, an association has been found between low BIS values and postoperative cognitive dysfunction in elderly patients, although the reasons and true significance of this are yet to be determined. Thus, BIS monitor usage has now become very dependent on individual practitioner’s preferences.
BIS Monitor Operation The monitor consists of a sensor, placed on one side of the forehead, which detects a frontal electroencephalograph. The signal is then converted mathematically into a numbered continuous measure, scaled from 1 to 100 (BIS number). This conversion algorithm was derived from EEG data from about 5,000 volunteers. It is the propriety property of Aspect Medical and has been modified several times since the introduction of the monitor (Table 41.1).
Applying Sensors After cleaning the skin well with alcohol, the sensor, which consists of a strip of four gelled electrodes, should be applied to one side of the forehead as follows (Fig. 41.2): Sensor number 1: center of the forehead, 2 in (5 cm) above the nose Sensor number 4: directly above and adjacent to the eyebrow Sensor number 3: temple area between the corner of the eye and the hairline Sensor number 2: between sensor number 1 and sensor number 4.
TABLE 41.1 BIS SCALE GUIDELINES BIS NUMBER
STATE OF HYPNOSIS
90-100
Awake state
70-90
Light hypnotic state, light sedation
60-80
Deep sedation
40-60
General anesthesia with low probability of consciousness and explicit recall
10-40
Deep hypnotic state
0
Flat line EEG
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■ FIGURE 41.2 Correct bispectral index sensor placement on the forehead. (Image used by permission from Nellcor Puritan Bennett LLC, Boulder, Colorado, doing business as Covidien.)
Note that the sensors are not numbered sequentially. The edges of the sensors should be pressed down for 5 seconds to ensure adhesion of the sensors to the skin and sealing in of the electrode gel. Appropriate contact and proper positioning of the electrodes are critical to produce accurate BIS measurements. The electrode strip is then connected to the monitor. Once powered up, the monitor will display a message indicating the status of the electrodes: • PASS indicates that there is good contact between the electrodes and the patient. • HIGH indicates a need to reprep the skin under the electrode and reapply at it. The “high” indicates that the impedance (resistance to flow of electrical currents between the patient and the monitor) is high. • NOISE may appear in the status window if the electrode is pressed upon during the check or in the presence of a large external stimulus. • LDOFF indicates an electrode has become detached from the patient. The electrode status may be accessed at any time during use from the setup menu. The BIS monitor may be started at any time as there is neither calibration nor baseline required for its use. The BIS monitor shows the BIS number in the upper left hand corner of the screen (Fig. 41.3). The monitor displays an indication of which power supply is in use (AC electrical supply or battery). If possible, the BIS monitor should be connected to AC power as typical battery life is only about 1 hour. The monitor
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■ FIGURE 41.3 Bispectral index monitor screen. (With permission from Nellcor Puritan Bennett LLC, Boulder, Colorado, doing business as Covidien.)
will also display a warning if the sensor gets disconnected from the machine. The signal quality index (SQI) bar indicates the quality of the EEG signal over 60-second time increments. It is optimal when the bar extends all the way to the right. As the SQI decreases, the BIS numeric display changes form a solid to an outlined number. This should prompt a check of both sensors and connectors. Electrocautery may also interfere with BIS values. The electromyographic bar reflects muscle tone in the underlying frontalis muscle. Increased tone in the frontalis from light anesthesia or recovery from muscle relaxants may be interpreted by the machine as an EEG signal. This can artificially raise the BIS number.
Troubleshooting BIS Values BIS is higher than expected: • Increased surgical stimulus • Inadequate anesthesia: Vaporizers and IV lines should be checked to ensure that accurate doses are being administered. • Frontalis muscle twitching or shivering BIS: Check for EMG activity on the monitor. Possible neuromuscular blockage wearing off. • Interference from pacemakers and other electrical devices
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BIS is lower than expected: • Decreased patient requirements (e.g., decreased surgical stimulus) • Decrease in frontalis muscle tension: Check EMG tracing. • Hypothermia • Cerebral ischemia • Improper lead placement: Reposition or replace sensor.
■ INTRACRANIAL PRESSURE MONITORING The adult skull is a rigid box whose contents include the brain tissue (80%), the cerebrospinal fluid (CSF) (10%), and the blood vessels (10%). These volumes create a pressure inside the skull known as ICP. Any condition that increases the volume inside the skull will increase the ICP (e.g., brain tumors, bleeding into the brain, or brain swelling after a head injury). Normal values for ICP are 8-12 mm Hg. If the ICP becomes elevated, it can compromise blood flow to the brain and lead to cell damage, impaired neurologic function, or even death. The cerebral perfusion pressure (CPP) may be calculated according to the following formula: Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) − intracranial pressure (ICP) Most clinicians strive to keep the CPP greater than 50-60 mm Hg. Either hypotension or increased ICP can compromise the CPP; thus, the treatment for low CPP is to raise the blood pressure and/or decrease ICP. Devices to measure ICP include the following: • Catheter placed directly into the ventricle of the brain (an external ventricular drain [EVD]) • Small fiberoptic catheter placed inside the brain tissue (Camino catheter) • Pressure monitoring catheters placed either subdurally or epidurally The most commonly used devices today are EVD and Camino catheters. All methods require connection of the device to a transducer to convert the pressure signal to a waveform that can then be displayed on a screen.
EVD The EVD is placed through a small hole in the skull and passed directly into the ventricle of the brain. The catheter is attached to a transducer
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and also to a drainage chamber, which allows for removal of the CSF. CSF drainage may be necessary to decrease ICP. CSF drainage is gravity dependent, so the rate of drainage will depend on the height of the drainage chamber relative to the height of the patient’s head. Great care must be taken that the drainage device is secured at the proper height at all times. This is particularly true during patient transport. If the drain is placed too low, too much CSF can drain out with severe consequences for the patient. It may be safer to close the EVD drainage valve during transport, but this should only be done in consultation with all physicians taking care of the patient. If the drain becomes kinked off or is inadvertently closed for a long period of time when CSF drainage was necessary, ICP may rise to very high levels and compromise blood flow to the brain. It may be advantageous to monitor ICP during transport as sudden changes in ICP can occur. After transport, the transducer should be rezeroed, the drainage device adjusted to the appropriate height, reopened if it has been closed, and checked to ensure that it is dripping and working again.
Camino Catheter In the 1980s, researchers at Camino Laboratories developed a small fiberoptic device that could be directly inserted into brain matter. A bolt, which acts as a conduit for the catheter, is placed in a sterile fashion in a small hole in the skull. The catheter is then passed through the hole in the skull directly into the frontal lobe of the nondominant hemisphere of the brain. Before placement through the bolt, the cable connector end of the fiberoptic catheter is handed off to a nonsterile assistant. The assistant attaches the connector to the monitor. The sterility of the catheter must be maintained throughout the procedure. The device is zeroed relative to the atmosphere while being held at the level of the external auditory meatus. If the display on the monitor does not read zero, there is a zero adjustment screw that can be turned with a special tool provided with the insertion kit. The transducer is built into the tip of the catheter and requires calibration before insertion. It does not have to be leveled or recalibrated and cannot be calibrated in vivo. The catheter is then placed inside the bolt and secured. A strain relief sheath, which prevents kinking and bending of the catheter, is then slid
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Chapter 41 • Neurophysiologic Monitoring
down over the catheter. It is very important not to bend the fiberoptic catheter as the delicate transmission fibers can be easily damaged. The monitor can either be a free-standing screen or can be integrated with the bedside patient monitor using a standard interface cable. The monitor can display an ICP waveform, digital ICP, CPP, and brain temperature. For transport, the external monitor can be unplugged from the electrical outlet, the catheter can be disconnected from the cable, and the monitor can be transported to the new location and reconnected. No additional zeroing is required.
■ SUMMARY Surgery often can unintentionally damage peripheral or central nervous system structures with scalpels, retractors, electrocautery devices, or other surgical instruments. In addition, surgical procedures may interrupt the blood supply to the central nervous system. Neurophysiologic monitoring can be used as an early warning system to monitor the status of both the peripheral and the central nervous system. Anesthesia technicians should be familiar with the basic physiology of these techniques and the anesthetic implications if they are to be used. In addition, anesthesia technicians should be familiar with the setup, operation, and maintenance of ICP monitors and processed ECG (e.g., BIS) monitors.
REVIEW QUESTIONS 1. The following are common uses of neurophysiologic monitoring EXCEPT A) Assess the status of peripheral nerves, the spinal cord, and the brain during the surgical case. B) Monitor ICP during neurosurgery or when the brain is injured. C) Navigate through the brain by using computer images. D) Assess the depth of general anesthesia. E) None of the above. Answer: C. Neurophysiologic monitoring is routinely used for all the above except for navigation with computer images.
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2. The use of a NIM endotrachael tube utilizes which of the following type of neurophysiologic monitoring? A) Somoatosensory evoked potentials (SSEPs) B) Motor evoked potentials (MEPs) C) Brainstem auditory evoked potentials or responses (BAEPs or BAERs) D) Visual evoked potentials (VEPs) E) Electromyography (EMG) Answer: E. This special endotracheal tube is monitoring muscle activity in the vocal chords. It does not send out a signal to “evoke” a response; rather it is monitoring baseline muscle electrical activity (EMG). If the surgeon should stimulate the nerve to the vocal chords by compression or electrocautery (the nerve can be close to the surgical site), the monitor will detect the muscle activity. BAEPs involve an auditory stimulus with detection of the response in the brain. Likewise, VEPs involve a visual stimulus and detect a response in the brain.
3. When preparing for a case that will require neurophysiologic monitoring, the anesthesia technician should have all the following items available EXCEPT A) A multichannel infusion pump with appropriate tubing B) Extra propofol C) Transport equipment D) Long-acting muscle relaxants E) Phenylephrine infusion Answer: D. Long-acting muscle relaxants should be avoided in cases where muscle activity will be monitored as part of neurophysiologic monitoring (MEP or EMG). Muscle relaxants will paralyze the muscle and the muscle will not have any baseline activity that can be monitored on the EMG and muscle response cannot be evoked by a stimulus to a nerve and thus cannot be monitored with MEPs. In some cases, the anesthesia provider will use a muscle relaxant at the beginning of a case to facilitate endotracheal intubation; however, the effects will be allowed to wear off before neurophysiologic monitoring is instituted. The use of muscle relaxants will not interfere with the use of SSEP monitoring.
4. BIS is a monitor that measures true patient awareness. A) True B) False Answer: B. The BIS measures a processed EEG signal and is just another tool for the anesthesiologist to use to monitor the depth of anesthesia. Many other factors can affect BIS readings and must be taken into account when interpreting BIS values. In addition, the monitoring of BIS values does not guarantee lack of awareness.
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5. Normal values for ICP are A) 8-12 mm Hg B) 22-30 mm Hg C) 15-18 mm Hg D) 2-6 mm Hg E) None of the above Answer: A.
6. When transporting with an EVD catheter, it is important that the anesthesia technician A) Always place the drain very low in order to drain off the CSF B) Always close the drain C) Always make sure the catheter and the drain are not kinked D) B and C E) All of the above
SUGGESTED READINGS Avidan MS, Zhang L, Burnside BA, et al. Anesthesia awareness and the bispectral index. N Engl J Med. 2008;358: 1097–1108. Bedell EA, Prough DS. Neurological and intracranial pressure monitoring. In: Irwin R, Rippe JM, et al., eds. Procedures, Techniques and Minimally Invasive Monitors in Intensive Care in Intensive Care Medicine. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008. Devlin VJ, Schwartz DM. Intraoperative neurophysiologic monitoring during spinal surgery. J Am Acad Orthop Surg. 2007;15(9):549–560. Orser BA. Depth-of-anesthesia monitor and the frequency of intraoperative awareness. N Engl J Med. 2008;358: 1189–1191. Sloan T, Heyer E. Anesthesis for intraoperative neurophysiologic monitoring of the spinal cord. J Clin Neurophysiol. 2002;19(5):430–443.
Answer: C. It is important that the tubing and catheter are not kinked and that the drain is placed level with the patient’s head. Obstruction of the catheter or closure of the drain valve could cause CSF to build up within the brain and cause injury to the patient. If the drain is placed below the patient’s head, CSF can drain. This should only be done with close physician supervision. The patient can suffer severe injury if too much CSF is drained. Closure of the drain and positioning of the drain should only be performed under physician supervision.
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CHAPTER
42
Intra-aortic Balloon Pumps and Ventricular Assist Devices Laura Downey ■ INTRODUCTION Cardiac disease continues to be the number one cause of death in the United States, accounting for 34.3% of all deaths in 2006. Over 81.1 million American adults carry the diagnosis of one or more types of cardiovascular disease. As the incidence of cardiac disease grows, an increasing number of patients with heart disease undergo anesthesia and surgery every year for various procedures. These procedures range from coronary artery revascularization, coronary angioplasty, valve replacement surgery, repair of aortic aneurysms, correction and palliation of congenital heart disease, to heart transplantation. Despite the improvement in medical and surgical interventions for cardiovascular disease, the aging U.S. population has led to a steady rise in the incidence of heart failure. Data from the 2010 Centers for Disease Control and Prevention (CDC) Heart and Stroke Update estimated that approximately 5.8 million people are living with heart failure and approximately 25% have advanced or end-stage heart failure. The 1-year mortality rate for patients with heart failure is estimated at 20%, while the 5-year mortality rate is estimated to be as high as 59% for men and 45% for women. While advances in medical and surgical therapy have been effective in reducing the mortality and morbidity from heart failure, there is a subset of patients who develop severe cardiac failure in the setting of myocardial infarction (MI), following cardiopulmonary bypass, trauma, or advanced cardiomyopathies. Medical therapies for these patients are often limited, and patients may require artificial support to maintain their cardiac output and perfusion to their vital organs while awaiting recovery or definitive surgical treatment. The most common devices used to support these patients until recovery
or heart transplantation are an intra-aortic balloon pump (IABP) or a ventricular assist device (VAD). This chapter examines at the indications, setup, operation, maintenance, and troubleshooting for these devices. Depending on the institution, these devices may be managed by anesthesia technicians, cardiovascular technicians, or perfusionists. Of note, both intra-aortic balloon pumps and various VADs often require extra training to learn the specifics of individual devices. Therefore, please follow your institution’s requirements and ensure that you are properly trained in the equipment prior to using the device on a patient.
■ AORTIC BALLOON PUMPS The IABP is a device that augments blood flow to the heart by inflation and deflation of a balloon that sits in the thoracic aorta (Fig. 42.1). This device is used to augment cardiac output and coronary blood flow in patients with cardiogenic shock. The indications for an IABP include (1) cardiogenic shock, (2) failure to separate from cardiopulmonary bypass, (3) stabilization of a patient prior to the operating room (OR), or (4) as a bridge to transplantation. See Table 42.1 for a listing of the indications and contraindications for IABP placement. IABPs are usually placed by cardiothoracic surgeons or cardiologists in the cardiac catheterization lab, OR, or in the intensive care unit (ICU) where appropriate monitoring and emergency equipment are available.
■ CARDIAC CYCLE AND CORONARY PERFUSION As IABP therapy is based on the timing of the cardiac cycle, it is important to review the two major phases of the cardiac cycle: diastole and 411
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in the ventricles is still greater than that in the atria. Therefore, the mitral and triscuspid valves remain closed and the ventricular volume does not change. At the end of diastole, the pressure is called the left ventricular end-diastolic pressure (LVEDP). Coronary artery perfusion occurs during diastole.
■ FIGURE 42.1 Cutaway of heart and aorta showing placement of an IABP in aorta just distal to the subclavian artery.
systole (Fig. 42.2) (see Chapter 7). These phases are important for understanding the mechanism of the IABP therapy because it uses the cardiac cycle to augment cardiac output during systole and coronary blood flow during diastole, a process called counterpulsation.
Diastole The onset of diastole is noted by the relaxation of the ventricles. As the ventricular pressure falls below the aortic and pulmonary artery pressure, the aortic and pulmonic valves close. During the period of isovolumetric relaxation, the pressure
Coronary Perfusion It is important to understand that coronary perfusion occurs only during diastole, when the wall tension or the LVEDP is the lowest. During systole, the pressure generated by the contraction of the myocardium may completely stop blood flow to the coronary bed. When the diastolic blood pressure is higher than the LVEDP, blood flows into the coronary arteries, resulting in coronary perfusion.
Systole At the beginning of systole, the ventricles are full of blood from the previous diastolic filling period and the ventricles begin contracting, a period called isovolumetric contraction. As the pressure in the ventricles rises higher than the atrial pressure, the mitral valves and tricuspid valves close. The period of isovolumetric contraction accounts for approximately 90% of the myocardial oxygen consumption. Eventually, enough pressure is generated to open the aortic and pulmonary valves, leading to rapid ventricular
TABLE 42.1 INDICATIONS AND CONTRAINDICATIONS FOR IABP USE INDICATIONS FOR USE
CONTRAINDICATIONS
Cardiogenic shock Myocardial infarction Myocarditis Cardiomyopathy Cardiac contusion
Absolute Aortic valve insufficiency Aortic disease Aortic dissection Aortic aneurysm
Surgical indications Postsurgical myocardial dysfunction Failure to separate from CPB Procedural support during angiography or CBP or noncardiac surgery
Relative End-stage disease Severe peripheral disease Severe noncardiac systemic disease Massive trauma
Cardiac support for hemodynamically unstable patients prior to repair Valvular insuffiency: mitral Ruptured papillary muscle Ventricular septal defect
DNR patients Severe coagulopathy
Bridge device Bridge to ventricular assist device Bridge to transplant
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Chapter 42 • Intra-aortic Balloon Pumps and Ventricular Assist Devices Isometric contraction period Pressure (mm Hg)
413
Isometric relaxation period
120 Aortic valve closes
100 80
Aortic pressure 60 Aortic valve opens
40
Left ventricular pressure
20
Atrial pressure
100 Ventricular volume (mL)
80 40 R
R
P
T
P
ECG Q 1st Heart sounds
Systole 0
Q 4th
2nd 3rd
0.2
Diastole 0.4
0.6
0.8
Time (sec) ■ FIGURE 42.2 The cardiac cycle. Changes in aortic pressure, left ventricular pressure, left atrial pressure, left ventricular volume, the electrocardiogram (ECG), and heart sounds. (From Porth CM. Pathophysiology Concepts of Altered Health States. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2005, with permission.)
ejection, where approximately 65%-75% of the stroke volume is ejected. After the blood is ejected, the pressure in the ventricles drops dramatically, but blood continues to flow into the aorta until the end of systole. The end of systole is signaled by the onset of myocardial relaxation and closure of the aortic valve.
■ HOW DOES AN IABP WORK: COUNTERPULSATION HEMODYNAMICS The IABP is a mechanical device that increases blood flow to the coronary arteries during diastole and increases cardiac output during systole. The device is a flexible catheter with a balloon at the end that sits in the descending aorta just distal to the left subclavian artery. The balloon augments blood flow by volume displacement
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and pressure changes associated with rapidly injecting helium gas in and out of the balloon chamber, a principle called counterpulsation (Fig. 42.3). During diastole, the balloon is filled with helium (approximately 40 mL depending on the balloon size), thus causing the blood to be displaced by the increased balloon volume. This causes the aortic pressure to increase, which increases the driving pressure into the coronary arteries. The result is improved blood flow to the coronary arteries. During systole, the reverse occurs. The balloon deflates and the blood flows forward to fill the evacuated space. The fall in pressure decreases the amount of pressure the failing left ventricle (LV) has to generate, thus decreasing the oxygen demands of the heart and increasing cardiac output by as much as 40%. The balloon inflation can be triggered by the
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■ FIGURE 42.3 Counterpulsation. The image on the left shows thorax with intra-aortic balloon catheter introduced via the femoral artery. The image in the center shows aorta with catheter inflated as in diastole. The image on the right shows aorta with catheter deflated as in systole. (LifeART image copyright (c) 2012 Lippincott Williams & Wilkins. All rights reserved.)
patient’s electrocardiogram, a pacemaker, a set rate, or the patient’s blood pressure. Key Points: 1. During diastole, the balloon inflates and augments coronary perfusion. 2. At the beginning of systole, the balloon deflates and increases cardiac output while decreasing myocardial oxygen consumption. 3. The balloon is inflated with helium, a gas that can be easily absorbed by the body without damage in the case of balloon rupture.
■ SETUP AND PLACEMENT Prior to placement, a thorough physical exam is performed to assess the circulation to both legs and determine the best side for insertion. The femoral artery is accessed with a needle and a guide wire is placed through the femoral artery and into the thoracic aorta (see Chapter 34). The puncture site is then dilated with successive placement of a dilator/sheath combination until the balloon can be threaded through the puncture site into the central aorta. The balloon sits in the aorta, approximately 2 cm from the left subclavian artery and above the renal artery branches. A chest x-ray or fluoroscopy is used to confirm proper placement. Daily chest x-rays demonstrate the tip at the 2nd and 3rd intercostal spaces. Depending on the institutional practice,
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patients may be fully anticoagulated while the IABP is in place, in order to prevent clot formation on the balloon. However, anticoagulation may increase the risk of bleeding, especially in the postsurgical setting. While IABPs are usually placed by cardiothoracic surgeons or cardiologists, there is a wide variation in the technicians who may set up and prepare the IABP kits: perfusionists, scrub technicians, anesthesia technicians, and cardiovascular techs. Before setting up an IABP, be sure to read the instruction manual for details specific to the model you will be using as there are many different companies that manufacture IABP systems and each one will operate in a slightly different way. The general setup includes the following: 1. Electrocardiogram (ECG) leads 2. Arterial blood pressure waveform monitoring 3. Balloon volume monitoring 4. Electric console to adjust triggering and inflation timing of the balloon 5. Battery backup power 6. Gas reservoir Details of equipment setup for IABPs are listed in Table 42.2.
■ OPERATION AND MANAGEMENT OF AN IABP For the optimal effect of counterpulsation, the inflation and deflation of the balloon must be correctly timed to the cardiac cycle (Fig. 42.4). This is usually achieved by triggering the balloon’s inflation based on the patient’s ECG signal or the arterial waveform. Usually, the triggering signal is from the R wave on the ECG. The balloon is set to inflate in the middle of the T wave, coinciding with the aortic valve closure and beginning of diastole. Deflation occurs prior to the R wave, noted on the arterial waveform just before the arterial upstroke (Fig. 42.5). The balloon augmentation usually starts at a beat ratio of 1:2, which means every other beat is augmented by the IABP. This allows the provider to compare the patient’s inherent ventricular beats with the augmented beats and adjust the timing as necessary. A health care provider trained in IABP therapy will likely assess the effectiveness of the IABP and adjust the timing appropriately. Figure 42.6 demonstrates an arterial waveform generated by a correctly positioned and timed balloon.
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Chapter 42 • Intra-aortic Balloon Pumps and Ventricular Assist Devices
415
TABLE 42.2 PLACEMENT OF AN IABP The following steps are important in placing a percutaneous IABP Supplies: Betadine Lidocaine with syringe for topical anesthestic Suture material Sterile drapes, mask, gown, gloves, cap Sterile dressing material Heparinized saline flush solution in 10 to 20-mL syringe Pressure tubing, transducer, and continuous heparin flush solution for: Balloon catheter Central lumen Balloon pump console with patient cables ECG electrodes IABP kit (kits usually contain the following): Central lumen catheter 30- and 40-mL 7.5 intra-aortic balloon, uses an 8-French sheath 50-mL 9-French intra-aortic balloon, uses a 9-French sheath Introducer sheaths, with and without side ports Guide wires Preparation of IABP for insertion: 1. Establish power and verify power switch on controlling console 2. Establish helium gas pressure 3. Establish ECG and pressure 4. Zero transducer on arterial pressure source 5. Confirm initial control setting 6. Balloon preparation: Place IABP guide wire on the field Attach one-way valve to the IABP connector Connect the 60-mL syringe to the one-way valve and apply full vacuum Do not remove the one-way valve until the IABP is fully in the patient Flush through the central lumen with heparinized saline just prior to insertion Remove the IABP from tray immediately before insertion After the IABP is positioned in the patient: 1. Aspirate blood from central lumen and gently flush with 3-mL heparinized saline 2. Hook up pressurized heparin saline flush system to central lumen 3. Remove one-way valve and connect IABP to pump 4. Suture at both the sheath hub and the catheter site 5. Initiation of pumping: Attach IABP to appropriate connector Attach connector to safety disk/condensate removal module Press START and verify filling of balloon Verify optimal augmentation Fine- tune deflation time Assess hemodynamic benefits Please refer to your hospital’s Policy and Procedure Manual for sterile procedures. Please carefully follow detailed instructions included with each balloon pump catheter.
■ TROUBLESHOOTING While an IABP can be a life-saving device, a number of complications have been described when using the IABP. The most common vascular complication is limb ischemia or compartment syndrome. Therefore, the patient must be constantly observed for indications of ischemia, such as cold limb, color changes,
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decreased pulses, or pain in the affected limb. Vascular injuries can be life or limb threatening and require physician notification immediately. Other complications include bleeding, infection, or device malfunction such as balloon tear or perforation (Table 42.3). Device malfunctions can sometimes be prevented or herald an impending emergency, and
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Early Inflation
Correct Timing
Late Inflation
Correct Timing
Early Deflation
Correct Timing
Late Deflation
Correct Timing
■ FIGURE 42.4 The timing of balloon inflation and deflation is adjusted in the 1:2 mode. The inflation point is moved rightward (later) until it occurs in late diastole and the dicrotic notch is uncovered. The inflation timing is moved progressively earlier in the cardiac cycle until the dicrotic notch on the central aortic tracing just disappears. Examples of early, late, and correct inflation are shown in the top two tracings. Similarly, the deflation knob is moved leftward (earlier) and then slowly advanced toward the right (later in the cardiac cycle) until the end-diastolic pressure dips 10 to 15 mm Hg below the patient’s unassisted diastolic pressure. This will produce a maximal lowering of the patient’s unassisted systolic pressure. Examples of early, late, and correct deflation timing are shown in the bottom two traces. (From Baim DS. Grossman’s Cardiac Catheterization, Angiography, and Intervention. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2006, with permission.)
alarms should be taken seriously. A careful survey of the patient and device may elucidate the malfunction and help prioritize corrective measures. In order to mitigate complications, device management tips and precautions are listed below: 1. Patient’s physiologic parameters should be monitored frequently for evidence of ischemia or worsening cardiac function. 2. Frequently check pump activity. 3. Check helium level to avoid an empty tank. 4. Replace empty helium tanks in 14 y
>50
7.0-8.0
Miller/Mac 2-3
4
ETT, endotracheal tube; LMA™, laryngeal mask airway.
hypothermia during anesthesia and surgery. It is essential to prevent the increased heat loss by warming the operating rooms (ORs), covering the babies with blankets, and using convection forced air warmers.
Psychological Issues For children, the anxiety regarding surgery and its associated pain is often compounded by fear of separation from family, and cognitive limitations, which may impair their ability to understand the purpose of the anesthesia and surgery. Because of this, pediatric caregivers employ a number of techniques to minimize the stress experienced by pediatric patients. For example, attempts are generally made to make the general environment appear “kid friendly.” This can be done with soothing and entertaining pictures on the walls and ceilings, available toys for the children to play with, and even entertainment in the preoperative area (i.e., video games, live music). In addition, because children’s anxiety may be shared by their parents, an effort is made to provide the children’s parents with support. This can be facilitated with pamphlets, preoperative discussions with parents, and sometimes even tours of the various preoperative and postoperative areas. Finally, a number of measures are employed with the children themselves to lessen their anxiety and discomfort. Discussions with children are conducted using age-appropriate concepts
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and vocabulary. For example, children aged 2-4 years are often eager to engage in fantasy and magical thinking, and brighten at the prospect of “being told a story” in the OR. Older children may be helped by being given the choices, (i.e., a “flavor” for their breathing mask). Adolescents are very often concerned about waking up during surgery, and respond well to reassuring discussions. Children between the ages of 1 and 3 years are at the highest risk of emotional trauma upon separation from their parents, or upon being shown either a needle (for injection) or an anesthetic mask. Not only are children in this age group at risk for stormy anesthetic inductions, but they are also at increased risk for postoperative behavioral changes (i.e., tantrums, nightmares, regression in potty training), which can last weeks to months. With this in mind, pediatric facilities may include “induction rooms” separate from the surgical suites in which children can be anesthetized with a parent present. General anesthesia is typically induced by having the child breathe increasing concentrations of anesthetic agent; IV lines are often not started until after children are unconscious. Another strategy for calming children prior to separation from their families is the use of oral premedication, which is seldom administered in the adult population. Oral midazolam has been shown to greatly reduce separation anxiety and resisting the mask in the OR. In addition, there is evidence that this
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premedication lowers the incidence of untoward postoperative behavior changes.
Equipment Considerations Marked changes in anatomy and physiology occur from birth to adolescence. However, similar anesthesia equipment is used in patients of all ages. The differences in airway equipment and vascular catheters are chiefly in size rather than shape or type (Figs 46.1-46.3). In addition, IV administration kits for children younger than about 10 years of age feature “microdrips” and buretrols to help prevent fluid overload (Figs. 46.4 and 46.5). Children in general greatly fear needles. Hence, in most hospitals, the majority of children younger than about 12 years of age are brought to the OR without an IV having been inserted. General anesthesia is typically induced by having the child breathe oxygen with increasing percentages of anesthetic gases (nitrous oxide, sevoflurane) added. IVs are placed after the children are anesthetized. It is important to understand that during the initial period, while the anesthesia is “light,” the child is at greatest risk for adverse airway events. These include laryngospasm, apnea, and airway obstruction. This is particularly true prior to the
■ FIGURE 46.1 Variation in laryngoscope blade sizes.
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■ FIGURE 46.2 Variation in LMA™ sizes. LMA™, laryngeal mask airway.
insertion of the IV, as there is not yet a method of rapidly administering medications emergently.
■ SPECIFIC SURGERIES Neonatal and Infant Surgery Anesthesia-related morbidity and mortality are higher in infants, particularly the neonate. To reduce this risk requires a well-planned technique and a thorough understanding of the specific pathophysiologic conditions and surgical needs. The unique demands of infancy will require the appropriate age-related equipment and expertise that are best met by personnel trained to provide care to pediatric patients, neonates, and infants on a regular basis.
■ FIGURE 46.3 Variations in nasal and oral airway sizes.
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Chapter 46 • Pediatric Anesthesiology
■ FIGURE 46.4 Standard and microdrip chambers.
A number of conditions require urgent surgical treatment in the neonatal period. Congenital diaphragmatic hernia (CDH) is a defect in the diaphragm that allows the abdominal contents to herniate into the left chest cavity. CDH is most commonly diagnosed and repaired during early infancy. The cardiopulmonary compromise associated with CDH can be severe enough that neonates may require extracorporeal membrane oxygenation (ECMO).
451
Tracheoesophageal fistula (TEF) is an abnormal opening between the esophagus and trachea. It is usually associated with an undeveloped blind-end esophagus. The fistula between the trachea and the esophagus allows the esophageal or gastric contents to enter the lungs and compromise the baby’s pulmonary function. Omphalocele and gastroschisis are defects of closure of the abdominal wall that present with abdominal contents exposed at birth. The risk of contamination and infection require immediate containment of the exposed abdominal contents, which is often performed shortly after birth with a sterile plastic silo. The infant can be stabilized, resuscitated, and further evaluated for associated congenital anomalies and prepared for more elective complete repair of the abdominal wall defect. Other neonatal gastrointestinal conditions that will often require urgent surgical interventions include intestinal atresias, pyloric stenosis, volvulus, meconium ileus, inguinal hernia, and necrotizing enterocolitis (NEC). Each will have specific anesthetic needs and concerns to be addressed. The less mature hepatic and renal systems often require using different IV fluids and drugs than with adults. Neonates have a significantly limited ability to maintain and regulate body temperature; therefore, they are at much greater risk of hypothermia while under anesthesia. This results in an increased oxygen consumption, which must be addressed by the immature neonatal cardiopulmonary systems.
Pediatric Neurosurgery
■ FIGURE 46.5 Neonatal intravenous administration kit with a buretrol.
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Common pediatric neurosurgical conditions include trauma, brain tumors, hydrocephalus, and spina bifida (myelomeningocele). Pediatric head trauma is the most common cause of serious injury and death in children. Brain tumors are the most common solid tumor in children, with a significant number of these patients requiring surgical treatment. Hydrocephalus can result from congenital anomalies of the brain, bleeding within the brain, or tumor. Hydrocephalus is an increase in the CSF within the brain that leads to increased intracranial pressure (ICP), which requires treatment, usually involving shunting of CSF (usually into the abdominal cavity). As in adults, neurosurgery in children can involve neurophysiologic (brainwave) monitoring, which provides information
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to minimize injury to the nervous system during the procedure. This requires using anesthetic drugs that minimally affect brain wave signals. Myelomeningocele is a congenital spinal anomaly that causes varying degrees of spinal cord spinal bone malformation. The most common indication for urgent neurosurgery on neonates is a myelomeningocele with exposed spinal cord in the lumbar area.
Cardiac Pediatric patients undergo cardiac surgery for very different reasons than adult patients. Adults most often need cardiac surgery because of coronary artery disease or diseases of the heart’s valves. Children rarely suffer from coronary artery disease. They present with “abnormal plumbing.” This means that either the heart itself (atria, ventricles, and valves) or the major blood vessels (e.g., aorta, pulmonary artery) did not form correctly. Abnormalities include incompletely developed chambers and defects in the walls separating the chambers within the heart. Extreme vigilance must be maintained when preparing all IV lines and pressure tubing. Even small air bubbles can have devastating consequences (strokes) in children with certain heart defects. Invasive monitors like arterial lines, central venous lines, and transesophageal echocardiography (TEE) are common. The use of pulmonary artery catheters (Swan-Ganz catheters) is less common. All invasive monitors must be sized (diameter and length) appropriately for the patient.
Urology Pediatric urology procedures are often performed to correct developmental defects or remove tumors. Common procedures include complete or partial kidney removal (nephrectomy), testicular repair (orchiectomy, orchiopexy, etc.), ureteral reimplantation, and penile and vaginal surgery. Most of these procedures are performed under general anesthesia using either an ETT or an LMA™. Invasive monitoring is rarely necessary, unless the patient is extremely sick or the surgery is expected to result in significant blood loss. For many of these surgeries, anesthesiologists will use regional anesthesia—caudal blocks or epidurals—to minimize postoperative pain. Infants and small children are unable to sit still for procedures. Therefore, unlike adult patients,
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these blocks are typically performed in children after induction of general anesthesia.
Orthopedics Pediatric patients routinely undergo orthopedic surgery. Often times, these surgeries are to correct limb fractures from falls or other accidental traumas. Other procedures are performed to correct congenital skeletal deformities—scoliosis, hip dysplasia, etc. Children presenting for repair of fractures often have “full stomachs.” This means they have not been fasting for surgery (like most patients for elective surgery), and these children are at increased risk for aspiration during induction of general anesthesia. The anesthesiologist may request a rapid sequence intubation to minimize the chance of aspiration. One can assist the anesthesiologist by making sure all equipment for intubation is readily available (e.g., appropriately sized ETT with a stylette), or by performing cricoid pressure as directed. Regional anesthesia (peripheral nerve blockade) is often a consideration for orthopedic surgery, especially surgery on limbs. Some surgeries can be performed under regional anesthesia alone, and other procedures utilize a combination of general and regional anesthesia. Depending on the age and maturity of the patient, peripheral nerve blocks may be done prior to induction of general anesthesia or afterward. Many of the same tools (i.e., ultrasound, nerve stimulators, catheters, etc.) that are used in adults can be used in children. Children with spinal deformities often require surgical correction. Scoliosis, or lateral curvature of the spine, can impair a child’s cardiopulmonary functioning. These procedures are extensive, and at times require both posterior and anterior procedures to fully correct and stabilize the spine. As the spinal column is straightened, the spinal cord and nerves can be stretched or damaged. For this reason, neurologic monitoring is routinely used to detect nerve injury and correct it during the procedure. Neurologic monitors are sensitive to volatile anesthetics (sevoflurane, isoflurane, desflurane, etc.); therefore, anesthesiologists utilize either partial or total IV anesthesia with sedatives (propofol, dexmedetomidine) and analgesics (fentanyl, remifentanil, ketamine). The anesthesiologist may also choose to place one or more invasive
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monitors—arterial and/or central venous line— that can be used to monitor hemodynamics, draw blood for laboratory tests, and provide adequate access for infusion of anesthetics and vasoactive medications. Setup for these types of cases should include vascular access equipment, transducers, fluid warmers, and infusion pumps for medications. Anyone working in ORs, and orthopedic rooms in particular, should be mindful that x-rays are frequently taken during the procedure. For protection, always wear a leaded apron when entering these ORs, or be certain to clarify that x-ray equipment is not currently in use.
Otolaryngology Pediatric ENT (ear, nose, and throat) surgery is often one of the busiest services in the ORs. Procedures range from ear tubes and tonsillectomies to repairs of cleft lips and palates and other congenital malformations. In assisting an anesthesiologist in an otolaryngology room, it is important to appreciate the types of surgeries scheduled. One of the most common and quickest procedures performed in a children’s hospital is the placement of ear tubes (myringotomy tubes). Other short procedures include removal of the tonsils and adenoids (tonsillectomy and adenoidectomy). In a room with these cases, a premium is placed on rapid turnover of the room between cases to facilitate a large number of procedures. Other types of otolaryngology cases involve birth defects or congenital malformation. These are usually defects in the structure of the head, face, palate, lip, and jaw. Certain syndromes (i.e., Treacher Collins, Pierre Robin, and Goldenhar syndromes) are associated with facial deformities. Unique malformations can make placement of the ETT extremely difficult. Having specialized equipment ready to go (i.e., fiber-optic bronchoscope, glide scope, intubating stylets, exchange catheters, etc.) in these situations is imperative. Lastly, at times otolaryngology surgeons use specialized equipment such as lasers to work on tumors and other lesions in the airway. The topic of laser safety is covered in another section of this text. However, it is important to wear eye protection (specifically designed for the particular type of laser) when entering any OR with a laser in use.
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Ophthalmology Ocular procedures performed in pediatric patients range from basic eye examinations under anesthesia (EUA) to complicated intraocular surgery. Providing appropriate care for these patients requires a thorough understanding of intraocular pressure (IOP), potential ocular effects of anesthetics, as well as the continuing maturation of vision following birth and specific physiologic consequences of ocular surgery. Retinopathy of prematurity (ROP) is a frequent concern for babies born prematurely. Often, repeated EUAs and laser treatments under general anesthesia are needed. The precise role of oxygen in the pathogenesis of ROP is uncertain. Appreciation of the varying effects anesthesia may have on IOP is essential in providing care to children with eye disorders. Whether it is measuring IOP during a sedated eye exam to care involving a ruptured globe, the IOP may be influenced significantly by anesthetic management. One of the most frequent types of eye surgery for children is strabismus (“squint”) repair. Surgery for this condition generally involves the surgeon shortening or lengthening various muscles attached to the surface of the eye (extraocular muscles). Pulling on the extraocular muscles can result in a dramatic slowing of the HR (the “oculocardiac reflex”). This reflex is often seen during eye surgery and is addressed with medications that increase the HR (e.g., atropine, glycopyrrolate). Malignant hyperthermia (MH) is a rare, life-threatening disorder characterized by high fevers and cardiac arrhythmias following exposure to certain anesthetic agents. An association between strabismus and MH has been described. Every anesthesia department should maintain a collection of supplies and medications to treat MH.
Dental Increasing numbers of children are undergoing dental procedures under general anesthesia in the hospital. Historically, general anesthesia was reserved for children with significant behavioral or other health issues. However, it has become recognized that general anesthesia in children carries lower risk than unmonitored sedation in the dentist’s office. In addition, general anesthesia allows for longer and more thorough procedures to be performed without discomfort. Because of
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these factors, dental procedures under anesthesia are increasingly being performed on otherwise healthy children. Historically, the most common scenario involving pediatric dentistry and general anesthesia has involved children with neurodevelopmental issues (e.g., autism, cerebral palsy), which prevent them from being able to hold still. Indeed, some children are so combative as to not be able to take oral sedative medication or cooperate in breathing from an anesthetic mask. At times, intramuscular medication (e.g., ketamine) is administered to sedate the children enough to bring them to the OR. Common dental procedures include crowns, fillings, and removal of carious primary (“baby”) teeth. After induction of anesthesia, nasal RingAdair-Elwyn (RAE) ETTs are typically inserted for intubation. This allows for a protected airway and better access to the teeth for the dentist. Commonly used equipment for these cases also includes Magill forceps, lubricant, nasal airways (used to test the patency and dilate the nasal passage prior to intubation), and oxymetazoline (Afrin).
Anesthesia and Sedation Outside of the Operating Room Because young children are unable to tolerate or remain still for many procedures, they are often sedated or anesthetized. For brief procedures that are not painful, children are often given various combinations of oral, nasal, or IV sedatives to tolerate the procedure. This is termed moderate sedation. For longer or painful procedures, children are given IV and/or inhalation medications that render them fully unconscious. Deep sedation is the term for children who are more lightly unconscious and able to easily breathe without any airway support. General anesthesia is a state of deeper unconsciousness without response to painful stimulation and often requires help maintaining airway patency. All sedated and anesthetized children need to be supervised and monitored by personnel with special training and experience in pediatric resuscitation and airway management. The minimum equipment required for either sedation or anesthesia includes Suction, Oxygen, appropriate Drugs, and Airway equipment (SODA). Drugs include sedatives, narcotics, muscle relaxants, cardiac resuscitation
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medications, and medications for anaphylaxis. Airway equipment includes O2 tubing, bag-mask ventilation supplies (e.g., Jackson Reece, Ambu), laryngoscopes, ETTs, tape, stylettes, oral and nasal airways, and LMAs.
■ SUMMARY Differences between adults and children include size, cognitive ability, physiology, and anatomy. Awareness of these differences and the availability of appropriately sized equipment and monitors have been associated with both diminished risk and diminished discomfort of surgery and anesthesia in children. Those working in a pediatric environment should be aware of these differences and familiar with the various sizes of all available equipment.
REVIEW QUESTIONS 1. When are most regional anesthesia procedures (epidurals, peripheral nerve blocks, etc.) performed on children? A) In the preoperative area with the patient sedated B) In the OR with the patient sedated C) In the OR with the patient under general anesthesia D) In the postanesthesia care unit (PACU) with the patient sedated E) Regional anesthesia is not indicated for pediatric patients Answer: C. Young children are less likely to understand procedures and may not be able to cooperate. Unlike adults, most regional procedures are performed under general anesthesia in the OR.
2. Concerning younger pediatric patients and IVs, which of the following statements is/are true? A) All air bubbles must be removed from the tubing. B) Microdrip tubing sets are preferred to macrodrip sets. C) Buretrols are used only for older/larger children. D) All of the above. E) A and B only. Answer: E. Young children, particularly those younger than 2 years, may have a patent foramen ovale. A patent foramen ovale can allow bubbles to pass directly from the right atrium into the left atrium and from there to the systemic circulation where they could cause a stroke or other ischemic phenomenon. Because children are much smaller than adults, the anesthesia provider must maintain a careful eye on the amount of fluids that are administered. Microdrip tubing and buretrols are both devices that allow better control of fluid administration than a standard macrodrip set.
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Chapter 46 • Pediatric Anesthesiology 3. To prepare for a pediatric general anesthetic, an anesthesiologist is likely to need what airway equipment? A) Oral airway, multiple sizes B) Laryngoscope blade, multiple sizes/styles C) ETT, multiple sizes—cuffed and/or uncuffed D) All of the above E) B and C only Answer: D. Similar to an adult general anesthetic, a full range of airway management equipment must be available for every anesthetic. The major difference will be making appropriate sizes of equipment available for the pediatric patient.
4. In comparing the HR and RR of infants and small children to those of adults, which of the following statement is true? A) HR faster, RR slower than adults B) HR slower, RR faster than adults C) HR slower, RR slower than adults D) HR faster, RR faster than adults E) Both HR and RR are similar to those of adults
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SUGGESTED READINGS Downes JJ, Raphaely RC. Anesthesia and intensive care. In: Ravich MM, et al., eds. Pediatric Surgery. 3rd ed. Chicago: Yearbook Medical Publishers; 1979. Kain ZN, Wang SM, Mayes LC, et al. Distress during induction of anesthesia and postoperative behavioral outcomes. Anesth Analg. 1999;88:1042–1047. Kain ZN, Mayes LC, Wang SM, et al. Postoperative behavioral outcomes in children: effects of sedative premedication. Anesthesiology. 1999;90(3):758–765. Rabbitts JA, Groenewald CB, Moriarty JP, et al. Epidemiology of ambulatory anesthesia for children in the United States: 2006 and 1996. Anesth Analg. 2010;111(4):1011–1015. Rackow H, Salanitre E, Green LT. Frequency of cardiac arrest associated with anesthesia in infants and children. Pediatrics. 1961;28:697–704.
Answer: D. Infants and children manifest several differences in their basic physiology and metabolic rate when compared to adults. Both the HR and the RR are higher in children than adults.
5. Compared to adults, which statement regarding children’s body temperature under general anesthesia is true? A) Decreases more slowly than adults B) Decreases more quickly than adults C) Pediatric ORs should be warmed and intraoperative warming devices routinely used D) A and C only E) B and C only. Answer: E. Compared to adults, infants have a much greater surface area to weight ratio and they are particularly prone to heat loss in the cold environment of the OR. Special attention needs to be paid to maintaining temperature balance in children, and this often includes warming the OR as well as active warming devices.
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CHAPTER
47
Obstetric Anesthesia Karen Hand ■ INTRODUCTION The aim of this chapter is to introduce the anesthesia technician to the care provided to obstetric patients by the anesthesia team in the delivery suite. The unique environment, the unique condition of pregnancy, and the particular challenges of provision of safe anesthesia care in this specialty area are considered. When elderly women are asked to name the most memorable day of their lives, the most common response is the day of delivery of their first child. The birth of a child is usually a joyful time, although the experience may be attended with fear, anxiety, and severe pain. Historically, and in parts of the world still, childbirth is associated with a high maternal mortality rate and an even higher neonatal mortality rate. The safety of childbirth has improved considerably in developed countries (Fig. 47.1). Nonetheless, for the fetus, delivery remains a time of high risk. Delivery may be complicated by known or previously unknown congenital medical problems, in utero growth problems, placental or umbilical cord accidents, obstruction of passage through the birth canal, and related injuries. For the mother, childbirth remains a significant cause of mortality and morbidity even in wealthy countries. Complications occur related to preexisting medical conditions in the mother, especially cardiac disease, and medical conditions arising as a result of pregnancy, such as venous thromboembolism, as well as diseases unique to pregnancy such as preeclampsia and amniotic fluid embolus. Hemorrhage remains a major cause of maternal mortality, even in the best of settings. There are also increased risks associated with anesthesia during pregnancy to be considered. The role of the anesthesia team on the labor and delivery suite is to provide labor analgesia, safe anesthesia for surgical procedures, both
elective and unplanned, and to respond to any emergencies as they arise, to ensure the safety of both the mother and child. Careful planning and preparation is the key to safe provision of anesthesia services on the delivery suite.
■ DESIGN OF OBSTETRIC UNITS Obstetric units are often remote from the main operating suite; indeed, they may be in distant buildings. Staffing assignments must ensure that adequate anesthesia coverage and technical support are available day and night. In rural settings and in small hospitals, anesthesia providers may not always be in-house at night. There will be a clear local policy as to acceptable times for delivery of anesthesia services, but the American Society of Anesthesiologists (ASA), American College of Obstetricians and Gynecologists (ACOG), and Joint Commission standard that must be met is that for emergency cesarean sections equipment and personnel should be adequate to ensure that a decision to incision interval of less than 30 minutes can be achieved. This means that anesthesia supplies must be ready and accessible at all times, operating rooms (ORs) must be prepared to receive a patient requiring an emergency cesarean section, and the anesthesia team should be prepared to provide anesthesia, including general anesthesia, at short notice. Although anesthesia technicians are an important part of the anesthesia team, many institutions do not provide a dedicated anesthesia technician to cover the obstetric suite. The delivery suite is usually set up with delivery rooms, in which the anesthesia team may be involved in providing labor analgesia for labor and forceps or vacuum deliveries, and ORs in which both elective and emergency procedures are performed, including cesarean section, manual removal of placenta, tubal ligation, cervical suture, and in some centers fetal in utero
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1000
Rate
*
800 600 400 200 0
1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 Year * Per 100,000 live births ■ FIGURE 47.1 United States maternal mortality rate by year (1900-1997). (Centers for Disease Control. Healthier mothers and babies. MMWR Morb Mortal Wkly Rep. 1999;48(38):849–856. Available from: http://www.cdc.gov/mmwr/PDF/wk/ mm4838.pdf. Accessed March 3, 2002.)
procedures. In some units, ORs may be shared with the main operating area.
■ MONITORING Facilities for monitoring in delivery rooms may be limited to noninvasive monitoring including noninvasive blood pressure and pulse oximetry. Obstetric nursing staff routinely monitor these parameters during labor, along with cardiotocography, which measures both the fetal heart rate and uterine contractions (Fig. 47.2). Fetal heart rate monitoring (analysis of cardiotocography patterns) allows assessment of the adequacy of uterine contraction and fetal well-being during labor. A normal fetal heart rate is between 110 and 160 beats per minute, with variability, and with “accelerations.” The monitor may also show “decelerations” of various types, the most ominous of which are frequent late decelerations, which means that the deceleration occurs after the peak of the contraction. This suggests that uteroplacental perfusion is compromised during the contraction and the fetus may be at increased risk of a poor outcome including neurologic damage and even death (Fig. 47.3). The decision to proceed with urgent cesarean section is frequently made on the basis of this monitoring. A sustained fetal bradycardia suggests that the supply of oxygen to the fetus remains impaired and is a clear emergency requiring immediate delivery. Advanced monitoring such as electrocardiogram (ECG), and arterial or central venous
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pressure monitoring, may be possible in the delivery room, although the training of obstetric nursing staff may limit its use. In addition, the supplies for these procedures are usually stocked in the OR, and not the delivery suite. During labor and delivery, there are very large changes in physiologic parameters as a result of pain and the metabolic demands of the contracting uterus; for example, cardiac output, already increased 50% percent by pregnancy itself, increases another 40% during labor and delivery. While labor analgesia is known to reduce such changes, for some patients safe delivery requires additional monitoring. Other options are the use of specialist obstetric nursing staff with additional training, intensive care nursing support, or the continuous presence of the anesthesiologist. It may be preferable for patients requiring invasive monitoring to deliver in an OR or an intensive care unit (ICU) setting. When invasive monitoring is required for labor, it is usually for patients with severe cardiac or other underlying disease. Arterial lines and central lines are used more frequently than pulmonary artery catheters. Occasionally, arterial pressure monitoring may be required for women with severe hypertension.
■ THE PHYSIOLOGIC CHANGES OF PREGNANCY The risks associated with general anesthesia are increased during pregnancy because of major physiologic changes occurring in the mother as
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■ FIGURE 47.2 Conditions for cesarean section, fetal distress, and persistent and consistent late decelerations indicating fetal distress.
a result of the pregnancy. These changes include the following: 1. An increased risk of aspiration of gastric contents because of decreased stomach emptying. 2. Increased oxygen consumption and decreased functional reserve capacity leading to rapid desaturation during induction of general anesthesia. 3. Increased edema. Difficult intubation is about ten times more common in the obstetric population, partly because of increased airway edema, and partly because of increased obesity, positioning difficulties, and the need for rapid sequence induction with cricoid pressure. 4. Aortocaval compression, leading to decreased venous return, decreased cardiac output, and hypotension in the supine position, particularly in the presence of central neuraxial blockade. The mass of the enlarged uterus and fetus compresses the vena cava and aorta. The patient should be positioned
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in left uterine displacement when supine, with a wedge under the right hip or the table tilted to ensure that the gravid uterus is moved away from these major blood vessels (Fig. 47.4). 5. When possible, general anesthesia is avoided during pregnancy. Maternal mortality figures show declining mortality associated with anesthesia, in line with decreasing use of general anesthesia, and increasing use of regional anesthesia. In addition, general anesthesia is associated with increased risks for the fetus.
■ LABOR ANALGESIA Neuraxial analgesia is both the most effective and least invasive option for labor analgesia. Lumbar epidurals are commonly used. Other options are spinals or combined spinal and epidural techniques (combined spinal epidural [CSE]). Optimal labor analgesia gives pain relief without motor blockade.
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■ FIGURE 47.3 An early deceleration mirrors the contraction, is caused by head compression, and is benign, requiring no intervention. A late deceleration mirrors the contraction but is offset because a late deceleration begins after the contraction has started and ends after the contraction has ended. The cause is uteroplacental insufficiency, and interventions are aimed at improving blood flow to the placenta.
Labor is divided into three stages. The first stage occurs when the uterus is contracting regularly and painfully and the cervix dilates. The second stage occurs when the baby descends through the birth canal and the mother actively pushes. The third stage is the delivery of the placenta. The pain of the first stage of labor is transmitted via nerves supplying the fundus and body of the uterus, from T10-L1, whereas the pain of the second stage of labor is transmitted via nerves supplied by sacral nerve roots S2-S4. The pain of labor is described as being among the most severe of all types of pain. Women’s expectations of the pain of labor are varied, as are their attitudes to analgesia. Some women plan for as much analgesia as possible, while others aim for minimal analgesia, or only
noninvasive techniques (Table 47.1). Labor pain is particularly severe in the later first stage, as the cervix approaches full dilation. This may coincide with both mental and physical exhaustion, leading many to request epidural analgesia at this stage. The pain of labor is unique in pain treatment, in that provision of as much analgesia as possible is not necessarily what the patient desires. Many women want to feel contractions to be able to time pushing. The labor epidural rate is approximately 60%. Some women, particularly with psychological preparation, do very well with minimal analgesia. However, others benefit enormously from neuraxial analgesia. Some women will be advised that a labor epidural is the safest option for them, particularly if they are
■ FIGURE 47.4 Left lateral tilt to relieve aortocaval compression. (From MacDonald MG, Seshia MKK, et al. Avery’s Neonatology Pathophysiology and Management of the Newborn. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005, with permission.)
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TABLE 47.1 TECHNIQUES OF LABOR ANALGESIA COMPLEXITY, INVASIVENESS
EXAMPLES
ADVANTAGES/DISADVANTAGES
Least invasive
Relaxation techniques: breathing, massage, visualization
Effective, especially in early labor, education helpful
Water birth Transcutaneous electrical nerve stimulation (TENS) Acupuncture Intermediate Most invasive
Opioids: e.g., meperidine, fentanyl Nitrous oxide/oxygen
Used in some centers, requires scavenging
Epidural
Very effective, some contraindications
Spinal
Limited duration
Combined spinal and epidural
Flexible, quick-onset analgesia, increased risk of meningitis
at high risk of needing to be delivered by cesarean section, or if they have particular medical conditions.
Labor Epidurals General aspects of the procedure for siting an epidural are described in Chapter 21. The anesthesia provider must review the patient’s medical history, and examine the patient, including her airway and heart and lungs. The patient must give informed consent, after review of complications such as dural puncture headache, temporary or permanent nerve injury, infection and bleeding, as well as immediate risks such as hypotension. Full equipment for resuscitation must be available, including a tipping bed (capable of being put in the Trendelenburg position), suction apparatus, oxygen, and a code cart. Standard packs for epidurals, spinals, and CSEs are very helpful, as is a well-stocked, lockable, mobile cart. The ASA Practice Guidelines for Obstetric Anesthesia suggest that laryngoscopes and assorted blades, endotracheal tubes and stylets, a self-inflating bag and mask, medication for blood pressure support, muscle relaxation, and hypnosis, a carbon dioxide detector, and a pulse oximeter should all be available during the initial provision of neuraxial anesthesia. The epidural cart must be checked regularly, restocked, and outdated drugs and equipment replaced. Patients often have family members accompanying them during labor. If a family member is to accompany the patient during the procedure,
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it may be prudent to insist that they are seated, because vasovagal episodes are common. Good sterile technique is vital during epidural placement. The delivery room is a less sterile environment than an OR. Surfaces such as tables must be cleaned before use as a workstation. Hand washing with surgical scrub solution, caps, masks covering the nose and mouth, sterile gloves, individual packets of skin preparation, and sterile draping are all recommended. Chlorhexidine is preferred. A gown may be worn. The patient must have a functioning intravenous cannula and should have received 500 mL of intravenous crystalloid to prevent hypotension. She is positioned sitting or in the lateral fetal position. Positioning the parturient can be difficult, both anatomically and because of pain, and it may be difficult for her to keep still during contractions. Monitoring will include noninvasive blood pressure and pulse oximetry. Immediate Complications of Labor Epidurals After placement of the epidural catheter, an initial test dose of lidocaine with epinephrine is usually given. Immediate complications associated with epidural placement include both predictable responses to dosing an epidural catheter with local anesthetic solution and complications caused by incorrect location of the epidural catheter. The test dose is intended to identify misplacement of the catheter. Local anesthetic placed in the epidural space anesthetizes pain
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fibers but also sympathetic nerve fibers, which maintain vascular tone. Even when the catheter is correctly located in the epidural space, the patient may develop hypotension secondary to blockade of sympathetic nerve fibers, and this may occur with the test dose or with subsequent doses of local anesthetic. Aortocaval compression is an important contributing factor and predisposes laboring patients to become hypotensive with regional anesthesia. Hypotension may cause maternal nausea and vomiting, but in most healthy women, the most serious effect is likely to be on the fetus. Altered uterine artery blood flow may cause fetal bradycardia. Occasionally, if the fetal heart rate does not improve with changes in maternal position, oxygen, boluses of fluid, and drugs such as ephedrine or phenylephrine, the patient may need to be moved to the OR emergently for delivery by emergency cesarean section. High or Total Spinal Epidural catheters should always be aspirated to check for cerebrospinal fluid. However, occasionally a catheter is inadvertently placed intrathecally (through the dura and into the subarachnoid space), and its misplacement is not suspected. If a test dose of 3 mL of 1.5% lidocaine with epinephrine is administered into the cerebrospinal fluid in the subarachnoid space, the error will usually be obvious, with motor blockade, a higher sensory level than expected, and maternal hypotension. If intrathecal placement is not recognized and a large dose of local anesthetic is given, it is possible to develop a “high spinal” or “total spinal,” with severe hypotension, breathing difficulties or apnea, and loss of consciousness, as progressively higher spinal levels and ultimately the brain are anesthetized. This is an emergency requiring immediate measures to secure the airway, ventilate, restore blood pressure, and deliver the fetus. An unconscious obstetric patient who has stopped breathing should be ventilated with a mask and Ambu bag, and cricoid pressure should be applied while preparations are made for intubation. Ephedrine and phenylephrine are first-line drugs for the treatment of hypotension. Left uterine displacement should never be forgotten. Atropine and epinephrine should also be readily available. Preparations should be made to transfer the patient to the OR for immediate delivery if there
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are signs of fetal distress. It should be noted that the upper limit of the epidural space is at the foramen magnum. A high epidural block will not anesthetize the brain, but high spinals can. Intravascular Epidural Catheter Placement An epidural catheter located in an epidural vein may become apparent when a test dose of local anesthetic with epinephrine is given. The patient is asked to report any symptoms she notices, and her heart rate is observed. An increase in maternal heart rate of more than 15 beats per minute is considered a positive test because the intravenous epinephrine can raise the heart rate. However, heart rate changes with contractions are very common in labor, so the test dose may be less reliable in pregnancy. If local anesthetic is injected into a blood vessel instead of being slowly absorbed from the epidural space, toxic levels of local anesthetic may occur. The major consequences of a toxic dose of local anesthetic are neurologic and cardiac. Early symptoms of local anesthetic toxicity include tingling of the lips or tongue, because of the high blood supply to this area, and ringing in the ears. Such early signs are not always present, and the presentation may be with seizures secondary to central nervous system toxicity, arrhythmias or cardiac arrest. If a patient suffers a cardiac arrest, particularly after a dose of bupivacaine, advanced cardiac life support (ACLS) protocols should be followed, although resuscitation may need to be prolonged because bupivacaine binds tightly to cardiac myocytes. Intralipid has been reported to be valuable in displacing bupivacaine from its binding sites on the heart and should be available.
■ CESAREAN SECTION Cesarean section is a very common operation, with 32% of babies currently delivered by cesarean section in the United States. Indications for elective cesarean section include prior cesarean section, breech presentation, twins, cephalopelvic disproportion, and maternal request. Indications for unplanned cesarean section include dysfunctional labor and fetal intolerance of labor. Regional anesthesia for cesarean section includes spinal, epidural, and CSE techniques. General anesthesia is usually reserved for emergency situations when the life of the mother or fetus is in immediate danger and the fetus needs
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to be delivered as quickly as possible, or situations when there is a contraindication to regional anesthesia.
Spinal Anesthesia A detailed description of the procedure for subarachnoid anesthesia is given in Chapter 21. Spinal anesthesia is often the technique of choice for uncomplicated elective cesarean sections. The patient should have a freely running intravenous cannula of at least 18G. She will usually have already received 1 L of crystalloid to offset the anticipated vasodilation from a spinal, and she will receive a drink of sodium citrate to reduce the risk of aspiration pneumonitis. At a minimum, blood pressure and pulse oximetry are monitored during placement, which is often performed in the seated position. The obstetric team will monitor the fetal heart rate. Intrathecal local anesthetic is usually supplemented with opioid drugs, including fentanyl and preservative-free morphine. Obstetric patients are particularly prone to dural puncture headache; therefore, small gauge Whitaker and Sprotte-type needles (25G or smaller) are preferred. The most common early complication of subarachnoid blockade is maternal hypotension. Cesarean section requires extensive dermatomal blockade to ensure maternal comfort during the surgery. The patient will develop a dense motor block, and on testing, the block level will often extend from the sacral dermatomes to as high as T2, and there will be a rapid-onset sympathectomy, sometimes accompanied by bradycardia as the cardiac acceleratory fibers are blocked. Blood pressure should be monitored frequently initially, and the ECG should be placed. Careful attention should be paid to the patient, who will often demonstrate perioral pallor or complaints of nausea, even before the blood pressure cuff confirms a drop in pressure. Alteration in uterine blood flow is a major concern. The fetus should be monitored during this time, and the response to developing hypotension should be prompt, because even small drops in maternal blood pressure can have detrimental effects on the fetus. Spinal hypotension usually responds to fluid, phenylephrine, and ephedrine, and these should be readily available. Increasing left uterine displacement may be necessary. Obstetric patients do not usually receive sedation, and it is important for all staff in the OR to
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be aware of this. It is common practice for the patient to have a support person of her choice accompanying her during cesarean sections performed under regional anesthesia. Visitors are not usually brought into the OR if the patient is to receive general anesthesia, and will be asked to leave if the patient requires conversion to general anesthesia The extent and quality of the subarachnoid block are checked carefully before surgical incision. Delivery of the neonate usually proceeds promptly, although scarring and adhesions from prior procedures can slow delivery considerably. Following delivery of the baby, uterotonics will usually be given to help contract the uterus to prevent blood loss. Oxytocin is the drug most commonly used, usually as an infusion. A pressure bag or infusion pump may be useful. Drug errors are a particular problem in obstetric anesthesia. Talking to the patient and her partner can be distracting for the anesthesia provider. Vomiting, hypotension, pain, or bleeding may require urgent interventions, which also make errors more likely. The anesthesia cart and anesthesia machine should be tidy and well organized at all times, and particular attention should be paid to routines intended to minimize the risk of errors.
Epidural Anesthesia for Cesarean Section Epidural anesthesia is most commonly used for cesarean section in patients who have a functioning labor epidural in place. Epidural blockade can usually be rapidly extended to provide adequate anesthesia for cesarean section with administration of additional boluses of local anesthetic. In addition, an epidural catheter may be placed de novo in preference to a subarachnoid block for several reasons. Increments of local anesthetic can be given slowly, in a manner that minimizes the risk of severe hypotension. This is particularly important for patients who would not tolerate a rapid onset of sympathectomy, such as those with cardiac disease. Placement of an epidural catheter also allows the duration of neuraxial blockade to be extended, which is essential if a case is expected to be prolonged.
Combined Spinal Epidural A CSE combines the benefits of both spinal and epidural anesthesia and is an excellent option
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for many patients. The spinal component can include a standard subarachnoid dose of local anesthetic or a smaller dose, which can then be extended as necessary using the epidural catheter, the advantage being less risk of hypotension than with a standard subarachnoid block, but quicker onset and denser sacral block than with an epidural. An additional advantage of the epidural catheter is that it can be used to extend the duration of block. The disadvantage of this technique is the increase in complexity.
General Anesthesia General anesthesia is usually reserved for patients for whom regional anesthesia is contraindicated, and for emergencies necessitating very rapid delivery of the fetus, if the mother does not have a functioning epidural in place. Common examples of contraindications to regional anesthesia in obstetrics include cardiovascular instability, coagulation abnormalities, and sepsis. Examples of fetal emergencies include cord prolapse and abruption. Preparation of equipment is vital to ensuring that general anesthesia can be provided to obstetric patients safely. The anesthesia machine must be fully checked, including the breathing circuit, suction tubing, and suction apparatus. A common but potentially disastrous error is forgetting to replace suction tubing between cases. Airway equipment should be prepared ahead of time including laryngoscopes, a choice of blades, oral and nasal airways, an intubating bougie, and endotracheal tubes. Endotracheal tubes of a smaller size than standard are usually chosen, because of the airway edema often occurring in pregnancy. For an average size woman, a size 6.0 or 6.5 tube might be selected. For many anesthesiologists, video laryngoscopy (e.g., Glidescope) has become the technique of choice in situations where standard laryngoscopy is unsuccessful, although the use of this device has not been widely studied in obstetric patients. A difficult airway cart should be readily available. The ASA Practice Guidelines for Obstetric Anesthesia provide suggestions as to the contents of a portable storage unit, including alternative choices of rigid laryngoscope blades, laryngeal mask airways, endotracheal tube guides, retrograde intubation equipment, a device for emergency nonsurgical airway ventilation such as a supraglottic airway and a hollow jet ventilation stylet with transtracheal jet ventilator, fiber-optic
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intubation equipment, and emergency surgical airway access equipment, such as a cricothyroidotomy kit. It should be noted that obstetric patients presenting for emergency section are at high risk for difficult airways. Medications required for rapid sequence induction must be immediately available. Sodium pentothal is the classic induction agent described. Propofol and etomidate are more frequently used today. Ketamine is another option. Succinylcholine is the muscle relaxant of choice in most cases. Other emergency drugs such as atropine, epinephrine, ephedrine, and phenylephrine should also be readily available. When the decision is made to proceed with emergency cesarean, achieving the ASA, ACOG, and Joint Commission standard of decision to incision interval of less than 30 minutes demands excellent teamwork. All personnel should be alerted promptly and should respond as quickly as possible. A team effort to move the patient into the OR and onto the operating table rapidly and safely is important. During transfer intravenous lines must be protected. The obstetric team may reassess the situation on arrival in the OR, including reevaluating the fetal heart rate tracing or repeating the vaginal examination, or may begin immediate preparation for cesarean section, including placing a urinary catheter, cleansing the abdomen with surgical antiseptic solution, and placing sterile drapes. During these preparations the anesthesia team will proceed expeditiously, but without compromising safe anesthesia practices. Whenever possible, the anesthesia team will have seen and assessed the patient previously, although it may be necessary to perform a rapid history and examination. It is vital that the patient is properly positioned on the operating table, with her head on the adjustable headpiece, and with elevation of her head and shoulders such as to achieve the “sniffing the morning air” intubating position. Proper patient positioning is especially important in pregnancy because of enlarged breasts, increased obesity, and increased incidence of difficult intubation. Left uterine displacement must not be omitted. For most healthy women, induction of general anesthesia is accomplished with a rapid sequence induction with cricoid pressure. Pregnant women are assumed to have a full stomach. If they have been in labor, have received opioids, or have eaten, they are at particular risk of aspiration
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of gastric contents. Sodium citrate is given to reduce the acidity of stomach contents. Standard ASA monitors are applied. Suction apparatus is placed within easy reach. The patient is preoxygenated. Preoxygenation is with four vital capacity breaths or 3 minutes of breathing 100% oxygen with a good seal around the mask on the patient’s face. To minimize exposure of the fetus to anesthetic gases, induction is delayed until the obstetrician is ready to make the skin incision, although surgery will not begin until induction is complete and the airway secured. Cricoid pressure is applied during induction of anesthesia and must not be removed except at the anesthesiologist’s request. After induction, maintenance of anesthesia is usually with an inhalational agent at one half minimum alveolar concentration (MAC), with 50% nitrous oxide, until delivery of the fetus, then 70% nitrous oxide. In pregnancy, the MAC for inhalational agents is reduced, it is desirable to minimize anesthetic effects on the fetus, and inhalational agents relax uterine muscle, which may increase bleeding. However, cases of awareness under anesthesia have been reported during cesarean sections. Neurophysiologic monitoring may be helpful to monitor anesthetic depth (see Chapter 41). At the end of surgery the patient can usually be extubated. Assessment of residual neuromuscular blockade is very important. The patient should usually be extubated fully awake, with intact protective airway reflexes, to minimize the risk of aspiration. The patient should be recovered in a safe location by qualified staff. The risk of airway complications is as high during emergence and recovery as on induction, with complications arising related to problems such as airway edema, bronchospasm, pulmonary edema, and residual muscle relaxation. Local policies may distinguish between recovery after general anesthesia and regional anesthesia. In the event of a failed intubation, the ASA’s difficult airway algorithm is adapted for obstetric patients to allow the anesthesiologist to take account of the needs of the fetus. In the event of a failed intubation, two questions determine what should happen: 1.
2.
Is surgery required for an emergency that is an immediate threat to the life of the mother or the fetus? Is it possible to ventilate the patient?
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In a situation other than an emergency posing an immediate threat to the life of the mother or the fetus, in most cases the patient will be woken up, and either intubated awake using advanced airway techniques or a regional technique will be employed. The increased risk of aspiration in obstetric patients makes awake fiber-optic intubation preferable to asleep fiber-optic intubation in most cases. If the patient can be ventilated using a mask and airway or laryngeal mask airway, in a lifethreatening emergency situation it is acceptable to proceed with the surgery, maintaining cricoid pressure if that does not interfere with ventilation. If the patient cannot be ventilated with optimal techniques and cannot be woken up, an emergency surgical airway will be necessary.
■ OTHER OBSTETRIC EMERGENCIES Emergencies in the context of emergency cesarean section have been discussed, as have emergencies related to epidurals. In this section, seizures, hemorrhage, embolic events, and cardiac arrest will be considered. Hypertensive disorders, hemorrhage, and embolic disorders are major direct causes of maternal mortality and may present as these types of emergencies on the delivery suite.
Seizures Seizures occurring in obstetric patients may be caused by eclampsia, although epileptic seizures are also common. Eclampsia is a condition that only occurs in pregnancy, and the postpartum period. A seizure may be the first sign of the disorder, although it is frequently preceded by preeclampsia, which is defined as hypertension and proteinuria occurring after the 20th week of pregnancy. In severe preeclampsia, there are signs and symptoms of end-organ damage in multiple organ systems, including the central nervous system, which may progress to seizures. Severe hypertension in itself may be an emergency requiring immediate management with intravenous medication, and occasionally invasive monitoring. The treatment of eclampsia is oxygen, airway support as necessary, and magnesium. Magnesium is very effective in stopping eclamptic seizures, and particularly in preventing a second seizure. Eclamptic seizures are usually self-limiting. Intubation is not usually required, although airway equipment should be
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available and prepared. Benzodiazepines are the first-line drugs in epileptic seizure management but are usually avoided in eclampsia because they increase postictal sedation and increase the risk of airway complications.
Hemorrhage Hemorrhage in obstetric patients can be catastrophic. Hemorrhage is classified as antipartum or postpartum (before and after delivery respectively). Antipartum causes of hemorrhage include abruption, when the placenta separates prematurely from the wall of the uterus, placenta previa, where the placenta is abnormally situated over the cervical opening, and uterine rupture. Postpartum hemorrhage may be caused by uterine atony (failure of the uterus to contract), or retained placental products or blood clots, which prevent the uterus from contacting down in the usual manner, leaving large blood vessels open and bleeding. By the end of pregnancy, the blood flow to the uterus is increased to 1 L per minute, and so hemorrhage can be rapid. Hemorrhage may be the presenting problem when a patient arrives emergently at the hospital, may develop unexpectedly during or after cesarean section, and may occur unexpectedly after a normal vaginal delivery. The expected blood loss after a vaginal delivery is 500 mL, with 1,000 mL at cesarean section. Unusually rapid bleeding, or more than 700 mL or 1,200 mL, respectively, should prompt preparation for management of massive hemorrhage. Equipment for the management of massive hemorrhage must be assembled quickly. It will be a matter of local policy what equipment is kept on the delivery suite versus in a central location. Additional intravenous access must be secured promptly. Equipment for arterial and central line placement and monitoring should be available, including an ultrasound machine. In some cases, very large bore access, such as introducers for pulmonary artery catheters or trauma lines are required. A rapid infusion device may be necessary. Intravenous fluid warmers and a forced air body warmer should be available and applied early to prevent hypothermia. Blood should be immediately available, including O negative blood. Good communication with the transfusion service is vital. In cases of massive hemorrhage, obstetric patients can rapidly develop coagulation abnormalities.
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It may become necessary to give fresh frozen plasma and cryoprecipitate, as well as red blood cells. The use of the cell saver has been limited in obstetrics because of concerns regarding the infusion of amniotic fluid particles, although it is becoming more widely used. It appears that cell savers can be used safely in obstetric patients providing amniotic fluid is suctioned away from the field and the field is thoroughly irrigated first. An additional leukocyte depletion filter may be used as well. Cell savers may also be helpful in Jehovah’s witnesses who decline other blood products. In cases of uterine atony, drugs used to improve uterine contraction include oxytocin, methylergonovine (Methergine), misoprostol, and prostaglandin F2 alpha (Hemabate). Embolization of a uterine artery can be an effective way of halting obstetric hemorrhage. In this case, the patient may need to be transferred to the interventional radiology suite. An anesthesia machine should be prepared in that location along with monitoring equipment and equipment for managing hemorrhage, while preparations are made to transfer the patient. In some cases, the obstetrician may need to perform a hysterectomy to control hemorrhage. When the likelihood of massive hemorrhage is high, or if a patient develops massive hemorrhage after leaving the obstetric unit, management in the main operating suite may be preferable, if staffing and equipment are more easily accessible. In some cases, the placenta may be known to abnormally adhere to the uterine wall, and may even invade the uterine muscle or other organs. This is known as placenta accreta, increta, or percreta, with placenta percreta being invasion of other organs such as the bladder or bowel. This may necessitate a planned cesarean-hysterectomy, which may be scheduled in a main OR location.
Embolism Venous thromboembolism is more common in obstetric patients because of changes in coagulation factors during pregnancy, as well as mechanical obstruction of venous return by the pregnant uterus. Pulmonary embolus may present as chest pain, shortness of breath, or even cardiac arrest, at any stage of pregnancy, with a particular risk in those with abnormal blood clotting and after cesarean section.
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Amniotic fluid embolus is specific to pregnancy. Classically, this is described as sudden cardiovascular collapse, cyanosis, mental status changes, or massive hemorrhage in a parturient with forceful contractions, although it can occur at any time. Fetal cells from amniotic fluid are forced into the maternal circulation and can be found in the pulmonary vascular bed postmortem. The condition has a very high mortality for both mother and fetus. More recent research suggests that there may be an anaphylactoid response to amniotic material, rather than a mechanical obstruction of blood vessels. Treatment of amniotic fluid embolus includes management of cardiac arrest and support of the cardiovascular system, delivery of the fetus, management of hemorrhage, and support of the cardiovascular system. The patient is likely to require full invasive monitoring and ICU care if she survives the acute event.
Cardiac Arrest in Pregnancy Cardiac arrest is rare in pregnancy. Causes include underlying cardiac disease, embolic disease, massive hemorrhage, anaphylaxis, and toxic doses of local anesthetic. In an obstetric patient, ACLS guidelines should be followed, but in addition left uterine displacement should be instituted immediately. Aortocaval compression by the gravid uterus severely impairs venous return to the heart and hinders successful resuscitation. The outcome for the fetus is likely to be poor. However, to improve the chances of survival for the mother, the fetus should be delivered if a perfusing rhythm has not been reestablished after 4 minutes. To deliver the fetus rapidly, it should be possible to perform a cesarean section at the bedside, calling for personnel and the cesarean section tray as quickly as possible.
■ SUMMARY Obstetric emergencies can be extremely difficult to manage. This is because of the rapidity with which a situation can change from routine to emergency and error to care for two patients simultaneously, the mother and the fetus. As mentioned previously, anesthesia technicians are important members of the anesthesia team. All technicians who may be called to assist with a procedure or emergency in the obstetric suite should be familiar with the general layout, anesthesia machine, airway equipment, and vascular
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access equipment available in the obstetric suite. This is especially true if the anesthesia technician only occasionally works in the obstetric department. Obstetric anesthesia is a very rewarding specialty area in which to work. The anesthesia technician can be of great assistance as part of the anesthesia team as he or she provides labor analgesia and anesthesia for cesarean sections in what are often rapidly evolving situations, particularly by ensuring that equipment is well stocked and maintained, and by responding rapidly to emergencies as they arise.
REVIEW QUESTIONS 1. The following statements regarding obstetric units are true EXCEPT A) Obstetric units may be isolated. B) Obstetric units must have access to an OR 24 hours per day. C) ASA standards are relaxed on the obstetric unit. D) Anesthesia technicians should be familiar with the anesthesia equipment on the obstetric unit. E) The ASA provides guidance as to the contents of the difficult airway cart. Answer: C. Despite the unique environment and isolated nature of the obstetric suite, ASA standards for monitoring and care of patients still apply. In addition, the ASA provides guidance as to contents of a difficult airway cart. Obstetric surgical emergencies can occur at any time and access to an OR 24 × 7 is critical. Because emergencies are not uncommon on the obstetric unit, anesthesia technicians should be familiar with the operation and location of all anesthesia equipment on the obstetric unit.
2. For labor epidurals, which of the following statements is TRUE? A) The patient can deliver at home. B) The technique for placing labor epidurals is substantially different than placement for nonlaboring patients. C) The epidural must be discontinued if the patient requires a cesarean section. D) A test dose is not necessary for labor epidurals. E) Full equipment and facilities for resuscitation must be available. Answer: E. The placement and conduct of epidurals are essentially the same in laboring and nonlaboring patients. Placement requires qualified personnel in an appropriate setting with resuscitation equipment immediately available.
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Chapter 47 • Obstetric Anesthesia 3. Which of the following statements regarding tracheal intubation during pregnancy is FALSE? A) The rate of failed intubation is increased. B) Airway edema may make intubation more difficult. C) Cricoid pressure is not necessary in pregnant patients. D) The risk of aspiration is increased during pregnancy. E) Advanced airway equipment should be readily available in the obstetric suite. Answer: C. Pregnant patients are at an increased risk for difficult airway management and aspiration. Rapid sequence inductions with cricoid pressure are the general rule. Emergency airway equipment should be readily available.
4. All of the following are examples of obstetric emergencies EXCEPT A) Uterine atony B) Massive hemorrhage C) Fetal distress D) Failed intubation E) All of the above are obstetric emergencies Answer: E. All of the above are obstetric emergencies and require a coordinated team effort for a successful outcome.
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SUGGESTED READINGS American Society of Anestheiologists Task Force on Infectious Complications Associated with Neuraxial Techniques Practice advisory for the prevention, diagnosis, and management of infectious complications associated with neuraxial techniques: a report by the American Society of Anestheiologists Task Force on Infectious Complications Associated with Neuraxial Techniques. Anesthesiology. 2010;112(3):530–545. American Society of Anesthesiologists Task Force on Obstetric Anesthesia. Practice guidelines for obstetric anesthesia: an updated report by the American Society of Anesthesiologists Task Force on Obstetric Anesthesia. Anesthesiology. 2007;106:843–863. Singh GK. Maternal Mortality in the United States, 1935–2007: Substantial Racial/Ethnic, Socioeconomic, and Geographic Disparities Persist. A 75th Anniversary Publication. Health Resources and Services Administration, Maternal and Child Health Bureau. Rockville, Maryland: U.S. Department of Health and Human Services; 2010. Hauth JC, Merenstein GB. Guidelines for Perinatal Care. 4th ed. Elk Grove Village, IL: American Academy of Pediatrics and American College of Obstetricians and Gynecologists; 2002:147. Sullivan I, Faulds J, Ralph C. Contamination of salvaged maternal blood by amniotic fluid and fetal red cells during elective cesarean section. Br J Anaesth. 2008;101(2): 225–229.
5. A “code” is called on an obstetric patient on the delivery suite. Which of the following is TRUE? A) ACLS protocols do not apply. B) The baby should be delivered immediately. C) Defibrillation is contraindicated in pregnancy. D) Chest compressions are contraindicated in pregnancy. E) The patient should be placed in left uterine displacement. Answer: E. Aortocaval compression by the uterus significantly impairs venous return and compromises cardiopulmonary resuscitation. ACLS protocols apply, although with some modifications, including the recommendation that the baby be immediately delivered if the resuscitation is not successful within the first 4 minutes of cardiac arrest.
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CHAPTER
48
Anesthesia Considerations for Out of Operating Room (OOR) Locations Andrew J. Pittaway and Karen J. Souter ■ INTRODUCTION An “out of operating room” (OOR) location is an area located at some variable distance from a hospital’s operating rooms (ORs). In the last two decades, there has been considerable expansion in the services provided at OOR locations and consequentially the need for general anesthesia (GA) and sedation in these areas is growing exponentially. There are a number of synonyms for the term OOR including “anesthesia at alternate sites,” “non–operating room anesthesia,” and “remote location anesthesia.” In this chapter, we will use the terms OOR and “out of operating room anesthesia” (OORA). An OOR location may be a site within a large hospital that is separated from the general OR suite but is within the same hospital. This could include a cardiac catheterization laboratory (CCL), a radiology suite, or a gastrointestinal (GI) endoscopy suite. Alternatively, the OOR location may be a site that is completely separate from a main hospital with no OR facilities, such as a dental clinic or a radiation therapy unit. Office-based anesthesia also falls within this category, but it will not be discussed in this chapter. The most significant concern for the anesthesiologist related to OORA is providing patient care in a location where he or she does not routinely work. OOR areas are often unfamiliar to the anesthesiologist. The anesthesiologist may work in OOR locations infrequently. The personnel are not the ones the anesthesiologist works with on a regular basis, and they may not be as acquainted with anesthesia care as OR personnel. The equipment, including the anesthesia machine, cart, and available drugs, are often different or in different locations than those in the OR. This unfamiliar environment
requires extra vigilance to provide safe care. It is in the OOR arena that the skill and expertise of a trained anesthesia technician is perhaps most valued and the partnership between an anesthesiologist and technician is most important.
■ GENERAL PRINCIPLES The scope of cases performed in the OOR arena covers a wide range of procedures performed on an increasingly diverse group of patients. There are a wide variety of techniques, equipment, and approaches to be considered, and it is easy for the anesthesia team to become distracted. A simple three-step approach is suggested to help you remain focused and to avoid omitting any important aspects of the patient’s care (Table 48.1). When providing anesthesia services in an OOR location, always consider each of the following very carefully: • The environment • The patient • The procedure
■ THE ENVIRONMENT Considerations related to the environment of the OOR location include the following: • Diagnostic and imaging equipment • Provision of standard anesthetic equipment • Availability of appropriate anesthesia monitors including invasive monitors • Constraints related to diagnostic and therapeutic imaging techniques • Unfamiliarity of OOR technical staff with anesthesia requirements • Environmental hazards posed to anesthesia staff, especially ionizing radiation
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TABLE 48.1 A THREE-STEP APPROACH TO ANESTHESIA IN OUT OF OPERATING ROOM LOCATIONS ENVIRONMENT
PROCEDURE
PATIENT
Anesthetic machine and monitors • Availability • Maintenance • Familiarity Resuscitation equipment • Ambu bag • Suction • Code cart + Defibrillator OOR personnel • Familiarity with anesthesia • Training in emergencies Technical equipment hazards • Radiation safety • Magnetic resonance concerns (magnetic field noise) • Temperature control • Allergic reactions Postanesthesia care Transport to and from OOR
Diagnostic or therapeutic duration Level of discomfort/pain Position of patient Special requirements (e.g., functional monitoring) Potential complications Surgical support
Ability to tolerate sedation vs. general anesthesia ASA grade Comorbidity(ies) Airway assessment IV access Allergies—IV contrast Monitoring requirements—simple vs. advanced Pediatric considerations Postanesthesia care
ASA, American Society of Anesthesiologists; IV, intravenous; OOR, out of operating room.
Diagnostic Imaging Equipment OOR locations generally contain large heavy, immobile equipment used for procedures such as fluoroscopy, magnetic resonance scanning, and computed tomography (CT). Fluoroscopy is widely used in many OOR locations, including interventional radiology, cardiac catheterization, and in the gastroenterology suite. Fluoroscopy is a technique used to obtain realtime moving images of the internal structures of a patient by using a fluoroscope. The patient is positioned between the x-ray source and the fluorescent screen and by coupling the fluoroscope to an x-ray image intensifier and video camera the images can be recorded and played on a monitor. Large C-shaped mobile fluoroscopy devices (C-arms) are used to provide images in multiple dimensions; these are moved back and forth around the patient and take up large amounts of space. Advances in technology have resulted in increasingly complex imaging techniques for both diagnostic and therapeutic purposes.
Anesthetic Equipment The American Society of Anesthesiologists (ASA) Standards and Practice Parameters
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Committee issued guidelines for standards to be followed for all non-OR procedures involving anesthesiology personnel. These are outlined in Table 48.2. The Joint Commission requires that patients undergoing anesthesia or sedation receive the same care in OOR sites as they would in the OR. The anesthesia equipment and monitors in the remote location should be of the same standard as in the main OR. This creates a dilemma because OOR sites may only require anesthesia services intermittently. The anesthesia equipment, drugs, and monitors may be left in the OOR site for use when needed or all this equipment may be brought in each time an anesthetic is required. In areas where anesthesia is required on a fairly regular basis (at least 3-4 times a week) equipping and maintaining the OOR site with basic anesthesia equipment that can be quickly supplemented for a case is a reasonable model. However, problems may occur with this setup. Anesthesia equipment left in the OOR site may be damaged as a result of nonanesthesia personnel moving it, tampering with it, and/or borrowing pieces and not replacing them. Anesthesia machines and other anesthesia-related equipment need regular maintenance and can easily be overlooked if they are kept in
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TABLE 48.2 ASA GUIDELINES FOR MINIMAL STANDARDS OF CARE FOR ANESTHESIOLOGY PERSONNEL PROVIDING CARE IN NON–OPERATING ROOM LOCATIONS STANDARD/REQUIREMENT
COMMENTS
1. Oxygen—A reliable source of oxygen adequate for the length of the procedure
• Piped oxygen is strongly encouraged. • Prior to the anesthetic, the capacities, limitations, and accessibility of the oxygen supply must be considered. • Backup oxygen—at least a full E cylinder is essential.
2. Suction—A reliable and adequate source of suction
• Suction standards should meet OR requirements.
3. Scavenging—Where inhalation anesthetic agents are used, an adequate and reliable system for scavenging waste gases is required.
• Extra lengths of tubing may be required to reach the patient.
4. Resuscitation Equipment—A self-inflating hand resuscitator bag capable of administering at least 90% oxygen as a means to deliver positive pressure ventilation; an emergency cart with defibrillator, emergency drugs, and equipment to provide CPR must be immediately available.
• MH cart and difficult airway carts should also be available.
5. Anesthetic Drugs and Supplies
• A supply of all the standard anesthetic drugs as well as emergency rescue drugs. Ideally, a cart similar to those used in the OR.
6. Anesthetic Equipment
• A functional anesthesia machine, ideally similar to those used in the OR.
7. Monitoring Equipment
• Adequate monitoring equipment to meet the ASA standards for basic monitoring. Invasive monitoring equipment may also be required.
8. Electrical Outlets—The location must have sufficient electrical outlets to satisfy anesthesia machine and monitoring equipment requirements.
• Clearly labeled outlets connected to an emergency power supply must also be available. In a “wet location,” isolated electrical power or electrical circuits with ground fault interrupters should be provided.
9. Illumination—Adequate illumination of the patient, the anesthesia machine, and monitors is required.
• Backup illumination must be available.
10. Space—Sufficient space must be available to accommodate the equipment and personnel and allow expeditious access to the patient, anesthesia machine, and monitors 11. Trained Anesthesia Support Staff—Adequately trained support staff and a reliable means of two-way communication. 12. Building And Safety Codes—These must always be observed. 13. Postanesthesia Management—Appropriate care for patients recovering from anesthesia must be provided together with trained recovery staff and facilities for safe transport of patients to the postanesthesia care unit. CPR, cardiopulmonary resuscitation; MH, malignant hyperthermia; OR, operating room.
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an area not routinely serviced by anesthesiology technicians. Hospitals may be reluctant to finance state-of the-art anesthesia equipment for a site where it is used infrequently and often the older machines are “retired” to the OOR site. This can create problems, as anesthesia personnel may not be familiar with anesthesia machine and monitors if they are different than the ones routinely used in the OR. Additionally drugs left in a remote site may go out of date if not used regularly. The alternative solution is to bring all the anesthesia equipment, drugs, and monitors into the OOR each time an anesthetic is required. A number of small portable anesthesia machines are available for this purpose; this is a more practical approach if anesthesia is performed infrequently. This setup does require extra preparation time; it is easy to forget essential equipment requiring anesthesia staff to make multiple trips back to the central anesthesia supply room. The development of a standard anesthesia cart containing all the necessary equipment that is restocked after every case and the use of checklists for all the drugs and equipment to bring each time an OOR anesthetic is required are essential. Checklists and preprepared carts will help the anesthesia technician prepare for an OOR anesthetic quickly and efficiently. It is also important for the anesthesiologist and technician to communicate ahead of time to make sure extra equipment such as special monitors or advanced airway devices are readily available if the case requires them. The provision of anesthesia in the magnetic resonance imaging (MRI) suite is a special situation. The presence of a strong magnetic field prohibits the use of any equipment containing ferrous metal. Specially developed anesthesia machines, monitors, and ancillary equipment are available for use in the MRI scanner.
Constraints Related to Imaging Techniques In a regular OR the anesthesia station is usually well laid out with plenty of space so the anesthesia team has easy access to the patient and monitors. This may not be the case in an OOR site. Frequently, the anesthesia team, equipment, and monitors are crammed in around the bulky radiology equipment, and this may limit
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■ FIGURE 48.1 OOR location with radiology equipment and a limited anesthesia workspace.
the anesthesiologist’s access to the patient, especially in an emergency (Fig. 48.1). The imaging techniques often require the patient to be moved in and out of the imaging device or to have the fluoroscopic imaging equipment move around the patient’s body. This is particularly true in neuroradiological procedures and in CT and MRI. It is extremely important to make sure the anesthesia circuitry, intravenous (IV) lines, urinary catheters, and monitoring cables are all of sufficient length to accommodate the patient moving back and forth on the imaging table. If breathing circuit and IV line lengths are not checked prior to starting the procedure, they are at risk of being dislodged with potentially disastrous results. Other challenges related to space and layout of the OOR site include the need for the anesthesiology team to be shielded from radiation. Transparent leadlined screens are positioned to protect the anesthesia team, but these may limit access to the patient.
Out of Operating Room Staff In the OR, the nursing and technical staff are all very familiar with the role of the anesthesia team and are available to help in any anesthetic emergency. In the remote OOR sites, technical and nursing staffs have different skill sets and may not be so familiar with the conduct of anesthesia or how to help in an emergency. It is vital that the anesthesiologist has experienced anesthesia technical support immediately available to help and provide the correct equipment rapidly
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in case of emergencies. One area where both the anesthesiology technician and the anesthesiologist can bring additional value to the OOR sites is to lead team communication and efforts to train OOR staff in emergency protocols. The whole team needs to know where the code cart with defibrillator and resuscitation drugs is located; these items need to be checked daily. All the staff working in OOR areas should be able to provide support and help manage emergencies such as cardiac arrest, airway emergency, and anaphylaxis. The management of anaphylaxis is particularly important, as patients may be allergic to the IV contrast media used in a number of radiological procedures. Although OOR personnel’s lack of familiarity with anesthesia emergencies can be a serious problem, they may also not be familiar with procedures that are routine in the OR. For example, patient positioning and padding are closely monitored in the OR, whereas OOR personnel may not be familiar with proper positioning and padding techniques for the lateral or prone position.
Environmental Hazards Anesthesiology personnel are at risk from exposure to radiation every time they provide patient care in an OOR location that uses fluoroscopy or CT scanners. It is vitally important that all personnel are informed about the risks of radiation and the procedure to avoid exposure. The two most effective methods anesthesiology personnel can use to prevent occupational exposure to radiation are to (1) ensure they wear high-quality protective garments and (2) monitor their cumulative exposure using dosimetry badges. The risks of exposure to radiation are well known. Radiation directly damages cells in a dose-dependent manner, resulting in cell death. In addition, radiation causes defects in cellular DNA resulting in gene mutations, which can lead to the development of cancer, infertility, and in pregnant women, to fetal abnormalities. Recently, the eye has been recognized as being particularly vulnerable to radiation. Lens opacities and cataract formation are a significant risk for radiologists and other personnel working in radiology suites. Occupational exposure to radiation is carefully controlled and regulated by the National Council on Radiation Protection (NCRP). Personal dosimeters are small badges containing x-ray film; they are used to measure
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the radiation dose received. It is recommended that at least two dosimeters be worn, one under the lead apron and one at the collar above the lead apron. This allows an estimate of the amount of radiation delivered to unshielded areas as well as the integrity of protective lead aprons. It is important for the anesthesia team to be aware of, and to participate in, dosimetry monitoring if they routinely work in the radiology suite. The greatest source of radiation exposure for the anesthesiology team is scatter from the patient rather than being in the direct line of the x-ray beam. Controlling the dose delivered to the patient helps to reduce exposure for the staff, and protective shielding provides further protection. There are three types of shielding: 1. Shielding built into the wall of the procedure room. 2. Equipment-mounted shields: These include protective drapes that are suspended from the table or ceiling between the x-ray generating equipment and the staff. 3. Personal protective devices: These include lead aprons, thyroid shields, eyewear, and gloves; these should be worn by all staff. The added weight of the leaded aprons can increase fatigue in staff, and lightweight aprons made of metals such as barium, tin, antimony, and tungsten are available. Thyroid shields and leaded goggles should also be worn. Ordinary corrective eyeglasses offer very minimal protection to the eye from the damaging effects of radiation. Protective eyeglasses should have large lenses and side shields. Gloves are more important for the actual radiologist whose hands may be directly in the path of the radiation beam rather than the anesthesiology team who need to preserve their manual dexterity.
Temperature Control In most OOR sites, the temperature is maintained at low levels because of the excess heat generated by the technical equipment. Anesthetized or sedated patients are very susceptible to hypothermia, and care must be taken to ensure patients are adequately warmed. On the other hand, in interventional cases, patients may be completely covered by drapes and overheating is a risk; it is important therefore that body temperature is monitored in all patients.
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Anaphylactic Reactions Injectable dyes, known as contrast media, are used during many radiological procedures to enhance the imaging techniques. Radio-opaque materials contain iodine, and the agents used in MRI contain gadolinium and manganese. Side effects and reactions to these agents are relatively common including nausea and vomiting, urticaria, hoarseness, dyspnea, facial edema, and hypotension. Occasionally, a patient can develop an anaphylactic reaction to these substances requiring full resuscitation and the institution of cardiac arrest protocols (see Chapter 64 ).
■ PATIENT CONCERNS IN THE OOR ENVIRONMENT The procedures undertaken in OOR sites are for the most part not particularly painful; however, they often require the patient to remain motionless for long periods. The proceduralist may request the help of the anesthesia team to provide sedation or GA to ensure the patient remains completely still. Many patients experience anxiety and claustrophobia particularly when presented with the enclosed spaces of the CT or MRI scanners. It is not unusual for patients to request some form of sedation to make these experiences less frightening. The great expansion in therapeutic radiological procedures has meant that treatment options are being offered to patients who previously would have been considered too sick to withstand surgical treatment. Thus, many patients who present for OOR procedures have significant comorbidities and need expert anesthesia care throughout.
■ COMMON OOR PROCEDURES Table 48.3 outlines the common procedures that may require anesthesia or sedation in OOR locations. It is important for the anesthesiology team to understand each procedure and the conditions needed for optimum imaging and/or for fast and effective therapeutic interventions.
Radiological Procedures Radiological procedures include noninvasive imaging techniques such as CT, MRI, and interventional radiological (IR) procedures. Computed Tomography CT scanners produce a cross-sectional image of the body in a few seconds, and so for the most
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TABLE 48.3 COMMON PROCEDURES THAT MAY REQUIRE ANESTHESIA IN OUT OF OPERATING ROOM LOCATION Radiology • Computed tomography • Magnetic resonance imaging • Interventional radiology (including interventional neuroradiology) • Radiofrequency ablation Gastrointestinal (GI) endoscopic procedures (GI endoscopy) • Esophagogastroduodenoscopy (EGD) • Endoscopic retrograde cholangiopancreatography (ERCP) • Colonoscopy • Transjugular intrahepatic portosystemic shunt (TIPS) Interventional cardiology • Cardiac catheterization • Electrophysiology (EP)
part imaging sequences are fast. Most adult patients can tolerate CT scanning without anesthesia or sedation. More recently, radiologists are using the CT scanner to guide more invasive procedures such as abscess localization and drainage and radiofrequency tumor ablation in lung, liver, or metastatic cancers. These more invasive activities take longer and can be painful, and so patients may need sedation or anesthesia to tolerate the procedure. The CT scanner is also used for imaging in patients who are severely injured or who are undergoing intensive therapy on the intensive care unit (ICU). In both cases, these patients are at risk of becoming acutely unstable in the CT scanner and anesthesia support may be required to provide safe care while these very sick patients undergo scanning. During the scan very high levels of radiation are generated, 1,000 times or more than produced by a simple x-ray, and staff are at risk if they remain in the scanner with the patient during the scan. For patients undergoing sedation or GA, the anesthesia team will be able to monitor the patient from the shielded control room using standard monitors. When planning the anesthetic technique, the team needs to remember that there will be a delay in accessing the patient if an emergency occurs. The airway should be properly secured ahead of time especially if there is any suspicion that it may be difficult to manage in an emergency. Sick, unstable patients must
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receive resuscitation prior to being taken into the scanner. Resuscitation efforts in the CT scanner will be hampered by the confined space and can be extremely difficult. Magnetic Resonance Imaging (MRI) Briefly, when the atoms of hydrogen are subjected to a powerful magnetic field, they line up with the field. Subsequent exposure of these protons to a radiofrequency pulse changes their energy state and when the radiofrequency pulse is discontinued the protons drift back to their original low energy state. As they do this they emit energy, which is detected by the MR scanner and is translated into images. The more powerful the magnetic field the better images can be produced. The magnetic field in an MR scanner is continually present; to turn it off is associated with considerable “down” time and other potential hazards. The MR scanner is housed in a shielded room in a more isolated part of the hospital to prevent outside radiofrequencies from interfering with the MRI and to isolate the magnetic field. Surrounding the MR scanner is a so-called fringe field where the field strength gradually declines; concentric lines representing the declining field strength are often marked on the floor of the scanner room. For example, the 5G line marks the point beyond which pacemakers are considered safe and syringe pumps will operate up to the 30G line. Any objects containing iron will be attracted to the magnet, and anesthesia equipment such as oxygen tanks, IV poles, and laryngoscopes will become dangerous projectiles if brought within the vicinity of the magnet (within the 50G line). Fatalities have occurred; thus, access to the MR scanner is strictly controlled. Implanted medical devices are also a source of concern; cardiac pacemakers in particular can stop functioning in the presence of the magnetic field and implants such as aneurysm clips may be dislodged with disastrous consequences. All patients need to complete an exhaustive checklist questionnaire before they enter the scanner to make sure they have none of these devices in their bodies. Medical personnel need to be aware of these constraints for their own personal protection, and they must leave objects such as pagers, badges, and pens at the entry to the MR scanner. The MR scanner
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is a long, narrow cylinder and many patients experience claustrophobia or anxiety on being placed inside it; to compound this issue, the scans themselves often last for at least 45 minutes. Many adults and most young children require some form of sedation or even GA to tolerate the procedure and ensure immobility. If a patient moves during the scan, it will need to be repeated, wasting valuable scanning time in the busy MRI schedule, which in many units may run 24/7. Standard anesthesia machines and monitors cannot be used in the MR scanner, and a number of MRI-compatible machines are available with aluminum oxygen cylinders and MRI-compatible components. In addition, patient-monitoring devices, syringe pumps, and IV poles also need to be MR compatible. MRI-compatible monitors are for the most part as effective as the standard ones although the electrocardiogram (ECG) signal can be distorted and difficult to read in the magnetic field. To avoid the risks of bringing ferromagnetic objects such as laryngoscopes and other pieces of anesthesia equipment too close to the scanner, the standard procedure is for the anesthesia team to initiate sedation or induce anesthesia and secure the airway in a preparation area outside the MR scanner away from the fringe field. The patient is then transferred to an MR-compatible gurney, MR-compatible monitors are attached, and the patient is transported into the scanner and hooked up to the MR-compatible anesthesia machine. In planning the anesthetic technique, the anesthesia team must be aware that once started the MR imaging sequence takes several minutes to shut down. It is important that the airway is appropriately secured; in patients with more difficult airways, placing a definitive airway (such as an endotracheal tube or LMA™) at the beginning of the procedure will avoid the need to rescue the airway in challenging circumstances later on. Unlike other radiological imaging, MRI does not produce harmful radiation and is considered safe for patients and staff. Side effects do occur, however, including peripheral nerve stimulation resulting in tingling and discomfort, and even diaphragmatic stimulation. Patients and staff may experience vertigo, nausea, and a metallic taste in the mouth. There is currently some debate about whether safety
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standards need to be imposed. As the stronger 3T scanners become more widespread, this may become more of an issue. The noise generated by the MR scanner is another important consideration for both patients and staff. To protect against the noise, all patients are provided with earplugs. The anesthesia team must remember to insert these for the unconscious patient before he or she is transported into the scanner and remove them afterward. If the anesthesia team chooses to remain in the scanner with the patient (as may be the case for pediatric patients), they too need to wear earplugs. Another safety concern is the electrical current and heat that can be generated by the magnetic field. During scanning heat-generating electric currents may build up around loops of wire particularly those in the various patient monitors. Care should be taken with placement of the ECG electrodes and other wires to prevent the risk of tissue burns. Patients with large tattoos containing ferromagnetic inks may also be at risk of burns. Interventional Radiology Fluoroscopy is the mainstay of IR and in recent years the discipline has expanded rapidly. With great skill and expertise interventional radiologists can place microcatheters into most of the larger blood vessels in the body. This allows the injection of radio-opaque dye for diagnostic imaging and for a large number of therapeutic procedures that previously required invasive surgery or were simply not possible. These procedures include the following: • Revascularization of a blocked vessel, such as a carotid artery in a patient at risk of stroke • Insertion of a stent to maintain the patency of a previously blocked vessel • Embolization of a vessel or vascular malformation that is acutely bleeding or at risk of rupture such as a cerebral aneurysm • Embolization of a vessel that is feeding a malignant tumor prior to surgery to reduce bleeding The expertise of interventional radiologists is usually focused in one particular area of the body; for example, neuroradiologists work on the cerebral and spinal blood vessels and more general interventionalists work on major vessels in the abdomen, liver, kidney, and extremities.
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While the anatomy and pathology of the diseases treated by these various interventional radiologists differ widely, there are a number of commonalities in all IR procedures. Access to the patient’s arteries and/or veins is gained in most patients via the femoral vessels in the groin. In patients with disease of these vessels, other blood vessels may be accessed such as the subclavian artery or vein or internal jugular vein, although this is uncommon. Occasionally, a surgical cut-down is required to access the vessels. Access to the blood vessel is first gained using a small needle (in some cases, ultrasound guidance may be used) and once the needle is identified in the correct vessel, a thin flexible wire is inserted through it and the small needle is removed. With the wire resting in the target blood vessel, the radiologist dilates the opening to the vessel using a wide-bore sheath, usually 6 or 7 French gauge. This technique is known as the “Seldinger” technique after Dr. Sven-Ivar Seldinger, the radiologist who first developed it in 1953. The Seldinger technique is used widely throughout medicine as a safe way of accessing a blood vessel or other structure without having to use a large needle from the outset. Once the radiologist has accessed the blood vessel, he or she will advance a series of microcatheters into the blood vessel(s) of interest using fluoroscopy guidance. The radiologist will inject radio-opaque dye along the path of the blood vessels to make an image of these vessels. This image is then superimposed on the radiologist’s fluoroscopy screen to act as a “road map” for accessing the blood vessel(s) of interest. The patient is positioned on a moving x-ray table surrounded by the imaging equipment. The imaging equipment is static although it can rotate around various axes to provide different views of the patient. As the catheter is advanced from the groin to the vessels of interest, the table and the patient are moved so the progress of the microcatheter can be closely observed. As a result, the patient is frequently moved back and forth and to the side. The importance of closely watching the anesthesia circuits, monitoring equipment, and IV tubing so they are not dislodged cannot be overemphasized. In order to make sure the road map matches the path of the microcatheter, it is vital that the patient remains completely still and in most cases GA is preferred. In some cases, the movement of the patient’s chest may interfere
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with the procedure, and at certain stages of the procedure, the radiologist will ask the anesthesiologist to “hold the breathing” by turning off the ventilator for a short period. The positioning of monitors, especially ECG electrodes, must be carefully considered. If the ECG leads or electrodes overlie the area being imaged, they can produce radiological shadows and artifacts that interfere with the procedure. In neuroradiological procedures, the metallic spring in the cuff of the endotracheal tube may obscure the view of a cerebral vessel. Large amounts of the IV contrast dye may be used during an IR procedure. These compounds act as diuretics, making a Foley catheter a requirement for most of these procedures.
Interventional Cardiology The range of procedures and interventions performed by cardiologists is becoming increasingly complex and technically challenging and is being offered to increasingly sick patients. There are two main areas where interventional cardiology procedures are performed: the CCL and electrophysiology laboratory (EPL). While much of the work in these sites may be performed without sedation or using mild sedation undertaken by the CCL and EPL team, there is an increasing requirement for anesthesiology services to be involved. The general considerations related to providing anesthesia in an OOR location apply. Both the EPL and the CCL contain large amounts of technical monitoring and imaging equipment. Fluoroscopy is used for imaging the heart and the coronary blood vessels. In a similar manner to other IR procedures, the access point for the catheters is mostly the femoral vessels in the groin. If this access point is not available, the subclavian or internal jugular veins may be accessed. Cardiac Catheterization Laboratory Interventional procedures carried out by interventional cardiologists in the CCL include the following: • Percutaneous coronary interventions (PCIs) • Percutaneous insertion of ventricular assist devices (VADs) • Percutaneous closure of septal defects • Percutaneous heart valve repair and replacement
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Electrophysiology Laboratory The main procedures performed in the EPL are catheter ablations and insertion of implantable cardiac pacemakers. Cardiac ablation is an invasive procedure performed to remove an aberrant or faulty electrical pathway in patients with cardiac arrhythmias such as atrial fibrillation, atrial flutter, supraventricular tachycardias (SVT), and Wolff-Parkinson-White (WPW) syndrome. A flexible catheter is advanced from the femoral vein into the heart and high-frequency electrical impulses are used to induce the arrhythmia. Once the aberrant part of the cardiac conduction pathway is identified, it can be ablated. These procedures are extremely long, lasting on average 6-8 hours but have very high success rates. Apart from having to lie still for many hours, patients generally tolerate these procedures well with just mild sedation. Minimal sedation may be provided by the EPL team, although in certain circumstances the anesthesia team will need to be involved. This is usually in patients who have significant comorbidities such as congestive cardiac failure or airway concerns that exceed the limits of applicable sedation protocols followed by nurses and proceduralists. In some cases, cardiac arrhythmias induced during the procedure require cardioversion for termination; when this happens, sedation needs to be deepened so that the patient can tolerate the unpleasant sensation of receiving a direct current (DC) shock. The anesthesiology team needs to be aware of the progress of the procedure to be able to anticipate the need for changing the level of sedation; additionally they should avoid sympathomimetic drugs, which may interfere with mapping the aberrant cardiac foci. The technology related to cardiac pacemakers has seen much development in recent years. Implantable cardioverter-defibrillators (ICDs) are used increasingly to deliver immediate defibrillation in patients at risk for ventricular tachycardia (VT) or ventricular fibrillation (VF). Biventricular pacemakers are complex devices that attempt to mimic the normal cardiac contraction cycle to provide improved cardiac function. Pacemakers are increasingly being inserted into patients with multiple comorbidities and significant cardiac pathologies, including diminished ejection fraction (
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The Anesthesia Technician & Technologist’s Manual All You Need to Know for Study and Reference
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-V r i 9 . 9 & s r s i n h a i ta s r e p . p i v
Glenn Woodworth, MD
Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Shannon Sayers-Rana, BS, Cer AT Anesthesia Support Manager Oregon Health and Science University Past President, ASATT Portland, Oregon
Jeffrey R. Kirsch, MD Professor and Chair Department of Anesthesiology and Perioperative Medicine Associate Dean for Clinical and Veterans Affairs Oregon Health and Science University Portland, Oregon
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Acquisitions Editor: Brian Brown Product Manager: Tom Gibbons Vendor Manager: Bridgett Dougherty Senior Manufacturing Manager: Benjamin Rivera Marketing Manager: Lisa Lawrence Design Coordinator: Teresa Mallon Production Service: SPi Global © 2012 by LIPPINCOTT WILLIAMS & WILKINS, a WOLTERS KLUWER business Two Commerce Square 2001 Market Street Philadelphia, PA 19103 USA LWW.com All rights reserved. This book is protected by copyright. No part of this book may be reproduced in any form by any means, including photocopying, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. Printed in China
G R
-V r i 9 . 9 & s r s i n h a i ta s r e p . p i v
Library of Congress Cataloging-in-Publication Data The anesthesia technician and technologist’s manual : all you need to know for study and reference / [edited by] Glenn Woodworth, Jeffrey Kirsch. — 1st ed. p. ; cm. Includes bibliographical references and index. ISBN-13: 978-1-4511-4266-2 ISBN-10: 1-4511-4266-8 I. Woodworth, Glenn. II. Kirsch, Jeffrey, 1957[DNLM: 1. Anesthesia. 2. Allied Health Personnel—education. 3. Anesthesiology—methods. WO 18.2] 617.96—dc23 2011040962 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. Application of the information in a particular situation remains the professional responsibility of the practitioner. The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accordance with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new or infrequently employed drug. Some drugs and medical devices presented in the publication have Food and Drug Administration (FDA) clearance for limited use in restricted research settings. It is the responsibility of the health care provider to ascertain the FDA status of each drug or device planned for use in their clinical practice. To purchase additional copies of this book, call our customer service department at (800) 638-3030 or fax orders to (301) 223-2320. International customers should call (301) 223-2300. Visit Lippincott Williams & Wilkins on the Internet: at LWW.com. Lippincott Williams & Wilkins customer service representatives are available from 8:30 am to 6 pm, EST. 10 9 8 7 6 5 4 3 2 1
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Dedication Of course, as an editorial staff, we must dedicate this text to our loving families who put up with our countless hours hunched over our computers when we should have been eating dinner or relaxing at home. Without their love and support, we would have not had the will or energy to complete this text. Finally, we dedicate this text to the community of anesthesia technicians so that they will know of our commitment to their education and our appreciation for their expertise and the role they play in the care of our patients.
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Contributors Kenneth Abbey, MD, JD Clinical Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Mark J. Baskerville, MD, JD, MBA Critical Care Fellow Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Matthew Abrahams, MD Oregon Anesthesiology Group Portland, Oregon
Curtis Bergquist, AB Anesthesia Technician Oregon Health and Science University Portland, Oregon
Diane Alejandro-Harper, Cer AT Administrative Manager O.R. Anesthesia Stanford Hospital and Clinics Stanford, California Ahmed Alshaarawi, CRNA Instructor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Ryan B. Anderson, MD, PhD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Michael S. Axley, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Michael F. Aziz, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Mary A. Blanchette, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Richard Botney, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Valdez G. Bravo, BA Supervisor, Biomedical Engineering Portland VA Medical Center Portland, Oregon Guy Buckman, Cer ATT Certified Anesthesia Technician Portland VA Medical Center Portland, Oregon Mark D. Burno, MD Instructor Department of Anesthesiology Northwestern University Feinberg School of Medicine Chicago, Illinois
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Contributors
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Michelle Cameron, MD, PT Assistant Professor Department of Neurology Oregon Health and Science University Portland, Oregon
Arjun Desai, MD Chief Anesthesia Resident Department of Anesthesia Stanford University School of Medicine Stanford, California
Deborah Carter, RN, BSN Laser Safety Officer/Coordinator Department of Surgical Services Oregon Health and Science University Portland, Oregon
Richa Dhawan, MD Assistant Professor Department of Anesthesia and Critical Care University of Chicago Chicago, Illinois
Lisa Chan, MD Pediatric Anesthesia Fellow Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Dawn Dillman, MD Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Mark A. Chaney, MD Professor Department of Anesthesia and Critical Care University of Chicago Chicago, Illinois
Laura Downey, MD Chief Resident Department of Anesthesiology Stanford University Palo Alto, California
Matthew Chao-Ben Chia, BA Coordinator, Anesthesia Technicians Northwestern Memorial Hospital Chicago, Illinois
Brian N. Egan, MD Pediatric Fellow Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Sue Christian, Cer ATT Manager/Educator Department of Anesthesiology Vanderbilt University Medical Center Nashville, Tennessee Thomas W. Cutter, MD, MA Ed Professor and Associate Chairman Department of Anesthesia and Critical Care Pritzker School of Medicine University of Chicago Chicago, Illinois Shohreh Sadlou Daraee Operating Room Pharmacist Department of Pharmacy Oregon Health and Science University Portland, Oregon Asish Das, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
Dalia H. Elmofty, MD Assistant Professor Department of Anesthesia and Critical Care University of Chicago Chicago, Illinois Roy K. Esaki, MD, MS Resident Department of Anesthesiology Stanford University Stanford, California Josh Finkle Medical Student University of Illinois College of Medicine Chicago, Illinois Judith A. Freeman, MB, ChB Associate Professor of Anesthesia Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon tahir99-VRG & vip.persianss.ir
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Contributors
Ryan Goldsmith, MD Department of Anesthesia PGY-2 Resident University of Florida Gainesville, Florida Matthew J. Griffee, MD Assistant Professor Department of Anesthesiology University of Utah Health Care Salt Lake City, Utah Jared D. Grose, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Karen Hand, FRCA Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Casey A. Harper, BA Manager of Anesthesia Services Northwestern Memorial Hospital Chicago, Illinois Matthew Hart, MS, CRNA Chief CRNA Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Izumi Harukuni, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Michael T. Jamond, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Staff Anesthesiologist Portland VA Medical Center Portland, Oregon
Edward A. Kahl, MD Assistant Professor of Cardiac Anesthesia Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Markus Kaiser, MD Assistant Professor Department of Anesthesiology Medical College of Wisconsin Milwaukee, Wisconsin Angela Kendrick, MD Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Shaleha Khalique, BS, Cer AT Certified Anesthesia Technician New York Presbyterian Weill Cornell Medical Center New York, New York Vishal Khemlani, BS Oregon Health and Science University Portland, Oregon Tae W. Kim, MD Clinical Associate Department of Anesthesiology and Critical Care Johns Hopkins Medical Institutions Baltimore, Maryland Aaron Kirsch Medical Student Wayne State University School of Medicine Detroit, Michigan Jeffrey R. Kirsch, MD Professor and Chair Department of Anesthesiology and Perioperative Medicine Associate Dean for Clinical and Veterans Affairs Oregon Health and Science University Portland, Oregon Jodi Heather Kirsch, DC Chiropractic Physician National University of Health Sciences Lombard, Illinois tahir99-VRG & vip.persianss.ir
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Contributors
Pamela Kirwin, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Eve Klein, MD Anesthesia Fellow Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Ramon Larios, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Staff Anesthesiologist Portland VA Medical Center Portland, Oregon Dawn M. Larson, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Delbert K. Macanas Manager, Anesthesia Services Kuakini Medical Center Honolulu, Hawaii Alex Macario, MD, MBA Professor of Anesthesia Program Director, Anesthesia Residency Stanford University School of Medicine Stanford, California Jeffrey Mako, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Kim Mauer, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
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Terrence McGraw, MD, FAAP Associate Professor Department of Anesthesiology and Pediatrics Oregon Health and Science University Doernbecher Children’s Hospital Portland, Oregon Sameer Menda, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Brett Miller, MD Anesthesiology Resident Stanford University Stanford, California Brian Mitchell, MD Staff Anesthesiologist Portland VA Medical Center Portland, Oregon Jeffrey L. Moller, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon MicHael Moore, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Lori Nading, CRNA Instructor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon L. Michele Noles, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
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Contributors
Andrew Oken, MD Staff Anesthesiologist Portland VA Medical Center Portland, Oregon Amy J. Opilla, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Jorge Pineda, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Andrew J. Pittaway, BM, BS, FRCA Attending Anesthesiologist Seattle Children’s Hospital Seattle, Washington Donald S. Prough, MD Professor and Chair Department of Anesthesiology University of Texas Medical Branch Professor and Chair Department of Anesthesiology John Sealy Hospital Galveston, Texas Brenda A. Quint-Gaebel, RHIT, MPA-HA Quality Program Manager Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Bryan J. Read, CRNA Instructor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Victoria Reyes Assistant Director Kaiser Permanente Anesthesia Technology Program Kaiser School of Anesthesia Pasadena, California
Scott W. Richins, MD Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Berklee Robins, MD Assistant Professor of Anesthesia and Pediatrics Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Danny L. Robinson, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Stephen T. Robinson, MD Clinical Professor and Vice-Chair for Clinical Anesthesia Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Henry Rosenberg, MD, CPE Director of Medical Education and Clinical Research Chief Medical Information Officer Saint Barnabas Medical Center Livingston, New Jersey Adjunct Professor of Anesthesiology Columbia University School of Medicine New York, New York Shannon Sayers-Rana, BS, Cer AT Anesthesia Support Manager Oregon Health and Science University Past President, ASATT Portland, Oregon Katie J. Schenning, MD, MPH Anesthesiology Resident Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
tahir99-VRG & vip.persianss.ir
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Contributors
Eric Schnell, MD, PhD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Staff Anesthesiologist Portland VA Medical Center Portland, Oregon Peter Schulman, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Valerie Sera, MD Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon Sarah M. Shabot, MD Assistant Professor Department of Anesthesiology University of Texas Medical Branch Galveston, Texas David M. Sibell, MD Associate Professor Comprehensive Pain Center Oregon Health and Science University Portland, Oregon Wesley Simpson II, BCTS, Cer ATT Clinical Education Specialist Deltex Medical Group, SC San Diego, California Corey Sippel, BS Lead Anesthesia Technician Oregon Health and Science University Portland, Oregon Karen J. Souter, MB, BS, FRCA Associate Professor, Vice Chair for Education, and Residency Program Director Department of Anesthesiology and Pain Medicine University of Washington Seattle, Washington
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M. Christine Stock, MD, FCCP, FCCM James E. Eckenhoff Professor and Chair Department of Anesthesiology Northwestern University Feinberg School of Medicine Chicago, Illinois Anita Stoltenberg, RRT Supervisor of CV Surgical and ICU Respiratory Therapy Mayo Clinic Rochester, Minnesota Esther Sung, MD Staff Anesthesiologist Portland VA Medical Center Portland, Oregon Pedro Paulo Tanaka, MD, PhD Clinical Associate Professor Department of Anesthesia Stanford University School of Medicine Stanford, California Heather Taylor, MD Anesthesiologist Department of Anesthesiology Banner Estrella Medical Center Phoenix, Arizona Norman E. Torres, MD Assistant Professor and Consultant Department of Anesthesia Mayo Clinic St. Mary’s Hospital Rochester, Minnesota Charles A. Vacanti, MD Professor of Anaesthesia Harvard Medical School Chair, Department of Anesthesiology Brigham and Women’s Hospital Boston, Massachusetts Kamila Vagnerova, MD Assistant Professor of Anesthesiology Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
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xii
Contributors
David C. Warltier, MD, PhD John P. Kampine Professor and Chairman Department of Anesthesiology Medical College of Wisconsin Milwaukee, Wisconsin Mary Ellen Warner, MD Associate Professor Department of Anesthesiology Mayo Clinic Rochester, Minnesota
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David Wilson Glenn Woodworth, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University Portland, Oregon
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Acknowledgments
W
e extend our thanks to the many authors who contributed their time and effort to the creation of this text. Although many have written extensively on their respective topics, they enthusiastically embraced the challenge of reworking the material to better serve the
needs of anesthesia technicians. Thanks to Matt Schreiner for his tireless efforts to coordinate our authors and the many tasks associated with bringing a textbook with 65 chapters together. Special thanks to Claudia Woodworth for her monumental editorial efforts.
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Preface
T
he role of the anesthesia technician in the perioperative environment has been expanding to keep pace with the rapid innovations in anesthesiology and surgery. As the responsibilities and complexity of the job have increased, so has the visibility of the role of anesthesia technician within hospitals and other health care institutions. Much like other health care roles, the increased responsibilities and complexity of job requirements have put the role of anesthesia technician on the path of becoming a more widely recognized allied health profession. Associated with this is an increased requirement for education and training ranging from equipment maintenance to medication handling. More and more institutions are scrutinizing the education and training of anesthesia technicians, with some going so far as to require certification as a job requirement. The goal of this text was to fill a critical gap in the material available to support the education and training of anesthesia technicians and technologists. Currently, there is no single text directed specifically at this group of allied health professionals. Community college course students or individuals studying for a certification exam must often utilize textbooks directed at anesthesiologists. Although the material is similar, the focus of these texts is not directed at an anesthesia technician audience. The Anesthesia Technician and Technologist’s Manual is specifically directed at this audience and their background education. Section I provides an overview of the profession, while Section II covers basic anatomy
and physiology with an emphasis on highlighting the principles upon which anesthesia equipment or procedures are based. Section III covers the basic activities of anesthesia to give the technician a solid foundation for understanding the different aspects of performing an anesthetic including airway management, sedation, general anesthesia, regional anesthesia, fluid therapy, and patient positioning. Section IV is the bulk of the text and covers a wide variety of anesthesia equipment and procedures from anesthesia machines and vascular access, to neuromuscular monitoring and ventricular assist devices. This section places a heavy emphasis on anesthesia equipment setup, operation and maintenance— a priority for anesthesia technicians. This section will help anesthesia technicians understand why a procedure is performed, what equipment might be needed and why, as well as how to set up and troubleshoot the equipment. Section IV introduces the anesthesia technician to the operating room and hospital environment covering topics from fire safety to the special needs of performing anesthesia out of the operating room. The final section, Section V, covers several anesthesia emergencies with the goal of familiarizing the anesthesia technician with what is going on, what the priorities are during the crisis, and what equipment or other activities the anesthesia technician should be prepared for. It is our sincere hope that current and future anesthesia technicians and technologists will think of The Anesthesia Technician and Technologist’s Manual as the core resource text for this exciting and growing health care profession.
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Foreword
A
s anesthesiologists, we realize that the safety of the patient and the outcomes of procedures require the coordinated efforts of many individuals. Anesthesiologists need the cooperation of the surgical and nursing personnel to do their jobs and work with us. However, we absolutely depend on anesthesia technicians to skillfully provide the tools we need and the expertise and support we must have to perform our jobs successfully. This book is dedicated to supporting the continuing education of our friends and colleagues, the anesthesia technicians. It will provide the support they need while attending a formal anesthesia technician educational program, studying for certification, or for simply advancing their knowledge to help them better perform their duties. One of the challenges for any textbook is to stay current with the rapid introduction of new information. Of course the pace of the introduction of new equipment and technologies into
the operating room environment is ever accelerating. Because a large portion of this text deals with equipment issues, it will require frequent updates and constant vigilance for developments in our field to maintain its relevancy to anesthesia practice. True to the educational mission of the text, all royalties from the sale of this book are designated to be donated to the Foundation for Anesthesia Education and Research. We hope this book is helpful to all individuals interested in caring for perioperative patients and that it improves the care of our patients. Jeanine Wiener-Kronish, MD Anesthetist-in-Chief Massachusetts General Hospital Henry Isaiah Dorr Professor of Research and Teaching in Anaesthetics and Anaesthesia Harvard Medical School Boston, Massachusetts
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Contents Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vi Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xiv Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xv
SECTION
I
Careers in Anesthesia Technology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 1
The Anesthesia Technician and Technologist Shannon Sayers-Rana and Delbert Macanas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
2
Certification for Anesthesia Technicians and Technologists Sue Christian . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
3
The Surgical Experience Shannon Sayers-Rana and Shaleha Khalique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
SECTION
II
Anatomy, Physiology, and Pharmacology . . . . . . . . . . . . . . . . . . . . 15 4
Pharmacokinetics David Sibell and Ryan Anderson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16
5
Pharmacodynamics Pamela Kirwin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22
6
Efficacy, Toxicity, and Drug Interactions Amy Opilla and Kim Mauer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
7
Cardiovascular Anatomy and Physiology Glenn Woodworth, Asish Das, and Valerie Sera . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
8
Cardiovascular Pharmacology Markus Kaiser and David C. Warltier. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58
9
Cardiovascular Monitoring Richa Dhawan and Mark Chaney. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
10
Mechanical Cardiovascular Support Richa Dhawan and Mark Chaney. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74
11
The Respiratory System Mark Burno, Casey A. Harper, Matthew Chao-Ben Chia, and M. Christine Stock . . . . . . . . . . 79
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xvii
Acid and Base Physiology Aaron Kirsch and Jeffrey Kirsch . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101
13
Central Nervous System Josh Finkle and Jeffrey Kirsch . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
14
Autonomic Nervous System Lori Nading and Ahmed Alshaarawi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121
15
Peripheral Nervous System Eve Klein and Michelle Cameron . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
16
Neuromuscular Anatomy and Physiology Jodi H. Kirsch and Jeffrey Kirsch . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138
SECTION
III
Principles of Anesthesia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147 17
Sedation Angela Kendrick and Dawn M. Larson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
18
Principles of Airway Management Michael Aziz . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155
19
Patient Positioning: Common Pitfalls, Neuropathies, and Other Problems Mary Ellen Warner . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165
20
Overview of a General Anesthetic Dalia Elmofty and Thomas Cutter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175
21
Regional Anesthesia for Anesthesia Technicians Michael S. Axley . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190
22
Fluid Therapy Sarah Shabot and Donald Prough . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204
23
Transfusion Medicine Curtis Bergquist and Kamila Vagnerova . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210
SECTION
IV
Equipment Setup, Operation, and Maintenance . . . . . . . . . . . . . . 219 24
Infectious Disease Brett Miller. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220
25
Equipment Contamination and Sanitation and Waste Disposal Katie Schenning and Stephen Robinson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225
26
Overview of Anesthesia Machines Brian Mitchell and Michael Jamond. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
27
Anesthesia Machine Checkout Ramon Larios and Esther Sung . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240
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Contents
Vaporizers Roy Esaki and Alex Macario . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247
29
Anesthesia Breathing Systems Charles A. Vacanti . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255
30
Anesthesia Machine Ventilators Eric Schnell and Valdez Bravo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261
31
Anesthesia Machine Operation, Maintenance, and Troubleshooting Andrew Oken and Scott Richins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 270
32
Gas Analyzers Wesley Simpson II . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
33
Basic Monitoring Wesley Simpson II . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 286
34
Vascular Access Equipment and Setup MicHael Moore and Izumi Harukuni . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297
35
Airway Equipment Setup, Operation, and Maintenance Norman E. Torres, Anita Stoltenberg, and Glenn Woodworth . . . . . . . . . . . . . . . . . . . . . . . . 330
36
Infusion Pumps Victoria Reyes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 356
37
Blood Gas Analyzers and Point-of-Care Testing David Wilson and Guy Buckman . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363
38
Ultrasound Matthew Abrahams and Jorge Pineda . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 372
39
Transesophageal Echo Edward A. Kahl and Lisa Chan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391
40
Neuromuscular Blockade Assessment Ryan Goldsmith . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 398
41
Neurophysiologic Monitoring Judith A. Freeman . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403
42
Intra-aortic Balloon Pumps and Ventricular Assist Devices Laura Downey . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411
43
Defibrillators Matthew Griffee and Jeffrey Moller . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 426
44
Pacemakers and Implantable Defibrillators Jeffrey Mako and Peter Schulman . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 434
45
Device Malfunction Pedro Tanaka, Diane Alejandro-Harper, and Arjun Desai . . . . . . . . . . . . . . . . . . . . . . . . . . . . 442
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SECTION
xix
V
Operating Room and Hospital Environment . . . . . . . . . . . . . . . . . 447 46
Pediatric Anesthesiology Brian N. Egan, Terrence McGraw, and Danny L. Robinson . . . . . . . . . . . . . . . . . . . . . . . . . . . 448
47
Obstetric Anesthesia Karen Hand . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 456
48
Anesthesia Considerations for out of Operating Room (OOR) Locations Andrew J. Pittaway and Karen J. Souter. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468
49
Medication Handling Shohreh Sadlou and Corey Sippel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483
50
Patient Transport Matthew Hart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 489
51
Electrical Safety Richard Botney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 495
52
Fire Safety Richard Botney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 502
53
Laser Safety Sameer Menda, Berklee Robins, Deborah Carter, and Vishal Khemlani . . . . . . . . . . . . . . . . . 509
54
Electronic Medical Records Heather Taylor and David Sibell . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 515
55
Legal Aspects of the Operating Room Mark J. Baskerville and Kenneth Abbey . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 520
56
Continuous Quality Improvement and Risk Management Brenda Quint-Gaebel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 523
57
Accreditation Shannon Sayers-Rana . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 528
58
Simulation-based Training Bryan J. Read and Michele Noles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 532
59
BLS and ACLS Certification Glenn Woodworth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 537
SECTION
VI
Operating Room Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 543 60
Airway Emergencies Dawn Dillman . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 544
61
Cardiac Arrest Glenn Woodworth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 554
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62
Contents
Fire in the Operating Room Richard Botney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 559
63
Malignant Hyperthermia Tae W. Kim and Henry Rosenberg . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 566
64
Anaphylaxis Mary Blanchette . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 575
65
Massive Hemorrhage Jared Grose and Ryan Anderson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 581
Acronyms and Abbreviations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 587 Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 591
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SECTION
I
Careers in Anesthesia Technology
1
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CHAPTER
1
The Anesthesia Technician and Technologist Shannon Sayers-Rana and Delbert Macanas ■ INTRODUCTION What exactly is an anesthesia technician (AT) or anesthesia technologist? This role was first developed in hospitals as the complexity of anesthesia increased and the anesthesia care team required more assistance in and out of the operating room. The first ATs became responsible for the anesthesia equipment and medication cart, stocking supplies, and running small errands for the anesthesia team. Over time, the role has evolved into becoming a significant, integral part of the anesthesia care team with numerous clinical responsibilities. These responsibilities typically include maintaining the anesthesia machine, assisting with vascular access and regional anesthesia procedures, assisting with difficult airways, troubleshooting anesthesia equipment, assisting with resuscitations and other operating room emergencies, and running point-of-care lab tests. In some institutions, ATs operate sophisticated blood collection equipment or even intraaortic balloon pumps to support patients with severe congestive heart failure. The American Society of Anesthesia Technicians and Technologists (ASATT) has a recommended scope of practice for these roles, which are outlined below, but each institution will have its own unique job description and preemployment requirements. What are the qualities of an AT? An AT must possess detailed knowledge of anesthesia procedures; must have solid technical skills to be able to operate numerous electronic devices and equipment; must have good communication skills to interact with anesthesia staff and patients; must be able to think on his or her feet while working in stressful situations; and must be able to work well in a team environment.
■ ANESTHESIA TECHNICIANS AND TECHNOLOGISTS: SCOPE OF PRACTICE The ASATT’s recommended scope of practice details the duties at three levels of practice: the AT, the certified anesthesia technician (Cer.A.T.), and the certified anesthesia technologist (Cer.A.T.T.). As stated on ASATT’s Web site, “Their role is to assist licensed anesthesia providers in the acquisition, preparation and application of the equipment and supplies required for the administration of anesthesia.” Outlined below are the common duties and responsibilities for each position as well as their educational requirements. However, as stated above, job duties may differ depending upon where the AT works. AT Responsibilities • Providing support for routine surgical cases by assisting in the preparation and maintenance of patient equipment and anesthesia delivery systems before, during, and after anesthesia • Assisting the licensed anesthesia providers in various settings • Performing duties under the direct supervision of a licensed anesthesia provider and/or registered nurse (RN) • Performing first-level maintenance on anesthesia equipment, cleaning, sterilizing, disinfecting, stocking, ordering, and maintaining routine anesthesia equipment and supplies AT Education • A high school diploma or 2-year degree and previous work experience are preferred for entry-level employment.
2
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Chapter 1 • The Anesthesia Technician and Technologist
An AT should also show proficiency in basic life support, physiologic monitors relating to the administration of anesthesia, handling of biologic hazards, infection control practices, and safe use and handling of anesthetic gases. The AT should also be aware of the indications for local, regional, and general anesthesia. Cer.A.T. Responsibilities • All of the above for the AT as well as the items listed below • Demonstrate practical knowledge and expertise in all areas of anesthesia with a thorough experience of the setup, operation, and troubleshooting of anesthesia equipment and devices • Knowledge of institutional guidelines, policies, and safety requirements • Understanding of anatomy and physiology as it applies to anesthesia • Administrative duties that include scheduling, evaluations, payroll, job descriptions, etc. • Assisting the licensed anesthesia provider with patient assessments, evaluations, transport, positioning, insertion of intravenous and other invasive lines, as well as airway management and regional anesthesia procedures Cer.A.T. Education • Successful completion of the ASATT certification exam. (To qualify for the exam, you must have a high school diploma or greater, a minimum of 2 years of AT experience, or graduation from an approved AT program.) A Cer.A.T. will show the same proficiencies as an AT, in addition to demonstrating the ability to perform technical duties in complex clinical situations, coordinating daily routines of the AT staff, delegating responsibilities, understanding the expenses incurred for anesthesia procedures, participating in quality improvement, as well as ensuring a safe environment for patient care. Cer.A.T.T. Responsibilities • All of the above duties for the Cer.A.T. in addition to the items listed below • Assisting the anesthesia provider with intraoperative fluid management including volume resuscitation • Operating autotransfusion equipment • Maintaining current basic cardiac life support (BCLS) and/or advanced cardiac life support
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(ACLS) certification and maintaining current pediatric advanced life support (PALS) certification if required • Performing inspection and maintenance of the anesthesia gas delivery systems • Setting up and troubleshooting the intraaortic balloon pump • Providing point-of-care laboratory services, following all regulatory guidelines Cer.A.T.T. Education • Currently, the role of the Cer.A.T.T. is distinguished from that of the Cer.A.T. by additional levels of training and education. Successful completion of the technologist exam is required to be designated as a Cer.A.T.T.
■ OTHER ROLES WITHIN THE ANESTHESIA CARE TEAM There can be confusion as to the different nonphysician roles within the anesthesia care team. The two more commonly recognized positions include the anesthesia assistant (AA) and the certified registered nurse anesthetist (CRNA). The AA has completed an advanced degree, specializing in anesthesia. He or she is able to practice anesthesia under the direction of an anesthesiologist. There are currently six schools offering anesthesia assistant programs throughout the United States, with AAs currently practicing in 18 states (and growing). The CRNA is an RN with advanced practice training and a degree from a nurse anesthetist program. CRNAs may practice anesthesia independently in some states. Others require that they practice under the supervision of an anesthesiologist, but not necessarily an anesthesiologist. Individual institutions will further define the local scope of practice through their governing boards and credentialing committees. As of April 2011, there were 111 nurse anesthesia training programs in the United States. To gain additional detailed information about becoming an AT, a Cer.A.T., or a Cer.A.T.T., visit the ASATT Web site at www.asatt.org. To gain further knowledge about the position of AA or CRNA, visit the Web sites at www.anesthesiaassistant.com and www.aana.com, respectively.
■ SUMMARY The operating room is an exciting environment. Incredible advances in the surgical treatment
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Section I • Careers in Anesthesia Technology
of patients are being constantly introduced as new technology or techniques become available. Recent advances include robotic surgery, magnetic resonance image–guided neurosurgical procedures, and ultrasound-guided nerve blocks. The introduction of new technology, the complexity of these procedures, and the medical condition of the patients who receive them have increased the complexity of working in the operating room. Nowhere is this more true than providing anesthesia during these procedures. The anesthesia team is responsible for providing safe operating conditions, preventing awareness, controlling pain, and keeping a patient immobile, all the while monitoring multiple physiologic parameters (e.g., blood pressure, inhaled gas concentration, cardiac rhythm, blood oxygen saturation, exhaled carbon dioxide levels, urine output and renal function, and blood glucose and electrolyte levels). The anesthesia technicians/technologists play a critical role on the anesthesia team. They are responsible for the setup, operation, and maintenance of
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the majority of the equipment that the anesthesia team of today and the future will use to care for the patient. The AT must be capable of troubleshooting equipment on the fly, assisting with complex procedures, transporting patients, and assisting with monitoring physiologic parameters. In addition to on-the-job training, there are several educational programs to help prospective ATs obtain the necessary skills and knowledge to enter this field. This text was designed to serve as the go-to source for current and prospective ATs, covering everything from relevant anatomy, physiology, and pharmacology, equipment setup/ operation/maintenance, anesthesia machine function and checkout, procedures for obtaining vascular access, and infection control to operating room emergencies.
SUGGESTED READINGS AA. Retrieved from www.anesthesiaassistant.com. AANA. Retrieved from www.aana.com. ASATT. Retrieved from www.asatt.org.
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CHAPTER
2
Certification for Anesthesia Technicians and Technologists Sue Christian ■ INTRODUCTION The first recorded use of anesthesia support personnel occurred during the late 1930s in England. History of the specialty shows that Sir Robert Macintosh solicited the services of Richard Salt to take care of the equipment and facilitate the administration of anesthesia (McMahon & Thompson, 1987). Since that time, the administration of anesthesia has been supported by dedicated ancillary staff to address the maintenance and operation of equipment and supplies needed to administer a safe anesthetic. Over the years, the number and complexity of surgical interventions have grown. Along with the growth have come significant advances in instrumentation and technology. This has increased the complexity of administering modern anesthetics and increased the demand for qualified support personnel. During the majority of this period, anesthesia technicians lacked a formalized training program and were trained “on the job” (on-thejob training [OJT]).
■ BACKGROUND The American Society of Anesthesia Technologists and Technicians (ASATT) is a nonprofit organization whose primary focus is the education of anesthesia technologists and technicians. The organization was officially founded in October 1989 when a core group of technicians met in New Orleans, Louisiana. Due to the overwhelming need for a formalized training program, the charter leadership was determined to legitimize the profession as well as provide educational support for the professionals practicing in this area. Realizing that they would need the support of the anesthesia providers to succeed, the timing and location for this historical meeting were
fixed in conjunction with the annual meeting of the American Society of Anesthesiologists (ASA). As interest in the ASATT grew and a formalized training program was adopted, it was realized that to gain formal recognition of the importance of anesthesia support personnel, a process would need to be implemented demonstrating these individuals possessed the knowledge and qualifications to be employed as anesthesia technicians. In 1993, ASATT began laying the foundation for the development of a national certification examination. The entire process took 2 years to complete, and in May 1996, ASATT administered its very first written certification examination for anesthesia technicians. Due to the popularity of the certification exam, ASATT members expressed interest in an advanced level of certification, and in 2001, the first technologist-level exam was administered. After several years, interest waned and the exam was put on hiatus. However, as certification became more widely accepted, the technologist exam was reactivated in 2006 due to expressed interest from both technicians and employers. As a condition of employment, the demand for certification has increased, as has the number of individuals seeking certification and taking the exam. To meet this increased demand, the ASATT began to administer the exam via computer in 2003, making it accessible year round. Due to expanded interest on the international level, ASATT began to offer a Web-based exam to those candidates in 2006. ASATT has the only nationally recognized certifications for both anesthesia technologists and technicians. The technologist and technician certifications are endorsed by the ASA and the American Association of Nurse Anesthetists (AANA). 5
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Section I • Careers in Anesthesia Technology
■ CERTIFICATION PROCESS A Certification Test Development and Test Writing Committee evaluates and develops the ASATT certification standards and exam in conjunction with Applied Measurement Professionals (AMP), an organization that develops and administers certification exams. Test development is written in accordance with the standards set forth by the National Organization for Competency Assurance (NOCA), an organization dedicated to providing educational, networking, and advocacy resources for the credentialing community. The Certification Test Development and Test Writing Committee consists of the following: • Anesthesiologists • Certified registered nurse anesthetists (CRNAs) • Certified anesthesia technologists (Cer.A.T.T.s) and certified anesthesia technicians (Cer.A.T.s) • Corporate representatives • A professor of anesthesia education • A member of the professional development company (AMP) Test items are written in accordance with a detailed content outline that is specific to each level of certification. Topics include, but are not limited to, operating room (OR) environment, infection control, types of anesthesia, anesthesia machine and gas delivery, anatomy, monitors and ancillary devices, and intraoperative complications. The test items are taken directly from the suggested study reference books.
■ CERTIFIED TECHNICIAN EXAM The current qualifications to take the technician exam are as follows: the candidate must (1) be actively working as an anesthesia technician with a minimum of 2 years of clinical experience and (2) be proficient in English and possess a high school diploma or equivalent. Interested applicants must complete the registration form, submit a copy of their high school diploma, submit a letter from their employer detailing their work experience, and pay the required fees. Once the application is processed, applicants are notified via e-mail when they may register to take the examination. The applicant will then have 90 days to register for the examination. Candidates who do not register within that time limit will forfeit all fees and have to restart the process.
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The exam consists of 120 questions pulled from a bank of 1,575 questions ensuring that the same exam is not given twice. The candidate is then given 3 hours to complete the test. Candidates are only scored on 100 questions, with the remaining 20 anonymous questions being used for research purposes. These 20 questions are predetermined prior to the candidate taking the exam. Once the candidates have completed the test, they will receive a printout of their score. Candidates will not be given the questions or the answers to the test items that were incorrectly answered. The certification must be renewed every 2 years to the ASATT Certification/Recertification Review Committee. At the end of each two full calendar year period, Cer.A.T.smust show that they have 20 continuing education hours (CEHs) relevant to their level of certification. • Example: You passed the exam in January 2011. Your certification will expire on December 31, 2013 (certification is granted for 2 full years beginning with the year following the year in which the applicant meets all certification requirements). • 20 CEHs must be earned between January 1, 2012, and December 31, 2013. • CEHs’ content must be relevant to the Cer.A.T.
■ CERTIFIED TECHNOLOGIST EXAM Currently, to be eligible for this examination, the candidate must be a certified technician in good standing. The test consists of 125 questions that are randomly drawn from a bank of 700. The candidate is given 3 hours to complete the exam and is scored on all 125 questions. The technologist exam is significantly more difficult than the technician exam. Certification for the technologist is also granted for a 2-year period. In order to maintain certification, a minimum of 30 CEHs must be submitted to the ASATT Certification/ Recertification Review Committee. At the end of each 2-year period, Cer.A.T.T.s must reapply for certification. • Example: You passed the exam in January 2010. Your certification will expire in December 2012. (Certification is granted for two full years beginning with the year following the year in which the applicant meets all certification requirements).
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Chapter 2 • Certification for Anesthesia Technicians and Technologists
• CEHs must be earned between the period of January 1, 2011, through December 31, 2012. • CEHs must come from this 2-year period, and the content must be relevant to the Cer.A.T.T. Since the candidate took the exam earlier in the year, he or she has a longer grace period in which to earn CEHs compared to a candidate who passed the certification exam in November of 2010 because the 2-year certification period begins with the year following the year in which the applicant meets all certification requirements. Both candidates’ certification will expire on December 31, 2012.
■ EDUCATIONAL PROGRAMS In April 2010, the Commission on Accreditation of Allied Health Education Programs (CAAHEP) approved anesthesia technology as an official health science discipline. Schools that offer an associate’s degree in anesthesia technology must become accredited through ASATT and CAAHEP in order for their graduates to be eligible for the certification exam. As an official health science discipline, OJT will be phased out as college graduates enter the workforce. The ASATT has tentatively set a timeline of July 2015 to phase out the certified technician exam. The technologist exam will be the only exam offered after that date. To qualify for the exam, you will need to be a graduate from a CAAHEP-accredited program. While the certified technician designation will continue to be recognized by the society, it will be imperative that these individuals keep their certification status in good standing.
■ CERTIFICATION BENEFITS In the past 7 years, there has been a steady increase of employers requiring certification as a condition of employment. Salaries may be based on whether the technician holds certification for the technician or technologist level. While some employers do not mandate certification as a condition of employment, most have initiated a requirement for certification within a designated time period from the date of hire. In addition, many employers have developed a clinical ladder for advancement based on certification. There is also an added incentive for employers to hire and maintain certified technologists and technicians. These individuals are staying abreast on the latest technology employed in the OR environment and actively participate in
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quality assurance for the monitoring devices in use. This enables the anesthesia department to remain compliant with local and state regulations as well as the Joint Commission (formerly the Joint Commission on Accreditation of Healthcare Organizations) and College of American Pathologists (CAP) accreditation. Certified technologists and technicians are skilled individuals who assist the anesthesia provider in line placement, difficult intubations, and patient monitoring, thus improving patient safety. They reduce operating costs and facilitate room turnovers by properly ensuring that all needed equipment and necessary supplies are readily available. The acronym for ASATT, “Assisting with Safe Anesthesia Today and Tomorrow,” guarantees that these qualified individuals are readily available to assist in both emergent and nonemergent patient situations.
■ SUMMARY The majority of anesthesia technologists and technicians in practice today were trained on the job. Looking at the history of the profession, the complexity of the surgical procedures, the medical acuity of patients, and the advancement in technology, no one can argue that the job has evolved in the last 20 years. Taking these factors into account, many institutions are beginning to question if OJT is feasible in this day and age. Employers are seeking qualified anesthesia technicians, and the demand is currently greater than the supply. This may be attributed to the 2006 recognition from the Association of Operating Room Nurses (AORN) when it included anesthesia technologists and technicians in its position statement on allied health care providers and support personnel in the perioperative practice setting. Several Cer.A.T.T.s and Cer.A.T.s have also been asked to sit on a variety of committees for the Anesthesia Safety Patient Foundation (ASPF). CAAHEP accreditation not only provides opportunities for the profession to excel but also enables the employer to hire qualified individuals as anesthesia technicians, thereby phasing out the costly and time-consuming responsibility of OJT. The society’s original goal was to see certification to fruition. By all indications, this health science discipline will be one of the fastest growing disciplines the medical profession has experienced in the last decade.
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Section I • Careers in Anesthesia Technology
REVIEW QUESTIONS 1. The ASATT was established in this year: A) 1986 B) 1989 C) 1996 D) 2001 E) None of the above Answer: B. ASATT was established in New Orleans, LA, in 1989.
2. The first recorded use of anesthesia support personnel occurred in A) England B) Australia C) Louisiana D) China E) California Answer: A. The first recorded use of anesthesia support personnel occurred in England in the late 1930s.
3. ASATT issued its very first written certification exam for the technician in A) 1889 B) 1993 C) 1996 D) 2001 E) 2010 Answer: C. ASATT offered the first written exam for anesthesia technicians in 1996.
4. The certification exam is administered in accordance with standards developed by A) ASA B) AANA C) APSF D) NOCA E) JCAHO Answer: D. NOCA developed the standards on which the certification exams are administered.
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5. Certification for both the technologist and technician exams is granted on a A) Four-year basis B) Rotation of every other year C) Two-year basis D) Yearly basis E) None of the above Answer: C. Both the technician and the technologist must recertify every 2 years after completing the required number of CEHs for their discipline.
6. The test writing committee is composed of A) Anesthesiologists B) CRNAs C) Corporate representatives D) Anesthesia technicians and technologists E) All of the above Answer: E. The test writing committee consists of anesthesiologists, CRNAs, corporate representatives, anesthesia technicians and technologists, educators, along with a representative from the test writing development company.
7. A certified anesthesia technician must show proof of this number of CEHs in a 2-year period: A) 30 B) 20 C) 120 D) 125 E) 10 Answer: B. The anesthesia technician must show proof of 20 CEHs every 2 years as part of the recertification process. The anesthesia technologist must have 30 CEHs in the same time period.
SUGGESTED READING McMahon DJ, Thompson GE. A survey of anesthesia support personnel in teaching programs. Med Instrum. 1987;21(5):269–274.
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CHAPTER
3
The Surgical Experience Shannon Sayers-Rana and Shaleha Khalique ■ INTRODUCTION In order to better understand the role of the anesthesia technician (AT) as a member of the anesthesia team and the flow of patients through the operating room (OR), it is useful to understand the overall surgical experience. This chapter provides a description of the different phases of care a patient may experience while undergoing a surgical procedure. This will serve as an excellent introduction to the perioperative environment.
■ THE SURGEON’S OFFICE OR CLINIC Mr. Smith has been experiencing abdominal pain for several months. He finally went to his primary care physician. After an examination and preliminary testing, his doctor told him that he had a mass near his pancreas and that surgery would be necessary to remove it and to make a definitive diagnosis. Diagnosis is the identification of a specific disease or an illness gleaned from a history of signs and symptoms, a physical exam, and testing. A surgery patient is usually diagnosed prior to coming to the OR unless it is an emergency or the surgery itself is necessary to make the diagnosis. Once the decision to proceed with surgery has been made, Mr. Smith will consult with the surgeon’s office staff to schedule the surgery. The timing will depend upon the following: • The surgeon’s schedule • The urgency of the procedure • Availability of surgical facilities for which the surgeon has privileges and are appropriate for the planned procedure; that is, an outpatient procedure would not be appropriate for heart surgery. • The patient’s insurance coverage: The insurance may only cover certain facilities or the cost to the patient may differ depending upon which facility is chosen.
• The schedule of the patient and any caregivers who might be involved in the postoperative care of the patient. Prior to surgery, a patient may go through additional testing or consultations to make sure that the medical condition is optimized, as much as time permits, prior to surgery. Standard preoperative (preop) testing may include an electrocardiogram (ECG), lab work, blood pressure, x-ray, urinalysis, etc. The type of testing will depend upon the patient’s medical condition and the scheduled surgery. For many healthy patients, pre-op testing may not be necessary.
■ PREADMISSION: PRE-OP VISIT Preadmission is the period of time prior to admission to the surgical facility. If the procedure will not take place for several days, the patient may be asked to return to the surgeon’s office for a pre-op visit; otherwise, the pre-op instructions will be given during the current visit. At this time, the surgeon will update the history and physical, provide instructions to the patient, and make sure that the patient understands the risks and benefits of the procedure he or she is about to undergo. Most institutions require that a history and physical be performed within the 30 days prior to a surgical procedure. All necessary documentation, such as the consent form and any legal forms, can also be completed at this time. Patients receive pertinent information regarding what needs to be brought with them the day of the surgery, what to avoid (i.e., not have anything to eat or drink 8 hours prior to surgery), what to expect after surgery, whether or not medications should be continued, and also when they should plan on arriving at the hospital or outpatient surgical facility. The patient will often be given prescriptions for medications to be
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Section I • Careers in Anesthesia Technology
taken during the postoperative period and care instructions for the period following the procedure. The vast majority of surgical procedures today are performed on an outpatient basis, and all of the above information is essential to help the patient be prepared for the surgery and the postsurgical period. On rare occasions, an anesthesia consultation may be requested by the surgeon. These are reserved for patients with severe medical conditions or special considerations that affect anesthesia. For example, the patient may have a family history of a rare, but lethal, reaction to a certain anesthetic.
■ ADMISSION Mr. Smith arrives at 5:00 in the morning at Sunnyside Hospital. He proceeds through the admission process where paperwork is filled out and his insurance verified. Mr. Smith had to get up at 3:00 am to get ready and have his wife drive them to the hospital, which was an hour away from their home. They are both tired and anxious. To make matters worse, Mr. Smith is asked about his religious preferences and who to designate for power of attorney should anything bad happen to him during surgery. The admissions personnel give Mr. Smith an identifying wristband. Patients coming in for surgery are asked to arrive 1-2 hours prior to their scheduled surgery time. Upon arrival, the patient will be prepared for the OR. In many cases, the patient will have had an opportunity to fill out admission paperwork in advance. In other cases, the paperwork will need to be filled out at the surgical facility. At the appropriate time, the patient will be referred to the pre-op holding area.
■ PRE-OP HOLDING Mr. Smith and his wife wait in the waiting area for about 3 hours. Mr. Smith’s surgery has been delayed because his doctor, Dr. Martin, has been delayed due to an emergency surgery that was added on this morning. Finally, at 9:00 am, Mr. Smith and his wife are escorted to the pre-op holding area. The nursing staff in the pre-op holding area assign him to a bed and have him change into a hospital gown. The pre-op nurse goes over an exhaustive list of questions about Mr. Smith’s medical history and medications. He is told that someone from the anesthesia department will see him soon.
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In the pre-op area, patients will be asked to change into a hospital gown and wear a cap to cover their hair. They will also be asked to remove any items such as jewelry, hearing aids, contact lenses, glasses, and dentures, which will be stored away. Their identification bracelet will be checked. If there are any allergies, or any precautions, patients will receive an additional band to alert all medical personnel. A nurse will come in and take vitals, measure height and weight, measure body temperature, and note if there are any changes in health. An intravenous (IV) line will also be placed to keep the patient hydrated and also as a place for administering medications. The nurse will also confirm that the paperwork and the surgical consent form are in order and have been signed by the patient and the surgeon. Mr. and Mrs. Smith wait in the pre-op holding area for another 30 minutes. Finally, the surgeon arrives. She apologizes for the long delay and begins reviewing the procedure with the Smith’s. Dr. Martin puts her initials on Mr. Smith’s abdomen. Once all of the Smiths’ questions are answered, Dr. Martin hurries off. Shortly thereafter, Dr. Kirby, the anesthesiologist arrives. Once again, Dr. Kirby reviews Mr. Smith’s medical history with him and performs a brief physical examination, which includes asking him to open his mouth wide and extend his neck. Mr. Smith is given the option of an epidural to help him with pain control after the surgery. The Smith’s are unsure but decide to go ahead with the procedure because the doctor must know best. Dr. Kirby finishes up with a discussion of the risks and benefits of the anesthesia, the invasive lines that will be placed, and the epidural. All of the things that can go wrong are a bit scary to Mrs. Smith, but she says nothing so as not to alarm her husband. Dr. Kirby hurries off and says that he will be right back. Soon the surgical nurse arrives and again asks many of the same medical questions. She also verifies the consent form. Many things happen in the pre-op area. The pre-op nursing staff will take vital signs, go over the patient’s medical history, and start an IV line. They will also record information in the medical record and make sure all the paperwork is in order and up to date. In many cases, the patient will get to briefly meet with the surgeon. The surgeon will answer any last minute questions and “mark” the surgical site on the patient. Marking of the surgical site in cooperation with
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Chapter 3 • The Surgical Experience
the patient is to reduce the risk of wrong-site surgery. In addition to meeting the surgeon, the patient will meet some of the other members of the OR team. The circulating nurse in the OR will stop by and verify that everything is ready for the patient to proceed to surgery. This will also be the time that the patient will meet the anesthesiologist. During the pre-op evaluation, the anesthesia provider reviews the patient’s medical history and inquires if there were any family complications with anesthesia. Part of the pre-op evaluation includes evaluating the patient’s airway and reviewing all labs, x-rays, and all other tests relevant to the surgery. The anesthesiologist will have already formed a preliminary anesthetic plan based upon initial information. After review of the history with the patient, a physical examination, and review of any new test results, the anesthesiologist modifies the plan. Based on the type of procedure, along with the preferences of the anesthesiologist, the patient, and the surgeon, the type of anesthetic is chosen. This may include local, regional, general, or a combination of methods. In addition to the type of anesthesia, any special monitoring or vascular access will also be planned. The patient must participate in the choice of the anesthetic plan and be informed of important risks and potential benefits of the anesthesia type and any special procedures. To prepare the patient for the OR, the anesthesia care provider will inform the patient of what he or she can expect as he or she enters the OR. If a regional block is indicated, the anesthesiologist or the regional block team may place the block in the pre-op holding area before the patient goes to the OR. Procedures performed in the pre-op holding area by the anesthesiologist will be conducted with the assistance of an AT. The pre-op area will be the final destination where family members can be with the patient. After the patient is taken to the OR, family members will wait in the family waiting room. In many institutions, anesthesia functions as a care team with the anesthesiologist supervising a certified registered nurse anesthetist (CRNA). In these cases, the anesthesiologist may be supervising several different CRNAs simultaneously. The anesthesiologist discusses and formulates the anesthetic plan along with the CRNA. The physician is then present for all critical portions of the procedure and is available for consultation if the CRNA needs help with the cases.
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In other institutions, the CRNA may function independently.
■ THE OPERATING ROOM In preparation for a surgical case, the anesthesia provider and the AT will make sure all necessary equipment, medications, monitors, and supplies for the procedure are readily available. This is particularly important if special equipment or supplies will be needed based upon the planned surgical procedure or the medical condition of the patient. The AT should be able to anticipate special needs based upon the planned surgical procedure as described in the surgical schedule. The anesthesia provider should communicate with the AT any other special requirements based upon the patient’s medical condition. Communication between the anesthesia provider and the AT is essential to ensure an efficient and safe anesthetic. The anesthesia provider should also coordinate with the AT if the technician will be required to assist the provider with any procedures. When the OR is ready for the patient, a member of the surgical team will come to the pre-op area and transport the patient to the room. Once in the OR, the appropriate monitors are placed and the anesthesia provider will “induce” anesthesia with IV or inhalational anesthetic agents. The patient’s airway may require intubation or the use of other devices to ensure safe ventilation of the lungs. Invasive lines, such as arterial lines or central lines, are usually placed after the patient is asleep with the assistance of an anesthesia technician. In some cases, due to the patient’s medical status, venous access or monitoring lines may be placed while the patient is still awake. The next phase of the anesthetic is referred to as maintenance. The anesthesia provider will administer anesthetic gases, additional pain medications, and drugs to paralyze muscles as necessary for the procedure. The anesthesiology provider continuously monitors the patient’s vital signs during the procedure. The level of awareness is also monitored through measurement of vital signs and the reaction to surgical stimulation, agent monitoring, or through brain wave monitors. During the operative procedure, the anesthesia provider will assess the need for transfusion of blood products or other fluids. Lab tests drawn and reviewed during the surgery will
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Section I • Careers in Anesthesia Technology
aid in this evaluation. In addition to maintaining the anesthetic, the anesthesia provider will monitor the patient’s respiratory status and in many cases will ventilate the patient with a mechanical ventilator. The final stage of the anesthetic is awakening the patient from anesthesia. This process is referred to as “emergence.” Once the surgical case is coming to an end, the anesthesia provider will slowly reduce the anesthetic medications or even give an IV reversal agent to assist with the waking-up process. Once full strength and awareness is observed in the patient, the anesthesiology provider will remove the breathing tube/device. When the patient is stable, the team can transfer the patient to the postanesthesia recovery room (PACU) or directly to the intensive care unit (ICU). At any point during the surgery, the AT may be asked to come to the OR to assist with a procedure, bring additional medications, equipment, or supplies, or help deal with an equipment problem. In addition, the AT could be called to assist the anesthesia provider with a medical emergency taking place in the OR.
■ POSTANESTHESIA CARE UNIT The next thing Mr. Smith remembers is waking up in an unfamiliar area. He is confused. The PACU nurse is telling him to take a deep breath. He does not have much pain but cannot seem to move his legs. The nurse tells him he is in the recovery room and that he must keep the oxygen mask on. Can he rate his pain on a scale of 1 to 10? Mr. Smith is slowly waking up and he realizes it is early evening. Didn’t he just go into surgery around lunchtime? He is a bit sick to his stomach and dizzy. The nurse tells him he is on his way to the ICU. Following anesthesia, some patients will be transported to the PACU for recovery. This is an area that monitors and supports patients as they recover from the immediate effects of anesthesia and surgery. Patients’ vital signs are continually monitored, and pain medication is administered as needed. Pain medication is given in the form of oral medication, injection, or a patient-controlled analgesia (PCA) pump. In some cases, a nerve block will be performed in the PACU to assist with pain that cannot be controlled with standard measures. When patients are stable, they are either discharged (referred to as “ambulatory” or
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“outpatients”) or transferred to a surgical ward in the hospital or an ICU (inpatients). An ambulatory patient is a patient who comes in for a procedure and leaves the facility the same day. An inpatient is a patient who was either already a patient in the hospital or a patient who was coming in for surgery but expected to stay in the hospital.
■ THE ANESTHESIA TECHNICIAN The anesthesia team consists of several different personnel with different job titles and descriptions who work together in order to provide anesthesia care to patients undergoing medical procedures. An important part of the anesthesia care team is the AT. ATs are the support service providers to the anesthesiologist and/or the nurse anesthetist who provide anesthesia care. The day-to-day tasks of the AT may vary based on the roles defined by each institution. Despite the differences, ATs do have a set of responsibilities that are often associated with them as part of their everyday routine. Some of these include resource planning, anesthesia machine checkout, covering multiple areas, assisting the anesthesia provider, turning over rooms, and supply management.
■ RESOURCE PLANNING Resource planning is a significant part of the job of an AT. It deals with analyzing available resources and making certain that the anesthesia team is fully prepared for the day’s cases as well as for emergencies or unanticipated cases. With experience, the ATs can anticipate what will be needed and prepare accordingly.
■ ANESTHESIA MACHINE CHECKOUT The anesthesia machine checkout is the full inspection of the anesthesia machine according to the manufacturer’s recommended procedure. This complete workup needs to be performed every morning by the AT and/or the anesthesia care provider. See Chapter 27 for details on the anesthesia machine checkout.
■ COVERING MULTIPLE AREAS ATs work in all areas where the anesthesia team is needed. These can include holding areas, ORs, PACUs, block rooms, obstetrics rooms, MRI/ CAT scan rooms, nuclear medicine suites, interventional radiology suites, cardiac procedure suites, electrophysiology labs, gastrointestinal
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Chapter 3 • The Surgical Experience
(GI) procedure areas, special procedure rooms, ICUs, and many more. With advances in modern-day medicine and technology, the areas covered by the anesthesia team are constantly growing; therefore, the areas covered by the AT are also growing. Chapter 48 provides an excellent overview of the special challenges associated with providing care in these areas.
■ ASSISTING THE ANESTHESIA PROVIDER A large part of the AT’s day is taken up by assisting the anesthesia provider directly. This may include assisting with regional blocks, transporting patients, placement of monitoring equipment, airway management, invasive line placement, use of ultrasound devices, and troubleshooting equipment. All of these will be covered individually in later chapters.
■ ROOM TURNOVER Room turnover is the term used to indicate that an OR is being cleaned and prepped for the next case. Room turnovers can be very quick and often require the AT to assist in making sure all disposables that have been used in the last case are discarded. All monitoring cables, screens, and surfaces of the machine and cart need to be cleaned with a hospital-approved disinfectant. Following the appropriate dry time, a new circuit, EKG pads, and suction are placed for the next patient. A leak test should be performed to
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make sure that there are no leaks in the new circuit. The CO2 absorbent should be checked to make sure it is not saturated. Requests for any supplies for the next case should be brought to the room following completion of the room turnover.
■ SUPPLY MANAGEMENT The AT should be involved on a daily basis in making sure adequate supplies are available. This may entail direct ordering or communication of needs to a purchasing department. It is important that there be a process in place that ensures products are continually checked for expiration dates.
■ EQUIPMENT STERILIZATION Nondisposable devices used by anesthesia need to be sterilized between uses. Sterilization means to get rid of any bacteria or virus that may have been exposed to that tool or device. Depending on the product being cleaned, there can be different methods of decontaminating them.
■ SUMMARY This chapter provides an overview of the surgical experience from the perspective of the patient, the anesthesia provider, and the AT. It is intended to introduce what goes on in the pre-op holding area, the OR, and the PACU. In addition, this chapter introduces several routine types of tasks performed in the OR by the anesthesia provider and the AT.
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SECTION
II
Anatomy, Physiology, and Pharmacology
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CHAPTER
4
Pharmacokinetics David Sibell and Ryan Anderson ■ INTRODUCTION The terms pharmacokinetics and pharmacodynamics are often confused or used interchangeably, but they are two distinct concepts. Pharmacodynamics examines how drugs affect the body—induce unconsciousness, relieve pain, increase blood pressure, etc. Pharmacokinetics is the study of how the body affects the drug—the process by which drugs are absorbed, distributed throughout the body, metabolized, and excreted from the body. The practice of anesthesia involves the administration of a large number of drugs that have a significant impact on patients’ physiology and behavior. These effects are influenced not only by dose, route, and timing of administration but also by each patient’s physiology and anatomy, as well as coexisting disease. This chapter introduces some of the more important concepts in pharmacokinetics.
■ ROUTES OF ADMINISTRATION In anesthesia, most drugs are given as intravenous (IV) injections, but they can also be given orally (PO, from Latin per os, or “by mouth”), inhaled into the lungs, or given by other numerous other routes (see Table 4.1). Most drugs are delivered to their sites of action by the bloodstream. Therefore, the initial distribution and onset time of the drug will be determined by how long it takes the drug to get into the bloodstream. This depends on the route of administration. Drugs that are injected intravenously are delivered directly to the bloodstream (intravascular space, central compartment). Inhaled gases are rapidly absorbed into the bloodstream in the alveoli. Sublingual drugs, like nitroglycerin, are absorbed by the oral epithelium and then move quickly into the bloodstream (within seconds). Transdermal and oral routes are much slower. Drug patches must diffuse the drug out of the patch, through the
skin (an excellent barrier to the outside world), through subcutaneous fat and fascial layers, and into the bloodstream, which usually takes hours. The oral route has a unique set of obstacles that must be overcome before a drug can get to its target organs. A tablet of gabapentin must be dissolved by gastric fluid, move to the small intestine where it is absorbed, and then move through the epithelial layers to eventually diffuse into the bloodstream, taking roughly 30-60 minutes. Unlike most other tissues, the venous drainage of the gut does not go directly back to the heart. Instead, it flows into the portal circulation taking nutrients and drugs, which are absorbed from the gut, to the liver where they are processed. One of the main functions of the liver is to detoxify the blood, by chemically altering (metabolizing) foreign substances. Therefore, with oral administration, the liver can remove a portion of drug from the bloodstream before the drug ever makes its way to the systemic circulation and target organs. This is known as first pass clearance. Much of the drug can be lost not only to first pass clearance but also to other factors. Gastric contents are highly acidic and can chemically degrade the drug. Additionally, other compounds in the gut can bind to the drug and prevent its absorption by the small intestine. Absorption can be impaired if the patient’s gut does not work properly or has unusual anatomy. Because of all of these factors, the oral route of administration leads to decreased bioavailability, which is the fraction of drug that is distributed in the systemic circulation relative to the total amount of drug given. This is why IV and PO dosing of medications is usually very different. Some drugs are delivered directly to their sites of action. Local anesthetics are injected subcutaneously to anesthetize the area around the injection site (local infiltration). They can be injected around a large nerve (nerve block) or
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Chapter 4 • Pharmacokinetics
17
TABLE 4.1 ROUTES OF DRUG ADMINISTRATION, THEIR ABBREVIATIONS, AND
EXAMPLES OF COMMON ANESTHETIC MEDICATIONS GIVEN BY EACH ROUTE ROUTE
ABBREVIATION
EXAMPLES OF ANESTHESIA MEDICATIONS
Intravenous
IV
Propofol, esmolol, fentanyl
Oral
PO
Bicitra, gabapentin
Inhaled
Isoflurane, nitrous oxide, albuterol
Subcutaneous
SC/SQ
Lidocainea, insulin
Intramuscular
IM
Ketamine, methylprednisolone
Transdermal
Scopolamine, fentanyl, nitroglycerin
Sublingual
SL
Nitroglycerin
Intraosseous
IO
Epinephrine, atropine (emergency drugs)
Rectal
PR
Acetaminophen
Intrathecala
IT
Bupivicaine, fentanyl
Epidurala
Bupivicaine, fentanyl
Perineurala (nerve block)
Chloroprocaine, bupivicaine
a
Works at the site of delivery.
into the epidural space to anesthetize an entire limb or portion of the torso. They can be injected into the subarachnoid space (intrathecal space), where they will act directly on the nerves that make up the spinal cord. In these situations, the drug remains where it was injected in order to work. It is also important to know that some drugs have multiple uses and multiple sites of action. Lidocaine is a local anesthetic that can be injected for local infiltration or nerve blocks. It is also frequently given intravenously to anesthetize the vein and reduce the pain on injection of induction agents. It can also be given intravenously to treat cardiac arrhythmias or chronic pain. It is always important to know where the drug you are injecting is going. Most catheters, whether leading into a vein or epidural or intrathecal space, have the same Luer-lock mechanism to attach syringes. The vast majority of medications used in anesthesia are given intravenously, but some are intended only for other routes. Giving a drug by the wrong route can have devastating consequences (like seizures, paralysis, and death). Drugs intended for other routes but accidentally given into the central nervous system (either intrathecal or epidural) tend to have the most serious consequences. However, drugs that are given intravenously (when intended for other routes) can also be very harmful. Institutional
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policy will vary as to whether the administration of drugs is in the scope of practice for anesthesia technicians. However, if not directly administering drugs, most anesthesia technicians are at least assisting with the administration of drugs. Great care must be taken to ensure that the right drug as well as the right dose is administered through the right route, even in emergencies. Good communication is essential when more than one person is involved in the administration of a drug. Errors in drug administration are one of the most common preventable errors in health care.
■ DISTRIBUTION As stated earlier, most drugs are delivered to their target organs by the bloodstream. It is important to know what happens to the drug after it is given. For example, general anesthesia is induced with an IV bolus of propofol. As soon as propofol has been injected, it starts mixing with the blood and will go where the blood goes. Peripheral veins drain into larger veins and eventually back to the heart, then lungs, heart again, and then to the systemic circulation. The propofol will soon mix evenly throughout the entire blood volume (30-60 seconds) and will reach a concentration in the blood dependent upon the dose given and the patient’s blood volume. The diluted propofol will start to make its way out of the bloodstream (at the capillary beds) and into
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the tissues of the body. This movement is driven by passive diffusion (force that drives molecules from compartments of high concentration to compartments of low concentration). As propofol moves from the bloodstream to the tissues, the concentration in each compartment (blood, fat, extracellular fluid) will gradually equilibrate. Within the systemic circulation, different organs get different fractions of the total blood flow (cardiac output). The organs that get the most blood flow are the brain, kidneys, liver, and heart, which are collectively known as the vesselrich group. Since the vessel-rich group gets most of the blood, it will get most of the propofol (initially). The tissue concentration of propofol in all the organs in the vessel-rich group will reach the concentration of propofol in the bloodstream rapidly. If the propofol concentration in the brain is high enough, it will render the patient unconscious.
■ REDISTRIBUTION The propofol concentrations rapidly equilibrate between the bloodstream (plasma concentration) and the vessel-rich group organs. It’s also equally important to know about the other organs in the body, those that get a smaller fraction of the blood flow. The muscle group gets the next largest fraction of blood flow, followed by the vesselpoor group (tendons, cartilage, and fascia). These tissues will continue to take up propofol as long as their propofol concentration is lower than the plasma level. As they absorb more propofol, the plasma level of propofol goes down, causing it to drop below the level in the vessel-rich group. The propofol in the vessel-rich group now diffuses down the concentration gradient back into the bloodstream, which takes it to the other tissues of the body. This is the concept of redistribution; a drug has an initial distribution to the vessel-rich group but then redistributes to other areas with lower blood flow. Redistribution is responsible for the offset of many short-acting drugs like propofol and thiopental. After an induction dose of propofol, a patient will lose consciousness because propofol above a minimum concentration interferes with the brain’s ability to maintain consciousness. The drug then redistributes, and its concentration in the brain drops below the minimum concentration and the patient will start to regain consciousness (8-10 minutes depending upon the dose of propofol).
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■ ELIMINATION As soon as a drug is given, physiologic processes involving several organ systems will start to remove it from the body through a process known as elimination. Even though the clinical effects of a drug may or may not have ended due to redistribution, the drug will still be present in the body until it has been completely eliminated, which can take hours to days. Some drugs must undergo several steps of chemical processing in order to be inactivated, while others are removed unchanged in the urine and feces. Biotransformation, the process by which drugs are chemically altered, either activates the parent compound (in prodrugs) or transforms active compounds into inactive substances that are excreted. Common locations for drug biotransformation include the liver and bloodstream. As previously discussed with first pass clearance, the liver is responsible for detoxifying the blood. Hepatic metabolism deactivates drugs and removes them from the bloodstream via numerous types of chemical reactions, most of which are categorized as Phase 1 or Phase 2 reactions. Phase 1 reactions alter the parent compound through oxidation/reduction (change in number of electrons), hydrolysis (breakdown by the addition of water), or the addition/removal of small functional groups (e.g., -OH, -COOH, and -NH2). In Phase 2 reactions, functional groups (e.g., glucuronic acid) are attached to the parent compound, thereby facilitating its excretion from the body. The family of enzymes that carries out the majority of hepatic metabolism is known as the cytochrome P450 (CYP) system. The functional level of these enzymes can vary greatly between patients and even within each individual. These differences can be due to genomic polymorphisms or acquired through the use of other medications or chronic exposure to toxins. A classic example is carbamazepine inducing the production of more CYP3A4 enzyme, causing increased metabolism of midazolam. Hepatic metabolism can also be significantly impaired in the setting of liver disease—hepatitis, alcoholic cirrhosis, liver cancer—or drugs or agents that interfere with the cytochrome P450 enzymes. Drugs can also be broken down by plasma cholinesterases (or pseudocholinesterases). Examples include some muscle relaxants (succinylcholine and mivacurium) and the opioid
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Chapter 4 • Pharmacokinetics
remifentanil. These compounds are all esters, which are cleaved at the ester linkage by plasma cholinesterases, rapidly inactivating them. The ubiquity of plasma cholinesterases accounts for the rapid breakdown of these drugs. There are very few acquired medical conditions, other than liver disease, that lead to reduced activity of these enzymes. Plasma cholinesterases are primarily produced in the liver, and alterations in liver function can decrease the amount of cholinesterases produced. In addition to liver disease, there are genetic defects that can cause either an atypical (poorly functioning) enzyme or a deficiency of the enzyme. Either situation may cause unexpectedly prolonged clinical activity of drugs that are metabolized by this class of enzyme. Many drugs and drug metabolites (breakdown products) are removed via renal clearance. The kidneys are constantly filtering the blood to control levels of water, electrolytes, pH, etc. within the body. As drugs are filtered by the kidneys, they end up in the urine and are soon eliminated. Some drugs are excreted unchanged in the urine, such as gabapentin, penicillins, and etomidate. However, this removal process does not work as well for drugs that are not easily filtered (those that are highly protein-bound or carry a strong electrical charge) or those that are reabsorbed by the kidney after filtering. Patients with impaired renal function will have a prolonged elimination phase for medications that are primarily excreted by the kidney, and their doses must be adjusted according to the degree of renal dysfunction.
■ VOLUME OF DISTRIBUTION Every drug has a unique set of chemical properties. They can carry a positive or negative charge or be electrochemically neutral. They can have regions with large polar functional groups, which make them dissolve easily in water (hydrophilic, “water loving”). They can have regions with large nonpolar groups, which make them repelled from water (hydrophobic, “water hating”) and more apt to dissolve in fat tissue (lipophilic). Some are bound up avidly by plasma proteins. These are the characteristics that determine how quickly a drug will start to work, how long it will work, and where the drug gets deposited until it is broken down and eliminated. Hydrophilic drugs tend to stay in the bloodstream, while hydrophobic drugs deposit themselves happily in fat tissue. Propofol is hydrophobic, which
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makes it able to cross membranes quickly (fast onset) and get deposited in fat tissue. The volume of distribution of a drug is the apparent volume into which a drug gets distributed. This is not an actual physical volume but rather one that is conceptual; it is calculated by the following equation: Vd = dose of drug given/initial drug plasma concentration Vd is the volume of distribution. This volume can be very small or several times the total volume of the patient (sufentanil’s is 195 L, while the total body volume of an adult male is about 70 L). For example, if a 1-mg dose of a drug were dissolved in a vat of blood, and the measured concentration of the drug was 0.5 mg/L, you could calculate that there must have been 2 L of blood in the vat. The 2 L is the volume of distribution. The experiment is repeated with the same vat of blood and a different drug; 1 mg of the new drug is mixed into the vat, and the concentration of this drug is measured. In this case, most of the drug sticks to the sides of the vat and very little is left in the blood. The measured concentration is 0.1 mg/L. The calculated volume of blood or volume of distribution would be 10 L (if 1 mg of drug were dissolved in 10 L, the concentration would be 0.1 mg/L). Of course, the vat does not contain 10 L of blood, only 2 L. The calculated volume of distribution is larger due to the sequestration of the drug on the walls of the vat. A similar phenomenon is what happens with sufentanil and many other lipophilic drugs. These drugs are highly sequestered into fat, leaving only a small amount in the bloodstream, which inflates the calculated volume of distribution.
■ HALF-LIFE The concentration of a drug in the body over a given time can be described through mathematical modeling. Most drugs follow first-order kinetics, which means that a constant fraction of drug is eliminated over a given time period (e.g., half of the drug is removed every 2 hours). Some drugs (e.g., ethanol, aspirin) follow zero-order kinetics, which means a constant amount of drug is eliminated over a given time period. So, stated another way, with first-order kinetics, the time that it takes the body to remove 50% of a drug is that drug’s half-life. For example, a patient is given 100 mg of a drug that has a 2-hour half-life.
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After 2 hours, only 50 mg will remain. Over the next 2 hours, the body will remove another half of what remains (25 mg), so after 4 hours, there is still 25 mg in the patient. After another 2 hours (three half-lives total), the remaining level drops to 12.5 mg. Mathematical formulas can be used to predict the amount of drug present at any time point following a dose. From these, we can establish dosing schedules to reduce the risk of reaching toxic levels of drugs in those patients with decreased ability to eliminate drugs.
■ STEADY-STATE CONCENTRATION If anesthesia providers want to maintain a steady concentration of a drug within a patient, there are different ways to achieve this. One way is to give a loading dose (initial dose of drug), which will reach a certain concentration in the blood (based on the dose and volume of distribution). The drug concentration will drop from elimination and redistribution. Additional doses of the drug can be given periodically to maintain the concentration of the drug at therapeutic levels. If we know how much drug is eliminated (e.g., 50 mg over a period of 30 minutes), then we can maintain a steady-state concentration, or constant level of drug in the bloodstream, by giving an additional 50-mg dose of the drug every 30 minutes. These doses are known as maintenance doses because they maintain the level of a drug in a desired concentration range. By knowing the volume of distribution and the half-life of a drug, we can calculate a loading dose, maintenance dose(s), and frequency of redosing in order to achieve and maintain a drug in a specific concentration range. While this strategy of drug dosing is frequently used, such calculations are not typically performed in clinical practice; it is described here to demonstrate these concepts. Another way to achieve a steady drug concentration in the blood is to administer a drug as a constant infusion. Typically, drug effects are initially achieved with a loading dose given as a bolus, and then the drug effect is maintained with an infusion. For example, general anesthesia can be induced with a bolus dose of propofol, and it can be maintained with infusion of propofol at a constant rate of administration. The benefit of the infusion is that it avoids the peaks and troughs of drug concentrations that come with repeat bolus dosing; peak drug levels can lead to pronounced side effects and toxic reactions,
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while trough drug levels can lead to inadequate drug effects, like light anesthesia. Ideally, the drug is infused at a rate that is equal to the rate of elimination. Remember, though, that shortacting lipophilic drugs redistribute from the vessel-rich group to other tissues much faster than they are eliminated from the body. So, infusion of propofol to maintain a constant plasma concentration is really just adding drug at the rate at which it redistributes to other tissues. If we were to continue a propofol infusion for several hours at the same rate, we would start to saturate the peripheral tissues. As more drug is redistributed over a long period of time, the level of drug in peripheral tissues will continue to rise until it is equal to the level in the bloodstream, at which time redistribution no longer occurs. Now, any additional drug that is administered will remain in the bloodstream and vessel-rich group until it is eliminated from the body (which takes much longer than the process of redistribution). If the infusion rate is not adjusted, the concentration of propofol in the bloodstream would begin to rise. When the infusion is stopped, the kidneys and liver remove drug from the central compartment (bloodstream), but more drug will continue to seep out of the peripheral tissues into the central compartment. The plasma concentration (and brain concentration) decreases very slowly. This demonstrates the concept of context-sensitive half-life, which describes how the half-life of a drug is proportional to the duration over which the drug has been administered.
■ CLEARANCE Clearance refers to the amount of a substance removed from the circulation, either by metabolism or by excretion, over a certain period of time. Drugs can be excreted with their chemical structures intact. Drugs can be filtered by the kidney and excreted in the urine, or they can leave the body in other fluids: tears, sweat, breast milk, etc. This is how some medications can be transferred from breast-feeding mothers to their babies, sometimes with harmful effects. Some drugs, like inhaled anesthetics, are eliminated by exhalation, again having undergone very little chemical degradation. Other drugs undergo metabolism as discussed above. The metabolites can then be eliminated by the kidney. All of these mechanisms of elimination lead to clearance of the drug from the circulation.
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Chapter 4 • Pharmacokinetics
REVIEW QUESTIONS 1. How would drug onset and duration of action be affected in a patient with heart failure (low cardiac output)? A) Speed drug onset B) Increase metabolism of the drug C) Shorten the duration of action D) Slow the onset E) Both A and C Answer: D. A patient with a reduced cardiac output, as in heart failure, will circulate the blood more slowly to the target organs, resulting in a delay in onset of action. The duration of action is usually, but not always, prolonged due to reduced blood flow to the liver (reduced metabolism) and kidneys (reduced elimination).
2. What process is responsible for the offset of effects of a bolus of propofol? A) First pass effect B) Redistribution C) P450 enzyme reduction D) Increased renal blood flow E) None of the above Answer: B. Redistribution. The bolus of propofol is mixed and distributed rapidly to the central compartment and to the vessel-rich group. Subsequently, the plasma level falls as the propofol is redistributed to muscles and the vessel-poor group.
3. Dysfunction of what organ systems will increase the elimination half-life of many anesthetic drugs? A) Liver B) Kidney C) Heart D) All of the above E) None of the above Answer: D. All of the above. Many drugs are metabolized in the liver, while many others are excreted unchanged by the kidneys. Any condition that reduces blood flow to the liver or kidneys can reduce the amount of drug that is cleared, which will cause an increase in the half-life of the drug.
4. Which of the following statements is FALSE? A) Oral administration of drugs may be subject to the first pass effect. B) IV administration is the route with the fastest onset of drug effects. C) Inhaled drugs cannot be absorbed into the bloodstream. D) Certain drugs may only be administered by certain routes. E) Appropriate drug dose may differ depending upon the route of administration.
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Answer: C. Inhaled drugs cannot be absorbed into the bloodstream. This statement is false. Many drugs including the inhaled anesthetics, nitric oxide, and lidocaine are all taken up into the bloodstream after inhaled administration. Orally administered drugs are absorbed by the gut and taken up into the bloodstream. From there, the blood passes through the portal circulation in the liver before mixing with the systemic circulation. As the blood passes through the liver, it has the opportunity to metabolize the drug. Drugs given intravenously have the fastest onset because drugs are delivered to their target organs by the bloodstream, so the rate of onset is largely determined by how long it takes for a drug to get to the bloodstream. A critical safety concern is making sure the right drug in the right dose is given by the right route. Some drugs are toxic if given by one route but not another. Other drugs have 100-fold different doses depending upon the route of administration.
5. Half-life is defined as A) Half way to the expiration date for a drug B) The time it takes the body to eliminate 50% of a drug C) The dose of drug that is effective in 50% of patients D) One half the volume of distribution E) None of the above Answer: B. Drugs are gradually eliminated from the body. Some are eliminated at a constant rate (xxx amount of drug per hour— zero-order kinetics). With the vast majority of drugs, the amount of drug eliminated is dependent upon the concentration of the drug—a fixed percentage of the drug, not a fixed amount, is eliminated each hour—first-order kinetics. The half-life is the amount of time it takes for 50% of the drug to be eliminated.
REFERENCES Davis L, Britten JJ, Morgan M. Cholinesterase: its significance in anaesthetic practice. Anaesthesia. 1997;52:244-260. Egan TD, Lemmens HJ, Fiset P, et al. The pharmacokinetics of the new short-acting opioid remifentanil (GI87084B) in healthy adult male volunteers. Anesthesiology. 1993;79(5):881-892. Evers AS, Crowder CM, Balser JR. General anesthetics. In: Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 11th ed. [online] 2006. Jackson, WY: Teton Data Systems; 2010. Available from.Accessed April 6, 2011. http://accessmedicine.com/content.aspx?aid=16664636 Gonzalez FJ, Tukey RH. Drug metabolism. In: Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 11th ed. [online] 2006. Jackson, WY: Teton Data Systems; 2010. Available from. Accessed April 6, 2011. http://accessmedicine.com/content.aspx?aid=16659426 Zhang L, Reynolds KS, Zhao P, et al. Drug interactions evaluation: an integrated part of risk assessment of therapeutics. Toxicol Appl Pharmacol. 2010; 243(2):134-145
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CHAPTER
5
Pharmacodynamics Pamela Kirwin
P
harmacodynamics is the relationship between the plasma drug concentration and the pharmacologic effect of the drug on the body, or more simply put, pharmacodynamics is the study of what drugs do to the body. Pharmacodynamics can be divided into three general areas: • The transduction of biologic signals: how drugs act at a cellular level to affect what is happening within the cell. A major component in understanding transduction is understanding how cellular receptors work. • Molecular pharmacology: the molecular properties of drugs and how they interact with organisms at a molecular level. • Clinical pharmacology: the clinical effects drugs have on an organism or organ system.
■ TRANSDUCTION AND RECEPTORS Receptors are external components of cells (in the cell membrane) that interact with compounds such as drugs or biochemical signals to start an intracellular cascade of reactions. There are three main components of the receptor theory. These include the quantitative actions of drug binding and the resulting effect, the selectivity of drugs and their ability to activate the cell, and the pharmacologic activity of those drugs at the receptor. The ability of drugs to bind to receptors is critical to their action. The specific receptor is an important determinant of what intracellular cascade gets triggered. Drugs that have similar biochemical structures often adhere to the same receptor. When a drug interacts or binds to a receptor, there is a quantitative relationship between the dose of the drug and the resulting effect of the intracellular cascade it sets off. In addition to the quantity of drug binding to receptors, drugs may bind with variable strength to a receptor. The biologic activity of a drug that strongly binds may be different than the activity of a drug that weakly binds. Drugs are sometimes
developed to bind selectively to certain subsets of receptors in order to either enhance drug effect or avoid drug side effects. A drug that binds to a receptor to initiate a cellular process is called an “agonist.” It is important to be aware that not all drugs bind to receptors to activate a process. Some drugs bind to receptors in order to inhibit a process from happening within the cell. These drugs are called “antagonists.” A cornerstone to receptor theory emerged from the work of Paul Erhlich. Erhlich studied the activity of curare on parts of the central nervous system and developed the concept that “agents cannot act unless they are bound.” This is the foundation on which the receptor theory was built. Classical receptor theory is best described through the mathematical relationship shown in Figure 5.1. In this equation, L is the ligand (the agent binding to the receptor), R is the receptor, Kon is the speed at which the ligand binds to the receptor, Koff is the speed at which the ligand is released from the receptor. The speed at which drugs bind and are released from receptors greatly impacts their effect on the receptor and the cell. This equation can be rearranged to form an equation that describes the relationship between the speed at which binding and release from the receptor takes place. This is called “Kd,” the dissociation constant (Fig. 5.2). From the dissociation constant, you can extrapolate the activity of the molecule and how it binds to a receptor. A low Kd means that the speed at which the drug binds to the receptor is much greater than the speed at which it is released from the receptor; therefore, not many molecules of the drug are required to occupy the majority of the target receptors. A low Kd indicates the drug tightly binds to the receptor. A higher Kd means that more molecules of a drug are required to occupy the majority of the receptors. Therefore, the drug is weakly bound to the
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Chapter 5 • Pharmacodynamics
■ FIGURE 5.1 Equilibrium for a ligand L binding to a receptor R.
receptor and falls off quickly. To have an equivalent activity to a drug with a high Kd, a drug with a low Kd would require many more drug molecules to keep attempting to bind to the receptor to make up for the weak binding. A great deal can be learned about a drug by measuring the amount of drug necessary to produce an effect on a cellular process. For example, how much drug is necessary to add to a group of cells in a test tube to get them to produce a certain quantity of hormone? How is receptor binding measured in actual humans? This is often accomplished by measuring an indirect action (secondary endpoint) as a result of receptor binding. A secondary endpoint is used to derive information about the way molecules bind to receptors. For example, to measure how a blood pressure medicine binds to a receptor and then compare it to another blood pressure medicine, which targets the same receptor, you might measure the percent and duration of a change in blood pressure not the actual binding of the molecule to the receptor. Measurement of drug activity at a receptor in actual humans can be very complicated. It may be difficult to find or measure secondary endpoints, the drug may require metabolism or shifting into other compartments of the body in order to finally bind to its receptor, or there may be physiologic delay in the actual effect.
Receptor Agonists and Antagonists Drugs are agonists of receptors if they attach to a receptor and create an effect. The effect may be excitatory or inhibitory on a process within the cell. In other words, an agonist may cause an effect that is inhibitory and still be considered an
■ FIGURE 5.2 Calculation of the Kd dissociation constant.
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“agonist” of that effect. Agonists of receptors fall into two common categories: partial agonists and full agonists. A drug that is highly effective at activating a receptor is called a full agonist. Any drug that activates the same receptor but has a significantly less effect on activating the receptor is considered a partial agonist. Buprenorphine is a partial opioid agonist that only partially activates the euphoria associated with opioids. Some believe partial agonists do not bind strongly to the receptor and this may be why their effect is more weakly produced. In addition, the partial agonist may be incompletely bound to the receptor or is unable to maintain the receptor’s activated shape after it is bound. Even at increasingly higher doses, partial agonists cannot fully activate a receptor. Antagonists bind to a receptor and prevent the receptor from causing a process to occur. Some antagonists bind irreversibly to the receptor, and in some cases this can be for the life of the cell. Others bind and release from the receptor (see disassociation constants above) and are called competitive antagonists. Competitive antagonists inhibit either endogenous molecules or other drug molecules from binding to the target receptor. Because there is a competition between agonists and antagonists for binding to the receptor, the competitive antagonists can be overwhelmed by giving higher and higher doses of an agonist. Noncompetitive antagonists, those that bind irreversibly to the receptor, cannot be overwhelmed by increasing the amount of agonist. An example of a noncompetitive antagonist is aspirin, which fully antagonizes the blood clotting function of the platelets after it binds to the cyclooxygenase receptor. Once aspirin binds to the platelet cyclooxygenase receptor, it is irreversible. This is why aspirin is usually withheld for 5 to 7 days prior to surgery. The body needs 5 to 7 days to generate new platelets that have not been exposed to aspirin and can help the patient clot during surgery. The use of competitive antagonists can be found in the administration of anesthesia. One example is nondepolarizing muscle relaxants (e.g., rocuronium, cis-atracurium, and vecuronium). These drugs are frequently used in the operating room to create muscle paralysis. Muscle paralysis may be necessary to intubate a patient or to create relaxed muscles that will make it easier for the surgeon to perform surgery.
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These muscle relaxants are competitive antagonists that compete with acetylcholine for the nicotinic receptor on muscle cells. This concept is more fully discussed in Chapter 16. αq/11 β GDP
αq/11
γ
Inactive state
Active state
A
Agonist (histamine)
αq/11 β GDP
Receptor States
GTP
Histamine
αq/11
γ
GTP
Inactive state
Active state
B H1-antihistamine Inverse agonist (H1-antihistamines)
αq/11 β GDP
Most receptors remain in the inactivated state and spontaneously cycle through to the activated conformation (shape); however, the receptor is only in the activated form for the minority of its time. Therefore, only a small percentage of a type of receptor is usually in its activated state. This percentage represents the receptors’ baseline state of activation. When a ligand binds to a receptor, the receptor is stabilized in the active state. In the activated state, receptors will interact with intermediate proteins within the cell wall and the cell, thus initiating the response cascade within the cell. Many classic antagonists are now considered to be inverse agonists. An inverse agonist is thought to bind to the receptor and stabilize the inactivated state of the receptor. This reduces the number of receptors in the activated state, which brings the activity of the receptor below its usual baseline (see Fig. 5.3).
αq/11
γ
Receptor Structure
GTP
Inactive state
Active state
C ■ FIGURE 5.3 Stabilization of a receptor in its inactivated state by an antagonist. (With permission: Figure 42-3: Adapted with permission from Leurs R, Church MK, Taglialatela M. H1-antihistamines: inverse agonism, antiinflammatory actions and cardiac effects. Clin Exp All. 2002;32:489–498, Figure 1.)
α
β
There are four types of receptor channels that are important in anesthesia. These include membrane receptor (G-protein coupled), ligand-gated ion channel, voltage-sensitive ion channel, and enzyme receptors (see Fig. 5.4). Membrane receptors on cell membranes are typically structured with a water-loving (hydrophilic) portion of the receptor, which is outside
γ
GDP
A
B
C
D
■ FIGURE 5.4 Four different types of drug receptors. (From Golan DE, Tashjian AH, Armstrong EJ. Principles of pharmacology. The Pathophysiologic Basis of Drug Therapy. 2nd ed. Baltimore, MD: Wolters Kluwer Health, 2008, with permission.)
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Chapter 5 • Pharmacodynamics
of the cell membrane. The external hydrophilic portion is able to bind water-soluble ligands. These ligands would otherwise be unable to cross into the cell that has a lipid interior. In the cell, just like in your kitchen, oil (lipid or hydrophobic molecules) and water (ionized or hydrophilic molecules) do not mix. Therefore, ligands that are water loving or hydrophilic cannot cross into the lipid portion of the cell membrane. To cross the membrane without any help, the molecule must be able to dissolve in fat (lipophilic). The receptor serves as the messenger system across the lipophilic cell membrane and allows the ligands to send its message without entering the cell itself. Some membrane receptors couple with G proteins to create their message within the cell. The most common version of the G-protein–coupled receptor is the cyclic adenosine 3’5’–monophosphate system “cAMP.” In this chain reaction, the ligand binds to a receptor that causes G proteins to activate the enzyme responsible for synthesizing cAMP. Many drugs are coupled to this enzyme system including betaagonists like epinephrine. The ligand-gated ion channel opens an ion channel when the ligand binds to the receptor. The opening of the channel will cause ions (molecules with a positive or negative charge) to flow into or out of the cell. The ions flowing into the cell can cause a process to occur within the cell or at the cell membrane. γ-Aminobutyric acid is a ligand-gated ion channel and it is the location of action of most hypnotic drugs such as benzodiazepines, barbiturates, propofol, and etomidate. Another method of cellular messaging is when a change in the electrical potential across a cell membrane changes and is propagated along the length of the cell. The electrical potential across a cell membrane is determined by the concentration of charged ions on either side of the membrane. When a ligand-gated channel opens, the concentration of ions across the cell membrane changes, which changes the membrane potential. This change in membrane potential can cause a change in conformation of a nearby voltagesensitive channel and allow the transit of molecules across the channel. In some cases, these are ions that can cause further membrane potential changes and so on. The end result is the membrane potential change (depolarization) is propagated along the cell membrane for the length of the cell. One example of this type of cellular
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messaging is a nerve cell. Eventually the cell must restore the ion concentrations across the cell membrane (repolarization) in order to reset the voltage-dependent channels, and be prepared to send another message. Local anesthetics target voltage-gated receptors. These agents often work by binding to a receptor on voltage-gated sodium channels. Once bound to the receptor, the conformation of the channel changes and allows sodium to pass through the channel. Because the conformational change is slow to reverse, the cell cannot reset and repolarization is slow to occur, thus inhibiting further cellular signal transmission. The ion pump is another type of receptor, one example of which is the adenosine triphosphatase (ATPase) ion pump. This pump serves as a motor, which pumps sodium out of the cell in exchange for potassium moving into the cell. This pump requires adenosine triphosphate (ATP) to bind to a receptor on the inside of the cell to activate the pump.
■ PHARMACODYNAMICS AND CLINICAL PHARMACOLOGY Pharmacodynamics also looks at what happens after a drug has attached to its receptor and created a conformational change and the ensuing cellular response. What is the final effect that we see on the human body?
Dose-response Curves A dose-response curve looks at the concentration of drug versus the response in the individual. This relationship is based on dose and concentration but does not take into account the time course of the response. This effect is described through the “Hill” equation (see Fig. 5.5).
Potency and Efficacy Potency describes the dose versus response relationship. This is typically described best as a concentration versus response relationship. Efficacy is a measure of the ability of the drug to produce a physiologic effect (see below). If two drugs create the magnitude effect, the drug that creates that effect at a lower dose is more potent. Effective Dose and Lethal Dose Effective dose or ED 50 is the dose of a drug required to produce a specific effect in 50% of patients to whom it is administered. The LD 50 is the dose of a drug that would be expected to be lethal in 50% of patients to whom that dose is
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drug binding to receptors. Receptors mediate the action between the drug (or ligand) and the cellular cascade of events within the cell that are ultimately responsible for the drugs action at a cellular level. Drug action at a receptor can be as an agonist or antagonist. The relationship between how quickly a drug binds and releases from a receptor can be described by the disassociation constant. The potency and efficacy of a drug can be described by the ED 50, LD 50, and the therapeutic index.
A Linear 1.0 Drug A Drug B E
EMAX
0.5
0 EC50(A) EC50(B)
[L]
B Semilogarithmic 1.0
REVIEW QUESTIONS
Drug A Drug B E
EMAX
0.5
0 EC50(A) EC50(B) [L]
■ FIGURE 5.5 Hill equation for describing a dose-response curve. (From Golan DE, Tashjian AH, Armstrong EJ. Principles of pharmacology. The Pathophysiologic Basis of Drug Therapy. 2nd ed. Baltimore, MD: Wolters Kluwer Health, 2008, with permission.)
administered. The therapeutic index is the ratio of the LD 50 to the ED 50. The larger the therapeutic index of a drug, the safer it is for administration. Opioid-tolerant patients have a small therapeutic index or therapeutic window of administration. In the post anesthesia care unit (PACU), opioid-tolerant patients require higher doses of opioids than other patients. The opioid-tolerant patient can be sedated and difficult to arouse in the PACU, and as a consequence, when woken from sleep, they will describe intense pain. If they receive more opioids to treat their pain, they may be dangerously sedated and still not achieve proper pain control. These patients have a small therapeutic index and the risk may exceed the benefit of the medication.
■ SUMMARY Pharmacodynamics is the study of what drugs do to the body. Central to the understanding of how drugs work in the body is to understand
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1. What is pharmacodynamics? A) The effect of the drug on the body B) Drugs acting on a cell C) Drugs acting on a molecular level D) Drugs effect on an organ system E) All of the above Answer: E. All of the above. Pharmacodynamics is the result of the drug’s effects on the body that include actions on systems, cells, and molecules. Pharmacokinetics describe what the body does to the drug.
2. Receptors site are _____ and cell membranes are _____? A) Hydrophilic and hydrophobic B) Hydrophilic and hydrophilic C) Hydrophobic and lipophilic D) Lipophilic and lipophilic Answer: A. Hydrophilic and hydrophobic. Cell membranes are made of lipid and are hydrophobic (repels charged molecules or water). They are also lipophilic (accommodate fat-soluble molecules, those that are not charged). Receptors can attach to ionized molecules and send a message through the cell membrane to effect change within the cell.
3. Aspirin is a _____ of platelet clotting function. A) Competitive agonist B) Competitive antagonist C) Noncompetitive agonist D) Noncompetitive antagonist Answer: D. Aspirin is a noncompetitive antagonist of platelet function. It attaches to platelets irreversibly; in other words, aspirin cannot be removed from its receptor on the platelet with another competitor ligand. Competitive antagonists compete for binding to the receptor with other molecules. The concentration of the molecules and the Kd of the molecules determine which competitor binds more receptors.
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Chapter 5 • Pharmacodynamics
REFERENCES 1. Booij LH. Neuromuscular transmission and its pharmacological blockade. Part 2. Pharm World Sci. 1997; 19(1):13–34. 2. Eger EI, Saidman LJ, Brandstater B. Minimum alveolar anesthetic concentration: a standard of anesthetic potency. Anesthesiology. 1965;26:756–763. 3. Ghanouni P, Steenhuls JJ, Farrens DL, et al. Agonistinduced conformational changes in the G-proteincoupling domain of the beta 2 adrenergic receptor. Proc Nal Acad Sci USA. 2001;98:5997–6002. 4. Hall, R. Mazer, DC. Antiplatelet drugs: A review of their pharmacology and management in the perioperative period. Anesth Analg. 2011;112(2):292–318. 5. Hudson R. Basic principles of clinical pharmacology. In: Barash PG, Cullen BF, Stoetling RK, eds. Clinical Anesthesia. Philadelphia, PA: Lippincott Williams & Wilkins; 1997:253–260. 6. Lai J, Hunter JC, Porreca F. The role of voltage-gated sodium channels in neuropathic pain. Curr Opin Neurobiol. 2003;13:291–297. 7. Pasternak GW. When it comes to opiates, just say NO. J Clinl Invest. 2007;117(11):3185–3187.
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8. Mason RP, Giles T, Sowers J. Evolving mechanisms of actions of beta blockers: focus on Nebivolol. J Cardiovasc Pharmacol. 2009;54(2):123–128. 9. Rolley E, Fudala P. Bruprenorphine: considerations for pain management. J Pain Symptom Manage. 2005;29(3): 297–326. 10. Sadean MR, Glass PSA. Pharmacokinetic– pharmacodynamic modeling in anesthesia, intensive care and pain medicine. Curr Opin Anaesthesiol. 2009; 22:463–468. 11. Shafer SL, Flood P, Schwinn D. Basic principles of pharmacology. In: Miller RD, et al., eds. Anesthesia. 6th ed. New York, NY: Churchill Livingstone; 2005: 495–507. 12. Skrabanja ATP, Bouman EAC, Dagnelie PC. Potential value of adenosine 5’-triphosphate (ATP) and adenosine in anesthesia and intensive care medicine. Br J Anaesth. 2005;94(5):556–562. 13. Swaminath G, Deupi X, Lee TW, et al. Probing the beta adrenoreceptor binding site with catechol reveals differences in binding and activation by agonist and partial agonists. J Biol Chem. 2005;280:22165–22171.
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CHAPTER
6
Efficacy, Toxicity, and Drug Interactions Amy Opilla and Kim Mauer ■ EFFICACY As introduced in the previous section, efficacy is the maximal effect produced by a drug. It is related to the ability of a drug to bind with the appropriate receptors to cause a desired effect. It is affected by the route of administration, volume of distribution, and clearance of the drug from the body. Therefore, efficacy of a particular drug can vary among patients depending on drug pharmacokinetics, pharmacodynamics, or both with respect to the individual patient. As the concentration of a drug increases, its effect also increases. However, there is a point when increased drug concentration does not produce any additional effect, which is defined as maximal efficacy. From this dose-response relationship, the value of ED 50 is derived (as stated in Chapter 5, this is the dose at which 50% of patients exhibit the desired effect of the drug). The dose-response relationship is also used to define the lethal dose of medications (again, as stated earlier, LD 50 is the dose that will cause mortality in 50% of the population). This is derived experimentally in rats or mice.
■ ADVERSE EFFECTS The desired effect of a drug is the effect that treats the patient’s symptoms or disease. In addition to the desired effects, drugs also can produce unwanted effects. When these unwanted effects are mild, they are called side effects and can include a myriad of symptoms such as dry mouth, headache, or nausea. However, these side effects also have the potential to be harmful or toxic and these are known as adverse effects. These adverse effects can be pharmacologic or dose related, meaning that giving an overdose of medication leads to toxic effects. Drugs with a narrow therapeutic index (ratio of LD 50 to
ED 50) are more likely to cause adverse effects due to overdose. For example, in anesthesiology, opioid medications (e.g., fentanyl and morphine) are commonly used to treat pain in the perioperative period. Opioids have a dose-related adverse effect of respiratory depression. Therefore, if too high a dose is given to a particular patient, the patient’s respiratory rate will decrease and he or she may stop breathing. Adverse effects are also related to lack of selectivity of drugs for the desired target. The target may be one organ or system, but the drug has the ability to interact with receptors all over the body, which may produce adverse effects in other organs. One example of this would be β antagonists, which is a drug commonly used in anesthesiology to treat tachycardia and hypertension. β receptors are located all over the body, and blocking all of these receptors may have adverse effects in other systems, such as triggering bronchospasm in patients with reactive airway disease. Adverse effects can also occur as a result of the metabolism of the drug. If drug breakdown produces a toxic metabolite, this can lead to adverse effects. In an acetaminophen overdose, enzymatic pathways are saturated, and a reactive toxic metabolite is formed, leading to liver injury. Allergic reactions to drugs are another form of adverse effect, the most severe being anaphylaxis, which is an immediate hypersensitivity reaction. In an anaphylactic reaction, the drug antigen activates the patient’s immune system, causing mast cells to release histamine via an IgE-mediated response. This leads to edema, vasodilation, hypotension, and shock. When the causes of adverse effects of a drug are not dose related or are unclear, they are called
28
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Chapter 6 • Efficacy, Toxicity, and Drug Interactions
idiosyncratic reactions and may be due to individual patient characteristics such as metabolism, receptor-drug interaction, immunologic factors, or a combination of multiple factors. Many common drugs in anesthesiology can lead to pathologic toxicity in different organ systems. Therefore, when administering a drug, the dose for each particular patient must be carefully calculated and the risk to benefit ratio must always be considered. In other words, does the benefit of the desired effect of this drug outweigh the risk of adverse effects for this particular patient?
■ DRUG INTERACTIONS The concept of drug interactions is very important in anesthesiology; a standard general anesthetic can include as many as 10 different drugs. Drug interactions can be due to a number of factors, such as pharmaceutical, pharmacokinetic, pharmacodynamic, or a combination thereof. Pharmaceutical drug interactions occur prior to the drug being administered or absorbed, such as the formation of a precipitate when mixing drugs in the same syringe. Pharmacokinetic factors of drug interactions include absorption, distribution, metabolism, and elimination. Absorption may be altered due to the effect of a drug on the body, such as in the gastrointestinal system, where certain drugs can alter the gastric pH or gastric motility, causing differences in absorption of other drugs administered by mouth. Another example of altered absorption is when anesthesiologists use local anesthetics combined with epinephrine. The epinephrine causes vasoconstriction, which helps to decrease absorption and prolong the effect of the local anesthetic. Distribution can be altered by competition at plasma protein binding sites or displacement from or alteration of tissue-binding sites. Metabolism of one drug can be altered by another drug administered concurrently. Drugs may induce or inhibit enzymes that break down drugs, such as cytochrome P450, causing an increase or decrease in efficacy. Pharmacodynamic factors of drug interactions include addition, synergism, or antagonism. Drugs that act on the same receptors are additive, whereas drugs that bind with different receptors but have the same effect are synergistic. Both of these types of drug interactions lead to an increase in the desired effect. Drugs that cause opposing effects are antagonists and may
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cause a reduced response of one drug or both when administered together. Anesthesiologists often utilize pharmacodynamic properties of drug interactions during administration of general anesthesia. For example, a volatile anesthetic, benzodiazepine, propofol, and an opioid can be combined to produce central nervous system (CNS) depression due to their additive and synergistic properties. Also, the reversal of neuromuscular blockade is an example of utilizing antagonistic drug interactions. Adverse effects of drugs can also be additive, such as both acetaminophen and alcohol can cause hepatoxicity, and this negative effect is greatly increased when both drugs are administered together. In addition to drug-drug interactions, herbal supplements can also interact with drugs to cause adverse effects. Herbal supplements, often identified as nutraceuticals, are consumed by a significant proportion of patients scheduled for surgical procedures. This is largely due to the use of herbal supplements in the United States, which has increased dramatically in recent years. The Food and Drug Administration (FDA) does not regulate these products with the same scrutiny as conventional drugs. This is concerning as some of these agents have the potential to cause serious drug interactions and hemodynamic instability during surgery. Thus, it is extremely important to identify patients self-administering these medications. Ginkgo, garlic, ginger, and ginseng increase the risk of bleeding when taken independently, and a provider should be aware of these substances before anesthetizing patients. Acetaminophen, when added to ginkgo, garlic, ginger and ginseng, further increases the risk of bleeding. The hepatotoxic herbs, echinacea and kava, become more hepatotoxic in combination with acetaminophen. Nephrotoxicity becomes a concern when acetaminophen is combined with herbs containing salicylate (willow and meadowsweet). The concomitant use of opioid analgesics with the sedative herbal supplements, valerian, kava, and chamomile, may lead to increased CNS depression. The analgesic effect of opioids may also be inhibited by ginseng. Aspirin interacts with the herbal supplements that are known to possess antiplatelet activity (ginkgo, garlic, ginger, bilberry, dong quai, feverfew, ginseng, turmeric, horse chestnut, fenugreek, and red clover) and with tamarind, enhancing the risk of bleeding.
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Herbals known to increase blood pressure include goldenseal, licorice, ephedra (Ma-Juang), and St. John’s wort. Kava kava may prolong the effect of certain anesthetics and increases the risk of suicide for people with certain types of depression.
■ SUMMARY The administration of anesthesia involves multiple drugs with multiple routes of administration. This chapter introduces the concepts of efficacy and toxicity, adverse reactions, and drug interactions. Anesthesia technicians will be more familiar with the perioperative environment if they have a basic understanding of the principals of pharmacology.
3. Which of the following is the correct definition of ED 50? A) The ratio of effective dose to lethal dose in 50% of the population B) The ratio of IV to oral medication that produces equivalent effect in 50% of the population C) The dose that causes mortality in 50% of the population D) The dose that produces the desired effect in 50% of the population E) The dose that produces adverse effect in 50% of the population Answer: D. This is the definition of ED 50.
SUGGESTED READINGS
REVIEW QUESTIONS 1. Which of the following can cause adverse drug reactions? A) Overdose B) Metabolites C) Allergy D) All of the above E) None of the above Answer: D. Adverse reactions can be dose related, and the more narrow the therapeutic window, the more likely that adverse reactions due to overdose will occur. Breakdown of drugs can form toxic metabolites, which may lead to adverse effects. Allergic reactions are a form of adverse reaction to a drug, the most severe being anaphylaxis.
2. Which of the following statements about drug interactions is TRUE? A) Drugs that act on the same receptors and cause the same response are antagonists. B) When two drugs mixed together form a precipitate, a pharmacokinetic reaction has occurred. C) Anesthesiologists commonly utilize drug interactions to their advantage in standard general anesthetics. D) Herbal supplements are natural and do not interact with drugs administered by anesthesiologists.
Gonzalez FJ, Coughtrie M, Tukey RH. Drug metabolism. In: Brunton LL, Chabner BA, Knollmann BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill; 2010. Gupta D, Henthorn T. Pharmacologic principles. In: Barash PG, Cullen BF, Stoelting RK, et al., eds. Clinical Anesthesia. 6th ed. Philadelphia: Lippincott, Williams & Wilkins; 2009:137–164. Munir Pirmohamed M, Breckenridge AM, Kitteringham NR, et al. Fortnightly review: adverse drug reactions. BMJ. 1998;316:1295–1298. Osterhoudt Kevin C, Penning Trevor M. Drug toxicity and poisoning. In: Brunton LL, Chabner BA, Knollmann BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill; 2010. Roscow RE, Levine WC. Drug interactions. In: Barash PG, Cullen BF, Stoelting RK, et al., eds. Clinical Anesthesia. 6th ed. Philadelphia: Lippincott, Williams & Wilkins; 2009:549–566. von Zastrow Mark, Bourne Henry R. Drug receptors & pharmacodynamics. In: Katzung BG, ed. Basic & Clinical Pharmacology.11th ed. Available from: http:// www.accessmedicine.com.liboff.ohsu.edu/content. aspx?aID=4509384.gff
Answer: C. Anesthesiologists commonly utilize drug interactions to their advantage in standard general anesthetics. This statement is true. For example, the drug interaction that occurs when intravenous (IV) and volatile anesthetics are combined is a form of synergism.
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CHAPTER
7
Cardiovascular Anatomy and Physiology Glenn Woodworth, Asish Das, and Valerie Sera ■ INTRODUCTION Anesthesia and surgery is a delicate dance with the cardiovascular system. The majority of anesthetics interact with the cardiovascular system by depressing sympathetic outflow, dilating blood vessels, or directly interacting with the heart. Surgical stimuli, blood loss, and anesthetic procedures have the further ability to interact with the patient’s cardiovascular system. This chapter introduces the anesthesia technician to the fundamental anatomy and physiology of this important body system.
■ SURFACE ANATOMY OF THE HEART The heart is a set of hollow muscular pumps combined into a single organ. It is located in the middle of the chest (the mediastinum) between the lungs and their pleural coverings. It is shaped like an upside down pyramid that is tilted to the patient’s left. The base of the heart lies superiorly, and the apex lies inferiorly and leftward (Fig. 7.1). The heart itself is covered in a thick sac called the pericardium. The heart is divided into two sides, a right and a left, and consists of a total of four chambers. The upper two chambers comprise the right and left atria, while the lower chambers are termed the right and left ventricles. The inferior and superior vena cava are connected to the right atrium (RA), and the pulmonary artery is connected to the right ventricle (RV). On the left side of the heart, the pulmonary veins are connected to the left atrium, and the aorta is connected to the left ventricle (LV) (Fig. 7.2). The heart is rotated slightly to the left, and the apex is tilted slightly anteriorly. Thus, the RA is anterior to the left atrium (LA), and the RV forms most of the anterior aspect of the ventricular mass. The LV is positioned on the left side of the
heart, but because of the rotation and the tilting, it is also positioned slightly posterior and inferior to the RV. An understanding of the position of the heart is important to properly read the electrical signals that are generated by the heart and recorded on an electrocardiogram (ECG). The ECG is discussed in more detail later in this chapter.
■ FETAL DEVELOPMENT Major organ development occurs between the 4th and 8th week of fetal life. The heart is the first organ to complete its development during fetal growth. The heart begins as a primitive vascular tube that curves back on itself and bends anteriorly and rightward to form three distinct portions called the single-chambered primitive atrium, a ventricle, and the truncus. These develop further into a right heart and a left heart, atria and ventricles with intervening atrioventricular (AV) valves, and the aortic and pulmonary trunks. Errors in fetal development of the heart can result in significant malformations. For example, the heart may fail to form two ventricles, or the aorta and pulmonary trunks may be fused into a single trunk arising from both ventricles. An average adult heart is 12 cm from base to apex, 8–9 cm at its broadest transverse diameter, and 6 cm anteroposteriorly. Its weight varies with average 300 g in male and 250 g in females, with adult weight achieved between the ages of 17 and 20 years.
■ PERICARDIUM The heart is enclosed in a three-layered sac called the pericardium. The outer fibrous layer of the pericardium is attached to the great vessels, the sternum, and the diaphragm. It secures the heart to the sternum anteriorly and to the diaphragm inferiorly. The inner serous layer 31 tahir99-VRG & vip.persianss.ir
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■ MYOCARDIUM
■ FIGURE 7.1 Normal heart anatomy, anterior view.
consists of a visceral and parietal portion. The visceral pericardium, also known as the epicardium, covers the entire heart and great vessels. The parietal pericardium forms an inner lining to the fibrous pericardium. The space between the two layers of the serous pericardium is called the pericardial space. Normally, the pericardial space contains 30–50 mL of serous fluid that acts as a lubricant to decrease friction while the heart beats. The fibrous layer of the pericardium is noncompliant (not easily expandable) and helps to prevent dilation of the heart and restrict cardiac filling beyond the normal range. When there is an acute collection of fluid or blood in the pericardial space, a clinical condition called cardiac tamponade develops. Rapidly accumulating fluid in the pericardial space can put pressure on the heart chambers, severely restricting blood from entering the heart, and can result in circulatory collapse. Surgical intervention is often necessary to relieve cardiac tamponade.
The heart wall consists of three layers. The outermost layer of the heart is the epicardium, consisting of epithelial cells that form a serous membrane that covers the entire heart. The innermost layer of the heart is the endocardium. It lines the inner surface of the heart, its valves, the papillary muscles, and the fibrous cords that connect the valves and continues into the major cardiac veins and arteries. The middle layer of the heart is the muscular layer known as the myocardium. It is responsible for the contractile action of the atria and ventricles. The human body contains three types of muscle: cardiac muscle, smooth muscle (found in other hollow organs like the bowel or bronchi), and skeletal muscle. Cardiac muscle cells are specialized muscle cells with amazing resiliency and capabilities. At an average heart rate (HR) of 60 beats per minute, the heart beats 3 billion or more times without resting in one’s lifetime. To accomplish this incredible feat, myocardial cells function in a slightly different manner than do skeletal muscle cells. Myocardial cells are rich in mitochondria, the energy engine of the cell. The large number of mitochondria makes the cells resistant to fatigue. This allows myocardial cells to perform almost continuous work as long as they have a rich supply of oxygen and nutrients. Unlike skeletal muscle, myocardial cells rapidly become unable to function if their blood supply is interrupted. In addition to extra mitochondria, myocardial cells have other unique properties. For example, they have the intrinsic ability to contract in the absence of stimuli in a rhythmic manner and have the ability to conduct electrical impulses from one myocardial muscle cell to the next. Both of these functions play an important role in the cardiac conduction system described below.
■ CARDIAC CHAMBERS AND THE CIRCULATION OF BLOOD As described above, the heart has four chambers: the RA, the RV, the LA, and the LV. The purpose of the heart is to circulate blood throughout the body where it can deliver oxygen and other nutrients, as well as pick up waste products like carbon dioxide. The blood circulates through the body in two loops or systems: the pulmonary circulation and the systemic circulation (Fig. 7.3). Beginning with the terminal portion of the systemic circulation, blood is drained into the venous
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Chapter 7 • Cardiovascular Anatomy and Physiology
33
NORMAL HEART ANATOMY
Cross Section
Superior vena cava Aorta Pulmonary trunk Right atrium Left auricle Pulmonary valve
Mitral valve
Tricuspid valve
Left ventricle
Inferior vena cava
Right ventricle
■ FIGURE 7.2 A coronal cut through the heart demonstrating the four chambers of the heart and their vascular connections.
system from the various organs and extremities. Blood from the lower portion of the body eventually drains into a large vein, the inferior vena cava (IVC). Blood from the upper portion of the
body, including the upper extremities and the head and neck, drains into the superior vena cava (SVC). This venous blood has had much of its oxygen removed (deoxygenated) by the tissues
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Section II • Anatomy, Physiology, and Pharmacology
Superior vena cava Aortic arch
Pulmonary arteries Pulmonary arteries
Pulmonary veins
Pulmonary veins
Left atrium Bicuspid (mitral) valve
Right atrium
Tricuspid valve
Left ventricle Right ventricle
Inferior vena cava
■ FIGURE 7.3 Blood circulates through the heart in two loops forming the pulmonary and systemic circulations.
and contains extra waste products like additional carbon dioxide (CO2). The systemic venous blood from both large veins drains into the RA. Contraction of the RA pushes the deoxygenated blood through the tricuspid valve into the RV. Contraction of the RV forces the blood forward past the pulmonic valve into the pulmonary artery, the beginning of the pulmonary circulation. The pulmonary arteries branch into ever smaller arteries and arterioles before turning into capillaries. Capillary blood flows close to the pulmonary alveoli. The blood can now add oxygen from the alveoli and discharge CO2 into the alveoli (see Chapter 11). Once the blood has been oxygenated and discharged some of its CO2, it begins to collect from the capillaries into venules and eventually into the large pulmonary veins. The four large pulmonary veins drain into the left side of
the heart and the LA. Contraction of the LA forces the oxygenated blood forward through the mitral valve and into the LV. The forceful contraction of the LV can generate high pressures, and the blood is ejected out of the LV through the aortic valve and into the aorta. From the aorta, the blood flows out to the systemic circulation, where it can perfuse the body. The blood can then return to the heart to complete the two loops. It is the continuous forward pumping action of the heart that keeps blood flowing through the body where it can deliver nutrients and pick up waste products.
Right Atrium The RA is a thin-walled muscular chamber. It receives deoxygenated venous blood from the SVC, the IVC, and the coronary sinus. The coronary sinus empties into the RA just above the
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Chapter 7 • Cardiovascular Anatomy and Physiology
tricuspid valve. In addition to the main chamber of the atrium, the RA has a small muscular pouch, the right atrial appendage. The RA is separated from the LA by the septum. The septal wall has an oval depression, the fossa ovalis. There are no true one-way valves in the venae cavae; thus, when the right atrial pressure rises, elevated pressure is reflected into the IVC and the SVC. Venous distention and systemic venous congestion are commonly seen when pressures are elevated in the heart as in congestive heart failure. Normal right atrial pressure ranges from 2 to 10 mm Hg.
Right Ventricle The RV extends from the tricuspid valve nearly to the apex of the heart. The tricuspid valve prevents flow of blood backward from the RV into the RA. At the base of the heart, the RV extends to the left to form the infundibulum. The pulmonary valve prevents the flow of blood from the pulmonary artery backward into the RV. In addition to the main muscular walls of the RV, the RV contains two major papillary muscles and a third smaller papillary muscle. The papillary muscles connect the chordae, fibrous collagenous cords, to the leaves (cusps) of the tricuspid valve. The RV receives blood from the RA through the tricuspid valve and ejects it through the pulmonic valve into the pulmonary artery where it can flow to the lungs. The resistance to flow in the pulmonary circulation is approximately 1/10th that of the systemic circulation. Therefore, the RV does not need to generate as much pressure to pump blood to the lungs as the LV needs to pump blood to the body. This also explains why the RV muscle is much thinner than the thick muscular wall of the LV. Systolic pressure in the RV ranges from 15 to 25 mm Hg with end-diastolic pressures from 0 to 8 mm Hg (the concepts of systolic and diastolic pressures are discussed in detail below).
Left Atrium The LA is the smaller of the two atria but has thicker walls. Its cavity and walls are mostly formed by the proximal part of the pulmonary veins, which are incorporated into the atria during fetal development. The left atrial aspect of the septum between the atria has a rough appearance and marks the site of the foramen ovale. In fetal life, the foramen remains open and is essential for fetal circulation. At birth, this foramen closes spontaneously, but in about 20%–30% of
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the normal population, the defect may persist without any symptoms. Although asymptomatic, a patent foramen ovale presents a potential passageway for gas bubbles or debris to pass from the right side of the heart to the left side without passing through the lungs. Under normal circumstances, most debris, like small blood clots or gas bubbles, will be stopped by the pulmonary microcirculation before they can reach the left side of the heart. Under abnormal circumstances (i.e., conditions in which the right atrial pressure is elevated), passage of gas or debris from the RA across the foramen ovale to the LA becomes a real possibility. This is important as any debris or bubbles in the left side of the heart could flow out of the heart and directly into the brain, causing a stroke. The LA receives oxygenated blood from the lungs through pulmonary veins. Normal filling pressure ranges from 4 to 12 mm Hg. Like the RA, the LA also has an appendage. The LA appendage forms a portion of the left heart border as seen on a chest x-ray. In atrial fibrillation (disorganized electrical activity of the heart), it can be a source of intracardiac blood clots. These clots can embolize systemically, causing a stroke or limb ischemia. When the atria fibrillates, it loses its contractile function and the left atrial appendage is less able to empty blood into the atrial main cavity. Blood pooling in the atrial appendage is prone to clotting.
Left Ventricle The LV wall is almost three times thicker than the RV wall. It is designed to be a powerful contractile chamber that can maintain flow in the high-pressured systemic arteries. The LV cavity extends from the AV groove to the cardiac apex. The mitral valve forms the inlet to the LV. The outlet region is formed by the aortic valve. The septum dividing the right and left ventricles is thick and is functionally more a part of the LV than the RV (Fig. 7.4). A ventricular septal defect is the most common congenital heart defect in children younger than 2 years of age. Most small defects close spontaneously. Only the larger defects need surgical correction. The normal thickness of the LV wall is between 0.8 mm and 1.1 cm. In hypertrophic cardiomyopathy, the septum may get disproportionately thickened. When the ventricle contracts, the hypertrophic septum can obstruct the outflow of blood from the ventricular cavity into the aorta (dynamic
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Section II • Anatomy, Physiology, and Pharmacology
Cardiac Skeleton The heart’s fibrous skeleton, the “annulus fibrosus,” is a firm anchor to which most of the heart’s muscles and valves are attached. The annulus fibrosus gives structure to the heart and acts as an insulator. Because the annulus fibrosus is not made up of myocardial muscle cells it does not conduct electrical impulses from one region of the heart to another. This ensures that electrical impulses traveling from the atria myocardial cells to the ventricular myocardial cells must move through a specialized pathway, the AV node. This system helps the heart regulate electrical signaling to coordinate contraction of the atria and ventricles as well as to help prevent abnormal electrical heart rhythms (arrhythmias).
Cardiac Conduction System
■ FIGURE 7.4 Cross-section of the heart demonstrating right and left ventricles.
subaortic obstruction). This clinical condition may cause sudden death and requires medical treatment. The LV receives blood from the LA through the mitral valve and ejects blood through the aortic valve to the systemic circulation via the aorta. The mitral valve prevents the flow of blood backward into the LA during contraction of the LV. There are several fibrous chords attached to papillary muscles in the ventricle that support the mitral valve cusps. These chordae are essential for the proper functioning of the mitral valve. Pressure in the LV is high during muscular contraction (“systole”) and equals systemic blood pressures. When the ventricle relaxes (“diastole”), the pressure falls. Normal end-diastolic pressures in the LV range from 4 to 12 mm Hg. The smooth left ventricular outflow tract ends at the cusps of the aortic valve. The cusps of the aortic valve are attached in part to the aortic wall and in part to the supporting ventricular structures. The aortic valve in its closed position has three coronary sinuses (out pouching between the aortic wall and the cusp).
Myocardial muscle cells differ from skeletal muscle cells because of their inherent ability to spontaneously depolarize and repolarize in a rhythmic fashion (automaticity). Ventricular muscle cells spontaneously depolarize at a lower frequency (30–40 beats per minute) than atrial muscle cells, but in the intact heart, both are synchronized to a more rapid rhythm, generated by pacemaker cells in the RA. The pacemaker cells, called the sinoatrial (SA) node, and the specialized myocardial cells, which conduct the electrical signals to synchronize the contraction of all myocardial cells, make up what is known as the “cardiac conduction system” (Fig. 7.5). The SA node is located in the high RA near the junction of the SVC and the RA. These “pacemaker cells” spontaneously depolarize and initiate contraction of the myocardial cells in the atria. Because all myocardial cells can conduct the electrical impulse and cause adjacent myocardial cells to depolarize, the electrical depolarization and subsequent contraction of atrial cells spreads like a wave beginning at the SA node. Several other specialized myocardial conduction cells conduct the electrical impulse from the RA to the LA (Bachmann’s bundle). The depolarization must also be conducted from the atria to the ventricles and more importantly the timing of atrial and ventricular contractions synchronized (see “Cardiac Cycle” below). If the atria and ventricles contract simultaneously, blood would not flow from the atria into the ventricles. The speed of conduction of electrical impulses through normal atrial and ventricular cells is about 0.5 m/s. The speed of
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Chapter 7 • Cardiovascular Anatomy and Physiology
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Sinoatrial node
Interatrial septum Atrioventricular node
Atrioventricular bundle (bundle of His)
Right and left bundle branches
Interventricular septum
■ FIGURE 7.5 The myocardial conduction system is made of specialized myocardial muscle cells forming the pacemaker region (the SA node), the AV node, the bundle of His, and the Purkinje fibers.
conduction of the electrical signal is much faster than the time it takes for muscular contraction; thus, the electrical signal from the SA node would reach the ventricle rapidly, long before the atrium has contracted. This would cause near simultaneous contraction of the atria and ventricles. In the normal functioning heart, this does not happen because the fibrous annular tissue that separates the atria from the ventricles does not conduct the electrical impulse. Instead the impulse must pass through a region of cells in the inferior posterior portion of the atrial septum called the AV node. This group of specialized myocardial cells conduct the impulse at 1/10th the speed of normal myocardial cells. This has the effect of slowing the electrical signal before reaching the ventricles. This gives the atria a chance to contract and eject blood into the relaxed ventricle before the ventricle begins its contraction. In order to efficiently eject blood and generate pressure within the ventricle, the septum and apex
of the ventricles must contract first, followed by the base of the heart. This coordination of contraction would not occur if the depolarization wave spread from the AV node through the ventricles from one cell to another. The heart utilizes additional specialized myocardial cells to rapidly conduct the electrical signals to the different portions of the ventricle to achieve effective contraction and blood ejection. These cells conduct the electrical signal 10 times faster than normal myocardial cells. After leaving the AV node, the electrical signal passes through the bundle of His to reach the base of the heart. It then passes on the endocardial side of the interventricular septum using specialized myocardical conduction cells (Purkinje fibers). It then moves along the endocardial side of each of the ventricles from apex to base using right and left branches of Purkinje fibers. The SA node, Bachman bundle, the AV node, the bundle of His, and the Purkinje fibers make up the myocardial conduction system.
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Wolff-Parkinson-White and other syndromes have abnormal electrical pathways in the heart that lead from the atria directly to the ventricles bypassing the AV node. These conditions can lead to very fast heartbeats (tachycardia) and even to life-threatening abnormal heart rhythms.
Coronary Arterial Supply The right and left coronary arteries arise from the ascending aorta just above the aortic valve. The coronary arteries supply the capillaries of the myocardium with oxygenated blood. One might think that the LV would not need any arteries because it could obtain oxygen directly from the oxygenated blood that flows through the ventricular cavities. However, the walls of the ventricles are too thick to obtain sufficient oxygen or eliminate waste products, like carbon dioxide, by diffusion. Arteries branching into arterioles and then capillaries must do the job. The blood is then collected into veins, which drain into the coronary sinus. The left coronary artery (LCA) has two main branches: the left anterior
descending (LAD) and the left circumflex (LCX) arteries (Fig. 7.6). The right coronary artery (RCA) and the LCX course around the heart in opposite directions in the AV groove. These two arteries throw off branches, with the terminal portions of the arteries meeting on the posterior aspect of the heart at an important landmark known as the crux of the heart. At this point, either the RCA or the LCX supplies the posterior descending artery (PDA), which descends in the interventricular groove toward the apex of the heart. This terminal branch supplies the posterior and inferior parts of the heart. Right or left coronary dominance is determined by which artery supplies the PDA. Seventy percent of people are RCA dominant, 10%–15% are LCA dominant, and 10%–15% have mixed right and left dominance. This is an important anatomical fact as the PDA supplies the crux and the posterior third of the ventricular septum. The AV node is located at the crux and is nourished by the PDA. Obstruction of the blood supply to the AV node can cause malfunction of the
Anterior view
Right coronary artery
Left coronary artery Circumflex artery
Branch to sinoatrial node Left marginal branch Right ventricular branch Diagonal branch Right atrial branch Posterior interventricular branch Anterior interventricular artery Right marginal branch
■ FIGURE 7.6 Coronary artery anatomy.
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Chapter 7 • Cardiovascular Anatomy and Physiology
node and prevent electrical impulses from traveling from the atrium to the ventricle properly (AV block). The RCA supplies the RA, RV, and inferior wall of the LV (if right coronary dominant). The LAD runs in the anterior interventricular groove and supplies the anterior wall of the LV. Along its course, it gives off diagonal arteries, which supply the lateral LV wall, and septal arteries, which supply the anterior two-thirds of the ventricular septum. The LCX artery supplies the LA and the lateral and posterior walls of the LV. The LAD, LCX, and RCA are considered major arteries because of their large area of distribution. Blockage in the proximal portion in any of these arteries can cause a large amount of myocardial cell death (myocardial infarction) and can significantly affect the heart’s ability to contract.
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Coronary Venous Circulation The venous system of the heart consists of the thebesian veins, the anterior cardiac veins, and the coronary sinus (Fig. 7.7). The coronary sinus is located in the posterior AV groove near the crux and collects about 85% of the blood from the LV. It opens into the RA at the coronary sinus ostium near the orifice of the IVC. During cardiac surgery, the coronary sinus must often be cannulated. Anomalies in coronary sinus anatomy can present significant challenges for both the anesthesiologist and the cardiac surgeon.
Innervation The heart is richly innervated by the autonomic nervous system to provide control of HR and the force of cardiac contractions (see Chapter 14).
Posterior view
Great cardiac vein Posterior vein of left ventricle
Anterior interventricular vein
Coronary sinus
Small cardiac vein
Middle cardiac vein
■ FIGURE 7.7 The coronary venous circulation.
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Section II • Anatomy, Physiology, and Pharmacology
Autonomic influence on the heart can modify cardiac function appropriately to meet the changing supply and demand of the body for blood flow. All portions of the heart are richly innervated by sympathetic fibers. When active, these sympathetic nerves release norepinephrine to act on the myocardial cells. Norepinephrine binds to β1-adrenergic receptors on cardiac muscle cells to increase the HR (chronotropy), increase the conduction velocity of electrical signals (dromotropy), increase the force of contraction (inotropy), and increase the speed of contraction and relaxation (lusitropy). Cholinergic parasympathetic innervation to the heart arises from the right and left vagal nerves and innervates the SA node, the atria, and the AV node. When active, these parasympathetic nerves release acetylcholine to act on myocardial cells. Acetylcholine interacts with muscarinic receptors on these cells to decrease the HR (SA node) and decrease the velocity of electrical signals moving through the AV node. Parasympathetic nerves may also act to decrease the force of contraction of atrial (not ventricular) muscle cells. Overall, parasympathetic activation acts to decrease cardiac pumping.
■ CARDIAC PHYSIOLOGY Cardiac Action Potential Like skeletal muscle, myocardial cells are able to contract due to the interaction of cellular proteins, actin and myosin. This interaction and subsequent contraction is dependent upon calcium for it to occur. As discussed above, the initiation of normal myocardial contraction begins with an electrical signal from the SA node. The electrical signal travels through the myocardial conduction system before reaching the rest of the myocardium. Upon reaching the myocardial cells, the electrical signal depolarizes the cell membrane, which opens channels to allow extracellular sodium and calcium to flow into the cell (Fig. 7.8). The inward flow of calcium causes additional calcium stores within the cell to be released. The calcium causes the cell to contract by promoting a temporary binding between actin and myosin. The calcium must be actively sequestered back into storage units within the cell to allow the muscle cell to relax. In addition, the myocardial membrane must be repolarized to prepare for another electrical signal. This sequence of events is called the cardiac action potential.
■ FIGURE 7.8 The cardiac action potential demonstrates cell membrane potential changes over time caused by changing flows of ions into and out of the cell. A) standard action potential. B) action potential from a cell with automaticity-automatic depolarization. Note how phase 4 shows the cell slowly depolarizing until it reaches a threshold to initiate phase 0. (From Topol EJ, Califf RM, et al. Textbook of Cardiovascular Medicine. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.)
The relative ratios of ions (molecules with strong positive or negative charges) like sodium, potassium, and calcium, inside and outside of the myocardial cell membrane create small electrical potentials or voltages across the membrane. For example, if there are more net positive ions outside of the cell than inside the cell, the cell would have a negative potential (the cell is polarized). By custom, the “positive” or “negative” potential of a cell is determined by the charge of the interior of the cell compared to the outside. At rest, myocardial cells have a negative potential called the resting membrane potential. Because of the charge differential between the inside and outside of the cell, the resting myocardial cell is a minibattery. Ions are kept inside and outside of the cell because the cell membrane is not permeable to ions. If an appropriate cellular channel for that ion is open, ions will flow into or out of the cell, depending upon the charge and concentration gradients. Once a sufficient electrical signal reaches the myocardial cell, it triggers a sequence of actions that open and close ion channels. The flow of ions across the channels causes the cell membrane potential to change over time resulting in the cardiac action potential. The phases of the cardiac action potential are as follows (Fig. 7.8): • Phase 4: Resting membrane potential • Phase 0: An electrical signal has caused the cell to open sodium channels and sodium rushes into the cell, depolarizing the membrane.
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Chapter 7 • Cardiovascular Anatomy and Physiology
• Phase 1: Fast sodium channels close. Small movements of potassium and chloride cause a slight dip in the membrane potential. • Phase 2: The membrane is kept depolarized by the inward flow of calcium ions balanced by an outward flow of potassium. • Phase 3: Repolarization occurs as the calcium channels close, but potassium continues to flow out of the cell. The cell must reset the ion balance by actively pumping sodium out of the cell and potassium into the cell. The cell must also restore calcium gradients by actively pumping calcium into storage. The cardiac action potential is much longer than that of skeletal muscle, and during this phase, cells remain unresponsive to further excitation. This is the refractory period.
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Supplemental right precordial leads
V5R
V4R V3R V2R V1R
Mid-clavicle Anterior axillary line Horizontal plane of V4–V6 RA
LA V1 V2 V3 V4 V5
Cardiac Electrophysiology During the phases of the cardiac action potential, ions move in and out of the cell, causing changes in membrane potential and causing small electrical currents. When the tiny electrical currents from multiple myocardial cells are added up, the currents can be measured with electrodes. A machine with lead wires and electrodes attached to the surface of the chest can measure these currents, amplify them, and record them on a graph, the ECG. The electrodes are small adhesive pads with electroconducting gel. They are attached to the ECG machine with lead wires. Each lead wire, with its attendant electrode, is attached to the body in a specific arrangement (Fig. 7.9). The specific location of the electrodes allows monitoring of signals from different directions and can be used to monitor different regions of the heart. Two or more electrodes are combined to form a “lead,” which should not be confused with a single lead wire. Each lead monitors the electrical signals from a specific direction. For example, the electrodes and lead wires from the right arm and the left arm are paired to create lead I. Electrical signals that travel along the axis from the right arm toward the left arm are measured and displayed as lead I. Signals traveling toward the designated electrode will be recorded as positive or upward deflections on the ECG. Therefore, electrical signals traveling toward the left arm electrode along the axis formed by the right arm and left arm electrodes will be recorded as upward deflections on the ECG. If the electrodes and lead wires for the right arm and the
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ECG strip
ECG machine RL
LL
■ FIGURE 7.9 Electrode placement in different positions to generate a 12-lead (ECG). (Adapted from Molle EA, Kronenberger J, West-Stack C et al. Lippincott Williams & Wilkins’s Pocketguide to Medical Assisting. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.)
left arm are placed properly, lead I will measure electrical forces in the heart that are traveling toward the left. In another example, the electrodes placed on the right arm, left arm, and left leg are combined into a single reference point in the center of the chest that is paired with the left leg electrode to form lead II. The axis from the reference point in the center to the left leg points leftward and inferiorly. Therefore, if the electrodes are properly placed, lead II will measure electrical forces in the heart that are traveling leftward and inferior. A standard ECG uses 10 electrodes (with 10 lead wires) in specific locations. The lead wires are used in various
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Section II • Anatomy, Physiology, and Pharmacology
Views reflected on a 12-lead ECG
Lead
View of the heart
Limb leads (bipolar) I
Lateral wall
II
Inferior wall
III
Inferior wall
aVL aVR
I
Augmented limb leads (unipolar)
III
aVR
No specific view
aVL
Lateral wall
aVF
Inferior wall
II aVF
Precordial, or chest, leads (unipolar) V1
Septal wall
V2
Septal wall
V6
V3
Anterior wall
V5
V4
Anterior wall
V5
Lateral wall
V6
Lateral wall
V4
V1 V2
V3
■ FIGURE 7.10 The spatial orientation of the 12 standard ECG leads. (From Springhouse. ECG Facts Made Incredibly Easy. 2nd ed. Ambler: Wolters Kluwer Health; 2010, with permission.)
combinations to produce 12 standard “leads.” Each lead measures the electrical forces from a specific direction. Figure 7.10 demonstrates the spatial orientation of the electrical forces measured by each of the standard 12 leads. Figure 7.11 shows a 12-lead ECG. Each small 1-mm box on the vertical axis of the ECG is 0.1 mV in a standard ECG (the sizing can be
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changed). By convention, most clinicians refer to the size of the waves in millimeters and not millivolts. The ECG waves are recorded over time, with the paper moving at 25 mm/s. At that paper speed, each large box (5 mm) represents 0.2 seconds; each small box (1 mm) represents 0.04 seconds. In this way, we can measure various features of waves on the ECG. If two events on the
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Chapter 7 • Cardiovascular Anatomy and Physiology
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■ FIGURE 7.11 Standard 12-lead ECG.
ECG are separated by four small boxes, the time separating the events is 0.16 seconds. Just as the size can be changed from the standard 1 mm equal to 0.1 mV, the speed of the paper (or tracing on a monitor) can be changed. The clinician needs to be aware of the size and speed settings to properly interpret the ECG. Typical 12-lead ECGs measure and record from three leads simultaneously for about 2.5 seconds, before switching to three more leads, and so on until all 12 leads are recorded over about a 10-second period on a single sheet of specialized graph paper. The leads are displayed in a standardized pattern as illustrated in Figure 7.11. In addition to graphing the standard 12 leads, most ECGs graph 2 or 3 of the leads over the entire 10-second period. They are graphed at the bottom of the ECG printout. Although these recordings are a subset of the same leads, graphed above, they represent a continuous 10-second period. These long recordings are useful in the diagnosis of abnormal electrical rhythms (arrhythmias). ECG monitors in the perioperative setting usually use a 3, 4, or 5 lead wire system. Depending upon how many lead wires you are using, they can be combined to produce anywhere from 3 to 12 modified leads. These monitors can display one or more leads continuously on the screen, as well as print one or two leads on a “strip” that may be easier to analyze than by looking at the monitor.
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Basic ECG waveform The typical ECG wave for one cardiac cycle includes a “P” wave, a “QRS” complex, and a “T” wave (Fig. 7.12). The SA node initiates the cardiac cycle and causes the atria to depolarize followed by atrial contraction. Because the SA node is located in the high RA, the atrial depolarization wave spreads from superior to inferior and from right to left. If you imagine a clock face on a patient’s chest, lead II measures electrical forces heading toward 5 o’clock, inferior and
■ FIGURE 7.12 The ECG wave is formed by the P wave, the QRS complex, the ST segment, and the T wave. (From Weber J, Kelley J. Health Assessment in Nursing. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003, with permission.)
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slightly leftward. Therefore, atrial depolarization creates a small positive wave in lead II (the “P” wave). This is why lead II is frequently monitored to determine if the SA node is driving the cardiac rhythm. It is an excellent lead to monitor atrial depolarization. As discussed earlier in the chapter, the myocardial conduction system funnels the electrical depolarization to the AV node where the signal is slowed to allow the atria to contract. The signal is then transmitted to the ventricles using the His-Purkinje bundles. The ventricular septum is the first to depolarize followed by the walls of the ventricles. The walls depolarize from the inside of the ventricular wall (endocardium) to the outside of the wall (epicardium). The depolarization of the septum from the left to right produces a short, small electrical signal that is directed anterior, rightward, and slightly superior due to the tilt of the heart in the chest. This electrical signal is moving away from lead II and produces a short, small downward deflection called a “Q” wave. The right and left ventricular depolarizations produce much larger waves due to their larger muscle mass compared to the atria. The RV depolarization is a rightward, anterior signal. The LV depolarization produces a large left, inferior, and slightly posterior signal. Because the LV is much more muscular than the RV, the electrical signal from the LV overwhelms the RV signal. Think of the electrical signals
being added together, except they are in opposite directions. Therefore, the RV signal slightly reduces or subtracts from the large LV signal. This combined signal produces a large upward deflection in lead II, which detects leftward and inferior signals. This upward deflection is the “R” wave. Following the R wave, there is often a small negative deflection called the “S” wave. Combined, these three deflections constitute the “QRS” complex. After a short delay, ventricular repolarization follows ventricular depolarization. This repolarization produces the “T” wave. The atria also repolarize; however, this occurs during ventricular depolarization and the small electrical signal of atrial repolarization is masked by the large ventricular depolarization signal. In addition to the P wave, QRS complex, and T wave, clinicians examine the intervals between the waves. The time from the beginning of the P wave to the beginning of the QRS complex is called the “PR interval.” The PR interval represents the time it takes for the electrical signal to travel from the SA node through the AV node and the rest of the myocardial conduction system before reaching the ventricles. The time from the end of the QRS complex to the beginning of the T wave is called the “ST segment.” These waves and intervals are used by clinicians to diagnose problems with the myocardial conduction system and heart muscle (Table 7.1).
TABLE 7.1 SEVERAL EXAMPLES OF DIAGNOSTIC INFORMATION DERIVED
FROM THE ECG ECG MEASUREMENT
DIAGNOSTIC INFORMATION
P wave
Large or broad P waves can indicate atrial hypertrophy. Abnormally shaped P waves can indicate an abnormal focus serving as the pacemaker for the heart instead of the SA node. The relationship between the P wave and the QRS complex can help determine the rhythm.
PR interval
A prolonged PR interval can indicate disease or medication-induced problems in the AV node. A short PR interval may indicate an abnormal connection between the atria and ventricles that bypasses the AV node.
QRS complex
Large amplitudes in the QRS complex can indicate ventricular hypertrophy. The changing shape of the QRS complex across leads can indicate a loss of electrical forces due to loss of active heart muscle from a heart attack. A prolonged duration of the QRS complex is common with abnormal function (blocks) of the Purkinje fibers (right and left bundles of the myocardial conduction system)
ST segment
ST-segment elevation or depression commonly occurs when myocardial cells have insufficient blood and oxygen (ischemia) or are injured (infarction). ST-segment abnormalities are also common with hypertrophied ventricles or bundle branch blocks
T wave
The shape of the T wave can be diagnostic for myocardial ischemia or infarction. It is also abnormal in bundle branch blocks or hypertrophied ventricles as well as electrolyte abnormalities.
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Chapter 7 • Cardiovascular Anatomy and Physiology
■ ABNORMAL HEART RHYTHMS Normal adult hearts beat between 60 and 85 beats per minute according to the rhythm set by the SA node. The HR can be accelerated or slowed by actions of the autonomic nervous system. For example, a vigorously exercising adult can have a HR of 140 beats per minute. HRs above 100 beats per minute are referred to as tachycardia. HRs below 60 beats per minute are referred to as bradycardia. Adults are rarely symptomatic until the HR decreases below 50 beats per minute. Some degree of bradycardia and tachycardia is normal in healthy populations (i.e., bradycardia during deep sleep and in a well-trained athlete; tachycardia following extreme emotion, excitement, after strenuous exercise, or with a fever). The SA node is the normal pacemaker for the heart. Several conditions are characterized by abnormalities with the origin of the pacemaker signal in the atria. One common condition is atrial fibrillation. In the normal heart, the SA node pacemaker initiates the signal, which then spreads like a wave across the atria. In this condition, the individual atrial myocardial cells are depolarizing and contracting completely independent of one another. The end result is that there is no coordination between the cells, a wave of depolarization is not produced, and the atria fail to contract. The independently depolarizing and contracting atrial muscle cells produce quivering atria. The disorganized atrial muscle cell depolarizations can be seen on the ECG as a fine wavy line (Fig. 7.13). Because the atria are not depolarized in a wave, the P wave is absent on the ECG. Besides lack of atrial contraction, another consequence of disorganized atrial depolarizations is that these electrical signals can be conducted through the AV node and produce irregular ventricular depolarizations and contractions. This might not seem like a bad thing; however, the atria can produce electrical signals at a rate of over
■ FIGURE 7.13 ECG demonstrating the lack of a P wave and an irregular heart rate characteristic of atrial fibrillation. (From Springhouse. ECG Facts Made Incredibly Easy. 2nd ed. Ambler, PA: Wolters Kluwer Health; 2010, with permission.)
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500 per minute. If these signals were conducted to the ventricles, the heart would beat too fast. At rates above 180–200 beats per minute, the ventricles do not have enough diastolic time to fill and forward flow begins to fall. The faster the rate, the more forward flow falls. The heart will rapidly reach the point where it cannot produce enough cardiac forward flow to perfuse the major organs. The heart attempts to protect itself from too many atrial signals reaching the ventricles by blocking them at the AV node. With very fast atrial signals, the AV node is unable to conduct every signal and begins “dropping” signals (beats) so that the ventricular rate is much slower than the atrial rate. In addition, the pattern of dropped or conducted signals can be variable, producing irregular ventricular contractions. Other atrial arrhythmias include atrial flutter and multifocal atrial tachycardia. Both of these rhythms have abnormal P waves. Because the atrial signal is conducted through the myocardial conduction system to the ventricles, the shape of the QRS complex will be relatively normal. These atrial arrhythmias usually produce fast HRs with normal (narrow) QRS complexes and are termed narrow complex tachycardias. Disease- or drug-induced reductions in conduction velocity through the AV node can cause serious problems. When conduction through the AV node slows to the point where the PR interval exceeds 0.2 seconds or the AV node fails to conduct normal atrial beats, it is referred to as heart block or AV block. When the AV node fails to conduct any atrial signals to the ventricle, the patient has “third degree” or “complete heart block.” Disease in the Purkinje bundles can cause abnormal transmission of the electrical signal to the ventricles (a “bundle branch block”). Often one or the other of the bundles is malfunctioning and failing to conduct the signal. In this condition, the normal bundle conducts the signal to its ventricle and then the signal must spread to the other ventricle through the heart muscle. Because the heart muscle conducts the signal 10 times slower than the myocardial conduction system, the ventricle supplied by the blocked bundle will depolarize later and more slowly than the other ventricle. This will result in a broad QRS complex, reflecting the slowed conduction, and an abnormally shaped QRS complex, reflecting the altered timing in depolarization of the ventricles.
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Section II • Anatomy, Physiology, and Pharmacology
■ FIGURE 7.14 ECG demonstrating wide QRS complexes at a fast rate characteristic of ventricular tachycardia. (From Springhouse. ECG Facts Made Incredibly Easy. 2nd ed. Ambler, PA: Wolters Kluwer Health; 2010, with permission.)
Arrhythmias can also originate in the ventricles. When an organized fast rhythm originates in the ventricle, it is called ventricular tachycardia (V tach) (Fig. 7.14). As mentioned above, fast ventricular rhythms can be associated with low cardiac output (CO) due to insufficient time to fill between contractions. In V tach, the ECG demonstrates a wide QRS complex tachycardia reflecting the slow conduction of the electrical signal through the heart muscle, even though the HR is fast. V tach is life threatening and requires immediate treatment. The most dangerous arrhythmia is ventricular fibrillation (V fib). This condition is physiologically similar to atrial fibrillation. The ventricular muscle cells depolarize and contract in a completely disorganized and independent fashion, producing a quivering ventricle that cannot generate any forward blood flow. The ECG demonstrates a completely disorganized electrical signal (Fig. 7.15). V fib produces no forward blood flow and is a life-threatening arrhythmia. Treatment for V fib requires application of an immediate electrical shock to the heart that causes all of the ventricular muscle cells to simultaneously depolarize. In many cases, after the shock (defibrillation) is delivered to the heart, the heart’s natural SA node pacemaker can take over and begin sending signals to coordinate the depolarization of the ventricles. One way to illustrate this concept is to think about a stadium filled with people. Each person represents an individual muscle cell. Beginning at one
■ FIGURE 7.15 ECG demonstrating a bizarre disorganized signal characteristic of ventricular fibrillation. (From Springhouse. ECG Facts Made Incredibly Easy. 2nd ed. Ambler, PA: Wolters Kluwer Health; 2010, with permission.)
WoodWorth_Chap07.indd 46
end of the stadium, the fans stand up and initiate the “wave.” As fans stand up and sit down raising their arms in order, the wave travels around the stadium pushing a beach ball in front of it. This is a coordinated contraction. Now imagine that every fan in the stadium is standing up and down randomly in a completely disorganized fashion. The stadium would appear to be quivering or fibrillating. A wave would not be produced, and the beach ball would not be pushed smoothly around the stadium. Now imagine someone got on the public address system and screamed, “SIT DOWN.” All the fans suddenly sit (depolarized by the shock), and the stadium is quiet. Then, the fans at one end of the stadium stand up and initiate the wave again (the SA node takes over as the pacemaker). The stadium has been successfully “defibrillated,” and we have the return of normal sinus rhythm. V fib is a life-threating event and if not treated promptly, the patient will die. Although many things can cause arrhythmias, some of the most common causes include the following: • Myocardial ischemia or infarction: Myocardial cells starved of oxygen do not function normally. They will not contract normally or conduct electrical impulses normally. The same is true for dead myocardial cells that have turned into a scar. These abnormal cells can be the origin of an arrhythmia or can alter conduction of a signal, causing an arrhythmia • pH or electrolyte imbalances: Normal pH and electrolyte levels are important for the myocardial cells to maintain their membrane potentials. Abnormalities in membrane potentials can cause abnormalities in the cardiac action potential and subsequent arrhythmias. • Overstretching of the heart due to valvular disease. Incompetent cardiac valves can cause blood to flow backward in the heart, stretching and overfilling chambers. These stretched and overfilled chambers are prone to abnormal heart rhythms.
■ CARDIAC CYCLE The cardiac cycle is defined as the period from the beginning of one heartbeat to the beginning of the next heartbeat. It includes systole
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Chapter 7 • Cardiovascular Anatomy and Physiology
the coronary arteries and then into the small arterioles and capillaries that feed the heart muscle itself. The capillaries are where the distance between the myocardial cells and blood flowing through the capillaries is short enough that gas and nutrient exchange can occur. During systole, ventricular pressures are high and essentially obstruct blood flow though the small arterioles and capillaries. This means that ventricular heart muscle is only supplied with oxygen and nutrients during diastole. Higher HRs can eventually lead to insufficient diastolic times to perfuse the heart muscle. To better understand the cardiac cycle, examine Figure 7.16. This figure depicts several simultaneous things happening during the course of two heartbeats. The top line represents the pressure in the aorta. The next line, the blue line, represents the pressure inside the LV, while
(i.e., contraction) and diastole (i.e., relaxation). The duration of each cycle is variable depending upon the HR. For example, with a HR of 72 beats/min, the cardiac cycle is 0.8 seconds (e.g., 60 Seconds per minute divided by 72 beats per minute = 0.8 seconds per beat). During this 0.8 seconds, the ventricles are in systole 0.3 seconds and in diastole 0.5 seconds. Although cardiac muscle contracts and relaxes faster at higher HRs, there is a limit. In general, as the HR increases, forward blood flow also increases. However, at HRs above 180–200 beats/min, the heart does not have enough time in diastole to fill before the next contraction begins. At HRs above this range, cardiac function progressively declines. Another important aspect of the HR is that the amount of time the heart spends in diastole affects myocardial perfusion. As mentioned earlier, blood flows from the aorta through Isometric contraction period Pressure (mm Hg)
47
Isometric relaxation period
120 Aortic valve closes
100 80
Aortic pressure 60 Aortic valve opens
40
Left ventricular pressure
20
Atrial pressure
100 Ventricular volume 80 (mL) 40 R
R
P
T
P
ECG Q 1st Heart sounds
Systole 0
Q 4th
2nd 3rd
0.2
Diastole 0.4
0.6
0.8
Time (sec) ■ FIGURE 7.16 The cardiac cycle depicted by measuring the pressures in the cardiac chambers during a heartbeat. (From Porth CM. Pathophysiology : Concepts of Altered Health States. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005, with permission.)
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the gray line below it represents the pressure in the LA. The red line represents the volume of blood within the LV. Although similar things are happening with the RA and RV, in order to simplify the diagram, the figure depicts only the LA and LV pressures. The dark blue line represents the ECG tracing from a single lead. Finally, the last gray line shows the phonocardiogram and depicts the sounds of the heart during the cardiac cycle. The mitral and tricuspid valves are often referred to as the AV valves and they are labeled on the diagram as the AV valves.
Ventricular Systole The first section of the diagram in Figure 7.16 represents ventricular systole, which is divided into three phases: isometric contraction, rapid ejection, and slow ejection. • Isometric contraction phase: This phase represents the beginning of ventricular contraction. The increase in pressure within the ventricle causes the mitral valve to close, preventing the flow of blood backward into the LA. The beginning of ventricular contraction is seen on this ECG as the R wave, a large positive upstroke created by the depolarization of the muscular ventricle. The sound of the closure of the AV valves can be detected on the phonocardiogram or heard with a stethoscope. AV valve closure produces the first heart sound (S1). S1 is a low, slightly prolonged “lub” caused by the vibrations of the sudden closure of the AV valves. They can best be heard with a stethoscope over the apex of the heart. The isometric contraction phase is also called the isovolumetric contraction phase because all the valves are closed and there is no ejection of blood. The volume of blood in the ventricle does not change until the ejection phase. During the isometric contraction phase, the ventricular pressure rises. The pressure in the ventricle must rise above the aortic pressure to get the blood to flow into the aorta. The atrial pressure has also started to rise, not because of atrial contraction, but rather because the blood pouring in from the vena cava is filling up in the RA and the blood from the pulmonary veins is filling up the LA. • Rapid ejection phase: When left ventricular pressure exceeds aortic pressure and right ventricular pressure exceeds pulmonary artery
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pressure, the aortic and pulmonic valves open. Blood ejects out of the ventricles into the aorta and pulmonary arteries, respectively. The majority of the ventricles’ blood is emptied during the first third of the ejection period, rapid ejection. The aortic pressure curve peaks sharply because the rapid flow of blood flow out of the ventricle into the aorta soon and causes the pressure within the ventricle to fall. • Slow ejection phase: A small amount of additional blood is ejected during the latter twothirds of the ejection phase. This is referred to as the slow ejection phase. Even though the ventricles continue to contract during this phase, very little blood is ejected during this period. The total volume of blood ejected during the rapid and slow ejection phases is called the stroke volume (SV). During the slow ejection phase, a slow broad wave appears on the ECG, the T wave. The T wave is the detection of the electrical currents created by the repolarization of the ventricles. Once repolarization occurs, the ventricular muscle starts to relax.
Ventricular Diastole Ventricular diastole can be divided into four phases: isovolumetric relaxation, rapid ventricular filling, slow ventricular filling, and atrial systole. • Isometric relaxation phase: The isometric or isovolumetric relaxation phase is the beginning of diastole. The ventricular pressure has fallen due to left ventricular relaxation to a point where it is lower than that in the aorta (lower than that in the pulmonary artery for the RV). The aortic valve and the pulmonary valves snap shut due to the pressure gradient and prevent the backward flow of blood. This pressure reversal, and closure of the aortic and pulmonary valves, produce the second heart sound (S2) as shown on the phonocardiogram. S2 is a shorter, high-pitched “dup,” caused by the vibrations of the closing aortic and pulmonic valves just after the end of ventricular systole. They can be easily heard with a stethoscope at the left second intercostal space. During the isometric relaxation phase, the ventricular pressure curve falls close to 0 mm Hg. • Rapid ventricular filling phase: When ventricular pressure falls below atrial pressure, the AV valves open and blood enters rapidly from
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Chapter 7 • Cardiovascular Anatomy and Physiology
the atria into the ventricles. The rapid flow of blood out of the atria into the ventricles causes the pressure in the atria to fall. This is the downward slope of the V wave on the atrial pressure tracing. • Slow ventricular filling phase: The slow ventricular filling phase is also known as diastasis or the last part of diastole. During this phase, only a small amount of blood drains from the lungs and peripheral circulation into the atria and into the ventricle. The rising pressure in the ventricles reduces the pressure gradient from the atria to the ventricles, resulting in reduced flow. Toward the end of this phase, atrial depolarization occurs and is seen as a small upward deflection on this ECG (the P wave). • Atrial systole phase: Atrial contraction begins during the last phase of ventricular diastole and contributes 10%-25% of the total amount of blood that fills the ventricles in a normal individual. Atrial contraction begins about the time of the peak of the P wave. When individuals lose their regular atrial contraction (e.g., atrial fibrillation), they often underfill their ventricles, leading to a reduction in cardiac function. The “a” wave of the central venous tracing correlates to atrial contraction just before the closure of the AV valves.
■ CARDIAC VOLUMES AND CARDIAC OUTPUT The blood volume in the ventricles at the end of diastole is approximately 120 mL. This volume is called end-diastolic volume (EDV). Sixty percent of the total blood volume in the ventricles is ejected out during systole, and the residual volume after ventricular systole is approximately 50 mL. The difference between the EDV and the end-systolic volume (approximately 70 mL) is known as the SV and is equal to the amount of blood ejected after each ventricular contraction. To determine ejection fraction (EF), SV is divided by EDV. The normal adult EF is approximately 50%-70% depending upon hemodynamic and volume status. The EF is a good indicator of cardiac function because cardiac disorders (e.g., ischemic heart disease, cardiomyopathies, valvular heart disease, or congestive heart failure) can markedly reduce the EF. The volume of blood the heart pumps in liters per minute is called CO. It is equal to the SV multiplied by the HR. A person with a HR of
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72 beats/min and a SV of 70 mL has a CO of 5.0 L (CO = HR × SV). This value is within the normal range for a resting average-size adult; however, CO can vary significantly with exercise, fever, or metabolic conditions like hyperthyroidism or hyperthermia. During periods of strenuous exercise, a well-trained athlete’s CO can reach as high as 35 L/min. Decreases in CO can be produced by a variety of physiologic and pathologic conditions. For example, arrhythmias (abnormal heart rhythms), ischemic heart disease, or valvular heart disease can produce significant reductions in CO. CO can also vary based on the size of the individual. The cardiac index (CI) is a measurement used by clinicians to adjust for individual differences in body size (CI = CO/body surface area [BSA] or SV × HR/BSA) and is the CO per square meter of BSA. The CI is therefore expressed in liters per minute per meter squared. The CI gives a better representation of perfusion than CO alone. The normal CI is 2.5–4.0 L/min/m2 of BSA.
■ FACTORS AFFECTING CARDIAC OUTPUT There has been a great deal of research into the major physiologic factors that affect CO. These include the HR, the EDV of the ventricle (preload), the force with which the ventricle can contract (contractility), and the resistance against which the heart must eject blood (afterload). The description of how these factors affect cardiac function is the cornerstone of cardiac physiology.
Preload The total volume of circulating blood affects preload. The greater the venous return to the heart, the more the myocardial fibers will stretch to accommodate the load on the heart. According to the Frank-Starling law, the greater the initial myocardial fiber length the greater will be the force of contraction. This mechanism has been compared to the increased recoil of a rubber band when stretched. The increase in contractile force is related to an increase in sarcomere length (the contractile unit of a cardiac muscle cell). After a certain point, the sarcomere can become overstretched and the contractile force will decrease. In conditions where there is decreased filling of the heart (e.g., hypovolemia), the sarcomeres are short and the force of contraction is diminished. With increasing blood volume (increasing preload) the contractile force increases. When the
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Normal
D A
E
C
HF with positive inotrope Untreated HF
Symptoms of high end-diastolic pressure
Normal
Cardiac output
Cardiac output
Symptoms of high end-diastolic pressure
F G
HF with ACE inhibitor Afterload reduction
C
Untreated HF
Preload reduction
B
Ventricular end-diastolic pressure
Ventricular end-diastolic pressure Symptoms of low cardiac output
Symptoms of low cardiac output
■ FIGURE 7.17 The physiologic relationship between the Starling Law of the heart and venous return pressure and volume. (With permission Figure 24-11: Adapted with permission from Harvey RA, Champe PC, eds. Lippincott’s Illustrated Reviews: Pharmacology. Philadelphia, PA: Lippincott Williams & Wilkins; 1992:157, Figure 16-6.)
blood volume is too high and there is excessive filling and stretching of the heart, the force of contraction begins to fall and is referred to as congestive heart failure. The ventricular function curve as depicted in Figure 7.17 shows the relationship between fiber length and the force of contraction. The left panel of the figure depicts ventricular end-diastolic pressure graphed against CO on the y axis. The upper “normal” curve demonstrates that increasing end-diastolic pressure (a measure of the preload volume in the ventricle) increases to a point. After that point, even with increasing end-diastolic pressure, the CO begins to fall as the ventricle becomes overstretched. Clinically, preload is estimated by measuring the pulmonary capillary wedge pressure. A catheter is placed in the pulmonary artery (pulmonary artery catheter or PAC) and a small balloon is inflated (see Chapter 34). The balloon wedges in a small pulmonary artery. The pressure from the LA is transmitted backward through the pulmonary circulation and is measured by the pulmonary artery capillary wedge pressure (PCWP). Higher PCWP can correspond to a higher preload. Another way to measure the volumes of the heart (preload) is to use echocardiography (see Chapter 9). Echo machines can use sound waves to image the heart and examine the size and contractile function of the cardiac chambers.
Afterload Afterload is an indication of the amount of wall tension that is produced by the ventricle.
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Clinically, afterload cannot be directly measured, and as a surrogate, clinicians think of afterload as the amount of pressure the ventricle must generate to eject blood. Anything that impedes the ability of the heart to eject is referred to as increasing afterload. For example, a constricted aortic valve or narrowed peripheral arteries would make it harder for the heart to eject blood, and thus increase afterload. The LV would compensate by working harder to generate higher pressures to overcome the increased resistance to ejection. Because increasing afterload increases the work of the heart, it also increases myocardial oxygen consumption. Conversely, decreasing afterload makes it easier for the heart to eject blood and decreases myocardial oxygen consumption. Afterload is an important concept. Many clinical conditions and drugs, including anesthetic agents, can increase or decrease afterload. Clinicians will often administer different medications in order to manipulate afterload. For example, a clinician may administer an arterial vasodilator to decrease afterload in a patient with a failing heart. The goal in this case is to ease the burden on the heart. Figure 7.17 demonstrates the effect of afterload reduction in the panel on the right. The failing heart is depicted in the bottom Frank-Starling curve. When the angiotensin-converting enzyme (ACE) inhibitor is given, the heart changes to the middle curve. Even with a lower end-diastolic pressure, the heart is able to produce a higher CO because of the afterload reduction.
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Chapter 7 • Cardiovascular Anatomy and Physiology
Contractility Myocardial contractility is the intrinsic ability of the heart to contract. We have already seen how preload and afterload can affect contractile function. Independent of these factors, the heart is able to produce a stronger or weaker contraction depending upon its contractility. In other words, if preload and afterload are kept constant, the “contractility” of the heart can affect the force of contraction. Many drugs change the intracellular amount of myocardial calcium and can increase contractility (e.g., epinephrine, norepinephrine, milrinone). Another word for contractility is “inotropy”; thus, drugs that increase contractility are referred to as positive inotropes. It is also important to understand that increasing contractility increases myocardial oxygen consumption. The left panel of Figure 7.17 demonstrates the effects of giving a positive inotrope to a patient with heart failure. Once the inotrope is given, the patient moves to the middle curve. Now for the same end-diastolic pressure the heart is able to produce a greater CO. Agents that reduce intracellular calcium decrease contractility. Examples of negative inotropes include calcium-channel blockers and beta-blockers. Acidosis and hypoxemia also negatively affect the contractility of the heart. One way to quantify contractility is through measurement of the EF with echocardiography. Under resting conditions, normal EF is between 50% and 70%. If afterload and preload are the same, a change in EF is a sensitive indicator of a change in contractility.
■ CARDIAC REFLEXES As discussed above, the heart is innervated by the autonomic nervous system. This innervation is responsible for several reflex changes in cardiovascular function. These reflexes are often feedback loops that help the body maintain normal HR and blood pressure. In the aortic reflex, a rise in blood pressure stimulates baroreceptors (pressure or stretch receptors) in the aortic arch and carotid sinuses. These baroreceptors stimulate the brainstem, causing a reflex parasympathetic outflow through the vagal nerve that slows the HR. Conversely, decreases in blood pressure cause decreases in baroreceptor output, resulting in decreased parasympathetic outflow and a resultant increase in HR in an attempt to restore blood pressure. The vagus nerve is responsible
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for the effector outflow to the heart. Any stimulus that leads to changes in vagal output can affect the heart. For example, carotid sinus massage (pressure in the neck over the carotid artery) can activate the carotid baroreceptors, resulting in increased vagal output and a slowing HR. In the past, this maneuver was used to intentionally increase vagal outflow to the AV node to attempt to disrupt certain kinds of tachyarrhythmias. The valsalva maneuver is another method to attempt to increase vagal output. A sustained increase in intrathoracic pressure causes an acute reduction in CO (reduced flow of blood into the heart). The sympathetic system is briefly activated to stimulate the heart and increase CO. When the intrathoracic pressure is released, blood flows rapidly back into the heart, increasing preload and blood pressure. The body responds with parasympathetic outflow, resulting in bradycardia. The sustained increase in intrathoracic pressure can be achieved by asking patients to “bear down” while holding their breath. In intubated patients, the anesthesia provider can deliver a large tidal volume and hold the inspiratory pressure for several extra seconds before releasing it. Other reflexes that result in increased parasympathetic flow include stimulation of ocular structures (pressure on the globe, cornea, eye muscles), stretch of hollow organs in the abdomen, traction on the attachments of the intestines to the abdomen, or even application of ice water to the face. One example of a reflex that decreases parasympathetic outflow and increases sympathetic outflow is the Bainbridge reflex. This reflex is triggered by high venous blood pressure that stimulates venous stretch receptors in the venae cavae and the RA.
■ MYOCARDIAL OXYGEN SUPPLY AND DEMAND When myocardial cells have insufficient blood supply and begin to dysfunction, it is referred to as myocardial ischemia. When the myocardial cells sustain irreversible damage and die, it is referred to as a myocardial infarction, more commonly known as a heart attack. The sudden onset of either of these conditions is referred to as acute coronary syndrome. Common symptoms include chest pain, shortness of breath, arm pain, and nausea. An ECG can be useful in making a diagnosis. Because the heart muscle is constantly
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contracting, it requires a continuous supply of blood flow and oxygen to support its metabolic demands. The balance between myocardial oxygen supply and oxygen demand determines whether the oxygen delivered to the heart is sufficient for the work it is doing. This is an important concept in understanding and treating heart disease. The major determinants of myocardial oxygen supply are the blood flow to the heart cells and the oxygen content of the blood.
Blood Oxygen Content Ventilation and gas exchange in the lungs affect the amount of oxygen in the blood (see Chapter 11). Even with sufficient inspired oxygen concentration and a perfectly functioning respiratory system, very little oxygen dissolves in blood. The body overcomes this limitation with hemoglobin. Hemoglobin is a protein within red blood cells that has a very high affinity for oxygen. Therefore, the total amount of blood oxygen content comes from dissolved oxygen and oxygen bound to hemoglobin. With normal lung function and inspired oxygen, hemoglobin is fully saturated (carries as much oxygen as it can). With hypoxic inspired gas mixtures or abnormal lung function, hemoglobin may not be fully saturated with oxygen. Clinicians frequently monitor the percentage of oxygen saturation of blood with a pulse oximeter, with normal values ranging between 97% and 100%. At this level of saturation and a normal hemoglobin level (14–15 g/dL), there is 20 times as much oxygen bound to hemoglobin as there is dissolved oxygen. Even when fully saturated, if the hemoglobin level falls to less than 6 g/dL, there may be insufficient oxygen to supply the heart. If the oxygen saturation of the hemoglobin is less than 97%, values of higher than 6 g/dL may be required to supply the heart. To summarize, the oxygen content of blood is determined by the inspired oxygen level, the function of the lungs, and the amount of hemoglobin.
Myocardial Blood Flow Oxygen delivery to the myocardium is determined by the amount of oxygen in the blood and by how much blood flows to the myocardium. As described earlier in this chapter, the coronary arteries deliver blood to the myocardium. The major coronary arteries (RCA, LCA, LCX) branch like a tree to form multiple smaller arteries,
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arterioles, and eventually capillaries. If a blood vessel supplying the myocardium is obstructed, the myocardium supplied by that artery may become ischemic, or even infarcted. The amount of heart muscle affected is determined by how much myocardium is supplied by that vessel and the presence of any collateral circulation. The closer the obstruction occurs to the root of the tree (the origin of the major artery), the greater the amount of myocardium that will be affected. For example, an obstruction near the origin of the LCA will damage a very large portion of the heart and is often fatal. Even an obstruction in smaller arteries can be important, for example, if they supply a critical portion of the heart such as the myocardial conduction system. The heart has a backup system to protect against obstructions in arteries. This is accomplished by forming multiple cross-connections between arteries, collateral circulation. This way, if an obstruction occurs, it is possible that another artery is connected to the obstructed artery below the obstruction and can supply blood flow to that part of the heart. Even if coronary arteries are unobstructed, the amount of blood flowing through them will depend upon aortic pressure. Recall that the coronary arteries originate from the proximal aorta. Any condition causing low blood pressure (hypotension) reduces the driving pressure that causes blood to flow through the coronary arteries. It is important to remember that many drugs can affect the coronary circulation. Vasodilators such as nitrates, including nitroglycerin, can dilate coronary vessels and increase coronary blood flow. Other drugs that are commonly used to raise blood pressure can constrict coronary arteries and reduce coronary blood flow. These drugs are discussed in more detail in the section on cardiovascular pharmacology. Finally, recall the earlier discussion about diastole. The majority of myocardial perfusion occurs during diastole because of compression of arterioles within the myocardium during systole. Therefore, high HRs, which minimize overall diastolic time, can reduce myocardial perfusion.
Myocardial Oxygen Demand The other side of myocardial oxygen balance is demand. The amount of oxygen the heart consumes is related to the HR (doubling the HR doubles oxygen consumption), the amount of
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Chapter 7 • Cardiovascular Anatomy and Physiology
resistance the heart must pump against (afterload), the force and speed with which the heart generates pressure (contractility), and the size of the cardiac chambers. Atria or ventricles that are stretched utilize more oxygen in order to generate the same amount of pressure as normalsized chambers. Increases in any of these factors increase myocardial oxygen consumption.
Myocardial Infarction Maintaining the balance between myocardial oxygen demand and supply is crucial to normal cardiac function. One of the most common causes of cardiac dysfunction is an acute interruption of coronary blood flow to the heart. Either with aging or disease, lipid material (like cholesterol) can build up within the wall of an artery. The body’s response to the lipid forms what is knows as an atherosclerotic plaque. The buildup of plaque within the wall of a coronary vessel can gradually obstruct the vessel. This can gradually lead to ischemia of the region supplied by the vessel. A more dangerous condition occurs when the plaque “ruptures.” The narrowing of the vessel lumen by the plaque causes turbulent blood flow. This turbulence can disrupt the cells covering the plaque and expose material to the blood that initiates clotting of blood. Clot formation by platelets and clotting proteins can rapidly cause complete obstruction of the vessel, leading to ischemia or infarction of myocardial tissue. This often requires emergent treatment. If the region of ischemia or infarction is large enough, it can impair the heart’s ability to pump. In addition, even small regions of ischemic tissue can interfere with the electrical activity of the heart and produce a sudden, life-threatening arrhythmia. The treatment for myocardial ischemia is to attempt to restore the balance between myocardial oxygen supply and demand. Reducing demand starts with a resting patient and drugs to reduce the HR (e.g., beta-blockers), contractility (e.g., beta-blockers, calcium-channel blockers), and afterload (e.g., calcium-channel blockers, alpha-blockers, nitrates). Care must be taken in the administration of these drugs because they can also decrease blood pressure and cardiac filling. If oxygen saturation or hemoglobin levels are low, these need to be addressed as well. In many cases, these treatments may not be enough and an attempt will be made to improve coronary
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blood flow by relieving an obstruction with clotbusting drugs, a percutaneous intervention by a cardiologist, or surgery. Drugs like aspirin (interferes with platelets) or heparin (interferes with clotting proteins) can reduce further clot formation. Other drugs (thrombolytics) directly attack the clot itself. In many cases, testing is necessary to determine which arteries are obstructed. A cardiologist or radiologist can inject dye into the circulation, which can be viewed by fluoroscopy or a computed tomography (CT) scan. Cardiologists can then attempt to expand a narrowing in a coronary artery with a balloon (angioplasty) and then keep it open with an expandable mesh (stent). In other cases, surgery is required to place a graft from one coronary artery to below the obstruction to create an alternative blood supply to the affected area.
■ VALVULAR HEART DISEASE As described earlier, the valves of the heart perform the important function of preventing backward flow of blood within the heart. Dysfunction of heart valves can occur when they become narrowed (stenotic) or incompetent (allow backward flow of blood). Both conditions can severely impair cardiac function and represent important challenges to the anesthesiologist. In the following section, we briefly discuss some of the more important valvular conditions.
Aortic Stenosis Aortic stenosis (AS) is one of the most common valvular problems. Rheumatic heart disease or degeneration of congenitally malformed valve leaflets is often the cause of the stenosis. The narrowing of the aortic valve impedes the outflow of blood from the LV. The worse the stenosis, the more the LV must work to eject blood. Early on in the progression of this disease, the LV becomes thick (hypertrophied) and generates very large pressures to overcome the obstruction. The thick ventricle is also stiff and does not relax as well as a normal ventricle. This makes it more difficult to fill the ventricle. The heart becomes very dependent upon preload and, in turn, left atrial contraction to fill the stiff ventricle. Patients without AS can often tolerate loss of atrial contraction (e.g., atrial fibrillation), whereas patients with AS are acutely sensitive to changes in preload or atrial fibrillation. In addition, the hypertrophied heart working against
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high resistance consumes more oxygen and is susceptible to ischemia. As the stenosis becomes worse, the heart can no longer compensate with ventricular hypertrophy and the patients become more symptomatic. The LV begins to dilate and the increased end-diastolic pressure causes the LA to dilate and often fibrillate. In addition, the increased diastolic pressure within the atrium backs up into the lungs, causing congestion. This congestion and the significant decrease in CO is referred to as congestive heart failure. Ischemia is also common with moderate to severe stenosis. These patients can have difficulty with even minimal exertion. Patients reaching this stage require repair or replacement of the stenotic valve. Whether presenting for valve surgery or noncardiac surgery, anesthetic management of these patients is complex and the stress of surgery can often prove fatal. Anesthetic goals include maintenance of preload at the right level (not too much, not too little), avoidance of arrhythmias (may require urgent cardioversion), maintenance of contractility (must be able to generate enough pressure to overcome the obstruction), avoidance of tachycardia (need time for ventricular filling), and avoidance of peripheral vasodilation and hypotension (maintain sufficient aortic pressure to maintain coronary blood flow). These patients will often require invasive monitors (arterial line, central venous pressure) and in severe cases transesophageal echocardiography (TEE). One of the biggest concerns is the lack of reserve in these patients. They can rapidly go from maintaining CO to severe congestive heart failure.
by increasing the HR. This increases the CO and reduces the amount of time the heart spends in diastole, thus reducing the amount of regurgitation. Unlike AS, the heart can compensate for aortic regurgitation for some time. By the time symptoms appear, the disease is usually severe and the heart quite dilated. Anesthetic management includes the following: maintain adequate HR (reduces regurgitation and maintains CO), ensure adequate preload, avoid hypertension, and reduce afterload (reduces back pressure causing regurgitant flow). The anesthesia technician should consult with the anesthesia provider about the need for invasive monitoring (e.g., arterial line, central venous line) and vasoactive infusions (vasodilators, inotropes).
Mitral Stenosis The most common cause of a stenotic mitral valve is rheumatic heart disease. Much like AS, the LA must work harder against the obstruction to flow into the ventricle. The heart compensates with dilation of the LA and pressures within the LA rise. As the disease progresses, congestion in the lungs and atrial fibrillation are common. The good news about this disease is that left ventricular function is preserved. Anesthetic concerns surround avoiding or treating volume overload and tachyarrhythmias that reduce diastolic time. The heart requires adequate diastolic time to fill the LV when the mitral valve is obstructed. The anesthesia technician should be ready for invasive monitoring. Although venodilators to reduce preload may be required, vasoactive infusion is not needed as often as in other valvular conditions.
Aortic Regurgitation Rheumatic heart disease, trauma, aortic dissection, and congenital abnormalities are the most common causes of an aortic valve regurgitating blood backward into the LV. This regurgitation occurs during diastole when the aortic valve is supposed to be closed. The regurgitating blood overloads the LV and it dilates over time. The increased end-diastolic volumes and pressure can back up into the LA and the lungs. The heart must eject a much larger amount of blood (SV) because a significant portion can flow right back into the heart after ejection due to the incompetent valve. The amount of backflow depends on how leaky the valve has become. In addition to increased SV, the heart attempts to compensate
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Mitral Regurgitation Mitral regurgitation is common and can be caused by multiple factors. Similar to aortic regurgitation, the regurgitant flow from the LV back into the LA overloads the LA. Pressures within the LA are significantly increased, and the LA can be dramatically dilated. The increased LA pressures commonly cause congestion in the lungs. The reduction in forward flow from the LV to the aorta (much is lost due to the backward flow into the LA) reduces CO. As in aortic regurgitation, the heart requires an adequate preload and a normal atrial rhythm and contraction to fill. Afterload should be slightly reduced to promote forward blood flow. The anesthesia
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Chapter 7 • Cardiovascular Anatomy and Physiology
technician should be ready for invasive monitors and vasoactive infusions. TEE may be required in severe cases (see Chapter 39).
■ SUMMARY Anesthesiologists deal with patients who have cardiac disease on a regular basis. In addition, surgery and multiple drugs, including anesthetic agents, can severely affect cardiovascular function. Anesthesia technicians should have a working knowledge of cardiovascular anatomy and physiology to better understand the effects of surgery and drugs on the cardiovascular system. This knowledge will also help the technician understand why particular forms of cardiovascular monitoring are utilized. This chapter introduces the anesthesia technician to cardiac anatomy, the circulation of blood through the four cardiac chambers, the innervation of the heart, the myocardial conduction system and cardiac rhythms, the cardiac cycle and the pressures within the heart, the factors that affect cardiac function (preload, afterload, contractility), myocardial oxygen balance, and valvular dysfunction.
REVIEW QUESTIONS 1. Which of the following is TRUE about how blood flows through the heart? A) RA to RV to LV to LA to aorta B) RV to RA to pulmonary artery to LV to LA to aorta C) RA to RV to pulmonary artery to LA to LV to aorta D) RA to LA to pulmonary artery to RV to LV E) None of the above Answer: D. Blood flows from the RA into the RV where it is ejected into the pulmonary artery and lungs. Oxygenated blood returns from the lungs into the LA and then into the LV where it is ejected into the aorta.
2. Which of the following veins return blood DIRECTLY into the RA? A) SVC and IVC B) Pulmonary veins C) Femoral vein D) Subclavian vein E) Internal jugular vein Answer: A. The SVC collects blood from the upper extremity through the subclavian vein and from the head and neck from the internal jugular vein. The SVC then drains directly into the
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superior RA. The blood from the lower extremities drains into the femoral vein and eventually into the IVC. The IVC drains directly into the inferior portion of the RA.
3. Which of the following statements are TRUE about the ventricles? A) The ventricles have thicker walls than the atria. B) The LV has much thicker walls than the RV. C) The right and left ventricles are separated by the interventricular septum. D) The ventricles receive blood from the atria. E) All of the above are true. Answer: E. The ventricles receive blood from the atria after which they pump the blood into a major artery. This pumping action requires a larger pressure and thus the ventricles have thicker, more muscular walls than the thin-walled atria. The LV must pump blood into the aorta at very high pressures and is much more muscular than the RV, which pumps blood into the lower pressure pulmonary circulation.
4. Which of the following is TRUE regarding the myocardial conduction system? A) The system is composed of specialized nerve cells that conduct impulses. B) The conduction system conducts blood from the LA into the LV. C) The conduction system conducts electrical impulse from the autonomic nervous system to different portions of the heart. D) The conduction system is made up of specialized myocardial muscle cells. E) None of the above. Answer: D. The myocardial conduction system is made up of specialized myocardial muscle cells that are responsible for pacing the heart and conducting electrical impulses to synchronize and coordinate the contraction of the atria and ventricles.
5. Which of the following statements are TRUE regarding the coronary circulation? A) The RCA, the LAD coronary artery, and the LCX are the major “trunk” arteries that supply large areas of the heart. B) The right and left coronary arteries originate from the aorta. C) The heart protects itself with cross-connections between arteries (collateral circulation). D) The majority of myocardial blood flow occurs during diastole. E) All of the above are true. Answer: E. All of the above statements are true. The right and left coronary arteries originate from the proximal aorta. The LCA branches into the LAD and circumflex arteries. These are all major arteries, and an obstruction in one of these arteries will damage a very large portion of the heart,
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Section II • Anatomy, Physiology, and Pharmacology possibly resulting in death. The heart protects itself from obstructions in its blood supply by connections between arteries (the collateral circulation). The majority of blood flow through the myocardial arterioles and capillaries occurs during diastole, when the ventricular pressure is lower.
6. The cardiac action potential represents the changes in membrane potential in myocardial muscle cells from the flow of ions across the membrane. A) True B) False Answer: B. True. The myocardial cells maintain a resting membrane potential like a minibattery. When the membrane is depolarized from an electrical signal, ion channels open, allowing the flow of ions across the membrane further depolarizing the membrane. Eventually, the membrane is repolarized by changing which ion channels are open, allowing the flow of ions.
7. Which of the following statements are TRUE regarding the ECG? A) The ECG machine amplifies and measures tiny currents generated by the depolarization of myocardial cells. B) A “lead” is formed by two or more electrodes. C) Currents flowing toward a lead are displayed as positive deflections on the ECG. D) The spatial orientation of the leads can help monitor electrical currents generated by different portions of the heart. E) All of the above are true. Answer: E. All of the above are true. The ECG measures the tiny electrical currents produced by depolarizing myocardial cells. A lead is formed by at least two electrodes (more than one electrode can be combined to form a reference electrode). The electrical forces traveling toward a lead are displayed as upward deflections on the ECG; therefore, the spatial orientation of the leads is important. The leads are positioned so that each lead displays the electrical forces coming from a different region of the heart.
8. The ECG is useful for monitoring which of the following? A) The pressure in the central venous circulation B) Arrhythmias C) The PCWP D) Cardiac output E) None of the above Answer: B. The ECG is useful for monitoring the rhythm of the heart, the function of the myocardial conduction system, and myocardial ischemia (insufficient oxygen delivery to myocardial cells). The central venous pressure and the PCWP are measured with catheters placed in the central circulation and pulmonary artery, respectively. CO can be measured with a PAC or echocardiography.
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9. Which of the following statements is FALSE regarding the cardiac cycle? A) As blood flows from the atria into the ventricles, the ventricular pressure rises. B) After the atria contracts, the ventricles reach their EDV. C) When the LV contracts, the pressure rises in the ventricle until it overcomes the aortic pressure and it begins ejecting blood into the aorta. D) Systole is defined as when the ventricles begin to relax. E) None of the above. Answer: D. Systole is defined as when the ventricles are contracting. Diastole is when the ventricles are relaxing. Blood flows from the atria into the ventricle. As the volume increases in the ventricle, the pressure rises. Just before systole begins the atria contract to add more blood into the ventricles. The volume in the ventricles just before they contract is the EDV and determines the end-diastolic pressure.
10. Which of the following statements are TRUE about the cardiac cycle? A) Valves within the heart prevent the flow of blood backward. B) EF is defined as the amount of blood ejected from the heart during diastole. C) CO is equal to the EF times the HR. D) Diastole is when the heart is contracting. E) None of the above. Answer: A. The valves within the heart are very important as they prevent blood from flowing backward into the atria during ventricular contraction and backward into the ventricles from the pulmonary artery and aorta. The EF is the fraction of the end-diastolic ventricular blood that is ejected during systole. In normal resting patients, around 50% of the blood in the heart at end-diastole is ejected during systole. CO is equal to the SV (the amount of blood ejected with each heartbeat during systole) times the HR.
11. Which of the following factors DO NOT affect the force of contraction of the heart? A) The AV node B) Preload C) Contractility D) Drugs E) Afterload Answer: A. The AV node is a portion of the myocardial conduction system that regulates the speed of conduction from the atria to the ventricles. Preload, afterload, and contractility are the major determinants of the force of myocardial contraction and can be explained by using Frank-Starling curves. Drugs can both positively and negatively affect contractility as well as affect preload and afterload.
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Chapter 7 • Cardiovascular Anatomy and Physiology 12. Which of the following are potentially lethal cardiac arrhythmias? A) Ventricular fibrillation B) Ventricular tachycardia C) Sinus bradycardia D) A and B E) A and C Answer: D. Both ventricular fibrillation and ventricular tachycardia may not produce any forward blood flow. Unless the ventricular tachycardia is slow, the patient will die.
13. Which of the following is NOT a determinant of myocardial oxygen supply? A) Hemoglobin level B) Afterload C) Blood oxygen saturation D) Coronary blood flow E) Diastolic time
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SUGGESTED READINGS Agur AMR, Dalley AF. Grant’s Atlas of Anatomy. 11th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005: Chapter 1 Thorax. Guyton AC, Hall JE. Textbook of Medical Physiology. 11th ed. Philadelphia, PA: Saunders Elsevier; 2005. Kaplan J, Reich D, Lake C, Konstadt S. Cardiac Anesthesia. 5th ed. St. Louis, Missouri: Saunders Elsevier; 2006. Barrett K, Barman S, Boitano S, Brooks H. Section VI: Cardiovascular physiology. In: Ganong’s Review of Medical Physiology. 23rd ed. McGraw-Hill Companies; 2010. Warwick R, Williams P (Eds). The anatomical basis of clinical practice. In: Gray’s Anatomy. 35th ed. Toronto, Ontrario, Canada: Elsevier Churchill Livingstone; 2005: Chapter 60. Widaier EP, Raff H, Strang KT. Vander’s Human Physiology: The Mechanisms of Body Function. 12th ed. London: McGrawHill; 2011: Chapter 12. Cardiovascular Physiology.
Answer: B. Afterload is a determinant of myocardial oxygen demand (the harder the heart works, the more oxygen it uses). Oxygen is supplied to the blood by binding to hemoglobin in the blood. Low hemoglobin levels can result in insufficient oxygen for the heart. In normal humans, hemoglobin is 97%-100% saturated with blood. If insufficient oxygen is loaded onto hemoglobin in the lungs, the heart may not get enough oxygen. Finally, coronary blood flow during diastole is what brings the oxygen in the blood to the myocardial cells. High systolic pressures compress the coronary arterioles and prevent blood from flowing to the heart muscle during systole.
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CHAPTER
8
Cardiovascular Pharmacology Markus Kaiser and David C. Warltier ■ INTRODUCTION The cardiovascular system can be influenced by a variety of medications used in the operating room and intensive care units. Pharmacologic agents may change the contractility of the heart (inotropy), heart rate (chronotropy), conduction of electricity through the atrioventricular (AV) node (dromotropy), or relaxation of the heart in diastole (lusitropy). Vasoactive drugs may constrict (vasopressors) or widen (vasodilators) blood vessels either by influencing receptors of the autonomic nervous system (alpha1, beta1, and beta2 receptors) or by direct actions on the smooth muscle of the vascular wall. Maintaining a normal heart rate and rhythm is essential for optimal cardiac function. Antiarrhythmic agents are commonly used in the perioperative period to accomplish this. Drugs impacting the cardiovascular system are used to overcome the sequelae of cardiovascular disease, the effects of cardiovascular-depressant drugs (e.g., anesthetic agents), physiologic reflexes, and/or any combination of these. This chapter introduces the anesthesia technician to the mechanism of action and uses of positive inotropic agents, vasoactive drugs, and antiarrhythmic agents. The cardiovascular actions of anesthetic drugs are described elsewhere.
■ POSITIVE INOTROPIC AGENTS Drugs that increase the force of myocardial contraction are called positive inotropic agents and include catecholamines, phosphodiesterase (PDE) inhibitors, and myofilament calcium sensitizers. Catecholamines and PDE inhibitors increase calcium concentration in the cytoplasm of cardiac muscle cells by different mechanisms to help generate a greater force of contraction. Myofilament calcium sensitizers enhance the interaction between the contractile proteins within myocardial cells without increasing intracellular calcium.
Stimulation of beta1-adrenergic receptors that are coupled to G proteins activates the enzyme adenylyl cyclase, which, in turn, forms cyclic adenosine monophosphate (cAMP) from adenosine triphosphate (see Fig. 8.1). cAMP increases contractility (via increased intracellular calcium concentration) of cardiac muscle while also causing relaxation in smooth muscle (e.g., in blood vessels). It is metabolized by the enzyme PDE. PDE is targeted by a variety of drugs called PDE inhibitors that increase cAMP levels by inhibiting PDE and preventing breakdown of cAMP.
■ CATECHOLAMINES The naturally occurring catecholamines epinephrine, norepinephrine, and dopamine are produced in the medulla of the adrenal gland. Norepinephrine is also synthesized in adrenergic nerves and functions as a neurotransmitter in the sympathetic division of the autonomic nervous system (see Chapter 14). Epinephrine and norepinephrine are considered stress hormones when released into the bloodstream from the adrenal gland. The half-lives of endogenous as well as synthetic catecholamines, such as dobutamine and isoproterenol, are short (minutes), and these drugs are quickly deactivated primarily by reuptake into presynaptic neurons or metabolism by enzymes. The metabolites can be detected in the urine and are elevated in patients with catecholamine-producing tumors such as pheochromocytoma. The drugs stimulating alpha and beta adrenoceptors to produce their actions have proportionally different effects on heart, vasculature, and other smooth muscles dependent on their affinity for receptor types (see Table 8.1).
■ EPINEPHRINE Epinephrine is a naturally occurring catecholamine that is produced from its precursor, norepinephrine, exclusively in the adrenal medulla.
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stimulation of these receptors by low doses of epinephrine produces vasodilation. Epinephrine also influences metabolism by increasing glycogenolysis in the liver and lipolysis in adipose tissue. In anesthetic practice, epinephrine may be used intravenously in life-threatening situations including cardiac arrest, low cardiac output syndromes, anaphylaxis, or bronchospasm. Added to solutions of local anesthetics in a concentration of 1:200,000, it prolongs the action of the anesthetic by constricting surrounding blood vessels and decreasing systemic reabsorption. In cardiopulmonary resuscitation, epinephrine is administered intravenously in 1-mg (0.02 mg/kg) increments every 3 minutes per advanced cardiac life support (ACLS) guidelines in a dilution of 1:10,000 (0.1 mg/mL) (see Chapter 61). At this high dose, the arterial vasoconstrictor properties predominate causing increased diastolic pressures, which improve coronary artery perfusion. As a continuous infusion, epinephrine is usually administered between 0.03 μg/ kg/min and 0.15 μg/kg/min. At lower doses, the effects on beta1 and beta2 adrenoceptors (bronchodilation, inotropy, and chronotropy) usually predominate, while at high doses epinephrine can cause profound vasoconstriction through alpha1 activation. Epinephrine can produce cardiac arrhythmias, especially in the presence of the anesthetic halothane. Increases in heart rate in patients with coronary artery disease may cause myocardial ischemia. In general, the betaadrenergic stimulant properties of epinephrine
■ FIGURE 8.1 Function of catecholamines and phosphodiesterase inhibitors in the myocyte. Catecholamines increase cAMP through an energy-dependent pathway. In the presence of phosphodiesterase inhibitors, the breakdown of cAMP to AMP is slowed and the effect of catecholamines potentiated. (AMP, adenosine monophophate; ATP = adenosine triphosphate; β1, β1 adrenoreceptor; cAMP, cyclic adenosine monophosphate, Gs, Gs protein; PDE3, phosphodiesterase [isoenzyme 3]). (Adapted from Klabunde RE. Cardiovascular pharmacology concepts. Available from: www.cvpharmacology.com)
It has a wide range of physiologic effects including increasing heart rate, myocardial contractility, and conduction in the heart by stimulating primarily beta1-adrenergic receptors. Increased peripheral vascular tone (afterload) is mediated by the activation of alpha1-adrenergic receptors, while relaxing bronchial smooth muscle (bronchiodilation) is caused by the activation of beta2 receptors. Beta2 receptors are also located on vascular smooth muscle cell membranes, and
TABLE 8.1 PHARMACOLOGY OF ALPHA- AND BETA-ADRENERGIC AGONISTS RECEPTOR FUNCTION
PHYSIOLOGIC EFFECT
DOSING RANGE
DRUG
a1
b1
b2
SVR
MAP
CO
BOLUS (mg/kg)
Epinephrine
+
++
++
+/−
+
++
0.2 (1 mga)
0.03-0.15
+++
++
0
+++
+++
+/−
NR
0.03-0.15
++
++
+
+
+
++
NR
1-10
Norepinephrine Dopamine
INFUSION (mg/kg/min)
Isoproterenol
0
+++
+
++
+/−
+++
0.02-0.1
0.01-0.05
Dobutamine
(+)
+++
(+)
+/−
+/−
+++
NR
2-10
++
+
+
+
++
+
0.15-0.4
NR
+++
0
0
+++
+
−
0.5-0.2
0.5-2.0
Ephedrine Phenylephrine a
For cardiopulmonary resuscitation SVR, systemic vascular resistance; MAP, mean arterial pressure; CO, cardiac output; NR, not recommended. Modified from Stoelting K, Hillier S, eds. Pharmacology & Physiology in Anesthetic Practice. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.
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and other catecholamines will be diminished in patients taking beta-blocking drugs. There is a very high variability in the response between patients, and thus this drug should always be titrated carefully to the desired effect. Infusion through a central venous line is recommended for higher concentrations as extravasation can cause tissue necrosis. In general, solutions containing catecholamines for infusion should be prepared in 5% glucose to avoid deactivation in alkaline solutions.
■ NOREPINEPHRINE Norepinephrine is an endogenous hormone secreted from the adrenal medulla and is the neurotransmitter released from postganglionic adrenergic nerve endings following sympathetic nervous system stimulation. In addition, norepinephrine plays a role in the stress response and is secreted from noradrenergic neurons in the central nervous system. Norepinephrine must be infused intravenously (approximately 0.05-0.15 μg/kg/min) and has dose-dependent effects mediated via alpha1- and beta1-adrenergic receptors. In the lower dose range, increased heart rate and contractility through beta1 activation may result in a higher cardiac output. Unlike epinephrine, norepinephrine has little to no activity at beta2 receptors. Norepinephrine is a positive inotrope and is an excellent drug for the treatment of lowoutput, low vascular resistance heart failure. In higher doses, alpha1 activity predominates and norepinephrine causes a profound vasoconstriction in the vasculature of the kidney, liver, skeletal muscle, and skin. The resulting increase in systemic vascular resistance, reduced venous return, and increased arterial pressure can elicit reflex bradycardia (baroreceptor reflex), and cardiac output may actually decline. Norepinephrine is a drug of choice in shock states characterized by diminished peripheral vascular resistance such as severe septic shock. Like epinephrine, it reduces renal and splanchnic perfusion and may contribute to organ dysfunction particularly if the patient is hypovolemic. This can lead to renal failure and mesenteric infarction. In the pulmonary vasculature, norepinephrine increases vascular resistance by stimulation of alpha1 receptors that may contribute to pulmonary hypertension and right heart failure. Patients should be carefully monitored
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while receiving norepinephrine, and due to its very short half-life (approximately 2 minutes), a continuous infusion is recommended.
■ DOPAMINE Dopamine is an endogenous catecholamine and an important neurotransmitter in the central nervous system. It is the direct precursor in the biosynthesis of norepinephrine and has a highly dose-dependent effect on cardiac, vascular, and endocrine functions. In addition to beta1 and alpha1 activity, dopamine has specific effects on a group of dopaminergic receptors. Due to its fast metabolism, dopamine has to be given as a continuous intravenous (IV) infusion. In lower dose ranges of approximately 1-3 μg/kg/min, dopamine activates mainly dopamine-1 (D1) receptors that cause vasodilation and increased blood flow in the coronary, renal, and splanchnic vascular beds. Higher doses stimulate beta1 (3-10 μg/kg/min) and alpha1 adrenoceptors (>10 μg/kg/min). Dopamine at midrange doses will increase cardiac output by increasing stroke volume, but at higher doses, characterized by increased peripheral vasoconstriction, impedance to ejection may limit this action. Like other catecholamines, dopamine has arrhythmogenic properties at high doses. Because of the individual variability of effects of dopamine, the dose should always be titrated to effect.
■ SYNTHETIC CATECHOLAMINES AND PHOSPHODIESTERASE INHIBITORS Dobutamine Dobutamine is a selective beta1 agonist and must be given by continuous infusion due to its short half-life. This drug has predominantly beta1 activity. It is used to treat ventricular failure by increasing cardiac output by increasing myocardial contractility and heart rate. Doses between 2 and 10 μg/kg/min are commonly used. Lower doses have beta2 effects and can cause additional vasodilator actions, reducing systemic and pulmonary vascular resistance. Compared to dopamine, dobutamine is a coronary vasodilator improving blood flow to myocardium. Its use does not lead to significant increases in vascular resistance even at higher doses as does dopamine. Higher doses of dobutamine commonly cause tachyarrhythmias and ventricular ectopy, especially in the presence of myocardial ischemia. Similar to other catecholamines,
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Chapter 8 • Cardiovascular Pharmacology
dobutamine will increase oxygen demand of the heart and is often used in nonexercise cardiac stress testing. Dobutamine and other positive inotropic drugs can be combined with different pharmacologic agents such as vasodilators to enhance their actions to increase cardiac output.
Isoproterenol The clinical value of isoproterenol for improving contractility has diminished with the introduction of other inotropic drugs. It is the most potent agonist of beta1 and beta2 adrenoceptors and is primarily used to increase heart rate to overcome heart block. Due to its short halflife (5 minutes), it must be given by continuous infusion (1-5 μg/min) but may be injected intramuscularly or subcutaneously (0.2 mg). A low-dose infusion should be started and titration slowly increased to the desired ventricular rate. Isoproterenol increases heart rate and myocardial contractility while decreasing arterial pressure. These hemodynamic effects can cause large increases in myocardial oxygen demand and decreases in oxygen supply resulting in myocardial ischemia in patients with coronary artery disease.
Milrinone Milrinone is a PDE inhibitor indirectly leading to increased intracellular cAMP concentrations in cardiac and vascular smooth muscle. This subsequently increases contractility of the heart and causes vasodilation in arterial blood vessels resulting in afterload reduction. Milrinone is frequently used in cardiac surgery to improve ventricular pump function, particularly of the right heart, while simultaneously reducing pulmonary vascular resistance (and right ventricular afterload). In addition, this drug may have a positive effect on diastolic function. Milrinone is usually administered in a loading dose of 50 μg/kg followed by a maintenance infusion of 0.375-0.75 μg/kg/min. It is commonly used in combination with catecholamines. It will potentiate the effect of these agents by blocking the metabolism of cAMP, the concentration of which is increased by stimulation of beta adrenoceptors. Patients should be closely monitored during drug administration and the dose adjusted to hemodynamic or clinical endpoints, so as to avoid excessive hypotension and cardiac arrhythmias.
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■ MYOFILAMENT CALCIUM SENSITIZERS Levosimendan Levosimendan is member of a new group of inotropes termed myofilament calcium sensitizers. It increases the contractility of muscle cells by binding to a regulatory protein. This allows actin and myosin filaments to contract more quickly and with greater force without increasing the intracellular calcium concentration. Levosimendan also opens adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle and has PDE inhibition properties, which facilitate vasodilation of coronary, pulmonary, and systemic blood vessels, thereby reducing right and left ventricular afterload. This overall function leads to an increase in cardiac output while minimizing the risk of arrhythmias and with a more favorable balance of oxygen supply and demand as compared to catecholamines and PDE inhibitors. In clinical trials, this drug has been given as a loading dose of 6-12 μg/kg over 10 minutes followed by a continuous infusion of 0.05-0.2 μg/kg/min. Levosimendan is not yet FDA approved but has gained significant use in Europe and Asia.
■ VASOPRESSORS Vasopressin Vasopressin (arginine vasopressin [AVP]) is a hypothalamic peptide hormone released from the posterior pituitary gland in response to hyperosmolarity and hypovolemia. It regulates urine output in the kidney and is a very potent arterial vasopressor, which is mediated through receptors in blood vessel walls. Vasopressin is used clinically to counteract the profound vasodilation in septic shock or catecholamine-resistant, postcardiopulmonary bypass shock. Vasopressin demonstrates variability in arterial vasoconstriction with greater effects in the skeletal muscle and splanchnic vasculature and much less in coronary, cerebral, and pulmonary blood vessels. In cardiopulmonary resuscitation, vasopressin (40 U IV) is considered an alternative to the first or second dose of epinephrine in the treatment of pulseless cardiac arrest.
Phenylephrine Phenylephrine is an alpha1-adrenergic receptor agonist. Clinically, this drug has no positive inotropic activity in contrast to norepinephrine.
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It has similar actions to norepinephrine in the presence of blockade of beta receptors, only it is less potent and has a longer duration of action. It causes greater vasoconstriction in veins than in arteries and thus can increase cardiac output by increased venous return and stroke volume. Large increases in arterial pressure, however, can affect the increase in cardiac output by reflexively decreasing heart rate. All pure vasoconstrictors including phenylephrine when given in high doses can cause reduced blood flow to a variety of tissues resulting in ischemia. Vasoconstrictor agents are best used to reverse hypotension caused by reduced peripheral resistance.
Ephedrine Ephedrine is an indirect acting sympathomimetic agent and is commonly used by anesthesiologists to treat intraoperative hypotension secondary to general or regional anesthesia. It stimulates alpha and beta receptors directly and also increases norepinephrine concentrations at these receptors by releasing norepinephrine from adrenergic nerve terminals and therefore has actions very similar to those of norepinephrine. Bolus doses (5-10 mg IV) increase heart rate, blood pressure, and cardiac output similarly but of lesser magnitude as compared to epinephrine, and its duration of action is approximately 10-15 minutes.
■ ANTIHYPERTENSIVE MEDICATIONS Achieving hemodynamic stability of patients in the perioperative period can be challenging. Perioperative stress through anesthetic or surgical manipulation often contributes to high sympathetic nervous system activity with elevated arterial pressure and heart rate on the day of surgery. Large increases in blood pressures can cause significant morbidity and even mortality in conditions associated with cardiac and cerebrovascular events. Several classes of drugs have antihypertensive properties and can be used to manage blood pressure. These include direct vasodilators, beta-adrenergic blocking agents, and calcium antagonists.
■ VASODILATOR AGENTS Nitroprusside Nitroprusside is a direct vasodilator with a very rapid onset (1 minute) and very short duration of action (1-2 minutes) and should only be given by continuous infusion. Nitroprusside reduces pulmonary as well as systemic vascular resistance and
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is frequently used when fast and reliable reduction of blood pressure is needed. Although this agent is used to reduce afterload to enhance left ventricular ejection, nitroprusside also reduces preload. Reduction of arterial pressure in chronically hypertensive patients should be done with caution, as a rapid decrease in pressure may lead to ischemia in brain, kidney, or heart. Nitroprusside may cause vascular steal by diverting blood flow away from ischemic areas of myocardium. Doses from 0.1 to 2 μg/kg/min should be carefully titrated to the desired level of blood pressure and/or other hemodynamic parameter. Nitroprusside is deactivated by light, and thus the drug infusion reservoir must be adequately protected from light to prevent degradation and loss of potency. The nitroprusside molecule contains cyanide, and cyanide toxicity can develop from the breakdown of the drug, particularly after long-term or high-dose infusions. Cyanide toxicity leads to tissue hypoxia and acidosis despite high oxygen saturations by interrupting intracellular oxygen utilization.
Nitroglycerin Nitroglycerin directly relaxes vascular smooth muscle and has a greater effect on the venous versus arterial vasculature. This leads to pooling of blood in venous capacitance vessels and subsequent reduction in venous return to the heart with a decrease in right and left ventricular filling pressures. The latter results in a reduction in wall stress during systole and less energy consumption of the heart muscle. Nitroglycerin reduces pulmonary vascular resistance, increases coronary blood flow, and improves perfusion to ischemic regions of the heart. Stroke volume and cardiac output will decrease with lower preload in normal individuals, but in patients with myocardial ischemia improvement in coronary perfusion can result in increased cardiac output. All these effects make nitroglycerin a drug of choice in the management of chronic heart failure (CHF) and acute myocardial infarction. Higher doses of nitroglycerin can cause a decrease in blood pressure by reducing systemic vascular resistance, which may compromise coronary perfusion. Low doses of this drug in hypovolemic patients can also cause profound decreases in pressure. The onset of action is rapid, and the half-life of nitroglycerin ranges from 1 to 3 minutes. IV bolus doses of 20-100 μg can be used to titrate to
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effect, while continuous infusions range between 0.1 and 7.0 μg/kg/min and often provide more stable hemodynamic conditions. Nitroglycerin also dilates the cerebrovasculature, which may lead to increased intracranial pressures through increases in intracranial blood volume.
Hydralazine Hydralazine is a direct vasodilator and has a greater effect on arterial vessels than the venous system and is mainly used in acute hypertension. Blood vessels in muscle and skin are less affected than coronary, cerebral, and renal vessels. Hydralazine can trigger sympathetic nervous system stimulation by the baroreflex with an increase in heart rate and cardiac output. Compared to other direct vasodilators, the onset of action is relatively slow (5-15 minutes), which may make treatment of acute hypertension more difficult. In addition, hydralazine has a longer duration of action and therefore moment-to-moment control of arterial pressure as with nitroprusside is impossible. Finally, the efficacy of hydralazine is considerably less than that of other vasodilators.
Fenoldopam Fenoldopam is an agonist of D1 receptors (and to a lesser extent of alpha2-adrenergic receptors) and a rapidly acting vasodilator. It is approved for the management of severe hypertension when a rapid, easily reversible reduction in arterial pressure is warranted. It has strong vasodilator effects on the splanchnic and renal arterial vessels and increases renal perfusion, diuresis, and natriuresis. In the cerebral circulation, fenoldopam reduces global and regional blood flow. The half-life of fenoldopam is approximately 5 minutes, and infusion rates are commonly started at 0.05 μg/kg/min and subsequently titrated to the desired blood pressure response with doses up to 1.6 μg/kg/min. The diuretic effect is readily observed at lower doses. Compared to nitroprusside, fenoldopam does not carry as much risk of systemic toxicity especially at high doses.
■ CALCIUM CHANNEL BLOCKERS The ability of cardiomyocytes and vascular smooth muscle cells to contract is directly related to the intracellular concentration of calcium. Calcium enters the cardiomyocyte through special Ca2+ channels, which triggers an additional boost of Ca2+ release from stores in the sarcoplasmic reticulum. During systole, the Ca2+
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63
concentration increases and during diastole Ca2+ is pumped back into the sarcoplasmic reticulum enabling cardiac muscle to relax. Calcium channel blockers reduce the flow of Ca2+ into the cell and in turn cause a much smaller release of Ca2+ from the sarcoplasmic reticulum. All calcium channel blockers produce vasodilation and reduce arterial pressure, which leads to a reduction in left ventricular afterload. Calcium antagonists are used to reduce peripheral resistance in the management of hypertension and to treat cerebral vasospasm after subarachnoid hemorrhage. They also slow conduction and impulse formation in areas of the heart and can be used as antiarrhythmic agents. The various calcium channel blockers show differences in their affinity for vascular smooth muscle and cardiac muscle cells. Nifedipine and nicardipine are much more effective vasodilators than myocardial depressants, while verapamil is used for its ability to slow conduction through the heart and has little effect on vascular muscle tone. Diltiazem has vasodilator action as well as antiarrhythmic effects. In patients with acute heart failure, calcium channel blockers should be avoided due to their negative inotropic effects.
Nicardipine In clinical practice, nicardipine is a prototypical calcium channel blocker and is very effective in controlling perioperative hypertension, improving coronary perfusion in myocardial ischemia, or treating cerebral vasospasm after subarachnoid hemorrhage. It is associated with less rebound hypertension than other vasodilators, has a short half-life, and can be effectively titrated by continuous IV infusion (1-4 μg/kg/min).
■ BETA ADRENERGIC ANTAGONISTS (BETA BLOCKERS) Beta adrenergic blocking agents have a variety of effects on the cardiovascular system including reduction in heart rate, contractility, and myocardial oxygen consumption. Beta blockers play a role in the treatment of hypertension and have antiarrhythmic properties used mainly to treat atrial (supraventricular) arrhythmias. Due to their effect to slow conduction between atria and ventricles, these drugs can cause severe bradycardia and different severities of AV block (see Chapter 7). By antagonizing the effects of endogenous catecholamines on beta2 receptors,
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bronchospasm may be triggered in susceptible patients. The use of beta-blockers has been shown to reduce mortality in a variety of medical conditions, including hypertension, postmyocardial infarction, and CHF, and in high-risk vascular surgery patients. Beta-blockers differ in their affinity for betaadrenoceptor subtypes (e.g., beta1 selective), duration of action, coactivity on alpha-receptors (combined alpha- and beta-receptor antagonists), and intrinsic sympathominetic activity or the ability to both stimulate and block receptors (partial agonist properties). Beta-blockers are commonly used perioperatively to reduce and/or prevent excessive increases in heart rate.
Metoprolol Metoprolol is a cardioselective beta-blocker commonly used in the management of hypertension and coronary artery disease. Like most beta-blockers it undergoes extensive metabolism in the liver when given as an oral dose (first pass effect) reducing drug bioavailability. Effective oral doses are much higher (100-200 mg/d) compared to the IV dosing at 2.5-5 mg every 510 minutes. With its high affinity for beta1 receptors, this drug carries a smaller risk for bronchospasm in patients with asthma.
Labetalol Labetalol has nonselective competitive beta1-, beta2-, and selective competitive alpha1-adrenergic receptor blocking activity. Depending on oral or IV administration, the ratio of alpha to beta blockade is either 1:3 or 1:7, respectively, due to a profound first pass effect. Labetalol produces a dose-dependent reduction in blood pressure without reflex tachycardia. Doses of 0.25-0.5 mg/kg decrease arterial pressure within 5 minutes, and subsequent doses can be repeated in 5- to 10-minute intervals until the target blood pressure is reached. Cumulative doses of more than 3 mg/kg may be necessary in severe hypertensives. The duration of action of labetalol may be up to 18 hours.
Esmolol Esmolol is a cardioselective beta1 antagonist that has to be administered intravenously. Its popularity is due to a very rapid onset (25 mL), or if the aspirate contains particles such as chunks of food. A fiberoptic bronchoscope may be used to remove particulate matter.
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Bronchospasm occurs when the circumferential muscles lining the airways constrict and decrease airway diameters. This increases the resistance to airflow and makes both spontaneous and mechanical ventilation significantly more difficult. Bronchospasm can be accompanied by airway inflammation and edema, particularly with asthma or an infection. A foreign body in the airway can be a trigger for bronchospasm. In patients with reactive airway disease, the stimulation of an endotracheal tube in the airway can trigger bronchospasm. There are multiple other causes of bronchospasm. Treatment consists of inhaled and intravenous bronchodilators and anti-inflammatory medications (i.e., corticosteroids). Laryngospasm and stridor most commonly occur during induction or emergence from anesthesia. Laryngospasm is a spasmodic closing of the vocal cords spasmodically due to mechanical stimulation of the airway. The vocal cords are more sensitive to stimulation during emergence than they are at other times. The vocal cords may partially close, resulting in a high-pitched sound during inspiration called stridor. The vocal cords may close completely and prevent any gas movement. Treatment of laryngospasm includes positive pressure using a bag-mask system or muscle relaxation. Partial or complete upper airway obstruction may occur due to residual anesthesia or muscle relaxants. Methods of relieving upper airway obstruction include a jaw thrust maneuver to lift the tongue forward and create a patent passage for gas movement, or the insertion of a device into the airway (“oral airway”) that pushes the tongue forward to allow space for gas flow. A nasal airway that stents open the oropharynx can be used as well. Hypoventilation is common after anesthesia due to the effects of anesthetic agents and opioids used for pain relief. These medications decrease the drive to breathe by affecting areas of the brain that are responsible for regulating carbon dioxide levels. Patients may have a slow respiratory rate and/or small tidal volume, which results in hypoventilation. CO2 levels in the blood can rise significantly, and if the hypoventilation is severe, blood oxygen levels will fall. In some cases, oversedated patients can stop breathing (apnea).
Abnormalities in a patient’s upper airway anatomy can make either mask ventilation or endotracheal intubation difficult. The inability to ventilate a patient during the induction of anesthesia is a true emergency and if not corrected can lead to severe patient morbidity or even death. Airway management is covered in Chapter 18, and airway emergencies are covered in Chapter 60.
■ SUMMARY One of the roles of an anesthesia provider in the operating room is to ensure that patients maintain optimum respiratory function, despite the physiologic aberrations that result from sedation, analgesia, general anesthesia, or muscle relaxation. Understanding upper and lower respiratory anatomy, respiratory physiology, and perturbations caused by anesthesia, respiratory pharmacology, surgery, and patient comorbidities help the anesthesia provider formulate an effective anesthetic plan that decreases the risk of perioperative complications. The anesthesia plan will include the type of anesthetic, a plan for airway management, and a plan for managing ventilation. During the course of the anesthetic, the anesthesia provider will make use of multiple devices to monitor respiratory function.
REVIEW QUESTIONS 1. Which of the following are functions of the lung? A) Warm and humidify inspired gases B) Deliver oxygen to the blood C) Remove carbon dioxide from the blood D) Filter inspired air E) All of the above Answer: E. All of the above represent the main functions of the lung.
2. Which of the following are functions of the UPPER airway? A) Prevent alveoli from collapsing B) Deliver oxygen to the blood C) Remove carbon dioxide from the blood D) Filter inspired gases E) None of the above Answer: D. Both the nose and the mouth, parts of the upper airway, play a role in filtering inspired gases. Oxygenation of blood and removal of carbon dioxide occur in the alveoli that are part of the lower airway.
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Chapter 11 • The Respiratory System 3. Which of the following structure is NOT a part of the upper airway? A) Nose B) Mouth C) Trachea D) Pharynx E) Larynx Answer: C. The nose, mouth, pharynx, and larynx constitute the upper airway. The trachea is part of the lower airway.
4. What is the purpose of the conducting airways? A) Filter gases B) Heat gases C) Direct gases to the respiratory airways D) Participate in gas exchange E) None of the above Answer: C. The conducting airways do not participate in gas exchange and form part of the anatomical dead space of the lung. They are conduits to direct gases to the respiratory airways and alveoli where gas exchange occurs. Filtration and heating of gases occur primarily in the nose.
5. What is the main muscle of respiration? A) Diaphragm B) External intercostal muscle C) Internal intercostal muscle D) Sternocleidomastoid E) None of the above Answer: A. The diaphragm is the main muscle of respiration. Contraction of the diaphragm pushes the chest wall out and the abdominal contents down. These actions cause an increase in intrathoracic volume and a decrease in intrathoracic pressure. The intercostal muscles and the sternocleidomastoid muscle are accessory muscles of respiration. They are utilized to augment the diaphragm if a larger inspiration is necessary.
6. What determines the oxygen reserve available in the lungs after induction of general anesthesia? A) Total lung capacity B) Functional residual capacity (FRC) C) Tidal volume D) Inspiratory reserve volume E) All of the above Answer: B. The FRC is the volume of gas in the lungs at the end of a normal exhalation. If a patient were to become apneic, this volume of gas and its residual oxygen form a reserve of oxygen that can be taken up into the bloodstream. Once this oxygen reserve is exhausted, the blood oxygen will fall. Patient factors like morbid obesity that reduce the FRC increase the risk of desaturation during the induction of general anesthesia.
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7. What is the term for the volume of gas moved during quiet ventilation? A) Tidal volume B) Total lung capacity C) Expiratory reserve volume D) Residual volume E) Inspiratory reserve volume Answer: A. The tidal volume is the volume of gas moved during a normal inhalation and exhalation. The inspiratory reserve volume is the amount of extra gas that can be taken in from a maximal inspiration. The total lung capacity is the total volume in the lungs after a maximal inspiration. The residual volume is the volume left in the lungs after a maximal exhalation. The extra amount of gas that can be expired after a normal exhalation is the expiratory reserve volume.
8. What structures protect the trachea from aspiration of stomach contents? A) Tongue B) Alveoli C) Conducting airways D) Vocal cords E) Mainstem bronchus Answer: D. The epiglottis and the vocal cords work in concert to occlude the entrance to the trachea to prevent aspiration. The vocal cords close and the epiglottis covers the vocal cords.
9. Where in the lungs does gas exchange occur? A) Trachea B) Carina C) Conducting bronchioles D) Alveoli E) All of the above Answer: D. The trachea, the bronchi, and the conducting bronchioles all are conducting airways that direct the gas to the alveoli. Gas exchange occurs in the alveoli where the lung tissue is very thin and the capillaries come in close contact with the alveoli to allow gases to diffuse. The carina is the junction where the distal trachea divides into the two mainstem bronchi.
10. What is dead-space ventilation? A) Ventilation during basic life support B) Regions of the lung that receive ventilation but not perfusion C) Regions of the lung that receive perfusion but not ventilation D) The volume in the lungs after a maximal expiration E) The volume in the lungs after a maximal inspiration Answer: B. When alveoli are ventilated but not perfused, no gas exchange takes place and it is referred to as dead space. When alveoli are perfused but not ventilated, no gas exchange takes place and it is referred to as shunt. It is as if
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11. How does the respiratory system participate in maintaining a physiologic pH? A) Respiratory function maintains CO2 homeostasis. B) CO2 can form carbonic acid. C) The brainstem modulates respiratory function in response to pH changes. D) Hyperventilation can decrease CO2 levels in response to acidosis. E) All of the above. Answer: E. All of the above. The respiratory system plays a critical role in acid-base balance. Because CO2 can be converted to carbonic acid, CO2 levels affect the pH of the blood. The brainstem adjusts minute ventilation in response to pH changes in the blood. Changing minute ventilation, either up or down, will affect CO2 levels and can compensate for the pH change. Hyperventilation decreases CO2 levels and decreases carbonic acid in the blood.
12. Which monitor is NOT used to monitor ventilation? A) End-tidal carbon dioxide B) Esophageal stethoscope C) Pulse oximetry D) Arterial blood gas E) Central venous pressure Answer: E. The central venous pressure is used to monitor blood volume. The remaining monitors are all used to monitor ventilation.
SUGGESTED READINGS Barrett KE, Barman SM, Boitano S, et al. Pulmonary function. In: Barrett KE, Barman SM, Biotano S, et al., eds. Ganong’s Review of Medical Physiology. 23rd ed. New York, NY: McGraw-Hill Medical; 2010: Chapter 35. Boer F. Drug handling by the lungs. Br J Anaesth. 2003:91(1):50–60. Conti G, Dell’Utri D, Vilardi V, et al. Propofol induces bronchodilation in mechanically ventilated chronic obstructive pulmonary disease (COPD) patients. Acta Anaesthesiol Scand. 1993;37:105–110. Hashiba E, Hirota K, Suzuki K, et al. Effects of propofol on bronchoconstriction and bradycardia induced by vagal nerve stimulation. Acta Anaesthesiol Scand. 2003;47(9):1059–1063. Kabara S, Hirota K, Hashiba E, et al. Comparison of relaxant effects of propofol on methacholine-induced bronchoconstriction in dogs with and without vagotomy. Br J Anaesth. 2001;86(2):249–253. LeBlond RF, Brown DD, DeGowin RL. The chest: chest wall, pulmonary, and cardiovascular systems; the breasts. In: LeBlond RF, Brown DD, DeGowin RL, eds. DeGowin’s Diagnostic Examination. 9th ed. New York, NY: McGrawHill Medical; 2009:302–332. Levitsky MG. Pulmonary Physiology. 7th ed. New York, NY: McGraw-Hill Medical; 2007. Morgan GE Jr, Mikhail MS, Murray MJ, eds. Respiratory physiology: the effects of anesthesia. In: Clinical Anesthesiology. 4th ed. New York, NY: McGraw-Hill Medical; 2005: Chapter 22. Prendergast TJ, Ruoss SJ, Seeley EJ. Pulmonary disease. In: McPhee SJ, Hammer GD, eds. Pathophysiology of Disease. 6th ed. New York, NY: McGraw-Hill Medical; 2003.
13. Which medications cause bronchodilation? A) Beta agonists B) The volatile anesthetics sevoflurane and isoflurane C) Neostigmine D) A and B E) B and C Answer: D. Beta agonists (e.g., albuterol, epinephrine) are potent bronchodilators. Volatile anesthetics (e.g., sevoflurane and isoflurane) cause bronchodilation. Desflurane produces minimal bronchodilation and is a potent airway irritant (causes coughing and breath holding). Neostigmine blocks the breakdown of acetylcholine, which is a potent vasoconstrictor.
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CHAPTER
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Acid and Base Physiology Aaron Kirsch and Jeffrey Kirsch ■ INTRODUCTION There is a vast amount of water in the human body, distributed as the cytoplasm within cells (intracellular fluid) and the extracellular fluid, which includes plasma. Dissolved in all of this water are a wide variety of solutes. Among the most important solutes are acids and bases. Acids are compounds that, when dissolved in water, will donate a hydrogen ion (H+). Bases are compounds that, when dissolved in water, will accept an H+ from an acid. Examples of acids include hydrochloric acid (HCl) or carbonic acid (H2CO3); examples of common bases include ammonia (NH3) or sodium hydroxide (NaOH). We measure the concentration of acid in the body fluids using the pH scale. The pH of a solution is defined as follows: pH = − log ⎡⎣H + ⎤⎦ where [H+] is the concentration of H+. If there is an abundance of acid in the fluid, there will be a high [H+]. This corresponds to a low pH. Therefore, the lower the pH measurement, the more acidic is the fluid. If there is an abundance of base in the solution, there will be a relatively lower [H+], because bases will eagerly accept and incorporate free H+. This corresponds to a high pH. Therefore, the higher the pH measurement, the more alkaline (basic) is the fluid. In chemistry, a pH of 7 is considered neutral, a pH less than 7 is considered acidic, and a pH greater than 7 is considered alkaline. In human physiology, however, the optimal pH of arterial blood is 7.4 or slightly alkaline. Venous blood will have a lower pH, as it is carrying waste from the periphery for removal by the lungs, kidneys, liver, and bowel. The balance between acids and bases is crucial to proper body functioning. Even slight deviations from a pH of 7.4 can result in serious pathologic consequences. For example, reduction in
pH to less than 7.0 can be fatal. This is because the organs and tissues of the body depend on the functionality of their cells. The functional actors in cells are enzymes, special proteins that catalyze chemical reactions. Alterations to the body’s acid-base balance change the chemical structure of enzymes, rendering them dysfunctional. This may result in organ malfunction. When the pH of the plasma is less than 7.4, the plasma is acidotic. When the pH is greater than 7.4, it is alkalotic.
■ PHYSIOLOGIC CONSEQUENCES OF ACID-BASE DISTURBANCES In the operating room (OR), acidosis produces its most significant and obvious effects on the cardiovascular system. As pH drops to 7.2, there is a noticeable reduction in heart muscle contractility and at a pH of 7.1, the entire cardiovascular system becomes much less responsive to catecholamines, making it very difficult for the anesthesiologist to treat hypotension with commonly used agents (e.g., norepinephrine, phenylephrine, ephedrine). Acidosis also causes hypotension due to peripheral arteriolar dilatation and constriction of the pulmonary arteries. Importantly, acidosis results in shifting of potassium out of cells and into the general circulation, which then may result in additional cardiac dysfunction.
■ RESPIRATORY ACID-BASE DISTURBANCES The acids in the body come from a variety of sources. When proteins are metabolized, weak acids are released into the bloodstream. But the main contribution of acid comes from a gas. When cells metabolize fats and carbohydrates, carbon dioxide (CO2) gas is produced. Inside of cells, this CO2 dissolves in the cytoplasm, producing H2CO3. 101 tahir99-VRG & vip.persianss.ir
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The enzyme carbonic anhydrase (CA) rapidly converts this H2CO3 into H+ and HCO3− (bicarbonate), which can be illustrated as follows: CA CO2 ↔ H2CO3 ↔ H + + HCO3 − As illustrated above, CO2 production results in an increase in [H+]. This translates into a lower pH. Therefore, excess CO2 leads to acidosis. If CO2 were not removed from the body, acid would build up and pH would decrease dramatically. Fortunately, the CO2 produced in metabolism is transported in the bloodstream to the lungs. Here, it is removed from the blood in exchange for oxygen (O2) and is breathed off into the environment. CO2 travels in the blood in three forms. The majority of CO2 dissociates into H+ + HCO3−. The H+ binds to hemoglobin molecules (Hb⋅H+), while the HCO3− travels freely in the plasma. Once at the lungs, the H+ and HCO3− recombine to form CO2, where it is exhaled. A small amount of CO2 also travels as dissolved CO2, and a small amount binds directly to hemoglobin (Hb⋅CO2). When acidosis is caused by the lungs being unable to breathe off CO2, it is termed respiratory acidosis. When alkalosis is caused by the lungs breathing off too much CO2, it is termed respiratory alkalosis. Respiratory acidosis occurs when ventilation is impaired. For instance, the diaphragm or intercostal muscles may be paralyzed or too weak. A paralyzed diaphragm can be commonly observed following interscalene blockade, whereas intercostal muscles become weak in patients with a high spinal anesthetic. Patients who are administered opiate drugs will also have a predictably depressed breathing rate. Patients with respiratory acidosis may appear anxious or delirious, or even have myoclonic convulsions or seizures in extreme cases. The acidosis is best treated by increasing ventilation (breathing rate), by treating the underlying cause, or, if necessary, by mechanically ventilating the patient (oxygen treatment). Other common causes of respiratory acidosis include pulmonary disease that impairs gas exchange (e.g., chronic obstructive pulmonary disease). Respiratory acidosis also occurs when there is excess production of CO2, beyond the ability of the patient’s ventilatory ability. For example, in patients who are anesthetized and mechanically ventilated (i.e., have a fixed ventilation), excess CO2 production may occur
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from high fevers or malignant hyperthermia. Decreased ability to clear CO2 from the lungs may occur secondary to extremely compromised pulmonary function. Respiratory alkalosis occurs due to hyperventilation (breathing too fast). This happens in patients suffering anxiety attacks. It is also seen in patients with pulmonary embolisms (blood clots that typically travel from the legs to the lungs), liver failure, pregnancy, and an overdose of aspirin. Patients might present with arrhythmias (irregular heartbeats), muscle cramps, tingling sensations, or even seizures. Although correcting the underlying cause is essential, hyperventilation can be urgently treated with sedating drugs if necessary. Oxygen (O2) is another important gas in maintaining acid-base balance. It is inhaled from the environment and enters capillaries in the lungs in exchange for CO2. If breathing is impaired, O2 cannot enter the lungs to be exchanged with CO2. As shown above, the buildup of CO2 in the blood results in acidosis. Furthermore, O2 is essential for aerobic metabolism. When cells lack O2, they produce energy via anaerobic glycolysis. Prolonged glycolysis causes the accumulation of lactic acid. This results in further acidosis. Low O2 supply to the tissue may result from systemic hypoxia (e.g., high altitude, poor pulmonary gas exchange) or compromised circulation to an individual body region (local ischemia). Global ischemia may be caused by overall poor circulation (e.g., cardiac failure or severe hypotension), while local ischemia may be secondary to surgical intervention (e.g., aortic cross-clamp, limb tourniquet) or patient disease (arterial blood clot, peripheral vascular disease, trauma, etc.).
■ ARTERIAL BLOOD GASES Because O2 and CO2 are important factors in determining acid-base balance, being able to measure their partial pressures (concentrations) in the bloodstream can provide valuable insight into the physiologic condition of the patient. This is accomplished by arterial blood gas measurement (ABG). A sample of blood is drawn from an artery and is placed into a blood gas analyzer device (See Chapter 37). This device uses a variety of electrochemical probes to measure the pH and the partial pressures of O2 and CO2. It is important to understand that the [HCO3−] is
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calculated and not directly measured by most blood gas machines. Assessment of a patient’s acid-base status from a reading on the blood gas analyzer can depend on the temperature of the patient and the temperature setting on the machine performing the measurement. Two different approaches exist: “alpha-stat” and “pH stat.” In blood, the pH changes inversely with temperature. Thus, at temperatures below 37°C, a pH of 7.4 would be considered acidotic. With the pH-stat approach, the anesthesia technician will run the blood sample entering the patient’s temperature into the blood gas machine, while with the alpha-stat approach, all blood gases are run at 37°C. Since there is great controversy among anesthesiologists regarding the best approach (alpha or pH-stat), the anesthesia technician should ask anesthesiologists their preference before analyzing the sample blood on the blood gas machine. When obtaining a patient’s vital signs during an operation or at the bedside, oxygen saturation (“pulse ox”) is often measured by clipping a pulse oximeter probe to the fingertip (see Chapter 33). Both the red and infrared waves emitted by this probe allow for the measurement of the amount of hemoglobin in the blood that is bound to the oxygen (Hb⋅O2). This defines oxygen saturation (SaO2). Although this gives us a good estimate of oxygenation, it does not tell us anything about CO2 or acid-base balance. This is why we must examine the ABG. ABG is obtained in the following manner. First, you must evaluate the arteries of the patient. Because of ease of access and the presence of a redundant circulation to the hand via the ulnar artery, the radial artery is typically used. You can palpate the radial artery pulse by placing one or two fingers just proximal (above) to the hand on the anterior-lateral (front, thumb side) surface of the wrist. Next, some clinicians try to assess the collateral circulation of the hand. They argue that if the radial artery is damaged during the procedure, it is important to be assured that collateral circulation to the hand via the ulnar artery is intact. The test that is done is called the Allen test. Those who use this test will choose an alternate site (e.g., femoral artery) for drawing an ABG if the Allen test demonstrates poor collateral circulation in the hands. However, a number of authors have demonstrated that the Allen test has very limited predictive value, regardless
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of whether it demonstrates good or poor collateral circulation via the ulnar artery. Therefore, this test is not used very often in clinical practice. In order to perform the Allen test, 1. The patient should extend the hand at the wrist 2. The patient should make a fist 3. The clinician should compress both the radial and ulnar arteries at the patient’s wrist 4. Have the patient open and close a tight fist several times 5. The palm should appear white, as it is not receiving any blood flow 6. Release your hold on the ulnar artery, restoring ulnar blood flow If there is good ulnar circulation, the palm should become red within 5-10 seconds (maximum of 15 seconds) after restoring ulnar blood flow. A palm that remains white constitutes a failed Allen test, meaning that ulnar flow is too poor for an ABG to be measured in this hand. If your hospital has preassembled kits for ABG measurement, they should be used. A 23-gauge (or smaller) needle is used, along with a preheparinized syringe, containing 30-100 units of heparin per milliliter of blood to be obtained. A syringe with too much heparin risks diluting the sample. When preassembled kits for ABG measurement are not readily available, the inside of a regular syringe can be lightly coated or rinsed with heparin (usually 1,000 unit/mL strength), taking care to remove as much liquid heparin from the syringe as possible. Glass syringes are preferable to plastic. The ABG sample is obtained as follows: 1. Clean the wrist with chlorhexidine, alcohol, or betadyne. 2. Prepare the puncture site with sterile drapes (towels). 3. The clinician should be wearing sterile gloves and a face mask. 4. Extend the patient’s wrist 30-45 degrees. 5. Your nondominant hand should palpate the point of maximal pulsation over the radial artery. 6. Local anesthetic should be infiltrated at the site prior to arterial puncture. 7. With your dominant hand, position the needle at an angle of 45 degrees and enter the radial artery just distal to where your other hand is palpating.
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8. Blood will fill the syringe spontaneously in specialized ABG syringes but will need to be withdrawn in standard syringes. 9. Expel any air bubbles from the syringe. 10. Send the sample (be sure it is labeled correctly) immediately to the laboratory for analysis. 11. After removing the needle, have the patient apply direct pressure over the site for 5 minutes. In the OR many patients who require frequent analysis of an ABG will have an indwelling catheter in a peripheral (usually radial) artery. Some institutions use arterial monitoring sets that include a blood withdrawal chamber in a closed system that minimizes blood wastage and contamination. With these sets, blood is drawn back into the chamber and the arterial blood sample is withdrawn from a special sampling port. Withdrawal of the appropriate amount of blood into the chamber ensures that pure blood is at the sampling site and not blood that has been mixed with the arterial line flush solution. After obtaining the blood sample for ABG analysis, the blood in the chamber, which will be a mixture of blood and dead-space fluid from the catheters, is infused back toward the patient. Finally, the catheter is flushed using a pressurized fluid system (using a pressurizing compression bag) to prevent blood clotting in the tubing system. Some institutions do not utilize the closed system tubing configuration. In this situation, the clinician will attach a sterile syringe to the stopcock that is most proximal to the patient and withdraw at least three times the amount that is included as dead space in the tubing system. The withdrawn blood must then be discarded and additional blood drawn to fill the ABG syringe. Finally, flush the tubing system with saline (or heparinized saline) to prevent blood from clotting in the tubing. There are certain pitfalls in ABG measurement that should be avoided. First, there should be minimal delay in transporting the sample to the analyzer. Within the blood sample, there are cells whose metabolic activity will alter the partial pressures of CO2 and O2. If you anticipate a delay of more than 10 minutes, the sample should be cooled on ice for no more than 1 hour to slow this metabolic activity. In cases of delay, glass syringes are superior as gases may dissolve over
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a short period of time in plastic. Additionally, any small air bubbles should be expelled from the syringe, as they result in inaccurate analysis (gas from the bubble can diffuse into the blood or gas in the blood can diffuse into the bubble). Large air bubbles indicate an unusable sample that should be discarded. Complications for the patient include mistaken venous sampling, hematoma, excessive bleeding, occlusion of the artery, and infection. A venous blood sample will have higher pCO2 and lower pO2 than arterial blood, and the values may not correspond to the patient’s clinical condition.
■ ABG INTERPRETATION The first step when evaluating an ABG is to determine if the pH is in the normal range of 7.35–7.45. Thus, if the patient’s pH is below 7.35, the patient is acidotic, and if it is higher than 7.45, the patient is alkalotic. Next, review the pCO2. When deviations in pCO2 account for changes in the pH, the patient is said to have a respiratory acid-base disorder. If the pCO2 is above 45 in acidotic patients, the patient has respiratory acidosis; if the pCO2 is below 35 in alkalotic patients, the patient has respiratory alkalosis. Next, it is important to analyze the HCO3- (normal 22-26 mEq/L). When the direction of change in HCO3- matches that of the pH, the patient is said to have a metabolic acidbase disorder. If HCO3- is below 22 in acidotic patients, the patient has metabolic acidosis, and if HCO3- is above 26 in alkalotic patients, the patient has metabolic alkalosis. Finally, patients may have alterations in both CO2 and HCO3-. In some cases, this is due to disorders in different organ systems. In other cases, the patient’s body is attempting to compensate for an acid-base disorder and restore the pH to as close to normal as possible. In these patients, the primary cause of the disorder (respiratory or metabolic) tracks the change in pH. Thus, a patient who has a low pH, a high pCO2, and a high HCO3- is said to have a primary respiratory acidosis with a compensatory metabolic alkalosis. Similarly, a patient who has a low pH, a low HCO3-, and a low pCO2 is said to have a primary metabolic acidosis with compensatory respiratory alkalosis.
■ METABOLIC ACID-BASE DISTURBANCES Besides the H+ generated from CO2, other metabolic processes—such as protein breakdown—generate
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acids such as H2SO4 and H3PO4. It is the responsibility of the kidneys to excrete enough H+ in the urine to ensure that excess acid is not retained in the body. Furthermore, feces are rich in HCO3−, and so every bowel movement results in loss of HCO3−, a base. Again, it is the responsibility of the kidneys to reabsorb enough HCO3− to balance these losses. When the kidneys are unable to adequately excrete H+ or fail to reabsorb enough HCO3−, acidosis results. This sort of acidosis is termed metabolic acidosis. Added H+ is moderated to a limited extent by the body’s buffer system. Buffering is the process by which increases in H+ concentration are partially bound to other molecules to reduce the amount of free H+ and its attendant impact on pH. Buffers can also absorb HCO3−. Finally, molecular buffers can release H+ or HCO3− to counteract pH changes when the concentration of H+ or HCO3− is falling. Hemoglobin buffers pH by directly binding H+. Bone can buffer pH during extreme acidosis by releasing HCO3− into the circulation. But the most important buffer is plasma HCO3−. As acid accumulates in the bloodstream, H+ combines with HCO3−. H2CO3 forms almost immediately and becomes CO2, which can be exhaled. Yet, if the body is overloaded with acid, the HCO3− buffer is exhausted and ceases to be effective. It is then that metabolic acidosis seriously affects the pH. When attempting to find the cause of a metabolic acidosis, you will find valuable clues in the concentrations of electrolytes (ions) in the patient’s blood. Plasma is electrically neutral— all of its positively charged constituents (cations) are balanced by an equal number of negatively charged constituents (anions). The major cations are sodium (Na+), potassium (K+), calcium (Ca2+), and magnesium (Mg2+). The major anions are HCO3−, chloride (Cl−), and proteins. Out of all these ions, Na+, HCO3−, and Cl− are considered the major, “measured,” ions. And, the difference in concentration between the measured cations and the measured anions is called the anion gap. Anion gap = ⎡⎣Na + ⎤⎦ – ( ⎡⎣ HCO3 − ⎤⎦ + ⎡⎣Cl − ⎤⎦ ) Normally, the anion gap ranges from 8 to 12. This reflects the concentration of the so-called unmeasured anions, mainly proteins. In a patient with diarrhea, extensive amounts of base, HCO3−, are lost in the stool. This results
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in a metabolic acidosis. As HCO3− is lost from the bloodstream, Cl− shifts from within cells to the bloodstream, replacing the lost negative charges, thus preserving electrical neutrality. Because the rise in [Cl−] offsets the fall in [HCO3−], there is no change in the anion gap. This is termed normal anion gap metabolic acidosis. It is treated by replacing lost fluids and electrolytes and quieting the underlying gastrointestinal disturbance. In severe cases, NaHCO3 (a base) may be gradually infused to raise the pH. Normal anion gap metabolic acidosis also occurs when the kidneys fail to reabsorb HCO3− due to damage to kidney tubule cells, when the CA enzyme is inhibited by medications (e.g., acetazolamide), and when there are deficiencies in the hormone aldosterone. One of the most common causes of metabolic acidosis in the OR is excessive infusion of chloride-containing fluid. This usually results from the anesthesiologist administering intravenous (IV) fluid in the form of normal saline (0.9% sodium chloride). Increases in blood chloride concentration causes the kidneys to excrete HCO3−, and the patient can become acidotic. Unfortunately, this acidosis is often not recognized to be secondary to excess chloride administration, with clinicians confusing this acidosis as being secondary to poor perfusion. The clinician may administer “volume resuscitation” with normal saline, making the acidosis and patient’s condition worse. When acids are added to the plasma, the acid dissociates into its ionic components. H − A → H+ + A − The added H+ combines with plasma HCO3−, depleting it. But, since the acid’s dissociation produces an anion (A−), there is no need for Cl− to shift from the cells to the plasma, because the lost negative charges of HCO3− are balanced by the added A−. Since neither [Na+] nor [Cl−] changes, while [HCO3−] decreases, the anion gap becomes larger. Such a situation is labeled increased anion gap metabolic acidosis. Certain causes of increased anion gap metabolic acidosis are commonly encountered. In the perioperative setting, the most common cause is lactic acidosis from poor perfusion. In patients whose tissues are starved of oxygen (e.g., systemic hypoxia, decreased blood flow to organs, or rarely carbon monoxide poisoning), anaerobic
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glycolysis predominates. The end product of this process is lactic acid, which results in an increased anion gap metabolic acidosis. In the OR, lactic acidosis is most common during prolonged periods of hypotension or when a large percentage of the body is excluded from normal circulation (e.g., aortic cross-clamp during aortic artery surgery). Severe ischemia, hypoxia, or shock is likely to increase the blood concentration of lactic acid. In critically ill patients, a lactic acid concentration of less than 2 mmol/L can be considered normal. With lactic acid levels of 2-5 mmol/L, the body can usually compensate and the patient may not present as being acidotic. However, lactic acid levels of greater than 5 mmol/L are usually associated with systemic acidosis. Treatment includes improvement of circulation (e.g., pharmacologic treatment of hypotension or removal of cross-clamps) and IV fluid rehydration (for decreased blood flow to organs). In the case of systemic hypoxia (e.g., congestive heart failure or poor lung function), treatment includes administering 100% oxygen therapy by using mechanical ventilation with aggressive use of positive end-expiratory pressure. Other causes of increased anion gap acidosis occur when acids other than lactic acid accumulate in the body. Aspirin (aminosalicylic acid) overdose decreases the pH and fills the blood with salicylate anions. This is best treated by preventing further aspirin absorption (using activated charcoal) and by alkalinizing blood and urine to encourage salicylate elimination (administer NaHCO3 until the blood pH is higher than 7.45). Patients with kidney failure are unable to excrete H3PO4 or H2SO4, resulting in the accumulation of metabolic acids. This is remedied by hemodialysis. Patients with poorly controlled type-1 diabetes mellitus accumulate keto acids (e.g., acetoacetic acid) leading to the emergency situation of diabetic ketoacidosis. This is best treated with insulin and IV fluid rehydration. When the kidneys excrete too much H+, the result is alkalosis. This sort of alkalosis is termed metabolic alkalosis. When a person vomits, HCl is expelled from the stomach. Similarly, inserting a suctioning nasogastric (NG) tube into the stomach to relieve a patient’s gastrointestinal distress also removes HCl. This loss of acid causes metabolic alkalosis. In order to reclaim the fluid volume lost, the kidneys reabsorb more Na+ and water. The Na+ is reabsorbed in exchange for H+, which is excreted
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from the bloodstream into the urine, exacerbating the metabolic alkalosis. This latter sort of alkalosis is also caused by diuretic drugs (e.g., furosemide) that cause volume loss by increasing urination. Properly rehydrating the patient with IV fluids corrects all of these alkaloses. Certain tumors produce an excess of the hormone aldosterone. Increased aldosterone results in metabolic alkalosis by causing increased Na+ reabsorption in exchange for H+. Aldosterone’s actions can be blocked by medications (e.g., spironolactone) or by surgical removal of the tumor. Although there are many causes of pH disturbances, ABG results, analysis of electrolytes and the anion gap, and patient history can point you toward a diagnosis and direct subsequent treatment.
■ COMPENSATION Changes in pH disrupt healthy body functioning. Fortunately, the body has built-in mechanisms to correct disturbances to its acid-base balance. In patients who are not anesthetized and have metabolic acidosis or alkalosis, ventilation (breathing rate) rapidly adjusts. Breathing faster expels CO2 more rapidly with each exhalation. The removal of CO2 is equivalent to breathing off H+, which makes the pH less acidic. Breathing rate, though, cannot increase infinitely, and this limits the effectiveness of respiratory compensation. On the other hand, breathing more slowly causes less CO2 to be exhaled. Thus, more H+ is retained, and the pH becomes more acidic. Breathing rate can only decrease a certain amount to compensate for alkalosis. This is because a decrease in ventilation also causes a decrease in O2 intake. Consequently, decreased ventilation never lowers the pH quite to 7.4. The body acts as its own blood gas analyzer by using chemoreceptors. A chemoreceptor is an apparatus that detects concentrations of chemicals. It consists of a sensor that relays information to an integrator. This integrator then instructs an effector to respond accordingly. There are two groups of chemoreceptors in charge of ventilation: peripheral and central. The peripheral chemoreceptors are located in the aortic body (near the heart) and the carotid body (in the neck). They detect pO2, increasing ventilation when pO2 decreases. The central chemoreceptors are located in the medulla of the brainstem (between the cerebrum and the spinal cord). They detect pCO2 and strive to maintain it at 40 mm Hg.
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In metabolic acidosis, when H+ is increased, increased CO2 is present in the central nervous system. Central chemoreceptor sensors send a signal to the respiratory centers of the brainstem, which instruct the lungs to increase ventilation. This increase in ventilation, which occurs minutes after the pCO2 is increased, decreases the pCO2. In this way, pH change is minimized. When metabolic or respiratory acid-base balance is disturbed for a prolonged period of time, further compensation is provided by the kidneys. They are responsible for maintaining optimal concentrations of electrolytes in the blood. Although their function is very complex, they essentially act as intelligent filters. As blood passes through the kidneys, electrolytes are reabsorbed back into the bloodstream, or they may be expelled by the kidney into the urine. The kidney senses alterations in voltage and pH and adjusts its filtering accordingly. For instance, if the blood pH is too acidic, the kidney secretes excess H+ into the urine, while simultaneously reabsorbing HCO3− back into the bloodstream. Nevertheless, this compensation never brings the pH back to a normal 7.4. In other words, a chronic (prolonged) acidosis will be compensated to a pH less than 7.4, while a chronic alkalosis will be compensated to a pH greater than 7.4.
■ SUMMARY Acid-base balance is crucial for normal physiologic functioning. Alterations in ventilation cause changes in pCO2. This results in respiratory acidosis or respiratory alkalosis. The loss of HCO3− via bodily excretions, and the accumulation of acids from metabolism and ingestions, results in metabolic acidosis. The body has its own mechanisms to compensate for alterations in pH. Within minutes, ventilation adapts to compensate metabolic acid-base disturbances. After 1 day, the kidney begins to compensate for both metabolic and respiratory acid-base derangements. Unfortunately, the body’s compensatory mechanisms can be overwhelmed. It is essential to treat the underlying cause of the acid-base disturbance, as it may easily become life-threatening. Measurement and analysis of an ABG, electrolytes, lactate level, and anion gap, as well as patient history, will guide diagnosis and treatment.
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REVIEW QUESTIONS 1. Infusing pure HCl will have what effect on H+ and pH? A) Increase H+; increase pH B) Increase H+; decrease pH C) Decrease H+; decrease pH D) Decrease H+; increase pH E) Unchanged H+; unchanged pH Answer: B. HCl is an acid. It will donate its H+, so that the concentration of H+ will increase. An increase in H+ translates to a decrease in pH. If a base were infused instead, there would be a decrease in H+, which translates into an increase in pH (option D).
2. Before attempting an ABG measurement in the right radial artery, you notice the patient fails the Allen test. What should you do next? A) Obtain a sample from the left radial artery. B) Obtain an ABG sample from the right radial artery. C) Obtain a sample from the right brachial vein. D) Measure oxygen saturation. E) Perform the Allen test on the left hand. Answer: E. A failed Allen test means that the arterial supply of the hand is inadequate, and this wrist is not suitable to be used for ABG sampling. The next step involves performing the Allen test on the patient’s other hand to see if it is a suitable site for ABG sampling (E). Most clinicians would support performing an Allen test before obtaining the ABG sample (option A). It is not appropriate to sample from a vein (option C). The oxygen and carbon dioxide contents differ in arterial and venous blood. Measuring oxygen saturation is not part of the protocol for obtaining an ABG sample (option D).
3. You are asked to see an anxious patient who you suspect may have respiratory alkalosis. Which of the following studies best assesses the patient’s acidbase status? A) Arterial blood gas (ABG) B) Pulse oximetry (Pulse ox) C) Lactic acid level D) Central venous pressure (CVP) E) Electrocardiogram (EKG) Answer: A. The ABG sample is passed through an analyzer machine, providing us with the arterial pH, pCO2, and pO2. This is the most informative study for the patient’s acid-base status. Pulse oximetry only measures oxygen saturation (SaO2). Decreased SaO2 will result in decreased tissue oxygenation and increased lactic acid levels. It is not as informative as ABG. Lactic acid levels increase when tissues are not supplied with adequate oxygen but do not give a good picture of global acid-base status. CVP is a measurement of body blood volume. It is decreased in hemorrhage, but it does not directly inform us about acid-base status. EKG findings are nonspecific and not very informative about acid-base status.
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SUGGESTED READINGS Adrogué HJ, Rashad MN, Gorin AB, et al. Assessing acid-base disorders. Kidney Int. 2009;76:1239–1247. Adrogue Horacio J, Madias NE. Management of life-threatening acid-base disorders: first of two parts. New Engl J Med. 1998;338:26–34. American Association for Respiratory Care. AARC clinical practice guideline: sampling for arterial blood gas analysis. Respir Care. 1992;37:913–917. Barthwal MS. Analysis of arterial blood gases: a comprehensive approach. J Assoc Phys India. 2004;52:573–577. Brackett NC. An approach to clinical disorders of acid-base balance. South Med J. 1974;67:1084–1101. Breen PH. Arterial blood gas and pH analysis: clinical approach and interpretation. Anesthesiol Clin North Am. 2001;19:885–902.
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Gehlbach BK, Schmidt GA. Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit – the role of buffers. Crit Care. 2004;8:259–265. Gluck SL. Acid-base. Lancet. 1998;352:474–479. Kellum JA. Clinical review: reunification of acid-base physiology. Crit Care. 2005;9:500–507. Koeppen B. The kidney and acid-base regulation. Adv Physiol Educ. 2009;33:275–281. Lahiri S, Forster RE II. CO2/H+ sensing: peripheral and central chemoreception. Int J Biochem Cell Biol. 2003;35:1413–1435. Shapiro BA, Harrison RA, Walton JR, Guidelines for sampling and quality control. In: Clinical Application of Blood Gases. 2nd ed. Chicago, IL: Year Book Medical Publishers, Inc; 1977: Chapter 14. Williams AJ. Assessing and interpreting arterial blood gases and acid-base balance. BMJ. 1998;317:1213–1216.
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CHAPTER
13
Central Nervous System Josh Finkle and Jeffrey Kirsch ■ INTRODUCTION The majority of anesthetic procedures involve the central nervous system (CNS), from inducing unconsciousness to performing regional anesthesia. In order to understand anesthesia, the anesthesia technician will need a basic understanding of the anatomy and physiology of the CNS. This chapter introduces the anatomy of the brain and spinal cord, which make up the CNS. The chapter also covers the physiology of the CNS beginning with the main cells of the CNS, neurons.
■ ANATOMY OF THE BRAIN The central and peripheral nervous systems together make up a complex network of cells and fibers that extends throughout the body. This network uses electrical and chemical signals to gather, interpret, and react to information from the external environment and from within the body. The CNS processes and integrates signals received by the peripheral nervous system and sends instructions to the rest of the body. Signals going into and out of the CNS are carried by peripheral nerves, which interact directly with the environment. The CNS can be divided into two distinct anatomic structures: the brain and the spinal cord. The brain is a complex organ with many functions, including the processing of sensory input, the generation of movement, and higher functions such as cognition, language, and emotions. The brain is functionally divided, with specialized regions that are primarily responsible for unique sets of functions. The structures that collectively make up the brain are the cerebral hemispheres, the central cerebral structures, the brainstem, and the cerebellum (Fig. 13.1). The cerebral hemispheres are the most prominent of the brain’s structures and consist primarily of the cerebral cortex, and some underlying
white matter, which are axons that serve to connect cells between brain regions. The cortical tissue of the cerebral hemispheres contains many folds, called gyri, and grooves, called sulci. The cerebral hemispheres can be divided into four major areas, or lobes: frontal, temporal, parietal, and occipital lobes (Fig. 13.2). Each lobe of the cortex contains specialized areas that are responsible for unique functions and responses, leading to a predictable distribution of the functional areas of the cortex. The occipital lobe is primarily associated with the processing of visual information and the formation of a coherent interpretation of the visual world. The temporal lobe is the primary site of auditory perception and contains a structure called the hippocampus, which is responsible for storage and retrieval of memories. The parietal lobe is a locus for integration of multiple senses and is responsible for the understanding of symbolic language and spatial relationships. The frontal lobe is responsible for executive functions, such as attention, conscious motor movement, and behavioral control. Knowledge of the link between structure and function allows the clinician to predict the location of pathology based on clinical presentation. It also allows the surgeon to warn patients preoperatively regarding expected postoperative neurologic deficits following brain tissue resection during tumor and seizure surgery. During any brain surgery, surgeons and patients are challenged with balancing the opportunity for cure (e.g., complete resection of a tumor with surrounding tissue) with the devastation that resection may cause to an individual’s postoperative cognitive and functional outcomes. Internal to the cerebral cortex, there are a number of structures that serve to connect and modulate the signals of the rest of the CNS. The basal ganglia, a set of nuclei below the cortex, are responsible for modulation of complex 109
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Section II • Anatomy, Physiology, and Pharmacology Cerebrum Diencephalon Thalamus Hypothalamus Pineal gland
Infundibulum Pituitary gland Cerebellum Brainstem Midbrain
Spinal cord
Pons Medulla oblongata
■ FIGURE 13.1 The brain (in situ; sagittal section). Showing the location of the four principal parts: cerebrum, diencephalon, brainstem, and cerebellum. (From Stedman’s Medical Dictionary. 27th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2000, with permission.)
Frontal motor control, some aspects of personality
Parietal sensation, some aspects of language
Occipital vision
Temporal speech, hearing The brain is divided into two hemispheres. The right half controls the left side of the body and the left half controls the right side of the body. Each hemisphere is divided into four lobes. Within the lobes there are even smaller areas, each associated with specific functions. ■ FIGURE 13.2 Segments of the brain and their role in the body labeled.
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motor signals sent from the frontal cortex. The thalamus is a large central structure within the cerebral hemispheres, and acts as a sensory integration point, with regions corresponding to inputs from various sensory modalities (vision, audition, touch, pain) on their way to the cortex. The hypothalamus is a region just below the thalamus with many important functions, the most notable of which is to connect the CNS to the endocrine system. The hypothalamus has direct input to the principal endocrine organ, called the pituitary gland, which sits just below the hypothalamus and controls chemically mediated signaling functions such as growth, metabolism, blood pressure, and sexual development. The cerebellum is in the posterior aspect of the skull, below the occipital lobe of the cortex. The cerebellum has connections to other CNS structures, including the cerebral cortex, the basal ganglia, and the spinal cord. The cerebellum’s major function is to integrate tactile and proprioceptive sensory inputs with motor signals for the
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production of smooth motion and the maintenance of balance and posture. The brainstem is the most caudal structure in the brain, and it connects the higher areas of the brain to the spinal cord. The sensory and motor pathways from the body (carried by the spinal cord) and the sensory pathways from the head (the trigeminal system) pass through the brainstem and make important functional connections. The brainstem is divided both structurally and functionally into three areas—the midbrain, pons, and medulla (from rostral to caudal). The medulla controls vital and unconscious functions, including breathing, heart rate, blood-vessel tone, and vomiting. Throughout the brainstem are nuclei (collections of cell bodies) for the cranial nerves, a set of nerves that control various functions within the head and neck, such as taste, audition, and sensation, as well as eye movements, vocalization, and facial expression.
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Within the cranial cavity there are structures that offer support to the tissues of the brain, namely, the meninges and the vasculature. The meninges are a set of three layers of protective tissue that surround the structures of the CNS (Fig. 13.3). The outermost of the meninges, the dura mater, is a thick protective layer that directly contacts the skull. Just below the dura mater is the arachnoid mater, which surrounds a fluidfilled cavity called the subarachnoid space. The subarachnoid space contains cerebrospinal fluid (CSF) that acts as a cushion for the brain against traumatic insults. The pia mater is a thin layer that runs along the surface of the brain, following the sulci and gyri of the cerebral cortex. The blood supply to the brain comes from the vertebral arteries and the internal carotid arteries, which meet on the ventral surface of the brain to form an arterial network, referred to as the circle of Willis. Branching off the circle of Willis are the arteries that supply the regions of the brain,
Dura mater Subdural space Arachnoid Choroid plexus
Subarachnoid space Pia mater
Arachnoid Subarachnoid space Pia mater Spinal cord Dura mater Subdural space
■ FIGURE 13.3 Meninges and cerebrospinal fluid flow.
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including the cerebral arteries, cerebellar arteries, and their branches. Blood returning from the brain enters a network of cavities within the dura mater, called venous sinuses, which collectively drain into the internal jugular vein.
■ CLINICAL IMPLICATIONS OF ANATOMY The rigid structure of the skull and meninges in combination with an increase in the intracranial volume of any component within the intracranial vault (e.g., brain, CSF, blood, or foreign bodies) will result in an increase in intracranial pressure and secondary brain injury. The brain component can increase because of abnormal growth (e.g., tumor) or swelling (e.g., from trauma or surgery). The blood component can increase because of ruptured blood vessels (i.e., ruptured aneurysm, hemorrhagic stroke, or trauma). Unfortunately, all of the inhaled (gas) anesthetics cause dilation of the cerebral blood vessels and an increase in intracranial pressure. Therefore, a typical neuroanesthetic will include an intravenous anesthetic (e.g., propofol, opiates) at concentrations that minimize the doses of inhaled anesthetic required to maintain a reasonable plane of anesthesia. The CSF component can increase from overproduction or poor reabsorption. Although each of these pathologies results in increased intracranial pressure, the definitive treatment is usually left to the discretion of the surgeon. Pressure within the brain can be measured via a catheter placed in the central CSF-containing spaces (e.g., lateral ventricles), or a “bolt” can be placed through the skull and a fluid connection with the CSF space is established through the dura and arachnoid tissues. In both cases, the device is attached to a transducer (as one would use for measurement of invasive blood pressure or central venous pressure) that is zeroed and balanced at the level of the external auditory canal. Alternatively, a fiber-optic Camino device can be placed by the surgeons into the brain parenchyma. Although all techniques provide an accurate assessment of intracranial pressure, only the catheter in the lateral ventricle can be used therapeutically to lower intracranial pressure by withdrawing CSF. Other means of decreasing intracranial pressure that are under the control of the anesthesiologist include hyperventilation (low pCO2 causes cerebral vasoconstriction and decreases blood
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volume in the brain) and intravenous administration of osmotic diuretics (e.g., mannitol and hypertonic saline), which reduce the amount of edema fluid in the brain. Because of the use of hyperventilation by anesthesiologists to lower intracranial pressure in patients having intracranial surgery, the anesthesia technician is likely to observe low arterial pCO2 values and high pH values on blood gases taken during the procedure. In addition, the administration of osmotic diuretics to neurosurgery patients will often result in an increase in the osmolarity measurement by the anesthesia technician.
■ ANATOMY OF THE SPINAL CORD The spinal cord begins just below the base of the brainstem, and continues down, through the vertebral column. The vertebral column is divided into four segments based on anatomic location (Fig 13.4). The cervical region of the vertebral column spans the length of the neck and has seven segments. The thoracic region spans the upper part of the back and is divided into 12 segments. The lumbar region spans the lower back and is divided into five segments. The sacral region of the vertebral column extends into the pelvis and is composed of five bones fused to form a single structure. A single coccygeal bone (referred to as the tailbone) is found at the end of the spinal column. Found within the vertebral column is the spinal cord itself. Although in the adult the spinal cord ends in the thoracic region of the vertebral column, the spinal cord levels are divided into segments based on the spinal column level for exit of their paired sensory and motor spinal nerves. Each of the four regions of the spinal cord controls motor and sensory functions for a specific part of the body. For example, the cervical spinal cord controls motion and sensation from the neck and upper extremities. The thoracic spinal cord controls motion and sensation from the trunk. The lumbar and sacral regions of the spinal cord control motion and sensation in the lower extremity and the pelvic/genital region. Within the spinal cord, there is gray matter and white matter. The gray matter is composed primarily of neuronal cell bodies, and the white matter is composed of long bundles of nerve cell tissue for signal conduction. The meningeal layers continue inferiorly and surround the spinal cord throughout its length. At the level of the spinal cord, the three layers of the meninges lie
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Spinal cord 1 2 3 Cervical cord
C2
4 5
Cervical
6 7 8 1 Thoracic cord
Vertebra
T1
2 3 4 5 6 7
Thoracic
8 9 10 11 12 Lumbar cord
Sacral cord
L1 1 2 Lumbar 3
4
5
Sacral S1
1 2 3 4 5
Spinal nerves ■ FIGURE 13.4 Segmental organization of the spinal cord. The spinal cord is divided into cervical, thoracic, lumbar, and sacral divisions (left). The right side shows the spinal cord within the vertebral column. Spinal nerves are named for the level of the spinal cord from which they exit and are numbered in order from rostral to caudal. (From Bear MF, Connors BW, Parasido MA. Neuroscience—Exploring the Brain. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001, with permission.)
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within the vertebral column and external to the spinal cord itself. As with the intracranial CNS, the meninges and CSF serve an important role to protect the spinal cord from trauma. The meninges and ligaments of the bones of the spinal canal are also used strategically by anesthesiologists for placement of spinal or epidural anesthesia. In the case of a spinal anesthetic, the needle is placed between the vertebral bones with the goal of advancing the needle (and medication) into the CSF (subarachnoid) space. When placing an epidural, the anesthesiologist places the needle (usually along with a catheter) in the epidural space, which is a potential space found as the needle passes past ligamentum flavum (the innermost ligament of intervertebral space), without penetrating the dura. The blood supply to the spinal cord comes from the vertebral arteries and a set of segmental branches off of the aorta, called medullary arteries. These arteries join at the surface of the spinal cord to form a network of arteries that invest the tissue of the spinal cord. Prominent in this network are the larger anterior and posterior spinal arteries, which run the length of the spinal cord, giving off smaller arterial branches at each level. Because of the anatomy of the spinal cord blood supply, patients are at great risk experiencing a critical reduction of blood flow and injury to the spinal cord during surgery that requires crossclamping of the thoracic aorta.
■ PHYSIOLOGY The CNS principally functions as a means to transduce and manipulate electrical information. This information can be used to quickly encode and interpret information from the external world, or allow for manipulation of the environment through motor functions or other complex activities such as language and cognition. The major functional cell type in the CNS is called the neuron. In the peripheral nervous system, neurons interact directly with the environment, acting as sensors for pain, temperature, and tactile information and directly innervating skeletal muscle as well as other muscles and glands that regulate automatic body functions (see Chapters 14 and 15). In the CNS, neurons interact with one another and with peripheral nerves to create and regulate the complex actions of the nervous system. The structure of a neuron reveals important functional properties (Fig. 13.5). A unique
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characteristic of neurons when compared with other cell types is the existence of a long cellular projection, called an axon. In the CNS, each cell’s axon terminates on other neuronal cells, forming an elaborate network of interactions among the cells of the CNS. Depending on the function of a neuron, its axon may be short (like some locally acting neurons in the brain) or as long as a meter (such as upper motor neurons, which can span the length of the spinal cord). An axon can also branch into hundreds of thousands of discreet terminals, making connections with other neurons in a local or diffuse pattern. Another important neuronal cell structure is the dendrite. Each CNS neuron has many dendrites that act as connecting points for the axons of other neurons. The most common neuronal interaction within the CNS is the axon of one neuron terminating on a dendrite of another neuron. The axon and dendrites of each neuron are projections off of a central structure, called the cell body (soma), that contains the nucleus and other important cell organelles and acts to integrate and process the incoming signals from the dendrites. Neurons function by propagating a signal in the form of an electrical impulse. The functional connection between two neurons is called a synapse. The most common type of synapse found in the CNS is the axon terminal of one cell (the presynaptic cell) contacting a dendrite of another cell (the postsynaptic cell). It is also possible for an axon terminal to synapse on a cell body or another axon. When a nerve signal reaches the end of the presynaptic axon, it causes release of chemicals, called neurotransmitters, from the axon terminal into the synaptic cleft, a small space between the presynaptic axon and the postsynaptic cell. These neurotransmitters interact with specialized receptors on the surface of the postsynaptic cell and ultimately affect the activity of the postsynaptic cell (Fig. 13.5). In addition to neurons, there are a number of cells in the CNS that function as supportive structures; these cells are collectively referred to as glial cells. Their functions include support of neuronal growth and signaling, scavenging neurotransmitters and other debris, and providing immunologic protection within the CNS. An especially notable glial cell type in the CNS is the oligodendrocyte. These cells produce a substance called myelin, which wraps neuronal axons and allows for greater speed and efficiency of nerve signal
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Impulses to cell body Nucleus Dendrites
Cell body Axon
Myelin sheath Impulses away from cell body
Direction of nerve impulse
Synapses
Postsynaptic neuron Synaptic cleft
Mitochondrion
Vesicles of transmitter substance Receptors on postsynaptic membrane ■ FIGURE 13.5 Structure of a motor neuron. A neuron or nerve cell is composed of a cell body having a nucleus and two types of processes—dendrites and axons. Impulses pass to the cell body through the dendrites (upper black arrows), and the axon carries impulses away from the cell body (lower black arrows). A neuron influences other neurons at junctional points or synapses. The detailed structure of an axodendritic synapse is illustrated (inset); neurotransmitter substances diffuse across the narrow space (synaptic cleft) between the two cells and become bound to receptors. (From Moore KL, Dalley AF II. Clinical Oriented Anatomy. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999, with permission.)
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conduction. Myelin is rich in lipids and gives white matter (primarily composed of axons) its color. Functional anatomy of the CNS can be divided into sensory systems, motor systems, and complex functions such as language, emotions, and memory. All of the body’s sensory systems feed into the CNS, where the signals are processed to form an internal representation of the environment and the body’s position relative to the environment. Somatosensory processes include mechanosensory (touch), pain, and proprioception (sensation of bodily orientation) and involve both the spinal cord and the brain. These pathways begin with mechanical and chemical sensors throughout the body as part of the peripheral nervous system (see Chapter 15) and ascend to the brain via the spinal cord. As the tracts ascend through the brainstem, the fibers carrying the signals for touch, pressure, and proprioception cross sides at the level of the medulla, and so above this level, somatosensory information within the CNS pertains to the sensation of the contralateral body. All the sensory fibers then synapse in the thalamus and from there travel to the primary sensory cortex in the parietal lobe, where the conscious feeling of sensation occurs. The control of voluntary motor function within the CNS begins in the primary motor
cortex in the frontal lobe, with motor planning and guidance coming from other areas of the frontal lobe including the premotor and prefrontal cortex. The axonal fibers from the primary motor cortex descend through the brainstem, crossing to the contralateral side at the level of the medulla and continue to descend in the lateral column of the spinal cord. These axons terminate within the ventral portion of the spinal cord at the appropriate vertebral level and synapse with lower motor neurons that exit the spinal cord within the spinal nerve to innervate skeletal muscle. Modulation of the motor pathway comes from various locations within the CNS, including the cerebellum, which is mainly involved in smoothing and coordinating movements, and the basal ganglia, which helps generate complex motor patterns. Reflexes are simple sensorimotor circuits that involve only the spinal cord and not the brain. In a reflex pathway, the sensory neuron synapses directly on a lower motor neuron in the spinal cord or on an interneuron that then inhibits a lower motor neuron (Fig. 13.6). For example, in the patellar tendon reflex, the tendon stretch sensory neuron directly activates the nerves that signal the leg to extend while acting to inhibit those that would flex the leg. To brain
1 Stretching stimulates sensory receptor (muscle spindle) Tapping the tendon stretches muscle
5 Effector, (quadriceps) contracts to relieve stretching
Inhibitory interneuron
2 Sensory neuron excited Spinal nerve 4 Motor neuron excited
Antagonistic muscles relax
3
Within integrating center (spinal cord)
Motor neurons to antagonistic muscles (hamstrings) is inhibited
■ FIGURE 13.6 Reciprocal innervation. (From Premkumar K. The Massage Connection: Anatomy and Physiology. Baltimore, MD: Lippincott Williams & Wilkins; 2004, with permission.)
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The CNS is also involved with the set of “special senses,” which includes vision, hearing, smell, and the vestibular sense. Each of these systems involves a specialized type of sensory receptor that encodes information from the environment (in the form of light, sound waves, ingested chemicals) into neural signals that are sent toward the brain. Aside from olfaction (smell), the pathways of all the special senses involve nuclei in both the brainstem and the thalamus before arriving at the cerebral cortex. The central olfactory pathway is the simplest of all the sensory pathways as it does not involve processing within the brainstem or thalamus. Specialized chemical sensors on the surface of the nasal cavity respond to interactions with specific chemical compounds in the inhaled air. These sensory neurons project to the olfactory bulb, a nucleus located within the cranial cavity directly above the nasal cavity. Neurons of the olfactory bulb project their axons directly to the primary olfactory cortex within the temporal lobe. The complex functions carried out by the CNS include memory, emotions, and language and mainly involve specialized areas of the cerebral cortex. Because of the complexities of these systems, all the pathways and interactions are not
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fully understood, but some important features of each system can be explored. Language is an important tool for communication among people, and it involves the production and comprehension of complex vocal and verbal patterns. Within the cerebral cortex, the areas involved with language fall within the temporal and frontal lobes, predominantly on the left side. Because of the importance of language in daily functioning, the left side of the cortex is considered the dominant hemisphere. The right hemisphere plays a role in language, but it is mainly involved with the emotional content rather than the semantic processing of language. There are two specific regions of the cortex that have been identified as major centers for language within the brain. The first, called Broca’s area, is in the left frontal lobe, anterior to the primary motor cortex, and it is involved with the efficient production of language and speech. Broca’s area is important for the motor planning involved in speech and for fluid expression of language. The second important area involved with language is Wernicke’s area, a region of the cortex in the left posterior temporal lobe. Wernicke’s area is important in the understanding of language and is associated with auditory cortex (Fig. 13.7). Damage to these areas of the cortex causes a specific language deficit, called aphasia,
Motor strip Sensory strip Frontal lobe Motor control of voluntary muscles Personality Concentration, organization Problem-solving
Parietal lobe Sensory areas of touch, pain, temperature Understanding speech, language Express thoughts Wernicke’s center Interpreting speech
Broca’s center Motor control of speech
Occipital lobe Visual recognition Focus the eye
Temporal lobe Hearing Memory of hearing and vision
Brain stem Controls heart rate and rate of breathing
Cerebellum Balance Coordinating muscle movement
■ FIGURE 13.7 Topical anatomy of the brain.
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which can present as difficulty in language production (if Broca’s area is affected) or language comprehension (if Wernicke’s area is affected). Within the brain, emotional responses are dictated by a set of structures collectively referred to as the limbic system. The limbic system consists of deep areas of the cortex, like the cingulate gyrus and the hippocampus, as well as structures like the hypothalamus that affect the autonomic nervous system (see Chapter 14). When confronted with an emotionally charged stimulus, the limbic system activates and sends signals to various brain centers, including the prefrontal cortex, which is involved with decision making, the pituitary, which controls the endocrine system, and the brain’s pleasure centers. Emotion and memory within the brain are intimately connected with many structures contributing to both processes. An important brain structure involved with memory is the hippocampus, an area of the cortex found within the temporal lobe. The hippocampus is activated during the storage and retrieval of memory, and it is especially associated with memory for locations and events. The cerebellum is involved with procedural memory, also called muscle memory, which is important in learning motor-oriented skills like riding a bicycle or playing a musical instrument. Strong emotional states encourage memory encoding, and so emotionally charged events are remembered more accurately and with more detail.
■ PHARMACOLOGY There are many pharmacologic agents that have effects on the CNS. Psychomotor stimulants are drugs that increase the overall activity within the CNS. They do so by increasing neuronal firing rate or promoting neurotransmitter release. Examples include caffeine and d-amphetamine, a drug commonly used to treat attention deficit/ hyperactivity disorder (ADHD). Anticonvulsants are drugs that decrease the overall activity within the CNS. They are used to treat seizure disorders, which involve abnormally increased neuronal firing in the CNS. Examples include sedatives such as barbiturates and benzodiazepines, as well as many other drugs that have been designed to treat specific types of seizures. Usually, these drugs decrease neuronal firing frequency and enhance the effects of inhibitory neurotransmitters. The CNS has an inbuilt array of molecules and receptors involved with analgesia (pain
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reduction). Specifically, three families of peptides, called endorphins, enkephalins, and dynorphins, are collectively referred to as the endogenous opioids and act on opioid receptors within the CNS with analgesic effects. Opioid agonists are a class of drugs that themselves bind to and activate the brain’s opioid receptors and are used for analgesia. Morphine is the prototypical drug in this class and is a strong opioid agonist. General anesthetics are a class of drugs used during surgeries for sedation, analgesia, amnesia, and muscle relaxation. These drugs are administered either through injection (usually intravenous) or inhalation. The inhaled anesthetics include isoflurane, sevoflurane, and desflurane. The inhaled anesthetics presumably do not act through a receptor-mediated pathway but by their direct interactions with cell membranes within the CNS. Propofol is a fast-acting injected anesthetic that is quickly cleared from the circulation, and so continuous administration is needed to maintain anesthesia. In adult patients requiring surgery for intracranial pathology, general anesthesia is often induced with a quick-onset intravenous anesthetic (e.g., propofol) and a neuromuscular blocking agent (e.g., rocuronium or succinylcholine) to allow the anesthesiologist an opportunity to quickly control ventilation, avoiding the dangers of hypoventilation (which can result in an increase in intracranial pressure). Intravenous opiates are administered in order to blunt the hemodynamic response to noxious stimuli (e.g., intubation, placement of the patient’s head in pins, and surgical incision). Hemodynamic stability is important, as hypertension may result in brain swelling in areas of brain damage (e.g., in the region of a tumor or trauma) and hypotension may result in poor perfusion to important areas of the brain. During brain surgery, anesthesia is often maintained using a combination of intravenous agents (e.g., propofol infusion and/or an opiate) and inhaled agents (e.g., desflurane) in order to minimize the detrimental effects of the inhaled anesthetic agents administered in high concentrations on brain blood volume. As discussed above, an increase in brain blood volume may result in an increase in intracranial pressure and secondary brain injury. Patients also often receive neuromuscular blocking drugs so that they will not move while the surgeon is operating within the brain parenchyma.
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■ INHERENT TOXICITY OF ANESTHETIC AGENTS IN THE CNS Although our previous understanding of the anesthetic agents was to “protect” the brain from injury by their ability to put the brain in a quiescent state, more recent investigations have demonstrated that all of the inhaled anesthetic gases and several of the intravenous anesthetic agents cause direct neurotoxicity. The mechanism of this toxicity appears to be related to their effect on the release of specific brain chemicals (neurotransmitters) within brain tissues. Current research suggests that patients at the extremes of life (i.e., neonates and the elderly) are most susceptible to the direct damaging effects of anesthetic agents. Unfortunately, there is no current consensus on anesthetic agents that are free of neurotoxic effects on the brain. Ongoing research is trying to establish which, if any, of the anesthetic agents is truly safe and if there are clinically applicable management strategies that can be applied for care of patients in the most vulnerable periods for anesthetic-induced brain injury. The strategies may include administration of additional drugs to protect the brain from anesthetic-induced brain injury (e.g., lithium has been suggested) or development of new anesthetic agents (e.g., xenon has been suggested). In the meantime, the most reasonable approach is to minimize exposure of patients to anesthetic agents during their most vulnerable age periods (i.e., neonates and the very old).
■ ANATOMY, PHYSIOLOGY, AND PHARMACOLOGY OF NAUSEA AND VOMITING Emesis (vomiting) is a process in which the normal direction of digestive propulsion is reversed and the contents of the stomach are brought upward through the esophagus and out of the mouth. The process is often forceful and unpleasant and can be induced by a number of factors including gastrointestinal irritation, motion sickness, and drug reactions. Emesis is usually preceded by a process called retching that involves a rhythmic contraction of the diaphragm and abdominal muscles. These muscles then undergo prolonged intense contractions, as the stomach contents are expelled upward. The lower and upper esophageal sphincters are relaxed as the contents are forcefully ejected from the mouth. Often a feeling of relief follows this process.
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Within the medulla, there is a nucleus called the chemoreceptor trigger zone (CTZ) that, when activated, triggers the emesis response. The CTZ has receptors for a number of neurotransmitters, including dopamine, acetylcholine, histamine, serotonin, and opioids. Drugs that modulate the effects of these chemicals and their receptors may alter the emetic response. Drugs with proemetic effects are often those that increase the activity of neurotransmitters to which the CTZ is sensitive. Opioid drugs can also activate the CTZ through its opioid receptors, but the proemetic effect of these drugs is not apparent in all patients. Other ingested substances, such as syrup of ipecac, trigger emesis by irritating the gastric mucosa. There are a number of drug classes that antagonize emesis, mainly by inhibiting the neurotransmitters and receptors within the CTZ. Dopamine receptor blockers are used as antipsychotics (see CNS pharmacology section) and have antiemetic effects by blocking dopamine 2 (D2) receptors within the CTZ. Scopolamine is a drug that is used to combat motion sickness through its anticholinergic effects at the CTZ. Additionally, selective serotonin antagonists (e.g., ondansetron) are often given to inhibit the nausea that occurs as a side effect of anesthesia and chemotherapeutic treatments.
■ SUMMARY In summary, the CNS is a complicated organ system that requires an in-depth understanding by anesthesiology staff in order to establish the desired operating environment for the surgeon and outcomes for our patients. Effective communication between members of the anesthesiology team will facilitate creating an anesthesia plan that minimizes the opportunity of CNS damage by our anesthetic agents by maximizing dosedependent anesthetic beneficial effects, while minimizing the inherent toxicity of each agent.
REVIEW QUESTIONS 1. Which of the following areas of the cortex is most likely to be involved with language production? A) Left frontal lobe B) Left temporal lobe C) Right frontal lobe D) Right temporal lobe E) None of the above
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Answer: A. Broca’s area is in the left frontal lobe, anterior to the primary motor cortex, and is involved with the efficient production of language and speech. Wernicke’s area, a region of cortex in the posterior temporal lobe, is important in the understanding of language and is associated with auditory cortex. The right hemisphere plays a role in language, but it is mainly involved with the emotional content rather than the semantic processing of language.
2. Blocking which of the following neurotransmitter receptors in the CTZ will have an antiemetic effect? A) Serotonin B) Acetycholine C) Dopamine D) A and C only E) A, B, and C Answer: E. There are a number of drug classes that antagonize emesis, mainly by inhibiting the neurotransmitters and receptors within the CTZ. Dopamine receptor blockers are used as antipsychotics and have antiemetic effects by blocking D2 receptors within the CTZ. Scopolamine is a drug that is used to combat motion sickness through its anticholinergic effects at the CTZ. Additionally, selective serotonin antagonists (e.g., ondansetron) are often given to inhibit the nausea that occurs as a side effect of anesthesia and chemotherapeutic treatments.
3. Which of the following correctly describes the path of the electrochemical signal through a single neuron as it is received, then processed, then relayed down the length of the neuron? A) cell body → dendrite → axon B) dendrite → cell body → axon C) cell body → axon → dendrite D) axon → cell body → dendrite Answer: B. Neurons receive most of their input signals through receptors on their dendrites. These signals cause changes in the cell’s electrical gradient, first within the dendrites themselves and then in the cell body. If the cell is depolarized past threshold, it will then send an action potential down the length of its axon.
4. Which of the following answer choices correctly matches the region of the spinal column with the number of vertebrae in that region? A) Cervical—12 B) Coccygeal—5 C) Lumbar—7 D) Thoracic—12 E) Sacral—7 Answer: D. The cervical region of the vertebral column spans the length of the neck and has seven segments. The thoracic region spans the upper part of the back and is divided into 12 segments. The lumbar region spans the lower back and is divided into five segments. The sacral region of the vertebral column extends into the pelvis and is composed of five bones fused to
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form a single structure. A single coccygeal bone (referred to as the tailbone) is found at the end of the spinal column. Found within the vertebral column is the spinal cord itself.
5. An endogenous peptide is discovered to act on receptors within the CNS and cause pain relief as well as euphoria and sedation. Which of the following CNS drugs acts on the same receptor as this molecule? A) Isoflurane B) Succinylcholine C) Lithium D) Morphine E) Scopolamine Answer: D. The endogenous opioids are peptides that act on opioid receptors within the CNS with analgesic effects. Opioid agonists, such as morphine, bind to and activate the brain’s opioid receptors and are used for analgesia. The inhaled anesthetics (such as isoflurane) directly interact with cell membranes within the CNS to cause analgesia and sedation. Succinylcholine is a neuromuscular blocking agent that interferes with cholinergic signaling between motor nerve terminals and muscles. Lithium can be used as a mood stabilizer to treat bipolar and other mood disorders. Scopolamine is a drug that is used to combat motion sickness through its anticholinergic effects at the CTZ.
SUGGESTED READINGS Clarke RS. Nausea and vomiting. Br J Anaesth. 1984;56(1): 19–27. Hanes DE. Neuroanatomy: An Atlas of Structures, Sections, and Systems. Philadelphia, PA: Lippincott Williams & Wilkins; 2010. Hickok G. The functional neuroanatomy of language. Phys Life Rev. 2009;6(3):121–143. doi: 10.1016/j.plrev. 2009.06.001. Huffman JC, Alpert JE. An approach to the psychopharmacologic care of patients: antidepressants, antipsychotics, anxiolytics, mood stabilizers, and natural remedies. Med Clin North Am. 2010;94(6):1141–1160, x. doi: S00257125(10)00143-4 [pii]. 10.1016/j.mcna.2010.08.009 Ishizawa Y. Mechanisms of anesthetic actions and the brain. J Anesth. 2007;21(2):187–199. doi: 10.1007/s00540-0060482-x. Llinas RR. The intrinsic electrophysiological properties of mammalian neurons: insights into central nervous system function. Science. 1988; 242(4886):1654–1664. Mansour A, Khachaturian H, Lewis ME, et al. Anatomy of CNS opioid receptors. Trends Neurosci. 1988;11(7): 308–314. Phillips ML, Drevets WC, Rauch SL, et al. Neurobiology of emotion perception, I: the neural basis of normal emotion perception. Biol Psychiatry. 2003;54(5):504–514. doi: S0006322303001689 [pii]. Purves D. Neuroscience. 4th ed. Sunderland, MA: Sinauer Associates, Inc.; 2008.
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CHAPTER
14
Autonomic Nervous System Lori Nading and Ahmed Alshaarawi
T
he autonomic nervous system (ANS) is a subdivision of the peripheral nervous system, which acts autonomously, or involuntarily, to control the visceral (internal) functions of the body. In other words, its effects on the body happen automatically without conscious actions. The ANS is separated into two divisions: the sympathetic system and the parasympathetic system. The sympathetic nervous system works to prepare the body for stressful situations. Thus, the sympathetic nervous system is also referred to as the “fight-or-flight” system. The parasympathetic nervous system counteracts the sympathetic nervous system and works to return the body to normal after a stressful situation, helping to maintain homeostasis. It is sometimes referred to as the “rest-and-restore” system. The ANS differs from the somatic nervous system in several ways. A brief review of the somatic system reveals a one-motor neuron system with a synaptic cleft. Acetylcholine is the primary neurotransmitter that allows for propagation of an impulse across the synaptic cleft. The effector site for the somatic system is skeletal muscle. The ANS is a two-motor neuron system comprised of a preganglionic neuron and a postganglionic neuron. Located between the two neurons is a ganglion, and it is within this ganglion that the synapse occurs. The postganglionic neurotransmitters (at the effector site) used in the ANS consist of acetylcholine and norepinephrine. The effector sites of the ANS are smooth muscle, cardiac muscle, and secretory glands. Ganglia are a collection of neuronal cell bodies outside the central nervous system (CNS). Sympathetic ganglia are also called paravertebral ganglia. The sympathetic paravertebral ganglia branch off the spinal nerves anterior to the ventral roots. The paravertebral ganglia are connected vertically, forming a chain lateral to the
spinal cord. This chain is referred to as the sympathetic chain or trunk. In the sympathetic nervous system, the firstorder neurons of the ANS arise from the CNS. The preganglionic fibers deliver impulses to second-order neurons or the paravertebral ganglia. These ganglia contain the cell bodies of the postganglionic fibers responsible for delivering the impulse to the effector organs. The preganglionic fibers of the ANS are myelinated, and the postganglionic fibers of the ANS are nonmyelinated. Postganglionic fibers of the sympathetic division are long and are spread throughout the body. They produce a more generalized mass response. The postganglionic fibers of the parasympathetic division are short with their terminal ganglia near the effected organ. Their effect is more localized.
■ ANATOMY OF THE AUTONOMIC NERVOUS SYSTEM The sympathetic nervous system preganglionic fibers originate in the thoracic (T1-T12) segments and the first three lumbar (L1-L3) segments of the spinal cord (Figure 14.1). For this reason, it is sometimes referred to as the thoracolumbar division. The myelinated effector nerves leave the spinal cord and enter the ganglia. After reaching the ganglia, the impulse may travel in one of three ways: (1) directly across the ganglion to synapse with cell bodies of the postganglionic fibers, (2) cephalad or caudad to synapse with a higher or lower postganglionic neuron, or (3) through the sympathetic chain without synapsing. Some preganglionic fibers exit the sympathetic chain and synapse with outlying ganglia such as the celiac ganglia or the superior and inferior mesenteric ganglia. Synapses with these outlying ganglia, sometimes also referred to as collateral ganglia, innervate the visceral organs below the diaphragm. Innervation of the adrenal 121
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medulla is unique in that the secretory cells are considered modified postganglionic neurons. Therefore, preganglionic fibers do not synapse prior to reaching the adrenal gland. Because the preganglionic fibers are myelinated, the signal speed is quick, causing a rapid release of norepinephrine and epinephrine from cells within the adrenal medulla. The parasympathetic nervous system cell bodies stem from cranial nerves III, VII, IX, and X and the sacral segment of the spinal cord Figure 14.1. It is sometimes referred to as the craniosacral
division. The preganglionic fibers of the parasympathetic system differ from those of the sympathetic system in that they travel uninterrupted to their effector organ before synapsing with a short postganglionic fiber. Parasympathetic stimulation arising from the cranial nerves innervate viscera of the head, thorax, and abdomen. A large percentage of parasympathetic innervation to the thorax and abdomen stems from the vagus (X) nerve. This includes parasympathetic stimulation to the heart, lungs, stomach, small intestine, liver, gallbladder, and pancreas.
Ciliary ganglion
Lacrimal gland
Midbrain Pterygopalatine ganglion
III
Submandibular gland
Submandibular ganglion
Pons
Sublingual gland
VII Parotid gland
IX Otic ganglion
Spinal nerves Medulla X To neck
C1
Vagus nerve
C2
Superior cervical ganglion
C3 C4
Pulmonary nerves
C5
To upper limb
C6
Middle cervical ganglion
C7
Bronchus
Inferior cervical ganglion
C8
T1
Larynx Trachea
Heart
Lung Cervical cardiac nn.: Superior Middle Inferior
T2
T3
Thoracic Celiac cardiac nerves ganglia
T4
T5
Liver
Greater splanchnic nerve
T6
Gallbladder Bile duct
Spleen
To body wall
Red lines - Sympathetic
Pancreas
T8
Lesser and least splanchnic nerve
T9
T10
Aorticorenal ganglia
Solid lines - Preganglionic motor neuron
Adrenal gland cortex
Esophagus Stomach
Kidney
Superior mesenteric ganglion
T12
L1
Bladder
L2
IX - Glossopharyngeal nerve X - Vagus nerve
L4 L5
To perineum
C Colon: Ascending-A Transverse-B Descending-C
Prostate
A
Rectum
Urethra
S1 S2 S3
B
Lumbar splanchnic Inferior nerves mesenteric ganglion
L3
Dashed lines - Postganglionic motor neuron III - Oculomotor nerve VII - Facial nerve
T11
To lower limb
KEY Blue lines - Parasympathetic
T7
Sympathetic ganglion
Pelvic splanchnic nerve
S4 S5
Uterus Testis Spinal cord
■ FIGURE 14.1 Spinal cord with medulla pons and midbrain, connecting parasympathetic and sympathetic nerves to the ganglion to the affected organs, glands.
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The eye receives parasympathetic stimulation via the occulomotor (III) nerve, and the lacrimal and salivary glands are stimulated through fibers from the facial (VII) nerve. Additionally, salivary glands also receive parasympathetic stimulation through the glossopharyngeal (IX) nerve. Parasympathetic nervous system fibers arising from the sacral portion of the spinal cord innervate the large intestine, rectum, and bladder.
■ PHYSIOLOGY OF THE AUTONOMIC NERVOUS SYSTEM The primary neurotransmitters released in the ANS are acetylcholine and norepinephrine. The preganglionic fibers of the sympathetic division and the preganglionic and postganglionic fibers of the parasympathetic division all release acetylcholine. Most of the postganglionic fibers of the sympathetic division release norepinephrine. There are a few exceptions such as the postganglionic fibers of the sympathetic nervous system that stimulate the sweat glands. These fibers release acetylcholine. Acetylcholine exerts its effect on cholinergic receptors found in the ganglia or in the effector organs. There are two types of cholinergic receptors, nicotinic and muscarinic. Nicotinic receptors are almost always excitatory. Acetylcholine released from preganglionic fibers act on nicotinic receptors found in the ganglia on the postganglionic fibers in both the sympathetic and parasympathetic nervous systems. Acetylcholine that is released from postganglionic fibers in the parasympathetic nervous system exerts its systemic effects by acting on muscarinic receptors. Muscarinic receptors can exhibit excitatory or inhibitory properties. Muscarinic activation in the heart causes decreased heart rate and contractility. Muscarinic activation also causes bronchoconstriction (e.g., wheezing), increased secretion by salivary glands, and intestinal and bladder contraction with release of their sphincter tone (often resulting in urination and defecation). Within the sympathetic nervous system, norepinephrine released from postganglionic nerves acts on adrenergic receptors. The two major classes of adrenergic receptors are alpha (α) receptors and beta (β) receptors. These receptors are further subclassified as α1 and α2 and β1 and β2. In general, stimulation of α1 receptors that exist outside of the central nervous system
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(CNS) results in constriction of blood vessels (hypertension) and relaxation of bladder and bowel, while at the same time causing constriction of the sphincters of the bowel and bladder. Stimulation of α2 receptors results in decreased release of norepinephrine from nerve terminals. Stimulation of β1 receptors causes increased heart rate and increased cardiac contractility, whereas stimulation of β2 receptors causes dilation of blood vessels (hypotension), dilation of bronchioles (i.e., good treatment for bronchospasm/wheezing), and increased blood glucose (from glycogenolysis and gluconeogenesis).
■ EFFECTS OF AUTONOMIC NERVOUS SYSTEM STIMULATION Unlike innervation of skeletal muscle, which is all excitatory, visceral organs receive both excitatory and inhibitory innervation. The two divisions of the ANS are responsible for this antagonistic innervation. As noted previously, the sympathetic system is usually excitatory and the parasympathetic system inhibitory. Stimulation of the sympathetic division of the ANS produces a physiologic response characterized by increased heart rate, increased force of contraction of the heart, increased blood pressure through constriction of blood vessels (vasoconstriction), increased blood sugar through release of glucose from the liver, inhibition of digestion, dilation of respiratory passageways, increased blood flow to skeletal muscle, and dilation of pupils (Table 14.1). The individual receptors involved in this effect of the sympathetic nervous system are outlined above. These functions are the classic “fight-or-flight” response. Although the stimulation of these organ systems can be helpful to escape a bear attack, they can also be detrimental. For example, surgical stimulation produces a pronounced sympathetic response. The increases in heart rate could increase myocardial oxygen demand, and the patient could suffer a heart attack if there is limitation in oxygen supply (e.g., if the coronary arteries are partially occluded). Activation of the parasympathetic nervous system generally counterbalances the sympathetic system. When not being chased by a bear, it is time for the body to take care of other physiologic needs like eating and storing energy. Stimulation of the parasympathetic system decreases heart rate and increases blood flow to the digestive track, increasing peristalsis. The parasympathetic
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TABLE 14.1 CHARACTERISTICS OF THE AUTONOMIC NERVOUS SYSTEM STRUCTURE/SYSTEM
SYMPATHETIC EFFECTS
PARASYMPATHETIC EFFECTS
Cardiovascular system
Increased heart rate and contractility Vasodilation and vasoconstriction of blood vessels
Decreased heart rate and contractility
Respiratory system
Increased bronchiole dilation and increased respiratory rate
Decreased dilation and respiratory rate
Digestive system
Decreased activity Increased glycogen breakdown Glucose synthesis and release
Increased activity Glycogen synthesis
Skeletal muscle
Increased force of contraction Glycogen breakdown
Not innervated
Eye
Dilation of pupil Focusing for distance
Pupil constriction Focusing for close-up Secretion of tear glands
Urinary system
Decreased urine production Relaxation of bladder and constriction of sphincter
Increased urine production Increased bladder tone and relaxation of sphincter
Reproductive system
Increased glandular secretions
Erection of penis or clitoris
nervous system is also responsible for relaxation of sphincters, allowing for urination and defecation (Table 14.1).
■ ANESTHETICS AND THE AUTONOMIC NERVOUS SYSTEM Most of the medications that are administered during anesthesia affect the ANS. This is especially true during general and neuraxial anesthesia (spinal and epidural anesthesia). Anesthetic interventions can directly reduce autonomic signals from the CNS (including the spinal cord), act at the ganglia, or act on the end-organ receptors for the neurotransmitters of the ANS. For example, the induction of general anesthesia often results in a generalized reduction in sympathetic outflow from the CNS. This results in hemodynamic changes such as a decrease in blood pressure. In this section of the chapter, we describe effects on the ANS of the different classes of medications that are utilized during general or neuraxial anesthesia.
■ GENERAL ANESTHESIA Benzodiazepines These medications (e.g., midazolam, diazepam) are often utilized in the preoperative area and during sedation cases. At low doses, they produce minimal reductions in sympathetic nervous system output from the CNS. When they are combined with narcotic medications, the reduction
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in sympathetic outflow can be more pronounced and can result in a significant decrease in blood pressure. The calming effects of the benzodiazepines—termed anxiolysis—may cause the heart rate to decrease and the blood pressure to drop as a result of decreased catecholamine production.
Opiates Fentanyl, hydromorphone, and morphine are opiates and are some of the commonly administered perioperative medications. Most commonly, opiate analgesics will produce a reduction in the sympathetic nervous system activity. And as noted above, when opiates are administered together with benzodiazepines, they cause a more pronounced reduction in the sympathetic outflow and corresponding decrease in blood pressure.
■ HYPNOTICS/BARBITURATES/ SEDATIVES Propofol, methohexital, and etomidate are classified as hypnotics and sedatives. They are potent depressants of the CNS and are used in anesthesia in low doses to produce sedation and in higher doses to produce unconsciousness. With the exception of etomidate, hypnotics usually produce a profound reduction in central sympathetic outflow, which can result in significant decreases in blood pressure, even in healthy
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patients. The reduction in sympathetic outflow reduces cardiac output and causes peripheral vasodilation. It is important to utilize these drugs judiciously, particularly in patients who may be more dependent on their sympathetic system to maintain blood pressure (e.g., a trauma patient) or in patients who may not be able to tolerate a significant decrease in blood pressure. Etomidate is the only hypnotic/sedative that does not result in significant attenuation of sympathetic outflow, and as a result, it is often chosen to induce anesthesia in hemodynamically precarious patients. Ketamine is a hypnotic anesthetic that is associated with sympathetic system stimulation, while at the same time causing direct myocardial depression. Thus, when given to normal patients, ketamine administration can be associated with hypertension and tachycardia. However, when administered to patients who have been in the intensive care unit for an extended period of time, ketamine causes direct myocardial depression and hypotension because these patients have often depleted their catecholamine stores.
■ INHALATION AGENTS Of all the currently utilized volatile inhalation agents, desflurane is the only agent that will produce an increase in the sympathetic outflow, causing tachycardia. However, this increase occurs only when there is a sudden elevated level of desflurane. Otherwise, all volatile inhalation agents will produce varying degrees of cardiovascular depression due to direct dilation of systemic blood vessels and reduced sympathetic nervous system activity. The result is often a drop in blood pressure that is antagonized with intravenous administration of a vasopressor drug (e.g., ephedrine or phenylephrine) or by release of endogenous catecholamines from painful stimuli such as surgical incision. Nitrous oxide is a nonvolatile inhalation anesthetic agent and is commonly associated with centrally propagated increase in sympathetic outflow, particularly when it is administered without other anesthetic agents. During noxious stimulation (e.g., tracheal intubation) patients who have nitrous oxide as part of their anesthetic have higher concentrations of blood catecholamines (particularly norepinephrine) due to direct effects of this drug on the sympathetic nervous system, but attenuated cardiovascular responses due to the anesthetic effect on the cardiovascular system.
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■ NEUROMUSCULAR JUNCTION BLOCKING AGENTS (MUSCLE RELAXANTS) In general, muscle relaxants do not exhibit significant effects on the ANS. That is especially true with rocuronium and vecuronium, two of the more commonly used muscle relaxants during anesthesia and surgery. Pancuronium is a long-acting muscle relaxant. Its administration is associated with tachycardia because of its effect to inhibit postganglionic muscarinic receptors on the heart. Succinylcholine, a depolarizing muscle relaxant, can produce dysrhythmias manifested as bradycardia, junctional rhythms, or ventricular dysrhythmias. As a depolarizing neuromuscular blocking agent, succinylcholine causes stimulation of both types of cholinergic receptors. Therefore, succinylcholine will activate both nicotinic ganglionic receptors and postsynaptic muscarinic receptors. The resulting stimulation of both sympathetic and parasympathetic nerves and muscarinic receptors in the sinus node of the heart the cardiovascular effects are unpredictable, but often result in bradycardia and cardiac arrhythmias.
■ MUSCLE-RELAXANT REVERSALS Neostigmine is one of the most commonly used medications in anesthesia to reverse the effects of the nondepolizer muscle relaxants (such as rocuronium, vecuronium, and pancuronium). This medication, which belongs to a class of drugs called anticholinestrases, has significant effects on the ANS, producing some of the most undesirable symptoms including salivation, bronchoconstriction, defecation, and bradycardia. These effects are counteracted by the concomitant administration of anticholinergic medications such as atropine and glycopyrrolate. The anticholinergics cause tachycardia and drying of secretions in order to oppose the effects of the anticholinesterases.
■ REGIONAL ANESTHESIA Epidural and spinal blocks involve injection of local anesthetics in close proximity to the CNS (spinal cord). These blocks are commonly used to inhibit sensory and motor transmission to various parts of the body. However, another important property of these procedures is the interruption of sympathetic (in the thoracic and lumbar region) and parasympathetic (in the
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TABLE 14.2 COMMON ANESTHESIA MEDICATIONS AND EFFECTS ON ANS ANESTHETIC-MEDICATIONS CLASS
EFFECTS ON THE AUTONOMIC NERVOUS SYSTEM
Benzodiazepines
Minimal reductions in sympathetic nervous system output from the central nervous system
Opiates
Reduction in the sympathetic nervous system activity
Hypnotics/barbiturates/sedatives
Profound reduction in central sympathetic outflow except for etomidate
Inhalation agents
Reduction in sympathetic nervous system outflow except desflurane (in sudden high concentrations) and nitrous oxide, both of which cause an increase in sympathetic nervous system outflow
Muscle relaxants
Negligible effects
Muscle relaxants reversals
Significant effects on the autonomic nervous system, causing profound dysrhythmias, gastrointestinal upset, and airway constriction
Epidural and spinal anesthesia
Chemical sympathectomy
sacral region) signals as well, as all transmission to or from the spinal cord can be blocked. When the level of anesthesia for a spinal or epidural anesthetic is allowed to ascend to the high thoracic region, the patient may experience a “chemical sympathectomy” because the spinal/ epidural anesthetic will inhibit all of the sympathetic outflow, since it originates in the thoracic and lumbar regions of the spinal cord. In this situation, the only part of the ANS that is functional is the parasympathetic system (cranial division), which in patients with a high spinal/epidural lacks the balance of the sympathetic nervous systems. Thus, during noxious stimulation above the level of spinal/epidural anesthesia (e.g., emergency tracheal intubation), the patient is more likely to exhibit bradycardia and hypotension from unopposed parasympathetic activity. On the contrary, paravertebral blocks may not inhibit sympathetic activity, as the sympathetic chain is anterior to the target for this block and there is much overlap of sympathetic innervation because of the sympathetic ganglia chain. Thus, even if the local anesthetic administered at a specific paravertebral level defuses anteriorly and anesthetizes the sympathetic ganglion at that specific level, the observed physiologic effect of that block will be minimal because sympathetic fibers will have likely reached the target via sympathetic ganglia more distant along the sympathetic chain. However, anesthetizing sympathetic ganglia outside of the sympathetic chain will have clear effects on target organs.
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For example, celiac ganglia, which provide sympathetic innervations to intraabdominal organs, are anesthetized to alleviate pain for patients who have cancer in these organs. It is important to recognize that, anatomically, celiac ganglia are also mixed with sensory nerves that originate in these organs. Table 14.2 in this chapter summarizes the commonly used medications in anesthesia and their effects on the ANS. In summary, the ANS is divided into two subdivisions. The sympathetic division arises from preganglionic fibers originating from the thoracic and lumbar segments of the spinal cord. The sympathetic division is activated during times of crises (“fight or flight”) and works to produce increased alertness, increased cardiovascular and respiratory function, and increased energy. The parasympathetic division arises from the preganglionic fibers originating in the cranial nerves of the brainstem and sacral segments of the spinal cord. Parasympathetic stimulation produces depression of cardiovascular function and promotes digestive function (“rest and restore”). These two divisions are antagonistic and work to counterbalance one another to regulate cardiovascular, respiratory, digestive, excretory, and reproductive functions. Most of the medications that are administered during anesthesia will affect the ANS. A general understanding of the ANS and the effects of medications will help the anesthesia technician participate in the anesthetic management of patients.
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Chapter 14 • Autonomic Nervous System
REVIEW QUESTIONS 1. The primary neurotransmitter released by the preganglionic fibers of the sympathetic nervous system and the preganglionic and postganglionic fibers of the parasympathetic nervous system is A) Epinephrine B) Acetylcholine C) Norepinephrine D) Dopamine E) None of the above Answer: B. Acetylcholine is the primary neurotransmitter for the preganglionic fibers of the sympathetic nervous system and the preganglionic and postganglionic fibers of the parasympathetic nervous system. Norepinephrine is released by most of the postganglionic fibers of the sympathetic nervous system. Epinephrine is released from the adrenal medulla after direct stimulation from preganglionic fibers.
2. Acetylcholine exerts its effect on which of the following receptors? A) Cholinergic B) Muscarinic C) Nicotinic D) Adrenergic E) A, B, and C Answer: E. Acetylcholine exerts its effect on cholinergic receptors of which there are two types: nicotinic and muscarinic. Nicotinic receptors are almost always excitatory. Muscarinic receptors exhibit both excitatory and inhibitory effects.
3. Which of the following effects is elicited by stimulation of the α1 receptors? A) Hypertension B) Hypotension C) Increased heart rate D) Dilation of bronchioles E) None of the above Answer: A. Hypertension and relaxation of bladder and bowel are effects caused by stimulation of the α1 receptor. Hypotension and dilation of the bronchioles is caused by stimulation of the β2 receptors. Increased heart rate is an effect of stimulating the β1 receptors.
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4. A patient with extremely poor cardiac function presents for surgery and requires a general anesthetic. Which of the following medications do you anticipate will likely be used during induction? A) Aspirin B) Etomidate C) Acetaminophen D) None of the above E) All of the above Answer: B. Etomidate is the only hypnotic/sedative that does not result in significant attenuation of sympathetic outflow, and as a result, it is often chosen to induce anesthesia in such patients. The other medications are not usually considered as anesthetic induction agents.
5. Which of the following inhalation anesthesia agents is considered to be the only inhalation agent that will produce an increase in the sympathetic outflow, causing tachycardia, when it is suddenly increased to high levels? A) Isoflurane B) Sevoflurane C) Desflurane D) Halothane E) None of the above Answer: C. Desflurane is the only agent that will produce an increase in the sympathetic outflow, causing tachycardia. Thus, it is not usually used as an induction agent.
SUGGESTED READINGS Boron WF, Boulpaep EL. Medical Physiology. Philadelphia, PA: Elsevier Science; 2003. Huether SE, McCance KL. Understanding Pathophysiology. 2nd ed. St. Louis, MO: Mosby; 2006. Martini FH, Bartholomew EF. Essentials of Anatomy & Physiology. 5th ed. San Francisco, CA: Benjamin Cummings; 2010. Morgan GE, Mikhail MS, Murray MJ. Clinical Anesthesiology. 4th ed. New York, NY: McGraw-Hill; 2006. Shier D, Lewis R, Butler J. Hole’s Human Anatomy & Physiology. 9th ed. New York, NY: McGraw-Hill; 2002. Stoelting RK, Hillier SC. Pharmacology & Physiology in Anesthetic Practice. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.
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CHAPTER
15
Peripheral Nervous System Eve Klein and Michelle Cameron
T
he nervous system transmits signals between different parts of the body and can be divided into the central nervous system (CNS), which includes nerves wholly contained in the brain and spinal cord, and the peripheral nervous system (PNS), which includes nerves outside of the CNS. The CNS and autonomic system are covered in Chapters 13 and 14, respectively, while this chapter focuses on the PNS, including anatomy, physiology, pathophysiology, and mechanisms of peripheral nerve blockade by local anesthetics.
■ PERIPHERAL NERVE ANATOMY Nerves of the PNS carry information to, or from, the CNS. The nerves that carry information to the CNS from the periphery are known as afferent nerves. Afferent nerves transmit a range of sensations, including touch, position, vibration, and pain. Sensory afferent nerves originate in the dorsal root ganglia just outside the spinal cord. The nerves that carry information from the CNS to the periphery are known as efferent nerves. Efferent nerves include both the somatic motor nerves that innervate skeletal muscles to make them contract voluntarily and the autonomic nerves that control involuntary muscles, such as smooth and cardiac muscle, and control glandular activity. Efferent somatic motor nerves originate in the anterior horn of the spinal cord.
■ NERVE CELLS Nerve cells, also known as neurons, are composed of a cell body, dendrites, an axon, and axon terminals (Fig. 15.1). The cell body contains the nucleus and various organelles (mitochondria, rough endoplasmic reticulum, ribosomes, and Golgi apparatus) needed to make proteins and process energy to maintain the nerve. The dendrites are branching and tapering extensions of the cell body that receive signals from other
neurons. The axon is a projection that carries signals from the cell body toward the axon terminals where signals are then transmitted to other nerves or to end organs such as muscles. Where the axon terminal of one neuron (the presynaptic neuron) meets an end organ or a dendritic ending or cell body of another neuron (the postsynaptic neuron) is known as a synapse, with the gap between the presynaptic neuron and the end organ or postsynaptic neuron referred to as the synaptic cleft. Neurotransmitters, proteins, and organelles are transported along axons using a system of microtubules and neurofibrils. Anterograde transport from the cell body of neurotransmitters and structures to replenish the plasmalemma is quick, whereas anterograde transport of proteins and organelles needed for axoplasm generation or replenishment (regenerating or mature neurons) is slow. Retrograde transport toward the cell body to return organelles to the cell body for disposal and to carry nerve growth factor toward the cell body also occurs slowly. Both anterograde and retrograde transport require an energy source that is compromised if the blood supply to the nerve is disrupted. A nerve is made up of multiple nerve cell axons. Each axon is surrounded by a delicate layer of loose connective tissue known as the endoneurium. Groups of axons are then arranged in bundles called fascicles, and each fascicle is surrounded by perineurium, which is composed of flattened cells, basement membrane, and collagen fibers. Groups of fascicles, with arteries and veins between them, are then held together by a layer of dense connective tissue known as the epineurium to form a nerve (Fig 15.2). It is important to know this anatomy when performing regional anesthesia, as inadvertent intraneural injection of local anesthetic—into the nerve itself—can cause mechanical or ischemic nerve injuries, which are discussed later in this
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Dendrites
Nucleus
Cell body
myelinated, the myelin wraps around the outside of the epineurium. Myelin is a lipoprotein that acts as an insulator for the axon. The myelin around peripheral nerves is made by Schwann cells. Each Schwann cell forms a segment of myelin about 1 mm long. There are small gaps of uncovered axon between each of these segments known as nodes of Ranvier. The segments of axon between the nodes are called internodes (Fig. 15.3). Myelin accelerates the transmission of signals along the axon because impulses can jump from one node to the next rather than having to traverse the entire length of the axon. This jumping is known as saltatory conduction. Unmyelinated nerve cell axons conduct nerve impulses much more slowly than myelinated nerve cell axons.
■ PERIPHERAL NERVE PHYSIOLOGY
Axon branch Axon covered with myelin sheath Myelin
Neuromuscular junction
Muscle ■ FIGURE 15.1 Components of the neuron: the cell body containing the nucleus and other organelles, dendrites to receive information, an axon to transmit information over a distance, and axon terminals to transmit a signal to an end organ. (From Cohen BJ. Medical Terminology. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003, with permission.)
chapter. Ultrasound is often used when performing regional anesthesia so that the anesthesia provider can visualize the location of the injection and thereby reduce the risk of intraneural or intrafascicular local anesthetic injection. Some peripheral nerve cell axons are wrapped in concentric layers of myelin. If a nerve is
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Two positively charged ions, potassium (K+) and sodium (Na+), are primarily responsible for the transmission of signals along nerves. At rest, when no signal is being transmitted, there is more sodium outside the neuron and more potassium inside the neuron. These concentrations are maintained by sodium-potassium adenosinetriphosphatase (ATPase) pumps on the cell membrane. These pumps use ATP as their energy source to pump three sodium ions out of the cell for every two potassium ions they pump into the cell. This results in the inside of the cell being less positively charged than the outside, which is considered a relative negative charge. This negative charge, of about −65 mV, is known as the resting membrane potential. When the nerve is sufficiently stimulated, sodium channels on the nerve membrane open allowing sodium ions to rapidly enter the neuron, causing the inside to become positively charged relative to the outside. More and more sodium channels open until all of the available channels are open. This causes a rapid rise in membrane potential, or depolarization, which is followed by sodium channel inactivation (closure). Once the sodium channels close, sodium ions no longer enter the neuron. Potassium channels then open, and potassium ions flow out of the nerve, causing the membrane potential to return to baseline. This sequential nerve depolarization and repolarization is known as an action potential (Fig. 15.4). To restore the membrane potential (repolarization), sodium is pumped
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Section II • Anatomy, Physiology, and Pharmacology Peripheral nerve
Epineurium Perineurium Fascicle Peripheral (myelinated) nerve fiber
Endoneurium
Blood vessels supplying nerve (vasa nervorum)
Myelin sheath (formed by neurolemma or Schwann cells) Axon ■ FIGURE 15.2 Arrangement and ensheathment of peripheral, myelinated nerve fibers. All but the smallest peripheral nerves are arranged in bundles (fascicles), and the entire nerve is surrounded by the epineurium, a connective tissue sheath. Each small bundle of nerve fibers is also enclosed by a sheath—the perineurium. Individual nerve fibers have a delicate connective tissue covering—the endoneurium. The myelin sheath is formed by neurolemma (Schwann) cells. (From Moore KL, Dalley AF II. Clinical Oriented Anatomy. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999, with permission.)
out of the cell and potassium is pumped into the cell. Action potentials can be initiated on the cell body or the axon, but they usually start at the axon hillock, the point where the axon leaves the cell body (see Fig 15.1) because this is the most readily excitable part of the nerve. Once an action potential occurs at any point on the axon, the resulting currents will trigger depolarization and an action potential on the neighboring stretch of membrane, with the signal then being propagated along the nerve in a domino-like fashion, until it reaches the end of the nerve. Since each action potential is generated anew along the next excitable stretch of axon, the signal does not decay in strength.
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Myelinated segments of axons are not excitable and do not produce action potentials. When an action potential reaches a myelinated segment, the current is quickly conducted, with some decay, to the next node of Ranvier where action potentials are generated to boost the signal. This saltatory conduction is much quicker than the sequential action potentials that occur along the entire length of unmyelinated nerves. When the action potential reaches the axon terminal it generally triggers release of a neurotransmitter from vesicles in the axon terminal into the synaptic cleft. The neurotransmitter binds to postsynaptic receptors, causing activation of the end organ or excitation or inhibition
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Chapter 15 • Peripheral Nervous System
Node of Ranvier
Schwann cell nucleus
Schwann cell nucleus
Layers of myelin
Axon
Layers of myelin Axon
■ FIGURE 15.3 The Schwann cell migrates down a larger axon to a bare region, settles down, and encloses the axon in a fold of its plasma membrane. It then rotates around and around, wrapping the axon in many layers of plasma membrane, with most of the Schwann cell cytoplasm squeezed out. The resultant thick, multiplelayered coating around the axon is called myelin.
of a postsynaptic nerve. A postsynaptic neuron or end organ may receive excitatory and inhibitory inputs from many other neurons. With a sufficient predominance of excitatory inputs, the end organ will be activated or an action potential will start in the postsynaptic neuron and propagate along the length of this nerve.
■ PERIPHERAL NERVE PATHOPHYSIOLOGY Damage to nerves of the PNS is known as peripheral neuropathy. Neuropathy is usually classified according to its distribution and its cause. The typical distributions of neuropathy are mononeuropathy, mononeuritis multiplex, polyneuropathy, and autonomic neuropathy. A mononeuropathy is a neuropathy that only affects one nerve. Mononeuropathies are usually caused by compression, for example, carpal tunnel syndrome at the wrist or peroneal nerve compression at the knee after prolonged compression during surgery. Mononeuritis multiplex is simultaneous or sequential involvement of multiple nerves that is asymmetric and evolves over time. Mononeuritis multiplex is associated with a range of medical conditions, including diabetes, HIV, and lupus. In contrast, in polyneuropathy, many nerve cells throughout the body,
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but not necessarily all neurons within a nerve, are affected. The most common form of polyneuropathy is a distal symmetric form in which the axons are affected in proportion to their length, with the longest axons being affected first. This type of polyneuropathy presents initially with symmetric distal symptoms and is most often caused by a disease process, most often diabetes. Autonomic neuropathy is a form of polyneuropathy that affects the autonomic nervous system. Autonomic neuropathy is usually seen in people with long-standing diabetes and usually develops after polyneuropathy affecting the sensory and motor nerves. Peripheral neuropathy can cause sensory, motor, and autonomic signs and symptoms. Sensory symptoms of peripheral neuropathy include those related to loss of function (negative symptoms) such as numbness or gait instability due to loss of proprioception (the sensation of where one’s body is in space) as well as those related to overactivity hypersensitivity of a nerve (positive symptoms) such as pain, itching, tingling, and skin hypersensitivity. Motor nerve involvement can also cause negative symptoms, including weakness and muscle fatigue, as well as positive symptoms, including cramps and fasciculations (small local muscle twitching). Autonomic nerve involvement can cause heart rate and blood pressure instability as well as constipation and urinary symptoms. The signs of peripheral neuropathy found during the neurologic examination typically include sensory loss, weakness, and reduced stretch reflexes (e.g., knee jerk and ankle jerk) in the area innervated by the involved nerve. There are many causes of peripheral neuropathy including metabolic diseases, genetically inherited disorders, toxins, inflammatory diseases, vitamin deficiencies, mechanical trauma, and a few others (Table 15.1). Diabetes mellitus is the most common cause of peripheral neuropathy. About 2% of the population and about 30% of people with diabetes have symptoms of peripheral neuropathy. Peripheral neuropathy is the most common complication of diabetes. Diabetes generally causes a symmetric length-dependent polyneuropathy that first affects sensation in the toes and feet, causing pain and numbness, and then gradually ascends up the legs. When the symptoms reach approximately to the midcalf they also start to
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Na+
Na+
Cl
Cl
Resting state (unstimulated state)
Excited state (stimulated state)
Action potential Depolarization Repolarization Resting potential Stimulus Na+
Hyperpolarization
Return to resting state
Nerve impulse Site of summation of multiple stimuli
All-or-none action potentials with transient reversal of polarity
■ FIGURE 15.4 Recording of electrical changes that occur at rest and on stimulation. (From Snell R. Clinical Neuroanatomy. Philadelphia, PA: Lippincott Williams & Wilkins; 2001, with permission.)
affect the fingers. This pattern of involvement is known as stocking-glove distribution. The progression of diabetic neuropathy can be controlled to some degree by good blood sugar control. With poor blood sugar control, the neuropathy associated with diabetes progresses to also affect the motor nerves, causing foot weakness, and
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the autonomic nerves, causing constipation and abnormal sweating and circulation. Charcot-Marie-Tooth (CMT) disease (also called hereditary motor and sensory neuropathy) is a group of inherited peripheral nerve disorders that can affect the sensory and/or motor nerves. It usually starts in the teens or twenties with distal
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TABLE 15.1 COMMON CAUSES OF NEUROPATHY AND EXAMPLES CAUSE OF NEUROPATHY
EXAMPLES
Metabolic diseases
Diabetes mellitus, hypothyroidism
Genetic disorders
Charcot-Marie-Tooth disease
Toxins
Alcohol, medications (e.g., certain chemotherapy agents), heavy metals, excess vitamin B6
Inflammatory diseases
Guillain-Barré syndrome, leprosy (Hansen’s disease)
Vitamin deficiencies
Vitamin B12, vitamin B1 (thiamine)
Mechanical trauma
Compression, traction, accidental injection, lacerations, ischemia
Other
Thermal injury, radiation, viral (varicella, HIV)
weakness and sensory loss and progresses gradually over the person’s lifetime. CMT is the most common inherited neurologic disorder in the United States, affecting approximately 1 in 2,500 (about 100,000) Americans today. Although CMT generally produces only mild weakness at onset, over a number of years some variants of this disease can progress to produce significant difficulties with walking and breathing. Alcoholic neuropathy presents with a gradual decrease in sensory and motor peripheral nerve function in patients who chronically consume excessive amounts of alcohol. About 10%-15% of chronic alcoholics have symptoms of neuropathy, and up to 75% show signs of neuropathy if they undergo sensitive sensory testing. Alcoholic neuropathy is more common in men than in women and increases in incidence with age and the amount of alcohol consumed. Patients present with symmetric distal sensory loss, weakness, and loss of reflexes, which progress in a stocking-glove distribution similarly to the neuropathy associated with diabetes. Guillain-Barré syndrome (GBS), also known as acute inflammatory demyelinating polyneuropathy (AIDP), is the most common cause of acquired acute and subacute areflexic paralysis in humans, with an annual incidence of 1-2 per 100,000. GBS is an autoimmune disease that generally causes demyelination, primarily of the motor nerves. The symptoms of GBS, primarily an ascending paralysis, come on over a few days and can progress to the point where the person cannot walk or breathe because of lower extremity muscle and diaphragm weakness. However, unlike the previously described types of neuropathy, after a few weeks, the signs and symptoms of GBS start to reverse, with full or almost full
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recovery occurring in most patients with GBS over weeks to months. Vitamin B12 and vitamin B1 deficiencies can both cause peripheral neuropathy. Vitamin B12 deficiency usually occurs in the elderly as a result of malabsorption and has a range of neurologic, psychiatric, and hematologic manifestations. Vitamin B12 deficiency can affect the peripheral nerves and the spinal cord and also cause anemia, mood changes, and psychosis. Vitamin B1 (thiamine) deficiency, also known as beriberi, usually occurs in alcoholics or in others with generally poor nutrition, and often occurs in conjunction with overall malnutrition. Thiamine deficiency can also cause the CNS disorders, Wernicke’s syndrome and Korsakoff’s syndrome, which are associated with confusion, ataxia, eye movement abnormalities, and memory loss. Mechanical trauma, usually from excessive compression or stretch, is a common cause of peripheral mononeuropathy. Most mechanically induced nerve injuries are also associated with inadequate blood supply to the nerve. Nerves may be injured by a single application of highforce compression or traction or by repeated or prolonged application of lower levels of compression or traction. Nerve compression may be caused by edema of surrounding soft tissue from acute or chronic inflammation, increased compartmental pressures, space-occupying lesions, contact against bones, entrapment within soft tissues, and iatrogenic causes such as tourniquets, blood pressure cuffs, or supports during surgery. The amount, distribution, and duration of compression force applied to a nerve affect the nature and degree of nerve damage. Ideally, the lowest effective pressure and the shortest necessary tourniquet times are recommended to reduce the risk
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of nerve injury. Use of a tourniquet for more than 2 hours and pressures of greater than 350 mm Hg in the lower extremity and more than 250 mm Hg in the upper extremity increases the risk of compression neuropathy. In patients with low baseline arterial blood pressure, lower cuff inflation pressures may be more appropriate. Classic teaching mandates that if a procedure requires that a tourniquet be applied for more than 2 hours, then it be deflated for 5 minutes each 30 minutes of inflation time. Some literature now suggests that tourniquets should not remain continuously inflated for longer than 60 minutes in the upper extremity or 90 minutes in the lower extremity. In addition, it is recommended that wide cuffs, or padding under the tourniquet, be used to distribute the pressure. Acute nerve stretching or traction injuries are associated with fractures, joint dislocation, extreme limb or body segment positioning, as can occur during positioning for surgical access, and pulling on a limb segment, as can occur in obstetrical brachial plexus injury. Traction that stretches the nerve a small amount may only impair circulation within the nerve. But a greater stretch can cause structural failure and complete conduction block and affect sensory and motor function. When a nerve is accidentally injected, it may be damaged by the physical trauma of the needle and by exposure to the drug or agent. Accidental injection injuries occur most often during medication delivery (intramuscular medications or regional anesthesia procedures), with the sciatic nerve being the nerve most frequently injured by injection. Needle-stick injuries to nerves during acupuncture are rare but have also been reported. Nerves can also be injured during vascular access procedures (e.g., starting peripheral intravenous [IV] lines, arterial lines). Injection of a substance into a nerve usually causes severe, radiating pain. Nerve lacerations can occur as a result of contact with a sharp object, such as a piece of glass, metal, knife, razor blade, or scalpel, or from contact with a blunt object, such as components of power tools or other machinery, and gunshot wounds. Sharp injuries may occur intraoperatively. Nerves may also be damaged by heat, either through direct exposure or by exposure to electrical current or radiation. Electrical currents
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tend to travel along neurovascular bundles, damaging the nerve directly by heating it and causing coagulation necrosis or by damaging the nerve cell membrane and increasing its permeability. Radiation injury to peripheral nerves can occur during cancer treatment, and when this occurs, the damage to irradiated nerves appears to be related to an increase in temperature and is generally permanent.
■ MECHANISM OF ACTION FOR PERIPHERAL NERVE BLOCKADE Local anesthetics may work either peripherally or centrally to block neural transmission. They do so by blocking sodium channels in neuronal cell membranes. When sodium ions cannot move freely in and out of cells, neuronal action potentials cannot form or propagate. When neuronal action potentials are blocked, nerve function is lost. Exactly how avidly a local anesthetic will block neuronal transmission depends on the size of the nerve fiber, the frequency of electrical stimulation of the nerve, and the particular local anesthetic. Local anesthetics may block nerves peripherally with local administration. Nerves may also be blocked in the spinal cord when medications are injected into the intrathecal or epidural space. When local anesthetics block the action of dorsal horn neurons in the spinal cord this results in blockade of nociceptive activity. When local anesthetics block activity in the ventral horn of the spinal cord, motor function is blocked. See Chapter 21 for an in-depth discussion of how local anesthetics are used in regional anesthesia.
■ PHARMACOLOGY OF LOCAL ANESTHETICS Pharmacodynamics Local anesthetics are weak bases. They may exist in either a neutral form, in which they are lipid soluble, or a charged form, in which they are hydrophilic. How much of the compound exists in each form depends on the pH of the environment and the dissociation constant specific to the local anesthetic in question. Generally, the charged form of the local anesthetic is the active form. However, local anesthetics in their lipid-soluble form more readily penetrate the nerve cell membrane to exert their blocking action on the intracellular side of
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Chapter 15 • Peripheral Nervous System
the sodium channel. The more lipid soluble the local anesthetic, the more likely it is to become sequestered in the myelin sheath of the nerve fiber or in other lipid-soluble compartments. Therefore, increasing lipid solubility of local anesthetics generally slows their rate of onset of action. More lipid-soluble local anesthetics also tend to have a longer duration of action because their sequestration in lipid-soluble compartments creates a repository from which they are slowly released. Increased lipid-solubility also predicts increased potency of local anesthetics via increased affinity for sodium channel receptors. Local anesthetics also exist in protein-bound and unbound forms. It is the unbound form of the local anesthetic that is pharmacologically active. Local anesthetics that are more highly protein bound are generally longer acting. Although the mechanism is uncertain, epinephrine when added to local anesthetics is reported to increase the duration of action and intensity of the block while decreasing systemic absorption. Epinephrine causes vasoconstriction, which may reduce systemic absorption, allowing more of the anesthetic to remain available for local nerve blockade. In general, the vasodilation caused by most local anesthetics is associated with a shorter duration of action of the anesthetic, whereas the vasoconstriction caused by epinephrine serves to prolong the duration of anesthetic activity. The vasoconstrictive effects of epinephrine are thwarted in acidic environments. The common practice of alkalinizing solutions containing local anesthetics with epinephrine serves to promote vasoconstriction and the resultant beneficial effects of epinephrine previously discussed. Regardless of whether epinephrine is present in the local anesthetic solution, alkalinization of the local environment in and of itself serves to inhibit neuronal conduction. Although no confirmatory data are available in humans, animal studies have shown that there is an increased risk of peripheral nerve injury associated with local anesthetics when mixed with epinephrine as compared to local anesthetics administered without epinephrine. Therefore, the decision as to whether or not epinephrine should be added to the local anesthetic solution requires a complex analysis of the relative risks and benefits by the anesthesia provider.
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Pharmacokinetics Because local anesthetics can be toxic when absorbed systemically, it is important to understand the pharmacokinetics of local anesthetic administration. Blood levels of a local anesthetic depend on absorption, distribution, and elimination of the local anesthetic. The rate of absorption of a local anesthetic depends on its site of injection, dose, and physiochemical properties, including whether or not it has been mixed with epinephrine. When local anesthetics are injected into more vascular areas, they will be more avidly absorbed systemically than when they are injected into areas containing more fat. Higher total doses of local anesthetics also result in greater absorption and higher blood levels. Increased lipid solubility and increased protein binding both result in less systemic absorption of local anesthetics. Distribution of the local anesthetic depends on organ blood flow, the partition coefficient specific to the particular local anesthetic, and the affinity with which the local anesthetic binds to plasma proteins. Once absorbed into the circulation, local anesthetics will tend to distribute most rapidly to highly vascular regions such as the heart and brain. Local anesthetics can be categorized as either aminoesters or aminoamides. Aminoesters include chloroprocaine, procaine, and tetracaine. Aminoamides include bupivacaine, lidocaine, mepivacaine, and ropivacaine. The elimination of aminoesters depends on their clearance by serum cholinesterases. Aminoamides, by contrast, are cleared by the liver. Thus, the elimination of aminoamides depends on liver function and protein binding. Pharmacokinetics also varies between individuals. Children and the elderly may experience increased systemic absorption of local anesthetics as well as decreased elimination rates. Individuals with cardiac or hepatic dysfunction will have altered distribution or elimination of local anesthetics. Therefore, these groups should be treated cautiously using lower doses.
■ CLINICAL USES OF LOCAL ANESTHETICS There are many different clinical uses for local anesthetics. Local anesthetics may be used neuraxially in epidural or intrathecal injections or infusions. They may be used in peripheral nerve blocks either as a single injection or as
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a continuous infusion through a catheter. Local anesthetics can also be administered topically to the skin or mucous membranes. IV administration of lidocaine can be used to decrease airway sensitivity preceding endotracheal intubation. IV lidocaine infusions or oral administration of mexiletine and tocaininde may be used to treat chronic neuropathic and central pain conditions.
■ LOCAL ANESTHETIC TOXICITY Local anesthetics readily cross the blood-brain barrier. Therefore, systemic absorption of local anesthetics may result in CNS toxicity. In addition, local anesthetics can affect heart function and conduction of electrical impulses within the heart. In general, local anesthetics with decreased rates of protein binding and clearance carry more risk for toxicity, while those with decreased systemic absorption and increased rates of elimination carry less risk for toxicity. With local anesthetic administration, careful attention must be paid to the route of administration and potential toxic doses. By decreasing systemic absorption, the addition of epinephrine to local anesthetics decreases the likelihood of toxicity. In hyperdynamic states, as during a physiologic stress response, cerebral blood flow is increased while hepatic blood flow is reduced. Such conditions increase the likelihood of local anesthetic toxicity by increasing the concentration of local anesthetic in the CNS and reducing the rate of local anesthetic clearance. Another way in which local anesthetic toxicity may occur is via inadvertent intravascular injection. A dose that is perfectly safe to administer as a nerve block can be lethal if injected into an artery or a vein. For this reason, prior to injection of local anesthetic, it is critical to aspirate through the needle to confirm that the needle position is not intravascular. Another technique commonly employed for ruling out inadvertent intravascular exposure is the administration of an epinephrine test dose. Intravascular epinephrine produces elevations in heart rate or blood pressure with 80% sensitivity. Although the two large case series available offer inconclusive results regarding its reliability, ultrasound guidance is another commonly accepted technique for the prevention of inadvertent intravascular injection of local anesthetics. Signs of systemic toxicity from local anesthetics range from sedation, lightheadedness,
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tinnitus, metallic taste, and perioral paresthesias at low doses, to seizures, coma, and cardiopulmonary arrest at high doses. At the doses and concentrations typically used clinically, local anesthetics are safe for peripheral nerves; however, at significantly higher concentrations, local anesthetics can cause nerve injury. Local anesthetics may also cause concentration-dependent damage to the spinal cord and nerve roots. There have been multiple case reports in which spinal infusion of lidocaine was associated with damage to the cauda equina, resulting in long-term bladder and gait dysfunction. By virtue of their sodium channel blockade, local anesthetics also produce dose-dependent cardiac conduction block. The degree of cardiotoxicity varies between local anesthetics by their relative potencies, with bupivacaine being relatively more potent and cardiotoxic and lidocaine being less. Toxic systemic effects of local anesthetics are exacerbated in the setting of hypoxia, hypercapnea, and acidosis. Therefore, when systemic toxicity does occur, supportive measures such as oxygenation and ventilation are critical. If cardiovascular depression occurs, resuscitation with a 20% lipid emulsion may be life saving. Traditional advanced cardiac life support (ACLS) interventions may be ineffective, although cardioversion or defibrillation often become effective after administration of the lipid emulsion. Therefore, maintenance of oxygenation and ventilation, high-quality cardiopulmonary resuscitation (CPR), and the lipid emulsion are the cornerstones of treatment for local anesthetic toxicity. Although propofol contains lipid, it does not constitute an effective lipid emulsion and can worsen outcomes if given for cardiac arrest from local anesthetic administration. Single enantiomeric preparations of local anesthetics, such as ropivacaine and levo-bupivacaine, are associated with decreased systemic toxicity. Anaphylactic allergic reactions to local anesthetics are rare and generally involve ester rather than amide compounds. Certain preservatives that may be added to local anesthetics can also cause allergic responses. Local and regional anesthesia plays an important role in perioperative pain management. The safe and effective provision of local and regional anesthesia is a complex task that demands knowledge of the anatomy and physiology of
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Chapter 15 • Peripheral Nervous System
the PNS, the mechanisms of action of local anesthetics, and the potential complications that can result from their use. Our understanding of these concepts is ever evolving as further data are published and newer, safer, and more effective local anesthetics are developed.
REVIEW QUESTIONS 1. Peripheral nerve myelin A) Is made by Schwann cells B) Has gaps known as nodes of Ranvier C) Speeds nerve conduction D) Slows nerve conduction E) A, B, and C Answer: A. Some, but not all, peripheral nerves are myelinated. Myelinated peripheral nerves are wrapped in concentric layers of myelin around the epineurium. The myelin is made by Schwann cells in about 1-mm long segments with gaps known as nodes of Ranvier between them. Myelin accelerates nerve conduction by allowing for saltatory (jumping) conduction of signals from one node of Ranvier to the next.
2. Which of the following statements are TRUE about nerve action potentials? A) A polarized nerve membrane is rapidly depolarized. B) Depolarization cannot be conducted from one stretch of nerve membrane to another. C) Phosphorus ions flowing into the cell cause depolarization. D) Phosphorus ions flowing out of the cell cause repolarization. E) None of the above. Answer: A. Nerves transmit signals from one area of the body to another with action potentials. At rest the nerve is polarized. During an action potential, sodium first rushes into the nerve to depolarize it and then potassium rushes out of the nerve to repolarize it. An action potential occurs in one place in the nerve and this then triggers depolarization and an action potential on the neighboring segment, propagating the signal along the nerve in a domino-like fashion.
3. All of the following paired definitions are correct EXCEPT A) Mononeuropathy: neuropathy affecting only one nerve B) Mononeuritis multiplex: simultaneous or sequential involvement of multiple nerves that is asymmetric and evolves over time
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C) Polyneuropathy: neuropathy affecting many nerve cells throughout the body, but not necessarily affecting all neurons within a nerve D) Autonomic neuropathy: a form of polyneuropathy that affects the autonomic nervous system E) Fasciculations: large involuntary muscle jerks or movements of an entire limb Answer: E. Fasciculations are small, involuntary muscle twitches that are not large enough to result in movement about a joint or movement of an entire limb. The other terms are correctly defined.
4. Signs of local anesthetic toxicity may include all of the following EXCEPT A) Tinnitus B) Burning smell C) Perioral numbness D) Respiratory arrest E) Metallic taste Answer: B. Auditory changes including tinnitus, perioral numbness, metallic taste, seizures, cardiac arrhythmia, coma, and respiratory arrest are all classically described signs of local anesthetic toxicity. A burning smell, which may precede a temporal lobe seizure, is a sign of a focal (starting in an isolated area of the brain) seizure rather than a generalized (whole-brain) seizure as would be expected due to local anesthetic systemic toxicity.
5. Which of these local anesthetics is associated with the highest risk of cardiotoxicity? A) Lidocaine B) Bupivacaine C) levo-bupivacaine D) Ropivacaine E) Mepivacaine Answer: B. In general, the cardiotoxicity of local anesthetics is proportional to their potency, with bupivacaine being more potent and more cardiotoxic than lidocaine or mepivacaine. The single enantiomeric local anesthetic preparations including ropivacaine and levo-bupivacaine are associated with decreased systemic toxicity.
SUGGESTED READINGS Barash P, Cullen B, Stoelting R. Clinical Anesthesia. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001. Henderson, CA. A Comprehensive Introduction to the Peripheral Nervous System. Medtutor.Com. 2010. Neal J, et al. ASRA Practice Advisory on Local Anesthetic Systemic Toxicity. Reg Anesth Pain Med. 2010;35(2): 152-161. O’Brien M. Aids to Examination of the Peripheral Nervous System. 5th ed. Elsevier; 2010.
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CHAPTER
16
Neuromuscular Anatomy and Physiology Jodi H. Kirsch and Jeffrey Kirsch ■ INTRODUCTION One of the key activities in conducting a general anesthetic for surgery can be to provide muscle relaxation (paralysis) in order to facilitate placement of an endotracheal tube in the trachea or to provide optimum operating conditions for the surgeon with quiet, soft muscles. This is accomplished with medications that interfere with normal functioning of the junction between nerves and muscles. Knowledge of the anatomy and physiology of the neuromuscular system will help anesthesia technicians understand the mechanism of how drugs affect the neuromuscular junction (NMJ) and how nerve stimulators can be used to monitor the condition of the neuromuscular system.
■ ANATOMY OF THE NEUROMUSCULAR SYSTEM The neuromuscular system, as implied by the name, is composed of nerves and muscles. These nerves are considered peripheral nerves. They exit from the spinal cord and then act upon the muscles of the body. There are three different types of muscle: cardiac muscle in the heart, smooth muscle, and skeletal muscle. Although similar, each of the different types of muscles has slightly different properties. Whereas skeletal muscle can be controlled at the desire of an individual, both cardiac and smooth muscle contraction and relaxation occur independent of direct individual control. Smooth muscle is an involuntary type of muscle that is controlled by the autonomic nervous system (see Chapter 14). Examples of smooth muscle include the walls of blood vessels, lymphatic vessels, bronchioles in the lungs, urinary bladder, and the reproductive tract of males and females. Contraction or relaxation of these muscles occurs in response to
activity/need, rather than by direct control of the individual. Cardiac muscle is also a type of involuntary muscle. While our body is composed of smooth muscle, cardiac muscle, and skeletal muscle, the majority of the body is skeletal muscle. Skeletal muscle is a voluntarily controlled, striated (under the microscope)-appearing tissue that enables our body to move. Skeletal muscles attach to bones by way of tendons. Skeletal muscle is composed of many muscle fibers, which are held together by protein and fibrous tissue (Fig. 16.1). These muscle fibers in turn are composed of multiple myofibrils (the actual individual muscle cells). Within each myofibril are abundant mitochondria (the energy-producing organelle in all cells), smooth endoplasmic reticulum (the cell organelle that produces lipids, metabolizes carbohydrates, and regulates calcium levels in the cell), and most importantly multiple nuclei. Multiple nuclei are imperative for skeletal muscle function due to the high activity level required of these muscles. The main contractile unit in skeletal muscle cells is called the sarcomere. There are many sarcomeres within one myofibril. When a sarcomere is further examined under an electron microscope, one observes repeating sections of light and dark areas. The light areas are the thin filaments. Thin filaments are composed of the protein, actin. The dark areas of the sarcomere are the thick filaments and are composed of the protein myosin. During contraction the myosin on the thick filaments binds to actin on the thin filaments. The binding of actin to myosin is a process that requires calcium and energy. The energy for the reaction is supplied by adenosine triphosphate. Overall, this process results in shortening of the sarcomere, which is anatomically
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Tendon
A dense, fibrous connective tissue that is continuous with the periosteum and attaches muscle to the bone
Periosteum
A tough, fibrous connective tissue that covers the surface of bones, rich in sensory nerves, responsible for healing fractures
Belly
Epimysium
Thick contractile portion (or body) of the muscle
Fibrous tissue enveloping the entire muscle and continuous with the tendon
Perimysium
Fibrous tissue that extends inward from epimysium, surrounding bundles of muscle. Each bundle bound by perimysium is called a fascicle.
Fascicle
A group of fibers that have been bound by perimysium
Endomysium
A delicate connective tissue that surrounds each muscle fiber
Z-line
Boundary of two sarcomeres
H-zone
Consists of stacks of myosin filaments
Z-line
Sarcomere
Portion of muscle fibers found between two Z-lines
Muscle fibers
Long, cylindrical, multinucleated cells with striations
Myosin Actin
Thick and thin filaments active during muscle contraction
■ FIGURE 16.1 Muscle anatomy.
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recognized as muscle contraction. The molecular basis of muscle contraction is explained by the “sliding filament theory.” This theory states that in the presence of calcium and energy, actin and myosin slide past each other and the sarcomere shortens. The protein filaments overlap but do not shorten. The overlap is what causes the sarcomere to shorten.
■ THE NEUROMUSCULAR JUNCTION The NMJ is composed of the terminal portion of a motor neuron axon and the motor end plate of a muscle fiber. The function of the NMJ is to allow the muscle to contract based on messages originating in the brain. Once the motor cortex of the brain sends the message, the message is delivered by way of action potentials (electrical signals) along the axons of motor neurons. When the action potential is sent down the axon, it eventually reaches the NMJ (Fig. 16.2). The junction across which one nerve sends a signal to another nerve, muscle, or gland is called a synapse. The terminal portion of the nerve where the signal originated is the “presynaptic” nerve. Once the nerve action potential arrives at the terminal portion of the presynaptic nerve, it causes acetylcholine (ACh) to be released from the axon terminal into an area between the axon and the motor end plate, called the synaptic cleft. The ACh then travels across this area to attach to nicotinic ACh receptors on the motor end plate of the muscle (Fig.16.3). Binding of ACh to these receptors causes sodium and potassium channels to open in the muscle cell membrane. Sodium and potassium travel opposite each other; sodium travels into the cell, and potassium trickles outward. Because sodium rushes into the motor cell much more quickly than potassium leaves the cell, the cell becomes more positively charged and
Peripheral nerve Neuromuscular junction Anterior horn cell
Muscle fiber
Ventral root ■ FIGURE 16.2 A motor nerve axon terminating at the junction between the nerve and muscle.
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depolarizes (a change in the charge of the interior of the cell membrane compared to the outside). Depolarization of the muscle cell then causes the release of calcium from sarcoplasmic reticulum in the muscle cell. Excess calcium in the muscle cell binds to the thin filament in the sarcomere, triggering a cascade of events resulting in muscle contraction. But how does our brain send a message to the many muscles of the body to contract or relax? Let us use the example of an anesthesia technician carrying an arterial line setup to an operating room. When the anesthesia technician wants to lift his or her arm, the bicep muscle must contract. A message is sent from the brain to tell the biceps muscle that it must shorten to accommodate the weight of the arterial line setup. The message originates in upper motor neurons in the motor area of the brain. The upper motor neuron crosses to the opposite side at the level of the brainstem and then synapses with a lower motor neuron in the anterior portion of the spinal cord, just before exiting the spinal canal. Thus, movement of the right side of your body comes from a message that originates in the left side of your brain. Because the movement of the arm happens almost instantaneously, the signal must travel very quickly from the brain to the muscles. This is why motor neurons are myelinated nerve fibers, to speed conduction (see Chapter 15). Myelin is an insulating material that covers nerve axons to increase the speed of signal transmission.
■ DISEASES THAT ALTER NEUROMUSCULAR FUNCTION Normal function of the complex transmission of information from the brain to muscle through the NMJ is essential to each individual for normal movement. Unfortunately, there are several disease processes that interrupt this normal function with defects that affect each of the steps along the way. Most proximal to the NMJ would be a defect in the motor cortex. For example, a stroke (an obstruction in a blood vessel or a ruptured blood vessel) in the motor cortex can prevent movement in the extremity on the opposite side of the body. This type of injury would present with upper motor neuron signs and symptoms (see below). The motor signals that originate in the cortex of the brain are sent out to the body through motor neurons. Disease of
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Nerve impulse Cerebral cortex
Axon motor neuron
Spinal cord
Motor end plate Packets of acetylcholine Nerve impulse From cerebral cortex Upper motor neuron
Lower motor neuron
Muscle cell nucleus
A
Axon branches
Acetylcholine receptors
Bundle of myofibrils
Neuromuscular junction
Synaptic space
Muscle fibers
Myofibril
Muscle fiber Type 1 fibers Type 2 fibers
Capillary
Nucleus
B ■ FIGURE 16.3 The neuromuscular junction with release of presynaptic acetylcholine binding to postsynaptic nicotinic receptors.
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the upper motor neurons themselves can affect transmission of the signal. Two of the most common central nervous system diseases affecting motor neurons include multiple sclerosis and Parkinson’s disease. A spinal cord injury could also interfere with upper motor neurons as they pass through the spinal cord. Because the nerves have already crossed over to the opposite side of the body at the level of the brainstem, a spinal cord injury will cause upper motor neuron signs and symptoms on the same side as the injury. Upper motor nerve signs and symptoms evolve over time (weeks to months) and include increased intensity of reflexes (e.g., knee jerk reflex) and muscle spasticity. Disease or injury can also affect lower motor neurons. Diseases that directly affect lower motor neurons include Lou Gehrig’s disease, Charcot-Marie-Tooth disease, and Guillain-Barré syndrome. Trauma is another common source of injury to low motor neurons after they leave the spinal canal. This can even happen in the operating room. For example, poor positioning of a patient on the operating room table can cause prolonged compression of a nerve, resulting in permanent injury. Patients with lower motor neuron injuries exhibit decreased reflexes and muscle wasting. Disorders of either upper or lower motor neurons can cause proliferation of ACh receptors on the muscle membrane. Finally, disease can strike the NMJ itself. There are two main diseases of the NMJ: Lambert-Eaton syndrome and myasthenia gravis. In LambertEaton syndrome, patients have antibodies to the mechanism that causes release of calcium within the presynaptic nerve cell. Patients with LambertEaton syndrome often have concurrent lung cancer. Although there are medications that make the symptoms (weakness and fatigue) better, the best treatment for weakness in patients with LambertEaton syndrome is to address the underlying cancer. In myasthenia gravis, patients have antibodies to nicotinic receptors on the postsynaptic side of the NMJ (muscle motor end plate). Efforts to treat patients with myasthenia gravis focus on preventing antibody attack of the nicotinic receptors, which ultimately improves transmission of nerve signals from the brain and strength/ endurance. Patients with myasthenia gravis are also treated with drugs that limit the breakdown of ACh (e.g., acethylcholinesterase inhibitors) in the synaptic cleft, which allows for a higher
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concentration of ACh and an increased ability to bind to the undamaged nicotinic receptors.
■ PHARMACOLOGIC NMJ BLOCKADE Anesthesiologists use their understanding of the anatomy and physiology of neuromuscular transmission and the NMJ to achieve muscle relaxation. In the clinical setting, muscle relaxation is important to prevent patient movement, to relax muscles and improve operating conditions for the surgeons, and to paralyze the laryngeal muscles (facilitate intubation). The agents used to achieve paralysis are referred to as neuromuscular blocking agents. Anesthesia providers must determine the proper way to block neuromuscular transmission. Insufficient paralysis may make intubation difficult, if not impossible, or a patient may move at an inopportune time during surgery and sustain an unintended injury. If too much neuromuscular blocking agent is given, the patient may have weak breathing muscles and respiratory insufficiency after surgery. It is by a thorough knowledge of the NMJ physiology and pharmacology that anesthesia providers can properly utilize neuromuscular blockers. There are two basic ways to block neuromuscular transmission: presynaptic inhibition of ACh release or postsynaptic blocking of the ACh nicotinic receptors on the muscle end plate. Although not used clinically in the operating room, one example of a substance that causes presynaptic inhibition of ACh release is botulinum toxin. Botulinum toxin can be administered in small doses to weaken overactive muscles in various muscle diseases (dystonias). This potent exotoxin works by destroying the proteins required for vesicles in the presynaptic nerve to release ACh. Other more commonly used medications that can cause presynaptic NMJ blockade are aminoglycoside antibiotics (e.g., streptomyosin, gentamicin). Aminoglycosides interfere with the movement of calcium, which limits the release of ACh into the synaptic cleft. Although these drugs are occasionally administered to patients in the operating room, they do not cause significant neuromuscular blockade, unless administered in very high concentrations or impaired kidney function decreases their elimination. In extremely rare situations, neuromuscular blockade caused by aminoglycoside antibiotics can cause respiratory depression. In order to limit the unwanted neuromuscular blockade that
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Chapter 16 • Neuromuscular Anatomy and Physiology
occasionally occurs with the administration of aminoglycoside antibiotics, the anesthesiologist may administer intravenous calcium or cholinesterase inhibitors (drugs that decrease the breakdown of ACh in the synaptic cleft). In the operating room, anesthesiologists administer NMJ-blocking drugs that primarily work on the postsynaptic side of the NMJ (they may also have very small effects on presynaptic nerves). Postsynaptic NMJ blockade falls into two main categories, with each achieving blockade by a different mechanism, depolarizing NMJ blockers and nondepolarizing NMJ blockers. Depolarizing agents (e.g., succinylcholine) bind to the nicotinic ACh receptor, causing a depolarization of the motor end plate. This causes the muscle to quickly contract and then relax. Continued presence of succinylcholine in the synaptic cleft with binding to nicotinic receptors prevents further stimulation of the muscle, resulting in paralysis. Whereas ACh is metabolized quickly to allow the muscle to quickly recover, metabolism of succinylcholine is much slower, which results in more prolonged (5-10 minutes) depolarization of the affected muscle cell and transient paralysis. Because succinylcholine causes depolarization of a large amount of muscle cells and the associated leakage of potassium out of the cell, its administration is associated with a small (0.7-1.0 mEq/L) increase in serum potassium level. This increase is generally not clinically significant; however, there are several groups of patients who are at risk for much greater increases in serum potassium. Any condition that results in a greater density of nicotinic receptors on the postsynaptic membrane is at risk for much greater rises in serum potassium after succinylcholine administration. Examples of patient groups with higher densities of nicotinic receptors include those with upper or lower motor neuron injury, prolonged periods of bed rest, or burns. Therefore, administration of succinylcholine is contraindicated in patients in these groups, as serum potassium may increase to levels high enough to cause cardiac arrest. Today in anesthesia, nondepolarizing agents are most commonly used to achieve NMJ blockade. Nondepolarizing NMJ blockers are often also called competitive blockers due to their mechanism of action. Competitive NMJ blockers compete against ACh for the ACh nicotinic receptor sites on the postsynaptic membrane.
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Nondepolarizing agents prevent the binding of ACh with nicotinic receptors; thus, depolarization does not occur and the muscle will remain in the noncontracted state. Various medications fall into the nondepolarizing category, including rocuronium, vecuronium, pancuronium, and atracurium. Nondepolarizing agents are longer acting than depolarizing agents due to their slower metabolism. They also have a slower onset time unless given in extremely high doses. For example, succinylcholine has an onset time of 30 seconds and will last for 7-10 minutes, whereas rocuronium has an onset time of 2-3 minutes and will last from 30 to 60 minutes. Both the onset time and the duration of action of nondepolarizing drugs are affected by the dose of the drug; the higher the dose, the quicker the onset and also the longer the duration of action. In addition, the duration of action of nondepolarizing agents can be prolonged even further in patients with certain medical conditions including kidney disease, liver disease, respiratory acidosis, metabolic alkalosis, hypothermia, presence of calcium channel blockers in the blood, increased magnesium in the blood, and decreased potassium in the blood. Due to the longer duration of action of nondepolarizing agents, it is often necessary to antagonize (“reverse”) the agent’s action. In order for the action of the NMJ-blocking agent to be antagonized, the patient must be given two different types of medications: acetylcholinesterase inhibitors (e.g., neostigmine or physostigmine) and anticholinergic agents (e.g., atropine or glycopyrolate). The acetylcholinesterase inhibitor prevents the metabolism of ACh in the synaptic cleft, which increases the amount of ACh in the synapse. The large amounts of ACh are better able to compete with the NMJ-blocking drug for the nicotinic receptor and initiate muscular contraction. Unfortunately, acetylcholinesterase inhibitors also increase ACh concentration at many sites in the body, not just at the NMJ. Due to binding with ACh receptors throughout the body, when used alone acetylcholinesterase inhibitors are associated with severe reductions in heart rate and gastrointestinal cramping referred to as a cholinergic crisis (see Chapter 14 for locations of cholinergic receptors in the body). In fact, anticholinesterases are commonly used as poisons. To prevent a cholinergic crisis, anticholinergic drugs that preferentially block
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muscarinic receptors for ACh (e.g., glycopyrolate or atropine) are administered simultaneously with the administration of an acetylcholinesterase inhibitor.
■ MONITORING NEUROMUSCULAR BLOCKADE The amount of neuromuscular blockade may be monitored by observing clinical signs or by objective assessment with a nerve stimulator. The use of objective means of measurement helps the anesthesiologist determine if the proper amount of blockade has been reached or to ensure that the blockade has been sufficiently reversed. As discussed earlier, the assessment of the degree of neuromuscular blockade is clinically important to prevent complications from insufficient blockade or inadequate reversal at the end of a case. Clinical signs can be used to estimate neuromuscular recovery. These signs include a head lift greater than 5 seconds, leg lift greater than 5 seconds, the patient holding a tongue depressor to the roof of his mouth while the anesthesiologist tries to pull it out, and lastly, a maximum inspiratory pressure of greater or equal to 50 cm H2O. They are often used as a measure of adequate reversal of neuromuscular blockade. Unfortunately, these signs require a cooperative patient and cannot be used during a general anesthetic to monitor the depth of neuromuscular blockade. The use of a nerve stimulator overcomes this limitation. These devices help to assess the function of the NMJ by stimulating a peripheral nerve and monitoring the effect on muscle innervated by the nerve (e.g., stimulation of the ulnar nerve and observation of the effect on the adductor pollicis muscle). After placing the stimulating electrodes near the peripheral nerve, the anesthesiologist will apply a train of four stimulations to the nerve. These stimuli are four equal impulses administered 0.5 seconds apart. The reaction of the muscle is used to determine the intensity of the block. The response of the muscle depends upon whether the neuromuscular agent administered was a nondepolarizing or depolarizing drug. Nondepolarizing agents are characterized by a response called fade; the muscle response to the stimulation decreases with repetitive nerve stimulation. With a train of four stimulations, the strength of each muscular contraction will
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diminish if there is residual neuromuscular blockade. The mechanism by which this fading occurs is controversial and may involve effects that the NMJ blockers have on presynaptic mechanisms of ACh release. Another characteristic of nondepolarizing agents is called posttetanic potentiation. If a tetanic stimulation is applied to a muscle and a single stimulus is immediately applied right afterward, the muscle twitch response to the single stimulus is greater than the previous tetanic muscle response. This response occurs because of an increase in presynaptic ACh release in addition to more ACh being present at the motor end plate. Depolarizing agents do not exhibit posttetanic potentiation or fade in response to a train of four stimuli. With depolarizing agents, the muscle response to all four of the nerve stimuli will be exactly the same.
■ SUMMARY As an anesthesia technician, it is imperative to understand the physiologic events leading to muscle contraction, what would happen if the normal neuromuscular response was blocked, the agents used to create the neuromuscular blockade, and how to measure the blockade during surgery. By understanding the fundamental general principles involved in the neuromuscular system and how it relates to anesthesia, it will better prepare anesthesia technicians to foresee what will be asked of them during many surgical procedures.
REVIEW QUESTIONS 1. Which of the following is the CORRECT order of events for muscle contractions? A) The motor cortex of the brain sends a message → Action potential sent down the axon → ACh attaches to the nicotinic ACh receptors on the motor end plate. B) ACh from the axon terminal goes to the synaptic cleft → Action potential sent down the axon → muscle contraction. C) ACh attaches to the nicotinic ACh receptors on the motor end plate → Action potential sent down the axon → muscle contraction. D) The motor cortex of the brain sends a message → ACh attaches to the nicotinic ACh receptors on the motor end plate → Action potential reaches the presynaptic terminal. E) None of the above.
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Chapter 16 • Neuromuscular Anatomy and Physiology Answer: A. The correct order of events is as follows: The motor cortex of the brain sends a message → Action potential sent down the axon → Action potential reaches the presynaptic terminal → ACh attaches to the nicotinic ACh receptors on the motor end plate→ muscle contraction.
2. If a patient were to have a stroke on the right side of the motor cortex, which area of the body would be affected and what would be the resulting symptoms? A) Right side of the body, lower motor neuron signs B) Right side of the body, upper motor neuron signs C) Left side of the body, upper motor neuron signs D) Left side of the body, lower motor neuron signs E) None of the above Answer: C. Due to crossover of nerve fibers, the motor cortex of the brain affects the opposite (contralateral) side of the body. Therefore, a stroke in the right motor cortex will affect the left side of the body. Upper motor neurons are in the brain. Lower motor neurons are in the nerves that leave the spinal cord.
3. What are the two basic ways to block neuromuscular transmission at the neuromuscular junction? A) Presynaptically block receptor release; postsynaptically block ACh nicotinic receptors on the muscle end plate B) Presynaptically block ACh release; postsynaptically block ACh muscarinic receptors on the muscle end plate C) Presynaptically block ACh release; postsynaptically block ACh nicotinic receptors on the muscle end plate D) All of the above E) None of the above Answer: C. The presynaptic neuron releases ACh as the neurotransmitter, which then binds to nicotinic ACh receptors on the motor end plate of the muscle. Muscarinic ACh receptors are present in other parts of the body. Receptors are not released; they are present on cell membranes.
4. Which of the following statements are FALSE regarding nondepolarizing agents? A) Examples of nondepolarizing agents include rocuronium, vecuronium, pancuronium, and atracurium. B) Nondepolarizing NMJ blockers are also called competitive blockers and are most commonly used in the operating room. C) Nondepolarizing agents are shorter acting and have a faster onset than depolarizing agents.
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D) Nondepolarizing agents can be reversed with anticholinesterases. E) All of the above are TRUE. Answer: E. All of the above statements are true regarding nondepolarizing neuromuscular blockers. These agents are competitive antagonists for the ACh receptor on the motor end plate. To reverse the effects of these agents, the administration of an anticholinesterase will prevent the breakdown of ACh and allow it to outcompete the nondepolarizing agent for the ACh receptor. The agent with the fastest onset and shortest duration of action is succinylcholine, which is a depolarizing agent.
5. Which of the following statement is TRUE when monitoring neuromuscular blockade on a twitch monitor? A) Nondepolarizing agents are monitored by placing the twitch monitor on the facial nerve only, while depolarizing agents are monitored by placing the twitch monitor on the ulnar nerve only. B) Nondepolarizing agents demonstrate a response called “fade” where the twitch response decreases with repetitive nerve stimulation. C) Depolarizing agents always cause “fade.” D) Neuromuscular blockade caused by nondepolarizing agents cannot be monitored with a nerve stimulator E) None of the above. Answer: B. Nondepolarizing agents cause the muscle response (twitch) to a stimulus applied to a nerve innervating the muscle to “fade.” The twitch strength will decrease with repetitive stimuli. This is a major method of monitoring the intensity of neuromuscular blockade caused by nondepolarizing agents. The nerve stimulator may be placed over a variety of nerves including the ulnar and facial nerves. Depolarizing agents, in most cases, do not cause “fade.”
SUGGESTED READINGS Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009. Chandler JT, Brown LE. Conditioning for Strength and Human Performance. Philadelphia, PA: Lippincott Williams & Wilkins; 2007. Fuchs-Buder T. Neuromuscular Monitoring in Clinical Practice and Research. Heidelberg: Springer; 2010. Neal MJ. Medical Pharmacology at a Glance. 5th ed. West Sussex, UK: Wiley-Blackwell; 2005. Subramaniam R. A Primer of Anesthesia. New Delhi, India: Jaypee Brothers Publishers; 2008.
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SECTION
III
Principles of Anesthesia
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CHAPTER
17
Sedation Angela Kendrick and Dawn M. Larson ■ INTRODUCTION Intravenous (IV) anesthetics may be used for induction of general anesthesia, maintenance of general anesthesia, and sedation. Sedation typically involves an agent called a “sedative-hypnotic” and refers to a state of calm and relaxation, whereas hypnosis refers to sleep. A sedative is often combined with an analgesic, which is used to treat pain. The combination of the two agents can be very effective; however, it may also potentiate each medication more than if they were given independently. Sedation involves a continuum from minimal sedation leading to moderate and deep sedation and eventually to general anesthesia. The definition of these states of consciousness has been published by the American Society of Anesthesiologists (ASA). In addition, the ASA has published practice guidelines for those who may administer sedation and standard monitoring required during a sedation case. The term monitored anesthesia care (MAC) does not refer to the depth of anesthesia but rather a sedation or service that is provided by an anesthesiologist. The term is falling out of favor and is being replaced by the term depth of sedation, regardless of who provides the service. Sedation is useful in a variety of settings: the intensive care unit (ICU) sedation for mechanical ventilation, sedation for procedures or imaging, and as an adjunct to regional anesthesia in the operating room (OR).
■ DEFINITION OF THE DEPTH AND LEVELS OF SEDATION/ANALGESIA Minimal Sedation (Anxiolysis): Cognitive function may be impaired, but there is a normal response to verbal stimuli with unaffected airway, ventilation, or cardiovascular function. Moderate Sedation/Anesthesia (aka Conscious Sedation): Purposeful response to verbal or tactile stimuli with airway, ventilation, and
cardiovascular functions that are adequate and should require no intervention. Deep Sedation/Analgesia: Purposeful response only following repeated or painful stimulation where the airway and ventilation often need support and the cardiovascular function is usually maintained. Providers who perform deep sedation should be qualified to respond to a patient who enters a state of general anesthesia. General Anesthesia: Unresponsive even to painful stimuli where the airway and ventilation are generally inadequate without intervention and the cardiac function may need intervention (Table 17.1).
■ PREEVALUATION FOR SEDATION CASES A task force of the ASA on sedation guidelines recommends that the clinician performing the sedation performs an assessment of the patient prior to administration of sedation. This should include the patient’s medical history, vital signs, allergies, current medications, response to previous sedation, and history of substance abuse. Additionally, a focused physical examination including heart and lung auscultation and airway evaluation should be included. An explanation of the risks, benefits, and alternatives of the level of sedation required should be provided to patients or their legal guardian prior to the procedure. Patients undergoing sedation should be advised not to eat solids or drink liquids according to the ASA guidelines for perioperative fasting. In emergency situations, the risks and benefits of sedation on nonfasted individuals should be considered and discussed with the patient or guardian regarding the potential for pulmonary aspiration of gastric contents (Table 17.2).
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TABLE 17.1 AMERICAN SOCIETY OF ANESTHESIOLOGY DEPTH OF ANESTHESIA
DEFINITIONS MINIMAL SEDATION (ANXIOLYSIS)
MODERATE SEDATION/ ANALGESIA (CONSCIOUS SEDATION)
DEEP SEDATION/ ANALGESIA
GENERAL ANESTHESIA
Responsiveness
Normal response to verbal stimulation
Purposeful response to verbal or tactile stimulation
Purposeful response after repeated or painful stimulation
Unarousable, even with painful stimulus
Airway
Unaffected
No intervention required
Intervention may be required
Intervention often required
Spontaneous ventilation
Unaffected
Adequate
May be inadequate
Frequently inadequate
Cardiovascular function
Unaffected
Usually maintained
Usually maintained
May be impaired
Monitoring is recommended by the ASA according to the level of sedation. Data should be recorded prior to the start of sedation, during the procedure, and after completion (Table 17.3). The personnel performing the sedation should not be the person performing the procedure and should be present to administer medications and monitor the patient during the procedure. This person may help with minor tasks related to the procedure when the patient is stable; however, he or she may not perform these tasks during a deep sedation. Additionally, he or she should be knowledgeable of the pharmacology of both sedating and analgesic medications as well as the reversal agents for those medications. There should be a basic life support (BLS) certified health care provider in the room, with advanced cardiac life support (ACLS) personnel available within
5 minutes. The exception is the administration of deep sedation, which requires the presence of an ACLS certified provider in the room.
■ SEDATION SCALES Many sedation scales exist to help categorize the level of arousal during a procedure or within the ICU. They attempt to standardize the level of consciousness to facilitate communication between providers. Two of the more common scales are the Ramsay Scale, which was introduced over 30 years ago, and the Riker SedationAgitation Scale (SAS) (Tables 17.4 and 17.5).
■ SUPPORT EQUIPMENT Because sedation is a continuum and medications are used that can cause respiratory depression and hemodynamic compromise, rescue equipment should be readily available (Table 17.6).
■ SEDATION AGENTS Propofol TABLE 17.2 AMERICAN SOCIETY
OF ANESTHESIOLOGY FASTING GUIDELINES INTAKE
MINIMUM FASTING PERIOD
Clear liquids
2h
Breast milk
4h
Nonhuman milk
6h
a
Light meal
6h
Heavy meal
8h
a
Light meal typically consists of clears and non–fat-based snack.
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Propofol is in the class of akylphenols and produces a state of anesthesia without analgesic (pain-relieving) properties. The mechanism of action is primarily by activation of γ-aminobutyric acid (GABA) receptors. It is lipid soluble and is prepared in an emulsion that consists of soybean oil, purified egg phosphatide, glycerol, and an inhibitor of antibacterial growth. It has a white milky appearance, is stable at room temperature, and once opened should be discarded after 6 hours to avoid bacterial contamination. It is also a potent antiemetic, even when used at dosing levels commonly used in sedation
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TABLE 17.3 SEDATION MONITORING – Pulse oximetry – Blood pressure and heart rate at 5-minute intervals – Electrocardiograph (EKG) for patients with cardiovascular disease and for all deep sedation procedures – Response to verbal commands if applicable – Adequacy of pulmonary ventilation (observation, auscultation) – Exhaled carbon dioxide monitoring when patients are at a distance from the sedation provider and for all deep sedation procedures (via nasal canula port or an angiocath inserted into a face mask)
dosing. Propofol may cause respiratory depression at therapeutic doses and a dose-dependent decrease in arterial blood pressure. Sedation dosing at 25-75 μg/kg/min is typically sufficient, although there is variability among patients. Metabolism occurs via the liver; however, other sites in the body may play a role as well. Propofol has a rapid onset and a short elimination half-life of 2-8 minutes, which is a desirable feature for sedation procedures. Because of propofol’s alternative use as an induction agent and its ability to continue into the level of general anesthesia, its use should follow guidelines for deep sedation regardless of the actual level of sedation planned.
Barbiturates Barbiturates are among the oldest IV anesthetics. They are still in use today but have been often supplanted by newer anesthetics. Barbiturates are hypnotics and do not possess analgesic properties. Their mechanism of action is mediated primarily on the neurotransmitter GABA; however, it is likely there are other neurotransmitters involved. They exist as sodium salts and are reconstituted for IV usage in sterile water or 0.9% sodium chloride solutions. As a basic solution,
TABLE 17.4 RAMSAY SCALE SCALE
DESCRIPTION
1
Anxious or restless or both
2
Cooperative, orientated, and tranquil
3
Responding to commands
4
Brisk response to stimulus
5
Sluggish response to stimulus
6
No response to stimulus
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this will precipitate when used with lactated Ringer’s solution or acidic medications such as pancuronium, rocuronium, alfentanil, sufentanil, or midazolam. The two classes of barbiturates are oxybarbiturates and thiobarbiturates, with the most commonly used being methohexital and thiopental, respectively. Thiopental was introduced into clinical practice in 1934. A sedation dose of thiopental is 50-100 mg IV. The onset of both medications is quick at 10-30 seconds, with the elimination half-life of 4 hours for methohexital and 12 hours for thiopental. Methohexital is commonly used in electroconvulsive therapy treatment for depression. Side effects include dose-dependent respiratory depression and hypotension. Metabolism for both classes is via the liver.
Benzodiazepines In addition to properties of sedation and hypnosis, all benzodiazepines have anticonvulsant activity. The mechanism of action for this group is mediated through activation of the GABA receptor. Of the many types of benzodiazepines, there are several that are more frequently encountered for sedation. The most widely used benzodiazepine in anesthesia practice is midazolam (Versed), which can be administered intravenously or orally (per os [PO]). It has a slower onset and metabolism than propofol but faster than other benzodiazepines, which makes it a desirable sedation medication. A typical IV sedation dose is 0.015-0.03 mg/kg in increments to achieve desired sedation. Lorazepam (Ativan) is an oral or IV medication and may be used frequently when only minor anxiolysis is required from an oral medication. Diazepam (Valium) is infrequently used because of its long halflife. Side effects of all benzodiazepines include dose-dependent respiratory depression and,
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TABLE 17.5 RIKER SEDATION-AGITATION SCALE SCORE
TERM
DESCRIPTION
+4
Combative
Overtly combative or violent; immediate danger to staff
+3
Very agitated
Pulls on or removes tube(s) or catheter(s) or has aggressive behavior toward staff
+2
Agitated
Frequent nonpurposeful movement or patient-ventilator dyssynchrony
+1
Restless
Anxious or apprehensive but movements not aggressive or vigorous
0
Alert and calm
−1
Drowsy
Not fully alert, but has sustained (>10 s) awakening, with eye contact, to voice
−2
Light sedation
Briefly ( 30 degrees) may also stretch the nerve.
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6. Which is the most common cause of perioperative peroneal neuropathy in a patient who is positioned in a lithotomy position? A) Compression of the nerve by a leg holder as the nerve wraps around the fibular head B) Hyperextension of the knee and ankle simultaneously C) Prolonged dorsiflexion of the foot in a leg holder D) Excessive hip flexion when the lower extremity is placed in a leg holder Answer: A. Leg holders should be padded to avoid direct pressure on the upper lateral leg when the peroneal nerve wraps around the fibular head. Peroneal neuropathies typically result in significant motor dysfunction, resulting in foot drop and difficulty with walking or running.
7. Which is the primary reason to pad peripheral nerves when positioning patients? A) The pad improves blood flow. B) The pad limits stretch of the nerve. C) The pad increases strain on the nerve. D) The pad distributes point pressure. Answer: D. Padding typically is used to distribute and disperse point pressure from hard surfaces. This dispersion of pressure reduces the risk of compressive injury to peripheral nerves. There are no studies that indicate any specific type of padding (e.g., gel, form, or other padding materials) to be any better than the others. The key is to distribute point pressure broadly or avoid pressure on a peripheral nerve entirely.
SUGGESTED READINGS American Society of Anesthesiologists Task Force on the Prevention of Perioperative Neuropathies. Practice guidelines for the prevention of perioperative neuropathies. Anesthesiology. 2000;92:1168–1182. Contreras MG, Warner MA, Charboneau WJ, et al. Anatomy of the ulnar nerve at the elbow: potential relationship of acute ulnar neuropathy to gender differences. Clin Anat. 1998;11(6):372–378. Litwiller JP, Wells RE, Halliwill JR, et al. Effect of lithotomy positions on strain of the obturator and lateral femoral cutaneous nerves. Clin Anat. 2004;17:45–49. Staff NP, Engelstad J, Klein CJ, et al. Post-surgical inflammatory neuropathy. Brain. 2010;133:2866–2880. Warner MA. Patient positioning and related injuries. In: Barash PG, et al, eds. Clinical Anesthesia. 6th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2009:793–814. Warner MA, Warner DO, Matsumoto JY, et al. Ulnar neuropathy in surgical patients. Anesthesiology. 1999;90:54–59.
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CHAPTER
20
Overview of a General Anesthetic Dalia Elmofty and Thomas Cutter ■ EARLY HISTORY OF ANESTHESIA AGENTS An anesthetic involves the administration of various intravenous and inhalational agents to produce a state in which a patient may safely and comfortably undergo a procedure. While the medical specialty of anesthesiology may be regarded as modern and “cutting edge,” many of the current medications have existed for centuries. The first known narcotic, opium, was found in a poppy plant, called the “joy plant” by the Sumerians, as far back as 3400 BC. In 1300 BC, the ancient Egyptians wrote about opium’s painrelieving or analgesic properties. In 40 AD, the Greek physician Pedanius Dioscordes noted the effects of the plant Atropa mandragora, when it was used in combination with alcohol prior to surgery, and coined the term “anesthesia” to describe its effect. In 1803, Friedrich Wilhelm Serturner of Germany extracted the active ingredient from opium and named it morphine, after Morpheus, the Greek god of dreams. The first inhalational anesthetic was described in 1800 by Sir Humphrey Davy as he personally experimented with nitrous oxide (“laughing gas”); he described it as producing a feeling of “well-being.” In 1818, Michael Faraday discovered that the volatile inhalational anesthetic ether could cause unconsciousness. In 1842, Crawford W. Long demonstrated ether’s effects on his colleagues during medical gatherings known as “ether frolics.” A dentist, William T. G. Morton, is credited with the use of the first inhalational anesthetic in a public demonstration at the Boston Massachusetts General Hospital in 1846 during a tooth extraction. The concept quickly spread and surgery flourished with the use of the new agents that could alleviate the pain and suffering of a surgical procedure (Figs. 20.1 and 20.2).
In Europe, chloroform was the preferred inhalational anesthetic. It was first described by Sir James Young Simpson, a Scottish obstetrician who administered it for labor pain. Dr. John Snow was recognized as the first professional anesthesiologist in England, when he provided a chloroform anesthetic to Queen Victoria during the birth of her children in 1853 and 1857. Intravenous anesthesia using sedative/hypnotic medications was not possible until the syringe and hypodermic needle were invented by Alexander Wood of Edinburgh in 1855. Barbituric acid, the source of the barbiturate sodium pentothal, was discovered in 1864 by Adolph von Baeyer, but it was another six decades before the first short-acting intravenous barbiturate was used to induce unconsciousness by the German obstetrician Rudolph Bumm in 1927. Barbiturates have been largely replaced by propofol, which was introduced in the 1980s. Benzodiazepines, which at low doses relieve anxiety but at higher doses may cause unconsciousness, have been available since 1960. Midazolam, the most commonly used benzodiazepine in anesthetic medicine, has been available for over 20 years. Curare was the first documented muscle relaxant, when, in 1800, Alexander von Humboldt wrote about a toxin from native plants by the Orinoco River that caused paralysis. It was not until the 1940s that curare was introduced into anesthesia as a muscle relaxant for surgery. Succinylcholine was introduced later by Bovet in 1949. The local anesthetic cocaine is derived from the leaves of the coca plant and has been used by Peruvians for centuries as a stimulant. It was isolated in 1860 and first used as a local anesthetic by Carl Koller in 1884. 175
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■ FIGURE 20.1 Morton’s ether inhaler (1846) consisted of a glass bulb, an ether-soaked sponge, and a spout to be placed in patient’s mouth. (From Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. Philadelphia, PA: Lippincott Williams & Wilkins; 2009, with permission.)
Inhalational gases, narcotics, local anesthetics, sedative hypnotics, and muscle relaxants are among the most commonly administered medications during anesthesia.
■ FOUR GOALS OF AN ANESTHETIC The four goals of an anesthetic are to provide a lack of awareness or amnesia, pain relief, immobility, and patient safety. Ideally, medications should have a fast onset, a predictable duration of action, and no side effects. Because no single medication can accomplish these four goals, an anesthesiologist often administers a “balanced anesthetic” with a small amount of a number of different drugs, thereby maximizing
■ FIGURE 20.2 Southworth and Hawes (1846) “Early operation using ether anesthesia.” The first public demonstration of inhalational anesthesia used during a tooth extraction by William T. G. Morton at Boston Massachusetts General Hospital. (Reproduced with permission from The J. Paul Getty Museum.)
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a drug’s positive effects while minimizing its side effects. The safe use of any anesthetic medication requires a thorough understanding of the drug’s pharmacology. Pharmacology can be divided into two parts: pharmacokinetics and pharmacodynamics (see Chapter 5). Pharmacodynamics is what the drug does to the body through interactions with receptors, cell membranes, enzymes and other proteins, and ion channels. The drug may either increase activity (agonist) or inhibit activity (antagonist). Pharmacokinetics is what the body does to the drug and includes the medication’s release from its formulation (liberation), its entry into the blood circulation (absorption), its spread through the fluids and tissues (redistribution), its breakdown (metabolism), and its elimination from the body (excretion).
Lack of Awareness Lack of awareness is on a continuum, ranging from fully awake to moderate sedation to deep sedation to unconsciousness/general anesthesia (GA) (Fig. 20.3). The effects of various anesthetic agents on consciousness have been studied using the electroencephalogram (EEG), an instrument that measures electrical brain activity. Modified EEGs such as the BIS monitor are also occasionally used in the operating room to measure brain activity as an estimate of the depth of anesthesia. Total unconsciousness is associated with a marked decrease in EEG activity. Other techniques to measure brain activity include positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). By definition, a general anesthetic results in total unconsciousness, while other anesthetic techniques may result in only sedation or no reduction in consciousness at all. For example, a spinal anesthetic for a woman undergoing a cesarean section may not include any drugs to diminish awareness because of the concern for their effects on the baby. Medications that can cause unconsciousness include both inhalational gases and injectable medications. Inhalational Gases Nitrous oxide is a relatively weak inhalational anesthetic and does not typically produce total unconsciousness; thus, it is never used alone in a general anesthetic but instead supplements other medications. It works through both ion channel
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■ FIGURE 20.3 Excerpted from Continuum of Depth of Sedation: Definition of General Anesthesia and Levels of Sedation/ Analgesia (Approved by the ASA House of Delegates on October 27, 2004, and amended on October 21, 2009) of the American Society of Anesthesiologists. A copy of the full text can be obtained from ASA, 520 N. Northwest Highway, Park Ridge, IL 60068-2573.
and receptor activity and has a relatively benign side effect profile. Sevoflurane, desflurane, and isoflurane are common volatile inhalational agents and can be used as the sole agent for a general anesthetic. The exact mechanisms by which these volatile inhalational agents work are not entirely understood, but several theories have been proposed. On a molecular level, Meyer and Overton suggested that anesthetics work at the lipid portion of the nerve cell membrane. Later, Franks and
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Lieb determined that the site of action is at the protein layer of the cell membrane. The main receptor involved is the γ-aminobutyric acid (GABA) receptor, which is an inhibitory receptor. It is thought that certain anesthetic agents increase the inhibitory action of this receptor, thereby decreasing nerve cell activity and consciousness. Volatile inhalational anesthetics must be vaporized from the liquid state and are administered from agent-specific vaporizers. A carrier gas
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(e.g., oxygen) passes through the vaporizer and takes up the inhalational agent, just as a breeze will carry steam. The agent will then be carried to the patient through the breathing circuit to enter the lungs. Once in the lungs, it diffuses into the bloodstream where it is carried to the brain and elsewhere throughout the body. The inhalational agent’s speed of onset is inversely proportional to its solubility, which is indicated by the blood/ gas coefficient (Table 20.1). The minimum alveolar concentration (MAC) is the concentration of the inhalational agent in the lungs that prevents movement in 50% of patients undergoing a surgical stimulus (e.g., being cut by a scalpel). Inhaled anesthetics are mainly eliminated from the body by exhalation, although there is some metabolism in the liver and excretion in the urine and through the skin. As with all medications, gases have side effects. In the brain, they increase cerebral blood flow and intracranial pressure while decreasing cerebral metabolic oxygen consumption. Their effect on the ventilatory system (airway and lungs) is to depress respiration and bronchodilate. The pungent nature of desflurane can cause airway irritation. They also can decrease systemic vascular resistance and the heart’s contractility, thereby lowering blood pressure (hypotension). Isoflurane and desflurane can cause increased heart rate, which can cause ischemia (inadequate blood flow) in a patient with coronary artery disease. Injectable Medications Common intravenous sedative hypnotic agents that produce unconsciousness include propofol, etomidate, benzodiazepines (e.g., midazolam), and barbiturates (e.g., sodium pentothal) (Table 20.2). These work by depressing the
reticular activating system, an area in the brain responsible for regulating arousal/wakefulness, and by increasing GABA action, inducing a loss of consciousness. Ketamine is an N-methyl D-aspartate (NMDA) antagonist that induces a state known as “dissociative anesthesia.” All of these agents are typically injected intravenously, although some can be injected intramuscularly or absorbed through moist surfaces (mucosa) such as those found in the nasal passages, the rectum, and the mouth. Their high lipid solubility in the brain results in a rapid onset of action. In many cases, their duration of action is primarily determined by redistribution (dilution) throughout the body rather than by metabolism or excretion. Thus, they accumulate when large doses are given and are more often used to start (induce) a general anesthetic than to maintain it. Propofol’s side effects include pain at the site of injection, so it is often preceded by or administered along with the local anesthetic lidocaine. It also produces a dose-dependent hypotension as a result of decreasing the heart’s contractility and lowering the systemic vascular resistance and causes significant ventilatory depression (i.e., the patient can stop breathing). Sodium pentothal’s clinical profile is similar to propofol’s, but it does not hurt when injected and it does not lower the blood pressure quite as much. Its disadvantage is that its sedating effects persist longer than those of propofol. Etomidate causes less hypotension than either propofol or sodium pentothal, but it can suppress hormone (steroid) production and is relatively expensive. Midazolam is noted to have less adverse cardiovascular and ventilatory effects than any of the preceding drugs, but the doses required to cause unconsciousness require a long time to wear off. Ketamine also maintains hemodynamic and
TABLE 20.1 BLOOD/GAS COEFFICIENT, MAC, AND SIDE EFFECTS OF INHALATIONAL
AGENTS INHALATIONAL AGENT
BLOOD/GAS COEFFICIENT
MAC (%)
SIDE EFFECTS HEART RATE
BLOOD PRESSURE
Desflurane
0.42
6.6
0-↑
↓
Sevoflurane
0.65
1.8
0
↓
Isoflurane
1.46
1.17
↑
↓
MAC, minimal alveolar concentration; ↓, decrease; ↑, increase; 0, no change. Adapted from Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:420.
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TABLE 20.2 COMMONLY USED INTRAVENOUS ANESTHETIC AGENTS INTRAVENOUS ANESTHETIC AGENT
DOSE (mg/kg)
Propofol
1–2
ONSET (s)
DURATION (min)
SIDE EFFECTS HEART RATE
BLOOD PRESSURE
15–45
5–10
0-↓
↓
Thiopental
3–6
100 beats/min)
Markedly increased (>120 beats/min)
Mental status
Awake, alert
Lethargic
Obtunded
Mucous membranes
Dry
Very dry
Parched
Urinary output
Mildly decreased
Decreased
Markedly decreased
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There are several laboratory measurements that aid in determining a patient’s fluid status. These include the hematocrit, serum sodium, creatinine, and blood urea nitrogen (BUN) levels. Serial arterial blood gases provide information regarding how well tissues are being perfused by circulating oxygen in the blood (as measured by the arterial pH, the arterial oxygen pressure [PaO2], and the base deficit). The urine can also be examined by assessing the urinary-specific gravity, urine sodium, and urine chloride concentrations. Visual inspection of the urine can also help the anesthesiologist determine how “dry” the patient is, with a low volume and dark color suggesting highly concentrated urine and a dehydrated patient. Invasive hemodynamic monitoring via a central venous pressure (CVP) catheter or a pulmonary arterial catheter may also assist in assessing intravascular volume status, but both entail the risks associated with cannulation. A central venous catheter is often placed into a large vein in the neck (internal jugular vein), chest (subclavian vein), or groin (femoral vein) when rapid infusion of fluid or blood is required, vasoactive or irritating medications are infused, or if invasive hemodynamic monitoring is indicated. CVP is measured from the tip of a central venous catheter that is properly placed at the junction of the superior vena cava and the right atrium. Theoretically, CVP measurements provide information regarding the volume of blood entering the heart. CVP monitoring must be assessed in conjunction with clinical signs. Normal values range from 5 to 12 mm Hg, but trends may be more useful than single measurements. A pulmonary arterial pressure catheter can be placed through central venous access, into the pulmonary artery, to assess volume status when the patient has right-heart dysfunction or to better assess pulmonary arterial pressures. Clinical correlation between data from pulmonary arterial catheterization and other diagnostic data is critical. Recently, transthoracic echocardiography and transesophageal echocardiography (TEE) have become useful tools in evaluating volume
status. A skilled clinician can assess the filling, emptying, and contractile function of the heart, in real time, with the use of these devices. During surgery, ongoing losses of fluid and blood must be monitored. The anesthesiologist must estimate the blood loss in the surgical field, even in cases in which little blood loss is anticipated. One can measure the blood that has collected in the surgical suction container (taking into account the amount of irrigating solution that has been added to the field by the surgeons), assess the number of laparotomy pads and sponges, along with the blood accumulated on them, and visually inspect the field regularly to detect bleeding into the wound or under the surgical drapes. Following serial hemoglobin and hematocrit levels is also helpful. The clinical signs mentioned previously (increased heart rate, decreased blood pressure, decreased urine output, etc.) are late signs of hypovolemia. By closely monitoring the blood loss throughout the procedure, one is able to continually replace the lost fluid, rather than “get behind” and expose a patient to the risks of insufficient fluid administration.
■ SUMMARY Surgical patients require intravenous access so that drugs can be administered promptly and necessary fluids can be infused. Fluid infusion should be regarded with the same seriousness as drug administration. Inadequate or excessive fluid administration is associated with complications, some of which are life threatening. During surgery, most anesthesiologists use crystalloid solutions, supplemented as necessary by colloids, which are more effective at maintaining plasma volume. Ongoing research is rapidly defining appropriate targets regarding fluid administration for specific types of surgery. Ultimately, fluid therapy can be personalized based on the characteristics of a patient and the type of surgery. Although considerable information is available to assist in monitoring the need of an individual patient for fluids, no single piece of information is sufficient—vigilance and close monitoring are always required.
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Chapter 22 • Fluid Therapy
REVIEW QUESTIONS 1. A 90-kg-male is scheduled for an inguinal hernia repair at 7 a.m. He has not had any food or water since dinner the night before (7 p.m.). What is his water deficit? A) 1,560 mL B) 850 mL C) 1,750 mL D) 550 mL E) 2,750 mL Answer: A. Using the 4:2:1 rule, this patient would have a deficit of 40 mL/hr for the first 10 kg, 20 mL/hr for the next 10 kg, and 70 mL/hr for the next 70 kg. This would total to 130 mL/hr multiplied by 12 hours, which equals 1,560 mL.
2. Which of the following physical exam findings suggests dehydration? A) Excessive sweating B) Clammy, moist hands C) Heart rate of 65 beats/min D) Blood pressure of 135/85 mm Hg E) Heart rate of 125 beats/min Answer: E. Tachycardia (fast heart rate) is a sign of dehydration as well as low blood pressure. In addition, patients who are dehydrated do not produce sweat.
3. If administering a citrated blood product, it is best to use lactated Ringer’s solution as a carrier. A) True B) False Answer: B. Lactated Ringer’s solution contains calcium, which can combine with the anticoagulant citrate used in blood products. This may cause the blood products to form clots.
4. Which of the following is NOT a means to assess ongoing blood loss intraoperatively? A) Monitoring suction canisters B) Periodically weighing the patient C) Counting soiled laparotomy pads D) Checking the hematocrit level E) All of the above Answer: B. It would be impractical to weigh the patient during surgery. In addition, changes in patient weight would be affected by fluid losses as well as blood losses (e.g., evaporative losses). Monitoring suction canisters and blood-soaked laparotomy pads is important to follow blood loss during surgery. Serial hematocrits are also useful to monitor blood loss.
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5. Which of the following statements are TRUE? A) Colloid solutions contain large-molecular-weight proteins or sugars. B) Lactated Ringer’s solution contains potassium. C) CVP can be used to monitor fluid status. D) Urine output can be used to monitor fluid status. E) All of the above. Answer: E. All of the above statements are true. The largemolecular-weight proteins and sugars in colloid solutions cause them to stay in the intravascular space longer than crystalloids. Lactated Ringer’s solution contains sodium, potassium, chloride, calcium, and lactate. Both CVP and urine output are commonly used to assess the volume status of a patient. Dehydrated patients do not make as much urine as they would normally.
SUGGESTED READINGS Boldt J, Mengistu A. Balanced hydroxyethyl starch preparations: are they all the same? In-vitro thrombelastometry and whole blood aggregometry. Eur J Anaesthesiol. 2009;26:1020–1025. Brandstrup B, Tonnesen H, Beier-Holgersen R, et al. Effects of intravenous fluid restriction on postoperative complications: comparison of two perioperative fluid regimens— a randomized assessor-blinded multicenter trial. Ann Surg. 2003;238:641–648. Finfer S, Bellomo R, Boyce N, et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004;350:2247–2256. Holte K, Klarskov B, Christensen DS, et al. Liberal versus restrictive fluid administration to improve recovery after laparoscopic cholecystectomy: a randomized, doubleblind study. Ann Surg. 2004;240:892–899. Magner JJ, McCaul C, Carton E, et al. Effect of intraoperative intravenous crystalloid infusion on postoperative nausea and vomiting after gynaecological laparoscopy: comparison of 30 and 10 ml kg−1. Br J Anaesth. 2004;93:381–385. Maharaj CH, Kallam SR, Malik A, et al. Preoperative intravenous fluid therapy decreases postoperative nausea and pain in high risk patients. Anesth Analg. 2005;100: 675–682. Nisanevich V, Felsenstein I, Almogy G, et al. Effect of intraoperative fluid management on outcome after intraabdominal surgery. Anesthesiology. 2005;103:25–32. O’Malley CM, Frumento RJ, Hardy MA, et al. A randomized, double-blind comparison of lactated Ringer’s solution and 0.9% NaCl during renal transplantation. Anesth Analg. 2005;100:1518–1524, table. Yogendran S, Asokumar B, Cheng DC, et al. A prospective randomized double-blinded study of the effect of intravenous fluid therapy on adverse outcomes on outpatient surgery. Anesth Analg. 1995;80:682–686.
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CHAPTER
23
Transfusion Medicine Curtis Bergquist and Kamila Vagnerova ■ INTRODUCTION Transfusion of blood products is a common occurrence during surgery. Anesthesia technicians may be called upon to retrieve blood products, help check them in, and help administer them. Transfusion of incompatible blood products to a patient can cause serious patient injury, and anesthesia technicians should be familiar with basic transfusion medicine. This chapter provides an introduction to the different types of blood products, what makes them compatible or incompatible with a patient, how they should be administered, and the potential complications or adverse reactions from the transfusion of blood products.
■ BLOOD TYPES The different blood types (blood groups) and their relationship to the immune system is the basis of transfusion science. Blood types are inherited and represent contributions from both parents. A total of 30 human blood group systems are now recognized by the International Society of Blood Transfusion (ISBT). A blood type is a classification of blood based on the presence or absence of inherited antigenic substances on the surface of red blood cells (RBCs). Antigens, which may be proteins, carbohydrates, glycoproteins, or glycolipids, are present on the cellular membrane of RBCs and are also secreted to plasma and body fluids. Antigens determine the blood group type. In 1900, Karl Landsteiner discovered the ABO blood groups for which he received the 1930 Nobel Prize in Medicine and Physiology. The ABO antigen system is the most important determinant of blood type grouping in transfusion medicine. The two major RBC antigens are known as A and B. The blood groups are A, B, AB, and O, where O is when the RBCs lack both A and B antigens. People with AB blood type have RBCs that have both antigens. People
with RBCs that only have the A or B antigen are blood type A and B, respectively. ABO compatibility remains the major safety consideration of blood product transfusions (Table 23.1). Compatibility means that the recipient does not recognize the blood transfusion as foreign. Immune systems of virtually all individuals produce antibodies directed against antigens they do not have (anti-B antibodies in type A individuals, anti-A antibodies in type B individuals, and anti-A and anti-B antibodies in type O individuals). The process whereby foreign antigens from blood groups cause production of antibodies directed against them in the recipient is called alloimmunization. This concept is extremely important to the understanding of transfusion medicine. If a patient receives blood (recipient) that has antigens that are foreign to the recipient, the recipient can mount a massive immune reaction (allergic reaction) against the foreign blood. These reactions are particularly severe if the recipient has preformed antibodies (a primed immune system) against the foreign antigen. This type of reaction is akin to an anaphylactic reaction except that the foreign antigen is the transfused blood. Humans form antibodies to A or B antigens in the first years of life if they do not have them on their own RBCs. This is thought to be from exposure to environmental antigens (food, bacteria, virus, etc.). Thus, humans are usually “primed” against ABO-incompatible blood. A reaction to ABO-incompatible blood is called an acute hemolytic transfusion reaction and is fatal in about 10% of cases. The recipient may not only manifest symptoms of an anaphylactic reaction (low blood pressure, fever, bronchospasm) from the immune mediators released but also suffer because his or her immune system attacks the foreign blood cells, causing them to hemolyze (rupture) and release free hemoglobin into the
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Chapter 23 • Transfusion Medicine TABLE 23.1. ABO COMPATIBILITY
CHART ABO COMPATIBILITY
Recipient
DONOR A
B
O
AB
A
Yes
No
Yes
No
B
No
Yes
Yes
No
O
No
No
Yes
No
AB
Yes
Yes
Yes
Yes
bloodstream. Free hemoglobin is a large protein and is very toxic to the kidney. It is not surprising that many of the first recipients of blood transfusions, before there was an understanding of blood group antigens, died from a severe transfusion reaction. Other types of transfusion reactions will be discussed below. The primary cause of transfusing ABO-incompatible units (incorrect blood type) is clerical errors in patient identification or errors in sample labeling. The second most important blood group system is the Rhesus (Rh) system. Rh positivity is indicated by the presence of D antigen in the membrane of the RBC; D antigen is absent in Rh (D)-negative individuals. About 15% of people are Rh (D)-negative. Unlike anti-A or anti-B antibodies, Rh (D)-negative individuals do not produce anti-Rh (D) antibodies until they are exposed to Rh (D)-positive blood. When an Rh (D)-negative individual is exposed to Rh (D)-positive cells, sensitization occurs and the immune system can produce anti-D alloantibody. Any subsequent exposure to Rh (D)-positive blood can result in a severe adverse reaction. Sensitization can occur by transfusion or during pregnancy. If an Rh (D)-negative mother is pregnant with an Rh (D)-positive baby (the baby inherited the Rh (D) antigen from the father), the mother will become sensitized to the Rh (D) antigen. This happens because there can be some mixing of the baby’s blood with the mother’s blood at delivery. Once a mother is sensitized to the Rh (D) antigen, she can form antibodies that can attack the blood of a subsequent fetus if the fetus is Rh (D)-positive. Even in emergencies, Rh (D)-positive blood should not be given to Rh (D)-negative patients to avoid sensitization. Typically, type-O Rh (D)-negative blood (O neg) is stored by hospitals for emergency transfusion
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because of its near-universal safety for patients with untyped blood due to its lack of AB or Rh (D) antigens. Several other blood group systems exist in addition to the ABO and Rh (D) systems: Lewis, I system, P system, MNSsU system, Kell Protein, and the Duffy and Kidd antigens. These antigens can be present on RBCs and result in incompatibility, but these are not necessarily tested for in every patient because they are either extremely rare, extremely common, or compatibility can be ensured by providing warmed blood (above 30°C). Patients who have received multiple transfusions over the course of their life are at higher risk of developing antibodies, and it may be more difficult to find a compatible unit. Procuring a compatible unit can take extra time and may result in a surgical delay.
■ COMPATIBILITY TESTING Before any RBC unit is given to a patient, it undergoes several different tests to ensure that it is compatible with the recipient. The tests are separate from the testing done for diseases such as hepatitis and human immunodeficiency virus (HIV). Screening of potential donors and rigorous testing of donated units have largely eliminated the risk of units containing HIV, hepatitis, and other infections. The first test, known as the type and screen, is done on donated blood before releasing the unit. This test determines the blood type—A, B, AB, O, and Rh (D)-positive/negative. This testing is also done on the patients to determine their blood type as well as screen for the presence of antibodies to A or B and antibodies against other antigens known to cause hemolytic reactions. The test is performed by mixing the sample blood (the patient’s blood or the donated blood) with a solution containing antibodies against the antigen being screened. For example, if one wants to determine if a patient has A antigen on his or her RBCs (he or she is blood type A or AB), a blood sample from him or her is mixed with a solution containing anti-A antibodies. If the resulting mixture agglutinates (clumps), it is because the antibodies have bound to cells with the A antigen. A second phase of the test involves mixing the patient’s plasma with commercially available O-negative RBCs that have approximately 20 different antigens that can cause a hemolytic reaction. If the patient’s plasma does not agglutinate these cells, the screen is negative.
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If the patient’s plasma does react to the cells, the patient possesses at least one antibody to a significant antigen and the screen is positive. If the screen is positive, further testing must be done to identify the antibody and to locate blood units that lack the antigen. The second test, the crossmatch, checks the patient’s blood against a specific donor unit for errors in ABO type. If the screen portion of the type and screen test was negative, the crossmatch consists of matching the patient with compatible donor blood. No real “test” is performed. The crossmatch involves matching the paperwork for the donor unit and the recipient. This step can even be performed by automated vending style machines that scan barcodes from the patient ID and the donor unit. If the patient’s screen was positive, a serologic crossmatch test is performed. This test is conducted by mixing the patient’s serum with a specific donor unit that has been selected because it lacks the antigens that the patient has antibodies against identified during the screen. A crossmatch is only necessary when the patient receives RBCs, as opposed to plasma or other blood derivatives. Compatibility of plasma is different from that of whole blood or RBCs. Plasma from an AB blood type donor can be transfused to a recipient of any blood group. This is because the AB donor plasma lacks A or B antibodies and will not react with the recipient’s RBCs even if he or she has the A or B antigen. Type O recipients already have A and B antibodies and can receive plasma from any blood type. The only problem is plasma from a type O donor. This donor has A and B antibodies in the plasma, and it cannot be given to a type A, B, or AB recipient. In emergency situations when RBC transfusion is immediately needed, abbreviated testing methods are necessary. Type-specific blood is always essential (unless the donor unit is O), but there are abridged versions of the crossmatch: Partial crossmatch checks for the most severe errors (ABO-Rh (D) blood type) and takes less than 10 minutes; uncrossmatched blood is less risky in previously untransfused patients and those who have not born children. The risk of complication from uncrossmatched blood varies between 1 in 1,000 to 1 in 100 patients depending on the history of previous exposure to donated blood. Trauma centers may also keep type O, Rh (D)-negative (“universal donor”) blood on hand for immediate use. Ideally, it should be
completely compatible, but it is always possible that there are anti-A or anti-B antibodies in the donor unit that could cause a reaction.
■ INDICATIONS FOR TRANSFUSION According to the list of guidelines provided by the American Society of Anesthesiologists in 2006, transfusion is rarely indicated when the hemoglobin concentration is greater than 10 g/dL and is almost always indicated when it is less than 6 g/dL, especially when the anemia is acute. However, the hemoglobin level should not be the sole consideration, as there are other patientrelated and surgical factors that help determine the “trigger” for transfusion. Patients can either receive his or her own previously donated blood (autologous blood) or someone else’s donated blood (allogenic, homologous blood). Autologous blood, which needs to be donated ahead of time, is considered safer than allogenic blood mainly due to lower risk of infection and is preferred over allogenic transfusion. However, there are complications related to autologous transfusion like anemia from the donation itself, the need for more frequent transfusions, and even febrile and allergic reactions. Autologous units are typed and crossmatched just as all allogenic units are.
■ COMPLICATIONS AND ADVERSE REACTIONS There are a variety of adverse reactions that come from a few basic sources: contaminated or infected blood (e.g., HIV or hepatitis), incompatible blood, and problems related to the infusion of RBCs (e.g., transfusion-related lung injury, volume overload, electrolyte disturbances, and coagulopathy). Table 23.2 summarizes some of the possible complications of transfusions. As soon as an acute adverse reaction to a transfusion is suspected, the first step is to stop the transfusion and call the blood bank. The three most common causes of transfusion-related deaths are hemolytic transfusion reactions, septic transfusions, and transfusion-related lung injury. Acute hemolytic transfusion reaction is caused by type incompatible blood, typically due to human error at some point between issuing the unit and transfusion. The body mounts an immune response to the offending blood, which can lead to severe coagulation issues, kidney failure, and even death.
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TABLE 23.2. OTHER ADVERSE REACTIONS Immune-mediated reactions Delayed hemolytic transfusion reaction Febrile nonhemolytic transfusion reaction Allergic reaction Anaphylactic reaction Alloimmunization—sensitization to antigens present in transfusion Posttransfusion purpura—caused by platelets’ transfusion Transfusion-associated graft versus host disease—immunocompromised at greatest risk Transfusion-related acute lung injury—causes pulmonary edema Nonimmunologic reactions Hypothermia, fluid overload, electrolyte toxicity, iron overload, and others Infections Transfusion-associated viral infections: HIV type 1; Hepatitis B, C, and G virus; cytomegalovirus (CMV) and other viral and bacterial infections
Other complications are more common during a massive transfusion (loss of at least one times the patient’s blood volume): • Hypocalcemia: The citrate used to preserve blood can bind calcium in the patient, leading to hypocalcemia. This is more common when the units are transfused quickly (>1 unit in 5 minutes), it is a massive transfusion, or the patient has liver dysfunction and has difficulty in metabolizing citrate. Monitoring of blood calcium levels will guide treatment with calcium. • Coagulopathy: Packed RBC units contain minimal platelets or plasma clotting factors. Patients who receive large transfusions will require replacement of platelets and clotting factors to avoid a dilutional coagulopathy. • Hyperkalemia: Typical blood units contain less potassium than normal blood; as the blood is stored, the RBCs release potassium. Rapid or large transfusions of RBC units, particularly older units, can lead to a significant potassium increase in the recipient.
■ HANDLING, VERIFICATION, AND STORAGE Retaining the oxygen-carrying capacity of blood throughout its shelf life is one of the primary problems of blood storage. Over time red cells lose their capacity to carry the same amount of oxygen as they could when fresh. It is hard to standardize the capacity of each unit because each starts from a different level and degrades at different rates. Different products are added
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to each unit to prolong the shelf life. One of the most common is citrate-phosphate-dextroseadenine (CPDA-1): Citrate is an anticoagulant, phosphate is added as a buffer, dextrose provides an energy source for the red cells, and adenine allows the cells to make adenosine triphosphate (ATP), a common cellular energy source. AS-1 (Adsol), AS-3 (Nutricel), and AS-5 (Optisol) are similar to CPDA-1 with slight variations. Storing the units between 1°C and 6°C slows down the metabolic processes of the red cells, but glycolysis (RBCs do not use the citric acid cycle because they lack mitochondria) still converts glucose to lactate. This accumulation of lactate lowers the pH of the unit and alters the intraand intercellular concentrations of sodium and potassium. The lower pH also contributes to the decreased oxygen-carrying capacity of the RBCs. If several units of plasma or packed red cells are needed in the operating room, they are often kept in a cooler or bucket with ice; the ice and blood product should be separated by a towel or other barrier to prevent the blood from freezing. The formation of ice crystals damages the RBCs. Another important reason to keep the blood cold for possible transfusion in the operating room is if the blood is kept cold, it can be returned to the blood bank if it is not used.
■ ADMINISTRATION Each unit must be checked at the bedside check before transfusing. The check consists of double checking the information on the unit and
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the paperwork that came with it. This procedure will vary from institution to institution, but typically requires two people, and often one of them must be licensed (e.g., a physician or a nurse). Commonly, the unit number, expiration date, blood type, and some type of patient identifier are used (Fig. 23.1). Blood products are typically administered through special blood administration tubing (Fig. 23.2). The vast majority of blood administration sets have an in-line filter to remove cellular debris and coagulated proteins. Most filters are designed for transfusion of two to four RBC units before they should be changed. Refer to the product information for specific guidelines. Some practitioners prefer to attach a separate blood filter to the spike. After multiple units have been transfused, the filter can be replaced without having to replace the entire tubing setup. Again, refer to the product information for the number of RBC units that can be transfused before filter replacement is recommended, as some filters allow up to 10 units. The tubing
■ Figure 23.1. Transfusion unit of red blood cells (RBCs). 1. Blood type: A Rh (D)-positive. 2. RBCs transfusion unit—leukoreduced. 3. Unit number. 4. Expiration date.
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■ Figure 23.2. Blood administration tubing. 1. Y connector. 2. Filter—holds debris and particles. 3. Chamber— blood can be pumped by squeezing the chamber to speed delivery. 4. Warmer—blood is warmed by passing through the hot-line system.
used in operating rooms usually has a Y connector with two separate “spikes” so that a unit or fluid can be prepared on one spike while the other is being actively used for transfusion or fluid administration. Typical blood administration sets used in the operating room also include a squeezable chamber that allows pumping the fluid or blood products to speed administration. Pediatric blood sets can come equipped with a chamber (buretrol) in which the provider can measure out a specific amount of blood product or fluid. This allows more precise administration of fluids or blood products, which can be critical in pediatric patients. Blood products are typically warmed before being given to a patient. This is often achieved with in-line heated tubing. The majority of these units utilize heated water, which is circulated outside an inner set of tubing through which the blood product or fluid is administered. As mentioned earlier, heating units above 30°C can reduce the risk of some complications. Additionally, blood is typically stored at 4°C and transfusing cold units to a patient could rapidly lower his or her body temperature. Platelets are the exception and are stored at room temperature. This is further discussed in the section on different blood products. There are many other transfusion devices that are mainly used during emergency situations, such as the Level One, Belmont, and pressure bags. These devices are covered in more detail in Chapter 34, but in essence, they provide heating, filtration, and the ability to rapidly administer blood products and fluid. It is routine practice to draw blood samples for laboratory testing of the patient’s blood before and after transfusion.
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Chapter 23 • Transfusion Medicine
Testing includes hematocrit and other values like electrolytes, glucose level, coagulation studies, etc., and it is often the anesthesia technician’s responsibility to run these samples if the operating room suites have their own blood gas analyzer machine.
■ DIFFERENT BLOOD PRODUCTS While blood donations typically consist of whole blood, or blood containing all of its normal components (red blood cells, plasma, etc.), they are routinely processed into several different products for clinical use. Today, whole blood is not readily available for transfusion and instead serves as the basis for further processing. Because the different components in blood differ in density, blood banks use centrifugation to separate the different parts, resulting in different blood products (see Table 23.3). • Packed red blood cells (PRBCs): PRBCs provide additional oxygen-carrying capacity because of the hemoglobin they contain. Transfusion of white blood cells (leukocytes) increases the risk of infection because they suppress the immune system of the recipient. Transfusion of leukocytes can also sensitize the recipient to leukocyte antigens. For these reasons, most PRBC units have the vast majority of leukocytes removed by filtration (leukoreduction). The hematocrit value of a PRBC is 70%. When RBCs are separated from whole blood, plasma and other blood components are retained for other use.
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• Fresh frozen plasma (FFP): FFP contains plasma proteins including factors V and VIII, which are needed for effective blood clotting. FFP replaces the coagulation factors lost with bleeding and can also be used as a reversal agent for anticoagulation drugs likewarfarin, in treatment of immunodeficiencies, in antithrombin III deficiency, in massive blood transfusion, and in other coagulation system deficiencies. FFP does increase the circulating volume but should never be used as primary volume expander. FFP is stored frozen and after thawing it must be used between 24 hours and 5 days, which will be indicated on the expiration date printed on the bag. Because of the time it takes to thaw stored FFP, there can be a delay in receiving FFP after it has been requested. As mentioned above, FFP must be compatible with the recipient’s ABO Rh (D) type. • Platelets: Platelets play a vital role in how the body forms blood clots. Platelets can be collected either from whole blood donations or from separately from platelet-specific donations. Because they are stored at room temperature (never place them in the refrigerator with other blood products), they present a higher risk of bacterial contamination. Indications for platelet transfusion vary but are guided by the patient’s platelet count (provided by the laboratory) and the extent of the surgical bleeding. It is not necessary to provide ABO-compatible platelets.
TABLE 23.3. DIFFERENT BLOOD PRODUCTS PRODUCT
STORAGE TEMPERATURE (°C)
VOLUME (ml)
SUPPLIES
HEMATOCRIT
Whole blood
4°C
500ml
Oxygen capacity, blood volume
40
PRBC Packed Red Blood Cells
4°C
300ml
Oxygen capacity, increases hematocrit 3%
70
Fresh frozen plasma
4°C
200ml
Factors V and VIII deficiency
—
Cryoprecipitate
4°C
10ml
Factor VIII and fibrinogen
—
Platelets
Room temperature
50–200ml
Increases platelet count 5,000–10,000/uL
—
Prothrombin complex
4°C
—
Factor IX
—
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• Cryoprecipitate: Cryoprecipitate contains high concentrations of clotting factor VIII and fibrinogen and is used to treat clotting factor deficiencies including hemophilia A. Cryoprecipitate also contains other clotting factors and plasma proteins. Cryoprecipitate should be filtered when administered, and it must be used within 6 hours of thawing. Cryoprecipitate is usually administered as ABO compatible, but it is not too important since the concentration of antibodies in cryoprecipitate is extremely low. • Prothrombin complex: Prothrombin complex is a mixture of clotting factors II, VII, IX, and X. It is used to treat factor IX deficiency, hemophilia B, and other bleeding disorders.
■ SUMMARY Blood cells are intimately related to the immune system and carry multiple antigens. Because of the presence of these antigens, the transfusion of foreign blood products may activate the immune system of the host, resulting in severe reactions, even death. Both patients and blood products prepared by the blood bank undergo extensive testing to ensure compatibility between the donor and the patient receiving the transfusion. This chapter introduced the basic concepts of transfusion medicine including blood types, compatibility testing, indications for transfusion, and potential adverse reactions to transfusions. Familiarity of these concepts is essential for all operating room personnel, including anesthesia technicians, who are involved with the transfusion process.
REVIEW QUESTIONS 1. What is an antigen? A) A unique cellular marker on cell surfaces B) A molecule made up from amino acids C) A part of the cell’s nucleus D) The oxygen-carrying part of a red cell Answer: A. Antigens are markers that are used by the body to identify different cells.
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2. Why is compatibility testing important? A) To avoid losing blood units at the blood bank B) To avoid adverse reactions, even death, from transfusion C) To screen for HIV-1 D) To prolong unit shelf life Answer: B. Compatibility testing ensures that patients will not receive incompatible transfusions, for this could cause death.
3. What are the primary causes of noncompatible transfusions? A) Bacterial contamination B) Excessively clumped platelets C) Clerical errors D) Expired crossmatch test tubes Answer: C. Compatibility testing is very sophisticated, but clerical errors can cause an incompatible transfusion.
4. What is FFP used for? A) Raising hematocrit B) Expanding blood volume C) Replacing clotting factors D) Lowering patient temperature Answer: C. FFP contains factors V and VIII, which aid clotting.
5. Why are O-negative patients considered universal donors? A) They have a lower hematocrit. B) They lack Rh (D) antigen. C) They lack antigens on their cell surfaces. D) They provide extra factor VII. Answer: C. Type O blood does not contain antigens that the recipient could recognize as foreign.
6. How is the shelf life of stored blood extended? A) The addition of nutrient supplements B) Repeated freezing and thawing C) Inverted storage freezers D) Constant centrifugation Answer: A. Nutrients help keep red cells alive while they are outside of the body.
7. What is the Rhesus blood group? A) The markers of the Kell blood group system B) What makes AB patients universal recipients C) The determinant of cryoprecipitate effectiveness D) Blood group with D antigens in cell membranes Answer: D. The Rhesus blood group is identified by the D antigen.
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Chapter 23 • Transfusion Medicine
SUGGESTED READINGS Dzieczkowski JS, Anderson KC. Transfusion biology and therapy. In: Fauci AS, Longo DL, eds. Harrison’s Principles of Internal Medicine. 17th ed. New York, NY: The McGrawHill Companies; 2008:707–712. Hess JR. Conventional blood banking and blood component storage regulation: opportunities for improvement. Blood Transf. 2010;8(suppl 3):s9–s15.
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Miller RD, ed. Transfusion therapy. In: Miller RD, Erikson LI, eds. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2009:1739–1766. Welsbay IJ, Bredehoeft SJ. Blood and blood component therapy. In: Longnecker DE, ed. Anesthesiology. China: The McGraw-Hill Companies; 2008:1892–1911.
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SECTION
IV
Equipment Setup, Operation, and Maintenance
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CHAPTER
24
Infectious Disease Brett Miller ■ INTRODUCTION Microorganisms are all around us. They are in the air, on our hands, on items we touch, and even in the food we eat. Many microorganisms are helpful (i.e., gut bacteria that aid in digestion); however, some microorganisms known as pathogens are capable of causing disease within humans. In health care settings, pathogens are very common and appropriate measures must be taken to protect our patients, our coworkers, and ourselves. The goal of this chapter is to • Identify the various types of pathogens that lead to infectious disease. • Describe the methods and precautions used to minimize the spread of infections in the health care setting. • Describe how to minimize transmission even after exposure.
■ PATHOGENS There are several types of organisms capable of producing disease (also known as pathogens): bacteria, virus, fungus, parasite, and prion. Bacteria are very small, single-celled organisms that lack a nucleus. They are extremely diverse and often very specialized. They are capable of utilizing many different energy sources such as oxygen, sunlight, and even geothermal heat. A single bacterium may trade DNA with another bacterium and confer traits to the recipient. A particularly important example of this capability is when one bacterium confers resistance to an antibiotic to another bacterium. Bacteria cause disease by producing toxins that interfere with cells, eliciting an inflammatory response, or invading host cells. Examples of bacteria include Staphylococcus aureus (methicillin-resistant Staphylococcus aureus [MRSA] is a common form of antibiotic-resistant bacteria found in health care settings), Streptococcus pneumoniae
(the most common cause of bacterial pneumonia), Clostridium difficile (common cause of diarrhea), and Mycobacterium tuberculosis (the cause of tuberculosis). Bacterial illness is generally treated with antibiotic medications (e.g., penicillin, vancomycin, azithromycin, and ciprofloxacin) that work by attacking specific bacterial cell targets that are not found in humans. A virus is even smaller than a bacterium and much simpler (Fig. 24.1). It is composed of RNA or DNA (genetic material) surrounded by a protein shell and a lipid envelope. Unlike other organisms, a virus does not contain the cellular machinery to produce energy, manufacture proteins, or even reproduce. In order to perform these functions, it must take over a host cell. A virus “infects” a cell by attaching to the host cell membrane and becoming incorporated into the cell. Once inside, the virus can use host enzymes and proteins to replicate its own genetic material and produce viral proteins. The virus eventually kills the host cell and is released. It is capable of infecting all kinds of living cells, including bacteria, plants, and animals. Examples of viruses that infect humans are influenza (cause of the flu), herpes virus (a viral class that may cause cold sores, chicken pox, genital herpes, and even a form of cancer), human immunodeficiency virus (the cause of acquired immunodeficiency syndrome or AIDS), and hepatitis viruses (cause liver inflammation and eventually cirrhosis). Antiviral medications (e.g., acyclovir, highly active antiretroviral therapy (HAART) are available to treat many illnesses caused by viruses. A fungus is a cellular organism containing a nucleus that shares many features of animals (i.e., they lack chlorophyll and require organic compounds as energy sources) and plants (i.e., presence of a cell wall and ability to reproduce sexually and asexually). It exists in many forms, including molds, yeast, and mushrooms. Only a
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prion can occur by grafting infected tissue (i.e., cornea transplant, dural grafts) or ingestion. Prions are extremely resistant to standard medical sterilization protocols. Presently, treatments for prion disease are only experimental.
■ PREVENTION OF HEALTH CARE– ASSOCIATED INFECTIONS
■ FIGURE 24.1 The HIV virus.
very small percentage actually causes disease in humans. Examples of fungal infections are tinea pedis (causes athlete’s foot), apergillosis (causes lung infections), and candidiasis (causes skin and mucous membrane infections). Antifungal drugs are available and include amphotericin, fluconazole, and caspofungin. Parasitic infections are often caused by organisms from the Protozoa kingdom. Protozoans are single-celled organisms with a nucleus that resemble yeast. Examples of Protozoan infections include malaria (an infection of red blood cells caused by Plasmodium) and amoebic dysentery (caused by Entamoeba histolytica). Other parasitic infections are caused by multicellular worms including hookworms (intestinal worm that can cause severe diarrhea, intestinal obstruction, and anemia) and tapeworms (intestinal worms usually from eating undercooked meat that can invade into tissues of the body such as muscles and brain). A variety of antiparasitic medications exist including quinine (for malaria infection) and mebendazole (for worm infections). Prions are the most recently discovered class of pathogens. They are proteins that have been folded into an abnormal shape. Once a prion has infected a cell, it induces host proteins to become misfolded, thereby producing disease. Creutzfeldt-Jakob disease is an example of a prion infection that causes progressive brain degeneration. In fact, all known prions affect brain and neural tissue. More importantly, prion infections are universally fatal. Transmission of a
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A health care–associated infection (HAI) is an infection that occurs during hospital admission with no evidence that the infection was present at the time of admission. In 2002, there were 1.7 million HAIs in the United States that led to 99,000 deaths. The most common types of HAIs are urinary tract infection (34%), surgical site infection (17%), pneumonia (13%), and bloodstream infection (14%). Remarkably, many of these infections are preventable. The United States Department of Health and Human Service and other international health care organizations have launched major initiatives to reduce or eliminate HAIs. One of the most common sources of HAIs are bloodstream infections caused by indwelling venous catheters, particularly central venous catheters. A bloodstream infection (also known as septicemia) is a life-threatening infection in which a pathogen can spread throughout the body by way of a patient’s blood. This can lead to severe sepsis, multiple organ dysfunction, and death. Central venous catheters (or central lines) place patients at increased risk for bloodstream infections because the catheter provides a direct route for pathogens to enter the bloodstream. Infections have been demonstrated to occur from organisms found on the hands of individuals placing central lines or injecting medications through ports on a central line, infected medications, or bloodstream infections that attach and grow on the central line. An important risk factor for the development of a catheter-related bloodstream infection (CRBSI) is the site of the catheter. Central lines placed in a femoral vein are associated with the highest risk of infection, whereas subclavian central lines are associated with the lowest risk. The Centers for Disease Control and Prevention (CDC) has recommended several techniques that have been proven to reduce the risk of CRBSI including hand hygiene before catheter insertion, maximal sterile barrier precautions (cap, mask, sterile gown, sterile gloves, and large
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sterile drape), and appropriate prep (chlorhexidine for patients >2 months old and povidone iodine, alcohol, or chlorhexidine for infants 0. The absorbent material can become dried out or desiccated if it is exposed to prolonged periods of fresh gas flow. Unfortunately, detection of desiccation is difficult. Some, but not all, absorbents change color with desiccation. Desiccation is also associated with heat formation. If either of these signs is noted after a prolonged period of machine inactivity, the absorbent should be replaced. The hazards associated with the use of a desiccated absorbent include carbon monoxide formation, compound A formation with sevoflurane, and fire within the canister. Compound A is a decomposition product of sevoflurane that is known to cause kidney injury in rats. Clinical vigilance is important, as desiccation is difficult to detect. This vigilance includes turning off the fresh gas flowmeters at the end of a case and replacing the absorbent when prolonged fresh gas flow may have occurred. The absorbent should also be replaced if the absorbent
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temperature is felt to be high or checked with a temperature probe and found to be greater than 50°C. A classic example of desiccation occurs with an anesthesia machine that is not used for surgery but accidentally left on with high gas flows over the weekend. If inspection of a machine indicates that this may have occurred, the absorbent should be replaced.
■ COMMON GAS OUTLET The common or fresh gas outlet receives the gas output from the anesthesia machine for delivery to the anesthesia circuit. When the outlet is in an external location, it may have a 15-mm female slip-joint fitting with a coaxial 22-mm male connector. As the common gas outlet contains the output of the vaporizers and various flowmeters, it should not be used to provide supplemental oxygen. This may lead to the unintentional administration of nitrous oxide or volatile anesthetic. A safer source of supplemental oxygen is the auxiliary oxygen connection or connection to an oxygen tank or wall source.
■ OXYGEN FLUSH VALVE The oxygen flush valve delivers high-pressure high-flow oxygen to the common gas outlet from either the tank or pipeline (see Fig. 26.6). Barotrauma of the patient’s lungs can occur if the oxygen flush valve is depressed during inhalation with a spontaneously ventilating patient. Barotrauma of the lungs is injury to the lung tissue caused by high pressure. The increased pressure can lead to a pneumothorax or hole in the lung. This can also occur if the valve is depressed when the ventilator is delivering a breath with some anesthesia machines.
■ BREATHING CIRCUIT The breathing circuit is the critical connection between the anesthesia machine and the patient and is discussed in more detail in Chapter 29. The most commonly used breathing circuit in the operating room is the circle system (Fig. 26.7). The basic circle system contains a Y-piece, inspiratory/expiratory tubes, unidirectional valves, fresh gas inlet, adjustable pressurelimiting (APL) valve, pressure gauge, reservoir bag, ventilator, bag/ventilator switch, airway gas monitor, airway pressure monitor, respirometer, and CO2 absorber. The design of the circle
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■ FIGURE 26.6 The oxygen flush valve introduces highpressure oxygen into the breathing circuit when depressed.
system allows for the conservation of heat, moisture, and volatile anesthetic because of the CO2 absorber and humidification devices. The APL valve, reservoir, and airway pressure monitor allow for the monitored delivery of positivepressure ventilation. The patient can be switched from spontaneous/manual ventilation to the ventilator with the bag/ventilator switch within the system. The other commonly used breathing circuits include Mapleson circuits. A common type of Mapleson circuit used in the perioperative setting is the Mapleson F or Jackson-Rees circuit. They are frequently used for transporting patients. The advantages of the Mapleson systems are that they are simple, lightweight, portable, and robust. The disadvantages include that they require high fresh gas flow, scavenging of gas is difficult, and rebreathing of gas can occur without high gas flows.
■ VENTILATOR A critical aspect of the practice of anesthesiology is the ability to ventilate patients. Anesthesia machines integrate the ventilator and its various
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controls and alarms. If the patient is unable to breathe adequately on his or her own, the ventilator can provide support and enhance the underlying pattern of breathing. If the patient is paralyzed or unable to adequately breathe for other reasons, the ventilator can serve the critical role of ventilation and subsequent oxygen delivery and carbon dioxide removal. The ventilator also serves to deliver and remove anesthetic gases. See Chapter 30 for a further discussion of anesthesia machine ventilators and ventilation modes. A simple distinction between the various ventilation modes is those with which the patient generates a breath versus those generated by the ventilator. The two basic modes of ventilation in which the anesthesia machine generates the ventilation are pressure control (a set pressure is delivered) and volume control (a set tidal volume is delivered). Another major type of ventilation mode involves augmenting a patient-initiated breath with a small amount of positive pressure (pressure support ventilation). This type of ventilation is sometimes combined with backup ventilator-generated breaths. Depending on the type of surgery, the patient, the patient’s comorbidities, and the anesthetic plan, the anesthesia provider will decide which type of ventilation is appropriate for the patient during the surgery.
■ SCAVENGING Scavenging systems remove the waste anesthetic gases from the operating room. This helps reduce exposure to nitrous oxide and halogenated anesthetic agents, which are potentially hazardous gases. These systems can be broken down into five basic components: 1. Gas Collection Assembly The gas collection assembly gathers the excess gas from the ventilator via the ventilator relief valve and from the manual side via the APL valve. Failure of these valves could lead to a buildup of pressure within the breathing circuit. 2. Transfer Tubing The transfer tubing carries the gas to the scavenging interface. It is of a specific size and rigidity to prevent easy kinking. If these tubes are blocked or kinked, there can also be a buildup of pressure in the breathing circuit. There is also tubing carrying gas from the gas analyzer to the scavenging interface.
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■ FIGURE 26.7 The circle breathing system is the breathing system used during most general anesthetics. (From Dorsch JA, Dorsch SE, eds. Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:239, with permission.)
3. Scavenging Interface The scavenging interface is either an open or a closed system. It protects the breathing circuit from excessive positive or negative pressure. An open interface is open to the atmosphere and has no valves. These are used with active disposal systems. A closed interface has valves to connect to the atmosphere. With passive disposal systems, there is a positive-pressure relief valve. With active disposal systems, there are both a positiveand a negative-pressure relief valve. The positive-pressure relief valve prevents the buildup of pressure within the scavenging system and back into the breathing circuit. The negative-pressure relief valve prevents the vacuum from emptying out the breathing circuit.
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4. Gas Disposal Assembly Tubing This tubing carries the gases from the scavenging interface to the gas disposal assembly. It is noncollapsible to prevent blockages. 5. Gas Disposal Assembly The gas disposal assembly is either an active or a passive system, which is the last step in removing the gas from the operating room. An active system uses a vacuum to induce flow and remove the gas. This can be through the regular suction outlets and couplings or through a waste anesthesia gas (WAG) line with its specific couplings and purple tubing. Typically two suction lines are needed for an anesthesia machine. One is used for patient suctioning equipment and the second for the waste gases. Some older machines only have one suction line, and the
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negative-pressure has to be balanced between the two uses. In active systems, there is an adjustable flowmeter showing the amount of negativepressure present, which should be checked to verify the presence of the vacuum. The gases are usually vented outside the building. A passive system does not use a vacuum to induce flow. The gases are pushed out through ventilation ducts as more gas flows from the anesthesia machine.
■ MONITORS Monitors form a critical connection between the patient, the anesthesia machine, and the anesthesia provider. They provide vital information needed to ensure safe care of patients. Monitors are discussed in depth in several chapters of this book. Chapter 32 discusses the gas analyzers used to monitor O2, CO2, N2O, and volatile anesthetic concentrations. Chapter 33 describes the basic monitors typically used during an operation. These monitors include electrocardiogram, which monitors the electrical activity of the heart, the arterial pulse oximeter, which monitors the oxygen saturation of arterial blood, the noninvasive blood pressure, capnography, which monitors the inspiratory and expiratory concentration of carbon dioxide, and temperature. Chapter 9 discusses more advanced invasive monitoring including arterial blood pressure and central venous pressure. Another important type of monitor incorporated in the anesthesia machine is an LCD, which contains information about the ventilation parameters and error messages from the machine. This functions as a monitor of the anesthesia machine and its various parts including the ventilator. In fact, there may be significant overlap between this monitor and patient-specific information displayed on a different monitor with the basic and invasive patient monitors. An example of the overlap is the anesthesia machine’s oxygen analyzer, which is displayed on the anesthesia machine’s LCD, and inspired oxygen concentration from the gas analyzer, which is usually displayed on the monitor with the patient’s vital signs. The anesthesia machine ventilator will also have a display for pressures and volumes monitored in the anesthesia circuit (see Chapter 30). In modern anesthesia machines with an LCD, the process of checking out the anesthesia machine usually includes a review of information displayed
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on this monitor. An understanding of the various machine-related error messages that are displayed is critical for proper machine operation and patient care. Chapter 31 discusses machine maintenance and troubleshooting and reviews common error messages and potential remedies.
■ SUMMARY The anesthesia machine is a critical component of the anesthesia work environment. These devices have grown in complexity and now often include not only the components necessary to deliver gas flows and anesthetic agents, but come bundled with sophisticated ventilators and monitoring equipment. Anesthesia technicians are intimately involved with working with anesthesia machines performing machine checkouts, routine maintenance, and troubleshooting. This chapter provides an overview of the basic machine components tracing them from the gas supply through the flowmeters, the vaporizers, the ventilator, and the breathing circuit to the patient and out through the waste gas scavenging.
REVIEW QUESTIONS 1. You are scheduled to work at your hospital’s ambulatory surgery center on Monday morning. As you start setting up equipment for the first case, you notice that the anesthesia machine is on and the oxygen is flowing at 10 L/min. You note that the operating room had not been in use since the previous Thursday when the surgery center was last open. What should you do? A) Turn off the oxygen. Finish setting out equipment for this room and then continue setting up the rest of the rooms for the day. B) Turn off the machine and the oxygen. Finish setting out equipment for this room and then continue setting up the rest of the rooms for the day. C) Do not touch the machine. Finish setting out equipment for this room and then continue setting up the rest of the rooms for the day. D) If the CO2 canister has not changed colors, do not replace it. Finish setting out equipment for this room and then continue setting up the rest of the rooms for the day. E) Replace the CO2 canister. Finish setting out equipment for this room and then continue setting up the rest of the rooms for the day. Answer: E. Prolonged fresh gas flows can lead to desiccation or dehydration of the carbon dioxide absorbent. If desiccation
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Chapter 26 • Overview of Anesthesia Machines is suspected, the absorbent should be changed. Desiccation can sometimes but not always lead to a change in the color of the absorbent. The hazards associated with the use of desiccated absorbent include carbon monoxide formation, compound A formation with sevoflurane, and fire within the canister.
2. At the end of a long operation, a new anesthetist calls you into the operating room. The anesthetist tells you that he is trying to switch volatile anesthetic agents from isoflurane to desflurane but is unable to turn the dial on the desflurane vaporizer to turn it on. He currently has the isoflurane vaporizer on. Both vaporizers are noted to be full of medication. The anesthetist wants to know if he needs a new vaporizer. What should you tell the anesthetist? A) Yes, the anesthetist needs a new vaporizer. You should be able to turn on both vaporizers at the same time to switch medications. B) Yes, the anesthetist needs a new vaporizer. There must be a leak in the vaporizer as the anesthesia machine has a safety mechanism that prevents the vaporizer from turning on if there is a leak. C) No, the vaporizer does not need to be replaced. You explain that there is a safety feature on the anesthesia machine that will not let him or her switch volatile anesthetics during an operation. D) No, the vaporizer does not need to be replaced. You explain that there is a safety feature on the anesthesia machine that will not let more than one vaporizer from being open at a time. E) No, the vaporizer does not need to be replaced. You tell the anesthetist that if he wants to switch medications, he should just add some desflurane to the sevoflurane vaporizer rather than use a different vaporizer. Answer: D. The vaporizers are properly functioning. When there is more than one vaporizer present on the anesthesia machine, there is a mechanical link called an Interlink that prevents more than one vaporizer from being opened at a time. This prevents the patient from receiving a simultaneous administration of two volatile anesthetics from the anesthesia machine.
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3. The Pin Index Safety System is designed for which purpose? A) To prevent the gas hose from one gas to be connected to another B) To prevent the backflow of gas from one cylinder to another C) To prevent the placement of gas tanks onto the wrong yoke D) To allow the quick release/connection of gas hoses to the machine E) To allow any gas tank to be connected to any yoke on the machine Answer: C. The Pin Index Safety System ensures that each gas tank can only be attached to the specific gas yoke for which it was designed. The Diameter Index Safety System prevents one gas hose from being connected to another. They can only be attached to the specific gas line they are made for. The backcheck valves prevent the flow of gas from one tank or gas line into another tank.
4. There are many parts to a scavenging system. Which part listed below is part of an active gas disposal system but not part of a passive system? A) Ventilator relief valve B) Rigid transfer tubing C) Adjustable pressure relief valve (APL) D) Vacuum system E) Positive-pressure relief valve Answer: D. The vacuum system is required for the active scavenging system and provides suction to draw the gases out of the building. The ventilator relief and APL valves allow the excess gas to flow from the breathing circuit to the scavenging interface. The rigid transfer tubing is part of all scavenging systems. The positive-pressure relief valve is part of a closed systems design in both active and passive systems.
SUGGESTED READINGS Baresh PG, Cullen BF, Stoelting RK, eds. Clinical Anesthesia. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006. Dorsch JA, Dorsch SE, eds. Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.
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CHAPTER
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Anesthesia Machine Checkout Ramon Larios and Esther Sung ■ INTRODUCTION The delivery of a safe anesthetic in modern-day practice begins with a checkout of the anesthesia machine. Improper or lack of inspection of anesthetic equipment prior to use has been associated with several significant incidents. Failure to check equipment clearly results in an increased risk of operative morbidity and mortality. With the large variety of anesthetic delivery systems available today, it is critical to understand the basic components of the system so that malfunctions can be detected prior to use or when failure occurs during use. Moreover, regular testing may lead to improved preventive maintenance and enhanced familiarity with the equipment. This chapter focuses on the fundamental components of the anesthesia machine checkout. Specific issues related to unique anesthesia delivery systems should be resolved by referring to the appropriate manufacturers’ operator manuals.
■ HISTORY OF MACHINE CHECKOUT RECOMMENDATIONS In 1993, a joint effort between the American Society of Anesthesiologists (ASA) and the U.S. Food and Drug Administration (FDA) resulted in the 1993 FDA Anesthesia Apparatus Checkout Recommendations. This simplified the initial 1986 preuse checkout and made it more userfriendly. At the time, the 1993 checklist focused on components that were immediately dangerous for patients and mechanisms that failed more regularly. This checklist was applicable to most commonly available anesthesia machines. Nevertheless, despite the recognized importance of an anesthesia machine checkout, available evidence suggests that the 1993 recommendations were neither well understood nor reliably used by anesthesia providers.
Moreover, because of recent and ongoing fundamental changes to the various anesthesia machine designs, the 1993 FDA preuse checklist may no longer be universally applicable to all anesthesia delivery systems. As more machines incorporate electronic checkouts, the user must determine which portions are automatically checked and which portions require manual checks. In such cases, the anesthesia care provider must be aware that the electronic machine check may not be a comprehensive preanesthesia checkout, and the user should follow the original equipment manufacturers’ recommended preuse checklist. As a result, in 2005, the ASA’s Committee on Equipment and Facilities, in conjunction with the American Association of Nurse Anesthetists (AANA) and the American Society of Anesthesia Technologists and Technicians (ASATT), began to develop a revised preuse checklist that was designed to be more workstation specific. These recommendations were published in 2008 and were intended to eventually replace the 1993 FDA Anesthesia Apparatus Checkout Recommendations. Rather than a checklist with specific instructions on how to perform each test, these new guidelines elaborate on specific systems and subsystems that must be evaluated. It is ultimately up to the user, along with the anesthesia machine manufacturer, to determine the actual mechanisms and/or specific checks that should be used to accomplish these subsystem evaluations. Appropriate personalized checkout procedures may need to be developed for individual machines and practices. The 1993 Anesthesia Apparatus Checkout Recommendations placed all of the responsibility for the preuse checkout on the anesthesia provider. The new 2008 recommendations identify certain aspects of the preanesthesia checkout that may be performed by a qualified anesthesia
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technician or a biomedical technician (http:// www.apsf.org/newsletters/html/2008/spring/ 05_new_guidelines.htm). Redundancy in the critical aspects of the checkout process makes it more likely that problems will be identified prior to use for a patient. Nevertheless, regardless of the additional support of technicians, the anesthesia care provider is ultimately responsible for the proper function of all equipment used to deliver anesthesia care.
■ ANESTHESIA MACHINE CHECKOUT PROCEDURE As stated earlier, the goal of the preanesthesia checkout is to allow for the safe delivery of anesthesia care. Requirements for safe delivery of anesthetic care include the following: • Reliable delivery of oxygen at any appropriate concentration up to 100% • Reliable means of positive pressure ventilation • Availability of functional backup ventilation equipment • Controlled release of positive pressure from the breathing circuit • Anesthesia vapor delivery (if intended as part of the anesthetic plan) • Adequate suction • Means to conform to standards for patient monitoring The new guidelines for the preanesthesia checkout procedures consist of 15 items. These items must be performed as part of a complete preanesthesia checkout on a daily basis. (Items that must be completed prior to each procedure are in bold). The 15 items are as follows: 1. Verify auxiliary oxygen cylinder and selfinflating manual ventilation device are available and functioning. Anesthesia ventilator failure resulting in the inability to provide patient ventilation is rare but can occur at anytime. For those situations where the problem cannot be immediately identified or corrected, a manual ventilation device (e.g., bag valve mask) may be necessary to provide positive pressure ventilation until the problem is resolved. As a result, a self-inflating manual ventilation device and an auxiliary oxygen cylinder should be available and checked for proper function at each anesthesia setting.
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In addition, the oxygen cylinder should have a regulator and a device to open the cylinder valve should be present. A full E cylinder of oxygen has a pressure of about 2,000 pound-force per square inch gauge (psig), which is equivalent to around 625 L of oxygen. After checking the oxygen cylinder pressure to ensure adequate supply, the cylinder should be stored with the valve closed in order to prevent unintended leakage or drainage of oxygen. 2. Verify patient suction is adequate to clear the airway. The immediate ability to clear airway secretions or gastric contents is essential for safe anesthetic care. Inability to visualize the glottic opening and therefore delay in timely acquisition of a secure airway can be dangerous and possibly fatal. Aspiration of gastric contents can cause prolonged intubation and airway complications. Adequate strength of the suction can be tested by occluding the suction tubing orifice with the underside of a thumb and determining if the weight of the suction tubing can be supported at waist height. Prior to anesthesia, adequate suction should be checked and a rigid suction catheter (e.g., Yankauer) should be available on the machine. 3. Turn on the anesthesia delivery system and confirm that AC power is available. AC power and the availability of backup battery power should be confirmed prior to the delivery of anesthesia. Visual indicators of the power systems exist on most anesthesia delivery systems. These should be confirmed as should appropriate connection of the power cord to a working AC power source. If the AC power is not confirmed, complete system shutdown is at risk when battery power is unknowingly depleted. Desflurane vaporizers, if used, should be checked for adequate electrical power source as well. 4. Verify availability of required monitors and check alarms. The patient’s oxygenation, ventilation, circulation, and temperature should be continually evaluated according to the ASA’s Standards for Basic Anesthetic Monitoring. Verification of the availability and proper function of the appropriate monitoring supplies should be performed prior to each anesthetic. Examples of necessary equipment include, but are not
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limited to, blood pressure cuffs, pulse oximetry probes, electrocardiogram (ECG) leads, and capnography. Moreover, the appropriate audible or visual alarms that would indicate problems with, or disruption of, patient oxygenation, ventilation, circulation, and temperature should be intact. It is prudent for the anesthesiology technician to turn off the monitors and then turn them back on between cases to be sure that alarms are reset to default values as designed by each individual institution. 5. Verify that pressure is adequate on the spare oxygen cylinder mounted on the anesthesia machine. Spare oxygen cylinders are mounted on anesthesia machines in the event that central oxygen supply is lost. Anesthesia machines require oxygen not only to provide oxygen to the patient but often to power pneumatically driven ventilators. The pressure of the oxygen cylinders should be checked to ensure an acceptable amount of backup oxygen is available. The oxygen cylinder valves should be closed after verification in order to prevent unrecognized depletion of the cylinder due to pressure fluctuations in the machine during mechanical ventilation or in the event of actual pipeline supply failure. Rarely, the cylinder is intended to be the primary oxygen source. In these cases, if the ventilator is pneumatically driven, then the oxygen cylinder supply may be depleted quickly. As a result, manual or spontaneous ventilation may be more appropriate in order to maximize the duration of oxygen supply. On the other hand, the duration of oxygen supply for electrically powered or piston-driven ventilators depends only on total fresh oxygen gas flow. 6. Verify that the piped gas pressures are ≥50 psig. Since there are many scenarios that may cause disruption of gas delivery from a central source, pressure in the piped gas supply should be checked at minimum once per day in order to ensure that adequate pressure is available for proper function of the anesthesia machine. If the pipeline hoses have been disconnected in order to move the anesthesia machine at any point during the day, the hoses should be reconnected to the central pipeline supply, and the fittings
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should be examined for firm connections without audible leaks. The pipeline pressure should be 50–55 psig. 7. Verify that vaporizers are adequately filled and, if applicable, that the filler ports are tightly closed. (Provider completes prior to each procedure; technician can complete daily.) Adequate supply of volatile anesthetics is requisite for vapor-based anesthetics in order to reduce the likelihood of inadequate anesthesia and recall under anesthesia. In addition, many vaporizers do not have low-agent alarms, so checking prior to usage is important. After filling the vaporizers, filler ports should be adequately tightened to prevent unrecognized leakage, especially for older vaporizers that do not have systems that automatically close after completion of refilling. Vaporizers should also be secured so that they cannot tilt or be lifted from their mounts. 8. Verify that there are no leaks in the gas supply lines between the flowmeters and the common gas outlet. (If the vaporizer has been changed, this should be rechecked prior to use.) The low-pressure component of the anesthesia machine circuit is located between the flow control valves to the common gas outlet. The leak test checks the integrity of the anesthesia machine in this part of the circuit. The components located within this area are subject to breaking and developing leaks. Leaks in the low-pressure circuit can cause leakage of oxygen from the inspired gas and delivery of a hypoxic gas mixture. Likewise, leakage of inhaled anesthetic can result in the patient receiving much less gas anesthetic than is indicated on the machine vaporizer, which places the patient at risk for awareness under anesthesia. In addition, each individual vaporizer must be turned on in order to check for leaks within each vaporizer or at the mount, and it is especially important to recheck this test whenever a vaporizer is changed. Several different methods have been used to check the low-pressure circuit for leaks. One reason for the large number of methods is that the internal design of various machines differs considerably. The clearest example is the difference between most GE Healthcare/Datex-Ohmeda and Dräger
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Chapter 27 • Anesthesia Machine Checkout
Medical workstations. Most GE Healthcare/ Datex-Ohmeda workstations have a check valve near the common gas outlet, whereas Dräger Medical workstations do not. The presence or absence of this check valve may determine which preoperative leak test is indicated. The check valve is located downstream from the vaporizers and upstream from the oxygen flush valve, and it is open in the absence of back pressure. Gas flow from the manifold moves a rubber flapper valve off its seat, thereby allowing the gas to proceed freely to the common outlet. The valve closes when back pressure is exerted on it, preventing the flow of gas back into the machine and through a leak. Examples of back pressure that can cause the check valve to close are oxygen flushing, peak breathing circuit pressures generated during positive-pressure ventilation, and the use of a positive-pressure leak test. Typically, the low-pressure circuit of anesthesia workstations without an outlet check valve can be tested with a positivepressure leak test (e.g., with Dräger Medical machine). When performing a positivepressure leak test, the operator generates positive pressure in the low-pressure circuit by using flow from the anesthesia machine or from a positive-pressure bulb to detect a leak. One common test is the retrograde fill test, which is performed by closing the adjustable pressure-limiting (APL) valve and occluding the patient port. Oxygen flow or flush is used to fill and distend the reservoir bag, and flow is adjusted so that a pressure of 30 cm H2O on the manometer is maintained in the breathing system. No more than 350 mL/min flow should be necessary to maintain a steady pressure. When complete, the pressure should be relieved by opening the APL valve, not by opening the patient port. Relieving the pressure by opening the patient port could cause CO2 absorbent dust to enter the system. Notably, the retrograde fill test checks both the lowpressure part of the machine and the breathing circuit and does not isolate the source of the leak. In addition, it is not very sensitive to small leaks. Machines with check valves must be tested with a negative-pressure leak test (e.g.,
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GE Healthcare/Datex-Ohmeda machine). When performing a negative-pressure leak test, the operator creates negative pressure in the low-pressure circuit by using a suction bulb to detect leaks. In order to do this, the machine’s master switch, flow control valves, and vaporizers should all be initially turned off. The suction bulb is attached by tubing and an adapter to the common fresh gas outlet, and the bulb is squeezed repeatedly until it is fully collapsed. This creates a vacuum in the low-pressure system. If the bulb stays collapsed for at least 10 seconds, the system is free of leaks, but if the bulb reinflates during this period, a leak is present. The test is repeated with each vaporizer individually turned to the “on” position because leaks inside the vaporizer can be detected only when the vaporizer is turned on. The negative-pressure leak test is the most sensitive leak test, as it can detect leaks as small as 30 mL/min. This test used to be considered the universal leak test since it works for machines with or without a check valve, but unfortunately, some new machines do not have accessible common gas outlets. For specific instructions, the appropriate anesthesia machine manual should be referenced, as there are many machines that have automated checks and/or variations to these procedures. 9. Test scavenging system function. To prevent room contamination by anesthetic gases, a functional scavenging system is necessary. The connections between the anesthetic machine and the scavenging system must be checked daily to ensure integrity of the scavenging system. The anesthesia technician should be particularly careful to remember to attach the scavenging system to the evacuation system when moving anesthesia machines to out-of-operating room (OR) locations of care. There are various scavenging system designs that may require that an adequate vacuum level be present. On active systems (e.g., full vacuum), vacuum pressure can be modulated by the screw valve. Most modern scavenging systems have positive and negative pressure relief valves. The positive relief valve allows exhaled gases to be released into the OR in the event of
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inadequate vacuum (usually occurs in an active system when someone inadvertently closes the screw valve). The negative relief valve prevents suction in an active vacuum system from affecting airway pressure in the breathing circuit for the patients. As these valves are important to protect the patient from pressure fluctuations coming from the scavenging system, they must be checked daily. The checks on these valves can be quite complex; therefore, the anesthesia technician should receive specific troubleshooting training from the hospital biomedical engineers and refer more complicated problems to them directly. 10. Calibrate or verify calibration of the oxygen monitor and check the low oxygen alarm. Calibration of the oxygen sensor is critical for safe patient care. Continuous monitoring of the inspired oxygen concentration helps prevent the delivery of a hypoxic gas concentration to patients. The oxygen monitor is crucial to detect any changes in the oxygen supply. Oxygen sensor calibration should occur at least once per day. Some anesthesia machines are self-calibrating. For these machines, they should be verified to read 21% when sampling room air. The oxygen sensor calibration can be performed by an anesthesia provider or anesthesia technician. If more than one oxygen monitor is present, the primary sensor that will be relied upon for oxygen monitoring during patient care should be the one checked. The low oxygen concentration alarm should also be checked at this time. This is done by setting the low oxygen alarm above the measured oxygen concentration and confirming that an audible alarm is generated. Detailed oxygen sensor calibration instructions can be found in the specific anesthesia machine’s operator manual. 11. Verify carbon dioxide absorbent is not exhausted. A circle breathing system relies on the removal of carbon dioxide to prevent rebreathing of carbon dioxide by the patient. There is a characteristic color change in the carbon dioxide absorbent, depending on the particular absorbent being used, that indicates depletion of the absorbent. When this color
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change occurs, it is a visual reminder that the absorbent must be replaced. Some newer absorbents change color when they become desiccated. If the carbon dioxide absorbent is exhausted or desiccated, it should be changed. It is possible that the carbon dioxide absorbent loses its ability to remove carbon dioxide without producing a color change. For example, an exhausted desiccated absorbent may return to its original color after a period of rest. Capnography, which must be used in every anesthetic, can be helpful in indicating the need to replace the absorbent. When the inspired carbon dioxide concentration is detected to be greater than 0, this indicates that the patient is rebreathing carbon dioxide and that the absorbent may be used up, and therefore, needs to be replaced. When replacing carbon dioxide absorbent canisters, it is important to install them correctly. Incorrectly installed carbon dioxide absorbent canisters are a common source of leaks within the anesthesia machine. 12. Breathing system pressure and leak testing. The breathing system leak test must be performed on the components that will be used during a particular anesthetic. If any portion of the circuit is changed after completing the leak test, the leak test must be performed again to ensure the integrity of the breathing system. The purpose of this test is to ensure that adequate pressure can be generated and maintained in the breathing system during assisted ventilation. Adequate pressure is usually considered to be greater than or equal to 30 cm H2O. This test also checks the ability to relieve pressure in the breathing circuit with the APL valve during manual ventilation. To manually check the breathing system for leaks, the APL valve is closed and the patient port is occluded at the Y-piece. The oxygen flush valve is used to instill 30 cm H2O pressure into the breathing circuit. If the circle system is free of leaks, the value on the pressure gauge should not decrease. Of note, newer machines may have automated testing that can be used to detect leaks. Additionally, they can also determine the compliance of the breathing system. Once adequate pressure is obtained in the circle
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Chapter 27 • Anesthesia Machine Checkout
system, it can be released by completely opening the APL valve. This step can test for proper functioning of the APL valve, ensuring that it entirely relieves the pressure in the circle system. 13. Verify that gas flows properly through the breathing circuit during both inspiration and exhalation. Although checking the breathing system for pressure and leaks is important, this test does not assess the function of the unidirectional inspiratory and expiratory valves. The presence of the valves can be assessed visually. To test for proper function of the unidirectional inspiratory and expiratory valves, first remove the Y-piece from the circle system. Next, breathe through the two corrugated hoses separately. The valves should be present, and they should move appropriately. The person performing the test should be able to inhale but not exhale through the inspiratory limb and able to exhale but not inhale through the expiratory limb. At the completion of this test, the breathing circuit should be changed to a fresh circuit prior to attaching the anesthesia machine to the patient. This flow test can also be performed by attaching a breathing bag to the Y-piece and using the ventilator. In addition, capnography can also be useful to detect an incompetent valve. For example, an incompetent inspiratory valve should be considered in situations of high (greater than zero) inspired carbon dioxide concentration. 14. Document completion of the checkout procedures. A printed copy of the preanesthesia checkout procedures should be retained near or in the anesthesia machine since an organized and systematic list may result in improved fault detection over memory alone. Moreover, a pictorial checklist may be helpful as it can be simpler to follow than a typewritten list. Documentation of checkout procedure completion should be performed and may be important in the case of an adverse incident, as omission of the checkout can by cited as evidence of substandard care. Dates and times of certain checkout procedures may be recorded automatically by some computerized checkout
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systems, but those that are not automatically recorded should be manually documented by the individual who performs the checkout procedure. Record keeping is important to provide supporting evidence that equipment is being appropriately maintained. Should service be necessary, this record may also be helpful for service representatives who come to repair the equipment, for providing a reminder to check on the repair that was done, and for referencing at a later date what was repaired and who performed the repair. A log of malfunctions may also help to determine if a particular piece of equipment warrants replacement. This record should be retained, should an adverse outcome lead to litigation. 15. Confirm ventilator settings and evaluate readiness to deliver anesthesia care. (Anesthesia provider should perform.) Prior to starting each anesthetic, the completion of the preanesthesia checkout procedures should be verified as well as the availability of essential equipment. Ventilator settings should be confirmed and pressure limit settings used as a secondary backup to prevent barotrauma once positive pressure ventilation is used. Specifically, the presence and functionality of appropriate monitors, the capnogram, and oxygen saturation by pulse oximetry should be checked. Proper flowmeter and ventilator settings, placement of the ventilator switch to manual, and adequate filling of the vaporizers should also be ensured before initiation of an anesthetic. The delivery of safe anesthetic care in modern practice begins with a thorough evaluation of the anesthetic delivery system being used. Anesthesia providers, along with trained anesthesia technicians and biomedical technicians, must have a thorough understanding of the fundamental components of the anesthesia machine. Thus, malfunctioning components can be repaired or replaced to decrease the potential for patient injury. These preanesthesia machine checks should be documented not only for maintenance records but also for medical-legal reasons. With the great variation in anesthesia machine design, it
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is important to always refer to the specific anesthesia machine manufacturer’s instruction manual for more detailed information and instruction.
■ SUMMARY The anesthesia machine is a critical component of the OR. Failures in the anesthesia machine have the potential to cause significant patient injuries. Proper maintenance and a thorough checkout procedure can identify many machine problems before they have a chance to cause problems in the OR. Multiple organizations and the anesthesia machine manufacturers have been instrumental in devising detailed anesthesia machine checkout procedures. Each machine will have a unique checkout procedure detailed by the manufacturer. This chapter presents an overview of the machine checkout procedure that should be customized for each anesthesia machine according to the manufacturer.
REVIEW QUESTIONS 1. Which organization(s) was involved in developing the 1993 Anesthesia Apparatus Checkout Recommendations? A) FDA B) American Medical Association (AMA) C) ASA D) A and C E) All of the above
Answer: D. It is important to check for adequate pipeline supply pressure for all gases connected to the anesthesia machine. Although failure of pipeline pressure is rare, it can affect the delivery of gases to the patient and function of the ventilator.
4. Who is qualified to perform portions of the anesthesia machine check? A) Anesthesia care provider B) Anesthesia technician C) Biomedical technician D) A and B E) All of the above Answer: E.
5. How often should the breathing system pressure and leak testing be performed? A) Once per day B) Prior to the start of each case C) Only at the end of the day D) A and B Answer: D.
6. Vaporizers should A) Be checked for adequate agent prior to each case B) Have filler ports tightened after filling to prevent leakage C) Never be tipped D) A and B only E) All of the above Answer: E. Not only should the vaporizers be checked for adequate agent prior to each case, but after filling, the filler ports should be tightened. Vaporizers should NEVER be tipped, as tipping may cause the internal wick to become saturated and the delivery concentration could become inaccurate.
Answer: D.
2. All anesthesia machines have a check valve in the low-pressure system. A) True B) False Answer: B. A check valve in the low-pressure system will negate a positive-pressure leak test. A negative-pressure leak test will be necessary to perform an adequate anesthesia machine checkout. Anesthesia technicians should consult the manufacturer’s operator manual for the presence of a low-pressure system check valve and the proper procedure for testing for leaks in this system.
3. Piped gas pressure should be A) 20–25 psig B) 30–35 psig C) 40–45 psig D) 50–55 psig E) Greater than 55 psig
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SUGGESTED READINGS Brockwell RC, et al., for American Society of Anesthesiologists. Recommendations for Pre-Anesthesia Checkout Procedures. 2008. Available at: http://www.asahq. org/For-Members/Clinical-Information/∼/media/ For%20Members/Standards%20and%20Guidelines/ FINALCheckoutDesignguidelines.ashx; 2008. Dorsch JA, Dorsch SE. Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008. Edward MG, Mikhail MS, Murray MJ. Clinical Anesthesiology. 3rd ed. New York, NY: McGraw-Hill; 2003. Miller RD. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2009. Standards for Basic Anesthetic Monitoring, Committee of Origin: Standards and Practice Parameters (Approved by the ASA House of Delegates on October 21, 1986, and last amended on October 20, 2010, with an effective date of July 1, 2011).
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CHAPTER
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Vaporizers Roy Esaki and Alex Macario ■ INTRODUCTION
Vapor and Vapor Pressure
Inhalational agents are drugs with anesthetic properties administered in the form of a gas. For a drug injected intravenously, the dosing relates to the mass the patient receives (e.g., in grams), in the form of a specific volume at a specific concentration. Inhalational agents, however, are delivered as a concentration in a volume of gas. The “volume” is being continuously delivered with each breath the patient receives. As these agents normally exist as liquids at room temperature and atmospheric pressure, a vaporizer is used to turn the liquid into a gas that the patient can inhale. In the middle of the 19th century, the first available “vaporizers” were merely devices that allowed the patient to breathe evaporated liquid agents. The device used by William Morton in the first public demonstration of ether anesthesia in 1846 was a container that contained a sponge soaked with ether (Fig. 28.1). The patient breathed in the agent as it evaporated off the sponge. Later, chloroform was administered by dropping the liquid agent using special dropper bottles (Fig. 28.2) over a cloth that was placed either directly over the patient’s mouth or draped over a wire mask. Although such devices allowed the liquid to evaporate into a gaseous form, the concentrations of the agent could not be controlled. Modern vaporizers were thus developed to deliver a precise and constant concentration of the agent.
A vaporizer turns the liquid anesthetic agent from a liquid form to a gas, or vapor. All substances can exist in liquid, solid, or gas forms, depending on the pressure and temperature of the substance. As a gas is compressed under increasing pressure, the particles are pushed closer together until the gas turns into a liquid. For example, when nitrogen gas is compressed enough, it turns into liquid nitrogen. For some gases, there is a critical temperature above which a gas cannot exist as a liquid, no matter how much pressure is applied. A vapor is a substance in the gaseous phase at a temperature below its critical point. That is, it is a gas that has the potential to become a liquid when compressed, or subjected to a higher pressure. When a volatile liquid is placed in a closed container, a certain percentage of the liquid molecules evaporate to become vapor. This vapor creates a pressure, called the vapor pressure. As more heat is applied, more molecules enter the gaseous phase, resulting in a greater pressure. As such, the vapor pressure of any substance increases with temperature. The concentration of an agent delivered by a vaporizer depends on the vapor pressure of the agent. Because different agents have different vapor pressures, each modern vaporizer is calibrated for use with a specific agent. Of note, desflurane has a much higher vapor pressure at room temperature than other agents, and thus requires a vaporizer with unique features (see below).
■ PHYSICAL CHEMISTRY
Gas Concentration: Partial Pressure and Volume Percent
To understand the basic principles of how modern vaporizers work, we need to review some principles of physical chemistry: the concepts of vapor, vapor pressure, and gas concentrations.
The concentration of a vapor can be expressed as either a partial pressure or a volume percent. In a mixture of gases, each gas independently
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body, concentrations delivered by a vaporizer are commonly expressed as a volume percent for practical convenience. Volume percent is the fraction of the total pressure attributable to the gas of interest expressed as a percent (partial pressure of gas/total ambient pressure × 100). This term may be a slight misnomer as the gas molecules are mixed together in a shared volume. Nonetheless, because the volume of a gas is proportional to the number of particles, given a constant pressure and temperature, the volume percent of an agent can be thought of as a percentage of the total number of gas molecules delivered to the patient.
■ PRINCIPLES OF MODERN VAPORIZERS ■ FIGURE 28.1 Early vaporizer. A replica of the inhaler used by Dr. William Morton to demonstrate the use of ether anesthesia in 1846. An ether-soaked sponge was placed inside, and the patient breathed in the evaporated vapor. (Photo courtesy of the Wood Library-Museum of Anesthesiology, Park Ridge, IL [http://www.woodlibrarymuseum.org/museum_view.php?id=2].)
contributes part of the total pressure, which is the sum of the partial pressures of all gases present. The portion of the total pressure created by any given vapor is called the partial pressure of that gas. Although the partial pressure of the gas is what actually corresponds to the clinical effect of an anesthetic gas in the
■ FIGURE 28.2 Chloroform dropper. From left to right: a chloroform drop flask, a drop bottle with a control valve, and an alembic flask. Such devices allowed careful titration of the liquid agent. (Photo courtesy of the Wood Library-Museum of Anesthesiology, Park Ridge, IL [http://www.woodlibrarymuseum.org/museum_view. php?id=25].)
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Vaporizers vary greatly in their design and construction. Figure 28.3 shows one common type of modern vaporizer. All modern (concentrationcalibrated vaporizers) are placed out of circuit— that is, between the flowmeter and the common gas outlet, rather than within the breathing system or between the common gas outlet and the breathing system. The intent of this chapter is not to go over the specifics of the operation of any specific vaporizer model but to provide an overview of the principles underlying the operation of modern vaporizers.
■ VARIABLE BYPASS VAPORIZERS As mentioned previously, the basic purpose of a vaporizer is to deliver a set concentration of anesthetic gas in a volume of inert gas, such as oxygen. Figure 28.4 shows the general schematic
■ FIGURE 28.3 The Drager Vapor 2000 series; from left to right, a desflurane, a sevoflurane (turned on), and an isoflurane vaporizer.
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the vaporization chamber and for the flow that would skip the chamber had to be manually adjusted to achieve a desired output gas concentration. Modern variable bypass vaporizers do this automatically when the concentration dial is set to a desired concentration. Although the input fresh gas flow rate theoretically can increase the output gas concentration, this effect is minimal with most modern vaporizers. The input gas composition (i.e., if nitrous oxide is used in addition to oxygen) can also affect the concentration. To account for these effects, many electronic vaporizers have a feedback system that adjusts its internal settings based on the actual gas output. In other types of vaporizers, such as the Tec 6 used for desflurane, there are two separate input circuits, rather than a single fresh gas flow that is split.
■ VAPORIZATION METHOD ■ FIGURE 28.4 Schematic of a variable bypass vaporizer. Simple schematic of modern vaporizer: Fresh gas flow enters the vaporizer inlet (top left) and is directed either down into the vaporizing chamber to become saturated with vapor or into a bypass chamber across the top. By varying the ratio of the split, the output vaporizer concentration (top right) can be changed. (Figure courtesy Dr. Guy Watney [http://www.asevet.com/resources/ vaporizer/index.htm].)
of a vaporizer. In this schematic, fresh gas flow enters from the top left, corresponding to the vaporizer inlet. The inert gas can then flow across the top bypass chamber, without being exposed to any volatile agent. Alternatively, some of the fresh gas flow can be diverted down into the vaporizing chamber, where it becomes saturated with a certain concentration of the volatile agent, as determined by the partial pressure of the agent. The concentration dial can vary the percentage of gas, called the splitting ratio that bypasses the vaporizing chamber; this construction is thus called the variable bypass vaporizer. The end result is that the partial pressure of the volatile agent in the vaporizing chamber is diluted by the fresh gas flow through the bypass to obtain the desired concentration of anesthetic. The gas with the desired vapor concentration exits through the outlet of the vaporizer, shown at the top right of the schematic. In an older type of vaporizer, called the copper kettle, the gas flows for both the flow directed to
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Older vaporizers such as the copper kettle bubbled the carrier gas up through the liquid anesthetic to saturate the carrier gas with the anesthetic. Most modern vaporizers have the carrier gas flow over the liquid agent where it takes up the anesthetic. Increasing the surface with internal wicks and baffles makes the vaporization and uptake of the anesthetic more efficient. To accommodate the higher vapor pressure of desflurane, the Tec 6 vaporizer uniquely uses a gas/vapor blender in which the desflurane is heated to a constant temperature to produce a vapor that is then injected into the gas flow in a regulated fashion (Fig. 28.5).
■ FIGURE 28.5 Schematic of Tec 6 desflurane vaporizer. The liquid desflurane (liquid) is heated (H) to a vapor form (gas), which is then mixed with the carrier gas to produce a vaporizer output of the desired concentration. (Figure courtesy Dr. Guy Watney [http://www.asevet. com/resources/vaporizer/index.htm].)
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TABLE 28.1 PROPERTIES OF VARIOUS VAPORIZERS VAPORIZER MODELS MOST MODERN VAPORIZERS*
COPPER KETTLE, VERNITROL
TEC 6 (DESFLURANE)
Carrier gas flow
Variable-bypass
Measured-flow (operator determines carrier gas split)
Dual-circuit (carrier gas is not split)
Method of vaporization
Flow-over
Bubble-through
Gas/vapor blender
Temperature compensation
Automatic temperature compensation
Manual (i.e., by changes in carrier gas flow)
Heated to a constant temperature
Calibration
Calibrated, agent-specific
None; multiple agent
Calibrated, agentspecific
Position
Out of circuit
Out of circuit
Out of circuit
*Tec 4, 5, 7, SevoTec, Aladin (ADU); Vapor 19, Vapor 2000. Table adapted with permission courtesy Dr. Michael Dosch (http://www.udmercy.edu/crna/agm/05.htm).
■ TEMPERATURE COMPENSATION Since vapor pressure depends on the temperature of the gas, the output vapor concentration of older vaporizers was often dependent on temperature. Modern vaporizers have an automatic mechanism built in that regulates the variable bypass to compensate for changes in temperature, keeping the gas concentration roughly constant over standard operating temperatures. The degree of temperature compensation depends on the specific vaporizer; some vaporizers have gas outputs that slightly increase as ambient temperature increases (Table 28.1).
vaporizer are potential causes of a vaporizer leak. Before mounting or detaching a vaporizer, it and all adjacent vaporizers should be turned off. The “travel” setting on the vaporizer should be used, if present, to prevent the agent from filling the bypass chamber (Fig. 28.6). Even with the travel setting in use, care should be taken to
■ OPERATION OF VAPORIZERS Anesthesia technicians know how to install and remove, transport, fill, operate, and drain vaporizers. It is important to be familiar with safety features and potential problems associated with each process.
Installation of Vaporizer Vaporizer mounting systems can be permanent or detachable. Permanent mounting systems have the advantage of less risk of physical damage and leaks, but the disadvantage is that vaporizers cannot be swapped out if a different agent is needed, or if a vaporizer malfunctions. Most modern anesthesia machines have detachable mounting systems, in which vaporizers can be mounted or removed without tools. In general, each vaporizer position has an input and output port valve, each with O-rings to prevent an air leak between the mounting system and the vaporizer. Missing or broken O-rings or improper mounting of the
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■ FIGURE 28.6 The concentration dial must be in the Travel (T) position of the Vapor 2000 vaporizer before the vaporizer can be unlocked from the machine. This isolates the vaporizer chamber to prevent liquid from entering the bypass chamber.
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Chapter 28 • Vaporizers
transport all vaporizers in an upright position to prevent liquid agent from entering inappropriate compartments.
Filling the Vaporizer As vaporizers are calibrated for use with specific agents with given partial pressures, an incorrect gas concentration will be delivered to the patient if an incorrect agent is used to fill the vaporizer. Because of this, the filling systems of modern vaporizers are designed to allow a vaporizer to be filled with only a specific agent. In a bottlekeyed system, each agent comes in a specifically designed bottle that may itself be used to fill the vaporizer or that uses an attachment (filler) that uniquely connects to the bottle of the agent and the filling port of the corresponding vaporizer. A common bottle-keyed system (Easy-fill system) uses a bottle collar that is color coded according to the anesthetic agent. The filling attachment of the same color as the bottle collar is designed in such a way that it can only screw onto the appropriate bottle (Figs. 28.7 and 28.8). There may be a metal block in some vaporizers that must be removed prior to attachment of the filling device. After the bottle-filler assembly is inserted into the vaporizer, some vaporizers have a latch that
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must be opened, after which the bottle is rotated up to fill the vaporizer as shown in Figure 28.9. Funnel-fill systems are less frequently used but exist in some older vaporizers; a screw-in plug is removed to expose the opening of the funnel, into which the liquid agent is poured. A screw-in adaptor can be attached to the funnel, for use with the bottle-keyed system. Desflurane vaporizers often use a Quick-Fill System in which the grooved filling attachment is permanently attached to the bottle. This is an extra measure to prevent desflurane from being poured into the wrong vaporizer (Fig. 28.10). The level of liquid agent remaining in the vaporizer may be displayed electronically on the anesthesia machine, or more commonly by a liquid fill indicator. The level of anesthetic agent remaining should be checked prior to the start of every case. Each type of vaporizer will have a different rate of consumption based on its efficiency, but a rough estimate of how long the liquid anesthetic should last is given by the following formula: 3 × Fresh gas flow (L/min) × volume% = milliliters of liquid used per hour Thus, a case using sevoflurane at 1.8% at 2 L/min fresh gas flow yields an hourly consumption
■ FIGURE 28.7 As an example of the bottle-keyed system, the collar of the sevoflurane bottle (left) has a color and spacing of protrusions that match an agent-specific filling attachment (right) with appropriately spaced indentations.
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block must be replaced snugly. This is a very common oversight that can create a leak in the system, resulting in anesthetic gas leaking out to the atmosphere when the vaporizer is turned on. Most modern vaporizers have a system to prevent the vaporizer from being overfilled, but care should nonetheless be taken to not fill the vaporizer above the fill line.
Delivery of Anesthetic ■ FIGURE 28.8 Filling attachment for use with a keyed filling system. The color-coded base attaches uniquely to the collared bottle, and the rectangular filling block is grooved to uniquely fit into a specific vaporizer.
of 10.8 mL. The capacities of vaporizers vary greatly from roughly 100 to 400 mL, but based on the equation above, a vaporizer filled to 200 mL would last about 18.5 hours. Gloves should always be used when filling the vaporizer, as the liquid agents can be caustic to skin. Whichever system is used, the cap on the vaporizer filling receptacle or the metal
■ FIGURE 28.9 After insertion of the filling attachment with the bottle upright, a latch is pulled to secure the attachment, and the bottle is rotated 180 degrees to an inverted position to fill the vaporizer.
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Modern vaporizers generally have a dial calibrated in terms of volume percent; a counterclockwise rotation of the concentration dial universally increases the concentration. Some vaporizers have a button on the dial that needs to be depressed while the gas is turned on as an additional safety feature. All vaporizers have a vapor exclusion, or interlock, system that mechanically prevents more than one vaporizer from being turned on at the same time. As mentioned earlier, there may be a discrepancy between the concentration dial setting and the actual vaporizer output as the vaporizer function may be affected by the fresh gas flow, the temperature of the gas, and the vaporizer itself. The gas composition (whether nitrous
■ FIGURE 28.10 A desflurane bottle with a permanently attached filling attachment that uniquely fits into a desflurane vaporizer.
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oxide is present in the fresh gas flow) may also slightly affect the vaporizer output.
Removal of Anesthetic The method of draining an agent from a vaporizer varies according to the vaporizer model. In general, there is a drain valve or nozzle that may simply require removal of a plug or insertion of a drain attachment (as with the desflurane QuickFill system). The removed agent can theoretically be set to evaporate in an area that people will not be exposed to the vapor. Alternatively, the agent could be poured into a container connected to the vacuum system, which will remove the vapor as the agent evaporates.
■ TROUBLESHOOTING An anesthesia technician will be called upon to help troubleshoot vaporizers when they malfunction. In diagnosing an issue, it is helpful to categorize the problem as one in which the vaporizer is delivering higher than expected vapor output or lower than expected output. These abnormalities can be detected when an agent monitor is utilized and the detected agent appears to be higher or abnormally lower than the concentration selected on the vaporizer dial.
Higher than Expected Vapor Output If the vaporizer is overfilled, or if the vaporizer is tipped, the liquid agent can spill into the bypass chamber. When this happens, the normally agent-free diluent (fresh) gas that “bypasses” the agent is now exposed to the anesthetic and picks up some vaporized agent. The result is that the vaporizer output contains more vapor than the vaporizer dial has been set for. As mentioned above, the “travel” setting on some vaporizers seals the vaporizing chamber during transport to prevent liquid from entering the bypass chamber. A failure of the vaporizer interlock system may also result in more than one vaporizer being turned on at the same time. This problem can be detected by an agent monitor (see Chapter 32). The monitor will display an error message or the presence of multiple volatile agents. Although a properly mounted vaporizer should not have this problem, the reversal of flow (i.e., fresh gas flow entering through the exit port) through a vaporizer can in some vaporizers cause excessive vapor pressure. Another cause of higher than expected agent readings occurs when an agent
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■ FIGURE 28.11 The yellow sevoflurane keyed filling device is incorrectly screwed onto an isoflurane bottle and a purple isoflurane keyed filling device is incorrectly screwed onto a sevoflurane bottle. (From Keresztury MF, et al. A surprising twist: an unusual failure of a keyed filling device specific for a volatile inhaled anesthetic. Anesth Analg. 2006;103(1):124–125.)
is used incorrectly in a vaporizer meant for use with an agent with a lower vapor pressure. In this case, the output gas concentration will be higher than expected. The keyed filling systems meant to prevent this problem can be circumvented (Fig. 28.11). This practice must be strictly avoided. The clinical effect of the increased concentration will depend on the relative potencies of the two agents, which is reflected by the minimum alveolar concentration (MAC) values.
Lower than Expected Vapor Output A simple and common cause of decreased vapor output is absent or low anesthetic agent levels in the vaporizer. Checking the agent level is a quick first step in troubleshooting decreased vapor output. Many modern vaporizers will sound an alarm when the agent level is low. Another cause of lower than expected output is if a vaporizer leak is present. The most common cause of a leak is a missing or loose cap on the filling port. Other sources of leaks
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are vaporizer misalignment (i.e., resulting from a foreign object wedged under the vaporizer), a damaged or missing O-ring in the vaporizer, or internal mechanical failure (e.g., from physical damage). A leak in the downstream circuit may also result in a lower agent level being detected by the agent monitor. If a leak is suspected, the gas sampling line can be used to “sniff” around the vaporizer and circuits to detect the source of the leak.
Other Problems A physically damaged vaporizer or particulate contaminants in the vaporizer may cause a multitude of nonspecific problems, and the vaporizer should be immediately set aside and sent out for appropriate repair. Regular maintenance should be performed according to the manufacturer’s guidelines and institutional protocols; in general, semiannual preventative maintenance with annual servicing would be appropriate.
■ SUMMARY Anesthetic agent vaporizers are a critical component of anesthesia machines. The laws of physics govern how liquid agents vaporize and this determines how liquid anesthetic agents function within a vaporizer. Modern vaporizers add anesthetic vapor to the fresh gas flow to deliver a desired concentration of anesthetic gas. A thorough knowledge of the inner workings of vaporizers will help an anesthesia technician troubleshoot vaporizer problems.
REVIEW QUESTIONS 1. Which of the following statements about filling an isoflurane vaporizer with sevoflurane are TRUE? A) Agent monitors cannot detect different anesthetic agents. B) The output of the vaporizer would be unchanged. C) The output of the vaporizer would change. D) The vaporizer would not output any vapor. E) None of the above. Answer: C. Sevoflurane has a much lower vapor pressure than isoflurane. Each vaporizer is calibrated for the specific vapor pressure of the agent intended for the vaporizer. If the vaporizer is filled with an agent of a different vapor pressure, the output will differ from what is set on the dial. Agent monitors are specifically designed to detect the amount of agent in the
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circuit and are the best way to determine if there is a discrepancy between the dial setting and the vaporizer output.
2. The majority of modern vaporizers have the following characteristics EXCEPT A) Agent-specific B) Variable bypass C) Temperature compensated D) In-circuit E) Flow-over Answer: D. Modern vaporizers are placed such that the agent is introduced into the system prior to the common gas outlet. Very old vaporizers injected agent directly into the breathing circuit (in-circuit design). All of the answers describe features of modern vaporizes.
3. Which of the following would be least likely to cause an overdose of anesthetic agent? A) Damaged O-ring on the vaporizer-mounting bracket B) Filled vaporizer that has been tipped over C) Vaporizer usage in an especially hot environment D) Failed interlock system E) All of the above. Answer: A. Damaged O-rings typically cause a leak with some of the gas containing anesthetic escaping (not added to the fresh gas). This will result in lower than expected vaporizer output. Vaporizers that have been tipped over can introduce the agent into the bypass circuit, causing the bypass gas to pick up the agent, resulting in a higher than expected vaporizer output. As temperature increases, the vapor pressure of liquids increases, which could increase the amount of agent added to the fresh gas. Most modern vaporizers compensate for temperature variations within a set range. A failed interlock system may allow multiple vaporizers to contribute agents to the fresh gas flow, potentially resulting in an overdose.
SUGGESTED READINGS Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Williams; 2009. Dosch M. The anesthesia gas machine. Available at: http:// www.udmercy.edu/crna/agm/05.htm. Accessed May 1, 2011. Ehrenwerth J, Eisenkraft J. Anesthesia Equipment: Principles and Applications. St Louis, MO: Mosby; 2007. Keresztury MF, et al. A surprising twist: an unusual failure of a keyed filling device specific for a volatile inhaled anesthetic. Anesth Analg. 2006;103(1):124–125. Rosch J, Dosrch S. Vaporizers in Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Wolters Kluwer/ Lippincott Williams & Williams; 2008.
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Anesthesia Breathing Systems Charles A. Vacanti ■ INTRODUCTION It is exceedingly important for anesthesia personnel to understand and become proficient at using a variety of breathing systems. Fortunately, anesthesia breathing systems represent very simple and logical devices and are consequently quite easy to learn. For the purpose of this chapter, anesthesia breathing apparatuses are defined as devices that enhance the ability to breathe a desired gas or vapor (including air or oxygen). The reader should note that this discussion does not include a detailed discussion of the anesthesia machine itself, but only the breathing circuit. Ventilators that assist breathing and masks and other aids for breathing (such as masks and nasal prongs) are discussed in Chapter 30 and Chapter 35, respectively. This chapter focuses on the development of anesthesia breathing systems from a functional perspective.
■ BREATHING DEVICE REQUIREMENTS One of the most straightforward breathing systems was demonstrated in an early Tarzan film when the “ape man” cut a long reed through which he was able to breathe while submerged in a pond, to elude the natives pursuing him. The reed functioned in a manner similar to a modernday snorkel. Thus, the simplest form of a breathing system may still be one of the most commonly employed, the snorkel. Today’s “standard” snorkel is about 50 cm in length, with an internal diameter of 2 cm, resulting in a capacity, or dead space, of about 150 mL. At a length of 7.5 ft and an internal diameter of 1 cm, Tarzan’s reed would have contained the same volume. He could have easily disappeared from view in a murky pond while submerged at over 7 ft. Although it helped Tarzan hide, snorkel-type breathing tubes suffer from two limitations: (1) as you further decrease the diameter of the breathing tube, there will be
significantly increased resistance to breathing (try breathing through a standard soda straw for any length of time) and (2) as you increase the volume of the breathing tube by increasing either the internal diameter or the length of the breathing tube, it increases the dead space in the breathing system. Most of us intuitively understand the concept of dead space. Imagine trying to breathe through a very long garden hose. How long would you be able to survive? Dead space in a breathing circuit is defined as the volume from the patient end to the point at which exhaled gas can be flushed out of the system and exchanged for fresh gas. Imagine that Tarzan is breathing with a tidal volume of 500 mL (volume of each breath). As Tarzan exhales through his 150-mL reed, it fills with his exhaled breath until it is flushed out at the end. Just before Tarzan inhales his next breath, the 150 mL volume of the reed (dead space) is filled with his last exhaled breath. When he begins to inhale, the first 150 mL he breathes in will be his previously exhaled breath, depleted of oxygen and containing carbon dioxide (CO2). The next 350 mL of his inhalation will come from the fresh jungle air. This 350 mL is plenty of air for Tarzan. Now imagine that Tarzan is hiding on the bottom of a lake and is using a reed that is 30 ft long and 1 cm in diameter. The dead space volume of the reed is now 600 mL. If Tarzan were to exhale a 500-mL tidal breath, it would fill the reed. When Tarzan inhaled, he would breathe back in his exhaled breath from the dead space in the reed and never get any fresh air! A large dead space would have prevented Tarzan from breathing fresh air. The exhaled gas in the dead space contains residual oxygen and large amounts of CO2. Rebreathing this gas would rapidly prevent Tarzan from eliminating CO2 from his lungs. For a short period of time he could utilize the residual oxygen that he 255
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exhales and reinhales. Therefore, if Tarzan were breathing through a system with a large dead space, he would rapidly become hypercarbic and soon become hypoxic. Fortunately, Tarzan learned that he could breathe quite comfortably through a reed that was very long, and thus contained a tremendous dead space, by inhaling though his mouth and then exhaling through his nose. In this way, the reed always contained fresh air. As illustrated in our Tarzan example, rebreathing of exhaled gases can be prevented by inhaling through the mouth and exhaling through the nose. The same thing can be accomplished mechanically, by adding a one-way valve to a snorkel that converts an open breathing system to a semiclosed system. This is also what is done when you change from breathing air from the atmosphere through a snorkel to breathing air from a tank, using a self-contained underwater breathing apparatus (SCUBA). The valve allows inspired air to flow into the lungs, and then diverts exhaled air into the water. These examples allow us to understand the critical elements of an effective anesthesia breathing system. The device must have the following: 1.
2.
3.
A reservoir: A sufficiently large reservoir of inhaled gas (air, when snorkeling) is needed to expand the lungs with minimum effort. This means that the reservoir of gas or air must be within a very compliant system, allowing it to be easily drawn into the lungs. When using a snorkel, there is a virtually unlimited supply of air above the water. The atmosphere serves as an extremely compliant reservoir of air, which is pulled directly into the breathing tube. Low resistance to breathing: A conduit of sufficient diameter to conduct the gas being breathed, without creating significant resistance. In Tarzan’s example, the reed diameter was a major determinant of resistance in the system. Low dead space or a mechanism to effectively prevent rebreathing of exhaled gases: This prevents rebreathing any unwanted exhaled gases (CO2 or possibly anesthetic agents) and provides fresh gas replenished with oxygen. A snorkel contains a dead space < 150 mL (much less than a normal adult tidal volume). Alternatively, adding a one-way valve will prevent rebreathing of CO2 by diverting
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the exhaled gas from reentering the breathing tube. This modification converts an open breathing system into a semiclosed breathing system. The advantage is that it virtually eliminates dead space in the breathing system. The only disadvantage of a one-way valve is that the valve will add some resistance to breathing, and being an active mechanical modification, it may malfunction; that is, it could stick open or stick closed.
■ BREATHING CIRCUITS To design an effective anesthesia breathing system, one must identify the ideal goals, evaluate the theoretical limitations of the device or modifications being proposed, and make appropriate accommodations to meet the need. This is indeed what occurred historically in the development of breathing devices used in anesthesia. So, why in reality were these devices not originally based on the simple breathing tube described above? As stated previously, specific breathing devices were designed to meet specific needs. In Tarzan’s case, the need was to use the breathing system to breathe air from the atmosphere while submerged in a shallow pond. For the purpose of delivering anesthetic agents, the goal is to deliver known mixtures of gases and vapors (e.g., oxygen and anesthetic agents), delivered not from the atmosphere, but usually from a pressurized source of gas and an anesthesia machine. Now let’s design a breathing system to anesthetize Tarzan rather than enable him to breathe underwater, by modifying a simple snorkel. Rather than inserting the tube into his mouth, we will place the breathing apparatus over his mouth and nose using a mask. We can now examine the most effective way to connect this simple breathing apparatus to the gas source. The simplest way to connect the gas source to the breathing tube is to run the gas outlet hose from the gas source (from the anesthesia machine) and connect it to the breathing tube (Fig. 29.1). This type of breathing system would be classified as a Mapleson E system. This system can be extremely effective depending on how close to the mask the fresh gas source is connected. If the fresh gas is connected to the breathing tube far away from the mask, the patient will breathe in exhaled air mixed with room air and very little fresh gas from the gas source hose. If the fresh gas is connected
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■ FIGURE 29.1 Mapleson classification of breathing systems. FG represents the fresh gas flow. P represents the patient and mask. The round ball represents a squeezable “bag.”
to the breathing tube close to the mask, the fresh gas will flush the exhaled gas out of the end of the breathing tube. The patient will then inhale mostly fresh gas. This design improves the delivery of fresh gas, and if the flow is sufficient, helps remove exhaled CO2 by blowing it out of the breathing tube. The dead space in the system, where rebreathing occurs, is the volume distal to the end of the gas source hose (includes the mask). When the flow of fresh gas is at least 1.5–2 times the minute ventilation, exhaled CO2 is effectively washed out of the breathing tube, preventing rebreathing. In a slight modification of this system, the fresh gas hose is directed through the breathing tube before it connects close to the mask. This system is referred to as a Bain circuit. The Bain circuit is one of the simplest and most effective “open circuit” breathing systems still used in anesthesiology. In the Mapleson E circuit described above, the patient breathes spontaneously through the corrugated breathing tube. Positive pressure ventilation cannot be provided. Consequently, the system can be again modified, by adding a breathing reservoir bag on the end of the breathing tube with a pop-off valve on the base of the bag (see Fig. 29.1—Mapleson F). This system is classified as a Mapleson F or the Jackson-Rees circuit. By partially closing the valve on the end of the bag, ventilation can be assisted. Other modifications have been made to the circuit with changes in the length to the exhalation tubing or the addition of a “pop-off” pressure relief valve at various
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positions (see Fig. 29.1—Mapleson D circuit). In one modification, the exhalation tube is very short and a pressure relief valve was added near the face mask (see Fig. 29.1—Mapleson C). This is the design of the popular Ambu bag-valvemask system. While these above circuits are effective and efficient, a high gas flow (1.5–2 times the minute ventilation) is necessary to prevent hypercarbia. Although high gas flows are not impractical in small children, fresh gas flows of 10–20 L/min would be required in adults. To maintain such high flows is expensive and inefficient and produces large amounts of waste gases to be scavenged. One way to reduce both rebreathing and gas flow is to add a reservoir bag to the end of the tube. Although this is helpful, it is only moderately effective. Other simple solutions to reduce gas flows and prevent CO2 buildup are to add a CO2 absorber, and/or one-way valves, to any of the aforementioned open circuit systems.
■ CO2 ABSORBERS
Adding a CO2 absorber results in what is called a “to-fro” system. The first to-fro canister was developed by Waters to deliver cyclopropane. The system is quite effective but results in less than optimal mixing of fresh and expired gases when low flows are used. In to-fro systems, the fresh gas inlet may be connected either proximal or distal to the CO2 absorber. An effective way to reduce the dead space in this system is to direct the expiratory gases back to the inspiratory limb of the system, after being channeled through the CO2 absorber by means of the one-way valves. These changes effectively create what is referred to as a “circle system,” which is described in the following section.
■ CIRCLE SYSTEM In 1926, Brian Sword developed a unidirectional rebreathing system referred to as a circle system (Fig. 29.2). The circle system consists of a fresh gas inflow directed to an inspiratory limb and unidirectional valve, an expiratory limb and unidirectional valve, a CO2 absorber, an expiratory pop-off valve, and a reservoir bag. Circle systems may be classified as semiopen, semiclosed, or closed, depending on the amount of fresh gas inflow. During inspiration, the fresh gas, along with the gas in the reservoir bag, flows through the
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■ FIGURE 29.2 Circle system. “V” represents the ventilator. “B” represents the reservoir bag.
inspiratory limb and its associated unidirectional valve to the patient. During expiration, the inspiratory unidirectional valve closes and the expired gas flows through the expiratory limb and through a unidirectional valve to the CO2 absorber and to the reservoir bag. The CO2 is absorbed in the canister. The fresh gas flow from the machine continues to fill the reservoir bag. When the reservoir is full, a relief valve opens and the excess gas is vented into the atmosphere or a scavenging system. This system has the advantages of requiring only very low fresh gas flows (as low as 250–500 mL of oxygen), less consumption of anesthetic agents, reduction in atmospheric pollution, and conservation of heat and humidity. Disadvantages of circle systems include a complex design with increased opportunity for malfunction, incorrect arrangement, slow changes in the inspired anesthetic concentration with low flows, and increased resistance to breathing due to the CO2 canister and valves in the system.
■ CO2 ABSORBERS
The CO2 absorber itself introduces potential problems including inhalation of soda lime dust and potential generation of other toxic compounds from interaction with anesthetic agents. Circle absorber systems have been used extensively in North America for more than 30 years. They were developed to reduce rebreathing of CO2, reduce the cost and use of expensive gases and inhalational anesthetic agents as well as reduce the amount of gas required to be
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scavenged, and ultimately reduce the extent of environmental pollution. Two types of absorbers are widely used: soda lime and baralyme. Both react with CO2 and contain 80% calcium hydroxide and some potassium hydroxide. Baralyme is more commonly used in the United States. In addition to 80% calcium hydroxide, soda lime contains water and sodium hydroxide (15% water, 4% sodium hydroxide, and 1% potassium hydroxide). Small amounts of silicate are also added to provide strength and prevent powdering as soda lime pellets are fragile. Conversely, in addition to the 80% calcium hydroxide, Baralyme contains 20% barium hydroxide and may contain some potassium hydroxide. The addition of silica to Baralyme granules is not necessary to ensure integrity of the granules. It is also not necessary to add water to Baralyme because it is liberated by a direct reaction of barium hydroxide and CO2. The reaction of CO2 with absorbers at first seems to be complex, but the basic reactions are actually straightforward and quite similar in the two systems. Both involve reactions of CO2 and water to form carbonic acid (CO2 + H2O− > H2CO3). In each system, carbonic acid in the granules reacts with both calcium hydroxide and potassium hydroxide (present in each mixture) to form calcium carbonate, potassium carbonate, water, and heat. In addition, the carbonic acid also reacts very quickly with either the sodium hydroxide of soda lime or the barium hydroxide of Baralyme to form the carbonate salt, that is, sodium carbonate or barium carbonate. In the case of Baralyme, this concludes the reaction. For soda lime, the sodium carbonate then reacts with a calcium hydroxide mixture (as does the potassium bicarbonate) to form calcium carbonate as well as to re-form the sodium hydroxide and potassium hydroxide found in the original mixture. To be effective, the granules in the absorbing canisters must be properly configured to minimize resistance to airflow and to maximize the mixing of gases with the absorbent. A larger cross-sectional diameter allows less turbulence, with reduced resistance and less dust. Baffles in the canisters reduce gas tracking down the walls and passing through the canister without encountering the absorbent. To prevent rebreathing, the intergranular space should be greater than the patient’s tidal volume.
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■ INDICATION OF ABSORBENT EXHAUSTION Soda lime absorbs up to 26 L of CO2 per 100 g; however, both absorbents become exhausted when sufficient CO2 has reacted with the original chemicals. If CO2 continued to pass through the absorbent canister, it would pass through unchanged. How does the anesthesia provider know that the absorbent is exhausted? When the canister can no longer absorb any more CO2, the CO2 will build up in the circle system and the patient will inspire it. This can be detected with a CO2 agent monitor in the circle system that graphs both inspired and expired CO2 (capnography—see Chapter 32). The majority of gas analyzer’s alarms will alert you to indicate the presence of inspired CO2. High fresh gas flows in the circle system will help flush the CO2 into the scavenging system; however, most anesthesia providers are using low flows. With low flows, the patient can inspire CO2 and eventually the expired CO2 levels will rise significantly as well due to the accumulation of CO2 in the patient. Clinical signs of hypercapnia, such as tachycardia, hypertension, cardiac arrhythmias, and sweating, appear after substantial rises in body CO2. Another method of detecting that the absorbent is exhausted is the condition of the absorbent granules. Soft and crushable granules are converted to hard ones (calcium hydroxide changes to calcium carbonate—limestone), indicating exhausted soda lime. This would be difficult to discern with visual inspection alone. To solve this problem, different manufacturers add different indicator dyes to the absorber. Some change from pink when fresh to white when exhausted. Others changed from white when fresh to purple when exhausted. The indicators are an acid or base whose color depends on pH. Interaction of CO2 with the absorbent changes the pH of the water in the canister. Color change may be misleading in certain circumstances. As indicated above, multiple chemical reactions are taking place in the canister. Many of these affect the pH. It is not uncommon for the absorbent to turn color, indicating exhaustion, only to turn back to the “fresh” color after a rest period. Additional chemical reactions have taken place to further change the pH. When the absorbent is truly exhausted, the color change will be sustained.
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Another method of detection of exhausted absorbent is a temperature rise in the canister. Because CO2 neutralization is an exothermic reaction (heat producing), changes in the absorbent temperature occur earlier than color changes. Studies have suggested that when the temperature of the downstream canister is higher than that of the upstream one, the absorbent should be changed in both canisters.
■ ABSORBENT REACTION WITH ANESTHETIC AGENTS It is important to reiterate that the absorbents will interact with inhaled anesthetics to some extent. In some circumstances, interaction of sevoflurane with the strong bases present in soda lime or Baralyme results in the formation of a chemical called “Compound A,” which has been shown to cause nephrotoxicity in animals. The circumstances where this occurs include (1) low total gas flow rate (below 1 L/min), (2) higher concentration of sevoflurane, (3) the use of Baralyme rather than soda lime, (4) higher absorbent temperatures, and (5) desiccated CO2 absorbent. Exposure of desflurane and isoflurane to soda lime and Baralyme results in formation of carbon monoxide. The factors predisposing to carbon monoxide production include (1) higher anesthetic concentration, (2) higher temperature, (3) dry absorbent, (4) the use of Baralyme rather than soda lime, and (5) the specific anesthetic agent. The magnitude of carbon monoxide production from greatest to least is as follows: desflurane > enflurane > isoflurane > halothane = sevoflurane. Other CO2 absorbers (e.g., Amsorb; Armstrong Medical, Londonderry, Northern Ireland) have come on the market during the past several years. They consist of calcium hydroxide with a compatible humectant (a hygroscopic substance with the affinity to form hydrogen bonds with molecules of water), namely calcium chloride. The absorbent mixture does not contain strong bases such as sodium and potassium hydroxide. They were designed to be effective CO2 absorbents while being chemically nonreactive with anesthetic gases.
■ SUMMARY In conclusion, by understanding a few relatively simple principles, one should be able to
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understand and quickly become proficient with breathing systems that he or she encounters. With such an understanding, you should be able to evaluate the advantages and disadvantages of any breathing system, and to effectively troubleshoot problems. I strongly recommend that those interested in pursuing the principles of breathing systems in more depth refer to http://www. capnography.com/. Despite the Web address that might lead you to think that this Web site is focused on capnography, the overall focus of the site is on anesthesia breathing systems.
REVIEW QUESTIONS 1. To be an effective anesthesia breathing system, a device must have A) A large reservoir B) Low resistance C) Low dead space D) All of the above E) None of the above Answer: D. A large reservoir, low resistance to airflow, and low dead space are all key design features of an effective anesthesia circuit.
2. Which of the following are FALSE regarding dead space in a circuit? A) A large amount of dead space contributes to rebreathing. B) The location of unidirectional flow valves does not affect dead space. C) The location of the fresh gas flow can affect dead space. D) High fresh gas flow rates can minimize rebreathing. E) All of the above are true.
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Answer: B. Unidirectional valves, as in a circle system, can direct exhaled gases in one direction and minimize rebreathing (reduces dead space). Locating the fresh gas flow near the breathing tube helps flush fresh gas near the breathing tube and minimize rebreathing as does high fresh gas flow rates.
3. Which item is NOT an indication of exhausted CO2 absorbent? A) Change in color of granules B) Increase in temperature of absorber C) Moisture in the circuit D) Increased inspired CO2 E) None of the above Answer: C. Moisture is not an indication of exhausted absorbent and is a natural byproduct of the chemical reactions of most absorbents. All other indicators are regularly used to judge exhaustion.
4. CO2 absorbent does not react with anesthetic agents. A) True B) False Answer: B. The most common reaction of anesthetic gases with CO2 absorbent is the production of carbon monoxide. All anesthetic gases currently on the market have some carbon monoxide production when CO2 absorbent is used.
SUGGESTED READING Shankar R, Kodali B. Anesthesia breathing system. Available at: h t t p : / / w w w. c a p n o g r a p h y. c o m / n e w / i n d e x . p h p ? option=com_content&view=article&id=288:maplesona-system&catid=79:-anesthesia-breathing-systems. Accessed on November 3, 2008.
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CHAPTER
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Anesthesia Machine Ventilators Eric Schnell and Valdez Bravo ■ INTRODUCTION A mechanical ventilator is a fundamental component of modern anesthetic practice. The ventilator performs two critical functions for an anesthetized patient: oxygenation and ventilation. Oxygenation supplies the lungs (and hence, the rest of the body) with oxygen. Ventilation delivers oxygen to the lungs and removes waste gases such as carbon dioxide from the lungs, allowing the body to maintain a physiologic acidbase balance. Additionally, ventilation can be used to administer and remove inhaled anesthetics. While awake, patients maintain spontaneous ventilation (breathing) by generating negative intrathoracic pressures with contractions of the diaphragm, causing air to flow into the lungs (see Chapter 16). After induction of general anesthesia, respirations are often depressed or absent, depending on the choice of anesthetics and muscle relaxants (i.e., neuromuscular junction–blocking agents). At this point, the airway is usually secured with an endotracheal tube (see Chapter 18). Ventilation and oxygenation are then accomplished by administering positive pressure to the patient’s airway, leading to the flow of oxygen and anesthetic gases into and out of the lungs. When the mechanical ventilator is not engaged, positive pressure can be manually delivered to the breathing circuit by squeezing the breathing reservoir bag with the adjustable pressure-limiting (APL or “pop-off”) valve partially closed (see Chapter 29). Alternatively, the breathing circuit can be placed in continuity with the ventilator, which delivers positive pressure breaths with a desired waveform and frequency. When the positive pressure is released, the patient passively exhales gases, including waste carbon dioxide, back into the breathing circuit.
Although both manual and mechanical ventilation are capable of providing oxygen, delivering anesthetic gases, and removing carbon dioxide, mechanical ventilation has several distinct advantages. First, it frees the anesthesia provider from having to perform continuous manual ventilation throughout the case. Second, it allows the anesthesia provider to set specific pressures and/or volumes for each breath, allowing for more precise control of ventilation than is possible manually. This fine control is critical when small changes in ventilatory parameters are required to optimize a complex patient’s respiratory function. Third, modern ventilators can deliver positive pressure waveforms that are difficult to achieve with manual ventilation, such as pressure control ventilation or end-inspiratory pauses (“holds”). Fourth, modern ventilators are linked to pressure monitoring systems that give important information about lung compliance. Thus, they are able to instantly release positive pressure if a threshold (maximum) pressure is reached, providing an additional measure of safety (for instance, when a patient coughs or strains against the ventilator). Finally, in certain modes, mechanical ventilators can even assist a patient’s spontaneous breathing by detecting a patient’s respiratory efforts and synchronously delivering positive pressure at the appropriate times.
■ VENTILATOR MODES Modern ventilators operate in specific modes that define the overall pattern of positive pressure delivery. The anesthesia provider independently programs parameters specific to each patient/procedure. Basic ventilator modes are distinguished based on two important characteristics: whether the ventilator delivers a fixed tidal 261
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volume or a specific inspiratory pressure and whether the ventilator is triggered by an internal timer or by the patient’s own respiratory efforts. Volume control ventilation delivers a set volume (also referred to as the tidal volume) with each positive pressure breath. These breaths are delivered at a provider-determined frequency, and thus provide a predictable minute ventilation (Minute Ventilation = Ventilator Rate × Tidal Volume). One major advantage of the volume control mode is the consistency of minute ventilation over prolonged periods of time, even during changes in lung expandability (known as lung compliance—see Chapter 11). For example, if a patient suddenly bears down and stiffens the chest muscles (making the lungs less compliant), the ventilator needs more pressure to expand the lungs than when the patient was completely relaxed. The ventilator will increase the pressure accordingly, and still deliver the same tidal volume as long as the inspiratory pressure limit
(Pmax, often set to 40 cm H2O in adults) is not reached. However, once the pressure limit is reached, the ventilator will stop delivering positive pressure and an alarm will sound, warning the anesthesia provider of the high airway pressure. One disadvantage of this mode is that it often requires slightly higher absolute peak pressures than other modes to achieve the same minute ventilation (Fig. 30.1A). Also, the lungs spend less time at larger lung volumes compared to pressure control ventilation, which may decrease the time available for gas exchange in some portions of the lung. Pressure control ventilation delivers a set plateau level of positive pressure with each inspiration (Fig. 30.1B). The actual tidal volume delivered depends on the patient’s lung compliance: A more compliant set of lungs will expand more easily and thus receive a higher tidal volume at the same pressure control settings than a less compliant (stiffer) set of lungs. One advantage
A Volume Control
B Pressure
Pressure Control
C Pressure Support
D SIMV
Time ■ FIGURE 30.1 Pressure-time waveforms of different ventilation modes. A: In volume control ventilation, pressure steadily increases during inspiration, as gas (typically at a constant flow rate) fills the lungs. During expiration, pressure drops quickly as the chest and diaphragm passively recoil. Breaths are delivered at regular time intervals. B: In pressure control ventilation, the ventilator quickly reaches the plateau (control) pressure and maintains this throughout the breath. This requires an increased respiratory flow at the outset of the breath and a small delay for the ventilator to reach the target pressure. Expiratory flows are passive and follow the same waveform as in volume control. C: In pressure support ventilation, the patient initiates each pressure-controlled breath by generating negative pressure (note the downward deflections prior to the pressure support), and thus inspiratory timing is dependent on patient effort. D: In SIMV, a volume-controlled breath is delivered with each inspiratory effort. If the patient fails to initiate a breath after a set interval, the ventilator will deliver a volume-controlled breath regardless.
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of this mode is that for any given peak pressure, the patient will spend a larger amount of time at larger lung volumes, and have a larger tidal volume, than that reached during volume control ventilation. It may be particularly useful in patients with very stiff lungs, or those in whom it is otherwise difficult to sustain adequate ventilation without resorting to very high inspiratory pressures. A disadvantage of this ventilator mode is that minute ventilation can change substantially if the patient’s pulmonary compliance changes. However, this can be easily countered by programming the alarms on the ventilator to notify the provider when tidal volumes or minute ventilation fall outside of a predetermined range. Both of the aforementioned ventilator modes are designed to deliver a set number of breaths per minute (the respiratory rate) on a regularly timed basis. This is absolutely necessary when an anesthetized patient is paralyzed and unable to breathe spontaneously. However, many anesthetics do not require complete muscle paralysis, and these patients may continue to make respiratory efforts while fully anesthetized. Modern ventilators are able to assist these efforts by synchronizing positive pressure delivery with a patient’s own respiratory rate. This assistance helps to counter the respiratory depressant effects of many anesthetics and the increased work of breathing through the resistance of an endotracheal tube. In pressure support ventilation (sometimes referred to as PSV-Pro ventilation), the ventilator senses a patient’s inspiratory effort as a drop in breathing circuit pressure and delivers a set level of positive pressure to augment the patient’s tidal volume (see Fig. 30.1C). In this mode, the patient is less likely to breathe in opposition to the ventilator, and thus less likely to cough or strain. As this mode depends on the patient’s effort to initiate an inspiratory cycle, if the patient stops making ventilatory efforts (or these efforts are too weak to trigger the ventilator), he or she receives no ventilation. For this reason, pressure support modes often have a backup mode that automatically begins timed positive pressure ventilation after a specified interval if no breaths are detected (often 30 seconds). One last commonly employed ventilator mode, synchronized intermittent mandatory ventilation (SIMV), delivers a specified volume synchronously with a patient’s respiratory efforts (Fig. 30.1D). However, it is also programmed to
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deliver the same volume after a specified time even if the patient has not made any inspiratory breaths during this interval. More advanced modern ventilators function using combinations of several of the above characteristics. Additionally, more detailed settings such as the ratio of time the ventilator spends in inspiration versus expiration during each respiratory cycle (the I:E ratio) can be changed, which may be useful in managing clinical situations such as bronchospasm. One commonly used, and clinically important, ventilator function is the ability to maintain positive pressure between breaths, called positive end expiratory pressure (PEEP). Without PEEP, the patient exhales gas back into the circuit until the airway pressure reaches atmospheric pressure. With PEEP engaged, expiratory flow is mechanically stopped when the desired expiratory pressure is reached, and thus positive pressure is maintained until the next inspiratory cycle. PEEP prevents lung alveoli from collapsing between breaths and can be of extreme utility in patients with pulmonary edema or obesity. In addition, it is critical in the management of ventilation during many thoracic surgery procedures. However, if the respiratory rate is set so high that the patient does not have time to exhale completely between breaths, the pressure may never fall back to the PEEP or atmospheric pressure, causing a phenomenon known as breath stacking and a gradual increase in pressures throughout the respiratory cycle.
■ VENTILATOR OPERATION Most mechanical ventilators used in operating room (OR) environments today can be categorized by the reservoir compressing the gas for each breath: bellows or piston. In each of these designs, the gas reservoir is in continuity with the breathing circuit and delivers whatever gas mix is in the circuit to the patient. During inspiration, external force compresses the reservoir, pushing the gas into the patient. At the beginning of expiration, the force is released, depressurizing the circuit. As the circuit pressure falls, gas moves out of the patient, driven by the patient’s elastic chest recoil. The ventilator’s gas reservoir refills with a combination of fresh gas from the anesthesia machine and expired gas returning from the patient (after having passed through the carbon dioxide absorption canister). Depending
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on the mode of ventilation, an inspiratory cycle may be based upon achieving a certain desired pressure or delivering a particular volume over a specified amount of time. Each ventilator model employs different designs to accomplish similar goals. However, all modern anesthesia machine ventilators share certain characteristics:
pressure measurement as well. A flow sensor is incorporated into the expiratory limb of the circuit and can be used by the anesthesia machine to calculate tidal volumes. • Pressure alarms and release valves to alert the provider of changes in lung compliance and to prevent pressure-related lung damage (barotrauma).
• A manual/mechanical control switch, which converts between manual and mechanical ventilation. This can be either a manual toggle or a digitally controlled servo. Thus, either the ventilator or the reservoir bag is able to ventilate the patient, but not both simultaneously. When the mechanical ventilator is engaged, the APL valve is bypassed, and compression of the bag does not cause gas to flow into the patient. • Check valves integrated into the inspiratory and expiratory limbs of the patient breathing circuit (see Chapter 29) to ensure unidirectional gas flow in all spontaneous, manual, and mechanical ventilatory modes. Although not part of the mechanical ventilator per se, properly functioning valves are critical to the function of anesthesia ventilators. • Excess gas scavenging. Fresh gas from the anesthesia machine is often supplied in excess of what is required for ventilation, so ventilators must have a mechanism to shunt excess gas (particularly at high gas flows) from the ventilatory circuit into the scavenging system (see Chapter 26). Additionally, ventilators must contain a valve that isolates the positive ventilator pressures from the scavenging system during inspiration, in order to allow the ventilator to deliver the positive pressure to the patient. • A PEEP valve, which is either a manual (rotary) valve or a digitally controlled expiratory valve that is able to stop gas return from the patient when a particular circuit pressure has been reached. In some older machines, PEEP is accomplished by attaching a mechanical ball valve to the expiratory limb of the circuit. • Flow and pressure sensors that measure circuit pressure and expiratory flow. At the very least, circuit pressure can be measured by the analog pressure gauge in line with the circuit, but newer machines often display a digital
A bellows-type ventilator uses pressurized gas to compress the bellows and thus deliver anesthetic gases to the patient. As mentioned above, bellows are simply a collapsible reservoir in which to store the mixed anesthesia gas. Older bellows ventilators do not require electricity but use manual controls to regulate the flow of pressurized gas into a sealed chamber surrounding the bellows. As the pressure in this chamber increases, the bellows are compressed and anesthetic gas inside the bellows flows into the breathing circuit. At the end of the inspiratory cycle, the pressure in the chamber is released, allowing the bellows to refill with gases from the patient and from the anesthesia machine. This functional bellows design has been in practice for many decades as a mechanical/pneumatic system and has since been enhanced through the addition of electromagnetic valves, which increase precision in gas flow delivery and pressure control. A diagram of a bellows-type ventilator is presented in Figure 30.2. Note that bellows-type ventilators necessitate an exhaust valve to separate the breathing circuit from the scavenging/ overflow system during inspiration. A typical bellows ventilator uses the increased drive gas pressure in the bellows chamber to close the exhaust valve, thus directly uncoupling the ventilator from the scavenging system during inspiration. In the event of a power failure, they do not require power to generate ventilator pressure. However, because they require pressurized oxygen, they will fail in the absence of pressurized gas and cause a backup tank to run out more quickly in the event of wall oxygen supply failure. Newer bellows ventilators are computer controlled, and thus require electrical power in addition to pressurized gas for operation (from wall outlets or a machine’s internal backup battery system). Piston ventilators use a motorized drive to compress a piston chamber, thus compressing the gas in the circuit. Newer piston-driven
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■ FIGURE 30.2 Bellows ventilator function: Inspiration and expiration. A: 1. During inspiration, bellows ventilators inject pressurized gas into the bellows’ housing chamber. 2. The bellows are compressed, forcing anesthetic gases inside the bellows into the breathing circuit, through the CO2 absorber, and into the patient. 3. Simultaneously, the ventilator drive pressure closes the overflow valve to the scavenging system, preventing gas from leaving the circuit. 4. Thus, during inspiration, all gas, including fresh gas from the machine, enters the patient. B: 5,6. During expiration, ventilator drive pressure is released, allowing gas to return and refill the bellows reservoir. 7. Release of bellows driving pressure also opens the scavenging valve, such that any additional anesthetic gases can exit the system once the ventilator bellows has filled.
ventilators provide more precise volume delivery, as the linear displacement of the piston allows the actual volume delivered to the circuit to be exactly determined. Additionally, piston ventilators are typically able to deliver higher peak pressures than many bellows ventilators, which may be of value in patients with lung disease but which also increase the potential for lung damage from the higher pressures. These ventilators do not need a gas source to power the ventilator but absolutely require electricity to run, from either a wall source or a battery backup. A typical piston ventilator design is detailed in Figure 30.3, which also shows how computer-controlled valves isolate the ventilator from the scavenging circuit as well as maintain PEEP.
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Other ventilator designs, for example, those employing turbines to deliver positive pressure, are not currently integrated into modern anesthesia machines. They are increasingly common in intensive care and transport ventilators, and thus might be used in the OR in rare circumstances, but are not be discussed here. Many modern ventilators have additional features that improve ease of use, safety, and accuracy. Commonly available features include the following: • Digital display/controls: Most modern ventilators incorporate a computerized control interface, which allows digital control of ventilator modes, pressures, volumes, PEEP, and alarm settings (see Fig. 30.4). Despite the fact that the most modern ventilators include digital readouts of tidal volumes and pressures, the bellows and pistons can be seen moving through a clear window, which serves as an important visual cue to confirm ventilator function. • Compliance compensation: Because the disposable breathing circuit tubing expands during inspiration, some of the measured tidal volume stays in the expanded tubing and never reaches the patient. Newer ventilators are able to measure circuit compliance (during machine checkout) and compensate for the volume lost in expanding the circuit by increasing the delivered tidal volume. • Fresh gas decoupling excludes fresh gas from the breathing circuit during inspiration. In older ventilator designs, fresh gas entering the circuit during inspiration was added to gas being delivered from the bellows, significantly (and potentially dangerously) increasing tidal volume when respiratory rates were slow or flow rates were high (Fig. 30.2). • Feedback compensation: Newer ventilators are able to dynamically regulate the delivered tidal volume in order to compensate for leaks in the circuit or the airway. These ventilators compare the tidal volumes returned from the patient with the programmed values and increase the volumes delivered in order to maintain the provider-specified volumes.
■ VENTILATOR MAINTENANCE The maintenance for both types of ventilators is the same: periodic replacement of parts on a maintenance schedule prescribed by the original
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■ FIGURE 30.3 Piston ventilator circuit example. A: 1. In this example of a piston-driven ventilator (Dräger Fabius GS), piston movement compresses circuit gases during the inspiratory phase of the cycle. 2. A computer-controlled valve (PEEP/PMAX control) closes during this phase, allowing pressure to increase in the circuit and expand the patient’s lungs. 3. A separate one-way (fresh gas decoupling) valve isolates the inspiratory flows to the patient from the fresh gas arriving from the anesthesia machine. B: 4. At the end of inspiration, the PEEP/PMAX valve opens, allowing expiration. 5. Gas returning from the patient passes through the CO2 absorber and returns to the piston reservoir. 6. In this particular model, the breathing bag actually stores anesthetic gases that can be used to refill the piston chamber during expiration, while in bellows design, the breathing bag is entirely removed from the circuit when the mechanical ventilator is engaged. 7. If PEEP is desired, the PEEP/Pmax valve closes when the circuit pressure reaches the desired PEEP pressure, thus maintaining this pressure until the next inspiratory cycle.
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■ FIGURE 30.4 A typical ventilator control screen. This image demonstrates features found on many computer-controlled ventilator interface screens. These include displays of the actual measured tidal volume, respiratory rate, and minute ventilation, and buttons (left to right on bottom) to set the peak inspiratory pressure limit (PMAX), tidal volume, rate, I:E ratio, an inspiratory pause, and PEEP. Also shown is a continuously charted graph of airway pressure versus time, with numerical readouts of the peak, plateau, and PEEP pressures. This ventilator is functioning in a volume control mode. The oxygen concentration measured from the oxygen sensor is displayed in the upper right corner.
equipment manufacturer (OEM). However, this level of maintenance will be performed by inhouse biomedical equipment specialists, support specialists, or vendor field service engineers. Obviously, any ventilator malfunction should be thoroughly diagnosed and repaired prior to administering an anesthetic if at all possible. In the event of an intraoperative ventilator failure, a patient can be manually ventilated with the breathing bag (or a separate Ambu-Bag or Jackson-Rees circuit) while troubleshooting the ventilator and perhaps arranging for an intraoperative machine switch. In the absence of malfunction, ventilators, either piston driven or a regular bellows, should have the rubber components of the gas reservoirs replaced regularly, often every 6 months. There may also be some O-rings/seals that are replaced in conjunction with the bellows. The discs that serve as the inspiratory and expiratory check valves are replaced on a periodic basis, although often less frequently than the bellows.
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Frequent problems with ventilators include holes in the rubber material, collapsed bellows that fail to compress gas, bellows that catch/hang on one side, thus preventing accurate gas delivery, or pistons that lose their calibration. Pistondriven vents typically have an electronic eye that looks for a sensor to be in a certain light path when in the start position. If this finely tuned measurement is compromised, the piston-driven ventilator will not know what location it is in and will display errors on the display screen. If any lubrication of piston rubber O-rings/seals/ hoses is needed, it should be done by trained service professionals. They have special instruments for the job and will use lubricants that are manufacturer approved for the oxygen-rich environment.
■ SUMMARY Mechanical ventilation is an essential component of anesthetic practice. Anesthesia technicians play a key role in assisting patient care by
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understanding the modes in which mechanical ventilation is delivered and how different ventilator designs accomplish this task. Although different ventilator models will vary slightly from the designs shown in this chapter, an understanding of the functional components of a standard ventilator will make it straightforward to contextualize these differences. With any particular model, a review of technical and functional specifications particular to that ventilator (provided by the manufacturer) will allow you to inspect, maintain, and ensure the safe and proper functioning of each machine.
REVIEW QUESTIONS 1. Which of the following ventilator modes requires patients to initiate a respiratory cycle? A) Volume control B) Pressure support C) Pressure control D) PEEP mode E) None of the above Answer: B. With pressure support ventilation, the ventilator senses a drop in circuit pressure initiated by a patient’s breath and then delivers the set pressure to augment the patient’s breath. This mode is often used to synchronize the ventilator with the patient’s respiratory efforts. Volume control delivers a fixed volume breath at a given rate regardless of patient effort. Pressure control delivers a fixed pressure breath at a given rate regardless of patient effort. PEEP is not really a ventilator “mode” but rather a setting for the ventilator to deliver a small amount of fixed pressure during expiration.
2. Which of the following is TRUE regarding pistondriven ventilators? A) Pressurized gas drives movement of the piston. B) They are unable to work in pressure-support mode. C) They require wall outlet electricity to be functional at all times. D) They require a servo-controlled valve that prevents the circuit pressure from exiting to the scavenging system during inspiration. E) None of the above. Answer: D. Piston control ventilators use a motorized drive to move the piston and deliver the breath. Bellows control ventilators, not piston control, use pressurized gas to collapse the bellows and deliver a breath. Piston control ventilators require electricity to drive the piston and will not work if there is a power failure. All anesthesia machine ventilators must have a mechanism to prevent a breath from escaping into the
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scavenging system instead of being delivered to the patient. Piston control ventilators have a servo-controlled valve that is triggered at the same time the piston is triggered. The valve shuts off flow to the scavenging system.
3. Why is fresh gas decoupling important? A) It prevents wall oxygen from mixing with the anesthesia gases. B) It allows patients to breathe spontaneously while the ventilator is active. C) It allows delivered tidal volumes to be independent of gas flow rate through the machine. D) It allows fresh volatile anesthetics to be separated from those exhaled from the patient. E) It allows ventilators to deliver positive pressure during both expiration and inspiration. Answer: C. In many older ventilators, the fresh gas flow continues to flow into the circuit while the ventilator is delivering a breath. This means that the fresh gas flow during inspiration will be added to the breath. At high fresh gas flows, this can significantly increase a delivered tidal volume if the ventilator is set to volume control. Fresh gas decoupling excludes fresh gas from flowing into the circuit during an inspiration from the ventilator.
4. What is the function of PEEP? A) It can improve patient oxygenation by preventing alveolar collapse. B) It prevents backward flow of ventilator gases through the vaporizer. C) It pushes breathing circuit gases through the CO2 absorber. D) High PEEP allows more comfortable breathing for lightly anesthetized patients. E) It accelerates the flow of gases at the beginning of the next inspiratory cycle. Answer: A. With PEEP, the breathing circuit is pressurized with a small amount of positive pressure (5–10 cm H2O controlled by the PEEP setting). When a patient exhales, the lungs deflate. Maintaining a small amount of pressure during exhalation prevents the lungs and alveoli from completely deflating. This can improve oxygenation in some patients.
5. Which of the following is NOT an advantage of mechanical ventilation? A) It allows precise control of tidal volumes. B) It allows precise control of minute ventilation. C) It allows the anesthesia provider to perform other tasks without manually ventilating. D) It prevents patients from trying to initiate spontaneous breathing. E) It allows fine adjustment of inspiratory and expiratory pressures. Answer: D.
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Chapter 30 • Anesthesia Machine Ventilators Mechanical ventilation can allow the anesthesia provider to control tidal volumes, respiratory rate, minute ventilation (rate × tidal volume), inspiratory pressure, and expiratory pressure. It also does not require the anesthesia provider to squeeze the bag and can free him or her up to perform other tasks. However, just because a patient is on a mechanical ventilator does not mean that the patient cannot attempt to breathe on his or her own. Patients can “fight” or “overbreathe” the ventilator as they attempt to take breaths. The clinician may need to paralyze the patient, or alter the ventilator settings or mode to achieve smooth ventilation, for example, changing to pressure support ventilation to augment the patient’s breathing efforts.
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SUGGESTED READINGS Barash PG, Cullen BF, Stoelting RK, et al. The anesthesia workstation and delivery systems. In: Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:Chapter 26. Dorsch JA, Dorsch SE. Anesthesia ventilators. In: Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:Chapter 12. Miller RD, Eriksson LI, Fleisher LA, et al. Respiratory care. In: Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2010:Chapter 93.
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CHAPTER
31
Anesthesia Machine Operation, Maintenance, and Troubleshooting Andrew Oken and Scott Richins ■ INTRODUCTION The anesthesia machine began quite humbly as a basic device to deliver anesthetic gases. It has evolved to a sophisticated integrated computerassisted physiologic monitoring system and anesthesia delivery system. Fundamentally, it continues to serve principally to facilitate gas exchange in the anesthetized patient; however, a number of functions have been integrated to improve the machine’s safety profile. Some of these improvements include agent-specific vaporizers, oxygen proportioning systems, oxygen analyzers, oxygen failure safety valves, breathing circuit pressure monitors, and the pin index safety system. The anesthesia machine consists of various components managing gas delivery and elimination, including a ventilator, gas inflows from a variety of sources, anesthetic vaporizers, scavenging system, breathing circuit, and CO2 absorption system. All these systems have appropriate check mechanisms and associated alarms or notifications to alert the medical providers to potential problems. While there are a number of machines available on the market, they principally share some very similar fundamental components and functionalities. It is therefore critical to have a basic understanding of the principles of the workings of the machine. Such a core base of knowledge is absolutely necessary to safe medical practice and the maintenance and evaluation/troubleshooting of anesthesia machines. Despite the similarities between anesthesia machines, it is important to recognize that machines have distinct differences. Anesthesia technicians should be thoroughly familiar with the unique properties of machines in use at their institutions.
The American Society of Anesthesiologists (ASA) and the Food and Drug Administration (FDA) have collaborated to develop recommendations for checking out an anesthesia machine prior to administering an anesthetic (see Chapter 27). Each manufacturer provides maintenance schedules, troubleshooting instructions, and guidelines for checkout of its specific machines. Internal machine designs vary and hence the need for specific manufacturer recommendations. In addition to testing machine components, the checkout will test associated alerts/ alarms. Anesthesia technicians should have detailed knowledge of the anesthesia machine checkout procedures as this can be the first indication that there is a problem with a machine. Anesthesia technicians will also be asked to troubleshoot machine problems between cases or even during a case. This chapter assists the anesthesia technician with the operation, maintenance, and troubleshooting of anesthesia machines.
■ BRIEF OVERVIEW OF THE ANESTHESIA MACHINE Although anesthesia machines can include several functions, the main function will always be to provide a controlled supply of oxygen and other anesthetic gases to the patient during surgery. The details of gas supply to the machine have been discussed previously; however, a short review is presented here to facilitate a troubleshooting discussion (see Fig. 31.1). The machine circuit can be broken down into high- and low-pressure circuits. The highpressure circuit starts where the gas enters the machine and ends at the flow control valves.
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N2O Cylinder Supply Check Valve
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■ FIGURE 31.1 Diagram of a generic gas anesthesia machine. (With permission from Barash P G, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.)
Gas enters the machine at a pressure near 50 psi from the pipeline. Gas can also be supplied from E cylinders, which supply a pressure of 2,200 psi for oxygen and 745 psi for nitrous oxide when tanks are full. This pressure is then further regulated to 45 psi downstream. Traveling toward the patient the next device is the fail-safe valve, which is downstream from the nitrous oxide source and serves to decrease the supply of nitrous oxide if the oxygen pressure drops. Most Datex-Ohmeda machines also have an oxygen supply alarm that sounds when the pressure drops below a safe level. Both these devices serve to decrease the potential for delivering a hypoxic mixture of gas. Gas then enters the flow control valves. The oxygen and nitrous oxide valves are coupled together to limit the percent of nitrous oxide that can be given as another
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means to reduce the risk of giving the patient a hypoxic mixture of gas. The low-pressure system of the anesthesia machine begins downstream of the flow valves. Gas travels through the flowmeters into a common manifold and then into one of the calibrated vaporizers. Between the vaporizers and the common gas outlet, which connects to the patient circuit, there is a check valve that prevents gas from flowing backward through the vaporizers. Exhaled gas passes through the carbon dioxide (CO2)-absorbing canister and rejoins the fresh gas here as well. The combined gas fills the ventilator or the bag depending on which manual ventilation or the ventilator is selected. If excess gas is present at this juncture, it overflows to the scavenging system past the adjustable popoff lever (APL), or through the ventilator relief
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⫹30 cm H2O Open Closed Closed
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■ Figure 31.2 Picture of circle system with ventilator. (From Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.)
valve. Gas then flows out through the inspiratory flow device past the oxygen analyzer to the patient through the inspiratory limb of the circuit. Expired gas is recycled as it flows back though the expiratory limb of the circuit, through the flow sensor, and then through the CO2-absorbing canister to ultimately rejoin the fresh gas from the common gas outlet prior to entering the ventilator or bag (see Fig. 31.2).
■ GENERAL AND DAILY MAINTENANCE Regular service should be performed by a machine representative according to the manufacturer’s recommendations. Daily maintenance
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by an anesthesia technician is crucial for proper function. Previous chapters have described sterilization techniques and daily machine checkout. These will not be covered in this chapter, but we will refer to the checkout process frequently because many of the problems that require troubleshooting can be prevented or later identified by the simple tests performed in a daily machine checkout. At the end of the day, further routine maintenance should be done. This includes removing the flow transducer to dry unwanted moisture, exchanging the CO2 absorber if it is exhausted, ensuring the gas flowmeters are off, and powering down the machine.
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273
■ TROUBLESHOOTING COMMON PROBLEMS Low Pressure If low pressure in the anesthesia machine is detected, the following items should be examined: • Check for low pressure leak. • Check for a circuit disconnect starting with the patient and working back to the machine. • Inspect bellows. • Inspect CO2 canister. • Check lids/coupling of vaporizers. • Inspect the flow sensor. • Check oxygen pressure from pipeline/cylinder. • Check for incompetent ventilator relief valve. The most common cause for a low-pressure alarm is a leak in the low-pressure circuit, and the most common cause of a leak is a disconnection or partial disconnection in the patient circuit. This is evaluated quickly starting at the patient and moving back to the machine evaluating the placement of the endotracheal tube (ETT), the ETT cuff pressure, the connection between the ETT and the circuit, the gas sample line port, and the connection of the inspiratory and expiratory tubing distal and proximal to the machine. If the leak is not resolved, continue to move upstream. Ensure the flow sensor is installed properly and tightly engaged. Check that the oxygen sensor is properly installed and all fittings are tight. Another common place for a leak is in the canister holding the CO2 absorber (see Fig. 31.3). Check to see that the latch is tight and there are no granules in the way of the seal with the gasket. Also, look and listen for cracks in the canister and ensure the condensation drain is closed. When the ventilator is turned off, if the pressure in the circuit returns to normal with hand ventilation, the leak can be isolated to the ventilator. The housing can be removed to look for cracks. This, along with poor seating of the plastic housing, can result in inappropriately low tidal volumes delivered to the patient because the driving gas is leaking into the room rather than compressing the bellows. Next, inspect the vaporizer lids to ensure they are on tight and inserted into the coupling system correctly. With the use of electronic flowmeters in newer machines there are no fluted tubes that can crack, but this is another place a leak can occur and should be examined when mechanical flowmeters exist.
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■ FIGURE 31.3 Carbon dioxide absorption canister in open/unlocked position (see space between plastic housing and blue plastic gasket); also condensation drain open at bottom.
It is uncommon for a low-pressure alarm to be due to problems in the high-pressure circuit, but they can occur. Pressure can be lost from inadvertent disconnects from the main supply, loss of the main supply pressure, or unrecognized depletion of a cylinder. Other less common causes may include a malfunctioning scavenging system or the vacuum is set too high such that the negative pressure from the scavenging system is able to lower the pressure in the circuit. Occasionally, high negative pressure in the scavenging system can also cause high pressure in the breathing circuit. In some machines, high negative pressure from the scavenging system can close the ventilator relief valve blocking excess gas from exiting the circuit, leading to increased airway pressures. Lastly, an incompetent ventilator relief valve can lead to hypoventilation because gas is delivered to the scavenging system instead of to the patient when the bellows collapse.
Hypoxic Gas Mixture • Turn on 100% oxygen and check for proper reading from the oxygen sensor. • Recalibrate the O2 sensor.
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• Replace O2 electrode if it does not appropriately recalibrate. • Check for main pipeline crossover. A common cause for a hypoxic gas mixture alarm is improper calibration of the oxygen sensor at the time of machine checkout. If the alarm sounds while a patient is connected to the circuit, the patient should be put on 100% oxygen (the patient may need to be ventilated with an alternative oxygen source during troubleshooting, e.g., bag-mask or replacement anesthesia machine). If the sensor does not read 100% after stabilizing for several minutes, the sensor should be recalibrated. If it will not recalibrate to the proper setting, the oxygen cell should be replaced. If there is a hypoxic reading, the highpressure circuit should be evaluated. If a central pipeline crossover is suspected, the oxygen tank should be opened and the pipeline supply disconnected. If oxygen levels are restored by this change, it is critical to alert the appropriate hospital staff to avoid further serious adverse events.
Flowmeter Problems • Check for a leak. • Check for a stuck bobbin. Flowmeter problems can often be detected during machine checkout. If the flowmeters are set to specific values and the oxygen or gas sensors are not reading the correct percentages of gas, either the sensors are malfunctioning or there is a problem with the circuit or flowmeters. Newer models of anesthesia machines are equipped with electronic flowmeters rather than the standard fluted glass tubes with a floating bobbin. Troubleshooting of electronic flowmeters should be done by the machine representative. The most common problem with fluted tube flowmeters is a float that is stuck from debris, leading to inaccurate readings. The quick fix is to gently flick the flow tube in an attempt to free the float from the debris. Ultimately, this should be brought to the attention of the machine representative for definitive cleaning and repair. The presence of a crack in the glass flow tube can cause a leak and thus a faulty reading. This can usually be detected during machine checkout when the low-pressure leak test is performed. Cracks that cause only a very small leak may be hard to detect. In some machines, a check valve, located between the
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common gas outlet and the flowmeters, prevents gas from flowing back through the vaporizer and into the flow tubes. In these machines, a positive-pressure leak test of the low-pressure circuit will not detect a leak in the flowmeters. A negative-pressure leak test should be performed on machines with a check valve in this location.
■ VENTILATORS For a full description of anesthesia machine ventilators, see Chapter 30. A brief review is provided in order to discuss how to troubleshoot common ventilator problems. The ventilator is typically pneumatically or mechanically driven. Mechanically driven ventilators use a pistondriven system to deliver a set volume or airway pressure to the circuit. Many current ventilators use an ascending pneumatically controlled bellow as part of a semiclosed circle system (Fig. 31.2). The pressure inside the clear plastic hood surrounding the bellows is regulated by a pneumatic circuit. During inspiration, gas enters the hood and the increase in pressure (1) closes the ventilator relief valve, blocking gas from going to the scavenging system, and (2) drives the bellows down, pushing anesthetic gas to the patient (older ventilators may have hanging bellows instead of standing bellows). During expiration, the pressure in the hood decreases, which allows fresh gas and scrubbed (i.e., CO2 removed) exhaled gas to fill up the bellows. The drop in pressure also opens the ventilator relief valve and when there is back pressure inside the bellows (inside the breathing circuit); excess gas overflows into the scavenging system. The ventilator system also incorporates airway volume and pressure monitors. Volume monitors often sense exhaled tidal volume and minute ventilation but can also sense inspiratory volumes. Pressure monitors sense expiratory and inspiratory peak and plateau airway pressures. Default alarm settings are programmed into the machine to sound when certain volumes and pressures exceed or fail to meet specified limits. The volume sensor is often in the expiratory limb of the circuit and is susceptible to errors when too much moisture is in the system.
Ventilator Maintenance Regular maintenance includes that performed by the manufacturer representative along with frequent visual inspections and functional testing,
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in addition to allowing the flow transducer and flow valves to dry at the end of the day.
Troubleshooting Common Ventilator Problems Ventilator will not fill: The most common cause is a leak in the system. Perform the same steps as above to investigate a low-pressure alarm. In addition, check for an incompetent ventilator relief valve. • Check for low-pressure leak. • Check for a circuit disconnect starting with the patient and working back to the machine. • Inspect bellows. • Inspect CO2 canister. • Check lids/coupling of vaporizers. • Inspect the flow sensor. • Check oxygen pressure from pipeline/cylinder. • Check for an incompetent ventilator relief valve. Ventilator will not deliver a breath • Look for inspiratory reverse flow/negative inspiratory flow alarm. • Check for high airway pressures. • Check for an incompetent expiratory valve. Sometimes, the ventilator is unable to deliver a breath even though it is able to fill. A common cause of this problem may be with the flow transducer or flow valves. Alarms such as “inspiratory reverse flow” or “negative inspiratory flow” can be displayed on the screen. In each case, too much moisture in the circuit can affect the flow transducer’s capacity to measure flow. This can be resolved easily by exchanging the flow sensor for a dry one. High airway pressures can also limit the ventilator from delivering a proper breath, particularly when using pressure control ventilation. This will be addressed further below. If the expiratory flow valve is incompetent, the ventilator will be able to deliver a breath, but it will be much smaller than programmed, as there will be volume lost into the expiratory limb. High airway pressures with mechanical ventilation • Check the breathing circuit from the machine to the patient for kinking or any type of obstruction. • Check the ETT for obstruction (kinking, secretions, mainstem intubation, etc.).
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• Consider patient pathophysiology (bronchospasm, tension pneumothorax, stone chest, etc.). • Check pop-off valve. • Check positive end expiratory pressure (PEEP) settings. • Check ventilator parameters. There are many common causes for ventilator alarms to sound. Low airway pressure was addressed previously under the gas delivery section and is most commonly due to a disconnection or leak in the system. High-pressure alarms can sound because of a number of patient-related processes, including bronchospasm and pneumothorax. These should be addressed by the anesthesia provider and are beyond the scope of this chapter (but cannot be disregarded). There are several equipment malfunctions that can trigger a high-pressure alarm. The most common is due to an occlusion in the breathing circuit. Commonly, this is due to a kinked or obstructed ETT or a kinked hose on the inspiratory or expiratory limb. Once this has been addressed, ensure the pop-off valve and PEEP are set appropriately. If a volume-controlled mode of ventilation is in use, ensure the tidal volume is correct. Other possible contributors include problems with the scavenging system, which will be addressed below. Lastly, the parameters of the preset alarms should be evaluated and reset as necessary for the clinical situation.
■ GAS ANALYZER Historically, operating room (OR) gas analyzers were separate devices from the anesthesia machine. Newer models have gas analysis incorporated into the main machine. These monitor the concentrations of CO2, oxygen, and inhaled anesthetics (see Chapter 32). A small gas sample line from the analyzer is connected to the end of the breathing circuit and samples are taken regularly from the inhaled and exhaled gas. The percent of gas is shown on the monitor. The continuous monitoring of CO2 levels is called capnography, and a tracing correlating to these levels is displayed on the monitor.
Maintenance of Gas Analyzers The gas analyzer should be serviced by a machine representative. The water trap and sample tubing should be replaced regularly, especially if condensation can be seen.
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Troubleshooting Common Problems with Gas Analyzers No CO2 tracing • Check that the gas analyzer has been turned on and has completed its warm-up cycle. • Check that the gas analyzer is not performing a temporary self-test. • Check for sample line disconnect or obstruction. • Anesthesia provider should confirm ETT placement. • Check for a circuit disconnect. Ensuring a proper CO2 tracing is part of the machine checkout and most, if not all, problems should be identified early and easily rectified. If no tracing appears, there are two very common causes. First, ensure the machine is on and has had time to calibrate. Next, examine the sample line to look for kinks, disconnects, or fractures in the tubing (Fig. 31.4). Other problems that can be quickly fixed include checking to see if the moisture trap is inserted properly and not full of water. If the CO2 tracing “stops working” (i.e., is not registering a positive number) during the time of patient care, it is critical to first confirm that it is not a lack of patient ventilation before checking for a machine problem. Inaccurate gas analyzer readings • Check water trap for condensation. • Check sample line for disconnect, obstruction, or condensation. • Check for recent aerosolized medication administration. • Check vaporizers (properly installed and not empty).
■ FIGURE 31.4 Gas sample line has been broken at the connection from surgeon leaning on line during case.
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A common cause for inaccurate readings from the gas analyzer is condensation in the sample line and/or an incomplete connection to the machine. Kinked, fractured, or poorly connected sample lines can also cause faulty readings (Fig. 31.4). If aerosolized medication is given through the ETT, the gas analyzer can often have trouble identifying the various gases. For example, aerosolized albuterol may give an endtidal reading of halothane, despite the complete absence of halothane. Less commonly, end-tidal and inspiratory gas readings may not correlate with the vaporizer dial. If desflurane is the gas, ensure the electronic vaporizer is plugged in. Alarms should sound from a battery if it is unplugged, but if the battery is depleted, no alarm will sound. Another cause related to the vaporizer is spilling of volatile agent when the machine is tipped. This can be rectified by flushing the system for 20 minutes at high flows with the vaporizer set at a low concentration.
■ CO2 ABSORBER
Exhaled gas from the patient travels back to the machine through the expiratory limb of the circuit and flows through the CO2 absorbent to be “scrubbed” of CO2. Most current anesthesia machines contain a clear cylinder into which prepackaged or loose CO2 absorbent can be placed. After flowing through the absorbent, the exhaled gas reenters the circle system and combines with the fresh gas to return to the bag or ventilator. The two absorbents used most commonly include soda lime and calcium hydroxide lime. The agent Baralyme was previously used; however, because of problems with adverse reactions with anesthetic agents it has been removed from the market. Other problems with CO2 absorbents are due in part to oxygen that had been left flowing for a long period of time after the completion of a case, causing the absorbent to dry out. It is very important that gas flow be turned off when a patient is not connected to the machine. The absorption of CO2 from exhaled gas occurs through several chemical reactions eventually forming sodium carbonate, or potassium carbonate and water. A chemical indicator ethyl violet is added to the absorbent and changes from white to purple as the absorbent becomes exhausted, signaling that it is time to be replaced (see Fig. 31.5).
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■ FIGURE 31.5 Partially exhausted granules; the exhausted granules will have purple tint in contrast to the white fresh granules.
Maintenance of CO2 Absorbers
The CO2 “scrubber” should be evaluated at least on a daily basis and should be part of the checkout between patients. When using low flows of fresh gas, a significant amount of absorber can become exhausted quickly. When replacing the canisters, ensure the plastic canister is closed (Fig. 31.3) and that there are no granules between the gasket and the plastic housing. If a drain is present in the bottom of the cylinder, water should be emptied daily.
Troubleshooting Common Problems with CO2 Elevated CO2 on capnography
• Replace the CO2 absorber. • Examine inspiratory and expiratory flow valves. If an exhausted CO2 absorber is not recognized and replaced during the machine checkout, it will often be recognized intraoperatively. The patient’s capnogram tracing will not fall to zero during inhalation. Although there are several other serious clinical scenarios that can cause this, commonly high inspired CO2 is due to exhausted absorber. Although not related specifically to the CO2 “scrubbing” system, another cause of elevated end-tidal CO2 is a faulty inspiratory or expiratory flow valve. The valves can become incompetent if they are damaged, dried out, cracked, or get stuck in an open position from too much moisture (Fig. 31.6).
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■ FIGURE 31.6 Moisture in inspiratory and expiratory valves causing incompetent valve.
Moisture in the CO2 canister • Drain the moisture or replace the canister. Because water is a by-product of the CO2 reaction with the absorbent, and the patient’s expired gas is humidified, condensation can accumulate below the CO2 canister. This can lead to higher airway pressures and sporadic PEEP pressures. A drain is often located at the bottom of the canister and can be opened to drain excess fluid that inhibits gas flow.
■ SCAVENGING SYSTEM There are three places exhaled gases can go when they leave the patient. Gas can escape into the room from a leak around a face mask or past a deflated ETT cuff. Gas can go back through the circuit into the bag and if the APL valve is open it will accumulate in the collecting assembly of the scavenging system. If the ventilator is engaged, the gas can fill the ventilator and then spill over to the collecting assembly through the ventilator relief valve. The scavenged gas then moves through the tubing into the scavenging interface or reservoir. Once in the reservoir, it is removed through a conduit to the disposal assembly, which is most often a central vacuum that pumps gas to the outside of the building. One of the safety features of the scavenging system exists in the interface. If the rate of flow is greater than the removal, a positive-pressure relief valve opens and gas spills out into the room, preventing an increase in the pressure in the patient circuit.
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Scavenging System Maintenance Maintenance is performed by service representative at regular intervals. The dial controlling the suction in the disposal conduit should be checked daily and set appropriately.
Troubleshooting Common Problems with Scavenging Systems Overwhelmed scavenging system • Turn down fresh gas flow if >10 L/min. • Check the vacuum control valve for proper adjustment (may need to increase the vacuum). • Check that the gas disposal conduit is working. An overwhelmed evacuation system most often presents with opening of the positive-pressure relief valve and the sound of escaping air into the room heard on expiration. The most common cause for an overwhelmed scavenging system is having high fresh gas flows with high minute ventilation. This can be checked by turning down the fresh gas flows and seeing if the evacuation system is capable of keeping the scavenging reservoir bag
■ FIGURE 31.7 Distended scavenging reservoir due to inadequate level of vacuum suction or impaired pop-off valve.
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from becoming overdistended. If not resolved, the next step would be to ensure that the vacuum control valve is adjusted correctly. If the control valve is set too low, it is unable to keep up with the regular gas flows and the amount of vacuum should be increased (Fig. 31.7). If the reservoir is still distended after increasing the vacuum flow, check that the gas disposal conduit is working properly. Assess for any kinks in the line that could limit the elimination of scavenged gas (Fig. 31.8). If the vacuum is weak even after maximal adjustment of the valve, a problem exists in the central gas disposal system and should be addressed quickly to avoid gas contamination of multiple ORs. Increased circuit pressures • Check the transfer means for kinks. • Check the vacuum control valve for proper adjustment. • Check the positive-pressure release valve for proper functioning. The most common cause for increased circuit pressures is typically not related to issues with the scavenging system. However, occasionally the scavenging system circuit may become
■ FIGURE 31.8 Kinked gas disposal tubing of scavenging system.
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Chapter 31 • Anesthesia Machine Operation, Maintenance, and Troubleshooting
occluded in a location proximal to the pressure relief valve of the scavenger and cause high circuit pressures. Alternatively, high pressures in the scavenging system may result from a malfunctioning pressure relief valve, thus allowing the high pressure in the scavenging system reservoir bag to translate to increased circuit pressure. In both these situations, increased airway pressures and barotrauma may result for the patient. The patient must be disconnected from the breathing circuit and ventilated by alternate means while the problem with the scavenging system is being corrected. If the problem cannot be immediately corrected, a new anesthesia machine will need to be brought into the room. Decreased circuit pressures • Check that the vacuum control valve is adjusted properly. • Check the ventilator relief valve. The most common cause for decreased circuit pressures is typically not due to problems with the scavenging system. But again, if the vacuum control valve is maladjusted, negative pressures may transfer to the main breathing circuit if the scavenger system has an incompetent check valve. This can be managed temporarily by adjusting the vacuum control valve so that the bag is not completely deflated with low circuit flows. An incompetent ventilator relief valve may also lead to lower pressures as gas is delivered to the scavenging system instead of the patient. As with the situation of an incompetent scavenger check valve resulting in high circuit pressures, when the incompetent valve results in low pressure the anesthesia provider should consider changing the anesthetic to intravenous agents and then ventilating the patient with an intensive care unit (ICU) ventilator or Ambu bag, until a new anesthesia machine can be brought into the room or the current machine fixed.
■ SUMMARY While equipment failure certainly does occur, many machine-related issues may be prevented through regular maintenance, a complete anesthesia machine checkout, and thorough understanding of the operation and design of anesthesia machines. The methodical completion of a thoughtfully tailored and specific checkout for your institution’s machines
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will help enormously to avoid many of the commonly encountered machine issues and complications. When such events occur, you will also be better prepared to address the circumstance at hand. A regular maintenance program, in tandem with vigilance from the anesthesia providers, will help to identify many issues before they become system-threatening failures, leading to potential patient injury. The collaborative team approach between the anesthesia technician and the anesthesia provider is clearly demonstrated in this particular arena with significant overlap of responsibilities. Prompt cooperation and collaboration of all parties will help remedy the situation in a timely fashion and thereby minimize and/or avoid clinical complications.
REVIEW QUESTIONS 1. Which of the following would correctly identify a leak in an oxygen flow tube? A) Positive-pressure leak check B) Oxygen analyzer C) Negative-pressure leak test D) All of the above E) None of the above Answer: C. Because most machines have a check valve between the patient circuit and the common gas inlet, a positive-pressure leak test will not identify a leak upstream. If a small leak was present, the oxygen analyzer would be unable to identify that 1 L of 100% oxygen instead of 5 L of oxygen was flowing through the circuit. Only a negative-pressure leak test will identify this.
2. The most common cause of improper delivery of oxygen to the patient is A) Improper gas cylinder connected to the machine B) Crack in oxygen flow tube C) Crossing of gas supply from the wall D) Disconnection of circuit from the patient E) Incompetent inspiratory flow valve Answer: D. Failure to properly deliver oxygen to the patient is most commonly caused by a disconnection in the patient circuit. Although A, B, and C can cause problems with delivery of oxygen, these are much less common causes. An incompetent inspiratory valve can lead to elevated baseline levels of carbon dioxide, but it should not cause poor oxygenation.
3. You are called into a room where the anesthesia staff complains that the airway pressure continues to rise in a relaxed patient with regular breath
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sounds. Which of the following problems with the machine could be causing this? A) A kink in the scavenging transfer means B) A faulty positive-pressure release valve in the scavenging system C) An incompetent pressure relief valve in the ventilator D) A and B E) All of the above Answer: D. If the scavenging transfer means is kinked, excess gas cannot be vented from the circle system to the scavenging system and barotraumas can occur from elevated airway pressures. This can also occur if flows are high in the system and the positive-pressure release valve does not function properly to vent the excess gas. An incompetent pressure relief valve in the ventilator will allow gas that is compressed by the ventilator to escape into the scavenging systems and would cause lower airway pressures and a leak in the circuit.
4. You are called into a room because of problems with the end-tidal carbon dioxide tracing not going back to a baseline of “0.” Which of the following could cause this? A) Incompetent expiratory valve B) Incompetent inspiratory valve C) Exhausted soda lime granules D) A and C E) All of the above Answer: E. The most common cause for elevated end-tidal carbon dioxide levels is exhausted absorbent, but improperly functioning inspiratory and expiratory valves can also cause this. Expired gas escapes down the inspiratory limb, and the patient is ventilated with this gas again. Inspired gas can also push a small amount of expired air back down the expiratory limb if the valve is incompetent. If this were to occur, the tracing would never reach “0” because small amounts of expired air would pass by the sampling port during inspiration.
5. The following steps should all be performed if a problem with the central gas supply is suspected in a room, EXCEPT A) Open the oxygen cylinder on the back of the machine B) Alert the OR front desk C) Disconnect the wall supply from the machine D) Ventilate the patient with a separate circuit E) All should be performed Answer: D. If a central pipeline crossover is suspected, the oxygen tank should be opened and the pipeline supply disconnected. If the pipeline supply is not disconnected, gas from the tank won’t be used. If oxygen levels are restored by this change, it is critical to alert the appropriate hospital staff to avoid
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further serious adverse events. There is no need to change to a separate circuit once a proper oxygen source is connected to the machine.
6. The safety and reliability of oxygen and anesthetic gas delivery are principal concerns and of critical importance to safe medical practice. Which machine improvements have been key components in helping to achieve this goal? A) Agent-specific vaporizers B) Oxygen proportioning systems C) Oxygen analyzers D) Oxygen failure safety valves E) All of the above Answer: E. There are many key safety developments that have been integrated into the modern anesthetic machine and importantly include the components noted above in addition to circuit pressure monitors, pin indexing systems, and central display and consolidation of assorted patient physiologic data points/trending.
7. Anesthesia machines have progressed in sophistication and complexity and routinely include a number of important components to manage gas delivery including A) Anesthetic vaporizers B) Ventilators C) Scavenging systems D) CO2 absorption E) All of the above Answer: E. While there are a number of anesthetic machines available and in use today worldwide, they principally share many similar fundamental components and functionalities. It is critical that one has a solid basic understanding of the principals of the workings of the anesthetic machine and its fundamental components.
SUGGESTED READINGS Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005;644–694. Dorsch JA, Dorsch SE. Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007. GE Health Care Aestiva/5. Anesthesia Delivery System Owner’s Handbook. Datex-Ohmeda, Inc; Madison WI, 2003. Miller DR, Eriksson LI, Fleisher LA, et al. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2009:Chapter 25. Morgan G, Mikhail M, Murray M. Clinical Anesthesiology. 3rd ed. New York, NY: McGraw-Hill; 2002:Chapters 1–4.
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CHAPTER
32
Gas Analyzers Wesley Simpson II
T
he primary difference between a device labeled an “analyzer” and one labeled a “monitor” is that a monitor includes adjustable low, or low and high alarm settings. In other words, a gas analyzer will measure whatever substances it is designed for but will not alert you if the values measured fall outside an acceptable range. Although the terms analyzer and monitor are frequently used interchangeably, a true analyzer should only be used in situations where continuous, uninterrupted observation is possible. Because the addition of alarm settings can contribute to vigilance, a monitor should always be used with patients undergoing an anesthetic. Gas monitors can measure either a single gas or multiple gases and are grouped into two general classifications: mainstream and sidestream. Although anesthesia providers can use mainstream monitors, the vast majority of monitors in current use are sidestream. Sidestream monitors divert gas mixtures from the breathing circuit by means of a continuous pump. The sample gas (normally 50–250 mL/min) is either returned to the breathing circuit or sent into the gas scavenger system. The exhaust from a sidestream monitor must be connected to one of these outflow sources. With the exception of a true emergency, it should never be allowed to empty into the room air. Mainstream monitors measure the gas of interest directly in the breathing circuit, usually consisting of a disposable cuvette and a reusable sensor cell. The primary limitations are that mainstream monitors are only capable of measuring one gas and there is a potential for interference caused by moisture collecting in the cuvette. The simplest form of gas analyzer/monitor, and the one that was used first by anesthesia providers, is the fractional inspired oxygen (FIO2) monitor. As its name implies, the FIO2 monitor
measures the fraction (displayed as a percentage) of oxygen present in the inspiratory limb of a breathing system. Human error or anesthesia machine malfunction could cause a gas mixture with insufficient oxygen to be delivered into the breathing system; therefore, inspired oxygen monitoring is essential to prevent hypoxia in an anesthetized patient. It is also a key component of both the American Society of Anesthesiologists (ASA) Standards for Basic Monitoring and Recommendations for Pre-Anesthesia Checkout. Anesthesia technicians have a responsibility to ensure that FIO2 monitors are properly calibrated prior to anesthesia machine use. At minimum, calibration to room air (21% oxygen) should be performed at least every 24 hours and prior to use on the first patient. Some monitors have the capability of performing a 100% oxygen calibration as well. This should be performed in addition to room air calibration and should not be performed in place of it. Be sure to follow the manufacturers’ recommendations when performing either a room air or 100% oxygen calibration. Keep the following key points in mind with all brands of FIO2 monitors you are working with or the type of sensor it uses: 1.
2.
3.
If you can access the sensor, remove it from the circuit and expose it to room air for several minutes prior to performing a 21% calibration. This allows time for the sensor to equilibrate and any trace gases to diffuse. Perform the room air calibration. This may be as simple as pushing a button with some monitors, or it may require a manual adjustment to obtain a reading of 21%. Whether or not the monitor provides for a 100% calibration, expose the calibrated sensor to pure oxygen. A final reading of 95%–100% is considered acceptable by most manufacturers. A sensor that has been calibrated to room air and then tested with 281
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Section IV • Equipment Setup, Operation, and Maintenance
100% oxygen and does not achieve a final reading of 95%–100% should be either serviced or replaced. If the FIO2 monitor is battery operated, check the battery level as part of the calibration procedure.
There are three primary types of sensor (measurement) cells used in oxygen monitors: polarographic, galvanic, and paramagnetic. Each type of sensor has strengths and drawbacks as well as specific concerns for the anesthesia technologist. Polarographic cells, sometimes referred to as Clark cells, use an anode and a cathode that are suspended in an electrolyte solution containing potassium chloride. The solution is separated from the inspiratory gases by a semipermeable membrane, usually made of Teflon or polypropylene. The strength of the current generated between the anode and the cathode is proportional to the concentration of oxygen in the gas mixture being analyzed. These sensors are highly accurate but can be slow to respond to rapid changes in gas composition. Polarographic cells are sold as either reusable or disposable. Cells that have reached the end of useful life can be placed in regular trash. Reusable sensors should be serviced whenever they fail to calibrate properly. Emptying the used electrolyte gel and using a soft cotton swab to clean the electrodes, membrane, and inner surface of the sensor capsule normally accomplish this. Fill the capsule with fresh electrolyte gel and replace the electrodes, being careful not to entrap any air bubbles. Galvanic or fuel cell sensors also use an anode and a cathode suspended in an electrolyte solution such as potassium hydroxide. The principle of operation is similar to that of the polarographic cell, and currents generated in the cell are in proportion to the concentration of oxygen molecules in the gas being sampled. Single-cell sensors can be slow to respond to changes in gas composition and are more prone to calibration drift. Newer dual-cell designs offer increased accuracy, faster response times, and greater stability. Galvanic cells are similar in composition to your car battery. The correct method of disposal will vary with state and local laws, but they should never be placed in regular trash, sharps, biohazardous, or pharmaceutical containers. Paramagnetic sensors expose the gas sample to an uneven magnetic field. Oxygen has a
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relatively high magnetic susceptibility as compared to nitrogen, carbon dioxide, nitrous oxide, and inhaled anesthetic agents. As the gas sample is sent through the sensor, oxygen molecules are attracted to the stronger of the magnetic fields. The resultant shifts measured in the sensor are proportional to the percentage of oxygen in the sample. Paramagnetic sensors react rapidly to changes in gas composition and have a long life span but are motion sensitive. As a result, they are not utilized within a breathing system because of the potential for movement of the breathing circuit during ventilation but are built into multiple gas monitors. They are not calibrated separately, but with other gases the monitor is designed to detect. This may be accomplished through an internal calibration standard or by using an external calibration gas. Since paramagnetic sensors are not used in discrete FIO2 monitors, they are an exception to the 24-hour calibration standard. The frequency for calibration will vary with the manufacturers’ recommendations and/ or department policies. In addition to monitoring FIO2, it is desirable for anesthesia providers to monitor other gases including carbon dioxide and a variety of anesthetic gases. The gas monitor can be as simple as a device that only monitors carbon dioxide (CO2) or as complex as a monitor capable of measuring multiple gases simultaneously. Monitoring of CO2 in the circuit is important because it provides information about the adequacy of ventilation for the patient and can detect conditions like apnea, underventilation, bronchospasm, or even circuit disconnects (see Chapter 33). Continual monitoring of end-tidal carbon dioxide (ETCO2) is a part of the ASA Monitoring Standards. Although the ASA guidelines are silent on the need to monitor other airway gases, in many instances it has become a “community standard of care” to do so. Monitoring of anesthesia gases can detect insufficient anesthetic gas delivery (i.e., the vaporizer is empty) or dangerously high anesthetic gas levels (i.e., vaporizer set inappropriately high or a machine malfunction). Carbon dioxide, as well as other common airway gases, can be measured by a variety of methods. The most common of these used in anesthesia is infrared monitoring. Infrared monitors employ the concept that most gases absorb infrared light, and the amount of light absorbed is in direct proportion to the concentration of
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Chapter 32 • Gas Analyzers
that gas (Beer-Lambert Law). Infrared monitors are capable of analyzing carbon dioxide, nitrous oxide, inhaled anesthetic agents, and alcohol vapors. Because oxygen does not absorb light in the infrared spectrum, a galvanic or paramagnetic cell must be used in an infrared multiple gas monitor. Other means of measuring multiple gases include Raman spectroscopy, which sends a laser beam through the gas sample; photoacoustic spectroscopy, which uses microphones to “listen” to the frequencies generated by gas molecule; and mass spectrometry in which differences in the molecular weight of gas molecules being monitored are separated. Regardless of the technology used, correct calibration of the monitor is the only way to ensure that accurate measurements are obtained. Manufacturer instructions must be followed exactly in order for an accurate calibration to be ensured. Although the details may vary from brand to brand, the following general principles should always be observed: 1.
2.
3.
4.
The sensor cell must “warm up” and obtain a stable temperature in order for calibration to be accurate. In some types of monitors, this interval can be as little as 5 minutes or as long as 45 minutes. If a calibration gas is used, it must be specific to the monitor being calibrated. Although most formulations (blends) of calibration gas can be used to “spot check” the accuracy of an analyzer, the only blends used for calibration must match manufacturer specifications. Calibration should be performed, at minimum, at the intervals specified by the manufacturer. Any monitor that fails manufacturer calibration standards should be removed from service immediately, or as soon as reasonably possible.
Taking time to make sure that gas monitors are properly calibrated and functional prior to use will minimize potential problems during an anesthetic. There will be times, however, when you will be asked to troubleshoot and repair a monitor while it is in use. Several of those requests are due to readings on the monitor that do not match the expected range for a particular patient, or if there has been a sudden change in
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the readings. In other words, what clinicians are seeing on the monitor does not correspond with what they think they should be seeing. Keep in mind that when troubleshooting, it is not always a monitor problem. There will be occasions when the abnormal reading truly reflects what is going on with the patient. When asked to evaluate a gas monitor problem, the following steps are suggested as a means of doing so quickly and efficiently: 1.
2.
3.
4.
5.
6.
7.
Be prepared and take everything you may reasonably need with you. For example: If a problem occurs with an FIO2 monitor, bring a fresh sensor cell, batteries, etc. For a sidestream monitor, you may need to replace the sample “T,” sample line, or water trap. When you arrive, take a moment to make your own assessment of the problem. The most important tools you bring to the situation are a fresh set of ears and eyes. The clinician may be involved with multiple tasks or problems and may not have been able to do a thorough analysis of the monitor problem. If there are multiple faults or alarm conditions, you will need to prioritize. If the patient is being adequately ventilated by a clinical evaluation, gas monitor alarms may be annoying, but may not be the highest priority. Use a standard approach to troubleshooting so that you do not miss any steps. For example: Check connections at the monitor first and then work your way one connection at a time until you reach the final connection to the breathing system. Alternatively, start with the connection to the breathing circuit and work your way back to the machine. When you remove the sample line or the water trap, cap off the sample port on the breathing circuit so that the resulting leak does not set off volume or pressure alarms. Have a backup plan in mind. If you cannot make an immediate repair, be prepared to give the anesthesia provider an accurate time estimate for replacement. Know where spare monitors are and how long it would take to get them ready for use. If you do remove a monitor from service, follow your facility’s defective equipment policy to facilitate repairs and minimize downtime.
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Most gas monitor alarms fall into one of three categories; the reading is lower than expected, higher than expected, or there is no reading. The following are common problems you may encounter in each category: If all or most of the readings are lower than expected: • Cracked sample line: This most commonly occurs where the sample line connects to the port on the breathing circuit. Even if you cannot see the crack, tightening the connection will not solve the problem and may actually make it worse. The crack or leak may also occur where the sample line connects to the monitor. • Leaking water trap or filter: This is easy to check, even if you cannot see the defect. Remove the sample line and cover the inlet of the trap/filter with your finger. If this does not create an occlusion alarm, replace the trap/ filter. • If you cannot find a leak, have the clinician check the cuff balloon on the endotracheal tube or supraglottic airway. • The monitor may not be properly calibrated, or the calibration may have failed. If only one gas is reading low: • Suspect that the monitor is not properly calibrated, or the calibration may have failed. If only the inhaled anesthetic is reading low, the vaporizer may be leaking or empty. Check the “sight glass” on the vaporizer. If the vaporizer is not empty, make sure it is securely mounted, listen for an audible leak, and smell for the presence of gas vapors. If all or most of the readings are higher than expected: • Check the exhaust port or line to make sure it is not occluded. An exhaust occlusion changes the flow of gas through the monitoring chamber and can result in false high readings. • Suspect that the monitor is not properly calibrated, or the calibration may have failed. • If only the inhaled anesthetic is reading high, the vaporizer may have failed. If the vaporizer is easily removed, replace it with another vaporizer and see if the readings become normal.
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If there is no reading: • There may be an occlusion. In some models of monitors, there is no occlusion alarm. Check for an occlusion at the sample port, in the sample line, and at the water trap/filter inlet. • The patient may have become unintentionally extubated (although this condition should also cause volume and pressure alarms on the anesthesia machine to respond). • The monitor’s calibration may have failed. • The internal pump may have stopped working. You can check this by occluding the inlet port with your finger to see if you can feel negative pressure. • The sample cell of a mainstream monitor may have failed or become disconnected. Disconnections can occur at either the breathing system connection or at the monitor.
REVIEW QUESTIONS 1. A sidestream gas analyzer A) Can measure only one gas B) Uses a continuous pump C) Should never be allowed to empty into room air D) B and C only E) All of the above Answer: D. Mainstream analyzers are limited to one gas. Sidestream monitors are able to monitor multiple gases.
2. When called into a room, you are told the O2 readings are lower than expected. Which of the following could be a likely cause? A) Failed vaporizer B) Occlusion C) Cracked sample line D) Patient extubation E) Exhaust port occluded Answer: C. With a cracked sample line, O2 could be leaking from the system, resulting in lower than expected O2 readings. A failed vaporizer may affect gas readings but not O2 readings. A patient or exhaust port occlusion may result in higher than expected O2 readings or no reading. A patient extubation should result in the absence of a reading altogether.
3. FIO2 monitors A) Should be calibrated to room air (21% O2) B) Should be calibrated at least every 24 hours C) Should be calibrated prior to use on the first patient D) A and C only E) All of the above
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Chapter 32 • Gas Analyzers Answer: E. All of the above is the standard recommendation from all manufacturers of FIO2 monitors.
4. The use of ETCO2 monitoring A) Is part of ASA monitoring standards B) Can detect conditions such as apnea, underventilation, bronchospasm, and circuit disconnect C) Can detect dangerously high anesthesia gas levels D) A and B only E) All of the above Answer: D. ETCO2 monitors do not detect agent. An agent analyzer may be incorporated into the ETCO2 monitor as a added system, but it is the ETCO2 portion that is an ASA standard and is able to detect noted conditions.
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SUGGESTED READINGS American Society of Anesthesiologists. ASA Recommendations for Pre-Anesthesia Checkout. 2008. Available at: https:// www.asahq.org/For-Members/Clinical-Information/2008ASA-Recommendations-for-PreAnesthesia-Checkout.asp. Accessed September 5, 2011. American Society of Anesthesiologists. Standards for Basic Anesthesia Monitoring 2011. Available at: http://www. asahq.org/For-Members/Clinical-Information/StandardsGuidelines-and-Statements.aspx. Accessed September 5, 2011. Simpson W. Need for FIO2 monitor strongly defended [letter to the editor]. APSF Newslett. 1993;8:1. Available at: http://apsf.org/newsletters/html/1993/spring/#art3. Accessed September 5, 2011.
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CHAPTER
33
Basic Monitoring Wesley Simpson II
This chapter is focused on basic monitors required for patient safety during the conduct of an anesthetic, as defined by the American Society of Anesthesiologists (ASA) Standards for Basic Monitoring and the role of the anesthesia technician in complying with these standards. The ASA standards were first approved in October 1986. The most recent update was completed in October 2010, and became effective July 1, 2011. Each of the five standards is discussed here. Standard I is a general statement, with standards II through V being specific to the monitoring techniques that should be used to assess a patient’s oxygenation, ventilation, circulation, and body temperature. These monitors are discussed in roughly the same order as the standards they fulfill.
■ ASA STANDARD I “Qualified anesthesia personnel shall be present in the room throughout the conduct of all general anesthetics, regional anesthetics and monitored anesthesia care.”
■ PULSE OXIMETRY (ASA STANDARDS II AND IV) Pulse oximetry is a noninvasive method used to determine oxygen levels in arterial blood. Similar to some gas analysis techniques, pulse oximetry is based on the principal that hemoglobin (Hgb) absorbs a specific wavelength of light differently whether it is saturated or desaturated with oxygen. Hgb is a protein contained in red blood cells (RBCs). Each Hgb molecule is capable of binding four oxygen molecules. Although oxygen dissolves in blood, binding oxygen to Hgb found in RBCs allows the blood to carry 70 times as much oxygen. In arterial blood, about 98.5% of the oxygen is bound to Hgb and only 1.5% is dissolved within the blood. Hgb that has bound
oxygen is termed oxyhemoglobin, and Hgb that does not have oxygen bound to it is termed deoxyhemoglobin. A standard pulse oximeter contains a light source and a sensor. The light is passed through a portion of the patient’s body that is small enough that some of the light can pass through the body part to be detected by the sensor on the other side. A pulse oximeter uses two bandwidths of light: infrared (660 nm) to measure oxyhemoglobin and nearinfrared (940 nm) to measure deoxyhemoglobin. The amount of light that is absorbed and the amount of light that passes through the body part are dependent upon the amount of oxygen bound to the Hgb within the RBCs. Sensor readings of the light absorbed for both wavelengths are processed through an algorithm that compares the ratio of absorption for the two wavelengths. The pulse oximeter can then calculate and display a value that represents the percentage of arterial blood oxygenation. Normal values for humans range from 95% to 100%. There are two types of pulse oximeter probes, transmission and reflection. Transmission probes were the first to be developed and remain the most common. Transmission probes have the light source on one side, with the detector directly opposite. Light from the source is transmitted through the tissues of interest to the detector, and the amount of light that reaches the detector is used for calculations. Transmission sensors can be placed anywhere near the light source, and the detector can be positioned on opposite sides of a pulsatile blood flow. Care must be taken when placing sensors, as both accuracy and stability depend on the transmitter and detector being directly opposite to each other. This is especially true for the newer cooximetry probes. Common sensor sites include fingertip, toe, nose, and earlobe for children and
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adults and foot and forearm for neonates. Less common sites include the cheek for adults and the penis for neonates. Reflection probes have both a light source and a detector placed near one another. The amount of light reflected to the sensor is used for calculations. The forehead is the most common site for reflectance sensors. Pulse oximeter probes can be either disposable or reusable (Fig. 33.1). Reusable probes are classified as “noncritical” items for disinfection purposes, and low-level disinfection between patients is suitable as long as the probe is placed over intact skin or does not become soiled with blood or body fluids. Any reusable probe that does become soiled should be treated with highlevel disinfection or sterilization. Regardless of the treatment used, make sure the probe has
■ FIGURE 33.1 Reusable and disposable pulse oximetry probes.
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dried completely before using it on the next patient.
■ LIMITATIONS OF PULSE OXIMETRY Although pulse oximetry information is extremely useful and has contributed to the safety of modern anesthesia, its limitations must be understood. A patient can have a reading in the normal range (95%–100%) and still have insufficient oxygen in the blood. What a pulse oximeter reading of 100% means is that of the Hgb that is available to transport oxygen in the arterial blood, 100% is occupied with oxygen. What it does not tell you is what percentage of Hgb is available to carry oxygen or what the total Hgb is. For example, if a patient’s Hgb is 16 g/dL and all of the available Hgb is carrying oxygen, the saturation reading would be 100%. If that same patient’s Hgb drops to 8 g/dL, the saturation reading can still be 100%, even though the total amount of oxygen carried in the arterial system has been reduced by half. Another important factor to consider is the effect of other substances and the ability of Hgb to bind oxygen and their simultaneous effect on pulse oximetry readings. Carbon monoxide binds to Hgb 20 times more strongly than oxygen. The presence of carbon monoxide effectively lowers the oxygen-carrying capacity of blood (available amount of Hgb to carry oxygen). In addition, carbon monoxide bound to Hgb (carboxyhemoglobin) absorbs one of the wavelengths of light used by the pulse oximeter and interferes with the calculation of oxygen saturation. Therefore, patients with high carboxyhemoglobin levels may not have enough oxyhemoglobin, yet still have high pulse oximetry readings (e.g., patients with carboxyhemoglobin concentrations of 70%—more than two-thirds of the Hgb is not available to carry oxygen—have had pulse oximetry readings of 90%.) Other forms of Hgb including methemoglobin and sulfhemoglobin also interfere with both the ability of oxygen to bind to Hgb and pulse oximetry readings. Patients with methemoglobinemia typically have pulse oximetry readings of 85% despite severe reductions in oxygen-carrying capacity. In most cases, a co-oximeter can be used to overcome the limitations of standard pulse oximeters mentioned above. Co-oximeters use multiple wavelengths of light (as many as eight) and can not only measure oxyhemoglobin but also
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provide values for other states of Hgb, such as carbhemoglobin, carboxyhemoglobin, methemoglobin, and sulfhemoglobin, as well as the total amount of Hgb. Co-oximeters are commonly available with blood gas machines; however, pulse co-oximeters are available for bedside use as well. Pulse oximeters also measure the volume of the sample body part and rely on the principle that during an arterial pulsation (increase in volume), the blood is fully oxygenated and this is when the reading should be taken. This is why most pulse oximeters provide a value for the heart rate and many display a waveform as they measure the rhythmic change in volume of the sample body. This property also leads to a limitation in pulse oximetry readings. When the pulse oximeter cannot detect regular, rhythmic changes in volume, it cannot give an oximetry reading. This can occur with peripheral vasoconstriction (peripheral vascular disease, vasospasm, cold body part, etc.), low blood flow (hypotension, reduced cardiac output), or arrhythmias that are irregular (atrial fibrillation, multifocal atrial tachycardia, etc.). There are several sources of interference that can affect the accuracy and usability of a pulse oximeter. Although all pulse oximeters can experience problems, newer models include features and software to help minimize them. The most common of these are light, motion, nail polish (some blues, reds, and browns), hypoperfusion, and intravenous dyes. Problems and possible solutions are presented below: • Light: Ambient light normally affects both the saturation reading and the pulse rate. Shield the sensor with a surgical towel, drapes, etc. or change the sensor site. • Motion: Motion of the probe interferes with readings. This can occur when the probe is jostled (e.g., surgical personnel leaning against the probe) or by medical devices that can cause patient movement (e.g., neuromuscular monitors or muscle-evoked responses). Use a disposable probe, secure the moving limb, or change the sensor site. • Nail polish: Nail polish, particularly dark red colors, can absorb the light emitted by the pulse oximeter. Change the sensor site or remove the nail polish. • Hypoperfusion: It can be caused by hypovolemia, hypothermia, vasoconstriction, or
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vascular blockage. If the patient is normothermic, but the sensor site is cool to the touch, cover the limb with warm blankets or a warm air blanket or change sensor sites. Other common problems encountered with pulse oximeters: • No light at sensor or light at sensor but the oximeter does not produce a reading or waveform—Check the cable connections at the sensor and monitor. If connections are not the problem, consider replacing the sensor, then the cable, then the monitor. • Erratic or suspected incorrect readings—Is the sensor placed correctly? Is it too tight? Is it on the same limb as the blood pressure cuff? Is the patient cold? Is the patient vasoconstricted? Modify the sensor placement or consider using a sensor on the earlobe, nose, or forehead.
■ CAPNOGRAPHY (ASA STANDARD III) Capnography is the measurement of carbon dioxide gas in the breathing system, with the measurements displayed in both numerical and graphic forms. The basic technology and related troubleshooting has been discussed in Chapter 32. In this chapter, we focus on the practical application of that technology in anesthesia. The role of capnography within the ASA standards is to help ensure a patient is adequately ventilated during all anesthetics. Continuous readings of exhaled carbon dioxide (CO2) can instantly communicate changes in the status of the patient and the anesthesia machine. Although the numerical readings from a capnometer will satisfy the basic requirements, a capnograph with a continuous waveform is preferred. The shape of the waveform can yield additional diagnostic information about how a patient is being ventilated. The “normal” capnogram is a waveform that represents the varying CO2 level throughout the breath cycle over time (Fig. 33.2A-E). Measured exhaled CO2 is a function of CO2 production by the body, delivery of the CO2containing blood to the lungs, gas exchange in the alveoli, and ventilation of the lungs to pick up CO2 from the alveoli and eliminate it to the outside. One of the most important functions of CO2 monitoring is to confirm the placement
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■ FIGURE 33.2 A-E: Normal capnogram. A,B: Baseline represents continued inhalation (value should be zero) or lack of gas movement. B,C: Expiratory upstroke (sharp rise from baseline represents the beginning of exhalation and consists of a mixture of air and alveolar gas. C,D: Expiratory plateau (continued exhalation of alveolar gas, should be straight or nearly straight). D: Endtidal concentration (value at the end of exhalation); D,E: Inspiration begins (sharp downstroke as fresh gas is inspired). (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
■ FIGURE 33.4 Rising ETCO2 levels as detected on a capnogram. (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
of an endotracheal tube into the trachea. If the tube is placed in the trachea and the patient is ventilated, and there is sufficient cardiac output to deliver CO2 to the lungs and there is sufficient gas exchange between the blood and the alveoli, the CO2 monitor will register CO2. If the endotracheal tube is placed in the esophagus, the CO2 monitor will not register sustained CO2 (Fig. 33.3). Although there may be some carbon dioxide in the esophagus and stomach, the concentration is normally low and will rapidly be depleted with ventilation of the stomach. Below is a discussion of the differential diagnosis of changes in measured CO2 values or waveforms. Increased CO2: An increase in the level of EndTidal Carbon dioxide (ETCO2) from previous levels can result from either an increase in the patient’s production of CO2 or a decrease in ventilation (Fig. 33.4):
• •
• Increased metabolic rate (rising body temperature from blankets or external warming
■ FIGURE 33.3 ETCO2 levels rapidly diminish or are not present with an esophageal intubation. (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
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• •
•
devices, thyrotoxicosis, malignant hyperthermia, etc.) Increased cardiac output Chemicals or metabolic products that have been administered to the patient that are converted to CO2 (bicarbonate, lactate, CO2 gas embolus, etc.) Decreased respiratory rate or tidal volume Decreased gas exchange with eventual rising CO2 blood levels (pulmonary failure, chronic obstructive pulmonary disease [COPD], bronchospasm, etc.) Machine problems leading to decreased ventilation (leaks, obstructions, depleted CO2 absorber, etc.)
Decreased CO2: A decrease in the level of ETCO2 from previous levels can result from a change in the body’s production of CO2 (rare), the delivery of CO2 to the lungs, or an increase in ventilation (Fig. 33.5): • Decreased metabolic rate or decreased core body temperature • Decreased cardiac output • Decreased pulmonary blood flow (pulmonary embolus) • Increased tidal volume or respiratory rate • Partial disconnect of CO2-monitoring tubing
■ FIGURE 33.5 Diminishing ETCO2 levels as detected on a capnogram. (Adapted from Capnography SelfStudy Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
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No CO2: A numerical reading of 0 or a flat waveform at 0 can indicate that CO2 is not being delivered to the monitor or a monitor malfunction. CO2 may not be delivered to the monitor/ sensor under the following critical conditions: • • • •
Circuit disconnect or sample line disconnect Apnea Cardiac arrest Total obstruction of the endotracheal tube, airway, or breathing circuit • Total obstruction of gas sampling (sample port, sample line, water trap) • Monitor malfunction Abnormal baseline CO2: Mechanical or anesthesia machine problems can often be a source of abnormal baseline CO2 readings (Fig. 33.6). Elevation of the baseline indicates rebreathing of CO2, which may also result in an increase in ETCO2. Possible causes include • Faulty expiratory valve on ventilator or anesthesia machine • Inadequate inspiratory flow • Exhausted CO2 absorbent • Partial rebreathing • Insufficient expiratory time Changes in the shape of the CO2 waveform: An obstruction to expiratory gas flow or differential emptying of obstructed small airways can present as a change in the slope of the expiratory upstroke of the capnogram (Fig. 33.7). The obstruction can be so severe that the CO2 wave never reaches a flat plateau before inhalation begins. Diagnoses to consider include • Obstruction in the expiratory limb of the breathing circuit • Presence of a foreign body in the upper airway
■ FIGURE 33.6 Elevated baseline CO2 levels as detected on a capnogram typical of rebreathing. (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
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■ FIGURE 33.7 ETCO2 waveform does not reach a plateau typical of bronchospasm or small airway obstruction. Electrocardiogram. lead color codes. (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
• Partially kinked or occluded endotracheal tube or supraglottic airway • Bronchospasm The “curare cleft” is seen in the plateau portion of the waveform. It is an indication that muscle relaxants are wearing off and the patient is returning to spontaneous ventilation (Fig. 33.8).
■ ELECTROCARDIOGRAM (ASA STANDARD IV—CIRCULATION) The electrocardiogram (ECG or EKG) is a record of the electrical activity of the heart over time. Although a “12-lead” ECG is traditionally used for diagnostic purposes, most anesthesia and critical care monitoring is accomplished using either a three-wire harness or a five-wire harness. The term ECG lead can mean different things to different people, often with confusing results. When people mention an ECG lead, it could mean the specific tracing, a specific wire on the ECG harness, or the adhesive electrode that attaches to the skin. To avoid confusion, we use the term leads to mean the specific tracings, lead wires to refer to the harness that connects from the monitor to the adhesive pads, and electrodes to refer to the adhesive pads that attach the lead wires to the skin. ECG lead wires are placed on patients
■ FIGURE 33.8 A “cleft” in the ETCO2 plateau. (Adapted from Capnography Self-Study Guide. Rev. 1. Smiths Medical; 2008. Used by permission.)
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in standard patterns. There are two primary color coding systems used throughout the world, American Hospital Association/Association for the Advancement of Medical Instrumentation (AHA/ AAMI) and the International Electrotechnical Commission (IEC). The AHA/AAMI colors are used in North America, while IEC colors are used throughout Europe. Other countries around the world vary in which standard they follow. Standard nomenclature is as follows: RA for right arm, RL for right leg, LA for left arm, LL for left leg, and V for any of the six cardiac lead positions. The standards are compared in Table 33.1. A three-wire harness is the most basic of ECG monitoring systems. The ECG display is limited to leads I, II, and III. Although ST-segment monitoring for cardiac ischemia can be done, the most sensitive leads (V1–V6) cannot be monitored. The standard three-lead harness consists of RA, LA, and LL, although some monitors may use RA, LA, and RL. A five-wire harness provides significant improvement in monitoring and diagnostic capabilities (Fig. 33.9). The addition of a ground lead (RL) and the cardiac leads (V1–V6) allow most modern monitors to display and print up to eight leads simultaneously. ST-segment and arrhythmia analysis is also improved with the additional leads. When placing the V lead wire on a patient, it can be in any one of six positions, V1–V6. • V1—Fourth intercostal space, right sternal border • V2—Fourth intercostal space, left sternal border • V3—Midway between V2 and V4 • V4—Fifth intercostal space, left midclavicular line • V5—Level with V4, left anterior axillary line • V6—Level with V4, left mid axillary line
TABLE 33.1 ECG LEAD WIRE COLOR
CODES LEAD
AHA/AAMI
IEC (EUROPE)
Right arm (RA)
White
Red
Right leg (RL)
Green
Black
Left arm (LA)
Black
Yellow
Left leg (LL)
Red
Green
Cardiac (V)
Brown
White
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■ FIGURE 33.9 Five-lead wire system with harness and electrodes.
The most common V lead wire positions used in critical care units are V1 and V2. The most common V lead wire positions used by anesthesia are V5 and V6, primarily due to the need for a clear surgical field and protection of the electrodes from surgical skin prep solutions. No matter which ECG monitoring harness is used, it is critical to place the lead wires in the proper position. Remember that the position of the lead wires is used to measure electrical forces from particular regions in the heart. Improper positioning of the leads can lead to abnormal ECG signals and errors in interpretation. Interference in the ECG signal usually stems from three primary sources: motion artifact, inadequate preparation and placement of the electrodes, and electronic interference. Movement of the lead wires can cause faulty electronic signals. Care should be taken that the lead wires are not being moved or in contact with moving or vibrating equipment. Even the respiratory movements of the chest can
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affect the ECG signal. Electronic interference is usually either 60 cycle (from faulty wiring) or excessive radio frequency (from electrocautery units). Options for minimizing electrical interference include changing the circuit the monitor is plugged into or adjusting the ECG filter on the monitor (although this can reduce diagnostic quality). Make sure cables and lead wires do not have breaks in insulating materials. Extreme instances may require use of a power conditioner. Correct skin preparation and lead placement are the key to obtaining quality ECG tracings. The signals received through the electrodes are relatively weak and can easily be obscured by impulses from other sources. In order to enhance the ECG signal quality and reduce artifact • Make sure the electrode gel has not dried out. • Shave or clip any excess hair. • Gently abrade the skin where the electrode will be placed (many electrodes have an abrasive area on the cover). • Wipe the area with an alcohol pad to remove skin oils.
■ NONINVASIVE BLOOD PRESSURE (ASA STANDARD IV) The arterial walls are muscular and elastic in the absence of vascular disease. Blood flows through the arteries in a pulsatile fashion as a result of pressure differences between the systolic and diastolic phases of the cardiac cycle (see Chapter 7). This flow pattern causes the arteries to alternately expand and contract, resulting in the pulse that we can feel with our fingertips. Blood pressure is not constant throughout the arterial system. In general, systolic pressure increases and diastolic pressure decreases the further blood moves from the heart. This is due to increasing resistance (friction) that blood encounters as it is forced through progressively narrower arteries. Changes in peripheral vascular resistance (vasoconstriction or vasodilation) can further alter these pressures. Mean arterial pressure (MAP) is not affected to the same degree, with a normal variation of only 1–2 mm Hg. Several noninvasive technologies have been developed to measure these pulsations and translate them into the blood pressure readings we are familiar with. The five most commonly
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used methods are pulse detection, auscultation, oscillation, applanation tonometry, and the volume clamp (photoplethysmographic or Penaz technique). Pulse detection, made practical by Dr. RivaRocci in 1896, was among the first techniques used for measuring blood pressure noninvasively. In this technique, a blood pressure cuff connected to a manometer is placed around a limb and a distal artery is palpated. The cuff is inflated about 20 mm Hg above the point where the pulse becomes absent. As the cuff is slowly deflated, the manometer reading at the point of pulse return is noted as the systolic pressure. Alternatively, the first “tick” in needle movement on an aneroid manometer or the point at which an SPO2 waveform returns can be noted as the systolic pressure. If a cuff or manometer is available, systolic pressure can be estimated by the body location at which a pulse can be palpated, as shown in Table 33.2. For example, if you can only obtain a carotid pulse, then the systolic pressure is at least 60 mm Hg. Similarly, a radial pulse is usually unobtainable below a systolic pressure of 80 mm Hg. Whenever you are palpating a pulse, make sure to use only the tips of your index and middle fingers. Never use your thumb to palpate a pulse. The artery in your thumb is large enough that you can mistake your own pulse for that of the patient. Unfortunately, palpation of pulses to estimate blood pressure is unreliable even when performed by health care providers. Auscultation, a refinement of the arterial occlusion technique, is the most frequently used method for noninvasive blood pressure monitoring. Auscultation, or “listening,” adds a stethoscope to the cuff and manometer. Dr. Nikolai Korotkoff developed this technique and described five distinct sounds that can be heard as a cuff is
TABLE 33.2 SYSTOLIC PRESSURE ESTIMATES ARTERY PALPATED
MINIMUM SYSTOLIC PRESSURE (MM HG)
Carotid
60
Femoral
70
Radial
80
Dorsalis pedis
90
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deflated over an occluded artery. These sounds result from the turbulent return of blood flow in the artery. The first sound is described as a clear snapping or tapping sound, and the manometer reading is noted as the systolic pressure. The second is a murmur that is heard for most of cuff deflation. The third marks a return of a clear, tapping sound. The second and third sounds have no known clinical significance. The fourth sound is referred to as thumping or muted and occurs within 10 mm Hg above the diastolic pressure. The fifth sound is silence as cuff pressure drops below diastolic pressure. This disappearance of sound is recorded as the diastolic pressure. The limitation of this method is dependence on proper technique and the differences in audio and visual acuity among clinicians. Despite these limitations, a cuff, manometer, and stethoscope should be readily available as a backup for automated systems. The oscillatory technique is used by the majority of anesthesia and critical care automatic blood presssure monitors. Although oscillometers still rely on the turbulent flow resulting from partial cuff compression, the form of energy measured (pressure vs. sound) differs from auscultation. Arterial pulsations create pressure variations (oscillations) that are transferred from the cuff to pressure transducers inside the
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monitor. These pressure fluctuations, along with their amplitude, are used to calculate displayed values. Although there is variation among manufacturers, systolic pressures are normally derived from the first significant oscillation detected, while diastolic pressures are calculated from the last. MAP is measured at the peak amplitude measured. Unlike auscultation techniques, oscillometers may have difficulty providing accurate readings in patients with arrhythmias or pulsus paradoxus. Most automatic oscillometers include a rapid determination, or STAT mode. These modes cycle the monitor continuously to provide frequent readings but sacrifice accuracy in the process. Despite manufacturers’ claims, when in STAT mode, you should only accept MAP readings (as a trend rather than as an absolute figure) after the first few minutes, as vascular congestion caused by continual, repeated cuff inflation makes systolic and diastolic readings less reliable. STAT modes should be reserved for emergent situations and used for the shortest possible amount of time. The difference between auscultation and oscillation measurements is demonstrated in Figure 33.10. Applanation tonometry provides a continuous noninvasive blood pressure (CNIBP) reading.
■ FIGURE 33.10 Simultaneous display of blood pressure cuff oscillations and auscultated blood pressure sounds.
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Although it can be used on most patients, it is especially useful for obese patients, patients where you have difficulty placing a cuff, and as an alternative for an invasive pressure line when deliberate hypotension is desired. In this technique, the radial artery is partially compressed against the styloid process of the radius. Physical location of the sensor is slightly distal to standard placement for a radial arterial line. In order to be accurate, tonometry requires entry of standard body mass index (BMI) information and relative position of the sensor in relation to the atria of the heart. MAP is directly measured. Systolic and diastolic values are calculated by processing BMI data through a nomogram. The volume clamp, also known as the photoplethysmographic or Penaz technique, can also be used to measure blood pressure. Like tonometry, it is designed to be used as a CNIBP device. Blood pressure is measured at the fingers using the principle of the “unloaded artery.” A small cuff containing a plethesmograph (similar to a pulse oximeter, but using only near-infrared light) is partially inflated around the finger(s) and maintained at a constant pressure. Pressure variations, along with changes in transmitted light, are used to determine MAP, which is calibrated against a standard cuff placed on the same limb. Comparisons between oscillations in the finger cuff and the arm cuff are used to estimate systolic and diastolic pressures. Although there have been improvements in recent years, estimates of systolic and diastolic pressures can be over- or underestimated. With the exception of tonometry, these technologies all rely on the use of a blood pressure cuff. A blood pressure cuff is basically an inflatable bladder encased in a sleeve that is wrapped circumferentially around an arm or leg. The accuracy of readings obtained is dependent on the selection of the correct cuff size. Although there is no industry standard for cuff sizes, most manufacturers follow the American Heart Association (AHA) guidelines, summarized in Table 33.3. It is critical to note that cuff sizes are designated based on the size of the internal bladder, not the external sleeve. A cuff that is labeled “long” is not the same as one labeled “large.” A long cuff has extra sleeve material to wrap around the limb, but the bladder dimensions
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TABLE 33.3 AHA BLOOD PRESSURE CUFF SIZE RECOMMENDATIONS EXTREMITY CIRCUMFERENCE (CM)
CUFF NAME
5–7.5
Newborn
7.5–13
Infant
13–20
Child
17–25
Small adult
24–32
Adult
32–42
Wide/large adult
42–50
Thigh
remain the same as a regular cuff of the same size. Using the correct cuff size is essential for accurate readings. A cuff that is too small will result in false high readings and one that is too large will result in false low readings. Using too small a cuff can also be very painful for an awake or lightly sedated patient. Most manufacturers include a printed index range on the sleeve as a visual confirmation of cuff size, making it easier to avoid size errors. If there is no index range, make sure that the end of the blood pressure cuff falls within the middle 75% of the bladder when it is applied. Proper cuff placement is also critical for accurate readings. In general, proper placement is approximately 1″ above the elbow for an arm cuff, 5″ below the elbow when using the forearm, and just below the groin fold for a thigh cuff. Most manufacturers include an “artery” marker in the center of the bladder. Placing this marker directly over the artery to be occluded results in even compression of the artery and helps limit artifact. Blood pressure cuffs can be either disposable or reusable. Reusable cuffs are classified as “noncritical” items for disinfection purposes, and low-level disinfection between patients is suitable as long as the cuff is placed over intact skin or does not become soiled with blood or body fluids. Any reusable cuff that does become soiled should be treated with high-level disinfection or sterilization. Regardless of the treatment used, make sure the cuff has dried completely before using it on the next patient. With the exception of tonometry, potential problems and related troubleshooting are similar
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regardless of which technique is used. Problems will usually present as an inability to obtain a reading. The basic troubleshooting questions to answer are as follows: • • • •
Is the cuff the correct size? Is the cuff placed correctly? Are all connections tight? Is a member of the surgical team leaning against the cuff? • Does the patient have excess muscle movement? If this sequence does not solve the problem, consider replacing the blood pressure cuff first. If replacing the cuff does not solve the problem, replace the tubing that connects the cuff to the monitor. If you are still unable to obtain a pressure, the problem may be internal to the monitor or related to the physical status of the patient. Consider a different cuff location, monitor, or technique.
■ TEMPERATURE (ASA STANDARD V) Temperature monitoring is key to the concept of temperature management. Consequences of unintended hypothermia can include increased oxygen demand, myocardial ischemia, platelet dysfunction, impaired renal function, delayed wound healing, and increased infection and mortality rates. Unintended hyperthermia can result in multiorgan failure. Temperature is normally expressed in degrees Celsius (C) rather than Fahrenheit (F) in anesthesia and critical care settings. Most monitors allow temperature to be displayed in either format, but the following formulas can be used to covert from one format to another: C = F − 32 × 5/9 and F = C × 9/5 + 32. Like arterial blood pressure, temperature is not constant throughout the body. For example, a core temperature of 36°C can result in temperature site readings of oral, 35.8°C; rectal, 36.5°C; axillary, 34.5°C; and skin surface, 33°C. Because of this, monitors should be labeled with temperature site whenever possible. Common monitoring sites for anesthesia include nasopharyngeal, esophageal, rectal, bladder, tympanic membrane, pulmonary artery (PA) catheter, and skin. Less common are oral, axillary, and vaginal. The most reliable site for monitoring core temperature is via the PA catheter.
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Most temperature monitoring is achieved using electronic and liquid crystal technologies. Electronic methods rely on either a thermistor “400 Series” probe or a thermocouple “700 Series” probe. Thermocouple probes are more accurate, but more expensive, so they are usually purchased when a reusable probe is used. Thermistor probes are less accurate, but significantly less expensive, and are normally purchased when disposable probes are used. Although most modern patient monitors are designed to work with either 400 Series or 700 Series probes, you may encounter some that only work with one or the other. Monitors that work with either series will have a soft key or physical switch that is used to select the correct type. Liquid crystal technology is used for disposable skin sensors. These are normally used on very short cases or as an adjunct to regional anesthesia. Interference with temperature monitoring is rare and primarily limited to heat sources affecting skin surface sensors. Temperature probes can be either disposable or reusable. Reusable probes are classified as “semicritical” items for disinfection purposes, and high-level disinfection between patients is suitable as long as the probe does not become soiled with blood or body fluids. Any reusable probe that does become soiled should be treated with high-level disinfection or sterilization. Regardless of the treatment used, make sure the probe has dried completely before using it on the next patient. Troubleshooting for temperature monitors is usually straightforward. If you have either no reading or an erratic reading, check the following to solve the problem: • Is the monitor correctly set for the series of probe being used? (check the 400/700 switch or soft key.) • Are all connections tight? • Is there an electronic short or frayed wiring? If checking these does not solve the problem, replace the probe/sensor. If replacing the sensor does not resolve the issue, replace the cable that connects the probe to the monitor. If that does not resolve the problem, consider an internal fault in the monitor. A spare module or standalone temperature monitor should be readily available for these needs.
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REVIEW QUESTIONS 1. You are called into the operating room (OR) and told that the pulse oximeter is broken. You look at the monitor and see that the reading is lower than expected with little, if any, waveform present. The likely cause(s) could be A) Cold body part B) Vasospasm C) Reduced cardiac output D) Patient disconnect E) A, B, and C only Answer: E. A patient disconnect would result in no reading and absence of waveform. All others could be likely causes of the scenario.
2. An elevation in the baseline of a CO2 monitor can be due to A) A faulty expiration valve on the ventilator B) Inadequate inspiratory flow C) Exhausted CO2 absorbent D) Insufficient expiratory time E) All of the above Answer: E. All of the above can cause an elevation in the CO2 baseline.
5. The most reliable site for monitoring core temperature is A) Esophageal B) Skin C) Oral D) PA E) Nasopharyngeal Answer: D. When measuring core temperature, the most reliable site is via the PA catheter.
SUGGESTED READINGS American Society of Anesthesiologists. Standards for Basic Anesthesia Monitoring 2011. Available at: http://www.asahq.org/For-Members/ClinicalInformation/Standards-Guidelines-and-Statements.aspx. Centers for Disease Control and Prevention. Guideline for Disinfection and Sterilization in Healthcare Facilities. 2008. Dorch JA, Dorsch SE. Understanding Anesthesia Equipment. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:776–795. Geddes LA. Cardiovascular Devices and Their Applications. New York, NY: John Wiley; 1984.
3. A three-lead EKG harness commonly consists of A) RA (white), LA (black), V (brown) B) RA (white), RL (green), LL (red) C) RA (white), LA (black), LL (red) D) RA (white), RL (green), V (brown) E) None of the above Answer: C. The RA, LA, and LL make up the common three-lead harness. The RL and V lead are added to make up the common fivelead harness.
4. Using a blood pressure cuff that is too small for the patient can result in false high readings. A) True B) False Answer: A. Conversely, a blood pressure cuff that is too large for the patient can result in false low readings.
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34
Vascular Access Equipment and Setup MicHael Moore and Izumi Harukuni ■ INTRODUCTION Anesthesia can be administered in multiple ways; however, regardless of the type of anesthesia, it is imperative to obtain vascular access to provide anesthesia care. The purposes of obtaining vascular access during anesthesia are (1) administration of fluid, (2) administration of medications, (3) administration of blood products, (4) blood sampling for laboratory testing, and (5) monitoring of hemodynamic parameters. Different types of vascular access may be required for each of these different activities. This chapter discusses the preparation, technique, and complications of different types of venous and arterial access. In addition, the associated equipment, setup, and troubleshooting for each technique are discussed as well.
■ PERIPHERAL INTRAVENOUS CATHETER Definition and Indications Peripheral intravenous (PIV) catheters are short, thin tubes (catheters) that are inserted into a peripheral vein (intravenous [IV]). Peripheral veins are those veins that are on, or near, the surface of the arms, hands, legs, and feet. The major deep vein in the leg and groin region is the femoral vein (FV), and it is considered part of the central venous system. PIV catheters are commonly used as they are usually easy to insert and associated with minimal complications. About 95% of hospitalized patients have PIV catheters. PIV catheters are usually placed in peripheral and superficial veins in the upper extremities. In some patients, they need to be placed in the lower extremities due to limitations or difficulty in obtaining access in the upper extremities (e.g., bilateral arm surgery may prevent extremity access; all the peripheral veins in the arms have been damaged).
PIV catheters vary in length. According to Poiseuille’s law, the rate of fluid flow that can be delivered through a tube is related to the diameter and the length of the tube, the pressure gradient (from one end of the tube to the other), and the viscosity of the fluid moving through the tube. The effect of the diameter of the tube on fluid rate is exponential to the fourth power. This means that a doubling in the diameter of a tube would result in a 16-fold increase in fluid rate (24 = 16). Therefore, small changes in the diameter of a PIV catheter will result in large changes in how fast fluid can flow through the catheter. The flow rate in a tube is inversely proportional to the length of the tubing. For example, doubling the length of the tubing cuts the flow rate by half. Taken together, fluid runs faster through a larger diameter and shorter length catheter. By convention, most catheters and needles in health care are sized according to the “Stubs iron wire gauge system,” which was first used to quantify the thickness of metal wire. In this inverse system, the smaller the “gauge,” the larger the diameter. When labeling catheters, the gauge is shortened to G. For example, a 14-gauge (14G) catheter is larger than a 20G catheter (Fig. 34.1). This can be confusing because there is a difference if you are referring to the actual gauge of a catheter or the Stubs gauge of a catheter. The actual gauge of a 14G catheter is approximately 2 mm. The actual gauge of a 20G catheter is 1 mm. When someone asks you for a larger gauge catheter, which should you get, the 14G or the 20G? By convention, when health care providers refer to smaller or larger “gauge,” they are referring to the actual size of the needle or the catheter. When they specify a number with gauge (e.g., 14G), they are referring to the Stubs gauge. Depending on the situation and purpose, 297
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■ FIGURE 34.1 Peripheral intravenous catheters. BectonDickinson Insyte Autogurad catheter in different sizes. The yellow catheter is 24G, the blue is 22G, the pink is 20G, the green is 18 G, the gray is 16G, and the orange is 14G.
the practitioner will decide on the size of the PIV catheter depending upon the desired potential flow rates required and the viscosity of the fluid to be used. Blood is much more viscous than saline and would run more slowly through the same tubing. If blood products or large volumes of fluids may need to be administered in a case, the anesthesia provider would opt for larger bore (smaller G) catheters. The indication for the placement of PIV catheters include • • • •
Administration of fluids Administration of medications Blood transfusion Blood sampling for laboratory testing
Contraindications for PIV catheters depend upon the site where the IV line will be placed. Common contraindications include • Massive edema • Burns or injury • Insertion site distal to the potential vascular injury (i.e., access in lower extremities when the patient sustained abdominal or thoracic trauma) • Local infection • Existing arteriovenous fistula • Previous radical axillary dissection
PIV Catheter Equipment All of the necessary materials and equipment should be available, prepared, and assembled at
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■ FIGURE 34.2 Setup for peripheral intravenous catheter placement.
the bedside prior to placement (Fig. 34.2). Basic equipment includes the following: • Appropriate size IV catheters (14–24G), at least two or three in each size. The full range of catheters should be available in the anesthesia cart; however, in most circumstances, it is not necessary to bring the full range of sizes to the bedside during a catheter insertion. The providers will have chosen a particular size they would like to insert. That size, and a couple of smaller catheters, should be ready at the bedside. The smaller catheters are ready in case the provider cannot locate a vein that can accommodate the desired size catheter. Two or three sizes of each of the appropriate catheters should be available in case more than one attempt at cannulation is necessary or a catheter is defective or inadvertently becomes unsterile. • Nonlatex tourniquet • Alcohol or chlorhexidine swab • Sterile or nonsterile gauze • Transparent dressing • Adhesive tape • IV fluid bag with IV infusion set (flushed with fluid) or saline lock (short tubing flushed with saline and saline syringe). Note that there are different types of IV sets that are used for different purposes. See Associated Equipment section below for additional information. • 3-mL syringe with a small needle (25G or 30G) and 1% lidocaine if local anesthesia at the insertion site is desired. • In rare cases, an ultrasound or other device may be necessary to assist in peripheral vein location.
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To prepare the IV infusion set, first, remove the protective cap on the IV fluid bag. Close the flowregulating clamp on the infusion set and insert the uncapped “spike” into the receptacle on the fluid bag. When “spiking” the bag, care should be taken that the spike on the infusion set remains sterile and does not touch anything other than the inner portion of the receptacle on the fluid bag. Once spiked, hold the fluid bag and drip chamber in an upright position and fill the drip chamber with fluid up to half of the chamber by squeezing the drip chamber a few times. Then, hang the bag on an IV pole and slowly open the regulating clamp to flush the entire tubing with fluid. While flushing, tap the tubing, stopcocks, and ports to remove small air bubbles trapped in these places. It is imperative to de-air the tubing when preparing the IV set for pediatric patients or adults with an intracardiac shunt (i.e., patent foramen ovale, atrial or ventricular septal defect) as even a small amount of air entering systemic circulation may cause an air embolism to vital organs.
Technique for Placing PIV Catheters Choosing the site and appropriate superficial vein is the first and most important step in placing PIV catheters. Superficial veins in upper extremities are the first choice unless there are contraindications. Generally, the most distal peripheral sites are chosen as the first attempt. This allows the practitioner to move to a more proximal site if the initial attempt fails (cannulating a vein distal to a recent prior attempt that drains the same vein can lead to fluid and medications leaking out of the prior cannulation site). In situations requiring large-bore IV access, such as trauma or cases in which the provider is anticipating significant blood loss, the median cubital vein is often preferred. These veins are usually large and stable. Unfortunately, infiltration (fluid or medications leaking out of the vein) can be harder to detect. In the circumstances where the veins of the upper extremities are not accessible, the saphenous vein of the lower leg or the veins of the lower leg and feet are the next choices. In difficult cases with poor peripheral venous access, the use of transillumination or an ultrasound-guided technique may be necessary. As with any other invasive procedures, universal precautions should be applied in placing PIV catheters (see Chapter 24). Because
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infection rates from PIV catheters are very low, full sterile technique is not necessary; however, the site is still prepped with alcohol and care is taken to maintain the sterility of the catheter and needle. Nonsterile gloves must be worn, and eye/ face protection is recommended. A gown should be considered in special circumstances.
PIV Catheter Procedure • Tightly apply a tourniquet to the extremity above the site (Fig. 34.3). • Identify the vein by visualization and/or palpation. • Cleanse the site with alcohol or chlorhexidine using an expanding circular motion. • In awake patients, consider infiltrating local anesthesia (i.e., 1% lidocaine with a 27 or 30 gauge needle) in the subcutaneous tissue at the insertion site, being careful not to enter the vein. • Unpack the needle catheter and inspect for any defect. • Insert the catheter (you will observe blood in the flow back in the needle hub chamber) and then advance the needle catheter a short distance into the vein (2–3 mm). Slide the catheter off the needle into the vein. • Release the tourniquet and retract the stylet needle (any sharp material should be discarded in the appropriate sharp container, including safety needles). Blood in catheter hub should be observed (Fig. 34.4). • Connect the IV set tubing or saline flush and ensure the correct placement of the IV catheter (observe free drip of fluid in the drip
■ FIGURE 34.3 Peripheral intravenous catheter placement: Preparation. The tourniquet is placed proximal to the venipuncture site.
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■ FIGURE 34.4 Peripheral intravenous catheter placement: Completing insertion. Once the catheter is in the vein, release the tourniquet. The blood in the hub of the catheter confirms that the catheter is in the correct position.
■ FIGURE 34.5 Peripheral intravenous catheter placement: Saline flush. The catheter is secure with Tegaderm and the tubing is attached. The blood is now flushed with saline.
chamber or flush without resistance or signs of infiltration). • Secure the catheter with a clear adhesive dressing (e.g., Tegaderm). The clear dressing allows for future inspection of the insertion site (Fig. 34.5) (some practitioners prefer to place a piece of tape over the catheter hub before applying the adhesive dressing). • Secure the IV tubing with tape over the skin. After applying the tape, check the security of the tubing, the connection to the catheter hub, and if fluid is infusing properly. • Adjust the flow rate with a regulating clamp.
• Local infection at the insertion site • Phlebitis/thrombophlebitis: inflammation or clotting (thrombosis) of the vein. Infiltration: leakage of fluid or medication into the subcutaneous tissue. Depending on the pH and other properties of the fluid or medication that has infiltrated into the subcutaneous tissue, infiltration may cause inflammation or even tissue necrosis. If a large volume of fluid infiltrates, it may result in compartment syndrome (severe swelling in the extremity, causing compression of blood vessels and potentially cutting off the blood supply to the extremity or tissues).
Removing PIV Catheters When a PIV catheter is no longer required, it is malfunctioning (infiltrating or occluding), or any complication is identified, the catheter should be removed. • Stop fluid infusion by occluding the regulating clamp. • Remove the tape and Tegaderm. • Place gauze over the IV site and remove the catheter while applying gentle pressure to the insertion site to stop any bleeding. You may need to apply pressure for 3–5 minutes until bleeding stops. Then, secure the gauze over the site with tape.
Complications of PIV Catheters Complications related to PIV catheters include the following: • Bleeding from the vein may result in bruises or a hematoma.
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Troubleshooting PIV Catheters Regardless by whom and where PIV catheters are placed, monitoring for proper functioning and any signs of complications should be performed on a regular basis. • Patient response: If the patient does not respond as expected to a medication administered through a PIV catheter, this may be the first sign that the IV is obstructed/kinked or has become disconnected or dislodged or is infiltrating (the medication is going into the subcutaneous tissue and not the vein). • Inspect the IV bag to make sure that it is not empty. • Inspect the insertion site for signs of infection or infiltration. • Inspect the fluid flow rate by observing the drip chamber (flow rates are frequently adjusted during cases and the provider may
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forget to return the flow rate to a desired level after making an adjustment). Also, checking that the IV fluid is flowing normally is reassuring that the IV line has not become disconnected or infiltrated. • Check the drip chamber to make sure it is half full and air cannot get into the infusion tubing. • It is also wise to keep IV lines labeled and untangled to prevent the injection of medications or infusions into the wrong IV. Administration ports should be readily accessible.
■ CENTRAL VENOUS CATHETER Definition and Indications “Central lines” or central venous catheters (CVCs) are invasive catheters placed directly into the patient’s central venous circulation. There are a variety of locations, methods of placement, and types of catheters available for use depending on the clinical circumstance. The choice of location and type of line can have a dramatic impact on proper patient care. Prior to setup, confirm the desired line type and location with the placing provider. Ideal placement of a central line leaves the catheter tip at a location in the superior vena cava, approximately 3–5 cm above the right atrium (RA), or the cavoatrial junction. This is always confirmed by chest x-ray some time after insertion. This location allows administration of medications with negligible circulation times so as to speed their onset. Based on their presence in the central circulation, central lines are a convenient location for blood sampling (discussed elsewhere in this chapter). With all blood returning to the heart via the inferior and superior vena cavae, the unique location of central lines also allows sampling of mixed venous blood for determination of SCVO2, or central venous oxygen saturation. While the uses of this laboratory value are beyond the scope of this chapter, it is important to be aware of this if assisting in blood sampling (see Chapter 9). The most common site for placement of a central line remains the internal jugular vein (IJV) in the neck. From the right side of the neck, the cavoatrial junction lies at a depth of approximately 16–18 cm from the right and 19–21 cm from the left side of the neck of adults. This difference is important to note as certain catheters may not have sufficient length for proper placement in the vein if using the left rather than
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the right side. Importantly, subclavian insertion locations affect the length of the catheter insertion similarly. Using a subclavian central line approach, the cavoatrial junction lies at a depth of approximately 13 cm from the right and approximately 16 cm from the left side of the chest wall (see below for proper placement location on the chest). A nice trick to estimate proper depth can be done by placing a catheter or a piece of string on the patient’s chest from the insertion site to approximately 2–3 cm below the sternomandibular junction and then measuring the length. While it is possible to place these catheters using physical landmarks, current recommendations are that internal jugular lines be placed using ultrasound guidance. The use of ultrasound in the placement of the central lines has been found to decrease catheter-related complications and time of insertion in some studies.
Central Venous Anatomy There are multiple locations for central line placement. This chapter provides brief anatomic descriptions of the three most common approaches. Internal Jugular Anatomy The IJV is the primary draining vein from the head and leaves the skull at the level of the jugular foramen. It follows into the neck, entering the carotid sheath along with the common carotid artery, vagus nerve, and deep cervical lymphatics (Fig. 34.6). The vein traverses below and medial to the sternocleidomastoid (SCM) muscle, to enter the anatomic triangle bound by the two muscle bodies of the SCM and the clavicle (an important fact for placing central lines). The IJV then joins with the subclavian vein (SCV) to form the innominate vein near the medial edge of the anterior scalene muscle. The innominate vein then follows into the superior vena cava entering the heart. Subclavian Vein Anatomy Primarily draining the upper extremities, the SCV is a continuation of the axillary vein. Importantly, it is attached by fibrous tissue to the posterior aspect of the clavicle for approximately 3–4 cm. These attachments do not allow the vein to collapse even in severely hypovolemic patients, making this technique beneficial in such situations. After passing medial to the clavicle, the SCV joins the IJV to form the innominate
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Digastric muscle (anterior belly)
Mandible Mylohyoid muscle Stylohyoid muscle Hyoid bone
External carotid artery Internal carotid artery
External jugular vein Thyroid cartilage
Superior thyroid vein
Sternocleidomastoid
Common carotid Left vagus nerve
Cricoid cartilage
Internal jugular vein
Sternothyroid muscle
Deep cervical lymph node
Brachial plexus
Middle thyroid vein
Trapezius muscle
Brachial plexus Thoracic duct
External jugular vein
Subclavian vein
Omohyoid muscle (inferior belly)
Thyroid gland
Trachea
Recurrent laryngeal nerve L. brachiocephalic vein
Inferior thyroid vein Anterior view
■ FIGURE 34.6 Internal jugular vein anatomy. (With permission from Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999.)
vein at the level of the sternoclavicular junction, then passing into the heart as the superior vena cava (Fig. 34.7). It is important to note that the subclavian artery, brachial plexus, phrenic nerve, and internal mammary artery lie just posterior to different regions of the SCV and are separated by the anterior scalene muscle, making damage to these structures a potential complication. Just inferior to the SCV lie the pulmonary apex and pleura, creating a higher potential for pneumothorax with this technique. Femoral Anatomy The FV anatomy is quite simple, which makes accessing this vein easier than many others. As a continuation of the popliteal vein from the lower extremity, the FV enters the femoral sheath in the thigh and continues to the level of the inguinal ligament (Fig. 34.8). Passing underneath this ligament, the FV becomes the external iliac vein, which then travels along the psoas muscle to join with the contralateral external iliac vein, forming the inferior vena cava. The femoral approach takes place in the inguinal region at the level of the femoral sheath. It is important to note that the femoral artery and nerve lie just lateral to the
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FV in this region, allowing for potential damage to these structures with a femoral access technique. The term NAVeL is a useful mnemonic for remembering the relative femoral anatomy. From lateral to medial —Nerve, Artery, Vein, empty, Lymphatics (Fig. 34.8).
CVC Types Triple-Lumen Catheter (Fig. 34.9) Size:
Length: Benefits:
Negatives:
7-French catheter with three lumens (proximal white and blue 18G, distal brown 16G) 15, 20, and 30 cm Provides ability to infuse multiple medications simultaneously and monitor the central venous pressure (CVP) Provides access to ports for blood sampling Does not allow rapid infusion of IV fluids
CVC Introducer (Fig. 34.10) Size: 8–10
Length: Benefits:
French single-lumen catheter typically used as a sheath for hands-free triplelumen or pulmonary artery catheter (PAC) insertion. It has an infusion side port. 10 cm Provides ability to rapidly infuse large amounts of IV fluids or blood products
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Sternocleidomastoid muscle (clavicular head) Sternocleidomastoid muscle (sternal head)
Anterior scalene muscle Clavicle
Index finger in jugular notch of manubrium
Right axillary vein
Superior vena cava
Right axillary artery Right subclavian artery and vein
■ FIGURE 34.7 Subclavian vein anatomy. (With permission from Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999.)
Negatives:
through the infusion side port. The main valved channel can be used to insert a PAC or hands-free catheter. Larger dilator with increased risk of injury to the cannulated vessel, especially if inadvertent intraarterial cannulation. By itself, it only provides one port for infusion. Insertion of a secondary catheter (hands-free triple-lumen or PAC) into the main introducer lumen decreases the flow rates that can be delivered through the infusion port.
Hands-Free CVC (Fig. 34.11) Single- or multilumen catheters are inserted through a CVC introducer and locked in place. Size: Length: Benefits:
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Vary, typically a 7 French double or triple lumen is used. 15–30 cm Allows addition of a multilumen catheter to an introducer without additional skin and vessel puncture.
Negatives:
Can be removed, while leaving the introducer in place (reduces the risk of CVC rupture). When inserted into a CVC introducer lumen, it decreases the flow rates that can be delivered through the infusion port. The lock is not tight enough and has a tendency to be pulled out with tension.
Peripherally Inserted Central Catheters These are longer, thin catheters typically placed by IV therapy teams in the hospital when longterm IV access is required or the patient has difficult venous access. As the name implies, they are placed peripherally, typically in the antecubital, basilic, or cephalic veins. Size: Length: Benefits:
2–6 French (adult and pediatrics) Vary by individual (typically 35–45 cm) Provides long-term venous access
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Anterior superior iliac spine
Inguinal ligament
Iliacus fascia and iliacus Deep circumflex iliac artery
Lateral cutaneous nerve of thigh
Femoral ring Lacunar ligament
Superficial circumflex iliac artery
Femoral
Pectineus and pectineal fascia
Nerve Artery Vein
Pubic tubercle
Deep artery of thigh
Obturator nerve, anterior division 1st perforating artery
Sartorius
Adductor longus
Rectus femoris
Gracilis Great saphenous vein
Iliotibial tract
Anterior femoral cutaneous nerves
■ FIGURE 34.8 Deep femoral vein anatomy. (With permission from Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999.)
Negatives:
without additional punctures Provides access to central circulation without risks of CVC placement Length and size limit flow rates (cannot be used for rapid infusion). Catheters are prone to clots and kinking.
Tunneled CVC Ports These are surgically placed, most often for infusion of chemotherapy and other caustic
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medications for long-term use. The infusion port is usually placed under the skin on the chest wall and can be accessed by placing a needle through the skin.
CVC Indications • • • •
Delivery of vasoactive medications Monitoring of intravascular volume Access for frequent blood draws Access for PAC
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■ FIGURE 34.9 Triple-lumen central venous catheter.
■ FIGURE 34.11 Hands-Off double-lumen central venous catheter.
• Inability to obtain peripheral venous access • Access for special CVC for potential aspiration of a venous gas embolus • Access for insertion of cardiac pacemaker wires or catheters • Access for long-term chemotherapy or parenteral nutrition • Access for dialysis or plasmapheresis • Infusion of medications that are irritating to peripheral veins
• CVC or CVC introducer
• 0.032″ diameter threading wire (straight of J-tip), usually contained within a special sheath • 7-French dilator • Scalpel • 18G thin-walled needle • 22G “finder” needle • 16G or 18G catheter-over needle • 10- to12-mL syringe (may be a special syringe that allows placement of the wire through the plunger) • Suture (possibly straight or curved) • Needle driver • Caps for infusion port • Gauze and sterile dressing material • Manometry tubing (may or may not be included in kit) • Large sterile drapes (may or may not be included in kit) • Prep sticks and solution (may or may not be included in kit)
■ FIGURE 34.10 Sheath introducer.
■ FIGURE 34.12 Central venous catheter insertion kit.
CVC Equipment Much of the equipment required for central venous access is contained in specialized kits. Contents of CVC kits vary slightly according to the type of catheter included in the kit. In addition, many manufacturers allow institutions to customize the contents of the kits. A description of a generic kit is included below. Generic CVC Kit (Fig. 34.12)
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• Local anesthetic (1% lidocaine), 25G needle, and a 5-mL syringe (equipment for local anesthetic infiltration may or may not be included in the kit) Additional equipment for CVC insertion that is usually not included in the kit: • Linear-array ultrasound with nonsterile ultrasound gel (nonsterile gel may be used for a “prescan” performed prior to the actual procedure). Sterile ultrasound gel is required for the actual procedure. • Sterile gown, mask, gloves • Sterile towels and sterile gauze pads • Pressure transducer setup (if needed) • Mobile table for setup of equipment • Sterile saline flushes • Sterile sleeve for the ultrasound probe • Sterile ultrasound gel • Additional sterile caps
Technique for CVC Insertion
•
•
The first steps are to assemble and prepare the necessary equipment for CVC placement. These steps are described below:
•
• Position the patient in 15 degrees of Trendelenberg for SVC or IJV placement (increases the size of the veins). Confirm with the provider if the Trendelenberg position is desired. • Turn on the ultrasound machine and place in position for easy viewing by provider. • Place a mobile table on the side of the provider’s dominant hand for ease of access. • In sterile fashion, open a central line kit, making sure not to touch the contents. Often, the providers will organize the contents of the kit how they prefer once it is opened. In other institutions, the anesthesia technician will don sterile gloves and organize the kit contents. • Place two sterile saline flushes and sterile ultrasound sleeve and gel onto the sterile field. • Some providers prefer to “prescan” the anatomy with the ultrasound before prepping the patient. If so, turn on the ultrasound, place a small strip of gel on the probe and hand to provider. • Once the “prescan” is finished, wipe gel off area and ensure the region is clean and clear of any debris. • If placing in the IJV, turn the patient’s head slightly to the contralateral side. It may also
•
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be necessary to remove the patient’s pillow if it is tilting the patient’s head too far forward or is in the way of the neck. If the patient is intubated, the circuit tubing should be moved so that it is out of the way and secure. In all of these steps, care should be taken to avoid dislodging the endotracheal tube. Using sterile technique, prep the region for at least 30 seconds. For IJV: prep from bottom of the ear to the clavicle and from the trachea to as far lateral as possible (Fig. 34.13). For SCV: prep from 1 to 2 inches above the clavicle to just above the nipple and from the anterior shoulder to the sternum. For FV: prep from just below the hip to approximately 6 inches below the inguinal crease and from medial groin to the lateral thigh. Assist the provider with gowning and gloving. Tie the gown in the back. Do not touch the provider’s arms, hands, or chest. Make sure the provider is wearing a mask and loose ties are not hanging down. Assist with draping, ensuring to only touch the underside of the drape when it is passed to you. Gently pull the drape until completely opened and the body covered (Fig. 34.14). When the provider is ready, place a small strip of nonsterile ultrasound gel on the probe. The provider will place his or her hand into the sterile sleeve and will grab the probe from you. As he or she passes the end of the sleeve to you, grab the very end and pull along the length of the cable, making sure no uncovered portion of the cable touches the sterile
■ FIGURE 34.13 Preparation of internal jugular vein: The skin is prepped with tinted chlorhexidine swab from just below the right ear and chin to the right nipple crossing the midline.
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■ FIGURE 34.14 Full-body drape. Patient’s entire body should be covered with a drape.
field (Fig. 34.15). Refer to Chapter 38 for the details on the operation of the ultrasound machine and transducer. The provider may ask for color Doppler during the procedure to confirm the location of vascular structures. • See below regarding the specifics of cannulating the vein and placing the catheter. • Once the vein has been entered and the guide wire is in place, the provider may ask you to take a picture with the ultrasound machine,
307
■ FIGURE 34.16 This photograph is the still shot of the ultrasound machine screen that demonstrated the presence of the wire in the internal jugular vein. The photograph is taken and placed in patient’s chart for the documentation. This is required for the billing of ultrasound-guided central venous catheterization.
showing the wire inside the vessel (Fig. 34.16). In many institutions, the picture is printed and placed in the patient’s chart. Ask the provider if a picture will be required and what to do with the print. In some institutions, the provider will want a personal copy of the print for anesthesia billing. • During insertion, the providers’ attention may be focused on the line placement itself. Periodically, review the patient’s status on the monitors and notify the provider of any significant changes in blood pressure, oxygen saturation, machine alarms, heart rhythms, etc. Be prepared to assist with drug administration (vasopressors or anesthetics) or adjustment of anesthetic agents if the provider requires it. • After the procedure is completed, carefully remove the drapes, making sure not to pull the line out and to avoid extubating the patient. • Connect the CVP transducer tubing to one of the flushed ports on the central line (preferably one of the 18G lumens), open all stopcocks, and zero the CVP transducer. Review the waveform and pressure reading (Fig. 34.17).
Provider Technique for Placing a CVC
■ FIGURE 34.15 Ultrasound transducer is covered in sterile sheath for use in the sterile field.
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The details of the placement of the central line are intended to give the anesthesia technician a basic understanding of the procedure. This information will help you to be able to assist the provider as needed, particularly if in your institution, the anesthesia technician gowns and
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CVP a
v
■ FIGURE 34.17 Central venous pressure normal waveform. (With permission from Springhouse. Lippincott’s Visual Encyclopedia of Clinical Skills. Philadelphia, PA: Wolters Kluwer Health; 2009.) CVP, central venous pressure; ECG, electrocardiogram.
gloves and actively hands in sterile equipment to the provider. After the setup above is completed and all ports of the CVC are flushed with saline, the provider will identify the vein with the sterile ultrasound probe in one hand and a needle/syringe in the other hand. Details change depending upon slight variations in technique. Here we describe the Seldinger technique (the catheter-over needle technique) using an 18G catheter and needle (if the kit does not contain an 18G catheter over a needle, a regular 2-inch 18G PIV catheter may be opened using sterile technique and placed on the provider’s tray). The needle is advanced with constant negative pressure in the syringe by slightly pulling on the plunger. The provider will monitor the advancement of the needle on the ultrasound monitor. Once a flash of blood is noted in the syringe, the angle of the needle is to be changed to a more shallow angle and the catheter is threaded into the vessel (if the provider is using only the thinwall needle without the catheter, this step will be skipped and the provider will proceed directly to passing the guide wire into the vein through the needle). The needle is removed, covering the end of the catheter with a finger (patients who are breathing spontaneously create negative intrathoracic pressure during inspiration and can entrain air into the circulation through an open catheter or needle). If using manometry, the tubing is connected to the catheter hub and lowered below the head to fill with blood. This tubing is then raised above the head, to confirm
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that the blood column falls slowly and that the pressure in the tubing is consistent with venous pressure (if the artery is accidentally cannulated, the pressure in the tubing will be much higher). Some providers ask to have the manometry tubing connected to a transducer to measure the pressure. The manometry tubing is removed and the wire is advanced into the catheter (and vein) to approximately 15–20 cm, and the catheter is removed over the wire. A small skin nick is made with the scalpel to make room for the CVC. The dilator is advanced over the wire to open a path for the CVC through the skin and deeper tissues. The dilator is removed over the wire. The CVC is fed over the wire until it almost reaches the skin. In most cases, the wire will need to be pulled back and fed back into the CVC until it emerges from the brown 16G port. Holding the far end of the wire (to avoid losing a wire into the central circulation), the central line is then advanced all the way over the wire and into the vein. The wire is then removed. Each port is flushed with sterile saline once ability to draw back blood is confirmed (many institutions preflush the catheter ports before the catheter is inserted). The ports are capped, the line is sutured in place, and the site is covered with a clear sterile dressing.
Complications Potential complications of CVC insertion include the following: • • • • • •
• • • • •
Hemorrhage Infection Damage to pleura, pneumothorax Arterial damage or arterial cannulation Thrombosis Arrhythmias: The wire can be advanced into the heart and cause an arrhythmia, particularly if it is advanced into the ventricle. A few premature ventricular beats are not uncommon. The wire should be withdrawn until the abnormal beats subside. On occasion, medications or further treatment will be necessary if the arrhythmia is serious (e.g., ventricular tachycardia). Nerve damage Vascular erosion with bleeding into the chest Cardiac tamponade and wall rupture Phlebitis Infection: local site infection or bloodstream infection
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Troubleshooting Most common problems encountered with central lines will be managed by the provider; however, a few common problems and possible solutions are shown in Table 34.1.
■ PULMONARY ARTERY CATHETER Definition and Indications The PAC, also known as the Swan-Ganz catheter named after its inventor, was introduced in 1970 and now is widely used as a diagnostic and monitoring tool in the management of critically ill patients. The PAC is a balloon flotation catheter. It has a small balloon on its tip that is inflated after insertion and floats the catheter along with the blood flow through the vena cava into the right heart. The PAC is then further advanced into the pulmonary artery (PA). If balloon flotation is unsuccessful, it can be placed with fluoroscopy or ultrasound at the bedside. Basic features of PACs are illustrated in Figure 34.18. The length of the catheter is 110 cm and the diameter is 7–8 French depending on the number of lumens and additional features. The basic catheter has at least three lumens, a distal port near the tip, a proximal port 30 cm from the tip, and a port for inflating the balloon. Inflation of more than 3 mL of air into the balloon port can rupture the balloon. It is important not to confuse the ports and inadvertently attempt to inject
■ FIGURE 34.18 Pulmonary artery catheter. This photograph shows Hospira Opticath thermodilution pulmonary artery catheter. The blue port is the proxymal port, the yellow is the distal port, and the clear is the infusion port. The red tube has a locking system for inflating/ deflating the balloon. This catheter is equipped with a fiberoptic cable to measure mixed venousoxygen saturation (black) and a thermistor (white) for measuring cardiac output by thermodilation technique.
medications or fluids through the balloon port. In addition to the ports, there is a thermistor (transducer that senses the temperature) 4 cm from the tip of the catheter. The newer catheters are equipped with more features such as an extra lumen for infusion or passing temporary pacemaker leads into the right ventricle (RV) (opens at 14 cm from the tip) and a fiberoptic system that allows continuous monitoring of mixed venous oxygen saturation.
TABLE 34.1 TROUBLESHOOTING FOR CENTRAL VENOUS CATHETERS ISSUE
PROBLEM
POSSIBLE SOLUTION
Wire will not thread.
Catheter/needle may not be in vein.
Check for continued flow of blood with syringe again.
Thrombosis in vessel
Repeat needle puncture if needed or change site.
Pulsatile flow in manometry tubing
Accidental arterial puncture
Immediately remove needle or catheter and hold pressure.
One or more lumens will not draw blood back.
Catheter may not be in vein. Clot/kink on catheter. Faulty catheter
Try gentle flush to clear clot and then draw back. Pull back catheter small distance. Replace catheter or change site.
CVP will not zero.
Air bubbles in line Closed stopcocks Kink in tubing. Faulty equipment.
Detach tubing and flush tubing. Open all stopcocks. Straighten tubing. Change CVP cable or transducer.
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PAC functions include the following: • Direct measurement of right atrial pressure (CVP), right ventricular pressure, and pulmonary arterial pressure • Indirect assessment of left atrial pressure via the pulmonary artery occlusion pressure (PAOP) (wedge pressure). This measurement is obtained by properly positioning the catheter in a branch of the PA and temporarily inflating the balloon while the measurement is taken. • Measurement of cardiac output by thermodilution and hemodynamic calculation • Mixed venous blood sampling Because of the potential complications associated with PACs (see below) and the introduction of transesophageal echo to monitor heart function, the indications for placement of PACs have diminished. Commonly accepted indications include • Management of complicated acute myocardial infarction with cardiogenic shock • Management of acute decompensation in severe heart failure • Management of noncardiogenic shock • Diagnosis of pulmonary hypertension Contraindications include • Mechanical prosthesis in tricuspid or pulmonary valve • Tricuspid or pulmonary endocarditis • Presence of right heart mass
■ FIGURE 34.19 Triple-pressure transducer. Each transducer is color coded. The most left is for arterial line (red), the middle is for central venous pressure (blue), and the most right is for pulmonary artery pressure (yellow).
Technique for PAC Insertion 1.
Determine the insertion site: The PAC is inserted most commonly in the IJV or the SCV as the course of venous return to the RA is more straightforward from these insertion
PAC Equipment Although placing the PAC is not complicated and easily done at the bedside, appropriate training and equipment are required. • All equipment needed for CVC insertion as previously described • Two pressure transducers so that pressure can be monitored in both the proximal and distal port (Fig. 34.19) • Introducer kit (8.5–9 French) (Fig. 34.20) • PAC • Thermodilution set (a bag of saline, injector, tubing) and cardiac output cable • Resuscitation equipment and external pacing device (in the event of vascular complications, or life-threatening arrhythmias during insertion (see complications below)
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■ FIGURE 34.20 Sheath introducer kit. The kit contains a 9-French sheath introducer, a dilator, a stopcock and caps, a manometry tubing, syringes, needles, a guide wire, a suture kit, a blade, gauze, dressing, 1% lidocaine (5-mL ampoule), a sterile cover, and a hub cap. Some kits also contain chlorhexidine preps and a full-body drape.
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sites. In the cardiac catheterization lab, the FV is often accessed for right heart catheterization. In addition, fluoroscopic guidance is used in the cardiology suite. Position the patient properly and obtain central venous access with an 8.5-French or a 9-French introducer as described above (Central Venous Access section). Once access is obtained, the operator will remain sterile and an assistant will perform nonsterile tasks. Just prior to the insertion, prepare the PAC. If it is equipped with a fiberoptic system for continuous mixed venous O2 saturation, connect the cable to the module and perform preinsertion calibration. Remove the PAC from the plastic packet and connect the thermodilution cable to the thermistor port. Check for the temperature to display on the monitor screen (should be room temperature before PAC insertion). Place the sterile cover over the catheter and lock it at 100 cm. Connect the pressure tubing from the transducers to each port on the PAC and flush with saline (the distal port for PA pressure, the proximal port is for CVP). If the PAC has an infusion port, connect a stopcock and a 3-mL syringe to the port and flush with saline. Lastly, inflate the balloon with 1.5 mL of air using the syringe provided in the kit (the syringe is equipped with a lock system to prevent overinflation of the balloon) (Fig. 34.21A). Check to see that the balloon has inflated evenly. Deflate the balloon by releasing the syringe plunger.
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Do not aspirate on the plunger to deflate the balloon. Most PACs have a mechanism to lock the balloon port to keep the balloon inflated (Fig. 34.21B). The operator is now ready to insert the catheter. Place the patient back to flat or in slight reverse Trendelenberg position. Slightly tilt the table to the right. This position assists the operator in floating the PAC into the PA. The operator inserts the catheter thorough the introducer up to 20 cm. Inflate the balloon slowly with 1.5 mL of air and lock the syringe. You should not feel resistance. If you do, stop inflating and notify the provider. Check the monitor for a venous waveform. As the catheter is advanced into the RV, the pressure waveform will change as shown in Figure 34.22. After advancing the PAC 30–35 cm in a normal-size adult, the catheter tip will enter the RV through the tricuspid valve. A pulsatile RV systolic pressure appears. The diastolic pressure is still equal to the RA pressure. Record the RV systolic and diastolic pressures. When the catheter is advanced across the pulmonic valve into the PA, the diastolic pressure rises whereas the systolic pressure remains unchanged. This occurs at around 45–50 cm in normal-size adults. Record the PA systolic and diastolic pressures. The catheter is then slowly advanced in the PA until the waveform changes again where the systolic pressure disappears and the waveform resembles the RA pressure waveform.
■ Figure 34.21 A: Inflating the balloon. The balloon at the tip of the catheter is fully inflated with 1.5 mL of air. Note that the syringe is locked. B: Deflating the balloon. The balloon is deflated when the syringe is unlocked and 1.5 mL of air is back in the syringe.
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■ FIGURE 34.22 Change in the pressure waveform correlates with the position of the tip of the pulmonary artery catheter.
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8.
This pressure is known as the pulmonary artery capillary wedge pressure (PACWP) or the PAOP. At this point, the operator will stop advancing the catheter. Record the pressure and then deflate the balloon by unlocking the syringe. Make sure that the same amount of air (1.5 mL) returns to the syringe without aspiration. If the air does not return, it can be a sign that the balloon has ruptured. The balloon should be deflated at all times while the PAC is left in place in the PA (prolonged inflation can cause PA rupture). Balloon inflation should be reserved for the measurement of PACWP. Inflate the balloon slowly until a wedge pressure tracing appears on the monitor screen. This can occur before the balloon is fully inflated. The catheter can migrate distally into a smaller portion of the artery. Overinflation can cause rupture of a PA. After the PACWP is recorded, the balloon should be deflated. Stretch the sterile cover toward the hub of the introducer and lock it over the hub. Lock the catheter by twisting the locking system on the cover to secure the catheter position.
■ FIGURE 34.23 Applying a sterile dressing over the pulmonary artery catheter insertion site.
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Apply the sterile transparent dressing at the insertion site (Fig. 34.23). 10. The catheter has multiple ports with multiple tubes and cables connected. The weight of these devices can pull on the catheter and dislodge it. To prevent this, secure the proximal end of the PAC with a securing device or clamp (use caution so that you do not clamp the catheter). 11. As noted above, the balloon should be deflated at all times while the PAC is left in place in the PA. The balloon inflation should be reserved for measurement of PACWP. After the PACWP is recorded, the balloon should be deflated.
Cardiac Output Measurement (by Thermodilution Technique) 1.
After the PAC is inserted, connect the thermodilution kit to the injection port (the proximal port) at the stopcock (Fig. 34.24), making sure that there is no air in the fluid bag and the tubing (de-airing the bag and tubing should be done prior to connecting). Stop the fluid infusion from the side port of the introducer to avoid a temperature
■ FIGURE 34.24 The thermodilution kit connected to a pulmonary artery catheter.
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change. Infusion of cold fluid through the infusion port will interfere with cardiac output measurements. Activate the Cardiac Output window on the monitor screen. Draw the fluid in the syringe (normally 5 or 10 mL, depending on the setup). Press the “Start” button on the monitor. After the beep and the prompt on the monitor screen (“Inject now!”), inject the entire amount of fluid in the syringe quickly but at a steady rate. You will see the curve of the temperature change on the screen. Wait for the monitor to come back to “Ready” before performing the next measurement. Perform three cardiac output measurements and record the average value.
PAC Complications The complications related to PAC placement include the complications related to CVC access as described above. PAC-specific complications are listed below: • Arrhythmias: Atrial or ventricular arrhythmias are the most common complications while placing or removing the catheter. The catheter can touch the endocardium and irritate it. Arrhythmias are normally transient and do not need intervention; however, in some cases, the arrhythmias can be serious (i.e., complete heart block or ventricular tachycardia/fibrillation) and require urgent treatment. • PA rupture: This is very rare but a catastrophic complication that carries a mortality rate of 50%-70%. Risk factors include pulmonary hypertension, hypothermia, and overinflation of the balloon. To minimize the risk, avoid overinflating the balloon and minimize PACWP measurements. • Pulmonary infarction: Overwedging of the catheter (prolonged balloon inflation) or overinflation of the balloon can cause pulmonary infarction. Prolonged inflation of the balloon usually occurs when a PACWP measurement was taken and deflation of the balloon was forgotten. • Catheter knotting: During insertion of the catheter, coiling of the catheter occasionally occurs in the cardiac chambers. This can lead to knot formation. If the catheter does not advance to the next chamber at the expected
length, it should be pulled back with the balloon deflated. Risk factors for knotting include a large RV, multiple attempts at passing the catheter into the PA, and a warm, flexible catheter.
PAC Troubleshooting • Cannot see the venous waveform: Make sure that the pressure transducers are connected to the correct ports and all transducers are zeroed. When any questions arise, withdraw the catheter and recheck by flushing each port. • On the inflation of the balloon, there is excessive resistance and very high pressure appears on the monitor: This could be caused by inflating the balloon in the sheath. Let the balloon deflate and advance the catheter to 20 cm. If it happens at 20 cm, the tip might be against the vessel wall. Deflate the balloon and reposition the catheter by rotating. • The catheter will not advance into the RV or the PA: Position the patient in reverse Trendelenberg position and slightly tilted to the right. Perform a Valsalva maneuver followed by release. This promotes the forward flow of blood in the right heart and can help float the catheter through the right side of the heart. Alternatively, temporarily increasing ventricular contractility by administering an inotropic agent may help advance the catheter into the PA. If still unsuccessful, transesophageal echocardiography may be helpful in guiding the catheter. In rare circumstances, fluoroscopy is necessary. • Unable to obtain a wedge pressure: In some patients, a typical PACWP waveform does not appear even at the maximum depth (60 cm in normal-size adult). The observed waveform could be a prominent v wave from significant mitral regurgitation or simply caused by nonuniform inflation of balloon, but the true cause is unknown in many cases.
■ INTRAOSSEOUS VENOUS ACCESS Definition and Indications The intraosseous route is one of the quickest ways to establish access for fluid infusion, administration of medications, or blood transfusions in an emergency situation, such as pediatric resuscitation. The bone marrow cavity is in continuity with the venous circulation; therefore, it can be used to administer medication, fluid, and blood. tahir99-VRG & vip.persianss.ir
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Intraosseous access can be obtained in the proximal tibia, the distal tibia, the proximal humerus, the femur, the iliac crest, or even the sternum. Intraosseous access sites can be used for blood samples for laboratory tests and cross match. Intraosseous access is indicated when emergent vascular access is required but peripheral or central access cannot be obtained or cannot be obtained in a timely fashion (i.e., life-threatening situation, pediatric emergency). It is not the first choice for access but after attempts to obtain vascular access fail, and time is limited, it can be a life-saving and efficient alternative. Intraosseous access takes less than 2 minutes to obtain. Contraindications include fractured bones, bones with osteomyelitis, and proximal bone fracture (i.e., do not use tibia if ipsilateral femur fracture is present).
Intraosseous Access Equipment • • • • •
Alcohol or chlorhexidine swab Local anesthetics (1% lidocaine) 5-mL syringe 50-mL syringe Intraosseous infusion needle (There are different needle sizes: 14G, 16G, and 18G. Smaller sizes are used for infants (Fig. 34.25). • Specialized intraosseous access tools (e.g., FAST1 and EZ-IO) (Figs. 34.26 and 34.27) are available, which may include special devices or handheld battery-operated drills to drive the needle system through the bone and into the intraosseous space.
■ FIGURE 34.25 Intraosseous infusion needle with Dieckmann modification and standard hub design (Cook Medical). (With permission from Tobias JD, Ross AK. Intraosseous infusions: a review for the anesthesiologist with a focus on pediatric use. Anesth Analg. 2010;110(2):391–401.)
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■ FIGURE 34.26 First Access for Shock and Trauma (FAST1) device (PYNG Medical). (With permission from Tobias JD, Ross AK. Intraosseous infusions: a review for the anesthesiologist with a focus on pediatric use. Anesth Analg. 2010;110(2):391–401.)
Technique 1.
2.
Determine the site. The anteromedial aspect of the tibia is most commonly used as it lies just under the skin and can be easily identified. Palpate the tibial tuberosity. The anteromedial tibial insertion site will be 1–3 cm below and 2 cm medial to the tuberosity.
■ FIGURE 34.27 EZ-IO device (Vidacare). (With permission from Tobias JD, Ross AK. Intraosseous infusions: a review for the anesthesiologist with a focus on pediatric use. Anesth Analg. 2010;110(2):391–401.)
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Wear sterile gloves and clean and then prep the skin by using an outward circular motion. In awake patients, inject local anesthetic in the skin and continue to infiltrate until the periostium (hard surface) is encountered. Position the lower extremity as flexing the knee and placing a pillow or sandbag behind the knee for support. If not available, have an assistant stabilize the lower leg by holding the knee and ankle from the other side. Hold the limb just above the insertion site and insert the intraosseous needle perpendicular to the skin and slightly caudal (toward toes) to avoid injury to the epiphyseal growth plate. Advance the needle with a drilling motion (or with the drill) until loss of resistance is felt when the needle penetrates the cortex of the bone and enters the marrow cavity. This may not be obvious in younger children. Remove the stylet and connect the 5-mL syringe. Confirm the correct position by aspirating blood. Inject 10 mL of saline to check for any signs of infiltration (swelling of limb or increase in resistance). In awake patients, inject 3–5 mL of preservative-free 1% lidocaine into the intraosseous space. The injection should be performed slowly to avoid patient discomfort. If not successful, remove the needle and try another site. Secure the needle in place with a clear dressing, sterile gauze, and tape.
Intraosseous Complications This is a relatively simple procedure, but there is the possibility of serious complications including • • • • •
Tibial fracture Compartment syndrome Osteomyelitis Skin necrosis Microscopic pulmonary fat and marrow embolism (not clinically significant)
The intraosseous needle should be removed as soon as peripheral or central vascular access is obtained, or within 24 hours, to minimize the risk of complications.
■ ARTERIAL LINE (A-LINE OR ART LINE) Definition and Indications An arterial line is an invasive catheter inserted into a peripheral artery that allows the provider to
directly monitor continuous real-time blood pressure changes. This provides beat-to-beat analysis of arterial blood pressure and allows continuous access to blood samples throughout surgery and afterward. The most common site chosen for placement of an arterial line, by far, is the radial artery given its superficial location and ease of access. Other potential sites include the brachial and axillary arteries in the upper extremities and the femoral, dorsalis pedis, and posterior tibial arteries in the lower extremities (see Table 34.2 for risks and benefits of each location). Umbilical and temporal arteries can be used in neonatal patients. Arterial lines are one of the most frequently placed invasive catheters and, as such, anesthesia technicians require a thorough understanding of why and how they are placed. The following indications for placement, general setup, technique for placement, and troubleshooting tips are general recommendations from our institution. Specific protocols may vary by hospital. The anesthesia technician should be familiar with local protocols for arterial line placement and management.
Indications for Arterial Line Placement There are multiple indications for the placement of an A-line including, but not limited to • Expected frequent or abrupt changes in blood pressure or hemodynamic instability • Expected large blood loss during surgery • Frequent need for blood draws (this prevents multiple arterial or venous sticks during surgery) • The need for titration of vasoactive medications to support blood pressure • Assessment of a patient’s intravascular volume status (“Systolic Pressure Variation”) • The need for blood gas monitoring
Contraindications to Arterial Line Placement • Infection or severe scarring at the site of expected placement • Coagulopathy or administration of tissue plasminogen activator • Substantial trauma in the same extremity • Arteriovenous fistula in the same extremity
Arterial Line Equipment (Fig. 34.28) • 20G Angiocath or Arrow kit (extra catheters and kits should be immediately available tahir99-VRG & vip.persianss.ir
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TABLE 34.2 RISKS AND BENEFITS FOR CHOSEN ARTERIAL LINE SITES SITE
BENEFITS
RISKS
Radial
Easiest to access and palpate
Bleeding, infection, thrombosis, embolism, vasospasm.
Good collateral flow
Short catheter can be inaccurate with high-dose vasopressors.
Accurate Brachial
Similar benefits to radial but can be harder to palpate
Often needs ultrasound for placement. Longer catheter needed.
Axillary
Larger diameter
Bleeding, infection, thrombosis, embolism, vasospasm.
Not many benefits
Difficult to place. Higher infection risk. Easy to dislodge.
Often a last-ditch effort
Can damage nearby nerves. Bleeding, infection, thrombosis, embolism, vasospasm.
Femoral
Often used if other sites are inaccessible
Higher risk of infection. Often needs ultrasound for placement. Patient must lie flat.
Dorsalis pedis/ posterior tibial
Can use if there are problems with upper extremity circulation
Bleeding, infection, thrombosis, embolism, vasospasm.
Ease of access and superficial
May not accurately represent systemic pressure.
Good if the provider will not have access to upper extremities during surgery
Easy to dislodge. Bleeding, infection, thrombosis, embolism, vasospasm.
as multiple attempts at cannulation are not uncommon). In addition, smaller catheters may be necessary, particularly in small patients, severe vascular disease, or pediatric patients. For femoral artery cannulation, most institutions have special femoral artery kits that contain a longer catheter, longer access needles, and other supplies. • Pressure transducer (compatible cable, IV pole attachment) • Threadable wire (64 mm) • Rigid pressure tubing with three-way stopcock. Many institutions utilize closed, needle-free, in-line reservoir tubing systems to avoid wasting of patient blood during blood sampling and to decrease the risk of accidental needle puncture. Examples include Safeset
•
• • • • • • •
and VAMP. Confirm with your institution on availability (see “Blood Sampling” section for further explanation). 500-mL bag of 0.9% NaCl. Some institutions utilize heparinized saline (heparin 2 units per milliliter), but it is not standard practice due to increased risk of heparin-induced thrombocytopenia (HIT). Check with your facility. Sterile prep (1% chlorhexidine) Sterile towels, gauze Sterile gloves (sterile gown is optional in most institutions) Mask, eye protection, and cap Arm board attached to operating room (OR) table Wrist immobilizer, tape to secure Pressure bag (capable of at least 300 mm Hg) tahir99-VRG & vip.persianss.ir
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■ FIGURE 34.28 Arterial line setup: The materials needed for arterial line placement are set up on the mobile cart for ease.
• Mobile table for easy access to supplies • Clear sterile dressing (e.g., Tegaderm or Opsite). • Tape • 2-0 silk sutures and needle driver, scissors • 1% lidocaine, 3-mL syringe, 25G or 30G needle • Ultrasound machine, sterile sleeve for the probe (ultrasound is used routinely by some providers and only for special circumstances with others). Ultrasound is almost always used for femoral artery cannulations.
Arterial Line Technique • Prepare transducer and monitoring line. For description of the proper setup of pressure transducers, please refer to “Pressure Transducers” section below. • Wash your hands and use gloves before handling or setting up any invasive device. • Identify the patient using hospital armband and, if able, the patient confirming his or her identity. • Confirm with the provider which artery on which extremity will be used. • Using tape, position patient’s arm on prepared arm board at an abducted position of less than 90 degrees on the OR bed (Fig. 34.29). In some cases, the femoral artery will be used. If so, slightly abduct the leg. • Clean the wrist of any obvious contamination; then, using sterile prep and sterile technique, clean arm for at least 30 seconds to 1 minute with enlarging outward circles. Include the area from the patient’s palm up
■ FIGURE 34.29 Preparation for radial arterial line placement. Patient’s upper extremity is secured on the arm board with tape proximally and distally with a roll under the wrist for extension. Supinate the lower arm so that the palm side of the wrist is in horizontal position. Tape the thumb to add more supination if necessary.
to approximately halfway up the forearm. Be sure to clean both medial and lateral aspects of hand and arm. If using the femoral artery, prep the groin area from 5 cm above the ilioinguinal ligament to the midthigh. • Using sterile gloves and towels, drape patient’s arm exposing only the desired field as shown in Figure 34.30. • Using sterile technique, open Angiocath or Arrow kit as well as sterile gauze. Have wire nearby as well. • Once the provider has successfully cannulated the artery and inserted the arterial catheter, remove the cap from the end of the rigid tubing and hand the provider the tubing without touching the end (Fig. 34.31).
■ FIGURE 34.30 Draping for radial arterial placement.
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■ FIGURE 34.31 Connecting the tubing to the radial arterial catheter.
• Confirm presence of a waveform on the monitor screen. • If desired by the provider, open and hand in the sterile needle driver and sutures. • Zero the arterial line. (See “Pressure Transducer” section.)
Placement of Arterial Line Once the proper setup is complete, the provider will place the arterial line by first palpating the chosen artery. After locating optimal pulse, the provider will insert the intended catheter or Arrow kit at a 30–45-degree angle until a flash of bright red blood is noted in the catheter. Using the Seldinger technique, leave the catheter in the vessel and withdraw the needle. Once pulsatile flow is noted from the catheter, a wire is threaded into the vessel and the catheter is advanced over this until securely inside the vessel. At this point, the wire is removed and pressure is placed just past the arterial catheter to avoid outflow of blood. The tubing is then connected to the catheter. Some providers attempt to advance the catheter needle assembly into the artery (specialized arterial line catheters have a self-contained wire that can be advanced at this point). The catheter is then advanced over the needle and into the artery in much the same way as PIV catheters are placed. If the catheter cannot be advanced off the needle into the artery, the catheter/needle setup is advanced, with the assumption that the operator has passed through the back wall off the artery. The needle is removed and the catheter is withdrawn as described above. When pulsatile flow is obtained, a wire is passed into the artery and then the catheter can be advanced over the wire
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into the artery. The wire can then be removed. Pulsatile flow should still be present. Securely attach the monitoring tubing to the catheter hub and check the monitor for an arterial waveform. For femoral arterial lines, the same basic technique is often utilized, with the exception that it is more common to use ultrasound to locate the artery. Prepare the ultrasound machine and probe as described in the section on central venous access. Prep and drape the patient as described above. The operator will attach a syringe to a needle and advance the needle under ultrasound guidance or by palpation into the artery. The syringe will be removed and pulsatile flow confirmed. A wire is passed into the artery and the needle removed. The specialized long arterial catheter can then be advanced over the wire and into the artery. The wire is removed and pulsatile flow is confirmed. The remaining steps are the same as those described for cannulation of the radial or brachial artery in the arm.
Arterial Waveform Basics The exact morphology of an arterial waveform can explain much about the arterial line setup, patient pathology, and hemodynamics. See Figure 34.32 for an example of a normal arterial waveform. The normal initial upslope indicates early systole with the opening of the aortic valve and left ventricular contraction. The peak indicates runoff after ventricular contraction and occurs during midsystole. The typical notch seen on the downward slope (dicrotic notch) indicates the closure of the aortic valve and indicates the beginning of diastole. The final downward slope indicates further diastole. Common variations in waveforms include both under- and overdampening. In a very simplistic sense, overdampening
■ FIGURE 34.32 Arterial pressure waveform.
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occurs when the transducer cannot sense the pulsation clearly. The waveform tracing will be flattened with a much smaller difference between systolic pressure and diastolic pressure. This can be due to kinked tubing or a kinked catheter, closed or partially closed stopcocks, flexed wrist, air bubbles or clots in the tubing, overdistensible tubing, underpressurized IV bag, vasodilation, or the catheter being up against the wall of the artery. This results in underestimation of blood pressure. Similarly, underdampening is an exaggerated peaked waveform that can overestimate blood pressure. This can be due to excessive tubing length, overly rigid tubing, vasoconstriction, kinked tubing, or partially closed stopcocks. Further explanation of waveform variation can be helpful but is beyond the scope of this chapter.
Arterial Line Complications Commonly cited complications can include bleeding, hematoma, and infection. It is critical to secure the tubing to the catheter as patients can lose blood upward of 500 mL/min if an arterial line becomes disconnected. Potential, but
less common, complications include damage to nearby structures (veins, nerves, tendons, etc.), decreased hand perfusion, air embolism, thromboembolism, and even compartment syndrome with hidden bleeding.
Arterial Line Troubleshooting Common conditions and troubleshooting tips are included in Table 34.3. Other items to consider include the following: • If the patient is awake, always introduce yourself and explain what you are doing and why. • The choice of artery remains up to the provider placing the line. In the vast majority of cases, the radial artery is chosen for convenience and safety. Other options include the ulnar, brachial, and axillary arteries in the upper extremities and the femoral, dorsalis pedis, and posterior tibial arteries in the lower extremities. • The site chosen for the catheter can be influenced by the surgical procedure, ease of access, and, in some cases, patient safety. Confirm the site with the provider prior to setup.
TABLE 34.3 TROUBLESHOOTING FOR ARTERIAL LINE PROBLEM
LIKELY ISSUE
SOLUTION
Inability to aspirate blood
Kink in tubing Closed stopcock No arterial placement Clot in catheter Faulty equipment
Flush tubing Straighten tubing Replace catheter/transducer Small traction on catheter Open all stopcocks
No waveform present
Kink in tubing Closed stopcock No arterial placement Clot in catheter Faulty equipment Disconnected tubing
Flush tubing Straighten tubing Open stopcocks Replace catheter/transducer Check all equipment
Unable to zero or reach baseline
Closed stopcock Air bubbles in line Not zeroed Faulty equipment
Open all stopcocks Disconnect and flush line Rezero line Replace catheter/transducer
Underdampened
Excess tubing Catheter movement Vasoconstriction
Remove extra tubing segments if able Secure catheter more Inform provider
Overdampened
Kink in tubing Air bubbles in line Closed stopcocks Vasodilation Clot in catheter Empty IV bag IV bag not pressurized
Straighten tubing Open stopcocks Flush line Repressurize bag (300 mm Hg) Replace IV bag Inform provider
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• Examine the arm for evidence of infection, trauma, existing vascular access, and arteriovenous fistulas prior to preparing the region. Miscommunications between the provider and the anesthesia technician can occur. If you observe a potential contraindication for placement of the arterial line in the location you are preparing, discuss the issue with the provider. • If the patient is alert and oriented, it can be helpful to ask about his or her handedness (which hand he or she brushes his or her hair or teeth with, etc.). It is more comfortable for the patient in the postoperative period if the catheter is placed in the nondominant arm. • Do not hyperextend the wrist if the radial artery is chosen as this can induce radial nerve injury. • Check for capillary refill in region distal to the catheter after insertion to ensure continued perfusion. • Arterial line transducers need to be changed out every 96 hours. • Change catheter to 22G in pediatric patients and 24G in the neonatal population.
■ ASSOCIATED EQUIPMENT Basic IV sets A basic IV setup consists of a bag of IV fluid; an IV infusion set that has a spike, a drip chamber, a tube, a regulating clamp, and injection ports; one or two three-way stopcocks; and an extension tube. Some of the sets are preassembled (Fig. 34.33); however, be sure to tighten and secure
■ FIGURE 34.33 Regular intravenous set. This shows a preassembled regular IV set with a macrodrip chamber, a clamp, double stopcocks, and an extension tubing.
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■ FIGURE 34.34 Macrodrip (right) and microdrip (left) IV sets.
all connections before clinical use. Additional IV setups include the following: • Microdrip (Fig. 34.34): The regular IV set (macrodrip) has a drip chamber that delivers 10, 12, or 15 drops equal to 1 mL. The microdrip IV set has a drip chamber that delivers 60 drops equal to 1 mL. Microdrip IV sets are used when small amounts and more exact fluid or drug administration are required (e.g., pediatrics or critical care settings). Because 1 hour is 60 minutes, the number of drops in 1 minute represents the milliliters delivered in 1 hour (100 drops in 1 minute is equal to 100 mL/hr). • Buretrol (Fig. 34.35): It is an in-line receptacle between the IV set and the IV fluid bag that has a maximum volume of 150 mL. It is a safety mechanism to avoid the overadministration of fluid to small patients (less than 15 kg). A defined amount of fluid is filled in
■ FIGURE 34.35 A preassembled intravenous set with a buretrol.
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■ FIGURE 34.36 Y-tubing blood transfusion set.
■ FIGURE 34.37 Infusion pump set.
the buretrol from the IV bag and then connecting tube to the bag is clamped off. Even with an IV pump malfunction, only the amount in the buretrol would be administered to the patient. • Basic blood tubing: The infusion set for blood transfusion is equipped with a 200-μm filter in the drip chamber. Some blood transfusion sets used intraoperatively also have a manual pressure pump for rapid infusion. • Y tubing (Fig. 34.36): It is used as the IV line when blood transfusion is anticipated. One side of Y tubing is spiked to normal saline and used to flush the tubing. When blood transfusion is needed, spike the blood bag with the other side of Y tubing to start blood transfusion. • Setups for infusions pumps (Fig. 34.37): Infusion pumps require specific tubing that fit certain pumps. Generally, it consists of a drip chamber, a regular tubing, a clamp, and the elastic tubing that lies inside of the pump.
■ FLUID WARMER
All IV sets should be primed prior to use to avoid injecting air into the patient. To flush the entire set with fluid, close the regulating clamp first and then spike the IV bag. Fill the drip chamber up to half of the capacity by squeezing and releasing the chamber. Then, open the clamp to flush the tubing until all air and bubbles have been removed from the tubing. The stopcocks and injection ports tend to trap the air. Tap these places with a finger or a surgical clamp to release bubbles. Once all air has been removed, close the clamp. Label the set with the date and the time as it should be used within 24 hours. Do not write on the fluid bags directly with markers.
Patients undergoing general anesthesia for operative procedures become hypothermic due to multiple reasons (i.e., lack of muscle activity, vasodilatation, hypothalamic depression, radiation, conduction, evaporation, convection of body heat). Administration of continuously warmed fluid has been shown to decrease the incidence of intraoperative hypothermia. Different types of fluid/blood warmers are available on the current market; however, they share several common characteristics. Most consist of a warming device and a disposal tubing component (e.g., HOTLINE, Level1) (Fig. 34.38). The IV tubing is connected to the proximal connector of the disposable warming tubing. The distal end of the warming tubing is connected to IV tubing, which is connected to the patient. They function by circulating warm sterile water through the outer lumen of the warming tubing, which surrounds an inner lumen through which the IV fluid flows. The Bair Hugger warming system uses a special coil of tubing that can be attached to the hose of the forced-air warming units. Another system is the Ranger fluid warming system that uses a proprietary cassette and highly conductive heating plates. All of these systems require special disposable components and wall socket power. Thermal Angel is a disposable, inline, battery-powered warming device. Its major advantage is that it can be used during transport of critically ill patients. Although it is very rare, there is a case report of a superficial burn caused by Hotline tubing touching the patient’s skin over a long period of time. Caution must be taken to prevent this type
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■ FIGURE 34.38 Hotline.
of complication. Setting up and troubleshooting vary in different brands and require in-service training by the manufacturer or distributor and referring to the manufacturer-specific manuals. However, the basic setup is very simple. After installing a prefilled tubing, coil, or cassette in the warming unit, simply turn the device on.
■ RAPID INFUSION SYSTEMS Rapid infusion systems are commonly used intraoperatively to transfuse massive amounts of fluids and of blood components rapidly. Some of the devices use pressure (e.g., Level1) (Fig. 34.39), and others use rotary pumps (e.g., Belmont) (Fig. 34.40). Both systems are equipped with filters, line pressure monitors, air detectors, and a warming device with temperature monitors. In addition, the Belmont system has a reservoir and a computer system to regulate flow rate. Both systems should not be used to transfuse platelets,
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■ FIGURE 34.39 Level1.
cryoprecipitates, or granulocyte suspensions. They should not be used where rapid infusion is medically contraindicated. Administration of blood (red cells) under pressure may cause hemolysis, resulting in hyperkalemia and hemoglobinemia. Continuous supervision by trained personnel is required in the use of these devices. General setting up is described below; however, it is essential to follow the manufacturer’s instruction for setup, operation, and troubleshooting. 1. 2. 3. 4. 5.
Inspect the system. Install the disposable set (including a reservoir for Belmont). Turn the power on. Spike the saline bag and prime the tubing (and fill the reservoir in Belmont). Connect extension tubing to the patient’s IV access and start infusing.
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■ FIGURE 34.41 Autotransfusion system (Cell Saver).
■ FIGURE 34.40 Belmont rapid infuser system.
■ CELL SAVER (AUTOTRANSFUSION SYSTEM) As a part of the effort to decrease the need for allogenic blood transfusion, autologous blood transfusion (autotransfusion) has been employed in surgeries since the early 19th century. A cell saver device consists of suction for the surgical field to collect the blood, a collection reservoir, a filter, a centrifuge, and a collection bag (Fig. 34.41). An anticoagulant (usually heparin) is added to the shed blood as it is collected. The blood is mixed with a washing solution to remove undesirable components such as debris from the surgical field, cytokines, free hemoglobin, and lipid microparticles. The mixture is then centrifuged to separate out the red blood cells. The red blood cells are transferred to a collection bag for transfusion. The end product will have very high hematocrit (60%-70%); however, it will lack platelets and clotting factors. The final concentration of red blood cells is dependent upon the amount of blood in the collection reservoir before the wash cycle is begun (the
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less blood in the reservoir, the lower the final hematocrit). The use of a cell saver is indicated for procedures in which anticipated blood loss is 20% or more of patient’s estimated blood volume (more than 1 L in adults). The type of procedure should be individualized by the institution and by surgeons. Contraindications include infection, topical anticoagulants (Avitene, Hemopad, Instat, etc.), liquid or soft bone cement (okay to use if the cement is hard) conditions that result in extensive hemolysis, topical antibiotics (can get concentrated to the point of nephrotoxicity), or where the suctioned blood is contaminated by sterile water, hydrogen peroxide, or alcohol. Relative contraindications include shed blood from obstetrics or malignancy. In all cases, if the washing process is not adequate, administration of cell saver blood could result in serious complications, such as hemoglobinemia, renal insufficiency, hyperkalemia, dilutional anemia, microembolism, and inadvertent anticoagulation. It is imperative that the cell saver be operated and monitored by trained personnel. Setup and operation vary in different brands; however, general operation is described as follows:
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Chapter 34 • Vascular Access Equipment and Setup
1. 2. 3. 4. 5. 6. 7. 8.
Turn the power on. Open the centrifuge lid. Install the disposable set (reinfusion bag, waste bag, washing chamber, pump adapter). Close the lid. Spike the saline bag. Start the priming procedure. Set up the blood collection reservoir and connect it to the disposable set. After sufficient blood is collected, start the wash program.
■ PRESSURE TRANSDUCERS A pressure transducer is a device containing a fluid-air interface that converts fluctuations in pressure to electronic data, which is then displayed on the patient monitor. The transducer contains a diaphragm with a silicon chip that continuously translates the pressure against the diaphragm from the column of fluid between the transducer and the patient’s circulation. The continuity of the fluid column is essential to proper functioning of the transducer, and, as such, any air bubbles, clots, or kinks in the tubing will cause inaccurate reporting of pressure changes. Also key to obtaining accurate information is properly “zeroing” the device. Gravity and the weight of the fluid in the column pressing against the diaphragm (if the fluid column is above the transducer) or pulling away from the diaphragm (if the fluid column is below the transducer) can affect pressure readings. To control for this effect, the transducer should be placed at the same height as the point in the body that will serve as the reference pressure, a point called the phlebostatic axis. For operations with the patient in the supine position, the phlebostatic axis is the point at which the fourth intercostal space intersects with the midaxillary line in order to use the RA as a reference point (zero level). It is important to maintain this relationship between the patient and the reference point. When the height of the operating table is changed, the transducer height will have to be changed as well. Small variations in the height of the transducer compared to the reference point will create inaccurate values in the measured pressure. Transducers can be used in the hospital to monitor a variety of pressures, including central venous blood pressure, arterial pressure, PA pressure, tissue compartment pressure, and even intracranial pressure.
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Setting up a Pressure Transducer • Connect the rigid tubing to the patient end (top) of the pressure transducer; also insert a three-way stopcock near the patient end of the tubing for blood sampling. If using VAMP, Safeset, or other in-line reservoir, ensure that the in-line reservoir is connected to the patient end of the pressure transducer (Fig. 34.42). • Connect the flexible tubing with the bag spike to the appropriate connection on the pressure transducer (bottom). • Spike normal saline or heparinized saline bag. Insert the fluid bag into the pressure bag and pressurize it to 200 to 250 mm Hg. Fill the drip chamber up to two-thirds of the capacity by squeezing the chamber a couple of times (Fig. 34.43). • Prime the entire tubing length with fluid by gently pulling on the red rubber tag on the pressure transducer (flush valve). If unable to prime, ensure all stopcocks and valves are open to the tubing. • VAMP and Safeset systems often come preassembled and you simply need to spike the IV bag and prime the tubing as above. • It is crucial to thoroughly flush the entire tubing and ensure there is NO AIR in the tubing as this can lead to severe patient complications. Periodically flick tubing and stopcocks with finger to release and remove any extra air bubbles. • Ensure arterial line transducer is attached to an IV pole at a point level with the phlebostatic axis.
■ FIGURE 34.42 Arterial line transducer and tubing (Safeset).
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2.
3.
ferent reference point than the RA—ask the provider if you are unsure). With the transducer patient tubing connected to the catheter, open the pressure transducer stopcock to the air. Then, press the “Zero” button on the monitor setup. Press the button appropriate for the line for which you are performing the zero. For example, for arterial lines, press “Zero ABP” button. At this point, the waveform should be flat. The numeric value on the monitor should read “0,” and most monitors provide an audible alert to indicate that the zeroing process is complete. Close the stopcock, positioned so that the transducer is open to the patient side. The waveform will reappear and give a digital display of the pressure
■ BLOOD SAMPLING
■ FIGURE 34.43 Fluid-filled drip chamber for pressure transducer to 250 mm Hg (green line).
• Certain arterial line tubing sets come with stopcock caps with holes in them that, when placed on the pressure transducer stopcock, allow for zeroing of the transducer without removal of the cap. It is important to ensure that these caps are only on the pressure transducer stopcock and not on the blood sampling stopcock near the patient end. If so, please replace with a yellow occlusive cap. • If asked to set up multiple invasive lines/ monitors, you will need a holder for multiple pressure transducers, as well as a single pressurized saline bag with the properly spiked flexible tubing (i.e., use 2:1 split tubing for an arterial line and CVP and 3:1 split for adding a PAC). Make sure to label each pressure transducer with the corresponding line it represents. Ensure that all lines and tubing are again properly flushed and contain NO AIR.
One of the benefits to placing an arterial line is that it allows repeated sampling of blood for arterial blood gases and other laboratory tests. With the proper technique, the patient risk associated with blood sampling will be minimized. Blood samples need to be drawn into tubes containing heparin or other anticoagulants to prevent hemolysis, unless otherwise specified for that particular test. For arterial blood gas samples, syringes that are preheparinized can be used or a small amount of heparin can be drawn up into a 1- to 3-mL syringe, coating the inside of the tube, and then squirted out. Of note, sterile procedure and universal precautions should be followed for all blood sampling. Withdrawing the blood sample in an open sampling set: 1. 2. 3. 4.
Zeroing the Pressure Transducer 1.
Set the transducer to the desired height in relation to the reference point (in some cases, the provider may want to use a dif-
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5.
Remove sterile cap from stopcock and wipe port with alcohol swab for 30 seconds. Attach 5- or 10-mL regular syringe to the port. Turn the stopcock off to the flush/transducer. Withdraw 5–10 mL of patient blood into syringe and then close the stopcock at 45-degree angle to prevent flush from flowing to patient (to avoid dilution of the sample, withdraw at least two times the dead space volume). Discard the waste syringe (the sample is diluted with flush solution) and attach an
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Chapter 34 • Vascular Access Equipment and Setup
6. 7.
8.
9.
appropriately sized syringe to the stopcock (blood gas samples must be drawn into heparinized syringes). Again turn the stopcock off to the flush and withdraw 1–3 mL of blood for the sample. Close the stopcock to the port and cap the sample syringe. Replace the sterile cap on the port. Pull the red rubber pigtail to flush the tubing until it is clear. Make sure to pull the red pigtail for only 2–3 seconds at a time, and repeat after a couple of seconds as needed to clear the line. Flushing the line for more than 3 seconds can push fluid back into the proximal arterial circulation as far as the aorta (or cerebral circulation in pediatric patients). Proper flushing of the tubing should require no more than one or two short pulls on the pigtail. If this is not clearing the tubing, ensure the saline bag is properly pressurized. Confirm the presence of a waveform.
Withdrawing blood in a closed sampling set: 1.
2.
3.
4.
When utilizing an in-line sampling set such as the Safeset, a blunt tip needle is necessary for the heparinized syringe. The Safeset system comes with an in-line syringe that collects the “discarded blood” into a 10-mL syringe. Five to ten mL of patient blood (at least two times the dead space volume) is slowly withdrawn into the syringe, and the stopcock at the end of the syringe is closed. After cleansing the closest Safeset port to the patient with alcohol, the blunt needle is inserted into the port and blood is removed for the sample. The syringe stopcock is then opened and the prior “discarded blood” is injected back into the patient, and the red rubber pigtail is pulled to flush the line until clear. Again confirm the presence of an appropriate waveform.
Withdrawing a sample from a PIV catheter: After placing a PIV catheter, venous blood sample can be obtained from the catheter before releasing the tourniquet and the infusion set is connected. After an infusion is started, a blood sample can also be obtained from a PIV catheter
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or central access catheter by the following procedure; however, small veins can collapse and blood sampling may not be possible in those circumstances. 1.
2.
3.
4.
5. 6. 7.
Stop all infusion at least 1 minute before sampling to avoid dilution. Make sure that the clamp flow through the IV is closed. Apply a tourniquet proximal to the IV insertion site if the sampling site is from a PIV catheter. If the blood pressure cuff is applied on the extremity that has the PIV catheter, the “Venipuncture mode” of the automated noninvasive blood pressure machine can be used. Attach a 10- to 20-mL syringe to the closest (to the catheter) stopcock or injection port and slowly withdraw at least four times the dead space volume. Discard the waste syringe and attach the sampling syringe (5–10 mL). Take caution not to apply excessive negative pressure as this will cause hemolysis of the sample. Collect the blood sample needed for the test. Release the tourniquet and turn off the “Venipuncture mode.” Open the regulating clamp and flush the blood in the tubing with IV fluid.
■ SUMMARY Obtaining vascular access, inserting CVCs, and starting arterial lines are extremely common procedures in anesthesia. In addition, the anesthesia provider may request a fluid warmer, rapid transfuser, or cell saver. The anesthesia technician will be frequently called upon to assist the anesthesia provider in obtaining and setting up equipment for these procedures, and the technician should be thoroughly familiar with the equipment. In addition, the technician should be familiar with sterile technique, different infusion sets, pressure transducers, and monitor operation for setting up, zeroing, and monitoring pressures. The anesthesia technician should also be prepared to troubleshoot a wide variety of equipment utilized for these procedures. Errors during equipment preparation or operation can have disastrous consequences, including air emboli in the arterial circulation, thrombosed or infiltrated catheters, or central bloodstream infections.
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REVIEW QUESTIONS 1. The rate of fluid flow in a catheter INCREASES with A) The fourth power of the increased radius of the catheter lumen B) Higher pressure applied to the fluid line (e.g., a pressurized IV bag) C) Increasing length of the catheter D) A and B E) All of the above Answer: D. The radius of the catheter is a critical determinant of fluid flow rates and is related to the fourth power of the radius. Increasing the catheter length would decrease the fluid flow rates.
2. In French sizes, the larger the number is, the larger the diameter is. A) True B) False Answer: A. In French sizes, the larger the number, the larger the catheter. This is in contrast to the Stubbs wire gauge system in which the larger the gauge, the smaller the catheter.
3. Which of the following are potential complications from the placement or use of a PAC? A) Carotid puncture B) PA rupture from balloon inflation C) Ventricular tachycardia D) Pulmonary infarction E) All of the above Answer: E. All of the above are potential complications.
4. Rapid infuser system is NOT equipped with A) Filter B) Heat exchanger C) Roller pump D) Reservoir E) Centrifuge Answer: E. The rapid infuser system is equipped with filters, line pressure monitors, air detectors, and a warming device with temperature monitors. In addition, the Belmont system has a reservoir and a computer system to regulate flow rate. The centrifuge is one of the features of an autotransfusion system (cell saver).
5. Which of the following is TRUE regarding setting up or using a transducer for an arterial line? A) Bubbles in the line can cause a venous embolus. B) The drip chamber should always be in the upright position. C) Damping of the signal will cause an overestimation of blood pressure. D) When flushing the line into the patient, hold the pressurized flush open for at least 6 seconds.
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E) The femoral artery should never be used for an arterial line. Answer: B. The drip chamber of the pressurized flush should be kept in the upright position to prevent air from entering the line to the patient. Bubbles in the line could cause an embolus in the artery and not the vein. In addition, bubbles in the line could dampen the signal (flatten the waveform), leading to an underestimation of the blood pressure. When flushing the line with pressurized fluid, the flush should not be applied for more than 3 seconds to prevent flush from reaching the central arterial circulation. The femoral artery is not uncommonly accessed for arterial pressures.
6. Which infusion set should be used to maintain strict control over the volume of fluid or medication delivered? A) Buretrol B) Microdrip C) Infusion pump tubing with an infusion pump D) Y-type blood administration tubing E) A, B, and C Answer: E. A buretrol is a 150-mL chamber that can be used to control medication or volume delivery, particularly in pediatric patients. A microdrip set has smaller drops (approximately 60 drops per milliliter) and can be used to deliver lower infusion rates. An infusion pump can be set to control infusion amounts and rates. A Y-type blood administration set would be used to deliver higher volumes of fluid or blood.
7. Which of the following statements are FALSE in regard to zeroing a transducer? A) The transducer should be opened to air to perform the zero. B) It is necessary to press a button on the monitor to initiate zeroing. C) Zeroing is not necessary the first time you set up and use a pressure transducer. D) The monitor should read “0” when the transducer is open to air. E) All of the above are FALSE. Answer: C. Every time you set up a transducer it must be zeroed. In addition, when the transducer cable is disconnected, the transducer may have to be rezeroed. To perform a zero, the transducer is opened to air and the monitor button for that particular line is pressed to initiate the zero. The monitor should give an audible beep when the zero process is complete and the monitor should read “0.”
8. Which of the following statements are TRUE with regard to central venous access? A) The internal jugular, subclavian, and femoral veins can be used for peripheral venous access. B) It is not necessary to gown when inserting a CVC.
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Chapter 34 • Vascular Access Equipment and Setup C) Manometry is used to verify the CVC is not in the lung. D) A cordis introducer CVC should be used if you do not expect large amounts of blood loss. E) All of the above are TRUE. Answer: B. It is necessary to use a sterile gown and gloves and use a mask when inserting a CVC to reduce the incidence of bloodstream infections. The internal jugular, subclavian, and femoral veins are used for central venous access. Once a CVC has been inserted, measuring the pressure in the line can help determine that the line was placed in a vein (low pressure) and not inadvertently in an artery (high pressure). A cordis introducer has a very large infusion channel (if nothing else is put into it, e.g., hands-free catheter or PAC) and can be used for high flow infusions.
9. Which of the following should be available to place a CVC? A) Ultrasound machine B) CVC kit C) Infusion setup D) IV fluids E) All of the above Answer: E. All of the above should be available for CVC insertion. Ultrasound is extremely common to identify the relevant anatomy and guide needle insertion into the vein.
10. Which of the following statements are TRUE with regard to peripheral venous access? A) A tourniquet should never be used. B) A transducer should be set up. C) Ultrasound can be used to identify the vein. D) The FV can be used. E) All of the above are TRUE. Answer: C. In rare circumstances, a peripheral vein can be difficult to see or palpate. In these cases, ultrasound can be utilized to identify a vein. A tourniquet is almost always used to enlarge the vein so that it can be more easily palpated and cannulated. A transducer is used to monitor CVPs and is not used for peripheral venous lines. The FV is part of the central circulation and is not considered a peripheral vein.
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SUGGESTED READINGS Atalay H, Erbay H, Tomatir E, et al. The use of transillumination for peripheral venous access in paediatric anaesthesia. Euro J Anaesthesiol. 2005;22:312–323. Celinski S, Seneff M. Procedures, Techniques, and Minimally Invasive Monitoring in Intensive Care in Intensive Care Medicine: Arterial Line Placement and Care. Philadelphia, PA: Lippincott; 2008. Chaney JC, Derdak S. Minimally invasive hemodynamic monitoring for the intensivist: current and emerging technology. Crit Care Med. 2002;30:2338–2345. Chatterjee K. The Swan-Ganz catheters: past, present, and future: a viewpoint. Circulation. 2009;119:147–152. Evans DC, Doraiswamy VA, Prosciak MP, et al. Complications associated with pulmonary artery catheters: a comprehensive clinical review. Scand J Surg. 2009;98(4):199–208. Goldstein JR. Ultrasound-guided peripheral venous access. Israeli J Emerg Med. 2006;6(4):46–52. Greenberg S, Murphy G, Venderm J. Standard monitoring techniques. In: Barash PG, Cullen BF, Stoelting RK, et al., eds. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott; 2009. Hasselberg D, Ivarsson B, Anderson R, et al. The handling of peripheral venous catheters—from non-compliance to evidence-based needs. J Clin Nurs. 2010;19:3358–3361. Hignett R, Stephens R. Radial arterial lines: practical procedures. Br J Hosp Med. 2006;67(5):M86–M88. Hocking G. Central venous access and monitoring. World Anaesth Online, 12:1–6, 2000. Available at: http://www. nda.ox.ac.uk/wfsa/html/u12/u1213_01.htm. Josephson DL. Intravenous Infusion Therapy for Nurses: Principle & Practice. 2nd ed. Clifton Park, NY: Delmar Learning; 2004. SAFESET Blood Sampling System. Critical Care Systems, San Clemente, CA: ICU Medical Inc.; 2005. Available at: http://www.icumed.com/criticalcare/safeset.asp. Silva A. Anesthestic monitoring. In: Basics of Anesthesia. 5th ed. Philadelphia, PA: Churchill Livingstone; 2007. Stoker M. Principles of pressure transducers, resonance, damping and frequency response. Anesth Intens Care Med. 2004;5(11):371–375. Tobias JD, Ross AK. Intraosseous infusions: a review for the anesthesiologist with a focus on pediatric use. Anesth Analg. 2010;110(2):391–401. Tokarczyk A, Sandberg W. Monitoring. In: Clinical Anesthesia Procedures of the Massachusetts General Hospital. 7th ed. Philadelphia, PA: Lippincott; 2007.
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CHAPTER
35
Airway Equipment Setup, Operation, and Maintenance Norman E. Torres, Anita Stoltenberg, and Glenn Woodworth ■ INTRODUCTION The management of the airway is one of the most important tasks of the anesthesia provider (see Chapter 18). Because of the complexity of airway management, manufacturers continue to produce an endless array of tools and equipment to aid in the management of the airway. This chapter introduces the most common types of airway equipment currently available as well as describes any special setup that might be required, how the equipment is generally used, and tips on maintenance and troubleshooting.
■ OROPHARYNGEAL AIRWAY In anesthetized or unconscious patients, the soft tissues of the oropharynx, especially the tongue, can obstruct the passageway between the mouth and the glottis. Oropharyngeal airways (OPAs) are used to stent open the oropharynx to allow passage of air/oxygen through the oropharynx. The majority of OPAs are made of curved hard plastic to conform to the oropharynx. They usually have an interior channel that allows the passage of gas or suction devices from the mouth opening through the channel into the posterior pharynx (Fig. 35.1). OPAs are used in anesthetized or unconscious patients who cannot be easily ventilated by bag/ mask ventilation or who are spontaneously breathing but have airway obstruction. They are usually not tolerated by awake patients and can cause gagging and even vomiting when used in a conscious or semiconscious patient. When inserting an oral airway, the anesthesia provider may use a tongue depressor to keep the oral airway from pushing the tongue back into the pharynx. Oral airways should be kept immediately available (easy to grab) in all settings in which airways are managed (e.g., operating room,
recovery area, emergency room, rapid response, or code carts). OPAs come in a variety of sizes from newborns to extra large adults and are often color coded to indicate the size of the airway. They are usually marked with the actual size in millimeters (50–100 mm) or with a number (5–10) that corresponds to the size in centimeters, with 8–10 the typical size range used in adults. OPAs generally cost between $0.30 and $3.00 each. The vast majority are disposable and latex free. Many institutions have single-use prepackaged disposable oral airways (Fig. 35.2). When removing the airway from the package, care must be taken to ensure that none of the packaging material remains attached to the airway prior to insertion in a patient. Plastic remnants from the packaging can be swallowed or aspirated into the patient’s lungs. Types of OPAs • Guedel airways have a single central channel with a reinforced bite block (Fig. 35.3). • Berman OPAs have dual-side channels (Fig. 35.4). Although many of these airways can be boiled or gas/cold sterilized, the majority OPAs are meant for single use only.
■ NASOPHARYNGEAL AIRWAYS Much like OPAs, nasopharyngeal airways (NPAs) are designed to be used in patients with airway obstruction. These airways are inserted through the nose and into the posterior pharynx where they can prevent the tongue from collapsing against the posterior wall of the oropharynx. NPAs are usually better tolerated than OPAs in awake or semiconscious patients with an intact gag reflex. NPAs are soft and flexible and have
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■ FIGURE 35.3 Guedel oropharyngeal airway. ■ FIGURE 35.1 Three different sizes of oropharyngeal airways.
an interior channel to permit the flow of gas, a beveled edge to ease passage through the nose, and a flared end to prevent the NPA from passing completely into the nose. Because of the flared end, many refer to them as a “nasal trumpet” (Fig. 35.5). Because NPAs can cause trauma to the nasal passages, a decongestant (e.g., phenylephrine nose drops) to shrink the nasal mucosa and lubricating jelly (e.g., “Surgilube” or 2% xylocaine jelly) can be used to facilitate passage of the NPA through the nose. NPAs come in a variety of sizes. They are often sized using the “French” scale, with sizes ranging from 12 to 36 French. Dividing the French number by 3 gives the diameter of the NPA in millimeters. The majority of modern NPAs are latex free and single use only. Older NPAs were made of rubber. Do not assume an NPA is latex free unless the packaging clearly states that it is. NPAs come individually packaged or can be purchased in bulk. Prices range from $3.00 to
■ FIGURE 35.2 Prepackaged disposable oral airway.
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$7.00 each. Some packages include a lubricant. As with many other medical products, the vast majority of NPAs are designed for single use and should not be cleaned and used in another patient.
■ FACE MASKS AND NASAL CANNULA Face masks and nasal cannula are used to deliver supplemental oxygen to the patient. One concept that is universal to all types of oxygen delivery systems is to make sure oxygen is flowing from the source. If a portable oxygen delivery source is to be used (oxygen tank), make sure it has sufficient oxygen for the trip. A full e-cylinder of oxygen at 1,900 psi contains about 660 L of oxygen. The amount of oxygen left in the tank is directly proportional to the amount of pressure left in the tank. If the tank reads about 950 psi, it is half full and contains about 330 L of oxygen. At 10 L/min flow through a simple face mask, this tank would have 33 minutes of oxygen left. If using wall-mounted oxygen, make sure the flowmeter is on and oxygen is flowing.
■ FIGURE 35.4 Berman oropharyngeal airway.
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■ FIGURE 35.5 Argyle nasopharyngeal.
■ PASSIVE OXYGEN DELIVERY— NASAL CANNULA Nasal cannulas are designed to supplement the flow of oxygen to the patient. In general, one end of the tubing is connected to a metered oxygen source and the nasal portion is secured to the patient’s head with the tips (“prongs”) of the nasal cannula resting a short way inside the patient’s nostrils (Fig. 35.6). The oxygen flow is adjusted between 2 and 6 L of oxygen per minute and delivers approximately 24%-44% oxygen to the patient. If the patient requires a higher concentration of oxygen, an oxygen face mask must be used. Delivering higher than 6 L of oxygen per minute through nasal cannula is irritating to the patient and can dry out the nasal mucosa, resulting in nosebleeds. This can happen even if the cannula is attached to a humidification system. Nasal cannulas are generally very similar in design and are usually made of a soft plastic material. They are intended for single patient use and prices range from $0.50 to $2.00 each. One of the major features of the cannula to consider
■ FIGURE 35.6 Nasal cannula. One end connects to the oxygen source, while the tips are secured in the entrance to the nostrils.
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is the length of the oxygen tubing, which can range from 7 to 100 ft. During patient transport, if the oxygen source is at the foot of the bed, the 7-ft length of oxygen tubing may be insufficient for the cannula to reach the patient’s head. Some anesthesia providers stretch the tubing to slightly increase its length. Other features to consider when using a nasal cannula include attaching the tubing to a breathing circuit or sampling exhaled carbon dioxide through the nasal cannula while it is delivering oxygen. Some nasal cannulas come with an adaptor to attach the oxygen source end of the tubing to the breathing circuit (Fig. 35.7). This will allow the anesthesia provider to control the upper limit of the percentage of oxygen delivered through the cannula. For example, the anesthesia provider may wish to control the percentage of oxygen to reduce the risk of fire during a head and neck procedure performed on an awake patient. Unfortunately, the control over the oxygen concentration is not very precise. During inhalation the entrainment of room air affects the delivered oxygen concentration. If the cannula does not come with an adaptor, tape can be wound around the oxygen source end of the tubing to increase its diameter to the point where it can be snuggly fit into the breathing circuit. Some nasal cannulas come with a gas sampling line built into the tubing. The sampling port is near the nostrils, and a separate connection port is near the oxygen source end of the cannula, which can be attached to a CO2 gas analyzer (Fig. 35.8). The sampling tubing can often be separated from the oxygen delivery tubing to facilitate attachment to the gas analyzer. These cannulas are extremely useful during procedures performed under sedation. The sampling line is connected to a CO2 gas analyzer and the anesthesia provider can monitor the respiratory rate,
■ FIGURE 35.7 Adaptor to connect oxygen tubing to the anesthesia breathing circuit.
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■ FIGURE 35.10 Venturi mask.
■ FIGURE 35.8 Nasal cannula with a CO2 sampling port.
• Simple face masks: These masks should be connected to an oxygen source delivering between 6 and 12 L of oxygen per minute. This corresponds roughly to an inspired oxygen concentration of 28%-50% (Fig. 35.9). • Venturi masks: These masks have a mechanism to adjust the inspired oxygen concentration (Fig. 35.10).
• Partial non-rebreathing masks: These masks have an attached reservoir of oxygen. When a patient inspires the oxygen from the face mask, the reservoir provides the majority of the gas flow. This limits the entrainment of air from around the mask. Any entrainment of air around the mask would dilute the oxygen delivered to the patient (this happens in a simple face mask). Non-rebreathing masks can deliver oxygen concentrations of up to 70% (Fig. 35.11). • Aerosol masks: Simple face masks and partial non-rebreathing masks can come with a device to deliver aerosolized medications including bronchodilators (or lidocaine in preparation for awake fiberoptic bronchoscopy) (Fig. 35.12). • Tracheostomy mask: This is a specialized mask that fits around a patient’s neck and is designed to cover a tracheostomy or stoma site. In normal breathing, the nose provides humidification to inspired gases. Because tracheostomy patients bypass the nose, the tracheostomy mask should be attached to a humidified oxygen source (Fig. 35.13).
■ FIGURE 35.9 Simple face mask.
■ FIGURE 35.11 Partial non-rebreathing mask.
a reasonable estimate of end-tidal CO2, and can detect airway obstruction.
■ PASSIVE OXYGEN DELIVERY— FACE MASKS Face masks come in two general types: those used for the passive delivery of oxygen and those used for assisted ventilation. Face masks designed for the passive delivery of oxygen consist of plastic tubing for attachment to an oxygen source (or humidified oxygen source) and the delivery end, which may cover the patient’s entire face, the nose and mouth, a tracheal stoma, or just the nose.
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■ FIGURE 35.12 Aerosol mask.
• Nose mask: For those patients who cannot tolerate nasal prongs or a face mask, masks are available that fit only over the nose. Features to consider when selecting or purchasing face masks include the length of oxygen tubing, the type of mask, and the concentration of oxygen that needs to be delivered. The majority of the face masks on the market are for single patient use only and should not be used on other patients.
■ MASKS FOR POSITIVE PRESSURE VENTILATION In order to deliver positive pressure ventilation via a mask, the mask must be able to form a tight seal around the patient’s mouth and nose. These masks tend to be of a more durable design than passive oxygen masks and also have an inflatable cuff around the edge of the mask to help form a seal with the patient’s skin (Fig. 35.14). The mask also has a port that accommodates a standard 15-mm inside/22-mm outside connector that fits into standard breathing circuits. Finally, many masks have four “prongs” around the connector opening. These prongs are used to attach
■ FIGURE 35.13 Tracheostomy mask.
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■ FIGURE 35.14 Plastic masks with four prongs for strap attachments.
a head strap to secure the mask to the patient’s face. Older mask designs were made of black rubber and were sterilized after use, so they could be used on another patient. The disadvantage of these types of masks include the cost of sterilization, the risk of disease transmission, the masks are not latex free, the inflatable cuffs would decay and lose their ability to stay inflated, and the masks may prevent the anesthesia practitioner from seeing vomit come out of the patient’s mouth and into the mask. Despite these drawbacks, many are still in use today. These masks cost in the range of $20-$40. When using one of these masks, take care to ensure that the cuff is inflated properly and can hold pressure. Follow the manufacturer’s recommendations for sterilization. Newer mask designs are made of plastic and are intended for single use only. They are typically used in the operating room with anesthesia breathing circuits or with bag-valve-mask ventilation systems. Before purchasing a new mask type, consult your anesthesia providers. Some of the masks are more difficult to hold with one hand because of the dome shape on the mask. When using a disposable mask, always check the cuff as it can lose cuff pressure when stored. The cuff can be easily inflated by attaching a syringe to the cuff port. If the cuff will still not hold pressure, the cuff may have a leak. Commonly, the valve used to inflate the mask has become incompetent and is allowing gas to escape from the cuff through the valve. These masks generally cost between $2.00 and $4.00 each. Some breathing circuits come packaged with a disposable anesthesia mask. When removing a mask from individual plastic packaging, it is critical to
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make sure that plastic remnants are not present on the mask. If not completely removed, these remnants could be aspirated into the patient’s lungs when the mask is used.
■ SPECIAL FACE MASKS Some specialized anesthesia masks (e.g., the endoscopy mask) have a port with a membrane for entry of a fiberoptic bronchoscope and a port to ventilate the patient without removing the mask from the patient’s face and without losing the ability to provide positive pressure ventilation (Figs. 35.15 and 35.16). Other face masks are designed to deliver continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BIPAP). BIPAP and CPAP are used to treat obstructive sleep apnea as well as respiratory failure in the intensive care unit (ICU). Both require a tight-fitting mask with a head strap to create a good seal to deliver positive pressure. These masks can cover just the nose or mouth. (Fig. 35.17).
■ LARYNGEAL AIRWAYS Intubating the trachea is considered the gold standard for securing the airway and minimizing the risk of aspiration once the airway is established. Many consider intubating the trachea to be “invasive” and not without risk. Glottic structures like the vocal cords or arytenoid cartilages can be damaged while attempting to pass a tube through the trachea. In addition, tracheal intubation is quite stimulating to the patient and can lead to catecholamine release and large swings in heart rate and blood pressure, which can be detrimental to many patients. Since the 1960s, inventors have been experimenting with a variety of methods to establish an airway that minimizes obstruction caused by oropharyngeal structures without inserting a tube through the vocal cords
■ FIGURE 35.15 Endoscopy mask.
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■ FIGURE 35.16 Endoscopy mask with a special port to admit a fiberoptic bronchoscope.
into the trachea. Because these devices are positioned above the vocal cords (glottic region), they are termed laryngeal or supraglottic airways. The term laryngeal airways would only include those devices that are positioned in the pharynx just outside the larynx and does not include devices like OPAs. There are many types of laryngeal airways. The basic design features that are present in many of these airways include the following: • Blind insertion technique: The glottis does not need to be visualized during insertion. The devices are inserted “blind” with visual markings and tactile feedback to indicate proper
■ FIGURE 35.17 CPAP and BIPAP mask.
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positioning. Proper positioning must be confirmed by listening to breath sounds and the presence of persistent end-tidal CO2. The ease of insertion of many of these devices has allowed them to be used effectively by nonanesthesia providers in emergency settings (emergency room, field airway management by paramedics or emergency medical technicians). Insertion of laryngeal airways does not require the use of paralytic agents to paralyze the vocal cords. Inflatable pharyngeal cuff: These devices include a “cuff” or balloon that is inflated after proper positioning of the device in the pharynx. Inflation of the cuff holds the device in position just outside the larynx and creates a seal to divert gas flow into the trachea and not into the esophagus. Because the device can also be taped in position, it frees up the medical provider to use both hands for other tasks once the airway has been established. At least one laryngeal airway has replaced the inflatable cuff with a proprietary gel material that conforms to the laryngeal inlet. Ventilation channel: All of the devices have a channel or tube through which ventilations or spontaneous ventilation can occur. The tube has a standard 15-mm/22-mm breathing circuit connector on the end. Esophageal suction channel: Many contain a separate tube or channel that will admit a suction device into the esophagus and from there into the stomach. This will allow partial removal of stomach contents and reduce the risk of subsequent aspiration. Intended for use in semiconscious, unconscious, or anesthetized patients: These devices are not tolerated by awake patients unless extensive topical anesthesia to the oropharynx has been applied. Positive pressure ventilation: These devices allow positive pressure ventilation with the caveat that, in general, only low airway pressures can be utilized. Modifications of these devices over the years have increased the amount of airway pressure that can be used to provide ventilation but not overcome the pharyngeal seal and begin pushing gas into the stomach. Intubation aid: During difficult intubations a laryngeal airway may be placed to establish ventilation. Once in place, many laryngeal airways can be used to facilitate insertion of
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an endotracheal tube. Because the laryngeal airway is placed close to the laryngeal inlet, an endotracheal tube or tube exchanger can sometimes be passed blindly through the ventilation channel into the trachea. In other circumstances, a flexible fiberoptic scope can be passed through the ventilation channel into the trachea and an endotracheal tube passed over the scope (see Chapter 18). Not all laryngeal airways have an opening near the laryngeal inlet that is large enough to permit passage of an adult-sized endotracheal tube. • Sizing: Laryngeal airways come in a variety of sizes and can be used in neonates to adults. Sizing nomenclatures are manufacturer specific. • Single use or multiuse: The early airways tended to be multiuse; however, many sites have switched to single-use airways to minimize sterilization costs and the potential for disease transmission. Follow the manufacturer’s instructions regarding single use or multiuse. If the device is multiuse, follow the manufacturer’s instructions for sterilization and the number of acceptable uses/sterilizations. Typical recommendations are between 30 and 50 uses. If the device is reused, care must be taken to clean the ventilation channel with a brush-type cleaner. • Troubleshooting: The most common fault observed with laryngeal airways is failure of the balloon or cuff to hold inflation. This can be due to a leak in the cuff or balloon; however, more commonly, the pilot valve used to inflate the cuff or balloon can become incompetent and leak. These problems occur more frequently with multiple reuses of the device.
■ LARYNGEAL MASK This device was introduced in the late 1980s and has become one of the most popular laryngeal airways worldwide, almost eliminating the use of prolonged mask ventilation. The laryngeal mask (LM) consists of a plastic, silicone, or rubber tube connected to an inflatable silicon “mask” that forms a seal around the laryngeal inlet (Fig. 35.18). A pilot tube with an inflation valve is connected to the cuff. The device is easy to insert and highly effective. Single-use disposable models are generally made of polyvinylchloride (PVC) and range in price from $5.00 to $10.00. Multiuse models generally have a silicone cuff and range in price from $100 to $250.
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■ FIGURE 35.18 LMA™.
Numerous manufacturers produce Several examples are provided below:
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■ FIGURE 35.19 LMA™ Fastrach.
LMs.
• Cuff design has been improved to allow higher positive pressures.
• Ambu: Full line of LM products • Merlyn Medical: ° Endomask Elite: silicone reusable, no laryngeal bars ° Endomask Essential: single-use PVC • Flexicare: Laryseal • Smiths Medical: Portex Soft Seal LM • Intersurgical: I-GEL • Intersurgical: Solus—full line of LMs • LMA™ North America/LMA™ International ° LMA™ Classic—multiuse, does not allow fiberoptic intubation ° LMA™ Unique—single use, latex free ° LMA™ Classic Excel—multiuse (up to 60), permits fiberoptic intubation ° LMA™ Supreme—single use, bit block, precurved, suction/gastric drain tube ° LMA™ ProSeal—multiuse, 30 cm H2O seal pressure for positive pressure ventilation, gastric drain tube ° LMA™ Fastrach
An additional modification has been made to the design of the LM to facilitate intubation (LMA™ Fastrach) (Fig. 35.19). Although blind or fiberoptic intubation can be accomplished with several current LM models, the “intubating” LM is specifically designed for this purpose. The intubating LM illustrated in Figure 35.19 has three components: the LM, a flexible endotracheal tube with removable airway adaptor, and an obturator. The device is first inserted into the oropharynx blindly and the cuff inflated to obtain a seal. The patient may be ventilated at this point with the anesthesia circuit or alternate breathing system. Once chest rise, maintenance of oxygen saturation with a pulse oximeter, and/or positive end-tidal CO2 measurement confirm adequate ventilation, the device can be used to blindly guide a flexible wire spiral endotracheal tube through the LM and into the larynx. Alternatively, a bronchoscope can be placed through the endotracheal tube to assist in guiding the tube into position. The intubating laryngeal mask device may be removed by first removing the endotracheal adaptor and pushing the endotracheal tube through and out of the LMA™ device with the obturator. The laryngeal mask portion of the device must be removed over the obturator while holding the endotracheal tube in position. Operators unfamiliar with this device can easily extubate the patient while attempting to remove the LM portion of the device over the endotracheal tube. After removal of the LM portion of the device, the endotracheal tube adaptor is attached to the endotracheal tube and ventilation is resumed. Breath sounds and end-tidal CO2 should be used to reconfirm tube placement.
• Cookgas: AirQ—disposable and reusable, precurved, bite block, permits bronchoscope • Winice Company • Ningbo TianHou Medical Supplies, Inc. • Teleflex Medical • Encore Several modifications have been made to the original design of LMs including the following: • The tubing can be reinforced with wire to prevent kinking. • The valve assembly can be made without metal to allow use in MRI suites. • The inflatable cuff has been replaced with a form-fitting gel material. • A gastric suction channel has been added.
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■ ESOPHAGEAL TRACHEAL COMBITUBE These devices were first described in the late 1960s. Their primary role has been to establish an airway in cases where a patient could not be intubated. Esophageal tracheal combitubes (ETCs) consist of a double-lumen tube with two inflatable balloons (Fig. 35.20). The “tracheal” lumen opens at the distal end of the ETC. The pharyngeal lumen opens in the lower pharynx via a series of side holes above the distal balloon. The ETC is inserted blindly into the oropharynx and should be advanced until the markings on the tube are at the teeth. The ETC may have been positioned in one of two locations: the esophagus (95% of the time) or the trachea. The large pharyngeal balloon is inflated (some ETCs require 70–100 mL of air to inflate the pharyngeal balloon) to seal the pharynx. The “tracheal” balloon is inflated with 7–10 mL of air. If positioned in the esophagus, the pharyngeal balloon seals the pharynx and ventilation can be accomplished with the pharyngeal lumen. Because the ETC is blindly placed into the esophagus 95% of the time, attempts to ventilate should be first made through the pharyngeal lumen. If breath sounds and end-tidal CO2 cannot confirm adequate ventilation via the pharyngeal lumen, the ETC may have gone into the trachea. In this case, the tracheal balloon would prevent gas from the pharyngeal lumen from entering the trachea. The user would then switch to attempt ventilation via the tracheal lumen. If the ETC is in the trachea, the tracheal lumen will function like a normal endotracheal tube. Note: the lumens are color coded and labeled. Because these devices are only used in emergencies, the operator may not be familiar with their use. The two lumens can confuse a
■ FIGURE 35.20 Esophageal tracheal Combitube.
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novice operator. These devices are single use, come in several sizes (adult only), are produced by several manufacturers (Mallinckrodt, Puritan Bennett, Kendall), and are generally priced between $70 and $100 each.
■ LARYNGEAL TUBE The laryngeal tube is made up of a single ventilation lumen surrounded by a proximal pharyngeal cuff and a distal esophageal cuff (Fig. 35.21). The ventilation tube is occluded at the distal end and like an ETC has a port above the distal cuff and below the pharyngeal cuff that is positioned in front of the laryngeal inlet. The major design advantage over the ETC is that the shape of the laryngeal tube causes it to pass into the esophagus almost 100% of the time. In addition, a single inflation tube will inflate both cuffs simultaneously. The tubes are generally color coded for size, and pediatric sizes are available. Some laryngeal tubes have an additional gastric suction port. Laryngeal tubes are commonly used to establish an emergency airway and have been found suitable for short periods of positive pressure ventilation. Some are advocating their use as a replacement for the LM and that they can be used for routine surgical cases in which a laryngeal airway is not contraindicated. It is important to note that many laryngeal tubes will not permit the passage of an endotracheal tube. In addition, although passage of a tube exchanger through the laryngeal tube into the trachea has been described, it can be very difficult. Laryngeal tubes are manufactured by several different companies including King Systems, VBM Medizintechnik, and Claflin Medical Equipment. They are intended for single use or multiuse, are latex free, and are generally priced between $40 and $75 each.
■ FIGURE 35.21 King laryngeal tube.
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Other laryngeal type tubes: Similar designs to the laryngeal tube include the Pharyngeal Airway Express (Vitals Signs Inc.), the Streamlined Pharynx Airway Liner (SLIPA), and the Glottic Aperture Seal Airway (Arizant Healthcare, Inc., formerly Augustine Medical, Inc.). As of press time, these airways have yet to gain significant popularity.
■ ENDOTRACHEAL TUBES A variety of endotracheal tubes are used in the practice of anesthesia and critical care medicine. This section will discuss the different types of endotracheal tubes available, their features, indication for use, setup, and their care. Endotracheal tubes are flexible, long, and hollow tubes made of PVC. They are usually equipped with an inflatable cuff, a pilot balloon, and an airway connector (Fig. 35.22). Inflation of the cuff will require a syringe. Common endotracheal tubes used in the operating rooms are described as High Low tubes. This means that the cuff may take high volumes of air (6–8 mL) to seal the trachea and protect the airway; however, cuff inflation generates low pressures on the trachea to minimize trauma to the airway. Placement may require the use of a stylet for guidance. Once the endotracheal tube is placed, correct tracheal positioning should be confirmed with positive bilateral breath sounds, positive end-tidal CO2 with a gas analyzer or colorimetric devices, or with bronchoscopy. The endotracheal tube needs to be secured with adhesive tape, a tube tie, or commercially available devices designed for securing endotracheal tubes. These endotracheal tubes come individually packaged, are disposable, and are meant for single use only. Cuffed endotracheal tubes come in a variety of sizes based on their internal diameter. Sizes
■ FIGURE 35.22 Single-lumen cuffed endotracheal tube.
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TABLE 35.1 THE AGE AND WEIGHT
OF PATIENTS CAN BE USED TO ESTIMATE THE APPROPRIATE SIZE OF ENDOTRACHEAL TUBE AGE
WEIGHT (KG)
ET TUBE INTERNAL DIAMETER (MM)
Newborn
2.0–3.0
3.0 uncuffed
Newborn
3.5
3.5 uncuffed
0–3 mo
6
3.5 uncuffed
1y
10
4.0 uncuffed
2–3 y
12–14
4.5 uncuffed
4y
16
5 uncuffed
6y
20
5.5
8y
24
6.0
10 y
30
6.5
Adult
40
7
Adult
50–60
7.5
Adult
60–70
8
Adult
>70
8.5–10
range from 4.5 to 10.5 mm. The size is labeled on the proximal end of the endotracheal tube. Table 35.1 presents the typical endotracheal tube sizes based on the approximate age and weight of the patient.
Parker Endotracheal Tubes Parker endotracheal tubes have an added feature of a downward curved, soft, midline, flexible tip that is designed to minimize trauma to glottic structures upon insertion (Fig. 35.23). These FlexTip tubes have been used when intubating over an intubating introducer or over a bronchoscope.
■ FIGURE 35.23 Parker Flex-Tip tube.
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Uncuffed Endotracheal Tubes Uncuffed endotracheal tubes are typically used in patients younger than 8 years of age to minimize airway trauma. The cricoid ring is located just below the larynx and is the narrowest portion of a child’s airway. Trauma to this portion of the airway can cause inflammation and narrowing of the trachea. These uncuffed tubes lack a cuff and pilot balloon (Fig. 35.24). With the endotracheal tube inserted into the trachea, a leak test is performed to check the seal on the airway. This is done by pressurizing the airway of the intubated pediatric patient and checking on the manometer at what pressure a small leak is detected. A leak at about 20–30 cm of water is considered acceptable. If the leak is not within this range, the clinician will need to repeat the intubation with a different size endotracheal tube until the appropriate fit occurs. Too much leak at low pressures will require a larger tube, while insufficient leak at appropriate pressure will require a smaller tube. In preparing for intubation in a pediatric case, several tube sizes should be available. A stylet should also be readily available to facilitate intubation. The size of the uncuffed endotracheal tube required will depend on the age and size of the child (Table 35.1). The endotracheal tube size for children older than 2 years of age may also be determined by the Cole equation: size = 4 + age/4. Some clinicians choose to use a cuffed endotracheal tube that is half or 0.5 tube size smaller than the estimated uncuffed endotracheal tube. This prevents the need for repeated intubations of a child and also may minimize trauma to the airway. The cuff will be used to provide a seal to the airway.
■ FIGURE 35.24 Uncuffed endotracheal tubes.
■ FIGURE 35.25 Right angle endotracheal (RAE) tube. Oral RAE tube pictured on the right. Nasal RAE tube pictured on the left.
Right Angle Endotracheal Tubes RAE tubes are cuffed endotracheal tubes with an over 90-degree bend near the connector (Fig. 35.25). These tubes are typically used in head and neck surgical cases where the right angle diverts the endotracheal tube away from the surgical field. RAE tubes may be inserted through the mouth or nose into the trachea. Oral RAE tubes direct the tube from the oropharynx toward the foot of the patient. Placement of an oral RAE tube may require the use of a stylet to shape the tube and facilitate intubation. Nasal RAE tubes direct the tube from the nares toward the top of the head. If a nasal route is chosen, the clinicians will require nasal spray phenylephrine, viscous lidocaine, and laryngoscope. In many cases, they may also require Magill forceps to facilitate endotracheal tube placement (Fig. 35.26). The forceps are used to grasp the distal end of
■ FIGURE 35.26 Magill forceps used to facilitate endotracheal tube placement.
tahir99-VRG & vip.persianss.ir
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the endotracheal tube under direct vision with a laryngoscope. The tube can then be directed to enter the trachea. RAE tubes are meant for single use only and are disposable.
the wire spiral endotracheal tube will need to be replaced immediately. It is highly recommended to place an oral bite block in a patient intubated with a wire spiral endotracheal tube.
Evac Tubes
Double-lumen Endotracheal Tubes
Special endotracheal tubes may be used in the ICU setting. The Mallinckrodt TaperGuard and TaperGuard Evac endotracheal tubes are endotracheal tubes with a large elliptically shaped opening on the back side of the endotracheal tube just above the cuff where secretions can pool in a supine patient. This opening is a drainage port through which secretions above the cuff may be suctioned through the evacuation lumen. This may reduce the number of ventilator-associated pneumonias in the ICU. This endotracheal tube may require a stylet to aid in placement and is disposable.
Double-lumen endotracheal tubes are used for clinical cases that require lung isolation and one-lung ventilation, or differential ventilation of the two lungs (Fig. 35.28). The doublelumen endotracheal tube may serve to protect one lung from the other with unilateral infection, abscess cavity, massive hemorrhage, or a large cyst or bulla that could rupture. Other indications for the use of these special endotracheal tubes are to provide ventilation if there is an opening in the conducting airways of the lung to the pleural cavity or outside of the body (e.g., bronchopleural fistula or bronchocutaneous fistula). These can occur from surgery or trauma. Double-lumen tubes are also used during surgery to facilitate surgical exposure by allowing one of the lungs to deflate while the other is ventilated so that the surgeon can visualize intrathoracic structures. Surgeries requiring double-lumen tubes include robotic cardiac surgery, thoracoabdominal aneurysm repairs, video-assisted thoracoscopic procedures, thoracotomies, and pneumonectomies. Double-lumen tubes come in a range of sizes; however, the 35 French size is commonly used in an average-size female and the 37 French size in an average-size male. The tubes come with a leftward-facing tip or a rightward-facing tip. The angle of the tip is designed to facilitate placement in either the right or left mainstem bronchus, depending upon the clinical situation. The tube will have both a tracheal cuff and a bronchial cuff. Each cuff is inflated separately. The double-lumen endotracheal tube has a special
Armored Endotracheal Tubes Armored endotracheal tubes have a spiral wire incorporated into the PVC tubing that reinforces the tube wall (Fig. 35.27). They are flexible and resistant to kinking. These may be either cuffed or uncuffed. They are used for flexible fiberoptic intubation or in airways that may have a tendency to collapse due to tracheal wall weakness or endobronchial tumors. They are also used in head and neck or oral surgery to prevent kinking with tube manipulation. Wire spiral endotracheal tubes may require either a fiberoptic bronchoscope or a semirigid stylet to facilitate placement. Most wire spiral tubes are single use only. Some may be sterilized and reused. One note of caution, if the patient actively bites down on the wire spiral endotracheal tube or the tube is kinked, the tube can remain kinked and the lumen can be significantly obstructed. In this clinical situation,
■ FIGURE 35.27 Wire-reinforced endotracheal tube.
■ FIGURE 35.28 Double-lumen endotracheal tube.
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while oscillatory ventilation could be applied to the other. In review, the following equipment may be necessary to facilitate the use of double-lumen endotracheal tubes:
■ FIGURE 35.29 Double-lumen endotracheal tube adaptor.
adaptor that allows for clamping of the airway and one-lung ventilation (Fig. 35.29). Double-lumen tubes may be placed with direct laryngoscopy or with the aid of a fiberoptic bronchoscope. Generally, the tube is placed through the glottis with the distal angle facing anteriorly. Once in the trachea, the tube is rotated so that the distal end enters the desired bronchus. A fiberoptic bronchoscope is used by the clinician to confirm the position of the tube. The tube is correctly positioned when the distal end of the tube is in the desired bronchus, the distal cuff is placed in the proximal bronchus just below the carina, and the bronchial cuff is not obstructing any distal bronchial openings. Many clinicians prefer to inflate the bronchial cuff while watching with the fiberoptic scope. The fiberoptic scope can be used to reposition the tube if necessary. Once properly positioned, the tube should be secured. Because these tubes may become slightly displaced during surgical manipulation or positioning of the patient, the fiberoptic bronchoscope should always be available in the operating room for the entire case. Once the adaptor is attached to the tube, both lungs can be ventilated. When one-lung ventilation is required, a clamp is placed over the tube leading to the lung that will not be ventilated. The cap over the lumen is opened to allow the desired lung to deflate. In some cases, one-lung ventilation is insufficient to maintain adequate oxygenation of the patient. The clinician may apply CPAP with oxygen to the “down” lung to slightly expand it with oxygen. In other special cases, each lung may be attached to a ventilator and differential ventilation applied to each lung. For example, standard ventilation could be applied to one lung,
• Appropriate size double-lumen tube • A right- or left-sided tube (check with provider which is desired) • Double-lumen tube endotracheal tube adaptor (comes with the tube) • Fiberoptic bronchoscope and all associated equipment (e.g., defogger) • Clamp • Lubricant to facilitate passage of the tube through the glottic opening • 10-mL syringe to inflate the tracheal cuff; 3- or 5-mL syringe for the bronchial cuff • CPAP device with a supplemental oxygen source • Tube exchanger (double-lumen tubes are frequently changed for single-lumen tubes at the end of the case)
■ ENDOTRACHEAL TUBE ADAPTORS Endotracheal adaptors connect the endotracheal tube to the airway circuit of the anesthesia machine or the mechanical ventilator. Most anesthesia circuits include an elbow connector. Other endotracheal adaptors serve specific purposes in the management of the airway. • A bronchoscope endotracheal adaptor allows the clinician to perform bronchoscopy on a patient airway while providing a sealed circuit to ventilate the patient (Fig. 35.30).
■ FIGURE 35.30 Bronchoscope adaptor.
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■ FIGURE 35.31 Endotracheal extender adaptor.
■ FIGURE 35.33 Heat and moisture exchanger.
• An endotracheal extender adaptor provides extra length from the endotracheal tube to the airway circuit (Fig. 35.31). • At times, special foam padding is used on the face of a prone patient. An extension adaptor may be used to connect an endotracheal tube in a prone patient through the padding to the airway circuit (Fig. 35.32). • Heat and moisture exchange (HME) adaptors are placed between the elbow connector of the endotracheal tube and the airway circuit of the anesthesia machine or the mechanical ventilator (Fig. 35.33). This allows the retention of warmth and humidity for the patient during ventilation. • Medication adaptors allow for the delivery of inhaled medications (e.g., bronchodilators) (Fig. 35.34). This adaptor is placed inline with the airway circuit just beyond the elbow connector. The drug is dispensed during the inspiratory cycle of ventilation.
■ STANDARD LARYNGOSCOPES
■ FIGURE 35.32 Endotracheal extender adaptor passing through padding for prone positioning.
■ FIGURE 35.34 Medication adaptor for the administration of inhaled medications.
The laryngoscope is an essential piece of equipment in the operating rooms and ICUs for airway management. The laryngoscope allows the clinician to directly visualize the glottic opening during intubations. A laryngoscope consists of a blade, light source, handle, and batteries. There are two basic rigid laryngoscope systems. The handle allows the clinician to manipulate the blade during intubation attempts. In addition, the handle serves as a power source for a bulb located at the blade tip (Fig. 35.35). The bulb is an incandescent tungsten filament surrounded by a halogen gas. The bulbs are either frosted or clear. In the other major laryngoscope system known as bulb-on-handle system, the laryngoscope handle not only serves as a power source but also provides a light source by using a light-emitting diode (LED). This light is then
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■ FIGURE 35.35 Laryngoscope handle for a regular blade.
transmitted to the tip of a special laryngoscope blade that has fiberoptic cables (Fig. 35.36). The special blades are referred to as fiberoptic blades. The LED light systems tend to last longer than the incandescent filament bulb, generate less heat, and use less energy. Both types of handles have either rechargeable or replaceable C- or D-size batteries. The rechargeable handles come with a recharging base (Fig. 35.37). After each use, the handles are wiped down with an antimicrobial wipe. Through the years, a variety of laryngoscope blades have been developed with minor variations in their designs. These include the Cranwall, Jackson, Janeway, Flange, Macintosh, Magill, Miller, etc. Despite the variations, blades come in two basic shapes: either straight (Fig. 35.38) or curved (Fig. 35.39). Both straight and curved blades come in a range of sizes: 0 (infants) through 4 (large adults). After each use,
■ FIGURE 35.36 Lighted handle for fiberoptic blade.
■ FIGURE 35.37 Rechargeable base for laryngoscope handle.
the laryngoscope blades are rinsed in an antimicrobial solution and dried. In preparation for every intubation, the laryngoscope must be inspected for proper working condition. If the laryngoscope fails to light up, several steps may be used to evaluate and remedy the situation: • Change the batteries in the handle (or recharge the handle). • Replace the handle.
■ FIGURE 35.38 Straight laryngoscopy blades sizes 1–3. tahir99-VRG & vip.persianss.ir
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■ FIGURE 35.39 Curved laryngoscopy blades sizes 2–4.
• • • •
Change laryngoscope blade. Change laryngoscope handle. Tighten the bulb on the blade. Change the bulb on the blade or the handle (bulb-on-handle system).
■ VIDEO LARYNGOSCOPES Rigid video laryngoscopes (RVLs) are transoral devices that can be used by the clinician to indirectly visualize the larynx during intubation with an endotracheal tube. Direct laryngoscopy with a standard laryngoscope allows the clinician to have a direct view of the vocal cords and the upper airway. Video laryngoscopes are composed of a light source, camera, video connector, video monitor, and electrical power source. The video monitor provides a real-time image useful in inspecting the upper airway and facilitating intubation. A flexible or rigid stylet (thick metal wire) placed inside the endotracheal tube is used to aid in the guidance of the endotracheal tube into the trachea. The RVLs that are currently available for clinical use include McGrath (LMA™ North America, Inc.), GlideScope (Verathon, Bothell, Washington), Storz DCI (Karl Storz GmbH & Co. KG, Tuttilngen, Germany), Airtraq (Prodol Meditech S.A., Vizcay, Spain), and PentaxAWS (Airway Scope; Pentax, Tokyo, Japan) (Figs. 35.40 and 35.41). RVLs cost between $10,000 and $20,000. The handling and maintenance of these devices are important. When provided separately, RVL blades and handles cost vary widely in price.
■ FIGURE 35.40 McGrath RVL.
Indications for the use of RVLs include the following: • Anticipated difficult airway (awake or asleep) ° Limited neck extension ° Upper airway (pharyngeal and laryngeal) partial obstruction Craniofacial abnormalities °
■ FIGURE 35.41 GlideScope.
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• As a rescue device for an unanticipated difficult airway Relative contraindications for the use of RVLs (mainly due to occlusion of the lens) include the following: • Massive upper airway bleeding • Upper airway (pharyngeal and laryngeal) total obstruction • Upper airway disruption from trauma • Need for emergent surgical airway All the videoscope systems require a brief warmup period prior to use. This prevents the clear plastic components from fogging during the intubation. If the user experiences difficulty with the image, check and clean all contacts and check the power source.
■ FIBEROPTIC SCOPES Indirect visualization of the glottic opening may also be done with fiberoptic scopes. Fiberoptic cables transmit light from a light source on the proximal portion to the distal portion of the scope. A different set of fiberoptic cables send an image from the distal portion of the scope to the eyepiece or camera and monitor. There are two varieties of fiberoptic scopes used in anesthesia: rigid and flexible. The Bullard scope is a rigid fiberoptic laryngoscope that is used for indirect visualization of the tracheal opening (Figs. 35.42 and 35.43). Figure 35.42 illustrates the three components that make up a complete Bullard blade: the power source (a regular rigid laryngoscope handle with two C-size batteries); the endotracheal tube stylet and guide; and the fiberoptic blade, handle,
■ FIGURE 35.42 Bullard scope components: handle, stylet, and fiberoptic laryngoscope.
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■ FIGURE 35.43 Bullard scope assembled.
and eyepiece. Figure 35.43 depicts a fully assembled Bullard scope with an endotracheal tube in position for intubation. This is a reusable device that requires germicidal cleaning of the blade, handle, and stylet sections of the Bullard blade in between use. The Wu scope is another rigid fiberoptic scope (Fig. 35.44). The Wu scope uses a short fiberoptic system that contains an eyepiece, a power source, and a light source. The eyepiece may be used directly, or a camera and monitor
■ FIGURE 35.44 Wu scope.
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system can be attached to the eyepiece. The flexible fiberoptic scope is placed into a rigid laryngoscope blade to provide the indirect image of the tracheal opening. This rigid blade contains another groove through which an endotracheal tube is passed into the airway. The component will also require germicidal cleaning in between uses.
■ FLEXIBLE FIBEROPTIC BRONCHOSCOPE The flexible fiberoptic bronchoscope has been the traditional gold standard in the management of a difficult airway either anticipated or nonanticipated (Figs. 35.45 and 35.46). The endotracheal tube may be placed into the trachea via an oral or nasal route with the guidance of the flexible fiberoptic scope. This scope is a steerable device that flexes and extends the tip by using a thumb control near the eyepiece. Rotation of the flexible fiberoptic scope clockwise or counterclockwise further refines the guidance of the scope. The light source may be an external device attached to the bronchoscope through a cable or directly attached with a small power source. The light is carried down to the distal tip of the bronchoscope by fiberoptic bundles. A different set of fiberoptic bundles carry the image to the eyepiece or camera at the proximal end of the scope. Care in handling of the fiberoptic bronchoscope is important since the fiberoptic bundles may break if bent too far. A separate channel is available to instill local anesthetic or oxygen to the distal tip and to serve as a suction port to clear secretions. The approximate cost of these scopes range from $10,000 to $15,000. Flexible fiberoptic scopes are useful for awake or asleep intubations. During an awake
■ FIGURE 35.46 Flexible portable bronchoscope disassembled.
intubation via the oral approach, the clinician will topicalize the airway with local anesthetics and place a bite block to prevent the patient from biting down on the scope or hand of the operator. The clinician may provide intravenous (IV) sedation to the patient if not contraindicated. An assistant may be necessary to displace the patient’s tongue forward with the use of clean gauze, laryngoscope blade, and/or Magill forceps. The technique for awake fiberoptic intubation is further discussed in Chapter 18. When performing a nasal fiberoptic intubation, various sized nasal airways, nasal vasoconstrictors (e.g., phenylephrine to shrink nasal tissues), and topical local anesthetics (e.g., cocaine-soaked Q-tips or 4% viscous lidocaine) are used to numb the airway and to facilitate intubation. After its use, the bronchoscope suction port should be cleared by holding the suctioning button and dipping the distal end of the scope into a container of water. The bronchoscope suction port should be cleaned to remove particulate matter with a long thin brush. This will prevent the solidification of material in the suction channel. Then, the entire scope, with the light source removed, is soaked in a bactericidal solution for several minutes, rinsed in clean water, suctioned with the use of a suction attachment, and then hand dried. A tray may be used to store, transport, and protect the bronchoscope in between uses.
■ OTHER AIRWAY ADJUNCTS Lighted Stylets ■ FIGURE 35.45 Flexible portable bronchoscope.
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There are several lighted stylets available for clinical use (Fig. 35.47). These include Trachlight (Laedral), Vital Light (Vital Signs),
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■ FIGURE 35.47 Trachlight.
■ FIGURE 35.48 Intubating bougie.
Trachlight (Rusch), and Surch-Lite (Aaron Medical Industries, Inc.). An endotracheal tube is placed on the flexible stylet but not over the lighted end. The lighted stylet is given a slight bend at the tip prior to insertion. The lighted stylets are blindly inserted devices through the mouth that use a bright light to transilluminate the anterior neck and to guide tracheal placement of an endotracheal tube. The ambient light in the room may need to be reduced when lighted stylets are used. Because the trachea is close to the surface of the skin, a small well-circumscribed glow in the anterior neck will occur when the stylet tip is located in the trachea. The tube can then be advanced into the trachea. If a dull diffuse light or no light is seen, then the tip of the lighted stylet is most likely within the esophagus.
need to be exchanged for different reasons (e.g., a different size tube, a broken pilot balloon, rupture endotracheal cuff, or exchange from a double-lumen tube to a single-lumen tube). In many cases, the original intubation was difficult, or subsequent swelling of airway structures may make laryngoscopy difficult while attempting to exchange an endotracheal tube. In these cases, a tube exchanger can be placed into the trachea via the original endotracheal tube. The endotracheal tube can be removed, and a lubricated endotracheal tube can be guided over the tube exchanger into the trachea. Tube exchangers have length measurements on the outer surface to estimate the depth of insertion. Tube exchangers come in a range of sizes and have either a luer lock or an airway attachment fitting that can be used for jet ventilation or insufflation of oxygen.
Intubating Bougie During direct laryngoscopy the clinician may have difficulty visualizing the glottis or passing an endotracheal tube. An intubating bougie is a long thin device with a slight bend at the distal tip that helps placement through the vocal cords (Fig. 35.48). In many cases, a bougie can be placed under direct visualization through the glottic opening even though the endotracheal tube could not. Once the bougie is in the trachea, an endotracheal tube can be placed over the bougie and into the trachea.
Tube Exchangers Tube exchangers are semirigid tubes that are used to exchange an existing endotracheal tube in a patient for another without the use of a laryngoscopy (Fig. 35.49). Endotracheal tubes
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■ FIGURE 35.49 Tube exchanger. (Courtesy of the Mayo Foundation.)
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■ CRICOTHYROTOMY
Direct Cricothyrotomy
The clinician is rarely confronted with a patient who cannot be intubated and cannot be ventilated despite the use of multiple different airway devices. This is an emergent situation that requires intervention to establish an airway within minutes or the patient may suffer irreversible brain damage or death (see Chapter 60). In this scenario, placing a large IV catheter (14G or larger), retrograde wire, or a cricothyrotomy tube through the cricothyroid membrane may be considered in attempting to establish an airway. The cricothyroid ligament is located between the thyroid cartilage and the cricoid ring in the upper airway (see Chapter 11).
An emergency cricothyrotomy kit consists of a catheter over a needle, stylet, syringe, guide wire, dilator, scalpel, soft neck strap, and a cricothyrotomy tube that attaches to an anesthesia circuit or a bag ventilation system (Fig. 35.50). The cricothyroid ligament is entered in a manner described above. The needle is angled toward the feet of the patient and a wire passed over the needle into the trachea. The scalpel is used to create a large opening into the trachea around the wire. The dilator is loaded inside the cricothyrotomy tube, and the entire unit is passed over the wire into the trachea. The dilator and wire are removed, and the breathing circuit is attached to the cricothyrotomy tube.
Cricothyrotomy and Jet Ventilation
Jet Ventilation Systems
An angiocatheter size 14G or larger may be placed in a sterile fashion through the cricothyroid ligament into the airway with the use of a fluid-filled syringe. The needle is angled toward the feet of the patient. As the needle enters the airway, bubbles will appear in the syringe, confirming proper entry. The angiocatheter is held in place by hand, and a lure locking jet ventilator is hooked to the catheter (see Jet ventilation below). This is only a temporary airway until a more definitive airway is established either surgically or via other techniques described in this chapter.
Jet ventilation systems are used to ventilate and oxygenate patients in both emergent airway situations and during surgeries in which traditional ventilation cannot be used. During emergencies jet ventilation via a catheter placed through the cricothyroid ligament can be life saving. Jet ventilators have a high-pressure hose that attaches to a wall cylinder (E or H size) oxygen source, a pressure regulator/gauge, an on/off valve, and a small-bore tubing assembly with a luer lock fit (Fig. 35.51). Once this device is hooked up to the catheter in the trachea, the on/off valve is pushed and the regulator is adjusted to the lowest pressure that allows for the patients’ chest to rise. The gas flow is delivered for about 1 second and released for 3 seconds to allow for passive exhalation through the mouth and nose. The catheter only allows flow into the patient. Expiration does not occur through the catheter, but rather through the patient’s nose and mouth. Another method of providing jet ventilation is the use of the oxygen flush valve of the
Retrograde Wire Cricothryotomy Another technique that is utilized if more time is available is to place a wire into the cricothyroid membrane. There are kits available that contain the necessary equipment. For the retrograde wire technique, the cricothyroid membrane is entered in a similar fashion described above except that the angle of the needle is toward the top of the head. Once the catheter is in the airway, a long flexible wire is passed into the oropharynx. When the wire is visualized in the oropharynx, Magill forceps are used to grasp the wire and deliver it out of the mouth. The endotracheal tube is then guided over the wire and into the trachea. In a modification of the retrograde wire-guided technique with the use of a fiberoptic scope, the wire is identified in the oropharynx. The wire is guided into the suction channel of the fiberoptic scope and the scope is advanced over the wire and into the trachea. The tube is then advanced into the trachea over the scope.
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■ FIGURE 35.50 Emergency cricothyrotomy kit.
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■ FIGURE 35.51 Jet ventilation system.
anesthesia machine. Here an adaptor must be fashioned to hook up the catheter luer lock to the anesthesia circuit. A 3-mL luer lock syringe with the plunger removed can be attached to the luer catheter. The endotracheal adapter for a size 7 French endotracheal tube is placed in the open end of the syringe to achieve a tight fit (Fig. 35.52). The adaptor is attached to the anesthesia circuit. Once properly attached to the
■ FIGURE 35.52 Jet ventilation adaptor using 3-mL syringe and size 7 endotracheal tube adaptor.
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circuit, the oxygen flush is held on for 1 second and released for 3 seconds to deliver high-pressure oxygen. Jet ventilation may also be accomplished with the use of an endotracheal tube exchanger passed through the vocal cords into the trachea. Some tube exchangers have a ventilating lumen and luer lock connector. The jet ventilator can be attached to the luer lock connector. Some neck and thoracic surgical cases are ventilated with this technique. A word of caution about the use of jet ventilation with a transcricothyroid ligament membrane catheter needs to be emphasized. If the catheter is not within the trachea, insufflation of oxygen in subcutaneous tissue, esophagus, blood vessels, and other solid structures may lead to damage to surrounding tissue and will not ventilate the patient. Furthermore, insufflation of gas into subcutaneous tissues can make further attempts establishing an airway even more difficult.
■ ROUTINE AIRWAY SETUP A routine airway checklist can be used prior to intubating a patient to ensure a safe intubation attempt. The checklist will cover the medications, equipment, and personnel that are important to have available during intubations. Setup for a routine intubation should include the following: • Functioning IV (checked that it runs well and is not infiltrated) • Anesthesia machine checked (if using) • Working suction with adequate tubing length and suction tip (e.g., Yankauer suction tip) • Bag-valve-mask as the primary or backup source of ventilation. Make sure the mask cuff is properly inflated. Mask cuffs can deflate over time. • Oxygen and a method to preoxygenate the patient (face mask, anesthesia mask, bagvalve-mask, etc.) • Appropriately sized oral airway or NPA • Appropriately sized endotracheal tube, cuff checked that it does not have a leak. If it is a cuffed endotracheal tube, a syringe to inflate the cuff should be ready (usually a 10-mL syringe). A backup endotracheal tube should be readily available. • Appropriate stylet for the endotracheal tube • Laryngoscope with appropriate blade. Light source and bulb have been checked. • Tape or other commercial device to secure the tube to the patient
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• CO2 monitor or colorometric CO2 detector to confirm tracheal intubation by the presence of CO2 • Stethoscope to evaluate breath sounds • Backup airway device available but not opened (e.g., laryngeal airway) • Intubation drugs: Succinylcholine immediately available for every intubation, other muscle relaxants as requested by the anesthesia provider, hypnotic (e.g., propofol or etomidate)
■ PLANNED DIFFICULT AIRWAY SETUP Once a patient has been identified as a difficult airway, patient positioning items, medications, adjunctive devices, videoscopes, flexible fiberoptic scopes, and alternative airway devices need to be available for the intubation attempt. The following should be available for a planned difficult airway: • Functioning IV (checked that it runs well and is not infiltrated) • Anesthesia machine checked (if using) • Working suction with adequate tubing length and suction tip (e.g., Yankauer suction tip) • Bag-valve-mask as the primary or backup source of ventilation. Make sure the mask cuff is properly inflated. Mask cuffs can deflate over time. • Oxygen and a method to preoxygenate the patient (face mask, anesthesia mask, bagvalve-mask) • Appropriately sized oral airway or NPA • Appropriately sized endotracheal tube, cuff checked that it does not have a leak. If it is a cuffed endotracheal tube, a syringe to inflate the cuff should be ready (usually a 10-mL syringe). A backup endotracheal tube should be readily available. The backup tube should be a smaller size and loaded with a stylet. • Appropriate stylet for the endotracheal tube • Laryngoscope with appropriate blade. Light has been checked. Difficult airways may require a variety of blades to be immediately available (different sizes or types from the primary blade). • Tape or other commercial device to secure the tube to the patient • CO2 monitor or colorometric CO2 detector to confirm tracheal intubation by the presence of CO2 • Stethoscope to evaluate breath sounds • Backup airway device available opened (e.g., laryngeal airway)
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■ FIGURE 35.53 Emergency airway cart with GlideScope.
• Intubating bougie/stylet available • Intubation drugs: Succinylcholine immediately available for every intubation, other muscle relaxants as requested by the anesthesia provider, hypnotic (e.g., propofol or etomidate) • Patient positioning devices (towels, blankets, specialized ramps) • Specialized laryngoscopes (videoscope and/or fiberoptic scope) • Airway adjuncts (lightwand, etc.) • Backup airway devices (laryngeal tubes, intubating laryngeal airway, emergency cricothyrotomy equipment) In most institutions, the majority of these items are assembled on a “difficult airway” cart that can be rapidly deployed to a location with a difficult airway (Fig. 35.53).
■ PLANNED FIBEROPTIC BRONCHOSCOPIC INTUBATION SETUP The planned fiberoptic bronchoscopic intubation may be done on either an awake or an asleep patient. If an awake intubation is planned, the difficult airway cart, if one is available, should be
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brought to the room. The most common method of awake intubation involves the use of the flexible fiberoptic bronchoscope. The following items should be set up to prepare for an awake intubation: • Functioning IV (checked that it runs well and is not infiltrated) • Anesthesia machine checked (if using) • Working suction with adequate tubing length and suction tip (e.g., Yankauer suction tip) • Bag-valve-mask as the primary or backup source of ventilation. Make sure the mask cuff is properly inflated. Mask cuffs can deflate over time. • Oxygen and a method to preoxygenate the patient (face mask, nasal cannula, anesthesia mask, bag-valve-mask). It is often desirable to be able to deliver oxygen to the patient while the awake intubation is being performed. The oxygen mask or nasal cannula should be fashioned to permit delivery of oxygen while the fiberoptic bronchoscope is being inserted into the patient’s mouth or nose. Some specialized masks are available to achieve this goal. They have a port to allow entry of the scope but still have the ability to maintain a tight mask fit around the patient’s mouth and nose. • Specialized equipment to assist in fiberoptic intubation ° Equipment to anesthetize the oropharynx: Topical anesthetic (2%-4% lidocaine solution, 2% lidocaine jelly) and a device to deliver the anesthetic (atomizer, nebulizer, cup for gargle and swallow, gauze and Magill forceps for possible glossopharyngeal nerve block, needle/syringe/catheter for possible transtracheal local administration, needle and syringe for possible laryngeal nerve block, etc). Tongue blade and gauze to open the mouth ° and possibly control the tongue ° Fiberoptic bronchoscope Light/power source has been checked. Video screen checked (if using) Test optics and focus of bronchoscope by using the scope to look at an object White balance the bronchoscope Specialized endotracheal tube (e.g., Parker endotracheal tube) to facilitate passage of endotracheal tube through the
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■
vocal cords. A regular endotracheal tube can be used as well. Scope has been lubricated to facilitate advancement of the endotracheal tube off the scope into the airway. Distal end of the scope has been treated with a defogger. Endotracheal tube is loaded onto the fiberoptic bronchoscope. The endotracheal tube should be secured to the handle of the bronchoscope to allow entry of the tip of the bronchoscope into the airway and prevent the endotracheal tube from slipping off the scope handle (Fig. 35.54). The cuff of the endotracheal tube checked and lubricated. Specialized oral airway to prevent the patient from biting on the bronchoscope as well as to guide the scope through the middle of the oropharynx (Ovassapian Airway, Williams Airway Intubator, Patil-Syracuse Oral Airway, Rapid Oral Tracheal Intubation Guidance System) (Fig. 35.55). These airway adjuncts allow for the forward displacement of the tongue along with a guide for the fiberoptic bronchoscope. These airways may be left in for a short duration of a surgical case or slipped out of the mouth over the endotracheal tube after the endotracheal tube adaptor is removed. Some clinicians will use a rigid laryngoscope blade (either Mac or Miller blade) to displace the tongue forward during fiberoptic intubation.
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■ ■
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■ FIGURE 35.54 Fiberoptic scope with endotracheal tube secured onto handle. (Courtesy of the Mayo Foundation.)
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•
■ FIGURE 35.55 Ovassapian airway. (Courtesy of the Mayo Foundation.)
10-mL syringe for possible injection of local anesthetic through the working or suction channel of the bronchoscope At the time of fiberoptic bronchoscopy, local anesthetic can be injected down the injection/suction port of the bronchoscope once the vocal cords or trachea have been visualized. About 1–2 mL of local anesthetic along with a few milliliters of air is placed into a 6- or 12-mL syringe. The air helps the local anesthetic to clear the injection port and to numb the area visualized by the operator of the bronchoscope. Some clinicians will pass an epidural catheter down the injection port and inject the local anesthetic through the epidural catheter, which is positioned just distal to the tip of the bronchoscope. Oxygen tubing and connector to allow possible oxygen administration through a port in the bronchoscope Suction and tubing that can be attached to the suction channel of the bronchoscope Stackable step stools to allow bronchoscopist to stand above patient Nasal fiberoptic intubation equipment ° Decongestant nasal spray (e.g., neosynephrine, 1% phenylephrine) to vasoconstrict the nasal passages and reduce bleeding Agents for anesthetizing the nasal passages (e.g., cocaine-soaked Q tips or ■
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viscous lidocaine applied with a nasal airway) Backup airway equipment ° Appropriately sized oral airway or NPA ° Appropriately sized endotracheal tube, cuff checked that it does not have a leak. The tube should be loaded with a stylet. Laryngoscope with appropriate blade. Light ° has been checked. Difficult airways may require a variety of blades to be immediately available (different sizes or types from the primary blade). Backup airway device available and opened ° (e.g., laryngeal airway, intubating laryngeal airway) Intubating bougie/stylet available ° Specialized laryngoscopes (videoscope and/ ° or fiberoptic scope) ° Airway adjuncts (lightwand, etc.) Tape or other commercial device to secure the tube to the patient CO2 monitor or colorometric CO2 detector to confirm tracheal intubation by the presence of CO2 Stethoscope to evaluate breath sounds Intubation drugs (succinylcholine immediately available for every intubation, other muscle relaxants as requested by the anesthesia provider) Sedatives (e.g., narcotic, propofol, etomidate, midazolam, dexmedetomidine) Drying agents to reduce oropharyngeal secretions (e.g., glycopyrolate) Infusion pump for delivery of medications
■ SUMMARY This chapter has outlined the airway equipment commonly used during the management of an airway including mask ventilation, laryngeal airways, and intubation of the trachea. The chapter covers equipment for routine, difficult, and emergent airways. It also includes checklists to aid the anesthesia technician in the setup, operation, and maintenance of airway equipment. It is intended to be a broad overview; however, due to the rapid introduction of new airway devices into the market, it cannot include all available airway devices.
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REVIEW QUESTIONS 1. Which of the following is NOT a feature of ALL common laryngeal airways? A) Inserted with a blind insertion technique B) Allows passage of an endotracheal tube through the ventilation channel C) Has a pharyngeal cuff or balloon to seal the pharynx D) Intended for semiconscious, unconscious, or anesthetized patients E) None of the above Answer: B. Some laryngeal airways have “ribs” or other design features that do not allow the passage of an endotracheal tube through the ventilation channel into the trachea. They all are inserted blindly (do not require a laryngoscope) and have a pharyngeal cuff or balloon to seal the pharynx. They are usually not well tolerated by awake patients unless the pharynx has been anesthetized.
2. SOME laryngeal airways have the following features: A) A channel for suctioning gastric contents B) A gel-based cuff that is not inflated with air for sealing the pharynx C) Allow positive pressure ventilation D) Are MRI compatible E) All of the above Answer: E. A few, but not all, laryngeal airways have a suction channel for gastric contents or a gel-based cuff. Many laryngeal airways are not MRI compatible. The pilot tube assembly may contain metal. Be sure to check the packaging on the airway before using it in the MRI suite. Almost all laryngeal airways allow some degree of positive pressure ventilation. Some are specifically designed with a pharyngeal seal to allow higher pressures during positive pressure ventilation.
3. Which of the following is NOT used as an emergency airway if initial attempts at intubation or ventilation fail? A) Laryngeal airway B) Esophageal combitube C) Laryngeal tube D) Venturi mask E) LM Answer: D. A venturi mask is a modification of a simple mask to deliver passive oxygen at specific oxygen concentrations. Use of the venturi mask requires a spontaneously ventilating patient. LMs and laryngeal tubes are two different kinds of laryngeal airways. Both are used to attempt to establish an airway if initial attempts at ventilation and intubation fail. An esophageal combitube is also used in emergencies. It can be placed blindly into the esophagus (95% of the time) or the trachea and can be used to attempt to establish an airway.
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4. Which of the following statements are TRUE about endotracheal tubes? A) All endotracheal tubes have a cuff that can be inflated to create a seal. B) All endotracheal tubes have a suction port above the cuff to prevent secretions from contaminating the airway. C) Parker endotracheal tubes have three lumens. D) RAE tubes are often used in oral and head/neck surgery. E) All of the above are TRUE. Answer: D. RAE tubes redirect the tube away from the surgical field and are often used in oral and head/neck surgery. Only a very few types of endotracheal tubes have special ports for aspirating secretions above the cuff. They are used in the ICU to reduce the risk of pneumonia. Parker tubes are similar to standard single-lumen endotracheal tubes except that they have a tapered tip to facilitate passage between the vocal cords.
5. Which of the following statements are FALSE with regard to double-lumen endotracheal tubes? A) Allow only one lung to be ventilated B) Can be used to ventilate both lungs C) Are positioned with a fiberoptic bronchoscope D) Allow each lung to be ventilated differently E) The distal tip is positioned in the trachea. Answer: E. The distal tip of a double-lumen tube is positioned in the right or left mainstem bronchus with the aid of a fiberoptic bronchoscope. Both lungs can be ventilated using a common anesthesia circuit, or each lung can be ventilated separately with a different kind of ventilator. The most common use of a double-lumen tube is to allow one lung to collapse during surgery (not be ventilated) to improve surgical visualization of intrathoracic structures.
6. Administration of inhaled medications through the anesthesia breathing circuit is best accomplished with a special adapter. A) True B) False Answer: A. True. Special adapters allow direct attachment of the inhaled medication delivery system to the breathing circuit near the endotracheal tube. In addition, they direct the flow of medication toward the endotracheal tube.
7. Which of the following statements are FALSE regarding RVLs? A) Often used for anticipated difficult intubations B) May be difficult to use with trauma or large amounts of oropharyngeal bleeding C) Have a flexible tip that can be manipulated D) Are used through the mouth, similar to other laryngoscopes E) None of the above
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Chapter 35 • Airway Equipment Setup, Operation, and Maintenance Answer: C. RVLs do not have a tip that can be manipulated. This is a feature of flexible fiberoptic scopes. RVLs are inserted into the mouth and provide a direct view of the larynx from the tip of the scope and can help the provider view the glottic structures. They are useful during difficult intubations. On occasion, blood can obscure the videoscope lens, making it difficult to see.
8. Which of the following airway adjuncts would NOT be useful during a difficult intubation? A) Heat and moisture exchanger B) RVL C) Flexible fiberoptic scope D) Intubating bougie E) Lighted stylet
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SUGGESTED READINGS Brown D, et al. Atlas of Regional Anesthesia. 2nd ed. Philadelphia, PA: Saunders; 1999. Cattano D, et al. The Cormak-Lehane Scale revisited. Br J Anaesth. 2010;105(5):698–699. Miller CG, et al. Management of the difficult intubation in closed malpractice claims. ASA Newslett. 2000;64(6):13–16, 19. Stone D, et al. Airway management. In: Miller RJ, ed. Anesthesia. 5th ed. Philadelphia, PA: Churchill Livingstone; 2000:1419.
Answer: A. An HME is a device that can be inserted into the breathing circuit to retain heat and moisture in the gas in the anesthesia circuit. This prevents some heat loss from the patient and prevents the respiratory mucosa from drying out. All of the other devices can be useful during a difficult intubation.
9. Which the following is part of an emergency cricothyrotomy kit? A) Scalpel B) Needle with syringe C) Wire D) Dilator E) All of the above Answer: E. A complete emergency cricothyrotomy kit includes a needle and syringe to puncture the cricothyroid membrane. The wire is inserted into the trachea. The scalpel is used to expand the hole in the tissues around the wire. The dilator tube assembly is passed over the wire and into the trachea. The wire and dilator are removed and the breathing circuit is attached to the tube.
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Infusion Pumps Victoria Reyes ■ INTRODUCTION Medication errors account for almost 20% of all medical injuries. Administration is the stage of the medication process most vulnerable to error, and the intravenous (IV) route of drug administration often results in the most serious patient injuries. IV infusion errors, which involve highrisk medications delivered directly into a patient’s bloodstream with an infusion pump, have been identified as having the greatest potential for patient harm. An understanding of the function, components, and use of medication pumps is essential for the anesthesia technician. Medication pumps are commonly used in the operating room (OR), obstetric suite (OB), and postanesthesia care unit (PACU). Infused medications include vasopressors, vasodilators, inotropes, antibiotics, chemotherapy medications, local anesthetics, sedatives, hypnotics, opioids, and muscle relaxants. Advances in the technology of medication pumps have introduced many new features. Today’s “smart pumps” have computer processors to provide decision support and fail-safe functions to improve patient safety. The anesthesia technician will be called upon to deliver pumps to the OR suite or off-site location and should be able to properly set up each device used in the facility. While the infusion pump is in use, the technician may need to troubleshoot alarms and nonfunctioning devices and be able to determine if the device needs replacement or service. Because the majority of anesthesia technicians will be involved in pump setup and troubleshooting, they should attend available opportunities for in-service training, particularly when new pumps are introduced into the department. The individual vendors are a great source of information and instruction on the use and maintenance
of the medication pumps used at your facility. In addition, anesthesia technicians will be involved in the maintenance of pump units stored in the department. The anesthesia technician must ensure that “smart pumps” are updated on a predetermined basis by the pharmacy and that they meet all standards set by governing entities. The technician should be sure that after pumps are used, they are returned to the workroom and cleaned according to the protocol at the facility.
■ MEDICATION PUMP SAFETY A major goal in the campaign to improve medication safety is to develop safer systems for the monitoring and delivery of drugs. IV medications administered through a pump must be delivered with precision due to the nature of the medications and the IV route of administration. IV administration results in a more rapid onset of drug effect; therefore, harmful side effects or the effects of drug toxicity may be more severe than when the same medication is administered orally. In addition, medication pumps deliver continuous infusions of medications. Thus, any error in dosing or formulation can be compounded over time. These issues effectively reduce the safety margin when medications are administered by IV infusion. The Joint Commission has noted that infusion pumps were frequently involved in medication errors that lead to serious patient injury. Experts reviewing these incidents have identified several human and mechanical errors. One of the most common problems was the use of pumps that do not provide protection from the free flow of IV fluid/medication into the patient. In addition, problems can occur when the wrong drug or concentration is administered, or the wrong rate is set. To address these issues, manufacturers of medication pumps have developed
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a number of innovations. For example, medication “smart pumps” were introduced in 2002 by Alaris Medical Systems, Inc. These computerized pumps for volume infusion and medication delivery utilize traditional infusion pump technology, while adding control over medication delivery based on predetermined clinical guidelines. Smart pump design improves medication safety by making it harder for the clinician to inadvertently enter the wrong information when programming the pump. This class of pumps utilizes drug libraries that include dosage parameters and alerts, requiring the clinician to intercede if the medication to be delivered is outside the dose recommended by the pharmacy and clinical advisory teams. Prior to smart pumps, most hospitals did not have drug dosing limits built into medication pumps, and drug information on high and low limits for IV medications was not available at the point of care. Other safety features of newer generation medication pumps include dosing alerts, continuously updated drug libraries, and treatment unit–specific programming. Requiring the provider to actively override alerts improves patient safety while allowing for flexibility in treating unique patient situations. For example, the pump may alert the provider that the programmed medication should be administered through a central venous line. The physician can override the alert based on clinical circumstances. Linking the smart pump to a computer network can allow drug library information to be automatically uploaded to the device as changes in practice, medication libraries, alert or dosing limits, or use of medications and practice guidelines occur. Medication pumps can be configured to fit the needs of the patients according to the unit in which they are receiving care, such as the OR, PACU, and the adult, pediatric, and neonatal ICUs. Alert limits and drug libraries can be tailored for each specific treatment unit. When a patient is transferred to a different treatment unit, care must be taken to exchange the pump for one that is appropriate to the new treatment unit, or, if possible, reset the pump for the new treatment unit. For example, when a patient is transferred to the OR from the floor, any medication pumps may need to be reset to OR settings to allow the anesthesia provider to access drug libraries and utilize alarm parameters that are appropriate to the OR and delivery of medications by
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anesthesia personnel. New technologies incorporate systems that will allow a single pump to follow the patients throughout their hospital stay by entering the hospital department into the “smart pump” via the data screen. The pump will change the drug library and parameters particular to that department’s protocols. An additional safety feature of modern medication pumps is the ability to continuously record similar to an airplane “black box.” The pump software allows the data to be retrieved for quality improvement purposes. This information can be used to review programming errors or identify treatment processes that could be improved and was unavailable prior to the introduction of smart pumps. One critical error that cannot be detected by the pump is the attachment of the wrong medication or concentration to the pump. For example, a provider wants to administer a normal saline and an epinephrine infusion. The pump is properly programmed to deliver a normal saline infusion at 100 mL/hr and epinephrine at 0.15 μg/kg/min; however, the bag of epinephrine is inadvertently attached to the tubing going to the pump for the normal saline and the normal saline is attached to the pump for the epinephrine. This situation would lead to a severe reaction in the patient due to an overdose of epinephrine.
■ TYPES OF MEDICATION PUMPS Manufacturers produce medication pumps that meet the needs of a broad range of settings including those that deliver medications in IV bags and/or syringes. This section will give examples of several different types of medication pumps and emphasize the features that are common to that class of pump; however, a comprehensive list of all currently available medication pumps is beyond the scope of this text.
Analog Pumps Analog pumps have a simple user interface controlled by dials (Fig. 36.1). For the majority of these pumps, the only allowable control is to adjust the flow rate. Some allow entry of patient weight and the dose of drug to be delivered per minute. Most bag infusion systems no longer use this technology; however, some analog syringe pumps are still in use (e.g., Baxter Bard Infus O.R. Syringe pump). These devices are mechanical
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■ FIGURE 36.2 Microcomputer-controlled pump with multiple channels.
■ FIGURE 36.1 Simple analog syringe pump.
doses, or rates outside of preset parameters in the library. The majority of modern infusion pumps for bags or syringes are microcomputercontrolled pumps. In addition to inpatient use, sophisticated microcomputer-controlled pumps are available for temporary home use or for implantation in the body (e.g., insulin pumps).
Patient-controlled Pumps and do not have the ability to make calculations regarding drug concentration.
Microcomputer Pumps Microcomputer-controlled pumps contain a limited microprocessor that controls pump function and can perform calculations. They can be syringe pumps or pumps designed for medication bags. Examples include the Baxter AS50 syringe pump and the Alaris PC point-of-care system (Fig. 36.2). The vast majority have a liquid crystal display (LCD) and keypad. The user interface usually allows entry of drug concentration, patient weight, dose of drug to be infused or rate, and total volume to be infused. The microprocessor can perform calculations, which gives the user some flexibility in entering data to achieve a desired infusion or dose. Most of these devices allow the user to program an optional loading dose (an initial rate or amount of drug delivery) followed by a continuous infusion (maintenance dose). In addition to the above features, these devices usually have an internal memory device for storing drug libraries and data. The user can select medications from the drug library and then confirm concentration and dosing information. The unit will alert the user to concentrations,
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Patient-controlled pumps use a syringe or medication bag for the source of medication and include a device to enable the patient to control the infusion or give boluses of medication (Fig. 36.3). These devices are generally used for postoperative and labor pain. Key features of these devices include the ability for the provider to set parameters that control basal infusion rates and the maximum amount and timing of bolus administrations triggered by the patient. They also include a “lock out” device to prevent tampering with the medication by unauthorized personnel.
Continuous Infusion Pumps The desire to send patients home with a temporary continuous infusion of medication led to the development of a variety of simple, lowcost pumps. Many of the early “home” pumps were simple devices with an elastic chamber that could be filled with a medication solution. These “elastomeric” pumps could then deliver a constant infusion that would last until the device was removed or the chamber was empty. Subsequent designs allowed adjustment of the basal flow rate and an on-demand bolus with a timed lockout (e.g., On-Q with Select-A-Flow) (Fig. 36.4). These pumps are frequently used to
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■ FIGURE 36.3 Patient-controlled pump.
deliver a continuous infusion of local anesthetics, with or without narcotics, for postoperative pain control. The infusion catheter can be placed directly in a wound or joint space, or in proximity to peripheral nerves that supply the painful region.
■ GENERAL OPERATING PRINCIPLES FOR INPATIENT MICROCOMPUTER PUMPS Before using a pump, the anesthesia technician will first verify that it has been charged. Since
■ FIGURE 36.4 Elastomeric pump.
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these pumps all have a battery backup system, they should be stored in an area where they can remain plugged in and ready for use. There should be a battery or charge light indicator on the front of the pump. If the pump has not been plugged in, turn on the device and determine battery life, before taking it into the OR. In addition to the pump, operation of the pump may require special syringes (20, 30, or 60 mL), infusion tubing (pump tubing or microbore tubing), or smaller IV bags to which medication can be added (50 or 100 mL normal saline or D5W). Some medications require special nonabsorbent infusion tubing (e.g., nitroglycerin). If multiple medications are to be administered, a stopcock or manifold assembly may be helpful. This equipment should be brought to the OR along with the pump. In the OR, the technician should ensure that the pump is attached to a designated IV pole, taking care that the IV pole is balanced and will not easily tip over. The pump should be plugged into a wall outlet or a hospital-grade multiport outlet extension. Take care to position power cords out of the way so that OR personnel do not trip on the cords. In addition, position the pump or IV pole on the side of the patient where the anesthesia provider will attach the infusion. Depending on the facility, the anesthesia technician may assist the anesthesia provider in setting up the pump. Consult with the provider to determine which drug(s) or fluids will be administered. The operator can enter the patient information required by the specific pump (e.g., patient’s name or initials, patient weight, medical record number). Most pumps will have a front panel with hard or soft keys to navigate through menus. In addition, a keypad can be used to enter numerical data (Fig. 36.5). For fluid administration, the operator will be required to enter an infusion rate and a volume to be infused. For drug administration, the operator can select the drug from the drug library. If a drug is commonly administered in different concentrations, most drug libraries include choices for selecting the concentration for the drug. Once a drug and a concentration are selected, the operator can select the infusion rate in milliliters per hour or the dosage (e.g., mcg/kg/min). The medication infusion tubing should be flushed (primed) and clamped off. The infusion tubing can then be inserted into the pump. In most pumps, the insertion of the
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■ FIGURE 36.5 Infusion pump front panel for data entry.
special manufacturer-specific infusion tubing is accomplished by either opening a door through which the tubing is threaded or by installation of a “cassette” (Fig. 36.6). Syringe pumps require attaching the syringe and the plunger into a cradle (Fig. 36.7). Some manufacturers require that tubing be flushed completely before starting the pump. Many will have an alarm if bubbles are detected as they pass through the pump. Other pumps have a priming function that will allow the operator to flush the tubing after it is inserted into the pump but before it is connected to the patient. Be sure to open the roller clamp or other device that is occluding the tubing before flushing or beginning an infusion. Many pumps will detect an occlusion (high pressure) in the line and sound an alarm (e.g., clamp closed, kink in the line, closed stopcock). Once the infusion tubing has been inserted into the pump and the line primed, the anesthesia technician must verify that all settings are correct. In addition, if
■ FIGURE 36.6 Infusion pump channel with the door open for insertion of infusion tubing.
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■ FIGURE 36.7 Syringe in pump cradle.
multiple pumps are in use, the technician should ensure that the correct medication is attached to the correct pump. The tubing can then be connected to the patient. Medication infusions should be attached to a port in the IV tubing as close to the patient is possible. This will allow changes in medication dose to reach the patient quickly. It is good practice to verify that the IV line into which the infusion tubing is attached is not infiltrated and runs well. Many medication infusions will require a “carrier” infusion to be flowing at a minimum rate, usually at least 75 mL/hr. This is because the medication infusion itself may only run at a few milliliters per hour. The carrier infusion will flush (carry) the medication through the IV tubing to the patient quickly. It is important to make sure that all medications that are infused through the same IV line are compatible with each other and the carrier fluid. If the pump has been correctly set up and verified by the provider, the technician will place the pump in standby mode. If the medication is needed immediately, the provider will press start to begin the infusion. Before starting the infusion, make sure all clamps or other devices are not obstructing flow to the patient. A common safety practice is to leave the infusion line
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clamped when not in use. This is because if the tubing is attached to the patient when the tubing is removed from the pump, it may be possible for an infusion to be “wide open” and administer a dangerous amount of medication into the patient. Most modern pumps occlude the infusion tubing with a special device when the tubing is removed from the pump to prevent this occurrence. The flow restriction must be opened manually to allow free flow of fluid through the infusion tubing.
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the wrong medication or the wrong dose is administered by IV infusion, anesthesia technicians should be thoroughly familiar with pump operation and troubleshooting. Anesthesia technicians should take advantage of opportunities to attend in-services offered by the vendors and facility educators to remain current with changes in pump technology and the operation of new devices.
■ TROUBLESHOOTING
REVIEW QUESTIONS
Most pumps have alarms for different conditions and will display an error message on the screen. Common problems that can cause alarms during use include the following:
1. Medications NOT commonly used in drug pumps include A) Vasopressors B) Heparin C) Sodium pentothal D) Muscle relaxants E) All of the above
• Air in the tubing (air detection alarm). Make sure the medication bag is not empty. Make sure the drip chamber is appropriately filled (fill to the appropriate level if necessary). Make sure no air or bubbles are in the line. If air or bubbles are found, a clamp should be applied to prevent flow into the patient, the infusion tubing removed from the pump, and the air or bubbles removed from the tubing by aspirating from a distal port. It may even be necessary to detach the infusion tubing from the patient and reflush the tubing. • High pressure in the line. Check for valves, clamps, or stopcocks that are closed, kinked tubing, infiltrated IV, or improperly installed infusion tubing in the pump. • Medication dosing outside of usual parameters—verify the settings with the anesthesia provider. Most pumps allow the provider to override the warning and continue the infusion. • Low battery. Make sure the pump is plugged in.
■ SUMMARY Medication infusion pumps are commonplace in hospitals and outpatient centers alike. The anesthesia technician plays an important role in the setup, operation, troubleshooting, and maintenance of these devices. Anesthesia technicians will also be responsible for making sure device maintenance meets regulatory requirements. Due to the complexity of these devices and the potential for severe complications when
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Answer: C. Sodium pentothal is not a common drug to be used in an infusion pump. All the others are common.
2. Medication pumps are configured generically to fit the average needs of the patient in any area of the hospital. A) True B) False Answer: A. Most pumps are configured with pharmacy-recommended dosages and concentrations based on generic populations.
3. If a pump sounds an alarm, the technician should check all of the following EXCEPT A) The data screen for message alerts. B) The medication is appropriate for this patient. C) Air in the tubing D) A clamp on the IV tubing has not been opened. E) The tubing is properly installed. Answer: B. The anesthesia technician may check any of the possible reasons for alarm other than if the medication is appropriate for the patient. The anesthesia provider is responsible for making sure that is the case.
4. Using the keypad, the following data may NOT be entered into the drug pump. A) Patient’s weight B) Volume to be infused C) Patient’s gender D) Desired dosage Answer: C. The patient’s gender is not needed in order to utilize any drug pumps.
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5. The leading cause of patient harm is medication errors. A) True B) False Answer: A. It has been reported that approximately 20% of medical errors are caused by medication errors, making it the single leading cause of harm to patients.
SUGGESTED READINGS Bates DW, Cullen DJ, Laird N, et al. Incidence of adverse drug events and potential adverse drug events: implications for prevention. JAMA. 1995;274:29–34. Eskew JA, Jacobi J, Buss W, et al. Using innovative technologies to set new safety standards for the infusion of intravenous medications. Hosp Pharm. 2002;37:1179–1189. General hospital devices and supplies/infusion pumps. Available at: www.fda.gov.
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Hatcher I, Sullivan M, Hutchinson J, et al. An intravenous medication safety system: preventing high-risk medication errors at the point of care. J Nurs Admin. 2004;34:437–439. Hicks RW, Cousins DD, Williams RL. Summary of Information Submitted to MEDMARX in the Year 2002. The Quest for Quality. Rockville, MD: USP Center for the Advancement of Patient Safety; 2003. Joint Commission. National patient safety goals. Available at: www.jointcommission.org. Leape LL, Brennan TA, Laird N, et al. The nature of adverse events in hospitalized patients: results of the Harvard Medical Practice Study II. N Engl J Med. 1991;324: 377–384. Williams C, Maddox RR. Implementation of an IV medication safety system. Am J Health Syst Pharm. 2005;62: 530–536. Wilson K, Sullivan M. Preventing medication errors with smart infusion technology. Am J Health Syst Pharm. 2004;61:177–183.
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Blood Gas Analyzers and Point-of-Care Testing David Wilson and Guy Buckman ■ INTRODUCTION Point-of-care testing (POCT) is defined as tests designed to be used at or near the site where the patient is located; they do not require permanent dedicated space, and they are performed outside the physical facilities of the clinical laboratories. POCT has grown in popularity as advancements in computer chip technology made POC devices more affordable, portable, and easy to use. Examples include circulating blood glucose monitors (glucometer), blood gas analyzers, activated clotting time (ACT) monitors, and heparin concentration monitors (Hepcon). There are a myriad of other POCTs that are used outside of the operating room but are not discussed in this chapter. Some examples of these POCT devices include those for testing hemoglobin A1c (Hb A1c), mircoalbumin, cardiac enzyme markers, cholesterol, infectious disease, etc. POCT can be found almost anywhere patients need quick and cost-effective testing such as a physician’s office, ICU, emergency rooms, hospital wards, and even in a patient’s home. However, this chapter gives a brief overview on POCT equipment that is commonly found in or around the operating room. The main emphasis of this chapter is on the organization of POCT from initial start-up to daily operations. The operating room is a unique environment in which a life-threatening situation needs to be identified and treated immediately. For example, hypoglycemia can lead to poor neurologic outcomes, cardiovascular collapse, and death if not identified and treated promptly. The clinician cannot wait for the long turnaround time required for tests sent to a central laboratory. Even STAT labs have a much longer turnaround time than POCT. A handheld glucometer allows
the clinician to quickly detect the patient’s circulating blood glucose and perform the appropriate intervention. The most efficient use of POCT occurs when an abnormality is quickly detected and an intervention is performed before any harm or escalation of patient care has occurred. POCT is composed of five essentials: equipment, personnel (not trained as certified laboratory personnel), procedure, quality control, and records and reports. It is governed by the College of American Pathologist (CAP) and Clinical Laboratory Improvement Amendments (CLIA). CLIA issues the certificate that allows the laboratory to function, and CAP is the regulatory body that governs daily operations. The POCT laboratory allows no disruption of patient care, samples never leave the immediate patient care area, and the results are immediate; however, clinicians must guard against interpreting POCT as the same accuracy as the main laboratory. When there is a question of the results, the best rule of thumb is to draw another sample and perform a test on the POCT machine and send a sample to the central laboratory for comparison.
■ BLOOD GAS MACHINE A blood gas machine is a portable system that analyzes whole blood for pH, partial pressure of CO2 and O2, bicarbonate levels (HCO3−), electrolytes, lactate, and hematocrit. There are a multitude of clinical scenarios in which an anesthesiologist may need to interpret the blood gas. A blood gas sample may be obtained from an artery or a vein depending on the clinical situation as the blood gas values will differ and will yield different information for the clinician. Arterial blood gases are more common and most often obtained from the radial artery as it is easily accessible. 363
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The blood sample is drawn into a heparinized syringe to prevent the blood from clotting. The blood sample is then taken to the blood gas analyzer where the sample is drawn into the machine for analysis. Blood gas analyzers today are fast and accurate. Most instruments are fully self-contained, consisting of the machine and disposable cartridges containing reagents, sensors, waste containers, and quality control (QC) pack. Usual systems are fully automated with self-calibration and self-quality control. Although today’s blood gas analyzers are accurate, there are many preanalytic errors that can occur, which can give erroneous results: 1. Make sure the correct patient’s blood is being sampled. Often, anesthesia technicians in a busy service area must multitask and perform multiple blood gas samples at one time. Reporting the results for the wrong patient could have serious consequences. 2. Excess anticoagulant. The heparin used to prevent the blood from clotting can cause erroneous low CO2, low bicarbonate levels, and low base excess. Excess heparin can also bind to cations, yielding a lower value. 3. Inadequate removal of flush solution during the blood draw can cause dilution of the sample, resulting in erroneously low values. 4. Air bubbles in the sample syringe normally cause an erroneous increase in PaO2 levels. 5. A delay of more than 10 minutes before running the sample can yield a PaO2 level difference of more than 10 mm Hg to the actual PaO2 level in plastic syringes. Malfunctions such as calibration errors, failed quality control, and bad sensors are usually identified during machine-initiated calibrations or quality controls. These problems are corrected by most current blood gas machines with a “lock-out” feature that will not allow further sampling. In some cases, the machine will allow a sample, but without the faulty “locked-out” analyte. High and low settings are set internally during the machine setup prior to initial use. The high/low settings are agreed upon with the main laboratory, and in the case of hematocrit and glucose, a reading outside those settings will require a sample to be drawn and double checked with the main laboratory. Note: High and low settings are set by the main laboratory and reflect the range of normal values.
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While the patient is in the operating room, it is not unusual for PCO2, PO2, hematocrit, and other values to be out of the “normal” range due to a variety of circumstances encountered during surgery.
■ ACTIVATED CLOTTING TIME The ACT detects clot formation. Patients who are having certain invasive procedures, such as cardiac bypass, require anticoagulation with heparin to prevent catastrophic thrombosis formation while on bypass. The heparin required to achieve a specific target level varies with individual patients and must be closely monitored. Clot formation is detected with an optical electromechanism located in an actuator block of the instrument. Single-use disposable cartridges contain the activator kaolin. The actuator mixes the kaolin with the blood sample and starts the timer. When blood is exposed to a foreign surface, the clotting process is triggered and fibrin forms. The optical system detects this change and displays the clotting time in seconds. As with many POCTs, there are some instances that can cause false values: 1. The ACT monitor is not warmed to 37°C. A monitor that is inadequately warmed will give an erroneously high ACT. 2. Inadequate removal of flush during the blood draw will give falsely elevated ACT. It should also be noted that there are two major manufacturers of ACT monitors. The ACT is not a standardized measurement, so an ACT of 300 seconds from one manufacturer does not correlate with an ACT of 300 seconds from another manufacturer.
■ HEPCON The heparin concentration (Hepcon) monitor is a device that measures the actual concentration of heparin in the patient’s blood. Hepcon is another POCT equipment that is used to gauge the adequacy of anticoagulation for certain procedures such as cardiopulmonary bypass. Hepcon is an integrated system consisting of a component for tracking clot detection and computing results, a component for sample delivery, and the single-use test cartridges for actual performance of the tests. The cartridge instructs the system, through an optical code, as to the type of test being performed, the calculations and the format
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required for results, and the volume of sample needed for each channel. The detection process uses the plunger assembly within the cartridge. This assembly is lifted and dropped through the sample/reagent mixture by a lifting mechanism actuator. As the sample clots, a fibrin web forms around the daisy located on the bottom of the plunger assembly and impedes the rate of descent of the assembly. This change in fall rate is detected by a photooptical system located in the actuator assembly of the instrument. The end point of the test is the time at which clot formation is detected; from these clotting times, derived results are calculated for all tests. The causes of faulty Hepcon readings are basically the same as those that occur with the ACT machine.
■ THROMBOELASTOGRAPHY Thromboelastography (TEG) is a device that allows the clinician to evaluate the patient’s ability to maintain hemostasis. In order for a patient to form a fibrin clot that is sufficient in strength to maintain hemostasis, the body depends on the interaction of enzymatic proteins (clotting factors) and platelets. Laboratory tests such as international normalized ratio (INR), partial thromboplastin time (PTT), ACT, and Hepcon measure the integrity of the clotting factors, whereas the TEG evaluates the entire coagulation process including platelet function. The TEG is generally used to monitor defects in the coagulation process and help guide the clinician to the appropriate treatment for those defects. Less commonly, the TEG can be used to monitor the adequacy of anticoagulation for patients undergoing procedures such as cardiac bypass. The TEG evaluates the ability to form clots by measuring the tensile strength of the fibrinplatelet complex. A sample of blood is placed into a cuvette with a metal pin in the center. The cuvette is slowly rotated at approximately 6 cycles/min. An activator is added to the sample and clot begins to adhere to the side of the cuvette and the metal pin. This creates resistance to rotation, which is then measured and plotted on a graph. The shape of the graph and time to when clot is formed gives the clinician information on the integrity of hemostasis and the presence of specific deficiencies. There are several preanalytical errors that can cause erroneous values for the TEG:
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1.
2.
3.
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Patient identification. As with all lab tests, care should be taken to make sure the sample and results are performed on the correct patient. Inadequate removal of flush solution during the blood draw can cause dilution of the sample, which will inhibit the sample from forming clots. Agitation, such as pneumatic tube transport of the sample, can cause the blood to prematurely start forming clots.
Appropriate blood samples for the TEG include whole blood, citrated blood, or heparinized blood. Each sample type is used in different clinical situations. Care should be taken to ensure the proper anticoagulant is used in the sample.
■ INTERNATIONAL NORMALIZED RATIO The INR is a test that measures the adequacy of anticoagulation for patients taking warfarin. Many patients presenting for surgery are taking warfarin for the treatment or prevention of thrombosis. Patients having invasive procedures or surgery normally stop taking warfarin 5–7 days prior to surgery. These patients need to have their INR checked the day of surgery as the effect of warfarin is highly variable from patient to patient. The INR is often sent to a central lab that may take hours to run the sample; POCT can give an accurate measurement of INR within minutes. This can decrease the time and complexity for patients who need to coordinate the timing of lab draws and the time of surgery. The INR is analyzed on a portable coagulometer much the same way that a patient’s circulating blood glucose is analyzed. A sample of blood is placed on a test strip after a finger stick is obtained. The test strip is then placed in the coagulometer at which time the sample is mixed with a thromboplastin reagent, causing a clot to form. There are several coagulometers available, and each has its own operating principles. However, all devices are accurate and can give results in under 3 minutes.
■ BLOOD GLUCOSE MACHINE (GLUCOMETER) Glucometer is a medical device for determining the approximate concentration of glucose in the blood. It is a key element of hospital and home blood glucose monitoring by people with
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diabetes mellitus or hypoglycemia. Glucometers are very accurate; however, a glucose reading from the main laboratory is always considered the gold standard. Clean the skin with an alcohol swab and allow the site to completely dry. Skin with alcohol may cause a faulty reading. A small drop of blood, obtained by pricking the skin with a lancet, is placed on a disposable test strip that is read by the meter and used to calculate the blood glucose level. The meter then displays the level in milligrams per deciliter or millimol per liter. With a hospital glucometer, daily quality controls are required prior to use and most meters have a lock-out system until the quality controls are complete. Quality control fluids are good for 90 days after opening unless the expiration date is before.
■ NEW EQUIPMENT Device Selection The key element to a successful program is a liaison between the main laboratory director, the POCT coordinator, and the anesthesia providers. POCT is a partnership between the main laboratory and anesthesia providers; however, inspectors hold the site performing the test and CLIA director responsible for noncompliance. This marriage of need is compelled from the moment the desire for a POCT site is recognized until the POCT site is decommissioned. Initial meetings between the main laboratory director, his or her POCT coordinator, and the anesthesia providers will establish a listing of acceptable analytic equipment. (1)(POC.06300) This analytic equipment must meet the standards of the laboratory and the needs of the anesthesia providers. Equipment standardization between the laboratory and POCT will minimize the number of different devices and be helpful when acceptance correlation verifications are required. With standardization, one policy can be shared among sites as well as a central data management system, operating procedures, clinical limitations, and reference intervals (normal values). Standardization will simplify training and competency for staff. When deciding on analytic devices, pay close attention to what extent they require operator interactions for calibration, quality control, temperature monitoring of the machine, quality controls that require monitoring of the expiration
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dates and materials that have opened dating, and special refrigeration or storage needs. Questions to ask when selecting a device are as follows: 1. 2. 3. 4.
5.
6.
7.
8.
9.
10.
11.
Can the product be trialed? What disposables are needed and their cost? What is the projected cost per test? Does the device self-prompt the operator and does the machine have automatic lockouts? These lockouts should include a lockout of anyone not qualified to operate the device and lockout a specific analytic if it fails quality control. Does the device perform automatic quality control or do personnel have to run daily shift quality controls? The automatic quality control mode with lockout would be the preferred since it eliminates human error and releases the staff to other work. What are the manufacturer’s requirements for calibration, quality control, and preventive maintenance? Will special power and/or computer hookup be required? An uninterrupted power supply system is highly recommended. Is there a secure data management system to capture quality controls and test results? Is there special software and licensing required? How much training will be provided to the operators? Who will perform this training? Will the manufacturer provide start-up assistance for the initial days? Contact the BioMedical repair department and ask BioMedical personnel to check medical device alerts for any product selected and establish any required training needed to maintain the device. Typically, BioMedical personnel check the device against the Emergency Care Research Institute (ECRI) database, which includes product repair information nationwide. Where will the quality control material be stored and what special handling will be required?
Once the device is selected, you should begin to write clear procedures and competencies and verify the procedure with the main laboratory POCT coordinator prior to going active, thereby reducing any problems that may arise. Define the quality control requirements and schedule,
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calibration cycle, and preventive maintenance schedule. The main laboratory may have a policy/procedure that can be tailored to the POCT area. At the very least, it will have a template for new lab policies and procedures that can be used as a starting point. The time spent in this initial phase will save the POCT director or his or her designee hours of time in the future. Once a good foundation is set, the program will run smoothly if you stay current with practices and perform internal audits. It may be helpful to establish a centralized POCT repository with all of the tools necessary to manage POCT.
Arrival of New Equipment Once newly purchased devices arrive, acceptance testing between the POCT device and the main laboratory device must be performed. Acceptance testing requires correlation verification between the POCT device and a main laboratory device. A minimum amount of acceptance testing is required and is set by the main laboratory or the manufacturer’s recommendations. In performing the test, a sample is drawn and run on the POCT device(s) and then the same sample is run on the corresponding main laboratory device. Results are documented between the POCT device(s) and the main laboratory device. Results must be within a set parameter established by the main laboratory or the manufacturer’s recommendations. These documented results are retained for the life of the device. Review the operating manuals to validate manufacturer’s requirements for calibration, quality control, and preventive maintenance. BioMedical repair personnel should be consulted for preventive maintenance (POC.06400). Identify the equipment using hospital-accepted identifying numbers for future preventive maintenance. Training for the operator prior to use must be accomplished and documented. A competency form for initial and ongoing training must be completed and retained for 3 years. The main laboratory POCT coordinator will initiate external proficiency testing (POC.03200). Review your policies/procedures prior to the activation date for the device.
■ PERSONNEL Operators need initial and ongoing training and certification. Identify only those operators who
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are required to perform the test to be authorized users (POC.06800). Large numbers of operators increase the amount of work to manage documentation and associated regulatory requirements. The job of training and proficiency testing will fall on the POCT director who is a physician or a doctoral scientist (POC.06600). The director or his or her designee will be responsible for developing initial training requirements, initial and ongoing competency, and the related documentation for both (POC.06700, .06850). This training must be accomplished prior to the initial use of any POCT device. Operators must document that they have read the policies and procedures for the facility, the main laboratory, and the new POCT. Each individual’s performance must be evaluated by an authorized user. This includes, but is not limited to, patient identification and preparation, specimen collection, handling, processing, and testing. Each individual must be monitored recording and reporting of test results. The POCT director ensures each operator conducts external proficiency testing and conducts ongoing monitoring of each operator performing tests, reporting results, and documenting results. This proficiency monitoring must be documented. A current list of POCT personnel that delineates the specific tests, levels, and methods that each individual is authorized to perform must be documented (authorized user list) and a copy sent to the main laboratory director (POC.06800). The competency of each person to perform the duties assigned must be assessed following training before the person performs patient testing (POC.06900). Semiannual competency during the first year of an individual’s duties is required. After an individual has performed duties for 1 year, competency must be assessed at least annually. Ongoing supervisory review is an acceptable method of assessing competency for certain elements. Competency assessment may be documented in a variety of ways, including a checklist completed by a supervisor.
■ QUALITY MANAGEMENT The quality management (QM) program for POCT must be clearly defined and documented. The program ensures quality throughout all phases of testing and should cover patient identification, specimen collection, identification
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and processing, as well as how to report results. The QM program must be capable of detecting problems and opportunities for system improvement. The POCT program must be able to develop plans of corrective/preventive action based on data from its QM system (POC.03500). Documentation should be maintained for all identified problems, corrective actions taken, and the outcome of those corrective actions. There must be a system in place that detects and corrects clerical errors and analytical errors in a timely manner (POC.03700). The usually accepted manner is to employ automatic quality controls with a lock-out feature that will not allow a specific analyte to be tested if an error is detected. Each device will also have internal high and low limits set for each analyte. The quality assurance test will indicate if an analyte is higher or lower than acceptable limits.
■ MANUFACTURER’S PROCEDURE MANUAL (USER MANUAL) A copy of the user manual should be located at the laboratory workbench for quick reference when there are questions or problems. A copy of the policies/procedures should be located with the user manual and reviewed annually by all authorized users. A copy of the annual review signature sheet should be retained with the user manual (POC.04100). When changes are made to the base policies/procedures, a review by the main laboratory director and the POCT director should document that the changes are acceptable (POC.04150).
■ SPECIMEN HANDLING A step-by-step procedure for specimen collections should be documented within the procedure and reference needle safety, how to identify the patient, how the test is requested, how the specimens are handled and identified, and how the results are reported (POC.04300).
■ RESULTS REPORTING Reference ranges specific for age, sex-specific normal values, and interpretive ranges (normal ranges) must be reported with patient test results; however, it is not necessary to include reference ranges when test results are reported as part of a treatment protocol that includes clinical actions (such as a surgical procedure), which are based on the test result. The test results must be recorded (POC.04500).
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After careful evaluation, the POCT site should set formal reference ranges and retain documentation of this evaluation. These reference ranges are set with the cooperation of the main laboratory (POC.04525). Critical limits must be established for appropriate tests, so immediate notification of a physician or other clinical personnel responsible for patient care occurs. These must be documented in the policies/procedures and within the procedures, a clear indication of how notification of a critical element is done and documented (POC.04550). The users must be familiar with critical limits for procedures that they perform (POC.04600). Personnel performing the test must be identified. This is usually accomplished with the assignment of a unique user code to access the test device (POC.04700).
■ QUALITY CONTROL Daily staff performing external controls must be run as follows (POC.07300): 1. For quantitative tests, two controls at two different concentrations must be run daily, except for coagulation tests (two controls required every 8 hours). 2. For qualitative tests, a positive and negative control must be run daily. Daily controls may be limited to electronic/procedural/built-in (e.g., internal, including built-in liquid) controls for tests meeting the following criteria: 1. For quantitative tests, the test system includes two levels of electronic/procedural/ built-in internal controls that are run daily. 2. For qualitative tests, the test system includes an electronic built-in internal control run daily. 3. The system is Food and Drug Administration (FDA)-cleared or approved and not modified by the laboratory. 4. The system is not classified as highly complex under CLIA. 5. The laboratory has performed and documented studies to validate the adequacy of limiting daily QC to the electronic builtin controls. Initial validation studies must include comparison of external and builtin controls for at least 25 samples. For validation of multiple identical devices, the 25-sample minimum applies to the initial
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device; the laboratory director is responsible for determining the sample size for the other devices. The laboratory director is responsible for determining criteria for acceptability and other details of the validation. 6. External controls are run for each new lot number or shipment of test materials and after major system maintenance and after software upgrades. Regarding the positive external control for qualitative tests, best practice is to run a weak positive control, to maximize detection of problems with the test system. 7. External controls are run at a frequency recommended by the test manufacturer or every 30 days, whichever is more frequent. Quality control data must be reviewed daily by testing personnel or supervisory technical staff to detect problems, trends, etc. The laboratory director or his or her designee must review QC data at least monthly (POC.07428). If the laboratory/POCT program uses more than one instrument to test for a given analyte, the instruments are checked against each other at least twice a year for correlation of results (POC.07568). This requirement applies to tests performed on the same or different instrument makes/models. This comparison must include all nonwaived instruments. The laboratory director must establish a protocol for this check. Quality control data may be used for this comparison for tests performed on the same instrument platform, with control materials of the same manufacturer and lot number. The use of fresh human samples (whole blood), rather than stabilized commercial controls, is preferred to avoid potential matrix effects. In cases when availability or preanalytical stability of patient/ client specimens is a limiting factor, alternative protocols based on QC or reference materials may be necessary but the materials used should be validated to have the same response as fresh human samples for the instruments/methods involved. Records of the correlations are required at least twice a year (POC.07568).
■ CALIBRATION A written procedure defining the use of appropriate calibration/calibration verification materials is needed. Criteria typically include the following:
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1. Changing of reagent lots unless the user can demonstrate that the use of different lots does not affect the accuracy of patient test results and the range used to report patient test data, or the control value. 2. When indicated by quality control data 3. After major maintenance or service 4. At least every 6 months 5. As recommended by the manufacturer
■ QUALITY IMPROVEMENT A successful quality improvement (QI) plan includes the monitoring of outcomes, events, problems, and utilization (benchmarks) with trends over time. Other aspects include the following: 1. QC documentation 2. Number of errors where wrong QC was analyzed 3. Percentage of QCs that fail 4. QC outliers with comment 5. Failed QCs with appropriate action (patients not tested) 6. Utilization (number of tests/site or device) 7. Tests billed versus tests purchased 8. Single lots of test and QCs in use at any time 9. Compliance 10. Untrained operators 11. Clerical errors or data entry errors 12. Medical record entry with reference ranges 13. Expired reagents and QC/reagents dated appropriately 14. Refrigerator temperature monitored 15. Proficiency testing successful Some or all of the QI information may be obtained from the computer systems (laboratory information system or LIS) when the POCT device is integrated into the hospital system.
■ REPORTS AND RECORDS Daily 1. Inspect the lab. 2. Review laboratory work. 3. Inspect blood gas machine and activated clotting machine. 4. Morning quality controls for each machine 5. Eight-hour quality controls 6. Refrigerator temperature checks for those that contain laboratory quality control products or test material.
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7. LIS (RALs) a. Data management b. Edit logs c. Flagged results d. Operators 8. Certification.
Weekly 1. Download glucometer results to laboratory information system or LIS.
Monthly 1. Activated clotting machine temperature checks 2. Activated clotting machine liquid quality control 3. Download stored laboratory test results into the LIS. 4. Records review 5. Review laboratory log sheets. 6. Laboratory results verification audit 7. Review competencies to ensure they are current. 8. Quality and performance report to main lab director. 9. Review refrigerator logs. 10. Operator reports 11. Cal reports 12. Levey-Jenning 13. QI reports
Quarterly 1. POCT director’s records review
Semiannual 1. 2. 3. 4.
Correlations Linearity studies Internal CAP audit of POCT Update authorized user list.
2. Initial validation records—5-year inspections 3. Response to inspection 4. Exception responses taken and follow-up RECORDS TO BE MAINTAINED
RETENTION (YEARS)
Policies and procedure
5
Current job descriptions of personnel and diplomas
5
Competencies
5
Personnel training and qualification
5
Signature, initials, and identification codes
10
Authorized user list
5
Equipment qualification/validation
5
Reviews and revisions of policies/procedures
5
■ SUMMARY POCT provides faster test results with the potential for improved patient outcome, but the quality of results is a concern. An organized POCT program is required to manage the quality of results supervised by laboratory staff (not dictated by the laboratory). This program should manage the validation of devices, training of operators, and day-to-day activities required for POCT to meet medical needs. POCT errors can occur in similar ways to laboratory errors. Training and QI programs should monitor the frequency of errors and act to improve detection and prevention of errors. Strategies to make POCT a part of routine patient activities have greater success at regulatory compliance and improved quality outcomes.
Annual 1. Competencies for operators, staff, and perfusionist for activated clotting, blood gas, and glucometer 2. Main laboratory audit of POCT 3. Records retention review 4. Policy/procedure review and signature
■ SAFETY Personnel Records 1. Competency records and what to include 2. Authorized user list
Records Retention 1. Equipment quality control, calibration, and preventive maintenance—include actions taken and follow-up
REVIEW QUESTIONS 1. All of the following can cause an erroneous value on a blood gas analyzer EXCEPT A) Excess anticoagulant in the sample tube B) Inadequate removal of flush solution during blood draw C) Excessive blood drawn into the sample tube D) Delay of more than 10 minutes before running blood gas sample E) None of the above Answer: C. Excess blood in the sample tube will not cause any problems. Flush solution can dilute the actual sample. A delay of more than 10 minutes can allow continued metabolism in the red blood cells and alter values.
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Chapter 37 • Blood Gas Analyzers and Point-of-Care Testing 2. Which of the following statement is TRUE regarding the ACT analyzer? A) The ACT measures the time to clot formation in seconds. B) The ACT analyzer should be cooled to 32°C prior to running the sample. C) Dilution of the blood sample has minimal effect on the results of the ACT. D) All ACT analyzers are standardized, so values from one manufacturer can be compared to values from another manufacturer. E) None of the above. Answer: A. The ACT is measured in seconds. The ACT analyzer should be warmed up prior to use. Failure to do so can produce faulty values. Similar to blood gas analysis, dilution of the sample can cause erroneous values. Two different ACT manufacturers have different methodologies to measure the ACT and the values cannot be compared.
3. Which of the following statements are TRUE in regard to the TEG? A) The TEG measures time to clot formation in seconds. B) The main advantage of the TEG compared to ACT is that heparin or citrated blood does not affect the results. C) The TEG does not evaluate the integrity of platelets on the clotting process. D) Excessive agitation of the blood sample can cause premature clot formation. E) All of the above. Answer: D. Agitation of the sample can cause premature clot formation and is a common source of errors with TEG measurements. The TEG results are plotted on a graph and not reported as a time. One of the advantages of the TEG is that it measures platelet function.
4. When there is a question about the validity of a test result, the best rule of thumb is A) Assume the values are true because today’s POCT machines are highly accurate and never give false values. B) Recalibrate the POCT machine in question.
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C) Draw two samples, reanalyze one on the POCT and send one to the central lab for comparison. D) Check to make sure the calibration reagents are not out of date. E) None of the above. Answer: C. If there is any doubt about the accuracy of a POCT device result, the best course of action is to perform another sample and compare the result to a result obtained from the central lab.
5. Which statement is TRUE regarding the INR? A) It is measured by a TEG. B) It evaluates the body’s ability to form clot as a whole dynamic process. C) It measures the adequacy of anticoagulation for patients taking warfarin. D) The blood sample must be drawn from an artery. E) None of the above. Answer: C. The INR is a measurement of a portion of the clotting cascade that is affected by warfarin. Thus, the INR is a common test for evaluating warfarin anticoagulation. The INR does not test the entire clotting process (e.g., another limb of the clotting cascade or platelet function). Blood samples for INR testing can be drawn from an artery or a vein.
SUGGESTED READINGS College of American Pathologist. Point-of-Care-Testing Checklist. Northfield, IL: College of American Pathologist; 2010. Hutchson AS, Ralston SH, DryBurgh FJ, et al. Too much heparin: possible source of error in blood gas analysis. British Med J. 1983;287:1131–1132. Mueller RG, Lang GE, Beam JM. Bubbles in samples for blood gas determinations—a potential source of error. Am J Clin Pathol. 1976;65(2):242–249. Picandet V, Jeanneret S, Lavoie JP. Effects of syringe type and storage temperature on results of blood gas analysis in arterial blood of horses. J Vet Intern Med. 2007;21(3): 476–481. Wallin O, Soderberg J, Grankvist K, et al. Preanalytical effects of pneumatic tube transport on routine haematology, coagulation parameters, platelet function and global coagulation. Clin Chem Lab Med. 2008;46(10):1443–1449.
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CHAPTER
38
Ultrasound Matthew Abrahams and Jorge Pineda ■ INTRODUCTION Anesthesiologists have recently started using ultrasound (US) for a variety of purposes. US can be used to evaluate a patient (diagnostic) or during procedures (interventional). US is a powerful tool that allows anesthesiologists to see structures beneath the skin, is noninvasive, and does not produce harmful radiation. Compared to other types of imaging, US is relatively portable and inexpensive. In addition, US images are generated nearly instantly, providing real-time information at the bedside. US equipment may appear complex at first, but by understanding a few basic principles and becoming familiar with your US machine’s basic controls, you can quickly become comfortable using it. Anesthesiologists may use US to determine the status of a patient’s medical condition. For example, US can be used to perform a detailed examination of the heart (echocardiography) either externally (transthoracic) or by placing a special transducer in the patient’s esophagus (transesophageal). US can also be used to evaluate the patient’s blood vessels for narrowing or blockage or to determine the patient’s volume status (do they have sufficient intravascular volume). It can be used to examine the patient’s internal organs or to look for fluid collections in the patient’s skin, muscle, or body cavities. US is also commonly used during procedures such as vascular access or nerve blocks. Specific uses of US are discussed in more detail in other chapters. This chapter focuses on the basic principles of US: the physics of US image formation, US machine controls, basic US terminology, storage of US images, tips for optimizing conditions during US exams and procedures, and proper use and maintenance of US equipment. In order to illustrate the concepts we discuss, we have included pictures showing various US machine
controls and sample US images. We made them using equipment available at our institution. This is not intended to be a comprehensive user’s manual for every US machine currently available. Different models of US machines have different types of controls, and the images may have a different “look.” It is important to become familiar with the machine(s) you will be using and apply the concepts in this chapter to understand how to use them.
■ BASIC US PHYSICS/MACHINE CONTROLS The basic underlying principle of US physics is that sound waves are emitted and received by the US transducer. A piezoelectric element (vibrates when an electrical current is applied) in the transducer emits sound waves that are reflected by the patient’s tissues. The reflected waves are received by the transducer, which measures the timing and strength of the reflected waves. The waves are emitted and received in a very thin beam, which is a flat plane about as thick as a piece of paper. The US machine then processes this information to produce the image on the US screen. The image produced is based on how fast the US waves move through various tissues and how much of the US energy the tissues reflect. US waves are above the range of normal human hearing (higher frequency) and so are not audible. The US transducer spends the majority of time receiving reflected US waves and is only emitting US energy about 0.1% (1/1000th) of the time. There are no known harmful effects to live tissue from exposure to US waves in frequencies used clinically.
Frequency of US Waves The behavior of US waves is governed by the simple equation: l = v/f. This describes the relationship between the frequency of US waves (f)
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and their wavelength (l). The velocity of US waves through tissue (v) is relatively constant at approximately 1600 m/s, though this varies slightly depending on the water content of the tissue. From this equation, you can see that the frequency and wavelength are inversely proportional, meaning that as the frequency increases, the wavelength becomes shorter. Conversely, as the frequency decreases, the wavelength gets longer. US waves’ ability to travel through tissue and the resolution (sharpness) of the US image also depend somewhat on the frequency and wavelength (Fig. 38.1). The resolution of the US image is approximately two wavelengths, so a shorter wavelength (higher frequency) will improve the resolution of the US image. The usual range of US waves emitted/received by US transducers commonly used by anesthesiologists is 2–15 megahertz (mHz) or 2– 15 million cycles per second. Unfortunately, higher-frequency US waves do not penetrate tissue well and are not capable of imaging deeper structures (Fig. 38.1). So it may be helpful to use a lower frequency to image these deeper structures, but the image will not be as sharp (lower resolution).
Gain The brightness of the US image can be adjusted using the gain controls on the US machine (Fig. 38.2). The gain is the amplitude of the US waves. Adjusting the overall gain control is similar to turning up the volume on a stereo. This makes the entire image brighter, but this may not improve the quality of the image, just as turning up the volume on a stereo may make the music louder but not improve the quality of the song. Fine gain controls such as time-gain compensation (TGC) or lateral gain compensation (LGC) can be used to brighten or darken specific areas of the image (Fig. 38.2). This is similar to adjusting equalizer settings on a stereo. To compensate for the effect of depth on signal strength, the TGC sliders are often arranged in a diagonal pattern to increase the brightness lower in the image (deeper). The most important point about TGC and LGC controls is that they should be checked to prevent overadjusting the image as this can produce significant artifacts and make US image interpretation more challenging. When in doubt, it is probably best to leave the sliders in a neutral position. Slight adjustments can then be made to “fine-tune” the US image as necessary.
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Depth The depth of the US image can be adjusted on nearly every US machine (Fig. 38.3). It is important to adjust the depth properly so that the structure(s) of interest is on the screen. Too much depth is not helpful as it makes the target structure(s) smaller in the US image, while deeper structures may not be relevant to the procedure being performed. In general, it is usually ideal to have the entire target structure(s) in the US image and adjust the depth so that the target(s) is roughly centered in the image. This allows the anesthesiologist to see other structures in the area that he or she may wish to avoid puncturing unintentionally, and to help visualize the needle if it is directed deeper than intended (Fig. 38.3).
Doppler/Color Another useful feature of most US machines commonly used by anesthesiologists is known as Doppler (or color) imaging. This uses a physical phenomenon known as the Doppler shift to measure movement. The Doppler shift describes the effect of an object’s direction and velocity on the sound emitted by the object as detected by the receiver. For example, as a train moves toward you, the sounds it makes have a higher pitch, while the sounds it makes have a lower pitch as it moves away from you. The faster the object is moving, the greater the change in pitch. The US transducer acts as the receiver. Objects moving toward the transducer reflect US waves at a higher pitch than emitted and those moving away at a lower pitch than emitted (Fig. 38.4). This phenomenon can be used to measure flow through blood vessels. The Doppler effect is displayed on the US screen as color, and the color scale can be used to show how fast blood (or any other substance) is moving toward or away from the US transducer. If the direction of flow is perpendicular to the transducer, flow is neither toward nor away from the transducer, and there may not be color on the US screen even though there is blood flowing through the vessels. Tilting the US transducer (discussed later) toward or away from the direction of flow may improve the color signal.
Focus The US waves emitted from the transducer are shaped like an hourglass (Fig. 38.5). The
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■ FIGURE 38.1 A: Schematic showing the relationship between frequency of US waves and tissue penetration. Red dots represent tissues/structures reflecting US waves (arrows). This shows that high-frequency waves are more likely to be reflected, preventing them from penetrating deeper. This is known as tissue attenuation. B: Controls for adjusting frequency on Sonosite (left) and Philips (middle, right) US machines. The Sonosite does not specify the actual frequency (in MHz) but uses a “Gen, Res, Pen” system. “Gen” is a midrange (general) frequency, “Pen” is a lower (penetrating) range, and “Res” is a high-frequency (resolution) range. The Philips machine also uses the “P,R,G” nomenclature on the US screen. C: US images of the same superficial area using high (left) and low (right) frequencies. The image on the left has better resolution.
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■ FIGURE 38.1 (Continued) D: US images of the same deep area using high (left) and low (right) frequencies. The image on the right shows the nerve better though the resolution is lower.
■ FIGURE 38.2 A: Pictures of gain controls for Sonosite (left) and Philips (middle, right) US machines. The Sonosite allows adjustment of overall gain and separate adjustment of gain in the near and far areas of the US image. The Philips unit allows for adjustment of overall gain as well as at different levels of the US image (time-gain compensation or TGC, top sliders, move side –to side) as well as on the edges of the US image (lateral-gain compensation or LGC, lower sliders, move up or down). The TGC and LGC sliders are arranged haphazardly in the middle, and more conventionally in the image on the right. B: Same US image with gain adjusted. On the left, the gain is too low, making the image dark and hard to interpret. On the right, the gain is too high, making the image too bright and again hard to interpret.
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■ FIGURE 38.2 (Continued) C: Same US image with TGC and LGC adjusted. The image on the left shows how improper use of the TGC controls can give the US image a “striped” appearance, making interpretation difficult. The image on the right shows how improper adjustment of the LGC controls can make one side of the US image too bright or too dark, again making interpretation difficult.
■ FIGURE 38.3 A: Depth controls for the Sonosite (left) and Philips (right) US machines. B: US images of the median nerve showing too little (left) and too much (right) depth. The nerve is not seen in the image on the left as the field of view is too shallow. The nerve appears very small in the image on the right as the field of view is too deep.
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■ FIGURE 38.4 A: Schematic showing the effect of movement of an object on the frequency of sound waves emitted or reflected by an object. The object (dot) is moving in the direction of the arrow (left) effectively compressing the sound waves moving in the same direction as the object (higher frequency) and dilating the sound waves moving in the opposite direction (lower frequency). This is known as the Doppler effect. B: Color imaging controls for the Sonosite (left) and Philips (right) US machines. C: Still image showing use of color imaging. The color denotes flow through blood vessels. In this image, the vein is blue and the artery is orange/red. This is due to the color scale seen in the upper right area of the US image. Veins may not always appear blue and arteries may not always appear orange/red depending on the color scale selected and the orientation of the US transducer relative to the vessels in the US image.
narrowest portion of the beam is known as the “focal zone.” In this area, there is the least interference among US waves and the US image is clearest. In general, the focus depth should be adjusted so that it is centered over the target structure(s). If multiple US beams are being used simultaneously (see below), the number of focal zones can be adjusted as well. If multiple beams
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are used, the focal zone can be made wider or narrower to include more or less of the US image.
Multibeam Many newer US transducers are capable of emitting multiple US beams simultaneously (Fig. 38.6). These may be oriented in slightly different directions or use frequencies that are
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■ FIGURE 38.5 A: The US beam has an “hourglass” shape that is focused where the beam is narrowest (the focal zone). The distance from the transducer at which the beam is focused (focal depth) as well as the number of beams that can be focused (number of focal zones) can be adjusted. If multiple focal zones are used, these can be tightly or widely spaced depending on the size of the area of interest. B: Focal zone controls for the Philips US machine. The focus depth controls are shown on the left, and the number of focal zones control is shown on the right.
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■ FIGURE 38.5 (Continued) C: Identical US images showing inappropriate (left) and appropriate focus depth (right). The nerve in the image on the right appears clearer. D: Identical US images using two (left) and four (right) focal zones. The number of focal zones is displayed on the right side of the US image (highlighted).
slightly different (harmonic imaging). This may reduce artifacts in the US image and may give the US image a “smoother” appearance. This also requires more processing of the image, and so the frame acquisition rate (number of times per second the US image is changed) may decrease. This can make movement within the image appear choppy. Multibeam imaging can usually be turned on or off easily, and there is usually a marker (varies depending on manufacturer) on the image to show if this feature is being used or not.
Compression Some US machines may allow for adjusting the compression or grayscale of the US image. A narrower grayscale (more compression) will
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make the image appear more homogeneous, while decreasing the compression (wider grayscale) will provide more contrast. Some types of US machines have different scales that can be selected from a menu, or filters that color the image differently (e.g., sepia or violet tone).
Presets Many US machines come equipped with “preset” combinations of the above settings to optimize the US image for specific types of procedures (Fig. 38.7). These have been created by the manufacturers to optimize imaging for specific types of exams or procedures without having to manually adjust all of the machine’s settings. Depending on patient-specific factors (such as size), the preset may or may not actually provide
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■ FIGURE 38.6 A: Schematic of multibeam imaging. The different colored areas below the US transducer represent distinct US beams, each oriented a slightly different direction. The US transducer receives reflections from each beam, and the machine combines the signals to reduce artifact and produce a “smoother” US image. Some anesthesiologists prefer not to use multibeam imaging, however. B: Multibeam controls for the Sonosite (left) and Philips (right) US machines. C: Identical US images with multibeam imaging turned on (left) and off (right). The appearance of the focus depth indicators (highlighted) is different if multibeam imaging is off or on.
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■ FIGURE 38.7 A: Presets button on the Philips US machine (highlighted). B: Screenshot showing presets menu on the Philips US machine. The appropriate preset can be selected for the procedure being performed.
optimal settings. Often the preset is a good way to start imaging, and fine adjustments (depth, frequency, gain, focus, etc.) can then be made to improve the image quality.
■ TYPES OF US TRANSDUCERS Different types of US transducers (probes) may be helpful for specific procedures (Fig. 38.8). Most US machines can be used with a variety of transducers. These may be all attached to the US machine at the same time or may need to be attached to the US machine separately. If multiple transducers are connected to the US machine, the transducer can be selected using a control on the machine. If only one transducer can be attached at a time, the transducer that is attached is obviously going to be the one being used. The interface between transducers and machines varies by manufacturer (Fig. 38.8). In general, manually changing transducers does not require any special tools and can be done in seconds. In general, US transducers can be divided into two main categories: linear array or curved array. Linear-array transducers emit and receive US waves directed perpendicular to the surface of the transducer (Fig. 38.8). This produces a squareor rectangular-shaped image on the US screen. Curved-array transducers emit and receive US waves directed radially from the surface of the transducer. This produces a wedge-shaped or semicircular image on the US screen. Lineararray transducers are most commonly used by anesthesiologists as they do not distort the image and allow straightforward needle guidance
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during procedures. Curved-array transducers may provide a wider field of view, which can be helpful in many circumstances. In addition, the curved-array transducer can be “rocked” from one side to the other to further widen the field of view. Due to distortion of the US image (especially near the edges), it may be more difficult to determine the correct angle for needle insertion/ advancement. Often the needle needs to be oriented more steeply than anticipated. Each transducer emits and receives US waves within a range of frequencies. Some transducers use low frequencies and are best suited for deeper exams and procedures. Others use higher frequencies and are best suited for more superficial procedures. The range of frequencies emitted/received by the transducer is usually written on the transducer and/or displayed on the US screen. Another feature of transducers relevant to their use by anesthesiologists is the size of the transducer. This is referred to as the transducer’s “footprint.” Wider transducers may provide a wider field of view but may be difficult to position in tight spaces such as between ribs. Most anesthesiologists will be able to do the majority of exams or procedures with a single transducer. As transducers are expensive (each one costs $3,000-$10,000), most practices will not use many transducers unless they use US very frequently. However, as more anesthesiologists use US and the applications for use of US continue to grow, more practices are likely to purchase and use a variety of transducers.
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■ FIGURE 38.8 A: Attachments for different transducers on the Sonosite (left) and Philips (right) US machines (both highlighted). B: Curved-array US transducers (left) and an US image obtained using a curved-array transducer (right). C: Lineararray US transducers (left) and an US image obtained using a linear-array US transducer (right). Both the curved- and linear-array transducers come in a variety of widths (see rulers in images). This is referred to as the “footprint.”
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■ US TERMINOLOGY Knowing the terminology used by anesthesiologists can help you communicate during US exams or procedures. Key terminology relates to the way structures are imaged, ways in which the US transducer can be moved during exams and procedures, and the orientation of needles relative to the US transducer during interventional procedures. Structures are usually imaged using a “shortaxis” or “long-axis” view (Fig. 38.9). The shortaxis view generally refers to a cross-sectional image. Advantages of the short-axis view are that it is often easier to recognize structures as well as the arrangement of adjacent structures in this view. In addition, the probe can be moved longitudinally along the patient’s surface to “follow”
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structures proximally or distally. This can help confirm the identity of a structure or plan a safe needle trajectory at a location where the target is close to a large blood vessel or other vital structure. The long-axis view involves rotating the transducer 90 degrees (see below) relative to its orientation during short-axis imaging to image a long section of a structure (Fig. 38.9). This may be especially useful for looking at blood vessels, as abnormalities (such as clots) may not be well seen using short-axis imaging. It may be difficult to keep structures in view, however, as slight tilting of the transducer (see below) may move the plane of the US beam so much that the structure of interest may no longer lie in the plane and so not appear on the US image.
■ FIGURE 38.9 A: Long-axis imaging of the median nerve in the forearm. The US transducer is oriented parallel to the nerve (left), producing an image of a section of the nerve that appears as a “stripe” on the US screen (right). B: Short-axis imaging of the median nerve in the forearm. The US transducer is oriented perpendicular to the nerve (left), producing a cross-sectional image of the nerve (right).
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The US transducer can be moved relative to the patient to optimize the US image. The basic moves that can be made are easily remembered using the “PART” mnemonic. The “P” refers to the amount of pressure used to make contact between the transducer and the patient (Fig. 38.10). Too little pressure can result in poor contact and lead to “shadowing” on the US image. This is an artifact cased by the inability of US
waves to travel through air. Too much pressure may be uncomfortable for the patient and can compress fluid-filled structures such as blood vessels (especially veins, which have thinner walls than arteries). The “A” refers to the alignment of the transducer relative to the target structure(s) (Fig. 38.10). The transducer can be moved from side to side and along the patient to fully evaluate the
■ FIGURE 38.10 The “PART” maneuvers. A: The amount of pressure applied to the US transducer can be adjusted. B: The alignment of the US transducer can be adjusted laterally or longitudinally.
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■ FIGURE 38.10 (Continued) C: The transducer can be rotated. D: The transducer can be tilted to either side.
anatomy of the area(s) of interest and to place the target(s) in an optimal position within the image on the screen of the US machine. The “R” refers to the rotation of the transducer relative to the target structure(s) (Fig. 38.10). Anatomic structures may be easiest to recognize in cross-section, so the transducer may need to be rotated relative to the patient’s surface in order to identify them. Once structures are identified, rotating the transducer 90 degrees will allow for evaluation of the structures using the long-axis view, which may provide additional
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information. Also, once the structure(s) of interest has been identified, the transducer can be rotated to produce an “oblique” image if this allows for a more advantageous needle trajectory during procedures. The “T” refers to tilting the transducer relative to the patient’s surface (Fig. 38.10). Again, as anatomic structures are often most easily recognized in cross-section, the transducer may need to be tilted if the structure is not parallel to the patient’s surface (moving deep to superficial or superficial to deep). Often structures can appear
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or vanish from the US image depending on the way in which the transducer is tilted. Another important area of terminology relates to the orientation of the needle relative to the US transducer during interventional procedures (Fig. 38.11). The “in-plane” technique involves inserting the needle in the center of the short side of the transducer and advancing the needle
so that its tip and the entire shaft (ideally) can be visualized within the plane of the US beam. The “out-of-plane” technique involves inserting the needle along the long edge of the US transducer so that it is oriented perpendicularly to the plane of the US beam. Each technique has advantages and disadvantages, and some anesthesiologists may prefer one technique over the
■ FIGURE 38.11 A: In-plane needle technique. The needle is inserted along the lateral edge of the transducer and directed parallel to the long axis of the transducer in order to place the needle’s shaft in the plane of the US beam (left). A US image showing the shaft of the needle approaching a nerve (right). The needle appears as a white stripe coming from the upper right portion of the screen toward the nerve in the center of the image. B: Out-of-plane needle technique. The needle is inserted along the long edge of the US transducer and directed perpendicular to the long axis of the transducer (left). This may not show the needle well as only a cross-section of the needle will be in the plane of the US beam. An US image of the out-of-plane technique (right) shows only a shadow where the needle’s shaft crosses the US beam, just to the right of the nerve in the center of the US image.
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other for specific procedures. In general, the inplane technique is most commonly used during nerve block procedures, and the out-of-plane technique is most commonly used during vascular access procedures. It is also important to be familiar with terminology used to describe the appearance of tissues or structures in the US image. The echogenicity of a tissue or structure refers to how strongly it reflects US waves. Hyperechoic structures reflect a large percentage of US waves that contact them, and as such they appear bright on the US screen. Conversely, structures that do not strongly reflect US waves appear dark on the US image and are described as hypoechoic. Different tissues or structures can be recognized as different parts may be hyper- or hypoechoic. For example, bones have a hyperechoic surface on the US screen but are hypoechoic below the surface as US waves bounce off the surface and do not penetrate deeper. In fact, US waves are not able to image past the surface of bone, producing a dark area below. This is known as acoustic shadowing, as it resembles a shadow formed as an object blocks light. Another important property of tissues and structures relevant to US is the ability of structures to be compressed or not. Fluid-filled structures usually are compressible, while solid structures usually are not. This can be helpful to distinguish nerves from blood vessels or muscles from fluid collections. Structures can be simply described as “compressible” or “not compressible.”
■ STORAGE OF US IMAGES Most machines have the capability of printing an image of interest. This is important for documentation and billing. It is easy for a provider to become engrossed in the procedure at hand to forget to ask for a print. It may be helpful to give a friendly reminder to the provider to print an image when appropriate. For central line placement, this image is typically an image of the guide wire or actual line in the vessel. For peripheral nerve blocks, this image is typically a picture of the needle near the nerve or with local anesthetic surrounding that nerve. Most modern machines are equipped with video capability. This is helpful for teaching and learning from the procedure. Not all machines are created equally, however. Some record
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antegrade (record images a preset limited amount of time after the record button is pushed), while others record retrograde (records a preset limited amount of time backward from the time the record button was pushed). The anesthesia technicians should be familiar with how the US machines in their facility record images and how long the preset recording times are. Be ready to push the record button frequently depending on the preset recording times.
■ TIPS FOR OPTIMIZING CONDITIONS FOR US EXAMS AND PROCEDURES Optimizing the US Image The first step is to select or attach the appropriate transducer. If a preset is available for the type of exam or procedure being performed, select it from the preset menu. The depth of the image should be then adjusted so that the entire target structure is seen in the US image. The frequency can be adjusted depending on the depth of the target structure. The frequency can be increased for more superficial structures and decreased for deeper structures. The focal zone(s) should be positioned over the target, and the gain and compression can then be adjusted to help distinguish structures from one another. A quick look with color imaging can help identify vessels that may not be easily seen. The anesthesiologist can then use the PART maneuvers to optimize image quality.
Ergonomics Proper placement of the machine in the room is essential. Ask the practitioner where they prefer to place it. Typically, this will be in a position near the patient and in the line of sight of the practitioner placing the line or block (Fig. 38.12). This avoids excessive turning of the head of the practitioner, which not only is uncomfortable and impractical but also draws attention away from the patient. Always position yourself near the US machine during the procedure should the need arise to make any adjustments or make use of other features on the machine.
■ PROPER USE AND MAINTENANCE OF US EQUIPMENT Preparation for Use To prepare the US machine, turn the power on (do this early as on some machines it takes a few minutes for the software to boot up), enter the
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acceptable. Affix a patient label on the form to ensure the image is charted and billed appropriately. The machine and transducers used should be wiped down between patients as explained in the following section. Time between patients is a good opportunity to restock supplies specific to the procedure. Specifically, in regard to the US machine, make sure the US gel (sterile and unsterile), sterile sheaths, or other means of probe cover are available for the next procedure. In order to improve efficiency, if the next patient name is known, this is a good time to enter demographic data, choose a preset, position the machine, and set up for the next procedure.
Maintenance ■ FIGURE 38.12 A block being performed using an advantageous ergonomic arrangement of operator, patient, and US machine. The picture is taken over the anesthesiologist’s shoulder to show how he is able to see the US image without turning his head. If necessary, he can check the position of his hands, the needle, or US transducer relative to each other or the patient with a quick glance down while still maintaining a view of the US image.
appropriate patient data for billing and study retrieval purposes, and ensure the appropriate US probes are available, functional, and clean. Make sure that adequate US gel (both sterile and unsterile) and sterile probe covers are available. Ask the provider what kind of procedure the US machine will be used for and on what location, including the side, if appropriate, of the patient it will be performed. If possible, position the machine on the correct side and select the proper probe and presets. Set the TGC sliders to the neutral position. Depending upon the type of procedure, assemble any other necessary equipment (e.g., block kits, vascular access kits, gloves, and gowns).
Following Use Once the exam or procedure is complete, ensure the images will be stored under the correct patient name. Prior to use, locate the save study button on the machine. This is typically easy to find and one push of the button will store all images and videos recorded for the patient. Make sure any pictures taken and saved have been printed, if necessary. Secure the printed picture to the appropriate institution-specific form. If one is not available, a progress note form is
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It is important to maintain the US machine in optimal condition and prevent potential damage as much as possible. The probes should be properly stored and protected when not in use. They are expensive and can be easily damaged. This is essential to providing safe, efficient patient care. Become familiar with any potential maintenance agreements your department has with the manufacturers of the machine. They often will provide a loaner machine for use while your department’s machine is either repaired or maintained. Some manufacturers recommend preventative machine maintenance and cleaning by a service representative on a quarterly basis. Contact information is frequently placed somewhere on the machine by the sales representative. Inspect the US machine daily. It may be easiest to do this at the beginning of the day. Ensure all connections such as probes and printers are plugged in properly. Evaluate the integrity of connection cables, wires, and transducers. Check the printer and make sure an adequate amount of printer paper remains. The machine and transducers should be wiped down, preferably with a nonalcohol-based solution. Alcoholbased solutions are effective but may decrease the life span of the transducers. Make sure to wear gloves when cleaning the US machine and transducers with hospital-grade cleaning wipes or cleaning solution. These wipes and solutions contain chemicals that can be caustic and irritating to the skin if direct contact occurs. Before each procedure, make sure to have some form of sterile covering available for the transducer, whether in the form of a sterile sheath or large clear adhesive. A brief inspection and thorough
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cleaning should occur between each patient and at the end of the day. Transesophageal echocardiogram probes should be sterilized between patients as per your institution’s protocol. Any problems encountered with the machine should be documented, and any significant issues should be reported to the sales representative as soon as possible. They can be helpful in organizing smooth and timely service to your machine and quick return for use. Some facilities choose not to obtain a maintenance agreement with the manufacturer of the machine, and instead choose an internal engineering department to handle all maintenance issues. US technology continues to evolve and many of today’s machines contain software that can be upgraded periodically. It is helpful to contact the sales representative to determine how often these upgrades should occur. Staying vigilant is the key to preventing or catching a problem with your machine early. Knowing the proper channels of communication will ensure timely service of your machine in order to avoid affecting appropriate patient care because a machine or probe is unavailable.
■ SUMMARY US is a powerful tool that can be used by anesthesiologists during a wide variety of procedures. US equipment may appear complicated, but a basic understanding of the physics of US image formation, machine controls, and terminology will allow you to properly use the equipment and assist during US exams and procedures. Proper use and maintenance of equipment will help provide safe and effective patient care.
REVIEW QUESTIONS 1. To adjust the brightness of the US image, which of the following controls on the US machine should be adjusted? A) Frequency B) Focus depth C) Depth D) Gain E) Focal zones Answer: D. Adjusting gain affects the brightness of the image. Gain may be adjusted overall or in specific areas of the image (near/far, TGC, or LGC). The other choices can all be adjusted on most
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US machines and are useful to optimize image quality, but they do not directly affect the brightness of the US image.
2. When using US to visualize deeper structures, which of the following adjustments are most likely to improve image quality? A) Decreasing depth, increasing frequency, decreasing focus depth B) Increasing depth, decreasing frequency, increasing focus depth C) Increasing gain, increasing frequency, decreasing focus depth D) Decreasing gain, increasing frequency, increasing focus depth E) Decreasing gain, decreasing frequency, decreasing focus depth Answer: B. To image deeper structures, there must be sufficient depth to the image to include the structure(s) of interest. Lower frequency US waves travel better through tissues and though they have by definition lower resolution than do higher frequency US waves, they can reach deeper structures better as they are less subject to tissue attenuation. Increasing the focus depth so that the US beams are focused at the depth of the structure(s) of interest will improve the quality of the image at that depth. Increasing or decreasing gain settings may or may not improve the ability to see deeper structures, depending on the specific sonographic properties of the particular structure.
3. Which of the following measures can help improve patient safety for US-guided procedures? A) Use of probe covers or other barriers, as well as cleaning the transducer between procedures to prevent cross-contamination B) Regular inspection and calibration of US equipment by the manufacturer or institutional biomedical engineering department to ensure proper function C) Presence of a practitioner experienced in USguided procedures to ensure adequate image acquisition and interpretation D) Archiving of images for possible future review as part of a teaching file of Continuing Quality Improvement mechanism E) All of the above Answer: E. All of these options are important safety measures associated with the use of US. Prevention of cross-contamination between patients will help reduce the risk of infectious complications. Ensuring proper function of US equipment will help to reduce the risk of error due to malfunctioning equipment and prevent risks of electrical shocks or other injuries. Knowledge of US imaging and US guidance techniques is essential for the safe use of US during patient care. Storage of images for periodic review can be helpful to determine potential causes of ineffective procedures or complications.
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4. With regard to probe manipulation during USguided procedures, the mnemonic “PART” stands for A) Polarity, activity, response, timing B) Power, arc, resonance, tension C) Pressure, alignment, rotation, tilting D) Positioning, access, reference, tone E) Point, aim, reflection, target Answer: C. The “PART” mnemonic stands for pressure, alignment, rotation, and tilting. The other choices are random words starting with the same letters.
5. US image formation at its most fundamental level involves a visual representation of the A) Direct measurement of the natural resonant frequencies of varying tissue compositions averaged over time B) Indirect measurement of electromagnetic waves emitted by movement of ions across cellular membranes C) Generation of sound waves by a piezoelectric element, the reflections of which are measured by the element and processed by a computer D) Direct measurement of microscopic oscillations of molecules, filtered through a white noise generator E) Generation of low-intensity ionizing radiation that penetrates tissues of varying density in a characteristic pattern
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Answer: C. The US image is a graphical representation of US waves that have been emitted from and received by the US transducer. The waves are generated by a piezoelectric element that vibrates when exposed to an electrical current. Waves are emitted for only a small percentage of the time, and the transducer is in the “receive” mode the majority of the time. The other choices are nonsense except for “E,” which describes the physics underlying roentgenograms (also known as x-rays).
SUGGESTED READINGS Guillory RK, Gunter OL. Ultrasound in the surgical intensive care unit. Curr Opin Crit Care. 2008;14(4):415–422. Neal JM, Brull R, Chan VW, et al. The ASRA evidence-based medicine assessment of ultrasound-guided regional anesthesia and pain medicine: executive summary. Reg Anesth Pain Med. 2010;35(2, suppl):S1–S9. Sites BD, Brull R, Chan VW, et al. Artifacts and pitfall errors associated with ultrasound-guided regional anesthesia, Part I: understanding the basic principles of ultrasound physics and machine operations. Reg Anesth Pain Med. 2007;32(5):412–418. Sites BD, Brull R, Chan VW, et al. Artifacts and pitfall errors associated with ultrasound-guided regional anesthesia, Part II: a pictorial approach to understanding and avoidance. Reg Anesth Pain Med. 2007;32(5):419–433.
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Transesophageal Echo Edward A. Kahl and Lisa Chan ■ INTRODUCTION There are several different vendors and models of transesophageal echocardiography (TEE) technology. This chapter provides a generalized overview of the basics of TEE, equipment setup, and handling. Equipment and protocols for handling TEE hardware and storing images vary from institution to institution, and it is recommended that the anesthesia technicians be familiar with these policies and practices at their institution.
■ BASIC PRINCIPLES OF ULTRASOUND AND TEE Energy is all around us in different forms. Heat from a fire and light from the sun are the most familiar examples; however, sound too is a form of energy. This form of energy is used frequently in nature by creatures like whales and dolphins. They emit sound waves underwater to detect objects in their surroundings. Submarines and ships have adopted a similar idea by emitting “pings” and gauging the distance to another object by the amount of time it takes for the “ping” to return. Closer objects will send the “ping” back sooner, whereas farther objects will cause the “ping” to return much later. This is because it takes the sound waves more time to travel to the farther object and then return back to the submarine. Somewhat similar to the submarine or the ship, the transesophageal probe (TEE) houses a crystal near the tip that generates several thousand “pings” per second and displays an image based on the time it takes for their return. The TEE probe is placed into the esophagus, and the crystal near the tip emits lots of tiny “pings” that travel through the wall of the esophagus and to the heart. When the “pings” bounce off the parts of the heart and return to the probe, the probe converts the “pings” to the image on the screen.
■ TYPES OF TEE: TWO-DIMENSIONAL AND THREE-DIMENSIONAL Two-dimensional (2D) TEE has been the imaging modality used most commonly for TEE procedures. More recently, three-dimensional (3D) TEE has made its way into mainstream cardiac operating rooms. 3D TEE is typically used in conjunction with 2D TEE to attempt to answer questions about structures of the heart that are not obvious with 2D images alone. TEE in general is helpful in evaluation of heart valves, heart function, cardiac masses, and even in evaluation of placing cannulae in the heart. If your institution has a limited number of 3D-capable TEE machines and probes, the 3D TEE machines should be reserved for valve surgeries or more complex procedures. However, one should always check with the anesthesia provider to inquire about whether 3D imaging will be necessary for a particular case. In cases that do not involve a valve, such as coronary artery bypass grafting (CABG), a 3D probe may not be necessary. For emergency cases that require TEE, the first TEE probe and machine available should be used, unless instructed otherwise. To obtain a 3D image, a 3D probe and an ultrasound machine that contains 3D software are required. If a 3D probe is placed in a patient and the ultrasound machine is not capable of 3D imaging, the probe may be disconnected from the machine (but kept in the patient) and reconnected to a machine that has 3D capability. However, if a 2D capable probe is inserted into a patient that requires 3D imaging, the probe will have to be replaced with a 3D probe connected to a 3D-capable machine for 3D imaging.
■ TEE PARTS The ultrasound machine is a computer processing unit. Some of the important components 391
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include a screen or monitor, keyboard, knobboard, pin ports for insertion of probe transducers (whether for TEE or other types of ultrasound probes), and outlets for transfer of information for digital storage. It is housed on wheels with a braking and locking system located at the bottom front of the machine. These machines can cost up to $250,000. The TEE transducer is a long, flexible probe that collects the picture information to be processed and viewed on the ultrasound machine. At one end of the probe is the housing unit that fits into the insertion port of the ultrasound machine. The locking mechanism on this housing unit should be set to “open” and once it fits snugly into the insertion port, the locking mechanism is turned 90 degrees to lock the connector into place. Different brands of TEE machines may have different mechanisms to engage the TEE probe onto the TEE machine. Further down the probe is the handle of the TEE. The handle consists of two rotating knobs and two rubber buttons. The rotating knobs control the movement of the tip of the probe anteriorly, posteriorly, left, and right. The larger knob moves the tip up (anterior) and down (posterior), whereas the smaller knob moves the tip left and right (Fig. 39.1). These knobs are also sometimes useful for distinguishing between 2D and 3D probes. For example, some vendors assign 2D probes black knobs and 3D probes gray knobs (Fig. 39.2). There is a locking lever located right next to the movement-control knobs that secures the probe tip in its current orientation. The lever should be released or “unlocked” and checked for resistance prior to placement of the probe in a patient. The probe should never be manipulated inside the patient with the tip in the locked position (Fig 39.3). In a fixed or locked position, the probe tip can damage the oropharynx, esophagus, or stomach. If the control knobs become incompetent, the probe loses its ability to be maneuvered and should not be placed in a patient. The two rubber buttons on the side of the probe control the plane of the sound beam emitted from the tip of the probe. The black cord between the handle and the tip contains electrical wires, which may become exposed after teeth repeatedly rub against the cord covering. Damage to the electrical cords may also occur if a patient bites
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■ FIGURE 39.1 TEE probe.
down with enough force. Therefore, in patients with teeth, it is prudent to place a bite guard to protect the cord from the patient. The tip of the probe houses the key elements that send out and receive the ultrasound waves. If the tip is broken, the probe requires repair. TEE probes themselves can cost up to $50,000.
■ FIGURE 39.2 3D TEE probe: Different-colored knob controls distinguish 3D from 2D probes. For this vendor, 3D probes have gray knobs and 2D probes have black knobs.
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Relative contraindications include: recent surgery in the throat, fragile veins in the esophagus (esophageal varices seen in liver disease), problems swallowing or pain on swallowing, neck arthritis, outpouchings in the esophagus or stomach, history of radiation to the chest or neck, or problems with bleeding.
■ COMPLICATIONS FROM TEE
■ FIGURE 39.3 Lever that locks the knob controls and hence locks the TEE probe tip in a fixed position. NOTE: TEE probe should NEVER be placed, removed, or manipulated inside the patient with the lever in the locked position.
■ INDICATIONS AND CONTRAINDICATIONS TEE is most commonly used in cardiac surgeries, liver and lung transplants, and major vascular surgeries. Specific guidelines for use can be found at the American Society of Anesthesia/Society of Cardiovascular Anesthesia/American Society of Echocardiography Web sites. Caution should be exercised in placement of the probe in conditions where the patient has had any neck, mouth, esophageal, stomach, or bleeding problems. Major complications include creating trauma or bleeding anywhere in the body where the probe comes into contact with. The question that must be always asked is: does the benefit of this procedure outweigh the risks? Some situations such as life-threatening emergencies may warrant the risk. Other options may be considered if a TEE cannot be placed safely, but information about the heart is needed. In these situations, transthoracic echocardiography (TTE) can be performed before surgery and/or an epiaortic exam (ultrasound of the heart and aorta in the surgical field) can be done once the chest is open. These technologies require different probes but can use the same ultrasound machine to process the signals and display an image. Absolute contraindications include: patient refusal, esophageal problems (esophageal stricture, tracheoesophageal fistula, postesophageal surgery, esophageal trauma, hole, rings/webs, tumor), unstable cervical spine, and previous esophagectomy or esophagogastrectomy.
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Fortunately, serious complications from TEE are rare. The following are the reported complications from TEE use: esophageal perforation, esophageal bleeding, problems swallowing (dysphagia), pain on swallowing (odynophagia), thermal burn injury to the esophagus or stomach from the probe tip heating up, lip trauma, dental damage, and rarely vocal cord damage from inadvertent endotracheal intubation.
■ TEE SETUP The TEE should be positioned in the room at or near where it will be located during the surgical procedure, especially if the machine is large and bulky. The initial step includes plugging the machine into a protected and grounded power outlet. The area around the TEE should be checked to ensure it is free of cords that would interfere with freely moving the TEE machine during the case. The next step is to ensure all network and/or media devices have been plugged in properly. Once this is accomplished, the TEE machine can be powered on. The startup time of the TEE from pressing the power button to entering patient data or being able to acquire images may take several minutes. Therefore, the technician should anticipate this delay in the emergent situation where TEE may be needed to make a fast therapeutic decision (i.e., used to diagnose the cause of hemodynamic instability). If TEE is needed in this situation, ensure that it is plugged in and powered on early, so there is no delay in waiting for it to power up. The next step after powering on the machine and ensuring its place in the operating room is to enter patient-identifying data. This information is required to associate the TEE images to the correct patient and to ensure they can be easily accessed in the future. The data elements collected vary from institution to institution. Therefore, it is up to the anesthesia technicians to be familiar with this process at their institution.
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If a TEE server/network is available at your institution, the proper network setup should be established. This includes ensuring that the network cable is connected to the TEE machine (usually in the back of the machine) as well as to the appropriate network jack in the operating room. The appropriate TEE jack in the operating room should be properly labeled to avoid confusion with other network jacks. Additionally, if a TEE network is not available at your institution, the proper media device should be available for saving the images if so required by your institution. These include DVDs, USB drives, and rarely VHS tapes or other media. Finally, connect the TEE probe to the machine as described above and ensure that the probe is recognized by the TEE machine. This step varies for different manufacturers. Once the probe is properly connected to the TEE machine, the integrity of the probe knobs should be checked for functionality. This means the locking lever should be in the unlocked position. Then, the large wheel and small wheels should be moved in both directions while inspecting the tip to ensure it moves appropriately. If the probe tip does not move properly, it should be sent for repair and should not be placed in a patient. Additionally, the locking lever should be in the unlocked position during placement to minimize trauma to the patient. Finally, the checked and ready TEE probe should be placed in a location where it is safe from damage. Probe covers are available to protect the crystal near the probe tip from inadvertent damage.
■ PREINSERTION CHECKLIST • Check that the TEE machine is the proper machine for the provider’s needs (i.e., does the provider require 3D capability?). • Check to ensure the proper TEE probe is available (i.e., 3D probe or 2D probe, epiaortic probe). • Be sure ultrasound gel is present near the TEE machine. • Have bite blocks or other probe protectors present. • Have an orogastric tube with lubricating jelly present (usually placed by anesthesia provider prior to TEE insertion to empty stomach contents). • Connect the power cord to the appropriate outlet and power up the machine.
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• Enter the required patient identification information as per your institution’s guidelines. • Ensure proper network setup and all necessary cables are connected; or check that proper media devices are available (DVDs, CDs, USB drives depending on institution). • Attach the ECG source (either ECG leads to be placed on the patient or connection to the anesthesia monitor ECG).
■ HELPING THE ANESTHESIOLOGIST PLACE THE PROBE AND ACQUIRE IMAGES The patient should be adequately anesthetized for this procedure. The jaw should be slack and easy to manipulate. The anesthesia technician should hold up the probe handle while the anesthesia provider inserts the TEE probe into the esophagus. Holding the handle up will prevent the tip from inadvertently being manipulated left, right, up, or down. This will also minimize the risk of the probe falling or twisting. Usually, the anesthesia provider will pull forward on the jaw to open up the back of the mouth during probe insertion. Other maneuvers that help placement are flexing the head so that there is a more gentle turn for the probe to make through the oropharynx. If these maneuvers fail, final attempts usually involve using a laryngoscope to find the esophageal opening. However, if there continues to be strong resistance to probe insertion, the procedure should stop. The probe should never be advanced forcefully. Additionally, the anesthesia technician can help the anesthesia provider acquire images by pressing the acquire image button on the TEE machine or adjusting the imaging depth. Also, the technician may help by turning on, off, or resizing the color flow windows or making caliper measurements of structures. The anesthesia providers should teach the anesthesia technicians how to perform these maneuvers as they differ from machine to machine. Some anesthesia providers may prefer to control these functions themselves.
■ END OF THE CASE Probe Removal Extreme care should be taken during TEE probe removal to protect both the patient and the TEE probe. During removal, the TEE probe is at risk of being damaged from the patient’s teeth and
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extra care should be taken during this process especially if a tooth guard has not been used. Even if it is common practice at your institution for anesthesia technicians to remove TEE probes from patients, still consult with the anesthesia provider before doing so. The locking lever should be checked to ensure it is in the unlocked position; and both knobs should be in the neutral position. The TEE probe should be removed slowly. Any amount of resistance should prompt the anesthesia technician to notify the anesthesia provider. After removal, the TEE probe should be examined for any signs of trauma to the probe and the patient. This includes looking for the presence of blood on the TEE probe. The “dirty” probe should be taken directly to central processing where it can be cleaned, unless there is a system in place that allows identification of dirty probes from clean ones. Leaving a dirty TEE probe lying around puts it at risk of being damaged or being inadvertently placed in another patient. Prior to removing the TEE probe or shortly afterward, the TEE exam should be ended. The images should be sent to the echo server/network if one exists, or the images should be saved onto a media device with a patient label placed on the media. It is important to save all images prior to powering down the ultrasound machine; otherwise, the images could be lost.
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contaminants. As such, it too should be cleaned in between patient use. Care should be taken to avoid using dirty gloves to handle the TEE probe or machine controls.
Probe Storage and Identification Once cleaned, the TEE probe should be stored in a clean place that is easily accessible and protects the probe from damage. A system should be in place to discern clean, postprocessed probes from dirty probes. This identification process is of utmost importance to avoid using a dirty probe in another patient.
■ SAFETY Safe handling of TEE equipment can save your institution tens of thousands of dollars or more. General rules, if followed, can ensure that the TEE probes and machines last at least their expected life span. These include the following: 1. Always keep the TEE machine and probe clear and safe from other equipment in the operating room (Fig. 39.4). 2. Never leave the TEE probe hanging loosely from IV poles or elsewhere without a tip protector because the probe tip (and the crystal inside it) can be damaged from contact with other objects.
Probe Processing TEE probe cleaning varies from institution to institution and from manufacturer to manufacturer. However, there are some general principles that should be followed: 1. Do NOT use bleach on any TEE transducer. 2. Do NOT use strong solvents such as acetone, freon, or other industrial cleaners on transducers. 3. Do NOT soak transducers for extended periods of time such as overnight. 4. Do NOT immerse or rinse the connector or cable portions near the connector. 5. Do NOT immerse or rinse the steering mechanisms. 6. Do NOT allow alcohol cleaning solutions or isopropyl alcohol to air-dry on the transducer. Additionally, the TEE machine itself may occasionally get soiled with blood or other
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■ FIGURE 39.4 TEE probe storage: The probe should be stored in a secure manner to avoid damage to the probe.
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3. Never leave the TEE probe lying on a tabletop where it could potentially be damaged by falling on the floor. 4. Always check the TEE probe controls and knobs prior to placing the probe into the patient. 5. Use caution when removing the TEE probe from patients with teeth, to avoid both dental injury to patients or damage to the TEE probe. 6. Never forcefully remove the TEE probe from a patient. It should come out with very little resistance. 7. Never insert, remove, or manipulate a TEE probe while in a patient if the lever that controls the knobs and the tip is in the locked position.
■ TEE IN EMERGENCIES TEE is sometimes needed emergently to diagnose hemodynamic instability either in the operating room or in the ICU. In these situations, keep in mind that the TEE machine may take several minutes to power up, so it should be promptly plugged in and powered on. Additionally, use caution to ensure the proper patient name is attached to the emergent study.
■ SUMMARY TEE is an established technology to evaluate the heart. The probe is inserted into the esophagus. Reflected sound waves are processed by the ultrasound machine and displayed on the monitor. The anesthesia technician should be familiar with the setup of the ultrasound machine, how to attach the probe to the machine, and how to operate the movement controls. TEE probes can be easily damaged. Anesthesia technicians should be familiar with how to properly handle, process, and store the probes. This chapter provides an overview of these topics.
REVIEW QUESTIONS 1. Which of the following should be available for a cardiac valve replacement procedure? A) Ultrasound gel B) Bite block C) Network connection or available media (DVD, USB drive)
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D) 2D or 3D TEE probe E) All of the above Answer: E. For a valvular procedure, a 3D machine and 3D probe are recommended if available but 2D is also acceptable. The rest of the options are part of the preinsertion checklist.
2. In which of these situations is it okay to continue placement of the probe? A) Strong resistance to probe insertion despite maneuvers B) On checking the knobs, the tip of the probe does not move. C) The probe insertion pins do not match up with the TEE machine insertion ports. D) The patient has consented for TEE and all necessary TEE equipment is available. E) The patient has a cervical spine injury. Answer: D. In Option A, when the probe is difficult to insert despite helpful maneuvers, do not force probe insertion. Option B is an example of a broken probe and should not be inserted into the patient. In Option C, the probe type and machine likely do not match one another or require an adapter. Option E is incorrect because TEE is contraindicated in cervical spine injury. Option D is true and correct as stated.
3. Why is it important to take extra care to ensure TEE equipment is clean and protected? A) There is a crystal in the TIP of the TEE probe that is expensive and can be easily damaged. B) Replacing broken TEE equipment can be very expensive. C) Ensuring probes are cleaned will avoid the complication of using a dirty probe on a patient. D) TEE is vulnerable to damage from surrounding operating room equipment. E) All of the above. Answer: E. All of the above are true.
4. Which of the following statements is FALSE? A) Purchase and maintenance of TEE machines and probes can cost hundreds of thousands of dollars. B) It is okay to insert a TEE probe into the patient with the tip in the locked position. C) Ultrasound gel should be available for TEE probe placement. D) An anesthesia technician can help the anesthesiologist with TEE probe placement by holding the handle of the TEE probe up while the anesthesiologist places the TEE probe into the patient. E) The TEE machine should be plugged into a grounded and protected outlet.
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Chapter 39 • Transesophageal Echo Answer: B. One should NEVER manipulate a TEE probe in the patient while the tip is in the locked position. All other lettered options are correct.
5. Which of the following statements is FALSE? A) TEE can be used to look at the heart’s valves and function. B) TEE is sometimes used in major vascular surgery. C) It is safe to leave the TEE probe hanging freely from an IV pole. D) 3D TEE is sometimes used to answer questions about the heart that 2D TEE is unable to. E) TEE is contraindicated in patients with recent stomach surgery. Answer: C. One should not leave the TEE hanging from an IV pole without a protective tip cover, as the tip can be damaged by surrounding operating room equipment. All other choices are true.
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SUGGESTED READINGS Practice Guidelines for Perioperative Transesophageal Echocardiography. An Updated Report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Copyright 2010, the American Society of Anesthesiologists, Inc. Philadelphia, PA: Lippincott Williams & Wilkins. Savage R. Organization of an intraoperative echocardiographic service. In: Savage R, ed. Comprehensive Textbook of Perioperative Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:3–41, 106–132. Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA guidelines for performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: recommendations of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography. J Am Soc Echocardiogr. 1999;12(10):884–900.
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Neuromuscular Blockade Assessment Ryan Goldsmith ■ INTRODUCTION Chapter 16 discussed the anatomy and physiology of the neuromuscular junction. In addition, Chapter 16 covered the clinical utility of neuromuscular blockade to induce patient paralysis, the medications used for this purpose, and the importance of monitoring the degree of neuromuscular blockade. This chapter focuses on how to use peripheral nerve stimulators to monitor neuromuscular blockade.
■ PERIPHERAL NERVE STIMULATORS There are multiple peripheral nerve stimulators on the market today; however, they share many common features. Peripheral nerve stimulators work by delivering a small electric current through the skin to a peripheral nerve. This electric current stimulates a muscle innervated by that nerve to contract. Various controls on the stimulator allow delivery of different types of electrical stimuli to the muscles in order to assess the degree of blockade between the neuron and the muscle. The different types of stimuli include single twitch, tetanus, and automatic train of four. Each type will be discussed below. Other controls on the nerve stimulator include power on/off and a control to adjust the intensity of the electrical current. These functions are easily selected on the face of most nerve stimulators by touching the membrane buttons or operating dials. The control to adjust the current usually allows the operator to adjust the output current from between 0 milliamps (mA) and 7.0 mA. The amount of current (in mA) that is delivered to the patient is often displayed on a digital LCD screen (less sophisticated nerve stimulators only indicate the mA on a dial and do not have a display). In addition, many nerve stimulators have an LED
light that flashes whenever a stimulus is sent. Others sound an audible beep each time a stimulus current is delivered (some systems do both). The loudness of the beep is often adjustable. All stimulators have a pair of lead wires that need to be attached to the stimulator and to the patient. The polarity of the electrodes is found on the stimulator box. The black polarity slot represents the negative lead, while red represents the positive lead. The lead wires can be attached and detached from the stimulator unit at the polarity connectors (Fig. 40.1). The lead wires attach to the electrodes using alligator clips or standard snap-on connectors. Some stimulators have an attachment that allows direct application of metal ball electrodes to the patient and do not require lead wires or electrode pads. Peripheral nerve stimulators can be purchased through most medical supply companies. To illustrate nerve stimulator functionality, we describe two popular nerve stimulators here: the MicroStim III and MicroStim Plus (Fig. 40.2). MicroStim III and MicroStim Plus have similar functionality. MicroStim Plus is smaller than MicroStim III and is easy to carry in a pocket. In addition, MicroStim Plus has metal probes that can be applied directly to the skin without the use of electrodes. The metallic probes attach to the nerve stimulator box at the polarity slots. The current is delivered through the probes. The current output is adjustable in 0.1-mA increments from 0 to 6.0 mA. The standby switch maintains power to the nerve stimulator without delivering a current. The twitch function delivers a pulse at 1 Hz (1 pulse per second) or 2 Hz (2 pulses per second). The tetanus function delivers 50 Hz (50 pulses per second) or 100 Hz (100 pulses per second). The twitch function
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delivers one pulse at a time, whereas the tetanus function delivers a sustained or constant stimulus. The train of four function key delivers four pulses every 2 seconds and then repeats every 10 seconds.
Electrodes are applied to the skin of the patient over a target nerve (nerve targets will be discussed below). The electrodes have an adhesive to attach to the skin. The center of the electrode that touches the patient has a conductive jelly to improve the conduction of the stimuli to the patient. The conducting gel area is small, approximately 7–11 mm in diameter. The other side of the electrode has a metallic nipple to allow the attachment of the lead wires (ECG electrodes can be used). The skin should be cleansed properly by rubbing it with an abrasive or alcohol swab and then dried before applying the electrodes. The nerve stimulator lead wires are then attached to the metallic nipples on the electrodes using the alligator clip (or snap-on connectors) on the lead wire (Figs. 40.3 and 40.4). The resistance to current at the skin ranges from 0 to 2.5 KΩ; however, with the body at cooler temperatures, the resistance can get as high as 5 KΩ. This can lead to misinterpretation of the response to a stimulus. Because of the resistance increase a stimulus may not elicit twitches that may be present at warmer skin temperatures. Some nerve stimulators have a display that shows the current delivered and alerts the user when the current selected is not being delivered due to an increase in resistance.
■ FIGURE 40.2 MicroStim Plus nerve stimulator.
■ FIGURE 40.3 Lead wires attached to electrodes over the facial nerve.
■ FIGURE 40.1 MicroStim III nerve stimulator.
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Black
Red
PULSE
DBS
TWITCH
TETANUS TOF
Path of ulnar nerve On-Off and intensity dial switch
■ FIGURE 40.4 Nerve stimulator box attached to the patient with lead wires over the ulnar nerve.
Once a nerve target is chosen, the negative (black) lead should be placed as close to the location of the nerve as possible. The positive (red) lead should be placed 3–6 cm proximal to the negative lead. The polarity is important. Nerve stimulators work better if the negative lead is placed over the nerve. Once the electrodes and leads have been attached, the unit can be turned on. Be sure the batteries are operational and the unit has power (the LED screen turns on or the power light turns on). The desired current output should be selected. A stimulus can then be applied by choosing a stimulus mode, and muscle twitches in response to stimuli can be observed.
■ SPECIFIC TARGET NERVES Several different nerves can be used to elicit a stimulated response from a muscle to evaluate neuromuscular function. The facial nerve, due to its accessibility during surgery, is one of the more common sites to stimulate and evaluate for muscle blockade. The temporal branch of the facial nerve can be found where the nerve emerges from the skull, approximately at the lower level of the ear. The nerve travels under the skin on the side of the face between the eye and ear. It supplies the muscles of the eyes, muscles around the ear, and the muscles on the side of the forehead. The negative electrode should be placed over the
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temporal branch of the facial nerve as close as possible to where it emerges on the face. A good landmark is the zygomatic arch (a bone just in front of the ear). The positive electrode can be placed on the forehead (Fig. 40.3). The location of the negative electrode is important. The intent is to stimulate the temporal branch of the facial nerve, which will then send the signal to the muscles around the eye, causing them to contract. If the neuromuscular junction is blocked, muscle contraction will be impaired. However, muscles can be stimulated directly by an electrical current (bypassing the motor nerve and any blockade at the neuromuscular junction), if the negative lead is placed close enough to the muscle. If placed too close to the muscle, a stimulus could be delivered and the muscle would contract, even though there was still neuromuscular blockade. This could lead a clinician to believe that a patient had recovered from a neuromuscular blocker, when in fact he or she had not. Another popular nerve to stimulate is the ulnar nerve (Fig. 40.4). With the arm placed in anatomical position, the ulnar nerve can be found as it runs along the medial and anterior side of the arm. The ulnar nerve supplies several muscles including muscles that flex the medial wrist, flex the 4th and 5th fingers, and adduct the thumb (pulls the thumb toward the 5th finger). For stimulation of this nerve, the electrodes are applied to the volar side (medial and anterior side) of the wrist over the ulnar nerve. The distal lead (negative/black) should be placed about 1 cm proximal to the point at which the wrist flexes (up the arm). Stimulation in this region may cause the wrist to flex due to direct stimulation of muscles in the forearm, particularly if the leads are placed too far proximally (up the forearm). Stimulation of the ulnar nerve at the wrist will cause the thumb to pull toward the little finger (adduction). The adductor muscles, which are responsible for this movement, are in the hand at the base of the thumb, far from leads placed on the wrist. Thus, assessment of the strength of thumb adduction is a good test of the neuromuscular junction between the ulnar nerve and the adductor muscles of the thumb.
■ NEUROMUSCULAR MONITORING After the administration of a nondepolarizing drug (e.g., rocuronium, cisatracurium), the muscle may experience different levels of paralysis
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including intense blockade, deep blockade, moderate blockade, and recovery. The nerve stimulator helps the anesthesiologist determine the level of neuromuscular blockade. If a sufficient initial dose of nondepolarizing neuromuscular blocker is administered, the muscle becomes flaccid or completely paralyzed. At this stage of intense blockade, the muscles will not respond (twitch) to a stimuli sent by a nerve stimulator. As the neuromuscular blockade begins to wear off, the muscle will begin to respond to a stimulus, but the twitch will be less than full strength. Additional stimuli administered immediately after the first twitch will either elicit progressively weaker twitches or fail to produce a muscle response at all (deep blockade). For example, most nerve stimulators produce four successive twitches, 0.5 seconds apart (2 Hz). During initial recovery, the four stimuli may only produce one or two weak twitches. After additional time has passed and the muscle has made further recovery (moderate blockade), all four stimuli may produce a twitch; however, each successive twitch will be progressively weaker. This is referred to as fade. The fade response is commonly used to assess the degree of neuromuscular blockade. Evaluation is accomplished by delivering four successive stimuli 0.5 seconds apart (referred to as the train of four [TOF]) to the target nerve and measuring the strength of any elicited muscle twitch. The strength of the muscle contraction can be measured by a special monitor, by feel, or by observation. An unblocked neuromuscular junction will produce muscle contractions with the greatest amplitude (strength of contraction), and subsequent contractions in the TOF stimulus will be just as strong (no fade). A common calculated measure is to divide the amplitude (strength) of the fourth muscle contraction in the TOF by the amplitude of the first muscle contraction (TOF ratio). One criterion for adequate recovery from neuromuscular blockade is that the TOF ratio is at least 0.7. For continuous monitoring of neuromuscular blockade, a TOF stimulus can be delivered automatically by the nerve stimulator every 10 seconds. Alternatively, the anesthesia provider may choose to monitor the TOF intermittently. Another useful nerve stimulator function is to deliver a tetanic stimulus, a 100-Hz or 50-Hz pulse to the nerve that will cause a normal muscle to spasm without relaxing (tetanus). Response
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to the tetanic stimulus, like the TOF function, is used to evaluate the level of neuromuscular blockade. Under an intense blockade, the muscle does not respond to either TOF or tetanus stimulus. Following intense blockade, the drug is metabolized over time and the ability for the muscle to respond to a nerve stimulus begins to recover. At this stage, the muscle will respond to a tetanus stimuli; however, the muscle will not be able to sustain the tetanic contraction. The ability to sustain a tetanic contraction is another criteria used to determine that a patient has sufficiently recovered from neuromuscular blockade.
■ MAINTENANCE FOR NERVE STIMULATORS Peripheral nerve stimulators should be stored in an organized storage box or shelf in order to decrease the damage to the stimulators, thus increasing the life of the stimulator. The leads should be coiled up and free from tangle in order to maintain their shelf life. Wires break frequently, and extra wires should be on hand. They can be purchased through medical supply companies. The power supply for most stimulators is a 9-V alkaline battery, and extras should also be available.
■ TROUBLESHOOTING If a stimulator does not appear to be working, check the following: • Check the batteries and replace if necessary. • Check all lead connections (stimulator to leads, leads to electrodes). • Check the lead wires. Try replacing the wires. • Check and replace electrodes if necessary (the conductive gel can become dried out and not transmit enough stimulus to the patient).
■ SUMMARY Neuromuscular blocking drugs are commonly used in anesthesia practice. Inadequate reversal or recovery from neuromuscular blockade can have severe clinical consequences. Peripheral nerve stimulators are an essential tool for anesthesia providers to monitor neuromuscular blockade, thus preventing clinical complications. A stimulus is applied to a nerve and the response of the muscle is an important indicator of the depth of blockade. Proper placement of the leads and electrodes is essential for proper interpretation of muscle responses.
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REVIEW QUESTIONS 1. Which of the following statements is TRUE regarding stimulation of the facial nerve to monitor neuromuscular blockade? A) The electrode should be placed directly over the muscle being monitored. B) The facial nerve is the ONLY appropriate nerve to stimulate. C) The facial nerve is a poor choice to monitor neuromuscular blockade. D) Both tetanus and TOF stimuli can be applied to the facial nerve. E) None of the above. Answer: D. Either TOF or tetanus can be applied to any nerve. The electrodes should not be placed directly over the muscle being monitored to avoid direct stimulation of the muscle (bypassing the neuromuscular junction). The facial nerve is a common location for monitoring because of its accessibility; however, many other nerves can be used.
2. Which of the following muscle responses indicate residual neuromuscular blockade? A) Fade to TOF B) Inability to sustain a tetanic contraction C) Twitch response is absent to a single stimulus D) Three out of four twitches are present after a TOF stimulus E) All of the above Answer: E. No muscle response to a stimulus indicates deep neuromuscular blockade. As the blockade begins to wear off, muscle
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twitches in response to stimuli will begin to appear; however, fewer than four twitches to a TOF stimulus still indicate a moderate blockade. A sustained muscle contraction without fade to a tetanic stimulus or four complete muscle twitches of equal and strong amplitude after a TOF stimulus indicate recovery from neuromuscular blockade.
3. A muscle does not respond to an apparent stimuli. Which of the following should NOT be performed? A) First, try a different nerve. B) Check that the power is on and the battery is functioning. C) Check that the stimulator box is delivering a stimulus (flashing indicator with each stimulus). D) Check the current setting. E) Check that the lead wires are properly attached to the box and to the patient. Answer: A. All of the other items should be checked first to ensure proper functioning of the nerve stimulator. If it appears to be functioning properly, check the position of the lead placement.
SUGGESTED READINGS Snell RS. Clinical Anatomy for Medical Students. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000: 668 pp. Viby-Mogensen J. Neuromuscular monitoring. In: Miller RD, Eriksson LI, et al., eds. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingston; 2009: Chapter 47.
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Neurophysiologic Monitoring Judith A. Freeman ■ INTRODUCTION Surgery often involves operating in close proximity to peripheral nerves, the spinal cord, and the brain, or their blood supply. These structures can be damaged unintentionally from scalpels, retractors, electrocautery devices, or other surgical instruments. Neurophysiologic monitoring can be used during surgery to assess the status of peripheral nerves, the spinal cord, and the brain. It can serve as an early warning system to alert the surgeon that something is wrong while there is still time for corrections to be made before permanent injury occurs. The basic technique is to apply a stimulus in the central or peripheral nervous system and to measure the response. The health of the system is determined from the nature of the measured response. Neurophysiologic monitoring may also be used to monitor intracranial pressure (ICP) during neurosurgery or when the brain is injured. Finally, neurophysiologic monitoring can be used to assess the depth of general anesthesia to reduce the risk of intraoperative awareness. This chapter provides an introduction to the major neurophysiologic monitoring techniques and their implications for anesthesia.
■ NEUROPHYSIOLOGIC STIMULUS AND RESPONSE Neurophysiologic monitoring involves the measurement of electrical signals generated along the entire length of motor or sensory neural pathways from peripheral nerves to the brain. Needle or surface electrodes may be used to both initiate the stimulus and measure the response. There are two basic methods of performing this type of monitoring. First, an electrical stimulus is applied to a peripheral sensory organ or nerve and the response signal is measured as it travels to the brain. In the second method, the stimulus is applied to the scalp over a particular
brain region and the response is measured as it travels along the nerve pathways to the periphery. Measurements are averaged with a computer, and the results are displayed on a screen as continuously changing waveforms (older systems recorded the signals on graph paper). Both the amplitude (the strength) and the latency (the time it takes to travel) of the signal yield important information about the health of the pathways (Fig. 41.1). Amplitude and latency are continuously measured during the surgery, and changes in either of these may indicate damage in the neuronal pathway. This type of monitoring will help to detect impending nerve damage along any part of the pathway produced by surgical manipulation of the brain, the spinal cord, peripheral nerves, or the blood supply to these structures. It provides an early warning system of altered nervous tissue function, thus allowing the surgeon to take steps to avoid permanent postoperative neurologic damage. Some examples of surgeries where neurophysiologic monitoring is utilized include carotid artery surgery (interrupts blood flow to the brain), spine surgery (the operation is in close proximity to nerves), and operations directly involving nerves, the spinal cord, or the brain. Although nerve damage causes changes in monitored waveforms, they are also affected by changes in the physiologic milieu. Hypoxia, hypotension, hypothermia, and anesthetic drugs (see below) all can alter signal latency and amplitude. These variables must be controlled as much as possible during surgery to avoid affecting neurophysiologic monitoring. Any changes in signal latency or amplitude must be interpreted by taking into account any changes in physiologic parameters or the administration of anesthetic agents. In most institutions, neurophysiologic monitoring is carried out by certified neurophysiology 403
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Motor Evoked Potentials Electrical stimulation of the scalp overlying the motor cortex of the brain produces a response passing through the spinal cord to the peripheral nerve and finally to the muscle. The response can be detected at any point in this pathway. Of particular importance to anesthesia providers is that stimulation of the motor cortex in the brain intending to stimulate nerves to the legs often stimulates the facial nerve as well. This may lead to jaw clenching during stimulation. A soft bite block should be placed, so that the tongue does not get bitten. ■ FIGURE 41.1 An example of the mixed peripheral nerve somatosensory evoked potential on stimulation of the posterior tibial nerve. The amplitude or strength of the response is represented by the height of the wave. The latency of the response is represented by the time in milliseconds that it takes for the response to be detected. (From Frymoyer JW, Wiesel SM, et al. The Adult and Pediatric Spine. Philadelphia, PA: Lippincott Williams & Wilkins; 2004, with permission.)
technicians under the guidance of an expert neurophysiologist and ultimately overseen by a physician. Arrangements are usually made between the surgeon, the anesthesiologist, and the neurophysiologist regarding the appropriate monitoring for the specific case. The following sections will briefly describe the major neurophysiologic monitoring techniques.
■ TYPE OF STIMULUS RESPONSE NEUROPHYSIOLOGIC MONITORING Somatosensory Evoked Potentials Repeated electrical stimuli are delivered to a peripheral nerve and the signal is recorded as it passes up the spinal cord into the cerebral cortex. For example, the stimulus could be applied to the posterior tibial nerve near the ankle because the surgeon is working on the spine near the spinal nerve roots. The roots may be difficult to see, and they contribute to the makeup of the tibial nerve. Somatosensory evoked potential (SSEP) waveform changes would alert the surgeon to potential injury to the nerve roots. In another example, the blood flow to the carotid artery must be interrupted during surgery. SSEP waveform changes could indicate that the brain is not receiving enough blood flow.
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Brainstem Auditory Evoked Potentials or Responses Repeated clicking sounds are delivered via an earpiece placed in the auditory canal, and the responses are picked up by electrodes on the scalp. This technique monitors the condition of the ear, the cochlear nerve, and the pathway to the auditory cortex through the brainstem. It is most useful during resection of acoustic neuromas (tumor on a nerve leading from the ear to the brain), brain surgery close to the junction of the brainstem and the cerebellum, and during decompression of certain cranial nerves.
Visual Evoked Potentials Lights are repeatedly flashed in front of the eyes, and the pathway to the visual cortex in the brain is recorded. Visual evoked potentials (VEPs) may be useful information in patients who have tumors involving the optic pathway (the optic nerve and the pituitary gland).
Electromyography The sensing electrodes are placed in the muscles innervated by the nerve at risk for damage. When the surgeon touches the nerve, an electrical signal will be generated in the muscle. This method is used in spine surgery, surgery where the facial nerve is at risk of damage, and more recently in thyroid surgery with the introduction of the NIM electromyography (EMG) endotracheal tube. The NIM endotracheal tube has two sensing electrodes just proximal to the cuff. When the tube is placed into the trachea with the cuff just past the vocal cords, the sensors will detect signals from the vocal cords. If the surgeon irritates the recurrent laryngeal nerve, the electrodes will sense vocal cord signals. EMG is a test involving
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motor nerves; therefore, muscle relaxants should not be used during the anesthetic.
■ IMPLICATION FOR ANESTHESIA PERSONNEL Anesthetic agents affect the evoked potential signals in varying degrees. Inhaled anesthetic gases have the greatest effect by depressing signal amplitude and prolonging latency. Low-dose intravenous (IV) agents have less effect on waveforms, but at higher doses, they can significantly decrease amplitude. Some IV agents (e.g., ketamine and etomidate) will even augment the signals. Not all evoked potential signals are equally susceptible to anesthetic agents. For most cases in which neurophysiologic monitoring will be utilized, anesthesia will consist of a small amount of inhaled anesthetic gas, supplemented by IV infusions, primarily propofol (some institutions require total IV anesthesia when monitoring MEPs). Opioids are frequently used to supplement the anesthetic. Muscle relaxants should be avoided in all cases where the motor response of a nerve will be monitored visually or by EMG or MEP. Because propofol infusions often cause hypotension, it is important to maintain perfusion of the brain and the spinal cord. A phenylephrine infusion may be required. Cases involving neurophysiologic monitoring are often complex and carried out for many hours; therefore, large amounts of propofol may be administered. At the end of the procedure, it may not be possible for the patient to rapidly emerge from anesthesia and undergo extubation of the trachea. Transport of an intubated patient to either the postanesthesia care unit or the intensive care unit (ICU) is always a possibility, and a transport monitor and an Ambu bag should always be available. Anesthesia technicians should prepare for these cases with the following: • A multichannel infusion pump with appropriate tubing • 100-mL propofol vials for infusion • Possible phenylephrine infusion • Soft bite block • Transport equipment for an intubate patient
■ OTHER BRAIN MONITORS Electroencephalography Electroencephalography (EEG) measures brain activity through an array of 20 electrodes placed
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at specific locations on the scalp. It may also be measured directly during a craniotomy by electrodes placed on the brain (electrocorticography). The standard recording has 16 channels and requires special training and experience to interpret. The signal may be processed to produce a single number, which may be more easily interpreted and indicates in which general direction the EEG is going. The bispectral index (BIS) monitor is a form of processed EEG. Hypoxia, hypotension, temperature changes, carbon dioxide tension, and all anesthetic drugs may affect the EEG. EEGs may be used during neurosurgical ablation of a seizure focus, awake craniotomy for resection of a tumor or vascular malformation, or carotid surgery.
Bispectral Index (BIS Monitor) Although anesthesia has been delivered safely for many years, there is no specific monitor for determining whether a patient is actually unconscious. Adequacy of anesthesia is based on a combination of knowledge of drug doses and monitoring of changes in heart rate and blood pressure. Many have argued that these are not reliable indicators of the depth of anesthesia. Multiple studies involving thousands of patients have estimated an incidence of awareness under anesthesia of between 1 in 1,000 and 1 in 10,000 patients anesthetized. Awareness mainly consists of remembering conversations and an inability to move or breathe while experiencing pain (this can happen if the patient is paralyzed with neuromuscular blocking agents). Subsequent significant long-term psychological sequelae including posttraumatic stress disorder may ensue in about 33% of these patients. The causes for awareness under anesthesia have been attributed to the following situations: • It was unsafe to administer deep anesthesia to the patient (e.g., very sick patients, severely injured trauma patients, emergency obstetric surgery where it is important to minimize drugs to the fetus). • Anesthesia machine malfunction (e.g., the vaporizer is not delivering the set amount of agent, problems with gas flows diluting a volatile agent) • Anesthetic has run out (e.g., an empty vaporizer or infusion pump that goes unrecognized). • Total IV anesthesia
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• Sedated patients where the patient experiences awareness. They sometimes do not understand that awareness is normal and common when a patient is sedated and not under general anesthesia (e.g., sedation only or sedation with regional anesthesia). • Partial awareness during emergence that is interpreted by the patient as intraoperative awareness • Patients using chronic opioids, alcohol, or other substances of abuse (these patients may be tolerant to the usual doses of anesthetic medications) The BIS was developed and introduced in 1994 as a more objective tool to monitor patients’ levels of consciousness and to decrease the level of awareness under anesthesia. In addition, the BIS monitor has been reported to assist anesthesia providers in optimizing anesthetic doses for individual patients, resulting in faster wake-up times and cost savings from decreased drug dosages. BIS has also been used to guide the management of sedation in critically ill patients in ICUs, especially during mechanical ventilation both with and without neuromuscular blockade and management of drug-induced coma. Another use of BIS monitoring is during anesthesia for neurosurgical procedures and in which it is necessary to induce pharmacologic EEG silence or burst suppression on the EEG (electrical silence with intermittent short bursts of EEG activity). Patients with increased ICP or sustained seizures fall into this category. This may be achieved by using BIS monitoring instead of the more complex full EEG monitoring. In recent years, awareness under anesthesia has received a great deal of media attention. In 2004, the Joint Commission deemed awareness under anesthesia a sentinel event and described and promoted a heightened attentiveness to this issue but did not mandate the use of brainmonitoring devices. The American Society of Anesthesiologists issued a practice advisory regarding BIS monitoring stating that it should be used at the discretion of the anesthesiologist. They also added a caveat that maintaining low brain function monitor values in an attempt to prevent intraoperative awareness may conflict with other anesthesia goals, for example, preserving vital functions. Many studies have now been carried out with conflicting results on the value of BIS monitoring
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in preventing awareness under general anesthesia and its usefulness in both decreasing levels of awareness and cost and time saving. In addition, an association has been found between low BIS values and postoperative cognitive dysfunction in elderly patients, although the reasons and true significance of this are yet to be determined. Thus, BIS monitor usage has now become very dependent on individual practitioner’s preferences.
BIS Monitor Operation The monitor consists of a sensor, placed on one side of the forehead, which detects a frontal electroencephalograph. The signal is then converted mathematically into a numbered continuous measure, scaled from 1 to 100 (BIS number). This conversion algorithm was derived from EEG data from about 5,000 volunteers. It is the propriety property of Aspect Medical and has been modified several times since the introduction of the monitor (Table 41.1).
Applying Sensors After cleaning the skin well with alcohol, the sensor, which consists of a strip of four gelled electrodes, should be applied to one side of the forehead as follows (Fig. 41.2): Sensor number 1: center of the forehead, 2 in (5 cm) above the nose Sensor number 4: directly above and adjacent to the eyebrow Sensor number 3: temple area between the corner of the eye and the hairline Sensor number 2: between sensor number 1 and sensor number 4.
TABLE 41.1 BIS SCALE GUIDELINES BIS NUMBER
STATE OF HYPNOSIS
90-100
Awake state
70-90
Light hypnotic state, light sedation
60-80
Deep sedation
40-60
General anesthesia with low probability of consciousness and explicit recall
10-40
Deep hypnotic state
0
Flat line EEG
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■ FIGURE 41.2 Correct bispectral index sensor placement on the forehead. (Image used by permission from Nellcor Puritan Bennett LLC, Boulder, Colorado, doing business as Covidien.)
Note that the sensors are not numbered sequentially. The edges of the sensors should be pressed down for 5 seconds to ensure adhesion of the sensors to the skin and sealing in of the electrode gel. Appropriate contact and proper positioning of the electrodes are critical to produce accurate BIS measurements. The electrode strip is then connected to the monitor. Once powered up, the monitor will display a message indicating the status of the electrodes: • PASS indicates that there is good contact between the electrodes and the patient. • HIGH indicates a need to reprep the skin under the electrode and reapply at it. The “high” indicates that the impedance (resistance to flow of electrical currents between the patient and the monitor) is high. • NOISE may appear in the status window if the electrode is pressed upon during the check or in the presence of a large external stimulus. • LDOFF indicates an electrode has become detached from the patient. The electrode status may be accessed at any time during use from the setup menu. The BIS monitor may be started at any time as there is neither calibration nor baseline required for its use. The BIS monitor shows the BIS number in the upper left hand corner of the screen (Fig. 41.3). The monitor displays an indication of which power supply is in use (AC electrical supply or battery). If possible, the BIS monitor should be connected to AC power as typical battery life is only about 1 hour. The monitor
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■ FIGURE 41.3 Bispectral index monitor screen. (With permission from Nellcor Puritan Bennett LLC, Boulder, Colorado, doing business as Covidien.)
will also display a warning if the sensor gets disconnected from the machine. The signal quality index (SQI) bar indicates the quality of the EEG signal over 60-second time increments. It is optimal when the bar extends all the way to the right. As the SQI decreases, the BIS numeric display changes form a solid to an outlined number. This should prompt a check of both sensors and connectors. Electrocautery may also interfere with BIS values. The electromyographic bar reflects muscle tone in the underlying frontalis muscle. Increased tone in the frontalis from light anesthesia or recovery from muscle relaxants may be interpreted by the machine as an EEG signal. This can artificially raise the BIS number.
Troubleshooting BIS Values BIS is higher than expected: • Increased surgical stimulus • Inadequate anesthesia: Vaporizers and IV lines should be checked to ensure that accurate doses are being administered. • Frontalis muscle twitching or shivering BIS: Check for EMG activity on the monitor. Possible neuromuscular blockage wearing off. • Interference from pacemakers and other electrical devices
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BIS is lower than expected: • Decreased patient requirements (e.g., decreased surgical stimulus) • Decrease in frontalis muscle tension: Check EMG tracing. • Hypothermia • Cerebral ischemia • Improper lead placement: Reposition or replace sensor.
■ INTRACRANIAL PRESSURE MONITORING The adult skull is a rigid box whose contents include the brain tissue (80%), the cerebrospinal fluid (CSF) (10%), and the blood vessels (10%). These volumes create a pressure inside the skull known as ICP. Any condition that increases the volume inside the skull will increase the ICP (e.g., brain tumors, bleeding into the brain, or brain swelling after a head injury). Normal values for ICP are 8-12 mm Hg. If the ICP becomes elevated, it can compromise blood flow to the brain and lead to cell damage, impaired neurologic function, or even death. The cerebral perfusion pressure (CPP) may be calculated according to the following formula: Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) − intracranial pressure (ICP) Most clinicians strive to keep the CPP greater than 50-60 mm Hg. Either hypotension or increased ICP can compromise the CPP; thus, the treatment for low CPP is to raise the blood pressure and/or decrease ICP. Devices to measure ICP include the following: • Catheter placed directly into the ventricle of the brain (an external ventricular drain [EVD]) • Small fiberoptic catheter placed inside the brain tissue (Camino catheter) • Pressure monitoring catheters placed either subdurally or epidurally The most commonly used devices today are EVD and Camino catheters. All methods require connection of the device to a transducer to convert the pressure signal to a waveform that can then be displayed on a screen.
EVD The EVD is placed through a small hole in the skull and passed directly into the ventricle of the brain. The catheter is attached to a transducer
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and also to a drainage chamber, which allows for removal of the CSF. CSF drainage may be necessary to decrease ICP. CSF drainage is gravity dependent, so the rate of drainage will depend on the height of the drainage chamber relative to the height of the patient’s head. Great care must be taken that the drainage device is secured at the proper height at all times. This is particularly true during patient transport. If the drain is placed too low, too much CSF can drain out with severe consequences for the patient. It may be safer to close the EVD drainage valve during transport, but this should only be done in consultation with all physicians taking care of the patient. If the drain becomes kinked off or is inadvertently closed for a long period of time when CSF drainage was necessary, ICP may rise to very high levels and compromise blood flow to the brain. It may be advantageous to monitor ICP during transport as sudden changes in ICP can occur. After transport, the transducer should be rezeroed, the drainage device adjusted to the appropriate height, reopened if it has been closed, and checked to ensure that it is dripping and working again.
Camino Catheter In the 1980s, researchers at Camino Laboratories developed a small fiberoptic device that could be directly inserted into brain matter. A bolt, which acts as a conduit for the catheter, is placed in a sterile fashion in a small hole in the skull. The catheter is then passed through the hole in the skull directly into the frontal lobe of the nondominant hemisphere of the brain. Before placement through the bolt, the cable connector end of the fiberoptic catheter is handed off to a nonsterile assistant. The assistant attaches the connector to the monitor. The sterility of the catheter must be maintained throughout the procedure. The device is zeroed relative to the atmosphere while being held at the level of the external auditory meatus. If the display on the monitor does not read zero, there is a zero adjustment screw that can be turned with a special tool provided with the insertion kit. The transducer is built into the tip of the catheter and requires calibration before insertion. It does not have to be leveled or recalibrated and cannot be calibrated in vivo. The catheter is then placed inside the bolt and secured. A strain relief sheath, which prevents kinking and bending of the catheter, is then slid
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down over the catheter. It is very important not to bend the fiberoptic catheter as the delicate transmission fibers can be easily damaged. The monitor can either be a free-standing screen or can be integrated with the bedside patient monitor using a standard interface cable. The monitor can display an ICP waveform, digital ICP, CPP, and brain temperature. For transport, the external monitor can be unplugged from the electrical outlet, the catheter can be disconnected from the cable, and the monitor can be transported to the new location and reconnected. No additional zeroing is required.
■ SUMMARY Surgery often can unintentionally damage peripheral or central nervous system structures with scalpels, retractors, electrocautery devices, or other surgical instruments. In addition, surgical procedures may interrupt the blood supply to the central nervous system. Neurophysiologic monitoring can be used as an early warning system to monitor the status of both the peripheral and the central nervous system. Anesthesia technicians should be familiar with the basic physiology of these techniques and the anesthetic implications if they are to be used. In addition, anesthesia technicians should be familiar with the setup, operation, and maintenance of ICP monitors and processed ECG (e.g., BIS) monitors.
REVIEW QUESTIONS 1. The following are common uses of neurophysiologic monitoring EXCEPT A) Assess the status of peripheral nerves, the spinal cord, and the brain during the surgical case. B) Monitor ICP during neurosurgery or when the brain is injured. C) Navigate through the brain by using computer images. D) Assess the depth of general anesthesia. E) None of the above. Answer: C. Neurophysiologic monitoring is routinely used for all the above except for navigation with computer images.
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2. The use of a NIM endotrachael tube utilizes which of the following type of neurophysiologic monitoring? A) Somoatosensory evoked potentials (SSEPs) B) Motor evoked potentials (MEPs) C) Brainstem auditory evoked potentials or responses (BAEPs or BAERs) D) Visual evoked potentials (VEPs) E) Electromyography (EMG) Answer: E. This special endotracheal tube is monitoring muscle activity in the vocal chords. It does not send out a signal to “evoke” a response; rather it is monitoring baseline muscle electrical activity (EMG). If the surgeon should stimulate the nerve to the vocal chords by compression or electrocautery (the nerve can be close to the surgical site), the monitor will detect the muscle activity. BAEPs involve an auditory stimulus with detection of the response in the brain. Likewise, VEPs involve a visual stimulus and detect a response in the brain.
3. When preparing for a case that will require neurophysiologic monitoring, the anesthesia technician should have all the following items available EXCEPT A) A multichannel infusion pump with appropriate tubing B) Extra propofol C) Transport equipment D) Long-acting muscle relaxants E) Phenylephrine infusion Answer: D. Long-acting muscle relaxants should be avoided in cases where muscle activity will be monitored as part of neurophysiologic monitoring (MEP or EMG). Muscle relaxants will paralyze the muscle and the muscle will not have any baseline activity that can be monitored on the EMG and muscle response cannot be evoked by a stimulus to a nerve and thus cannot be monitored with MEPs. In some cases, the anesthesia provider will use a muscle relaxant at the beginning of a case to facilitate endotracheal intubation; however, the effects will be allowed to wear off before neurophysiologic monitoring is instituted. The use of muscle relaxants will not interfere with the use of SSEP monitoring.
4. BIS is a monitor that measures true patient awareness. A) True B) False Answer: B. The BIS measures a processed EEG signal and is just another tool for the anesthesiologist to use to monitor the depth of anesthesia. Many other factors can affect BIS readings and must be taken into account when interpreting BIS values. In addition, the monitoring of BIS values does not guarantee lack of awareness.
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5. Normal values for ICP are A) 8-12 mm Hg B) 22-30 mm Hg C) 15-18 mm Hg D) 2-6 mm Hg E) None of the above Answer: A.
6. When transporting with an EVD catheter, it is important that the anesthesia technician A) Always place the drain very low in order to drain off the CSF B) Always close the drain C) Always make sure the catheter and the drain are not kinked D) B and C E) All of the above
SUGGESTED READINGS Avidan MS, Zhang L, Burnside BA, et al. Anesthesia awareness and the bispectral index. N Engl J Med. 2008;358: 1097–1108. Bedell EA, Prough DS. Neurological and intracranial pressure monitoring. In: Irwin R, Rippe JM, et al., eds. Procedures, Techniques and Minimally Invasive Monitors in Intensive Care in Intensive Care Medicine. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008. Devlin VJ, Schwartz DM. Intraoperative neurophysiologic monitoring during spinal surgery. J Am Acad Orthop Surg. 2007;15(9):549–560. Orser BA. Depth-of-anesthesia monitor and the frequency of intraoperative awareness. N Engl J Med. 2008;358: 1189–1191. Sloan T, Heyer E. Anesthesis for intraoperative neurophysiologic monitoring of the spinal cord. J Clin Neurophysiol. 2002;19(5):430–443.
Answer: C. It is important that the tubing and catheter are not kinked and that the drain is placed level with the patient’s head. Obstruction of the catheter or closure of the drain valve could cause CSF to build up within the brain and cause injury to the patient. If the drain is placed below the patient’s head, CSF can drain. This should only be done with close physician supervision. The patient can suffer severe injury if too much CSF is drained. Closure of the drain and positioning of the drain should only be performed under physician supervision.
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Intra-aortic Balloon Pumps and Ventricular Assist Devices Laura Downey ■ INTRODUCTION Cardiac disease continues to be the number one cause of death in the United States, accounting for 34.3% of all deaths in 2006. Over 81.1 million American adults carry the diagnosis of one or more types of cardiovascular disease. As the incidence of cardiac disease grows, an increasing number of patients with heart disease undergo anesthesia and surgery every year for various procedures. These procedures range from coronary artery revascularization, coronary angioplasty, valve replacement surgery, repair of aortic aneurysms, correction and palliation of congenital heart disease, to heart transplantation. Despite the improvement in medical and surgical interventions for cardiovascular disease, the aging U.S. population has led to a steady rise in the incidence of heart failure. Data from the 2010 Centers for Disease Control and Prevention (CDC) Heart and Stroke Update estimated that approximately 5.8 million people are living with heart failure and approximately 25% have advanced or end-stage heart failure. The 1-year mortality rate for patients with heart failure is estimated at 20%, while the 5-year mortality rate is estimated to be as high as 59% for men and 45% for women. While advances in medical and surgical therapy have been effective in reducing the mortality and morbidity from heart failure, there is a subset of patients who develop severe cardiac failure in the setting of myocardial infarction (MI), following cardiopulmonary bypass, trauma, or advanced cardiomyopathies. Medical therapies for these patients are often limited, and patients may require artificial support to maintain their cardiac output and perfusion to their vital organs while awaiting recovery or definitive surgical treatment. The most common devices used to support these patients until recovery
or heart transplantation are an intra-aortic balloon pump (IABP) or a ventricular assist device (VAD). This chapter examines at the indications, setup, operation, maintenance, and troubleshooting for these devices. Depending on the institution, these devices may be managed by anesthesia technicians, cardiovascular technicians, or perfusionists. Of note, both intra-aortic balloon pumps and various VADs often require extra training to learn the specifics of individual devices. Therefore, please follow your institution’s requirements and ensure that you are properly trained in the equipment prior to using the device on a patient.
■ AORTIC BALLOON PUMPS The IABP is a device that augments blood flow to the heart by inflation and deflation of a balloon that sits in the thoracic aorta (Fig. 42.1). This device is used to augment cardiac output and coronary blood flow in patients with cardiogenic shock. The indications for an IABP include (1) cardiogenic shock, (2) failure to separate from cardiopulmonary bypass, (3) stabilization of a patient prior to the operating room (OR), or (4) as a bridge to transplantation. See Table 42.1 for a listing of the indications and contraindications for IABP placement. IABPs are usually placed by cardiothoracic surgeons or cardiologists in the cardiac catheterization lab, OR, or in the intensive care unit (ICU) where appropriate monitoring and emergency equipment are available.
■ CARDIAC CYCLE AND CORONARY PERFUSION As IABP therapy is based on the timing of the cardiac cycle, it is important to review the two major phases of the cardiac cycle: diastole and 411
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in the ventricles is still greater than that in the atria. Therefore, the mitral and triscuspid valves remain closed and the ventricular volume does not change. At the end of diastole, the pressure is called the left ventricular end-diastolic pressure (LVEDP). Coronary artery perfusion occurs during diastole.
■ FIGURE 42.1 Cutaway of heart and aorta showing placement of an IABP in aorta just distal to the subclavian artery.
systole (Fig. 42.2) (see Chapter 7). These phases are important for understanding the mechanism of the IABP therapy because it uses the cardiac cycle to augment cardiac output during systole and coronary blood flow during diastole, a process called counterpulsation.
Diastole The onset of diastole is noted by the relaxation of the ventricles. As the ventricular pressure falls below the aortic and pulmonary artery pressure, the aortic and pulmonic valves close. During the period of isovolumetric relaxation, the pressure
Coronary Perfusion It is important to understand that coronary perfusion occurs only during diastole, when the wall tension or the LVEDP is the lowest. During systole, the pressure generated by the contraction of the myocardium may completely stop blood flow to the coronary bed. When the diastolic blood pressure is higher than the LVEDP, blood flows into the coronary arteries, resulting in coronary perfusion.
Systole At the beginning of systole, the ventricles are full of blood from the previous diastolic filling period and the ventricles begin contracting, a period called isovolumetric contraction. As the pressure in the ventricles rises higher than the atrial pressure, the mitral valves and tricuspid valves close. The period of isovolumetric contraction accounts for approximately 90% of the myocardial oxygen consumption. Eventually, enough pressure is generated to open the aortic and pulmonary valves, leading to rapid ventricular
TABLE 42.1 INDICATIONS AND CONTRAINDICATIONS FOR IABP USE INDICATIONS FOR USE
CONTRAINDICATIONS
Cardiogenic shock Myocardial infarction Myocarditis Cardiomyopathy Cardiac contusion
Absolute Aortic valve insufficiency Aortic disease Aortic dissection Aortic aneurysm
Surgical indications Postsurgical myocardial dysfunction Failure to separate from CPB Procedural support during angiography or CBP or noncardiac surgery
Relative End-stage disease Severe peripheral disease Severe noncardiac systemic disease Massive trauma
Cardiac support for hemodynamically unstable patients prior to repair Valvular insuffiency: mitral Ruptured papillary muscle Ventricular septal defect
DNR patients Severe coagulopathy
Bridge device Bridge to ventricular assist device Bridge to transplant
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413
Isometric relaxation period
120 Aortic valve closes
100 80
Aortic pressure 60 Aortic valve opens
40
Left ventricular pressure
20
Atrial pressure
100 Ventricular volume (mL)
80 40 R
R
P
T
P
ECG Q 1st Heart sounds
Systole 0
Q 4th
2nd 3rd
0.2
Diastole 0.4
0.6
0.8
Time (sec) ■ FIGURE 42.2 The cardiac cycle. Changes in aortic pressure, left ventricular pressure, left atrial pressure, left ventricular volume, the electrocardiogram (ECG), and heart sounds. (From Porth CM. Pathophysiology Concepts of Altered Health States. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2005, with permission.)
ejection, where approximately 65%-75% of the stroke volume is ejected. After the blood is ejected, the pressure in the ventricles drops dramatically, but blood continues to flow into the aorta until the end of systole. The end of systole is signaled by the onset of myocardial relaxation and closure of the aortic valve.
■ HOW DOES AN IABP WORK: COUNTERPULSATION HEMODYNAMICS The IABP is a mechanical device that increases blood flow to the coronary arteries during diastole and increases cardiac output during systole. The device is a flexible catheter with a balloon at the end that sits in the descending aorta just distal to the left subclavian artery. The balloon augments blood flow by volume displacement
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and pressure changes associated with rapidly injecting helium gas in and out of the balloon chamber, a principle called counterpulsation (Fig. 42.3). During diastole, the balloon is filled with helium (approximately 40 mL depending on the balloon size), thus causing the blood to be displaced by the increased balloon volume. This causes the aortic pressure to increase, which increases the driving pressure into the coronary arteries. The result is improved blood flow to the coronary arteries. During systole, the reverse occurs. The balloon deflates and the blood flows forward to fill the evacuated space. The fall in pressure decreases the amount of pressure the failing left ventricle (LV) has to generate, thus decreasing the oxygen demands of the heart and increasing cardiac output by as much as 40%. The balloon inflation can be triggered by the
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■ FIGURE 42.3 Counterpulsation. The image on the left shows thorax with intra-aortic balloon catheter introduced via the femoral artery. The image in the center shows aorta with catheter inflated as in diastole. The image on the right shows aorta with catheter deflated as in systole. (LifeART image copyright (c) 2012 Lippincott Williams & Wilkins. All rights reserved.)
patient’s electrocardiogram, a pacemaker, a set rate, or the patient’s blood pressure. Key Points: 1. During diastole, the balloon inflates and augments coronary perfusion. 2. At the beginning of systole, the balloon deflates and increases cardiac output while decreasing myocardial oxygen consumption. 3. The balloon is inflated with helium, a gas that can be easily absorbed by the body without damage in the case of balloon rupture.
■ SETUP AND PLACEMENT Prior to placement, a thorough physical exam is performed to assess the circulation to both legs and determine the best side for insertion. The femoral artery is accessed with a needle and a guide wire is placed through the femoral artery and into the thoracic aorta (see Chapter 34). The puncture site is then dilated with successive placement of a dilator/sheath combination until the balloon can be threaded through the puncture site into the central aorta. The balloon sits in the aorta, approximately 2 cm from the left subclavian artery and above the renal artery branches. A chest x-ray or fluoroscopy is used to confirm proper placement. Daily chest x-rays demonstrate the tip at the 2nd and 3rd intercostal spaces. Depending on the institutional practice,
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patients may be fully anticoagulated while the IABP is in place, in order to prevent clot formation on the balloon. However, anticoagulation may increase the risk of bleeding, especially in the postsurgical setting. While IABPs are usually placed by cardiothoracic surgeons or cardiologists, there is a wide variation in the technicians who may set up and prepare the IABP kits: perfusionists, scrub technicians, anesthesia technicians, and cardiovascular techs. Before setting up an IABP, be sure to read the instruction manual for details specific to the model you will be using as there are many different companies that manufacture IABP systems and each one will operate in a slightly different way. The general setup includes the following: 1. Electrocardiogram (ECG) leads 2. Arterial blood pressure waveform monitoring 3. Balloon volume monitoring 4. Electric console to adjust triggering and inflation timing of the balloon 5. Battery backup power 6. Gas reservoir Details of equipment setup for IABPs are listed in Table 42.2.
■ OPERATION AND MANAGEMENT OF AN IABP For the optimal effect of counterpulsation, the inflation and deflation of the balloon must be correctly timed to the cardiac cycle (Fig. 42.4). This is usually achieved by triggering the balloon’s inflation based on the patient’s ECG signal or the arterial waveform. Usually, the triggering signal is from the R wave on the ECG. The balloon is set to inflate in the middle of the T wave, coinciding with the aortic valve closure and beginning of diastole. Deflation occurs prior to the R wave, noted on the arterial waveform just before the arterial upstroke (Fig. 42.5). The balloon augmentation usually starts at a beat ratio of 1:2, which means every other beat is augmented by the IABP. This allows the provider to compare the patient’s inherent ventricular beats with the augmented beats and adjust the timing as necessary. A health care provider trained in IABP therapy will likely assess the effectiveness of the IABP and adjust the timing appropriately. Figure 42.6 demonstrates an arterial waveform generated by a correctly positioned and timed balloon.
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TABLE 42.2 PLACEMENT OF AN IABP The following steps are important in placing a percutaneous IABP Supplies: Betadine Lidocaine with syringe for topical anesthestic Suture material Sterile drapes, mask, gown, gloves, cap Sterile dressing material Heparinized saline flush solution in 10 to 20-mL syringe Pressure tubing, transducer, and continuous heparin flush solution for: Balloon catheter Central lumen Balloon pump console with patient cables ECG electrodes IABP kit (kits usually contain the following): Central lumen catheter 30- and 40-mL 7.5 intra-aortic balloon, uses an 8-French sheath 50-mL 9-French intra-aortic balloon, uses a 9-French sheath Introducer sheaths, with and without side ports Guide wires Preparation of IABP for insertion: 1. Establish power and verify power switch on controlling console 2. Establish helium gas pressure 3. Establish ECG and pressure 4. Zero transducer on arterial pressure source 5. Confirm initial control setting 6. Balloon preparation: Place IABP guide wire on the field Attach one-way valve to the IABP connector Connect the 60-mL syringe to the one-way valve and apply full vacuum Do not remove the one-way valve until the IABP is fully in the patient Flush through the central lumen with heparinized saline just prior to insertion Remove the IABP from tray immediately before insertion After the IABP is positioned in the patient: 1. Aspirate blood from central lumen and gently flush with 3-mL heparinized saline 2. Hook up pressurized heparin saline flush system to central lumen 3. Remove one-way valve and connect IABP to pump 4. Suture at both the sheath hub and the catheter site 5. Initiation of pumping: Attach IABP to appropriate connector Attach connector to safety disk/condensate removal module Press START and verify filling of balloon Verify optimal augmentation Fine- tune deflation time Assess hemodynamic benefits Please refer to your hospital’s Policy and Procedure Manual for sterile procedures. Please carefully follow detailed instructions included with each balloon pump catheter.
■ TROUBLESHOOTING While an IABP can be a life-saving device, a number of complications have been described when using the IABP. The most common vascular complication is limb ischemia or compartment syndrome. Therefore, the patient must be constantly observed for indications of ischemia, such as cold limb, color changes,
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decreased pulses, or pain in the affected limb. Vascular injuries can be life or limb threatening and require physician notification immediately. Other complications include bleeding, infection, or device malfunction such as balloon tear or perforation (Table 42.3). Device malfunctions can sometimes be prevented or herald an impending emergency, and
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Section IV • Equipment Setup, Operation, and Maintenance Balloon Timing
Early Inflation
Correct Timing
Late Inflation
Correct Timing
Early Deflation
Correct Timing
Late Deflation
Correct Timing
■ FIGURE 42.4 The timing of balloon inflation and deflation is adjusted in the 1:2 mode. The inflation point is moved rightward (later) until it occurs in late diastole and the dicrotic notch is uncovered. The inflation timing is moved progressively earlier in the cardiac cycle until the dicrotic notch on the central aortic tracing just disappears. Examples of early, late, and correct inflation are shown in the top two tracings. Similarly, the deflation knob is moved leftward (earlier) and then slowly advanced toward the right (later in the cardiac cycle) until the end-diastolic pressure dips 10 to 15 mm Hg below the patient’s unassisted diastolic pressure. This will produce a maximal lowering of the patient’s unassisted systolic pressure. Examples of early, late, and correct deflation timing are shown in the bottom two traces. (From Baim DS. Grossman’s Cardiac Catheterization, Angiography, and Intervention. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2006, with permission.)
alarms should be taken seriously. A careful survey of the patient and device may elucidate the malfunction and help prioritize corrective measures. In order to mitigate complications, device management tips and precautions are listed below: 1. Patient’s physiologic parameters should be monitored frequently for evidence of ischemia or worsening cardiac function. 2. Frequently check pump activity. 3. Check helium level to avoid an empty tank. 4. Replace empty helium tanks in 14 y
>50
7.0-8.0
Miller/Mac 2-3
4
ETT, endotracheal tube; LMA™, laryngeal mask airway.
hypothermia during anesthesia and surgery. It is essential to prevent the increased heat loss by warming the operating rooms (ORs), covering the babies with blankets, and using convection forced air warmers.
Psychological Issues For children, the anxiety regarding surgery and its associated pain is often compounded by fear of separation from family, and cognitive limitations, which may impair their ability to understand the purpose of the anesthesia and surgery. Because of this, pediatric caregivers employ a number of techniques to minimize the stress experienced by pediatric patients. For example, attempts are generally made to make the general environment appear “kid friendly.” This can be done with soothing and entertaining pictures on the walls and ceilings, available toys for the children to play with, and even entertainment in the preoperative area (i.e., video games, live music). In addition, because children’s anxiety may be shared by their parents, an effort is made to provide the children’s parents with support. This can be facilitated with pamphlets, preoperative discussions with parents, and sometimes even tours of the various preoperative and postoperative areas. Finally, a number of measures are employed with the children themselves to lessen their anxiety and discomfort. Discussions with children are conducted using age-appropriate concepts
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and vocabulary. For example, children aged 2-4 years are often eager to engage in fantasy and magical thinking, and brighten at the prospect of “being told a story” in the OR. Older children may be helped by being given the choices, (i.e., a “flavor” for their breathing mask). Adolescents are very often concerned about waking up during surgery, and respond well to reassuring discussions. Children between the ages of 1 and 3 years are at the highest risk of emotional trauma upon separation from their parents, or upon being shown either a needle (for injection) or an anesthetic mask. Not only are children in this age group at risk for stormy anesthetic inductions, but they are also at increased risk for postoperative behavioral changes (i.e., tantrums, nightmares, regression in potty training), which can last weeks to months. With this in mind, pediatric facilities may include “induction rooms” separate from the surgical suites in which children can be anesthetized with a parent present. General anesthesia is typically induced by having the child breathe increasing concentrations of anesthetic agent; IV lines are often not started until after children are unconscious. Another strategy for calming children prior to separation from their families is the use of oral premedication, which is seldom administered in the adult population. Oral midazolam has been shown to greatly reduce separation anxiety and resisting the mask in the OR. In addition, there is evidence that this
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premedication lowers the incidence of untoward postoperative behavior changes.
Equipment Considerations Marked changes in anatomy and physiology occur from birth to adolescence. However, similar anesthesia equipment is used in patients of all ages. The differences in airway equipment and vascular catheters are chiefly in size rather than shape or type (Figs 46.1-46.3). In addition, IV administration kits for children younger than about 10 years of age feature “microdrips” and buretrols to help prevent fluid overload (Figs. 46.4 and 46.5). Children in general greatly fear needles. Hence, in most hospitals, the majority of children younger than about 12 years of age are brought to the OR without an IV having been inserted. General anesthesia is typically induced by having the child breathe oxygen with increasing percentages of anesthetic gases (nitrous oxide, sevoflurane) added. IVs are placed after the children are anesthetized. It is important to understand that during the initial period, while the anesthesia is “light,” the child is at greatest risk for adverse airway events. These include laryngospasm, apnea, and airway obstruction. This is particularly true prior to the
■ FIGURE 46.1 Variation in laryngoscope blade sizes.
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■ FIGURE 46.2 Variation in LMA™ sizes. LMA™, laryngeal mask airway.
insertion of the IV, as there is not yet a method of rapidly administering medications emergently.
■ SPECIFIC SURGERIES Neonatal and Infant Surgery Anesthesia-related morbidity and mortality are higher in infants, particularly the neonate. To reduce this risk requires a well-planned technique and a thorough understanding of the specific pathophysiologic conditions and surgical needs. The unique demands of infancy will require the appropriate age-related equipment and expertise that are best met by personnel trained to provide care to pediatric patients, neonates, and infants on a regular basis.
■ FIGURE 46.3 Variations in nasal and oral airway sizes.
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Chapter 46 • Pediatric Anesthesiology
■ FIGURE 46.4 Standard and microdrip chambers.
A number of conditions require urgent surgical treatment in the neonatal period. Congenital diaphragmatic hernia (CDH) is a defect in the diaphragm that allows the abdominal contents to herniate into the left chest cavity. CDH is most commonly diagnosed and repaired during early infancy. The cardiopulmonary compromise associated with CDH can be severe enough that neonates may require extracorporeal membrane oxygenation (ECMO).
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Tracheoesophageal fistula (TEF) is an abnormal opening between the esophagus and trachea. It is usually associated with an undeveloped blind-end esophagus. The fistula between the trachea and the esophagus allows the esophageal or gastric contents to enter the lungs and compromise the baby’s pulmonary function. Omphalocele and gastroschisis are defects of closure of the abdominal wall that present with abdominal contents exposed at birth. The risk of contamination and infection require immediate containment of the exposed abdominal contents, which is often performed shortly after birth with a sterile plastic silo. The infant can be stabilized, resuscitated, and further evaluated for associated congenital anomalies and prepared for more elective complete repair of the abdominal wall defect. Other neonatal gastrointestinal conditions that will often require urgent surgical interventions include intestinal atresias, pyloric stenosis, volvulus, meconium ileus, inguinal hernia, and necrotizing enterocolitis (NEC). Each will have specific anesthetic needs and concerns to be addressed. The less mature hepatic and renal systems often require using different IV fluids and drugs than with adults. Neonates have a significantly limited ability to maintain and regulate body temperature; therefore, they are at much greater risk of hypothermia while under anesthesia. This results in an increased oxygen consumption, which must be addressed by the immature neonatal cardiopulmonary systems.
Pediatric Neurosurgery
■ FIGURE 46.5 Neonatal intravenous administration kit with a buretrol.
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Common pediatric neurosurgical conditions include trauma, brain tumors, hydrocephalus, and spina bifida (myelomeningocele). Pediatric head trauma is the most common cause of serious injury and death in children. Brain tumors are the most common solid tumor in children, with a significant number of these patients requiring surgical treatment. Hydrocephalus can result from congenital anomalies of the brain, bleeding within the brain, or tumor. Hydrocephalus is an increase in the CSF within the brain that leads to increased intracranial pressure (ICP), which requires treatment, usually involving shunting of CSF (usually into the abdominal cavity). As in adults, neurosurgery in children can involve neurophysiologic (brainwave) monitoring, which provides information
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to minimize injury to the nervous system during the procedure. This requires using anesthetic drugs that minimally affect brain wave signals. Myelomeningocele is a congenital spinal anomaly that causes varying degrees of spinal cord spinal bone malformation. The most common indication for urgent neurosurgery on neonates is a myelomeningocele with exposed spinal cord in the lumbar area.
Cardiac Pediatric patients undergo cardiac surgery for very different reasons than adult patients. Adults most often need cardiac surgery because of coronary artery disease or diseases of the heart’s valves. Children rarely suffer from coronary artery disease. They present with “abnormal plumbing.” This means that either the heart itself (atria, ventricles, and valves) or the major blood vessels (e.g., aorta, pulmonary artery) did not form correctly. Abnormalities include incompletely developed chambers and defects in the walls separating the chambers within the heart. Extreme vigilance must be maintained when preparing all IV lines and pressure tubing. Even small air bubbles can have devastating consequences (strokes) in children with certain heart defects. Invasive monitors like arterial lines, central venous lines, and transesophageal echocardiography (TEE) are common. The use of pulmonary artery catheters (Swan-Ganz catheters) is less common. All invasive monitors must be sized (diameter and length) appropriately for the patient.
Urology Pediatric urology procedures are often performed to correct developmental defects or remove tumors. Common procedures include complete or partial kidney removal (nephrectomy), testicular repair (orchiectomy, orchiopexy, etc.), ureteral reimplantation, and penile and vaginal surgery. Most of these procedures are performed under general anesthesia using either an ETT or an LMA™. Invasive monitoring is rarely necessary, unless the patient is extremely sick or the surgery is expected to result in significant blood loss. For many of these surgeries, anesthesiologists will use regional anesthesia—caudal blocks or epidurals—to minimize postoperative pain. Infants and small children are unable to sit still for procedures. Therefore, unlike adult patients,
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these blocks are typically performed in children after induction of general anesthesia.
Orthopedics Pediatric patients routinely undergo orthopedic surgery. Often times, these surgeries are to correct limb fractures from falls or other accidental traumas. Other procedures are performed to correct congenital skeletal deformities—scoliosis, hip dysplasia, etc. Children presenting for repair of fractures often have “full stomachs.” This means they have not been fasting for surgery (like most patients for elective surgery), and these children are at increased risk for aspiration during induction of general anesthesia. The anesthesiologist may request a rapid sequence intubation to minimize the chance of aspiration. One can assist the anesthesiologist by making sure all equipment for intubation is readily available (e.g., appropriately sized ETT with a stylette), or by performing cricoid pressure as directed. Regional anesthesia (peripheral nerve blockade) is often a consideration for orthopedic surgery, especially surgery on limbs. Some surgeries can be performed under regional anesthesia alone, and other procedures utilize a combination of general and regional anesthesia. Depending on the age and maturity of the patient, peripheral nerve blocks may be done prior to induction of general anesthesia or afterward. Many of the same tools (i.e., ultrasound, nerve stimulators, catheters, etc.) that are used in adults can be used in children. Children with spinal deformities often require surgical correction. Scoliosis, or lateral curvature of the spine, can impair a child’s cardiopulmonary functioning. These procedures are extensive, and at times require both posterior and anterior procedures to fully correct and stabilize the spine. As the spinal column is straightened, the spinal cord and nerves can be stretched or damaged. For this reason, neurologic monitoring is routinely used to detect nerve injury and correct it during the procedure. Neurologic monitors are sensitive to volatile anesthetics (sevoflurane, isoflurane, desflurane, etc.); therefore, anesthesiologists utilize either partial or total IV anesthesia with sedatives (propofol, dexmedetomidine) and analgesics (fentanyl, remifentanil, ketamine). The anesthesiologist may also choose to place one or more invasive
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Chapter 46 • Pediatric Anesthesiology
monitors—arterial and/or central venous line— that can be used to monitor hemodynamics, draw blood for laboratory tests, and provide adequate access for infusion of anesthetics and vasoactive medications. Setup for these types of cases should include vascular access equipment, transducers, fluid warmers, and infusion pumps for medications. Anyone working in ORs, and orthopedic rooms in particular, should be mindful that x-rays are frequently taken during the procedure. For protection, always wear a leaded apron when entering these ORs, or be certain to clarify that x-ray equipment is not currently in use.
Otolaryngology Pediatric ENT (ear, nose, and throat) surgery is often one of the busiest services in the ORs. Procedures range from ear tubes and tonsillectomies to repairs of cleft lips and palates and other congenital malformations. In assisting an anesthesiologist in an otolaryngology room, it is important to appreciate the types of surgeries scheduled. One of the most common and quickest procedures performed in a children’s hospital is the placement of ear tubes (myringotomy tubes). Other short procedures include removal of the tonsils and adenoids (tonsillectomy and adenoidectomy). In a room with these cases, a premium is placed on rapid turnover of the room between cases to facilitate a large number of procedures. Other types of otolaryngology cases involve birth defects or congenital malformation. These are usually defects in the structure of the head, face, palate, lip, and jaw. Certain syndromes (i.e., Treacher Collins, Pierre Robin, and Goldenhar syndromes) are associated with facial deformities. Unique malformations can make placement of the ETT extremely difficult. Having specialized equipment ready to go (i.e., fiber-optic bronchoscope, glide scope, intubating stylets, exchange catheters, etc.) in these situations is imperative. Lastly, at times otolaryngology surgeons use specialized equipment such as lasers to work on tumors and other lesions in the airway. The topic of laser safety is covered in another section of this text. However, it is important to wear eye protection (specifically designed for the particular type of laser) when entering any OR with a laser in use.
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Ophthalmology Ocular procedures performed in pediatric patients range from basic eye examinations under anesthesia (EUA) to complicated intraocular surgery. Providing appropriate care for these patients requires a thorough understanding of intraocular pressure (IOP), potential ocular effects of anesthetics, as well as the continuing maturation of vision following birth and specific physiologic consequences of ocular surgery. Retinopathy of prematurity (ROP) is a frequent concern for babies born prematurely. Often, repeated EUAs and laser treatments under general anesthesia are needed. The precise role of oxygen in the pathogenesis of ROP is uncertain. Appreciation of the varying effects anesthesia may have on IOP is essential in providing care to children with eye disorders. Whether it is measuring IOP during a sedated eye exam to care involving a ruptured globe, the IOP may be influenced significantly by anesthetic management. One of the most frequent types of eye surgery for children is strabismus (“squint”) repair. Surgery for this condition generally involves the surgeon shortening or lengthening various muscles attached to the surface of the eye (extraocular muscles). Pulling on the extraocular muscles can result in a dramatic slowing of the HR (the “oculocardiac reflex”). This reflex is often seen during eye surgery and is addressed with medications that increase the HR (e.g., atropine, glycopyrrolate). Malignant hyperthermia (MH) is a rare, life-threatening disorder characterized by high fevers and cardiac arrhythmias following exposure to certain anesthetic agents. An association between strabismus and MH has been described. Every anesthesia department should maintain a collection of supplies and medications to treat MH.
Dental Increasing numbers of children are undergoing dental procedures under general anesthesia in the hospital. Historically, general anesthesia was reserved for children with significant behavioral or other health issues. However, it has become recognized that general anesthesia in children carries lower risk than unmonitored sedation in the dentist’s office. In addition, general anesthesia allows for longer and more thorough procedures to be performed without discomfort. Because of
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these factors, dental procedures under anesthesia are increasingly being performed on otherwise healthy children. Historically, the most common scenario involving pediatric dentistry and general anesthesia has involved children with neurodevelopmental issues (e.g., autism, cerebral palsy), which prevent them from being able to hold still. Indeed, some children are so combative as to not be able to take oral sedative medication or cooperate in breathing from an anesthetic mask. At times, intramuscular medication (e.g., ketamine) is administered to sedate the children enough to bring them to the OR. Common dental procedures include crowns, fillings, and removal of carious primary (“baby”) teeth. After induction of anesthesia, nasal RingAdair-Elwyn (RAE) ETTs are typically inserted for intubation. This allows for a protected airway and better access to the teeth for the dentist. Commonly used equipment for these cases also includes Magill forceps, lubricant, nasal airways (used to test the patency and dilate the nasal passage prior to intubation), and oxymetazoline (Afrin).
Anesthesia and Sedation Outside of the Operating Room Because young children are unable to tolerate or remain still for many procedures, they are often sedated or anesthetized. For brief procedures that are not painful, children are often given various combinations of oral, nasal, or IV sedatives to tolerate the procedure. This is termed moderate sedation. For longer or painful procedures, children are given IV and/or inhalation medications that render them fully unconscious. Deep sedation is the term for children who are more lightly unconscious and able to easily breathe without any airway support. General anesthesia is a state of deeper unconsciousness without response to painful stimulation and often requires help maintaining airway patency. All sedated and anesthetized children need to be supervised and monitored by personnel with special training and experience in pediatric resuscitation and airway management. The minimum equipment required for either sedation or anesthesia includes Suction, Oxygen, appropriate Drugs, and Airway equipment (SODA). Drugs include sedatives, narcotics, muscle relaxants, cardiac resuscitation
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medications, and medications for anaphylaxis. Airway equipment includes O2 tubing, bag-mask ventilation supplies (e.g., Jackson Reece, Ambu), laryngoscopes, ETTs, tape, stylettes, oral and nasal airways, and LMAs.
■ SUMMARY Differences between adults and children include size, cognitive ability, physiology, and anatomy. Awareness of these differences and the availability of appropriately sized equipment and monitors have been associated with both diminished risk and diminished discomfort of surgery and anesthesia in children. Those working in a pediatric environment should be aware of these differences and familiar with the various sizes of all available equipment.
REVIEW QUESTIONS 1. When are most regional anesthesia procedures (epidurals, peripheral nerve blocks, etc.) performed on children? A) In the preoperative area with the patient sedated B) In the OR with the patient sedated C) In the OR with the patient under general anesthesia D) In the postanesthesia care unit (PACU) with the patient sedated E) Regional anesthesia is not indicated for pediatric patients Answer: C. Young children are less likely to understand procedures and may not be able to cooperate. Unlike adults, most regional procedures are performed under general anesthesia in the OR.
2. Concerning younger pediatric patients and IVs, which of the following statements is/are true? A) All air bubbles must be removed from the tubing. B) Microdrip tubing sets are preferred to macrodrip sets. C) Buretrols are used only for older/larger children. D) All of the above. E) A and B only. Answer: E. Young children, particularly those younger than 2 years, may have a patent foramen ovale. A patent foramen ovale can allow bubbles to pass directly from the right atrium into the left atrium and from there to the systemic circulation where they could cause a stroke or other ischemic phenomenon. Because children are much smaller than adults, the anesthesia provider must maintain a careful eye on the amount of fluids that are administered. Microdrip tubing and buretrols are both devices that allow better control of fluid administration than a standard macrodrip set.
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Chapter 46 • Pediatric Anesthesiology 3. To prepare for a pediatric general anesthetic, an anesthesiologist is likely to need what airway equipment? A) Oral airway, multiple sizes B) Laryngoscope blade, multiple sizes/styles C) ETT, multiple sizes—cuffed and/or uncuffed D) All of the above E) B and C only Answer: D. Similar to an adult general anesthetic, a full range of airway management equipment must be available for every anesthetic. The major difference will be making appropriate sizes of equipment available for the pediatric patient.
4. In comparing the HR and RR of infants and small children to those of adults, which of the following statement is true? A) HR faster, RR slower than adults B) HR slower, RR faster than adults C) HR slower, RR slower than adults D) HR faster, RR faster than adults E) Both HR and RR are similar to those of adults
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SUGGESTED READINGS Downes JJ, Raphaely RC. Anesthesia and intensive care. In: Ravich MM, et al., eds. Pediatric Surgery. 3rd ed. Chicago: Yearbook Medical Publishers; 1979. Kain ZN, Wang SM, Mayes LC, et al. Distress during induction of anesthesia and postoperative behavioral outcomes. Anesth Analg. 1999;88:1042–1047. Kain ZN, Mayes LC, Wang SM, et al. Postoperative behavioral outcomes in children: effects of sedative premedication. Anesthesiology. 1999;90(3):758–765. Rabbitts JA, Groenewald CB, Moriarty JP, et al. Epidemiology of ambulatory anesthesia for children in the United States: 2006 and 1996. Anesth Analg. 2010;111(4):1011–1015. Rackow H, Salanitre E, Green LT. Frequency of cardiac arrest associated with anesthesia in infants and children. Pediatrics. 1961;28:697–704.
Answer: D. Infants and children manifest several differences in their basic physiology and metabolic rate when compared to adults. Both the HR and the RR are higher in children than adults.
5. Compared to adults, which statement regarding children’s body temperature under general anesthesia is true? A) Decreases more slowly than adults B) Decreases more quickly than adults C) Pediatric ORs should be warmed and intraoperative warming devices routinely used D) A and C only E) B and C only. Answer: E. Compared to adults, infants have a much greater surface area to weight ratio and they are particularly prone to heat loss in the cold environment of the OR. Special attention needs to be paid to maintaining temperature balance in children, and this often includes warming the OR as well as active warming devices.
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CHAPTER
47
Obstetric Anesthesia Karen Hand ■ INTRODUCTION The aim of this chapter is to introduce the anesthesia technician to the care provided to obstetric patients by the anesthesia team in the delivery suite. The unique environment, the unique condition of pregnancy, and the particular challenges of provision of safe anesthesia care in this specialty area are considered. When elderly women are asked to name the most memorable day of their lives, the most common response is the day of delivery of their first child. The birth of a child is usually a joyful time, although the experience may be attended with fear, anxiety, and severe pain. Historically, and in parts of the world still, childbirth is associated with a high maternal mortality rate and an even higher neonatal mortality rate. The safety of childbirth has improved considerably in developed countries (Fig. 47.1). Nonetheless, for the fetus, delivery remains a time of high risk. Delivery may be complicated by known or previously unknown congenital medical problems, in utero growth problems, placental or umbilical cord accidents, obstruction of passage through the birth canal, and related injuries. For the mother, childbirth remains a significant cause of mortality and morbidity even in wealthy countries. Complications occur related to preexisting medical conditions in the mother, especially cardiac disease, and medical conditions arising as a result of pregnancy, such as venous thromboembolism, as well as diseases unique to pregnancy such as preeclampsia and amniotic fluid embolus. Hemorrhage remains a major cause of maternal mortality, even in the best of settings. There are also increased risks associated with anesthesia during pregnancy to be considered. The role of the anesthesia team on the labor and delivery suite is to provide labor analgesia, safe anesthesia for surgical procedures, both
elective and unplanned, and to respond to any emergencies as they arise, to ensure the safety of both the mother and child. Careful planning and preparation is the key to safe provision of anesthesia services on the delivery suite.
■ DESIGN OF OBSTETRIC UNITS Obstetric units are often remote from the main operating suite; indeed, they may be in distant buildings. Staffing assignments must ensure that adequate anesthesia coverage and technical support are available day and night. In rural settings and in small hospitals, anesthesia providers may not always be in-house at night. There will be a clear local policy as to acceptable times for delivery of anesthesia services, but the American Society of Anesthesiologists (ASA), American College of Obstetricians and Gynecologists (ACOG), and Joint Commission standard that must be met is that for emergency cesarean sections equipment and personnel should be adequate to ensure that a decision to incision interval of less than 30 minutes can be achieved. This means that anesthesia supplies must be ready and accessible at all times, operating rooms (ORs) must be prepared to receive a patient requiring an emergency cesarean section, and the anesthesia team should be prepared to provide anesthesia, including general anesthesia, at short notice. Although anesthesia technicians are an important part of the anesthesia team, many institutions do not provide a dedicated anesthesia technician to cover the obstetric suite. The delivery suite is usually set up with delivery rooms, in which the anesthesia team may be involved in providing labor analgesia for labor and forceps or vacuum deliveries, and ORs in which both elective and emergency procedures are performed, including cesarean section, manual removal of placenta, tubal ligation, cervical suture, and in some centers fetal in utero
456
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1000
Rate
*
800 600 400 200 0
1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 Year * Per 100,000 live births ■ FIGURE 47.1 United States maternal mortality rate by year (1900-1997). (Centers for Disease Control. Healthier mothers and babies. MMWR Morb Mortal Wkly Rep. 1999;48(38):849–856. Available from: http://www.cdc.gov/mmwr/PDF/wk/ mm4838.pdf. Accessed March 3, 2002.)
procedures. In some units, ORs may be shared with the main operating area.
■ MONITORING Facilities for monitoring in delivery rooms may be limited to noninvasive monitoring including noninvasive blood pressure and pulse oximetry. Obstetric nursing staff routinely monitor these parameters during labor, along with cardiotocography, which measures both the fetal heart rate and uterine contractions (Fig. 47.2). Fetal heart rate monitoring (analysis of cardiotocography patterns) allows assessment of the adequacy of uterine contraction and fetal well-being during labor. A normal fetal heart rate is between 110 and 160 beats per minute, with variability, and with “accelerations.” The monitor may also show “decelerations” of various types, the most ominous of which are frequent late decelerations, which means that the deceleration occurs after the peak of the contraction. This suggests that uteroplacental perfusion is compromised during the contraction and the fetus may be at increased risk of a poor outcome including neurologic damage and even death (Fig. 47.3). The decision to proceed with urgent cesarean section is frequently made on the basis of this monitoring. A sustained fetal bradycardia suggests that the supply of oxygen to the fetus remains impaired and is a clear emergency requiring immediate delivery. Advanced monitoring such as electrocardiogram (ECG), and arterial or central venous
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pressure monitoring, may be possible in the delivery room, although the training of obstetric nursing staff may limit its use. In addition, the supplies for these procedures are usually stocked in the OR, and not the delivery suite. During labor and delivery, there are very large changes in physiologic parameters as a result of pain and the metabolic demands of the contracting uterus; for example, cardiac output, already increased 50% percent by pregnancy itself, increases another 40% during labor and delivery. While labor analgesia is known to reduce such changes, for some patients safe delivery requires additional monitoring. Other options are the use of specialist obstetric nursing staff with additional training, intensive care nursing support, or the continuous presence of the anesthesiologist. It may be preferable for patients requiring invasive monitoring to deliver in an OR or an intensive care unit (ICU) setting. When invasive monitoring is required for labor, it is usually for patients with severe cardiac or other underlying disease. Arterial lines and central lines are used more frequently than pulmonary artery catheters. Occasionally, arterial pressure monitoring may be required for women with severe hypertension.
■ THE PHYSIOLOGIC CHANGES OF PREGNANCY The risks associated with general anesthesia are increased during pregnancy because of major physiologic changes occurring in the mother as
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■ FIGURE 47.2 Conditions for cesarean section, fetal distress, and persistent and consistent late decelerations indicating fetal distress.
a result of the pregnancy. These changes include the following: 1. An increased risk of aspiration of gastric contents because of decreased stomach emptying. 2. Increased oxygen consumption and decreased functional reserve capacity leading to rapid desaturation during induction of general anesthesia. 3. Increased edema. Difficult intubation is about ten times more common in the obstetric population, partly because of increased airway edema, and partly because of increased obesity, positioning difficulties, and the need for rapid sequence induction with cricoid pressure. 4. Aortocaval compression, leading to decreased venous return, decreased cardiac output, and hypotension in the supine position, particularly in the presence of central neuraxial blockade. The mass of the enlarged uterus and fetus compresses the vena cava and aorta. The patient should be positioned
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in left uterine displacement when supine, with a wedge under the right hip or the table tilted to ensure that the gravid uterus is moved away from these major blood vessels (Fig. 47.4). 5. When possible, general anesthesia is avoided during pregnancy. Maternal mortality figures show declining mortality associated with anesthesia, in line with decreasing use of general anesthesia, and increasing use of regional anesthesia. In addition, general anesthesia is associated with increased risks for the fetus.
■ LABOR ANALGESIA Neuraxial analgesia is both the most effective and least invasive option for labor analgesia. Lumbar epidurals are commonly used. Other options are spinals or combined spinal and epidural techniques (combined spinal epidural [CSE]). Optimal labor analgesia gives pain relief without motor blockade.
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■ FIGURE 47.3 An early deceleration mirrors the contraction, is caused by head compression, and is benign, requiring no intervention. A late deceleration mirrors the contraction but is offset because a late deceleration begins after the contraction has started and ends after the contraction has ended. The cause is uteroplacental insufficiency, and interventions are aimed at improving blood flow to the placenta.
Labor is divided into three stages. The first stage occurs when the uterus is contracting regularly and painfully and the cervix dilates. The second stage occurs when the baby descends through the birth canal and the mother actively pushes. The third stage is the delivery of the placenta. The pain of the first stage of labor is transmitted via nerves supplying the fundus and body of the uterus, from T10-L1, whereas the pain of the second stage of labor is transmitted via nerves supplied by sacral nerve roots S2-S4. The pain of labor is described as being among the most severe of all types of pain. Women’s expectations of the pain of labor are varied, as are their attitudes to analgesia. Some women plan for as much analgesia as possible, while others aim for minimal analgesia, or only
noninvasive techniques (Table 47.1). Labor pain is particularly severe in the later first stage, as the cervix approaches full dilation. This may coincide with both mental and physical exhaustion, leading many to request epidural analgesia at this stage. The pain of labor is unique in pain treatment, in that provision of as much analgesia as possible is not necessarily what the patient desires. Many women want to feel contractions to be able to time pushing. The labor epidural rate is approximately 60%. Some women, particularly with psychological preparation, do very well with minimal analgesia. However, others benefit enormously from neuraxial analgesia. Some women will be advised that a labor epidural is the safest option for them, particularly if they are
■ FIGURE 47.4 Left lateral tilt to relieve aortocaval compression. (From MacDonald MG, Seshia MKK, et al. Avery’s Neonatology Pathophysiology and Management of the Newborn. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005, with permission.)
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TABLE 47.1 TECHNIQUES OF LABOR ANALGESIA COMPLEXITY, INVASIVENESS
EXAMPLES
ADVANTAGES/DISADVANTAGES
Least invasive
Relaxation techniques: breathing, massage, visualization
Effective, especially in early labor, education helpful
Water birth Transcutaneous electrical nerve stimulation (TENS) Acupuncture Intermediate Most invasive
Opioids: e.g., meperidine, fentanyl Nitrous oxide/oxygen
Used in some centers, requires scavenging
Epidural
Very effective, some contraindications
Spinal
Limited duration
Combined spinal and epidural
Flexible, quick-onset analgesia, increased risk of meningitis
at high risk of needing to be delivered by cesarean section, or if they have particular medical conditions.
Labor Epidurals General aspects of the procedure for siting an epidural are described in Chapter 21. The anesthesia provider must review the patient’s medical history, and examine the patient, including her airway and heart and lungs. The patient must give informed consent, after review of complications such as dural puncture headache, temporary or permanent nerve injury, infection and bleeding, as well as immediate risks such as hypotension. Full equipment for resuscitation must be available, including a tipping bed (capable of being put in the Trendelenburg position), suction apparatus, oxygen, and a code cart. Standard packs for epidurals, spinals, and CSEs are very helpful, as is a well-stocked, lockable, mobile cart. The ASA Practice Guidelines for Obstetric Anesthesia suggest that laryngoscopes and assorted blades, endotracheal tubes and stylets, a self-inflating bag and mask, medication for blood pressure support, muscle relaxation, and hypnosis, a carbon dioxide detector, and a pulse oximeter should all be available during the initial provision of neuraxial anesthesia. The epidural cart must be checked regularly, restocked, and outdated drugs and equipment replaced. Patients often have family members accompanying them during labor. If a family member is to accompany the patient during the procedure,
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it may be prudent to insist that they are seated, because vasovagal episodes are common. Good sterile technique is vital during epidural placement. The delivery room is a less sterile environment than an OR. Surfaces such as tables must be cleaned before use as a workstation. Hand washing with surgical scrub solution, caps, masks covering the nose and mouth, sterile gloves, individual packets of skin preparation, and sterile draping are all recommended. Chlorhexidine is preferred. A gown may be worn. The patient must have a functioning intravenous cannula and should have received 500 mL of intravenous crystalloid to prevent hypotension. She is positioned sitting or in the lateral fetal position. Positioning the parturient can be difficult, both anatomically and because of pain, and it may be difficult for her to keep still during contractions. Monitoring will include noninvasive blood pressure and pulse oximetry. Immediate Complications of Labor Epidurals After placement of the epidural catheter, an initial test dose of lidocaine with epinephrine is usually given. Immediate complications associated with epidural placement include both predictable responses to dosing an epidural catheter with local anesthetic solution and complications caused by incorrect location of the epidural catheter. The test dose is intended to identify misplacement of the catheter. Local anesthetic placed in the epidural space anesthetizes pain
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fibers but also sympathetic nerve fibers, which maintain vascular tone. Even when the catheter is correctly located in the epidural space, the patient may develop hypotension secondary to blockade of sympathetic nerve fibers, and this may occur with the test dose or with subsequent doses of local anesthetic. Aortocaval compression is an important contributing factor and predisposes laboring patients to become hypotensive with regional anesthesia. Hypotension may cause maternal nausea and vomiting, but in most healthy women, the most serious effect is likely to be on the fetus. Altered uterine artery blood flow may cause fetal bradycardia. Occasionally, if the fetal heart rate does not improve with changes in maternal position, oxygen, boluses of fluid, and drugs such as ephedrine or phenylephrine, the patient may need to be moved to the OR emergently for delivery by emergency cesarean section. High or Total Spinal Epidural catheters should always be aspirated to check for cerebrospinal fluid. However, occasionally a catheter is inadvertently placed intrathecally (through the dura and into the subarachnoid space), and its misplacement is not suspected. If a test dose of 3 mL of 1.5% lidocaine with epinephrine is administered into the cerebrospinal fluid in the subarachnoid space, the error will usually be obvious, with motor blockade, a higher sensory level than expected, and maternal hypotension. If intrathecal placement is not recognized and a large dose of local anesthetic is given, it is possible to develop a “high spinal” or “total spinal,” with severe hypotension, breathing difficulties or apnea, and loss of consciousness, as progressively higher spinal levels and ultimately the brain are anesthetized. This is an emergency requiring immediate measures to secure the airway, ventilate, restore blood pressure, and deliver the fetus. An unconscious obstetric patient who has stopped breathing should be ventilated with a mask and Ambu bag, and cricoid pressure should be applied while preparations are made for intubation. Ephedrine and phenylephrine are first-line drugs for the treatment of hypotension. Left uterine displacement should never be forgotten. Atropine and epinephrine should also be readily available. Preparations should be made to transfer the patient to the OR for immediate delivery if there
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are signs of fetal distress. It should be noted that the upper limit of the epidural space is at the foramen magnum. A high epidural block will not anesthetize the brain, but high spinals can. Intravascular Epidural Catheter Placement An epidural catheter located in an epidural vein may become apparent when a test dose of local anesthetic with epinephrine is given. The patient is asked to report any symptoms she notices, and her heart rate is observed. An increase in maternal heart rate of more than 15 beats per minute is considered a positive test because the intravenous epinephrine can raise the heart rate. However, heart rate changes with contractions are very common in labor, so the test dose may be less reliable in pregnancy. If local anesthetic is injected into a blood vessel instead of being slowly absorbed from the epidural space, toxic levels of local anesthetic may occur. The major consequences of a toxic dose of local anesthetic are neurologic and cardiac. Early symptoms of local anesthetic toxicity include tingling of the lips or tongue, because of the high blood supply to this area, and ringing in the ears. Such early signs are not always present, and the presentation may be with seizures secondary to central nervous system toxicity, arrhythmias or cardiac arrest. If a patient suffers a cardiac arrest, particularly after a dose of bupivacaine, advanced cardiac life support (ACLS) protocols should be followed, although resuscitation may need to be prolonged because bupivacaine binds tightly to cardiac myocytes. Intralipid has been reported to be valuable in displacing bupivacaine from its binding sites on the heart and should be available.
■ CESAREAN SECTION Cesarean section is a very common operation, with 32% of babies currently delivered by cesarean section in the United States. Indications for elective cesarean section include prior cesarean section, breech presentation, twins, cephalopelvic disproportion, and maternal request. Indications for unplanned cesarean section include dysfunctional labor and fetal intolerance of labor. Regional anesthesia for cesarean section includes spinal, epidural, and CSE techniques. General anesthesia is usually reserved for emergency situations when the life of the mother or fetus is in immediate danger and the fetus needs
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to be delivered as quickly as possible, or situations when there is a contraindication to regional anesthesia.
Spinal Anesthesia A detailed description of the procedure for subarachnoid anesthesia is given in Chapter 21. Spinal anesthesia is often the technique of choice for uncomplicated elective cesarean sections. The patient should have a freely running intravenous cannula of at least 18G. She will usually have already received 1 L of crystalloid to offset the anticipated vasodilation from a spinal, and she will receive a drink of sodium citrate to reduce the risk of aspiration pneumonitis. At a minimum, blood pressure and pulse oximetry are monitored during placement, which is often performed in the seated position. The obstetric team will monitor the fetal heart rate. Intrathecal local anesthetic is usually supplemented with opioid drugs, including fentanyl and preservative-free morphine. Obstetric patients are particularly prone to dural puncture headache; therefore, small gauge Whitaker and Sprotte-type needles (25G or smaller) are preferred. The most common early complication of subarachnoid blockade is maternal hypotension. Cesarean section requires extensive dermatomal blockade to ensure maternal comfort during the surgery. The patient will develop a dense motor block, and on testing, the block level will often extend from the sacral dermatomes to as high as T2, and there will be a rapid-onset sympathectomy, sometimes accompanied by bradycardia as the cardiac acceleratory fibers are blocked. Blood pressure should be monitored frequently initially, and the ECG should be placed. Careful attention should be paid to the patient, who will often demonstrate perioral pallor or complaints of nausea, even before the blood pressure cuff confirms a drop in pressure. Alteration in uterine blood flow is a major concern. The fetus should be monitored during this time, and the response to developing hypotension should be prompt, because even small drops in maternal blood pressure can have detrimental effects on the fetus. Spinal hypotension usually responds to fluid, phenylephrine, and ephedrine, and these should be readily available. Increasing left uterine displacement may be necessary. Obstetric patients do not usually receive sedation, and it is important for all staff in the OR to
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be aware of this. It is common practice for the patient to have a support person of her choice accompanying her during cesarean sections performed under regional anesthesia. Visitors are not usually brought into the OR if the patient is to receive general anesthesia, and will be asked to leave if the patient requires conversion to general anesthesia The extent and quality of the subarachnoid block are checked carefully before surgical incision. Delivery of the neonate usually proceeds promptly, although scarring and adhesions from prior procedures can slow delivery considerably. Following delivery of the baby, uterotonics will usually be given to help contract the uterus to prevent blood loss. Oxytocin is the drug most commonly used, usually as an infusion. A pressure bag or infusion pump may be useful. Drug errors are a particular problem in obstetric anesthesia. Talking to the patient and her partner can be distracting for the anesthesia provider. Vomiting, hypotension, pain, or bleeding may require urgent interventions, which also make errors more likely. The anesthesia cart and anesthesia machine should be tidy and well organized at all times, and particular attention should be paid to routines intended to minimize the risk of errors.
Epidural Anesthesia for Cesarean Section Epidural anesthesia is most commonly used for cesarean section in patients who have a functioning labor epidural in place. Epidural blockade can usually be rapidly extended to provide adequate anesthesia for cesarean section with administration of additional boluses of local anesthetic. In addition, an epidural catheter may be placed de novo in preference to a subarachnoid block for several reasons. Increments of local anesthetic can be given slowly, in a manner that minimizes the risk of severe hypotension. This is particularly important for patients who would not tolerate a rapid onset of sympathectomy, such as those with cardiac disease. Placement of an epidural catheter also allows the duration of neuraxial blockade to be extended, which is essential if a case is expected to be prolonged.
Combined Spinal Epidural A CSE combines the benefits of both spinal and epidural anesthesia and is an excellent option
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for many patients. The spinal component can include a standard subarachnoid dose of local anesthetic or a smaller dose, which can then be extended as necessary using the epidural catheter, the advantage being less risk of hypotension than with a standard subarachnoid block, but quicker onset and denser sacral block than with an epidural. An additional advantage of the epidural catheter is that it can be used to extend the duration of block. The disadvantage of this technique is the increase in complexity.
General Anesthesia General anesthesia is usually reserved for patients for whom regional anesthesia is contraindicated, and for emergencies necessitating very rapid delivery of the fetus, if the mother does not have a functioning epidural in place. Common examples of contraindications to regional anesthesia in obstetrics include cardiovascular instability, coagulation abnormalities, and sepsis. Examples of fetal emergencies include cord prolapse and abruption. Preparation of equipment is vital to ensuring that general anesthesia can be provided to obstetric patients safely. The anesthesia machine must be fully checked, including the breathing circuit, suction tubing, and suction apparatus. A common but potentially disastrous error is forgetting to replace suction tubing between cases. Airway equipment should be prepared ahead of time including laryngoscopes, a choice of blades, oral and nasal airways, an intubating bougie, and endotracheal tubes. Endotracheal tubes of a smaller size than standard are usually chosen, because of the airway edema often occurring in pregnancy. For an average size woman, a size 6.0 or 6.5 tube might be selected. For many anesthesiologists, video laryngoscopy (e.g., Glidescope) has become the technique of choice in situations where standard laryngoscopy is unsuccessful, although the use of this device has not been widely studied in obstetric patients. A difficult airway cart should be readily available. The ASA Practice Guidelines for Obstetric Anesthesia provide suggestions as to the contents of a portable storage unit, including alternative choices of rigid laryngoscope blades, laryngeal mask airways, endotracheal tube guides, retrograde intubation equipment, a device for emergency nonsurgical airway ventilation such as a supraglottic airway and a hollow jet ventilation stylet with transtracheal jet ventilator, fiber-optic
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intubation equipment, and emergency surgical airway access equipment, such as a cricothyroidotomy kit. It should be noted that obstetric patients presenting for emergency section are at high risk for difficult airways. Medications required for rapid sequence induction must be immediately available. Sodium pentothal is the classic induction agent described. Propofol and etomidate are more frequently used today. Ketamine is another option. Succinylcholine is the muscle relaxant of choice in most cases. Other emergency drugs such as atropine, epinephrine, ephedrine, and phenylephrine should also be readily available. When the decision is made to proceed with emergency cesarean, achieving the ASA, ACOG, and Joint Commission standard of decision to incision interval of less than 30 minutes demands excellent teamwork. All personnel should be alerted promptly and should respond as quickly as possible. A team effort to move the patient into the OR and onto the operating table rapidly and safely is important. During transfer intravenous lines must be protected. The obstetric team may reassess the situation on arrival in the OR, including reevaluating the fetal heart rate tracing or repeating the vaginal examination, or may begin immediate preparation for cesarean section, including placing a urinary catheter, cleansing the abdomen with surgical antiseptic solution, and placing sterile drapes. During these preparations the anesthesia team will proceed expeditiously, but without compromising safe anesthesia practices. Whenever possible, the anesthesia team will have seen and assessed the patient previously, although it may be necessary to perform a rapid history and examination. It is vital that the patient is properly positioned on the operating table, with her head on the adjustable headpiece, and with elevation of her head and shoulders such as to achieve the “sniffing the morning air” intubating position. Proper patient positioning is especially important in pregnancy because of enlarged breasts, increased obesity, and increased incidence of difficult intubation. Left uterine displacement must not be omitted. For most healthy women, induction of general anesthesia is accomplished with a rapid sequence induction with cricoid pressure. Pregnant women are assumed to have a full stomach. If they have been in labor, have received opioids, or have eaten, they are at particular risk of aspiration
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of gastric contents. Sodium citrate is given to reduce the acidity of stomach contents. Standard ASA monitors are applied. Suction apparatus is placed within easy reach. The patient is preoxygenated. Preoxygenation is with four vital capacity breaths or 3 minutes of breathing 100% oxygen with a good seal around the mask on the patient’s face. To minimize exposure of the fetus to anesthetic gases, induction is delayed until the obstetrician is ready to make the skin incision, although surgery will not begin until induction is complete and the airway secured. Cricoid pressure is applied during induction of anesthesia and must not be removed except at the anesthesiologist’s request. After induction, maintenance of anesthesia is usually with an inhalational agent at one half minimum alveolar concentration (MAC), with 50% nitrous oxide, until delivery of the fetus, then 70% nitrous oxide. In pregnancy, the MAC for inhalational agents is reduced, it is desirable to minimize anesthetic effects on the fetus, and inhalational agents relax uterine muscle, which may increase bleeding. However, cases of awareness under anesthesia have been reported during cesarean sections. Neurophysiologic monitoring may be helpful to monitor anesthetic depth (see Chapter 41). At the end of surgery the patient can usually be extubated. Assessment of residual neuromuscular blockade is very important. The patient should usually be extubated fully awake, with intact protective airway reflexes, to minimize the risk of aspiration. The patient should be recovered in a safe location by qualified staff. The risk of airway complications is as high during emergence and recovery as on induction, with complications arising related to problems such as airway edema, bronchospasm, pulmonary edema, and residual muscle relaxation. Local policies may distinguish between recovery after general anesthesia and regional anesthesia. In the event of a failed intubation, the ASA’s difficult airway algorithm is adapted for obstetric patients to allow the anesthesiologist to take account of the needs of the fetus. In the event of a failed intubation, two questions determine what should happen: 1.
2.
Is surgery required for an emergency that is an immediate threat to the life of the mother or the fetus? Is it possible to ventilate the patient?
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In a situation other than an emergency posing an immediate threat to the life of the mother or the fetus, in most cases the patient will be woken up, and either intubated awake using advanced airway techniques or a regional technique will be employed. The increased risk of aspiration in obstetric patients makes awake fiber-optic intubation preferable to asleep fiber-optic intubation in most cases. If the patient can be ventilated using a mask and airway or laryngeal mask airway, in a lifethreatening emergency situation it is acceptable to proceed with the surgery, maintaining cricoid pressure if that does not interfere with ventilation. If the patient cannot be ventilated with optimal techniques and cannot be woken up, an emergency surgical airway will be necessary.
■ OTHER OBSTETRIC EMERGENCIES Emergencies in the context of emergency cesarean section have been discussed, as have emergencies related to epidurals. In this section, seizures, hemorrhage, embolic events, and cardiac arrest will be considered. Hypertensive disorders, hemorrhage, and embolic disorders are major direct causes of maternal mortality and may present as these types of emergencies on the delivery suite.
Seizures Seizures occurring in obstetric patients may be caused by eclampsia, although epileptic seizures are also common. Eclampsia is a condition that only occurs in pregnancy, and the postpartum period. A seizure may be the first sign of the disorder, although it is frequently preceded by preeclampsia, which is defined as hypertension and proteinuria occurring after the 20th week of pregnancy. In severe preeclampsia, there are signs and symptoms of end-organ damage in multiple organ systems, including the central nervous system, which may progress to seizures. Severe hypertension in itself may be an emergency requiring immediate management with intravenous medication, and occasionally invasive monitoring. The treatment of eclampsia is oxygen, airway support as necessary, and magnesium. Magnesium is very effective in stopping eclamptic seizures, and particularly in preventing a second seizure. Eclamptic seizures are usually self-limiting. Intubation is not usually required, although airway equipment should be
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available and prepared. Benzodiazepines are the first-line drugs in epileptic seizure management but are usually avoided in eclampsia because they increase postictal sedation and increase the risk of airway complications.
Hemorrhage Hemorrhage in obstetric patients can be catastrophic. Hemorrhage is classified as antipartum or postpartum (before and after delivery respectively). Antipartum causes of hemorrhage include abruption, when the placenta separates prematurely from the wall of the uterus, placenta previa, where the placenta is abnormally situated over the cervical opening, and uterine rupture. Postpartum hemorrhage may be caused by uterine atony (failure of the uterus to contract), or retained placental products or blood clots, which prevent the uterus from contacting down in the usual manner, leaving large blood vessels open and bleeding. By the end of pregnancy, the blood flow to the uterus is increased to 1 L per minute, and so hemorrhage can be rapid. Hemorrhage may be the presenting problem when a patient arrives emergently at the hospital, may develop unexpectedly during or after cesarean section, and may occur unexpectedly after a normal vaginal delivery. The expected blood loss after a vaginal delivery is 500 mL, with 1,000 mL at cesarean section. Unusually rapid bleeding, or more than 700 mL or 1,200 mL, respectively, should prompt preparation for management of massive hemorrhage. Equipment for the management of massive hemorrhage must be assembled quickly. It will be a matter of local policy what equipment is kept on the delivery suite versus in a central location. Additional intravenous access must be secured promptly. Equipment for arterial and central line placement and monitoring should be available, including an ultrasound machine. In some cases, very large bore access, such as introducers for pulmonary artery catheters or trauma lines are required. A rapid infusion device may be necessary. Intravenous fluid warmers and a forced air body warmer should be available and applied early to prevent hypothermia. Blood should be immediately available, including O negative blood. Good communication with the transfusion service is vital. In cases of massive hemorrhage, obstetric patients can rapidly develop coagulation abnormalities.
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It may become necessary to give fresh frozen plasma and cryoprecipitate, as well as red blood cells. The use of the cell saver has been limited in obstetrics because of concerns regarding the infusion of amniotic fluid particles, although it is becoming more widely used. It appears that cell savers can be used safely in obstetric patients providing amniotic fluid is suctioned away from the field and the field is thoroughly irrigated first. An additional leukocyte depletion filter may be used as well. Cell savers may also be helpful in Jehovah’s witnesses who decline other blood products. In cases of uterine atony, drugs used to improve uterine contraction include oxytocin, methylergonovine (Methergine), misoprostol, and prostaglandin F2 alpha (Hemabate). Embolization of a uterine artery can be an effective way of halting obstetric hemorrhage. In this case, the patient may need to be transferred to the interventional radiology suite. An anesthesia machine should be prepared in that location along with monitoring equipment and equipment for managing hemorrhage, while preparations are made to transfer the patient. In some cases, the obstetrician may need to perform a hysterectomy to control hemorrhage. When the likelihood of massive hemorrhage is high, or if a patient develops massive hemorrhage after leaving the obstetric unit, management in the main operating suite may be preferable, if staffing and equipment are more easily accessible. In some cases, the placenta may be known to abnormally adhere to the uterine wall, and may even invade the uterine muscle or other organs. This is known as placenta accreta, increta, or percreta, with placenta percreta being invasion of other organs such as the bladder or bowel. This may necessitate a planned cesarean-hysterectomy, which may be scheduled in a main OR location.
Embolism Venous thromboembolism is more common in obstetric patients because of changes in coagulation factors during pregnancy, as well as mechanical obstruction of venous return by the pregnant uterus. Pulmonary embolus may present as chest pain, shortness of breath, or even cardiac arrest, at any stage of pregnancy, with a particular risk in those with abnormal blood clotting and after cesarean section.
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Amniotic fluid embolus is specific to pregnancy. Classically, this is described as sudden cardiovascular collapse, cyanosis, mental status changes, or massive hemorrhage in a parturient with forceful contractions, although it can occur at any time. Fetal cells from amniotic fluid are forced into the maternal circulation and can be found in the pulmonary vascular bed postmortem. The condition has a very high mortality for both mother and fetus. More recent research suggests that there may be an anaphylactoid response to amniotic material, rather than a mechanical obstruction of blood vessels. Treatment of amniotic fluid embolus includes management of cardiac arrest and support of the cardiovascular system, delivery of the fetus, management of hemorrhage, and support of the cardiovascular system. The patient is likely to require full invasive monitoring and ICU care if she survives the acute event.
Cardiac Arrest in Pregnancy Cardiac arrest is rare in pregnancy. Causes include underlying cardiac disease, embolic disease, massive hemorrhage, anaphylaxis, and toxic doses of local anesthetic. In an obstetric patient, ACLS guidelines should be followed, but in addition left uterine displacement should be instituted immediately. Aortocaval compression by the gravid uterus severely impairs venous return to the heart and hinders successful resuscitation. The outcome for the fetus is likely to be poor. However, to improve the chances of survival for the mother, the fetus should be delivered if a perfusing rhythm has not been reestablished after 4 minutes. To deliver the fetus rapidly, it should be possible to perform a cesarean section at the bedside, calling for personnel and the cesarean section tray as quickly as possible.
■ SUMMARY Obstetric emergencies can be extremely difficult to manage. This is because of the rapidity with which a situation can change from routine to emergency and error to care for two patients simultaneously, the mother and the fetus. As mentioned previously, anesthesia technicians are important members of the anesthesia team. All technicians who may be called to assist with a procedure or emergency in the obstetric suite should be familiar with the general layout, anesthesia machine, airway equipment, and vascular
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access equipment available in the obstetric suite. This is especially true if the anesthesia technician only occasionally works in the obstetric department. Obstetric anesthesia is a very rewarding specialty area in which to work. The anesthesia technician can be of great assistance as part of the anesthesia team as he or she provides labor analgesia and anesthesia for cesarean sections in what are often rapidly evolving situations, particularly by ensuring that equipment is well stocked and maintained, and by responding rapidly to emergencies as they arise.
REVIEW QUESTIONS 1. The following statements regarding obstetric units are true EXCEPT A) Obstetric units may be isolated. B) Obstetric units must have access to an OR 24 hours per day. C) ASA standards are relaxed on the obstetric unit. D) Anesthesia technicians should be familiar with the anesthesia equipment on the obstetric unit. E) The ASA provides guidance as to the contents of the difficult airway cart. Answer: C. Despite the unique environment and isolated nature of the obstetric suite, ASA standards for monitoring and care of patients still apply. In addition, the ASA provides guidance as to contents of a difficult airway cart. Obstetric surgical emergencies can occur at any time and access to an OR 24 × 7 is critical. Because emergencies are not uncommon on the obstetric unit, anesthesia technicians should be familiar with the operation and location of all anesthesia equipment on the obstetric unit.
2. For labor epidurals, which of the following statements is TRUE? A) The patient can deliver at home. B) The technique for placing labor epidurals is substantially different than placement for nonlaboring patients. C) The epidural must be discontinued if the patient requires a cesarean section. D) A test dose is not necessary for labor epidurals. E) Full equipment and facilities for resuscitation must be available. Answer: E. The placement and conduct of epidurals are essentially the same in laboring and nonlaboring patients. Placement requires qualified personnel in an appropriate setting with resuscitation equipment immediately available.
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Chapter 47 • Obstetric Anesthesia 3. Which of the following statements regarding tracheal intubation during pregnancy is FALSE? A) The rate of failed intubation is increased. B) Airway edema may make intubation more difficult. C) Cricoid pressure is not necessary in pregnant patients. D) The risk of aspiration is increased during pregnancy. E) Advanced airway equipment should be readily available in the obstetric suite. Answer: C. Pregnant patients are at an increased risk for difficult airway management and aspiration. Rapid sequence inductions with cricoid pressure are the general rule. Emergency airway equipment should be readily available.
4. All of the following are examples of obstetric emergencies EXCEPT A) Uterine atony B) Massive hemorrhage C) Fetal distress D) Failed intubation E) All of the above are obstetric emergencies Answer: E. All of the above are obstetric emergencies and require a coordinated team effort for a successful outcome.
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SUGGESTED READINGS American Society of Anestheiologists Task Force on Infectious Complications Associated with Neuraxial Techniques Practice advisory for the prevention, diagnosis, and management of infectious complications associated with neuraxial techniques: a report by the American Society of Anestheiologists Task Force on Infectious Complications Associated with Neuraxial Techniques. Anesthesiology. 2010;112(3):530–545. American Society of Anesthesiologists Task Force on Obstetric Anesthesia. Practice guidelines for obstetric anesthesia: an updated report by the American Society of Anesthesiologists Task Force on Obstetric Anesthesia. Anesthesiology. 2007;106:843–863. Singh GK. Maternal Mortality in the United States, 1935–2007: Substantial Racial/Ethnic, Socioeconomic, and Geographic Disparities Persist. A 75th Anniversary Publication. Health Resources and Services Administration, Maternal and Child Health Bureau. Rockville, Maryland: U.S. Department of Health and Human Services; 2010. Hauth JC, Merenstein GB. Guidelines for Perinatal Care. 4th ed. Elk Grove Village, IL: American Academy of Pediatrics and American College of Obstetricians and Gynecologists; 2002:147. Sullivan I, Faulds J, Ralph C. Contamination of salvaged maternal blood by amniotic fluid and fetal red cells during elective cesarean section. Br J Anaesth. 2008;101(2): 225–229.
5. A “code” is called on an obstetric patient on the delivery suite. Which of the following is TRUE? A) ACLS protocols do not apply. B) The baby should be delivered immediately. C) Defibrillation is contraindicated in pregnancy. D) Chest compressions are contraindicated in pregnancy. E) The patient should be placed in left uterine displacement. Answer: E. Aortocaval compression by the uterus significantly impairs venous return and compromises cardiopulmonary resuscitation. ACLS protocols apply, although with some modifications, including the recommendation that the baby be immediately delivered if the resuscitation is not successful within the first 4 minutes of cardiac arrest.
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CHAPTER
48
Anesthesia Considerations for Out of Operating Room (OOR) Locations Andrew J. Pittaway and Karen J. Souter ■ INTRODUCTION An “out of operating room” (OOR) location is an area located at some variable distance from a hospital’s operating rooms (ORs). In the last two decades, there has been considerable expansion in the services provided at OOR locations and consequentially the need for general anesthesia (GA) and sedation in these areas is growing exponentially. There are a number of synonyms for the term OOR including “anesthesia at alternate sites,” “non–operating room anesthesia,” and “remote location anesthesia.” In this chapter, we will use the terms OOR and “out of operating room anesthesia” (OORA). An OOR location may be a site within a large hospital that is separated from the general OR suite but is within the same hospital. This could include a cardiac catheterization laboratory (CCL), a radiology suite, or a gastrointestinal (GI) endoscopy suite. Alternatively, the OOR location may be a site that is completely separate from a main hospital with no OR facilities, such as a dental clinic or a radiation therapy unit. Office-based anesthesia also falls within this category, but it will not be discussed in this chapter. The most significant concern for the anesthesiologist related to OORA is providing patient care in a location where he or she does not routinely work. OOR areas are often unfamiliar to the anesthesiologist. The anesthesiologist may work in OOR locations infrequently. The personnel are not the ones the anesthesiologist works with on a regular basis, and they may not be as acquainted with anesthesia care as OR personnel. The equipment, including the anesthesia machine, cart, and available drugs, are often different or in different locations than those in the OR. This unfamiliar environment
requires extra vigilance to provide safe care. It is in the OOR arena that the skill and expertise of a trained anesthesia technician is perhaps most valued and the partnership between an anesthesiologist and technician is most important.
■ GENERAL PRINCIPLES The scope of cases performed in the OOR arena covers a wide range of procedures performed on an increasingly diverse group of patients. There are a wide variety of techniques, equipment, and approaches to be considered, and it is easy for the anesthesia team to become distracted. A simple three-step approach is suggested to help you remain focused and to avoid omitting any important aspects of the patient’s care (Table 48.1). When providing anesthesia services in an OOR location, always consider each of the following very carefully: • The environment • The patient • The procedure
■ THE ENVIRONMENT Considerations related to the environment of the OOR location include the following: • Diagnostic and imaging equipment • Provision of standard anesthetic equipment • Availability of appropriate anesthesia monitors including invasive monitors • Constraints related to diagnostic and therapeutic imaging techniques • Unfamiliarity of OOR technical staff with anesthesia requirements • Environmental hazards posed to anesthesia staff, especially ionizing radiation
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TABLE 48.1 A THREE-STEP APPROACH TO ANESTHESIA IN OUT OF OPERATING ROOM LOCATIONS ENVIRONMENT
PROCEDURE
PATIENT
Anesthetic machine and monitors • Availability • Maintenance • Familiarity Resuscitation equipment • Ambu bag • Suction • Code cart + Defibrillator OOR personnel • Familiarity with anesthesia • Training in emergencies Technical equipment hazards • Radiation safety • Magnetic resonance concerns (magnetic field noise) • Temperature control • Allergic reactions Postanesthesia care Transport to and from OOR
Diagnostic or therapeutic duration Level of discomfort/pain Position of patient Special requirements (e.g., functional monitoring) Potential complications Surgical support
Ability to tolerate sedation vs. general anesthesia ASA grade Comorbidity(ies) Airway assessment IV access Allergies—IV contrast Monitoring requirements—simple vs. advanced Pediatric considerations Postanesthesia care
ASA, American Society of Anesthesiologists; IV, intravenous; OOR, out of operating room.
Diagnostic Imaging Equipment OOR locations generally contain large heavy, immobile equipment used for procedures such as fluoroscopy, magnetic resonance scanning, and computed tomography (CT). Fluoroscopy is widely used in many OOR locations, including interventional radiology, cardiac catheterization, and in the gastroenterology suite. Fluoroscopy is a technique used to obtain realtime moving images of the internal structures of a patient by using a fluoroscope. The patient is positioned between the x-ray source and the fluorescent screen and by coupling the fluoroscope to an x-ray image intensifier and video camera the images can be recorded and played on a monitor. Large C-shaped mobile fluoroscopy devices (C-arms) are used to provide images in multiple dimensions; these are moved back and forth around the patient and take up large amounts of space. Advances in technology have resulted in increasingly complex imaging techniques for both diagnostic and therapeutic purposes.
Anesthetic Equipment The American Society of Anesthesiologists (ASA) Standards and Practice Parameters
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Committee issued guidelines for standards to be followed for all non-OR procedures involving anesthesiology personnel. These are outlined in Table 48.2. The Joint Commission requires that patients undergoing anesthesia or sedation receive the same care in OOR sites as they would in the OR. The anesthesia equipment and monitors in the remote location should be of the same standard as in the main OR. This creates a dilemma because OOR sites may only require anesthesia services intermittently. The anesthesia equipment, drugs, and monitors may be left in the OOR site for use when needed or all this equipment may be brought in each time an anesthetic is required. In areas where anesthesia is required on a fairly regular basis (at least 3-4 times a week) equipping and maintaining the OOR site with basic anesthesia equipment that can be quickly supplemented for a case is a reasonable model. However, problems may occur with this setup. Anesthesia equipment left in the OOR site may be damaged as a result of nonanesthesia personnel moving it, tampering with it, and/or borrowing pieces and not replacing them. Anesthesia machines and other anesthesia-related equipment need regular maintenance and can easily be overlooked if they are kept in
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TABLE 48.2 ASA GUIDELINES FOR MINIMAL STANDARDS OF CARE FOR ANESTHESIOLOGY PERSONNEL PROVIDING CARE IN NON–OPERATING ROOM LOCATIONS STANDARD/REQUIREMENT
COMMENTS
1. Oxygen—A reliable source of oxygen adequate for the length of the procedure
• Piped oxygen is strongly encouraged. • Prior to the anesthetic, the capacities, limitations, and accessibility of the oxygen supply must be considered. • Backup oxygen—at least a full E cylinder is essential.
2. Suction—A reliable and adequate source of suction
• Suction standards should meet OR requirements.
3. Scavenging—Where inhalation anesthetic agents are used, an adequate and reliable system for scavenging waste gases is required.
• Extra lengths of tubing may be required to reach the patient.
4. Resuscitation Equipment—A self-inflating hand resuscitator bag capable of administering at least 90% oxygen as a means to deliver positive pressure ventilation; an emergency cart with defibrillator, emergency drugs, and equipment to provide CPR must be immediately available.
• MH cart and difficult airway carts should also be available.
5. Anesthetic Drugs and Supplies
• A supply of all the standard anesthetic drugs as well as emergency rescue drugs. Ideally, a cart similar to those used in the OR.
6. Anesthetic Equipment
• A functional anesthesia machine, ideally similar to those used in the OR.
7. Monitoring Equipment
• Adequate monitoring equipment to meet the ASA standards for basic monitoring. Invasive monitoring equipment may also be required.
8. Electrical Outlets—The location must have sufficient electrical outlets to satisfy anesthesia machine and monitoring equipment requirements.
• Clearly labeled outlets connected to an emergency power supply must also be available. In a “wet location,” isolated electrical power or electrical circuits with ground fault interrupters should be provided.
9. Illumination—Adequate illumination of the patient, the anesthesia machine, and monitors is required.
• Backup illumination must be available.
10. Space—Sufficient space must be available to accommodate the equipment and personnel and allow expeditious access to the patient, anesthesia machine, and monitors 11. Trained Anesthesia Support Staff—Adequately trained support staff and a reliable means of two-way communication. 12. Building And Safety Codes—These must always be observed. 13. Postanesthesia Management—Appropriate care for patients recovering from anesthesia must be provided together with trained recovery staff and facilities for safe transport of patients to the postanesthesia care unit. CPR, cardiopulmonary resuscitation; MH, malignant hyperthermia; OR, operating room.
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an area not routinely serviced by anesthesiology technicians. Hospitals may be reluctant to finance state-of the-art anesthesia equipment for a site where it is used infrequently and often the older machines are “retired” to the OOR site. This can create problems, as anesthesia personnel may not be familiar with anesthesia machine and monitors if they are different than the ones routinely used in the OR. Additionally drugs left in a remote site may go out of date if not used regularly. The alternative solution is to bring all the anesthesia equipment, drugs, and monitors into the OOR each time an anesthetic is required. A number of small portable anesthesia machines are available for this purpose; this is a more practical approach if anesthesia is performed infrequently. This setup does require extra preparation time; it is easy to forget essential equipment requiring anesthesia staff to make multiple trips back to the central anesthesia supply room. The development of a standard anesthesia cart containing all the necessary equipment that is restocked after every case and the use of checklists for all the drugs and equipment to bring each time an OOR anesthetic is required are essential. Checklists and preprepared carts will help the anesthesia technician prepare for an OOR anesthetic quickly and efficiently. It is also important for the anesthesiologist and technician to communicate ahead of time to make sure extra equipment such as special monitors or advanced airway devices are readily available if the case requires them. The provision of anesthesia in the magnetic resonance imaging (MRI) suite is a special situation. The presence of a strong magnetic field prohibits the use of any equipment containing ferrous metal. Specially developed anesthesia machines, monitors, and ancillary equipment are available for use in the MRI scanner.
Constraints Related to Imaging Techniques In a regular OR the anesthesia station is usually well laid out with plenty of space so the anesthesia team has easy access to the patient and monitors. This may not be the case in an OOR site. Frequently, the anesthesia team, equipment, and monitors are crammed in around the bulky radiology equipment, and this may limit
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■ FIGURE 48.1 OOR location with radiology equipment and a limited anesthesia workspace.
the anesthesiologist’s access to the patient, especially in an emergency (Fig. 48.1). The imaging techniques often require the patient to be moved in and out of the imaging device or to have the fluoroscopic imaging equipment move around the patient’s body. This is particularly true in neuroradiological procedures and in CT and MRI. It is extremely important to make sure the anesthesia circuitry, intravenous (IV) lines, urinary catheters, and monitoring cables are all of sufficient length to accommodate the patient moving back and forth on the imaging table. If breathing circuit and IV line lengths are not checked prior to starting the procedure, they are at risk of being dislodged with potentially disastrous results. Other challenges related to space and layout of the OOR site include the need for the anesthesiology team to be shielded from radiation. Transparent leadlined screens are positioned to protect the anesthesia team, but these may limit access to the patient.
Out of Operating Room Staff In the OR, the nursing and technical staff are all very familiar with the role of the anesthesia team and are available to help in any anesthetic emergency. In the remote OOR sites, technical and nursing staffs have different skill sets and may not be so familiar with the conduct of anesthesia or how to help in an emergency. It is vital that the anesthesiologist has experienced anesthesia technical support immediately available to help and provide the correct equipment rapidly
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in case of emergencies. One area where both the anesthesiology technician and the anesthesiologist can bring additional value to the OOR sites is to lead team communication and efforts to train OOR staff in emergency protocols. The whole team needs to know where the code cart with defibrillator and resuscitation drugs is located; these items need to be checked daily. All the staff working in OOR areas should be able to provide support and help manage emergencies such as cardiac arrest, airway emergency, and anaphylaxis. The management of anaphylaxis is particularly important, as patients may be allergic to the IV contrast media used in a number of radiological procedures. Although OOR personnel’s lack of familiarity with anesthesia emergencies can be a serious problem, they may also not be familiar with procedures that are routine in the OR. For example, patient positioning and padding are closely monitored in the OR, whereas OOR personnel may not be familiar with proper positioning and padding techniques for the lateral or prone position.
Environmental Hazards Anesthesiology personnel are at risk from exposure to radiation every time they provide patient care in an OOR location that uses fluoroscopy or CT scanners. It is vitally important that all personnel are informed about the risks of radiation and the procedure to avoid exposure. The two most effective methods anesthesiology personnel can use to prevent occupational exposure to radiation are to (1) ensure they wear high-quality protective garments and (2) monitor their cumulative exposure using dosimetry badges. The risks of exposure to radiation are well known. Radiation directly damages cells in a dose-dependent manner, resulting in cell death. In addition, radiation causes defects in cellular DNA resulting in gene mutations, which can lead to the development of cancer, infertility, and in pregnant women, to fetal abnormalities. Recently, the eye has been recognized as being particularly vulnerable to radiation. Lens opacities and cataract formation are a significant risk for radiologists and other personnel working in radiology suites. Occupational exposure to radiation is carefully controlled and regulated by the National Council on Radiation Protection (NCRP). Personal dosimeters are small badges containing x-ray film; they are used to measure
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the radiation dose received. It is recommended that at least two dosimeters be worn, one under the lead apron and one at the collar above the lead apron. This allows an estimate of the amount of radiation delivered to unshielded areas as well as the integrity of protective lead aprons. It is important for the anesthesia team to be aware of, and to participate in, dosimetry monitoring if they routinely work in the radiology suite. The greatest source of radiation exposure for the anesthesiology team is scatter from the patient rather than being in the direct line of the x-ray beam. Controlling the dose delivered to the patient helps to reduce exposure for the staff, and protective shielding provides further protection. There are three types of shielding: 1. Shielding built into the wall of the procedure room. 2. Equipment-mounted shields: These include protective drapes that are suspended from the table or ceiling between the x-ray generating equipment and the staff. 3. Personal protective devices: These include lead aprons, thyroid shields, eyewear, and gloves; these should be worn by all staff. The added weight of the leaded aprons can increase fatigue in staff, and lightweight aprons made of metals such as barium, tin, antimony, and tungsten are available. Thyroid shields and leaded goggles should also be worn. Ordinary corrective eyeglasses offer very minimal protection to the eye from the damaging effects of radiation. Protective eyeglasses should have large lenses and side shields. Gloves are more important for the actual radiologist whose hands may be directly in the path of the radiation beam rather than the anesthesiology team who need to preserve their manual dexterity.
Temperature Control In most OOR sites, the temperature is maintained at low levels because of the excess heat generated by the technical equipment. Anesthetized or sedated patients are very susceptible to hypothermia, and care must be taken to ensure patients are adequately warmed. On the other hand, in interventional cases, patients may be completely covered by drapes and overheating is a risk; it is important therefore that body temperature is monitored in all patients.
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Anaphylactic Reactions Injectable dyes, known as contrast media, are used during many radiological procedures to enhance the imaging techniques. Radio-opaque materials contain iodine, and the agents used in MRI contain gadolinium and manganese. Side effects and reactions to these agents are relatively common including nausea and vomiting, urticaria, hoarseness, dyspnea, facial edema, and hypotension. Occasionally, a patient can develop an anaphylactic reaction to these substances requiring full resuscitation and the institution of cardiac arrest protocols (see Chapter 64 ).
■ PATIENT CONCERNS IN THE OOR ENVIRONMENT The procedures undertaken in OOR sites are for the most part not particularly painful; however, they often require the patient to remain motionless for long periods. The proceduralist may request the help of the anesthesia team to provide sedation or GA to ensure the patient remains completely still. Many patients experience anxiety and claustrophobia particularly when presented with the enclosed spaces of the CT or MRI scanners. It is not unusual for patients to request some form of sedation to make these experiences less frightening. The great expansion in therapeutic radiological procedures has meant that treatment options are being offered to patients who previously would have been considered too sick to withstand surgical treatment. Thus, many patients who present for OOR procedures have significant comorbidities and need expert anesthesia care throughout.
■ COMMON OOR PROCEDURES Table 48.3 outlines the common procedures that may require anesthesia or sedation in OOR locations. It is important for the anesthesiology team to understand each procedure and the conditions needed for optimum imaging and/or for fast and effective therapeutic interventions.
Radiological Procedures Radiological procedures include noninvasive imaging techniques such as CT, MRI, and interventional radiological (IR) procedures. Computed Tomography CT scanners produce a cross-sectional image of the body in a few seconds, and so for the most
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TABLE 48.3 COMMON PROCEDURES THAT MAY REQUIRE ANESTHESIA IN OUT OF OPERATING ROOM LOCATION Radiology • Computed tomography • Magnetic resonance imaging • Interventional radiology (including interventional neuroradiology) • Radiofrequency ablation Gastrointestinal (GI) endoscopic procedures (GI endoscopy) • Esophagogastroduodenoscopy (EGD) • Endoscopic retrograde cholangiopancreatography (ERCP) • Colonoscopy • Transjugular intrahepatic portosystemic shunt (TIPS) Interventional cardiology • Cardiac catheterization • Electrophysiology (EP)
part imaging sequences are fast. Most adult patients can tolerate CT scanning without anesthesia or sedation. More recently, radiologists are using the CT scanner to guide more invasive procedures such as abscess localization and drainage and radiofrequency tumor ablation in lung, liver, or metastatic cancers. These more invasive activities take longer and can be painful, and so patients may need sedation or anesthesia to tolerate the procedure. The CT scanner is also used for imaging in patients who are severely injured or who are undergoing intensive therapy on the intensive care unit (ICU). In both cases, these patients are at risk of becoming acutely unstable in the CT scanner and anesthesia support may be required to provide safe care while these very sick patients undergo scanning. During the scan very high levels of radiation are generated, 1,000 times or more than produced by a simple x-ray, and staff are at risk if they remain in the scanner with the patient during the scan. For patients undergoing sedation or GA, the anesthesia team will be able to monitor the patient from the shielded control room using standard monitors. When planning the anesthetic technique, the team needs to remember that there will be a delay in accessing the patient if an emergency occurs. The airway should be properly secured ahead of time especially if there is any suspicion that it may be difficult to manage in an emergency. Sick, unstable patients must
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receive resuscitation prior to being taken into the scanner. Resuscitation efforts in the CT scanner will be hampered by the confined space and can be extremely difficult. Magnetic Resonance Imaging (MRI) Briefly, when the atoms of hydrogen are subjected to a powerful magnetic field, they line up with the field. Subsequent exposure of these protons to a radiofrequency pulse changes their energy state and when the radiofrequency pulse is discontinued the protons drift back to their original low energy state. As they do this they emit energy, which is detected by the MR scanner and is translated into images. The more powerful the magnetic field the better images can be produced. The magnetic field in an MR scanner is continually present; to turn it off is associated with considerable “down” time and other potential hazards. The MR scanner is housed in a shielded room in a more isolated part of the hospital to prevent outside radiofrequencies from interfering with the MRI and to isolate the magnetic field. Surrounding the MR scanner is a so-called fringe field where the field strength gradually declines; concentric lines representing the declining field strength are often marked on the floor of the scanner room. For example, the 5G line marks the point beyond which pacemakers are considered safe and syringe pumps will operate up to the 30G line. Any objects containing iron will be attracted to the magnet, and anesthesia equipment such as oxygen tanks, IV poles, and laryngoscopes will become dangerous projectiles if brought within the vicinity of the magnet (within the 50G line). Fatalities have occurred; thus, access to the MR scanner is strictly controlled. Implanted medical devices are also a source of concern; cardiac pacemakers in particular can stop functioning in the presence of the magnetic field and implants such as aneurysm clips may be dislodged with disastrous consequences. All patients need to complete an exhaustive checklist questionnaire before they enter the scanner to make sure they have none of these devices in their bodies. Medical personnel need to be aware of these constraints for their own personal protection, and they must leave objects such as pagers, badges, and pens at the entry to the MR scanner. The MR scanner
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is a long, narrow cylinder and many patients experience claustrophobia or anxiety on being placed inside it; to compound this issue, the scans themselves often last for at least 45 minutes. Many adults and most young children require some form of sedation or even GA to tolerate the procedure and ensure immobility. If a patient moves during the scan, it will need to be repeated, wasting valuable scanning time in the busy MRI schedule, which in many units may run 24/7. Standard anesthesia machines and monitors cannot be used in the MR scanner, and a number of MRI-compatible machines are available with aluminum oxygen cylinders and MRI-compatible components. In addition, patient-monitoring devices, syringe pumps, and IV poles also need to be MR compatible. MRI-compatible monitors are for the most part as effective as the standard ones although the electrocardiogram (ECG) signal can be distorted and difficult to read in the magnetic field. To avoid the risks of bringing ferromagnetic objects such as laryngoscopes and other pieces of anesthesia equipment too close to the scanner, the standard procedure is for the anesthesia team to initiate sedation or induce anesthesia and secure the airway in a preparation area outside the MR scanner away from the fringe field. The patient is then transferred to an MR-compatible gurney, MR-compatible monitors are attached, and the patient is transported into the scanner and hooked up to the MR-compatible anesthesia machine. In planning the anesthetic technique, the anesthesia team must be aware that once started the MR imaging sequence takes several minutes to shut down. It is important that the airway is appropriately secured; in patients with more difficult airways, placing a definitive airway (such as an endotracheal tube or LMA™) at the beginning of the procedure will avoid the need to rescue the airway in challenging circumstances later on. Unlike other radiological imaging, MRI does not produce harmful radiation and is considered safe for patients and staff. Side effects do occur, however, including peripheral nerve stimulation resulting in tingling and discomfort, and even diaphragmatic stimulation. Patients and staff may experience vertigo, nausea, and a metallic taste in the mouth. There is currently some debate about whether safety
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standards need to be imposed. As the stronger 3T scanners become more widespread, this may become more of an issue. The noise generated by the MR scanner is another important consideration for both patients and staff. To protect against the noise, all patients are provided with earplugs. The anesthesia team must remember to insert these for the unconscious patient before he or she is transported into the scanner and remove them afterward. If the anesthesia team chooses to remain in the scanner with the patient (as may be the case for pediatric patients), they too need to wear earplugs. Another safety concern is the electrical current and heat that can be generated by the magnetic field. During scanning heat-generating electric currents may build up around loops of wire particularly those in the various patient monitors. Care should be taken with placement of the ECG electrodes and other wires to prevent the risk of tissue burns. Patients with large tattoos containing ferromagnetic inks may also be at risk of burns. Interventional Radiology Fluoroscopy is the mainstay of IR and in recent years the discipline has expanded rapidly. With great skill and expertise interventional radiologists can place microcatheters into most of the larger blood vessels in the body. This allows the injection of radio-opaque dye for diagnostic imaging and for a large number of therapeutic procedures that previously required invasive surgery or were simply not possible. These procedures include the following: • Revascularization of a blocked vessel, such as a carotid artery in a patient at risk of stroke • Insertion of a stent to maintain the patency of a previously blocked vessel • Embolization of a vessel or vascular malformation that is acutely bleeding or at risk of rupture such as a cerebral aneurysm • Embolization of a vessel that is feeding a malignant tumor prior to surgery to reduce bleeding The expertise of interventional radiologists is usually focused in one particular area of the body; for example, neuroradiologists work on the cerebral and spinal blood vessels and more general interventionalists work on major vessels in the abdomen, liver, kidney, and extremities.
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While the anatomy and pathology of the diseases treated by these various interventional radiologists differ widely, there are a number of commonalities in all IR procedures. Access to the patient’s arteries and/or veins is gained in most patients via the femoral vessels in the groin. In patients with disease of these vessels, other blood vessels may be accessed such as the subclavian artery or vein or internal jugular vein, although this is uncommon. Occasionally, a surgical cut-down is required to access the vessels. Access to the blood vessel is first gained using a small needle (in some cases, ultrasound guidance may be used) and once the needle is identified in the correct vessel, a thin flexible wire is inserted through it and the small needle is removed. With the wire resting in the target blood vessel, the radiologist dilates the opening to the vessel using a wide-bore sheath, usually 6 or 7 French gauge. This technique is known as the “Seldinger” technique after Dr. Sven-Ivar Seldinger, the radiologist who first developed it in 1953. The Seldinger technique is used widely throughout medicine as a safe way of accessing a blood vessel or other structure without having to use a large needle from the outset. Once the radiologist has accessed the blood vessel, he or she will advance a series of microcatheters into the blood vessel(s) of interest using fluoroscopy guidance. The radiologist will inject radio-opaque dye along the path of the blood vessels to make an image of these vessels. This image is then superimposed on the radiologist’s fluoroscopy screen to act as a “road map” for accessing the blood vessel(s) of interest. The patient is positioned on a moving x-ray table surrounded by the imaging equipment. The imaging equipment is static although it can rotate around various axes to provide different views of the patient. As the catheter is advanced from the groin to the vessels of interest, the table and the patient are moved so the progress of the microcatheter can be closely observed. As a result, the patient is frequently moved back and forth and to the side. The importance of closely watching the anesthesia circuits, monitoring equipment, and IV tubing so they are not dislodged cannot be overemphasized. In order to make sure the road map matches the path of the microcatheter, it is vital that the patient remains completely still and in most cases GA is preferred. In some cases, the movement of the patient’s chest may interfere
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Section V • Operating Room and Hospital Environment
with the procedure, and at certain stages of the procedure, the radiologist will ask the anesthesiologist to “hold the breathing” by turning off the ventilator for a short period. The positioning of monitors, especially ECG electrodes, must be carefully considered. If the ECG leads or electrodes overlie the area being imaged, they can produce radiological shadows and artifacts that interfere with the procedure. In neuroradiological procedures, the metallic spring in the cuff of the endotracheal tube may obscure the view of a cerebral vessel. Large amounts of the IV contrast dye may be used during an IR procedure. These compounds act as diuretics, making a Foley catheter a requirement for most of these procedures.
Interventional Cardiology The range of procedures and interventions performed by cardiologists is becoming increasingly complex and technically challenging and is being offered to increasingly sick patients. There are two main areas where interventional cardiology procedures are performed: the CCL and electrophysiology laboratory (EPL). While much of the work in these sites may be performed without sedation or using mild sedation undertaken by the CCL and EPL team, there is an increasing requirement for anesthesiology services to be involved. The general considerations related to providing anesthesia in an OOR location apply. Both the EPL and the CCL contain large amounts of technical monitoring and imaging equipment. Fluoroscopy is used for imaging the heart and the coronary blood vessels. In a similar manner to other IR procedures, the access point for the catheters is mostly the femoral vessels in the groin. If this access point is not available, the subclavian or internal jugular veins may be accessed. Cardiac Catheterization Laboratory Interventional procedures carried out by interventional cardiologists in the CCL include the following: • Percutaneous coronary interventions (PCIs) • Percutaneous insertion of ventricular assist devices (VADs) • Percutaneous closure of septal defects • Percutaneous heart valve repair and replacement
WoodWorth_Chap48.indd 476
Electrophysiology Laboratory The main procedures performed in the EPL are catheter ablations and insertion of implantable cardiac pacemakers. Cardiac ablation is an invasive procedure performed to remove an aberrant or faulty electrical pathway in patients with cardiac arrhythmias such as atrial fibrillation, atrial flutter, supraventricular tachycardias (SVT), and Wolff-Parkinson-White (WPW) syndrome. A flexible catheter is advanced from the femoral vein into the heart and high-frequency electrical impulses are used to induce the arrhythmia. Once the aberrant part of the cardiac conduction pathway is identified, it can be ablated. These procedures are extremely long, lasting on average 6-8 hours but have very high success rates. Apart from having to lie still for many hours, patients generally tolerate these procedures well with just mild sedation. Minimal sedation may be provided by the EPL team, although in certain circumstances the anesthesia team will need to be involved. This is usually in patients who have significant comorbidities such as congestive cardiac failure or airway concerns that exceed the limits of applicable sedation protocols followed by nurses and proceduralists. In some cases, cardiac arrhythmias induced during the procedure require cardioversion for termination; when this happens, sedation needs to be deepened so that the patient can tolerate the unpleasant sensation of receiving a direct current (DC) shock. The anesthesiology team needs to be aware of the progress of the procedure to be able to anticipate the need for changing the level of sedation; additionally they should avoid sympathomimetic drugs, which may interfere with mapping the aberrant cardiac foci. The technology related to cardiac pacemakers has seen much development in recent years. Implantable cardioverter-defibrillators (ICDs) are used increasingly to deliver immediate defibrillation in patients at risk for ventricular tachycardia (VT) or ventricular fibrillation (VF). Biventricular pacemakers are complex devices that attempt to mimic the normal cardiac contraction cycle to provide improved cardiac function. Pacemakers are increasingly being inserted into patients with multiple comorbidities and significant cardiac pathologies, including diminished ejection fraction (
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