Massachusetts General Hospital Clinical Anesthesia Procedures PDF

Handbook of Clinical Anesthesia Procedures of the Massachusetts General Hospital TENTH EDITION Senior Editor Richard M. Pino, MD, PhD, FCCM Associate Editors Edward A. Bittner, MD, PhD, FCCM Hovig V. Chitilian, MD Wilton C. Levine, MD Susan A. Vassallo, MD Department of Anesthesia, Critical...

Handbook of Clinical Anesthesia Procedures of the Massachusetts General Hospital TENTH EDITION Senior Editor Richard M. Pino, MD, PhD, FCCM Associate Editors Edward A. Bittner, MD, PhD, FCCM Hovig V. Chitilian, MD Wilton C. Levine, MD Susan A. Vassallo, MD Department of Anesthesia, Critical Care, and Pain Medicine Harvard Medical School Massachusetts General Hospital Boston, Massachusetts 1 Copyright Acquisitions Editor: Keith Donnellan Senior Development Editor: Ashley Fischer Editorial Coordinator: Sean Hanrahan and Oliver Raj Marketing Manager: Kirsten Watrud Production Project Manager: Justin Wright Design Coordinator: Stephen Druding Manufacturing Coordinator: Beth Welsh Prepress Vendor: TNQ Technologies 10th edition Copyright © 2022 Wolters Kluwer. Copyright © 2016 Wolters Kluwer. Copyright © 2010, 2007 Lippincott Williams & Wilkins, a Wolters Kluwer business. Copyright © 2002 Lippincott Williams & Wilkins. Copyright © 1998 Lippincott-Raven. Copyright © 1994 JB Lippincott. All rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, 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. To request permission, please contact Wolters Kluwer at Two Commerce Square, 2001 Market Street, Philadelphia, PA 19103, via email at [email protected], or via our website at shop.lww.com (products and services). 9 8 7 6 5 4 3 2 1 Printed in China Library of Congress Cataloging-in-Publication Data ISBN-13: 978-1-975154-40-0 Cataloging in Publication data available on request from publisher. This work is provided “as is,” and the publisher disclaims any and all warranties, express or implied, including any warranties as to accuracy, comprehensiveness, or currency of the content of this work. This work is no substitute for individual patient assessment based upon healthcare professionals’ examination of each patient and consideration of, among other things, age, weight, gender, current or prior medical conditions, medication history, laboratory data and other factors unique to the patient. The publisher does not provide medical advice or guidance and this work is merely a reference tool. Healthcare professionals, and not the publisher, are solely responsible for the use of this work including all medical judgments and for any resulting diagnosis and treatments. Given continuous, rapid advances in medical science and health information, independent professional verification of medical diagnoses, indications, appropriate pharmaceutical selections and dosages, and treatment options should be made and healthcare professionals should consult a variety of sources. When prescribing medication, healthcare professionals are advised to consult the product information sheet (the manufacturer’s package insert) accompanying each drug to verify, among other things, conditions of use, warnings and side effects and identify any changes in dosage schedule or contraindications, particularly if the medication to be administered is new, infrequently used or has a narrow therapeutic range. To the maximum extent permitted under applicable law, no responsibility is assumed by the publisher for any injury and/or damage to persons or property, as a matter of products liability, negligence law or otherwise, or from any reference to or use by any person of this work. shop.lww.com 2 3 Contributors Mark Abraham MD* Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Christopher M. Aiudi MD, PharmD Resident in Anesthesia, Department of Anesthesia, Critical Care, and Pain Medicine , Massachusetts General Hospital , Boston, Massachusetts Daniel Ankeny MD, PhD Instructor in Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Cliodhna Ashe MD Resident in Anesthesia Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Aditi Balakrishna MD Assistant Professor Harvard Medical School Department of Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Xiaodong Bao MD, PhD Assistant Professor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital , Boston, Massachusetts Diana Barragan-Bradford MD Fellow in Critical Care Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts William Benedetto MD Assistant Professor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Gloria Nadayil Berchmans MD Resident in Anesthesia Department of Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Sheri M. Berg MD Assistant Professor of Anesthesia Harvard Medical School Director of PACU Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Edward A. Bittner MD, PhD, MSEd, FCCM Associate Professor of Anesthesia Harvard Medical School Program Director, Critical Care-Anesthesiology Fellowship Associate Director, Surgical Intensive Care Unit Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Juan M. Cotte Cabarcas MD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine , Massachussets General Hospital , Boston, Massachusetts Shika Card MD, MA Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Andrew N. Chalupka MD Assistant Professor of Anesthesia Senior Associate Consultant Department of Anesthesiology and Perioperative Medicine Mayo Clinic Rochester, Minnesota Marvin G. Chang MD, PhD , Instructor of Anesthesia, Harvard Medical School , Assistant Program Director, Critical Care Anesthesiology Fellowship, Department of Anesthesia, Critical Care and Pain Medicine , Massachusetts General Hospital , Boston, Massachusetts Frances K. W. Chen MD Resident in Anesthesia, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Jenny Zhao Cheng MD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts 4 Hovig V. Chitilian MD , Assistant Professor of Anesthesia , Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine , Neurosurgical, Vascular, and Thoracic Division Chief, Massachusetts General Hospital , Boston, Massachusetts Kate Cohen MD Instructor of Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine , Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts Devan Cote MD Resident in Anesthesia, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Jennifer Cottral MD Instructor of Anesthesia Harvard Medical School Department of Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Stephanie L. Counihan MSN, CRNA Staff Nurse Anesthetist, Massachusetts General Hospital, Department of Anesthesia, Critical Care, and Pain Medicine, Boston, Massachusetts Jerome Crowley MD, MPH* Instructor of AnesthesiaHarvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Adam A. Dalia MD, MBA, FASE Assistant Professor of AnesthesiaHarvard Medical School, Division of Cardiac Anesthesia , Department of Anesthesiology, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Michelle Dyrholm DO Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Dan Ellis MD Instructor of AnesthesiaHarvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine , Massachusetts General Hospital, Boston, Massachusetts Michael R. Fettiplace MD, PhD Resident, Department of Anesthesia, Critical Care and Pain Medicine , Massachusetts General Hospital , Boston, Massachusetts Gregory H. Foos MD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital , Boston, Massachusetts Hilary Gallin MD Resident in Anesthesia Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Erica L. Gee MD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine , Massachusetts General Hospital , Boston, Massachusetts Philipp Gerner MD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Gregory E. Ginsburg MD Assistant Professor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital , Boston, Massachusetts Paul D. Guillod MD Resident in Anesthesia, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Casey Hamilton MD Resident in Anesthesia , Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts David Hao MD Resident in Anesthesia, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Evan Hodell MD Resident in Anesthesia, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Ryan J. Horvath MD, PhD Instructor of AnesthesiaHarvard Medical School, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Omar Hyder MD, MS Instructor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Oluwaseun Johnson-Akeju MD, MMSc Anesthetist in Chief Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Alexander S. Kuo MS, MD Assistant Professor , Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Jean Kwo MD Assistant Professor in Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General 5 Hospital, Boston, Massachusetts Maximilian Frank Lang MD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital , Boston, Massachusetts Stephanie Lankford CRNA Certified Registered Nurse Anesthetist, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Thomas J. Lavin DO Resident in Anesthesia, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Johanna Lee MD Resident in Anesthesia Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Wilton C. Levine MD Assistant Professor of Anesthesia Harvard Medical School Medical Director Perioperative Services Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Jason M. Lewis MD Instructor of Anesthesia, Harvard Medical School, Director, Clinical Operations, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Rupeng Li MD, PhD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Lucy T. Li MD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts James Taylor Lloyd MD Instructor of Anesthesia Harvard Medical School Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Ying Hui Low MD Instructor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts Christopher J. Mariani MD, PhD Resident in Anesthesia Department of Anesthesiology, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts John Marota MD, PhD Associate Professor Harvard Medical School Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Lukas H. Matern MD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Joseph L. McDowell MD Instructor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine , Massachusetts General Hospital , Boston, Massachusetts Rebecca D. Minehart MD, MSHPEd Assistant Professor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Ilan Mizrahi MD Instructor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Miguel A. Patino Montoya MD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Jeremi Mountjoy MD Instructor of Anesthesia Harvard Medical School Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Eleanor M. Mullen MSN, CRNA Staff CRNA, Department of Anesthesia, Critical Care, and Pain Medicine, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts Alexander Nagrebetsky MD, MSc Assistant Professor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, 6 Boston, Massachusetts John H. Nichols MD Instructor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Raissa Quezado da Nobrega MD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Peter O. Ochieng MD Resident in Anesthesia, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Riccardo Pinciroli MD Instructor , Harvard Medical School, Research Staff, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Richard M. Pino MD, PhD, FCCM* Associate Professor of Anesthesia, Harvard Medical School, Division Chief, Critical Care, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Triffin J. Psyhojos MD Instructor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care, and Pain Medicine , Massachusetts General Hospital, Boston, Massachusetts Jason Zhensheng Qu MD , Assistant Professor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine,, Massachusetts General Hospital , Boston, Massachusetts Katarina Ruscic MD, PhD Instructor of Anesthesia Harvard Medical School Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts A. Sassan Sabouri MD Assistant Professor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Kyan C. Safavi MD, MBA Assistant Professor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Aubrey Samost-Williams MD, MS Instructor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine , Massachusetts General Hospital, Boston, Massachusetts Kendrick Shaw MD, PhD Instructor of Anesthesia, Harvard Medical School, Department of Anesthesia, Pain, and Critical Care Medicine, Massachusetts General Hospital, Boston, Massachussetts Jamie L. Sparling MD Instructor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Peter Stefanovich MD Assistant Professor of Anesthesia Harvard Medical School Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Rachel Steinhorn MD Cardiovascular Fellow, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Matthew W Vanneman MD Instructor of Anesthesia Harvard Medical School Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Susan A. Vassallo MD Associate Professor of AnesthesiaHarvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Rafael Vazquez MD Assistant Professor of AnesthesiaHarvard Medical School, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Elisa C. Walsh MD Resident in Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine , Massachusetts General Hospital , Boston, Massachusetts Jeanine P. Wiener-Kronish MD Distinguished Professor, Henry Isaiah Dorr Professor of Anesthetics and Anesthesia, Harvard Medical School, Emeritus Chair, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Shauna Williams CRNA Staff CRNADepartment of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts 7 Samuel Wood MD Resident in Anesthesia, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Jared R. B. Wortzman MD* Instructor of Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Nancy M. Wu MD Assistant in Anesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts Luca Zazzeron MD Resident in Anesthesia Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts 8 Preface Dr. Richard Kitz, as the Anesthetist-in-Chief at Massachusetts General Hospital, had a vision for a “manual of anesthetic practice that was written primarily by recent house staff” that was “intended to be the foundation of practical knowledge for the inexperienced or incompletely trained anesthetist.” The goal was to have each chapter written by a resident mentored by a faculty member. Although Dick is no longer with us, the legacy that he started in the 1970’s continues today with the 10th edition of Clinical Anesthesia Procedures of the Massachusetts General Hospital. These chapters have been passed on from generation to generation with updating to meet the needs of our ever-changing specialty. This 10th edition has several new features. Each senior author of the previous edition was given a choice to write a new chapter with the hope that new authors would significantly update each chapter as needed rather than just making minor edits of previous ones. Several of the chapters now have online links to videos and graphics. Anesthesia at MGH is conducted as a care team of residents, CRNAs, fellows, and staff anesthesiologists. Several of the chapters in this edition are now coauthored by a CRNA who has expertise of the subject matter. Finally, this edition was written almost entirely during the COVID-19 pandemic. During this time, all of the authors were administering to the needs of incredibly sick patients with respiratory and multisystem organ failure. The Tenth edition continues to focus on clinical fundamentals that are required for the safe administration of anesthesia and perioperative care. Each chapter reflects the current clinical practice at MGH that is the foundation of our residency and fellowship programs. It is designed to be an easily accessible and accurate source of information for practicing anesthesiologists, CRNAs, anesthesia assistants, learners in anesthesia and other disciplines, medical students, and healthcare professionals interested in perioperative care. The information should be augmented with consultation of other in-depth published works and online sources. I wish to gratefully acknowledge the many past editors of, and contributors to, the previous editions of this handbook. I have enjoyed working with Sean Hanrahan, Ashley Fischer, Oliver Raj, and Keith Donnellan at Wolters Kluwer. My executive assistant, Amanda Bourgeois, has been indispensable throughout the planning and organization of this book, communicating with the publishing staff, and “gently reminding” my colleagues to submit the chapters on time. During the writing of this book and the COVID-19 pandemic, the support of our families was essential for maintaining some semblance of normalcy. Thanks to my wife, Patti, and son, Daniel, for their continued love and support. I have been privileged to work with my mentors and friends, Hassan Ali, MD, and Jeanine Wiener-Kronish, MD. Thirty years ago, I purchased the third edition of Clinical Anesthesia Procedures of the Massachusetts General Hospital during an anesthesia elective with Mack Thomas, MD, at LSUMC in New Orleans. I am forever grateful for his teaching, enthusiasm that inspired me to become an anesthesiologist and critical care physician, and his continued friendship. Richard M. Pino, MD, PhD, FCCM 9 10 Contents Contributors Preface PART I: EVALUATING THE PATIENT BEFORE ANESTHESIA 1 Evaluating the Patient Before Anesthesia Michelle Dyrholm and Kate Cohen 2 Basics of Echocardiography Thomas J. Lavin and Alexander S. Kuo 3 Specific Considerations With Cardiac Disease Adam A. Dalia and Casey Hamilton 4 Specific Considerations With Pulmonary Disease Riccardo Pinciroli, Jeanine P. Wiener-Kronish and Rachel Steinhorn 5 Specific Considerations With Renal Disease Katarina Ruscic and Cliodhna Ashe 6 Specific Considerations With Liver Disease Mark Abraham and Jerome Crowley 7 Specific Considerations With Endocrine Disease Aubrey Samost-Williams and Jennifer Cottral 8 Infectious Diseases and Infection Control in Anesthesia Diana Barragan-Bradford and Jamie L. Sparling PART II: ADMINISTRATION OF ANESTHESIA 9 Safety in Anesthesia Miguel A. Patino Montoya and Rebecca D. Minehart 10 The Anesthesia Machine Samuel Wood and Jeremi Mountjoy 11 Administration of General Anesthesia Luca Zazzeron and Kendrick Shaw 12 Intravenous and Inhalation Anesthetics Juan M. Cotte Cabarcas and Gregory E. Ginsburg 13 Airway Evaluation and Management Gregory H. Foos and Jean Kwo 14 Neuromuscular Blockade Aditi Balakrishna and Matthew W. Vanneman 15 Monitoring Christopher M. Aiudi and Kyan C. Safavi 16 Monitoring Anesthetic Brain States Johanna Lee and Oluwaseun Johnson-Akeju 17 Intra-anesthetic Problems Frances K. W. Chen, Ying Hui Low, and Alexander Nagrebetsky 18 Perioperative Hemodynamic Control Devan Cote and William Benedetto 19 Local Anesthetics Michael R. Fettiplace and Xiaodong Bao 11 20 Spinal, Epidural, and Caudal Anesthesia Erica L. Gee and Joseph L. McDowell 21 Regional Anesthesia Lucy T. Li, Shika Card, and A. Sassan Sabouri 22 Anesthesia for Orthopedic Surgery Susan A. Vassallo, Philipp Gerner, and Shauna Williams 23 Anesthesia for Neurosurgery Eleanor M. Mullen and Daniel Ankeny 24 Anesthesia for Spine Surgery John Marota and Raissa Quezado da Nobrega 25 Anesthesia for Transplant Surgery Elisa C. Walsh and Hovig V. Chitilian 26 Anesthesia for Abdominal Surgery David Hao and Triffin J. Psyhojos 27 Anesthesia for Thoracic Surgery Peter O. Ochieng and Ryan J. Horvath 28 Anesthesia for Vascular Surgery Christopher J. Mariani and James Taylor Lloyd 29 Anesthesia for Cardiac Surgery Maximilian Frank Lang and Jason Zhensheng Qu 30 Anesthesia for Head and Neck Surgery Nancy M. Wu and Jason M. Lewis 31 Anesthesia for Urologic Surgery Jenny Zhao Cheng and Dan Ellis 32 Anesthesia for Obstetrics and Gynecology Hilary Gallin and Andrew N. Chalupka 33 Anesthesia for Pediatric Surgery and Care of the Neonate Rupeng Li and Chang A. Liu 34 Non-Operating Room Anesthesia Stephanie L. Counihan and Rafael Vazquez 35 Anesthesia for Trauma and Burns Evan Hodell, Stephanie Lankford, and Ilan Mizrahi 36 Transfusion Therapy Lukas H. Matern and Marvin G. Chang PART III: PERIOPERATIVE ISSUES 37 The Post-anesthesia Care Unit Jared R. B. Wortzman and Sheri M. Berg 38 Pain Management Gloria Nadayil Berchmans and Peter Stefanovich 39 Adult, Pediatric, and Newborn Resuscitation John H. Nichols and Paul D. Guillod 40 Vascular Access Omar Hyder Appendix I: Drugs With Narrow Therapeutic Ranges and Potential for Harm Richard M. Pino Appendix II: Commonly Used Drugs 12 Appendix III: Common Intravenous Antibiotics Index 13 PART I: EVALUATING THE PATIENT BEFORE ANESTHESIA 14 CHAPTER 1 15 Evaluating the Patient Before Anesthesia Michelle Dyrholm and Kate Cohen 16 I. Introduction The clinic model for anesthesiologists’ preoperative evaluation of patients is evolving. Historically, prior to the day of surgery, a patient was evaluated in person at an office. The visit established rapport and allowed the anesthesiologist to become familiar with the patient’s surgical illness, identify and medically optimize comorbidities, develop a perioperative management strategy, and obtain informed consent. Due to patient and hospital factors, this approach is being modified. Telemedicine consults are burgeoning as a cost- and time-saving method of accomplishing the same preoperative evaluation. Electronic consults, or eConsults, are also being used as a direct pathway of communication between the anesthesiologist and other patient providers. The anesthesiologist gathers clinical information through fragmented healthcare systems and synthesizes an overall clinical picture to determine optimization and complete workup prior to surgery. Physical examination and consent forms are completed on the day of surgery. Some centers with known low-risk patients and low-risk procedures defer the entire evaluation to the day of surgery. Regardless of the model of preoperative evaluation, the basic tenants remain the same. 17 II. History Relevant information is obtained through chart review followed by corroboration with the patient interview. When the medical record is not available, a history is obtained from the patient and supplemented by the patient’s other physicians. A. History of presenting illness. The anesthesiologist should review the symptoms of the present surgical illness, presumptive diagnosis, initial treatment, and diagnostic studies. B. Medications. The provider should establish the current dosing and schedules of all the patient’s medications. Antihypertensive, antianginal, antiarrhythmic, anticoagulant, anticonvulsant, and specific endocrine (eg, insulin and hypoglycemics) medications are especially important. Deciding to continue medication during the preoperative period depends on the severity of the underlying illness, potential consequences of discontinuing treatment, half-life of the medication, and likelihood of deleterious interactions with anesthetic agents. As a general rule, most medications may be continued up through the time of surgery (see Section VI). C. Allergies and drug reactions. True allergic reactions are relatively uncommon. Adverse reactions to perioperative medications are common, however, and may be reported by the patient. Therefore, it is important to obtain a careful description of the exact nature of the reaction. 1. True allergic reactions. IgE-mediated reactions and anaphylaxis can be presumed based upon characteristic symptoms that occurred within a narrow timeframe after exposure to an allergen. Multiple organ systems can be affected, and common symptoms include pruritic rash, urticaria, angioedema, bronchospasm, shortness of breath, wheezing, hypotension, persistent vomiting, and intestinal cramping. 2. Antibiotic allergy. Allergies to antibiotics, especially to sulfonamides, penicillins, and cephalosporin derivatives, are the most common drug allergies. While skin testing can help determine true penicillin allergy, 90% to 99% of patients with self-reported allergy have a negative skin test. Therefore, it should not be used as the sole predictor. In patients with a penicillin allergy, the major determinant of immunological reaction to a cephalosporin is the similarity between the side chain of first-generation drug rather than the β-lactam structure that they share. There is a 0.5% to 3% cross reactivity to first-- and second-generation cephalosporins. Some institutions implement a test dose procedure prior to administering a therapeutic dose and monitor for adverse reaction. However, anaphylaxis is not dose dependent. For patients with a penicillin allergy, there is a threefold increased coincidental risk of reaction to even an unrelated drug. That is, they are more likely to react to any medication. 3. Soybean oil and/or egg yolk allergy. Propofol is commonly formulated as an emulsion containing soybean oil, egg lecithin, and glycerol which has created concerns regarding its use in patients with a history of associated food allergies. Egg allergies are predominantly to the ovalbumin protein found in the egg white, rather than the lecithin in the egg yolk. Similarly, soy allergy is typically to the soy protein rather than the soy oil. Current data suggest low likelihood of adverse reaction to propofol in these patients. 4. Inhalational agent or succinylcholine “allergy.” A history of allergy to “anesthesia,” inhalational agents, or succinylcholine, in the patient or any close relative, may represent a history of malignant hyperthermia (Chapter 17) or atypical plasma cholinesterase. 5. Local anesthetic allergy. Allergy to ester-type local anesthetics can be anaphylactic (see Chapter 19), while allergy to the amide-type local anesthetics is exceedingly rare. Tachycardia or palpitations associated with perivascular injection of local anesthetic mixed with epinephrine may be reported as an occurrence during regional anesthetics. A history of local anesthetic systemic toxicity (LAST) can uncover relevant neurological or cardiac sequelae and inform patient preferences but is unlikely to recur. 6. Shellfish or seafood allergy. Patients with an allergy to shellfish, seafood, or topical antiseptic containing iodine are not at increased risk of adverse reaction to iodinated intravenous contrast. However, patients with a prior documented reaction to contrast are at risk if exposed to the same agent. It is important to note that there is no allergy cross reactivity between different classes of contrast, and alternate contrasts can typically be safely administered. 7. Latex allergy or hypersensitivity reactions. Latex allergy must be ascertained preoperatively to allow for preparation of a latex-free operating room. Additionally, banana, avocado, chestnut, kiwi, or papaya allergy should be elicited as 30% to 50% of individuals with these allergies have cross-reactive allergies to latex. Other risk factors for latex allergy include repeated exposure to latex (eg, healthcare workers or patients with multiple prior surgeries), atopy, and certain medical disorders, such as spina bifida. If these risk factors exist, and no prior skin or serologic tests have been conducted, it may be warranted to treat the patient as latex allergic. D. Anesthetic history. It is crucial to question the patient about their prior experience with anesthesia. Common descriptions of anesthetic problems include postoperative nausea and vomiting (PONV), sore throat, neuropathy, difficult intubation, and prolonged emergence. Reviewing previous anesthetic records can shed light on other patient-specific considerations. 1. Response to medications. Patient response to sedative, analgesic, and anesthetic agents varies widely among individuals. Cognitive changes, such as memory loss, delirium, or dullness, are frequently described in elderly patients and can be minimized by avoiding burst suppression, 18  anticholinergic drugs, and benzodiazepines. Intraoperative awareness may be reported. Describing to the patient the experience of sedation versus general anesthesia may clarify a prior experience and provide reassurance. Those with true recall may require higher doses of hypnotic medication, modified electroencephalographic (EEG) assessment, and other mechanisms of confirming depth of anesthesia. 2. Vascular access and invasive monitoring. Determining the need for ultrasound-guided IV placement or central access can help to avoid repeated attempts in a patient who is a “difficult stick.” In morbidly obese patients, noninvasive blood pressure (BP) monitoring may be impossible due to the conical shape of the upper extremity and an arterial line may be required. 3. Airway management. Determine past ease of mask ventilation, view obtained on direct laryngoscopy, size and type of laryngoscope blade and endotracheal tube, and depth of endotracheal tube insertion. A prior history of a difficult intubation is the primary predictor of a difficult airway. 4. Perianesthetic complications. Review prior records for complications such as adverse drug reactions, dental injury, protracted PONV, hemodynamic instability, respiratory compromise, postoperative myocardial infarction (MI), unanticipated admission to an intensive care unit (ICU), prolonged emergence, or need for reintubation. 5. Opioid requirements. Opioid administration perioperatiely can lend insight into future requirements and the need for alternative pain management strategies such as neuraxial anesthetics, peripheral nerve blocks, and multimodal pharmacology. E. Family history. A history of adverse anesthetic outcomes in family members should be assessed with open-ended questions, such as “Has anyone in your family experienced unusual or serious reactions to anesthesia?” Additionally, patients should be specifically asked about a family history of malignant hyperthermia. F. Social history and habits 1. Smoking. The perioperative period is a powerful time to provide counseling and support smoking cessation in patients and is associated with a higher rate of success. Smoking cessation reduces postoperative complications, and evidence suggests that abstinence should be encouraged regardless of surgical interval timing. A history of exercise intolerance or the presence of a productive cough or hemoptysis may indicate the need for further evaluation. 2. Drug and alcohol use. Although self-reporting of drug and alcohol intake typically underestimates use, it is a helpful start to define the type of drugs used, routes of administration, frequency, and timing of most recent use. Stimulant abuse may lead to palpitations, angina, and lowered thresholds for serious arrhythmias and seizures. Marijuana use can cause airway hyperreactivity and significantly increase the requirements of propofol and analgesics. Acute alcohol intoxication decreases anesthetic requirement and predisposes to hypothermia and hypoglycemia. Alcohol withdrawal may precipitate severe hypertension (HTN), tremors, delirium, and seizures and may markedly increase anesthetic and analgesic requirements. Risk of intraoperative awareness is also increased with chronic opioid or benzodiazepine use. 19 III. Review of Systems The purpose of review of systems (ROS) is to elicit symptoms of occult disease and to determine the stability of current disease. Coexisting illnesses should be evaluated by an organ-systems approach with an emphasis on recent changes in symptoms, signs, and treatment (see Chapters 3-7). A minimum ROS should seek to elicit the following information: A. Cardiovascular. 1. Coronary artery disease. Preexisting coronary artery disease (CAD) may predispose the patient to spontaneous myocardial ischemia, demand ischemia, or ventricular dysfunction. Angina, dyspnea on exertion (DOE), paroxysmal nocturnal dyspnea, and reduced exercise capacity can help characterize the severity of disease. 2. Pacemakers (permanent pacemaker, PPM) and implanted cardioverter-defibrillators (ICD). ICDs should be interrogated within 6 months of surgery, PPMs within 12 months, and cardiac resynchronization therapy (CRT) devices within 3 to 6 months. The decision to deactivate functions of an ICD or change a PPM to asynchronous mode via transcutaneous magnet placement should be made based on the likelihood of electrocautery interference (ie, distance from the generator) causing unwanted shocks or failure to pace. 3. HTN. Baseline blood pressure ranges should be established, and the perioperative goal should be to maintain pressures within 10% to 20% of the baseline. Poorly controlled HTN is frequently associated with marked preoperative HTN and labile intraoperative pressures. If the planned surgical position is prone or beach chair, the procedure may be delayed for BP optimization so the risk of blindness and stroke is minimized. 4. DOE. DOE is an important sign that can be caused by myriad underlying etiologies, including physical deconditioning, obesity, or cardiopulmonary pathology. If the DOE is acute or acute-on-chronic, the patient should be evaluated and referred for appropriate testing to determine etiology and treatment. 5. Exercise capacity. Assessment of functional capacity helps in risk stratification for predicting a perioperative cardiac event. Functional capacity is quantified in terms of metabolic equivalents of task (METs) rated on a scale of poor (1.6 cm; however, the major limitation of this measurement is that it only evaluates the free wall of the right ventricle, neglecting the contributions of the interventricular septum and right ventricular outflow tract. 4. Right ventricular wall thickness: Wall thickness is useful for evaluating the presence of right ventricular hypertrophy, which can result from pulmonary hypertension or chronic right ventricular volume overload. RV lateral wall thickness is best measured by TTE using the subcostal four-- chamber. Using M-mode, the measurement is made at end diastole at the level of the tip of the anterior tricuspid valve leaflet. The right ventricular wall is normally less than 5 mm thick. 5. Right ventricular dilation: Right ventricular size is best evaluated in the apical four-chamber view. During end diastole, one measures the diameter right above the tricuspid annulus along the base of the right ventricle. The normal value is less than 4.2 cm. Generally speaking, the normal RV is no more than two-thirds the size of the left ventricle in an apical four-chamber view. If the RV makes up the apex or is larger than the LV, then the RV is most likely significantly enlarged. D. IVC 1. The IVC can be readily assessed by surface ultrasound. The patient should be supine for measurements. The vena cava is a tubular structure that runs cephalad to caudad. Imaging is performed from the subcostal window to the right of midline in the sagittal plane to obtain LAX view of the IVC. The morphology of the IVC can provide insight into the filling pressures of the heart and provide supportive data for diagnoses such as tamponade, hypovolemia, or heart failure. 2. IVC diameter and central venous pressure (CVP) a. In spontaneously breathing patients, IVC diameter correlates to CVP. i. If the IVC diameter is less than 2.1 cm AND collapses more than 50% with sniff, this indicates filling pressures are normal, CVP < 5 mm Hg. ii. If the IVC diameter is greater than 2.1 cm AND collapses less 50% with sniff, this indicates elevated filling pressures, CVP > 15 mm Hg. iii. Other conditions are indeterminate, and filling pressures may be intermediate, CVP 5 to 10 mm Hg. 3. IVC for fluid responsiveness: In intubated patients without any spontaneous effort, variations in CVP diameter can be used to predict fluid responsiveness. Please see the section below on Hemodynamic Measurements and Fluid Responsiveness. 60 IV. Hemodynamic Measurements and Fluid Responsiveness 1. The difference in pressure between chambers can be assessed by measuring the velocity of fluid flow between the two chambers. This relationship is given by simplified Bernoulli equation. 2. Simplified Bernoulli equation (Figure 2.34): FIGURE 2.34 Bernoulli equation for calculating transvalvular gradients. where P1 – P2 is the difference in pressure between the two chambers in mm Hg and V is the velocity of the fluid flow jet between the chambers in meters per second. A common usage of this equation is in the measurement of right ventricular systolic pressure (RVSP). 3. RVSP measurement: The tricuspid regurgitant jet is measured in the apical four-chamber or parasternal RV-inflow view using continuous wave Doppler. The peak velocity is then inserted in the simplified Bernoulli equation. CVP is then added to the calculated pressure gradient, since the calculated pressure difference is between the RV and the right atrium and not the absolute pressure. If the fluid is starting with a significant initial velocity, a slightly more accurate modified Bernoulli equation must be used to account for this. An example of this would be measurement of the aortic stenosis with high cardiac output since the LVOT would have significant velocity. Modified Bernoulli equation: 1. Although ultrasound cannot measure flow directly, velocity can be measured and integrated over time, velocity time integral (VTI), to determine distance travelled. Multiplying the VTI by the cross-sectional area of the structure through which the velocity is measured yields the rate of flow. A common application of this approach is the measurement of stroke volume and cardiac output. 2. Stroke volume measurement: This is performed by measuring first measuring the LVOT diameter in the parasternal LAX view. Assuming the LVOT is a circle, the area can be calculated, LVOTarea. Then the flow in the LVOT from the apical five-chamber view using pulse wave Doppler. From the pulse wave Doppler waveform, the area under the curve of ejection is then measure to obtain the VTI. This VTI is then multiplied by LVOTarea to give the stroke volume (SV). The SV can then be multiplied by the heart rate (HR) to give the cardiac output. a. SVV: In order to calculate SVV, an apical five-chamber view is obtained to determine the blood flow through the LVOT using pulse wave Doppler. Placing the marker through the LVOT will produce a series of VTIs, and SVV is calculated by subtracting the maximum velocity by the minimum velocity divided by the average of the two velocities. Changes > 12% correlate with a likelihood of fluid responsiveness; however, this technique has only been validated for patients in sinus rhythm who are mechanically ventilated with neuromuscular blockade and receiving a tidal volume of 8 mL/kg. 61 b. IVC diameter variation is measured in a manner similar to the static assessment of IVC diameter. In the subcostal IVC LAX view, the M-mode beam is sited approximately 1 to 2 cm proximal to the cavoatrial junction and used to measure the change in maximum diameter (at the end of positive pressure inspiration) and minimum diameter (at the end of positive pressure expiration). A value greater than 12% after calculating the difference between the maximum and minimum diameters divided by the mean of each has been shown to predict fluid responsiveness to an 8 mL/kg intravenous (IV) volume bolus (Table 2.2). Although this technique has only been validated in mechanically ventilated patients, IVC diameter variation does not require sinus rhythm, unlike SVV. TABLE 2.2 Inferior Vena Cava Diameter correlation to Central Venous Pressure IVC Diameter Collapse With Sniff Approximate CVP Less than 2.1 cm AND Greater than 50% Normal, 0-5 mm Hg Greater than 2.1 cm AND Less than 50% Elevated, >15 mm Hg Does not meet both conditions above Indeterminate or intermediate CVP, central venous pressure; IVC, inferior vena cava. Derived from Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28(1):1-39.e14. c. PLR test is a reversible preload challenge that translocates approximately 300 mL of blood from the lower extremities by changing a semirecumbent positioned patient into a supine position with leg elevation. The maximal cardiac response to PLR occurs within 2 minutes of the positioning change. Similar to conventional SVV, a sonographer will calculate the LVOT velocity in the apical five-chamber view, both before and after the maneuver. An increase in the velocity by 10% to 15% corresponds with likelihood of fluid responsiveness. A meta-analysis of studies of PLR found the diagnostic value of this technique to be excellent. A particular advantage of this approach is the lack of requirement for mechanical ventilation, sinus rhythm, or normal pulmonary compliance. d. Fluid challenge: A final method is to measure CO before administration of an IV fluid bolus and then measure the CO after. If the cardiac output does not increase with the fluid challenge, the patient is presumed not to be fluid responsive and no further IV fluids are administered until there has been a change in physiologic state. Measurement of CO using echocardiography is describe the above in the section on “Flow Measurement.” A. Doppler ultrasound 1. Ultrasound cannot directly measure pressures or blood flow, but using Doppler measurements, velocity can be assessed and pressure and flows can be inferred. This is a powerful tool that allows for quantitative hemodynamic measurements. It is important to recognize that Doppler can only measure velocity along the direction of the ultrasound beam. Thus, measurement accuracy is dependent on angle and is most accurate when the angle of the transducer beam is less than 20° to the direction of blood flow. There are three main modes of Doppler used: continuous wave, pulse wave, and color. 2. Continuous wave Doppler continuously transmits and receives Doppler signals. This allows measurement of the highest velocity of blood flow along the path of the beam and is useful for assessing regurgitant jets or the flow through a stenotic aortic valve. However, it does not allow the position of the velocity measurement to be known. 3. Pulse wave Doppler allows velocity measurements at a specific location. However, due to the Nyquist limit, the maximum measurable velocity is limited by aliasing. Thus, only lower velocities flows can be measured, such as ventricular ejection or mitral inflow. 4. Color Doppler allows visualization of flow overlaid on the 2D image. Like pulse wave, it is also limited to accurate measurement of lower velocities. It is a very useful tool to qualitatively evaluate flow patterns. B. Pressure gradient assessment A. Flow measurements A. Fluid responsiveness 1. The concept of fluid responsiveness is central to optimizing fluid therapy. Fluid overload has been associated with prolonged duration of mechanical ventilation, in addition to increased overall morbidity and mortality; thus, fluids should only be administered to patients who are fluid responsive. The use of echocardiography for fluid responsiveness remains a controversial topic. 2. Fluid responsiveness is defined by a 10% to 15% increase in stroke volume after receiving a 500 mL fluid bolus over 10 to 15 minutes. Conceptually, administering additional fluid will only increase stroke volume if it increases stressed blood volume and if both ventricles are volume responsive and functioning on the ascending portion of the Frank-Starling curve. It is important to consider that a heart with impaired systolic function can respond to an increase in fluid; however, the overall response will be relatively reduced. 3. Static echocardiograph parameters: Overall, static parameters are poor predictors of volume responsiveness, but they do correlate with values such as central venous and pulmonary capillary wedge pressure. 4. Left ventricular end-diastolic area (LVEDA) is best measured in the parasternal SAX view at the midpapillary level and has been shown to more accurately reflect left ventricle preload relative to pulmonary capillary wedge pressure. A publication reviewing fluid responsiveness in intensive care 62  unit (ICU) patients included two studies that found patients more likely to respond to a fluid bolus if they had lower LVEDAs relative to individuals who would not respond; however, these two studies relied on TEE rather than TTE. Overall, LVEDA < 10 cm2 has been associated with severe hypovolemia, and conversely, >20 cm2 has been associated with volume overload. 5. Left ventricular end-systolic area (LVESA) is measured at the midpapillary level in the parasternal SAX views. Particular attention should be paid to the positioning of the papillary muscles. The classical teaching is that contact between opposing papillary muscles at the end of systole (“kissing papillary muscles”) is indicative of severe hypovolemia. There are various other factors that can also cause a small LVESA, including distributive shock, hyperdynamic left ventricle contractility, right ventricular failure, acute mitral regurgitation, or cardiac tamponade to name a few. 6. IVC diameter: Please see the section above on IVC assessment. 7. Dynamic echocardiographic parameters are more evidence supported indices for determining fluid responsiveness relative to static tests. Some examples of dynamic parameters of fluid responsiveness are stroke volume variation (SVV), IVC variation, passive leg raise (PLR) testing, and fluid challenge. 63 V. Conclusion Driven by progressive advances in ultrasound technology, the use of echocardiography and FoCUS by noncardiologists is rapidly expanding. This allows the clinician at the bedside to rapidly and repeatedly evaluate a patient. It supplements physical examination and obviates the potential risk involved in waiting for, or transporting an unstable patient for, additional forms of diagnostic testing. A focused bedside ultrasound examination does not replace the role of a comprehensive echocardiographic examination and care must be taken to practice within the limitations of one’s own expertise. Consultation of an expert echocardiographer is recommended when there is any question or complex diagnosis. However, point of care cardiac ultrasound is a powerful new tool for the bedside clinician, and the applications will continue to develop in the future. 64 Suggested Readings Beigel R, Cercek B, Luo H, Siegal RJ. Noninvasive evaluation of right atrial pressure. J Am Soc Echocardiogr. 2013;26(9):1033-1042. Cherpanath TG, Hirsch A, Geerts BF, et al. Predicting fluid responsiveness by passive leg raising: a systematic review and meta-analysis of 23 clinical trials. Crit Care Med. 2016;44(5):981-991. doi:10.1097/CCM.0000000000001556 Cherpanath TG, Geerts BF, Lagrand WK, Schultz MJ, Groeneveld AB. Basic concepts of fluid responsiveness. Neth Heart J. 2013;21(12):530-536. Feissel M, Michard F, Faller JP, Teboul JL. The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. Intensive Care Med. 2004;30:1834-1837. doi:10.1007//s00134-004-2233-5 Feissel M, Michard F, Mangin I, Ruyer O, Faller JP, Teboul JL. Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated patients with septic shock. Chest. 2001;119(3):867-873. Goldberg BB, Goodman GA, Clearfield HR. Evaluation of Ascites by ultrasound. Radiology. 1970;96:15-22. Kristensen JK, Buemann B, Kuhl E. Ultrasonic scanning in the diagnosis of splenic haematomas. Acta Chir Scand. 1971;137:653-657. Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr. 2010;23:1225-1230. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28(1):1-39.e14. McKaigney CJ, Krantz MJ, La Rocque CL, Hurst ND, Buchanan MS, Kendall JL. E-point septal separation: a bedside tool for emergency physician assessment of left ventricular ejection fraction. Am J Emerg Med. 2014;32(6):493-497. Monnet X, Marik PE, Teboul JL. Prediction of fluid responsiveness: an update. Ann Intensive Care. 2016;6(1):111. Michard F, Teboul JL. Predicting fluid responsiveness in ICU patients: a critical analysis of the evidence. Chest. 2002;121(6):2000-2008. Panoulas VF, Daigeler AL, Malaweera ASN, et al. Pocket-size hand-held cardiac ultrasound as an adjunct to clinical examination in the hands of medical students and junior doctors. Eur Heart J Cardiovasc Imaging. 2013;14(4):323-330. doi:10.1093/ehjci/jes140 Spencer KT, Kimura BJ, Korcarz CE, Pellikka PA, Rahko PS, Siegel RJ. Focused cardiac ultrasound: recommendations from the American Society of Echocardiography. J Am Soc Echocardiogr. 2013;26:567-581. Wetterslev M, Haase N, Johansen RR, Perner A. Predicting fluid responsiveness with transthoracic echocardiography is not yet evidence based. Acta Anaesthegiol Scan. 2013;57(6):692-697. doi:10.1111/aas.12045 Wojciech M, Dyla A, Zawada T. Utility of transthoracic echocardiography (TTE) in assessing fluid responsiveness in critically ill patients—a challenge for the bedside sonographer. Med Ultrason. 2016;18(4):508-514. doi:10.11152/mu-880 65 CHAPTER 3 66 Specific Considerations With Cardiac Disease Adam A. Dalia and Casey Hamilton 67 I. General Considerations An estimated one in three Americans has one or more types of cardiovascular disease (CVD). Mortality data show that one of every three deaths in the United States is secondary to CVD. 68 II. Coronary Anatomy The coronary arteries perfuse the myocardium. The left and right coronary arteries originate from the coronary sinuses distal to the aortic valve. The left main coronary artery (LMCA) branches into the left anterior descending artery (LAD) and the left circumflex artery (LCX) to supply most of the left ventricle (LV), interventricular septum (IVS), and the left atrium (LA). The right coronary artery (RCA) supplies the right atrium (RA) and ventricle (RV), as well as portions of the IVS, including the sinoatrial (SA) and atrioventricular (AV) nodes (Figure 3.1). In approximately 70% of the population, the posterior descending artery (PDA) is supplied by the RCA. This circulation is described as “right dominant.” The remainder of the population is either “left dominant,” with the PDA emerging from the LCX (10% of the population), or “codominant,” with the PDA receiving contributions from both the LCX and RCA (20% of population). FIGURE 3.1 Coronary anatomy. 69 III. Preoperative Cardiovascular Evaluation for Noncardiac Surgery The American College of Cardiology and the American Heart Association (ACC/AHA) have developed joint guidelines for the preoperative cardiovascular evaluation and management of patients undergoing noncardiac surgery. The initial evaluation consists of the patient’s history, focused physical examination, and routine laboratory investigation. Based on the patient’s history, cardiac risk factors, functional status, and the nature of the surgical procedure, the ACC/AHA guidelines provide a stepwise approach for identifying patients who may benefit from further cardiovascular testing (Figure 3.2). FIGURE 3.2 Stepwise approach to perioperative cardiac assessment for CAD from the latest ACC/AHA guidelines. Colors correspond to classes of recommendations. ACC/AHA, American College of Cardiology and American Heart Association; ACS, acute coronary syndrome; CAD, coronary artery disease; CPGs, clinical practice guidelines; GDMT, guideline-directed medical therapy; MACE, major adverse cardiac event; METs, metabolic equivalents. (Reprinted from Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. J Am Coll Cardiol. 2014;64(22):e77- e137. Copyright © 2014 American College of Cardiology Foundation and the American Heart Association, Inc. With permission.) A. Initial screening 1. The need for emergency surgery preempts further cardiac workup. The ACC/AHA guidelines define an emergency procedure as one that must be started within 6 hours. As there is little to no time, the patient must proceed often with no or very limited clinical preoperative evaluation. Emergent surgery should proceed with appropriate patient monitoring and management strategies based on the patient’s 70  clinical risk factors for coronary artery disease (CAD). Bedside focused cardiac ultrasound (FoCUS) via transthoracic echocardiography can be performed to rule out life-threatening cardiac conditions such as tamponade, aortic dissection, or myocardial infarction (MI) to help with perioperative management in the emergent setting. 2. If the surgery is not emergent, determine whether the patient has an acute coronary syndrome (ACS). An ACS is an unstable angina or an MI. The patient may present with chest pain, shortness of breath, diaphoresis, or nausea. The electrocardiogram (ECG) may show ST segment depressions or elevations. If the patient has an ACS, the surgical procedure should be postponed and the patient should immediately undergo cardiac evaluation and guideline-directed medical therapy (GDMT). If the patient does not have an ACS, then proceed with an assessment of the patient’s postoperative risk for a major adverse cardiac event (MACE). B. Risk of MACE. The patient’s risk of MACE should be determined based on clinical characteristics and the surgical procedure. Clinical risk factors for MACE include a history of heart failure, CAD, cerebrovascular disease, diabetes, and chronic kidney disease. Validated risk prediction tools, such as the Revised Cardiac Risk Index (RCRI) and the American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) Surgical Risk Calculator (riskcalculator.facs.org), can be used to help predict the risk of perioperative MACE. 1. If the patient has a low risk of MACE (2 mm, sustained into recovery, and/or associated with hypotension). The risk of perioperative cardiac events is increased significantly in patients who have abnormal exercise ECGs at low workloads. Radionuclide imaging or echocardiography can be combined with exercise stress testing for patients whose baseline ECGs render interpretation invalid. b. Pharmacologic stress testing can be conducted with either an agent that increases myocardial oxygen demand (dobutamine) or dilates coronary arteries and causes coronary steal from diseased vessels (dipyridamole or adenosine). Pharmacologic stress tests are suitable for patients who are unable to exercise. Dobutamine stress testing is typically combined with echocardiography to detect wall motion abnormalities brought about by the increased myocardial workload. Dipyridamole or adenosine stress tests are typically combined with radionuclide imaging to detect areas of myocardium that are at risk. Pharmacologic vasodilation has the risk of a false-negative test in patients with multivessel CAD where all vessels are 71  already maximally vasodilated. In both cases, perioperative cardiac risk is directly proportional to the extent of myocardium that is found to be at risk on imaging. 4. Cardiac catheterization is considered the “gold standard” for evaluating CAD. Information obtained includes coronary anatomy with visualization of direction and distribution of flow, hemodynamics, and overall function of the heart. Routine preoperative coronary angiography is not recommended. Revascularization before noncardiac surgery is recommended in circumstances in which revascularization is indicated according to existing clinical practice guidelines. 5. Noninvasive imaging including cardiac MRI (CMR) and coronary computed tomography angiogram (CCTA) have emerged as reasonable options for preoperative cardiac evaluation. CMR is usually reserved for patients after first-line imaging (echocardiography) is either inconclusive or indeterminant; it is generally reserved for patients with complex disease. Contraindications to CMR include the presence of implants or cardiovascular implantable electronic devices (CIEDs) that are not MRI safe. CCTA can be utilized to rule out obstructive CAD in low- to medium-risk patients, but it is not advised for high-risk patients; coronary catheterization remains the gold standard for high-risk patients. Contraindications to cardiac CTA include renal failure or allergy to contrast. 6. Cardiac consultation may be helpful in determining which tests will be useful and in interpreting the results. The consultant can help optimize the patient’s preoperative medical therapy and provide follow-up in the postoperative period. Such follow-up is crucial with the initiation of new drug therapies and often for patients with pacemakers and implantable cardioverter-defibrillator (ICD) devices (see Section XI). D. Indications for preoperative coronary revascularization with either coronary artery bypass grafting or percutaneous coronary intervention (PCI) are in general the same as in the nonoperative setting. Surgery, in and of itself, is not an indication for coronary revascularization, regardless of extent of vessel disease or left ventricular dysfunction. 72 IV. Preanesthetic Considerations A. Patients are likely to be anxious. Reassurance during the preoperative visit has been shown to be useful in decreasing anxiety. Anxiolytics may blunt rises in sympathetic tone and may be invaluable. B. Cardiac medications are usually continued perioperatively. Possible exceptions include angiotensin-- converting enzyme inhibitors (due to proposed prolonged vasodilation), sustained-release or long-acting medications, and diuretics. 1. β-blockers. While the evidence for initiating β-blockers in the perioperative period is mixed, there is a consensus that patients already taking β-blockers should continue them in the perioperative period. Initiating β-blocker therapy in the perioperative period has been associated with an increased incidence of MACEs such as nonfatal stroke and MI. In patients with moderate to high risk of perioperative myocardial ischemia or with three or more Revised Cardiac Risk Index (RCRI) risk factors (eg, diabetes mellitus, HF, CAD, renal insufficiency, cerebrovascular accident), it may be reasonable to start β-blockers before surgery. When possible, β-blockers should be started days to weeks before elective surgery and titrated cautiously. They should not be started on the day of surgery; starting β-blockers within 1 day or less of surgery increases the risk of stroke, death, hypotension, and bradycardia. 2. Statins. Patients taking statins should continue to receive statins perioperatively. Preoperative initiation of statin therapy is reasonable in patients undergoing vascular surgery as well as in patients with standard clinical indications for statin therapy who are undergoing elevated-risk procedures. 3. Aspirin. The efficacy of aspirin for the secondary prevention of MI in patients with ischemic heart disease has been well documented. Data on the risk of discontinuing antiplatelet therapy in patients with coronary stents have strongly suggested continuing aspirin in the perioperative period. The data on continuing aspirin in patients undergoing elective noncardiac, noncarotid surgery who have not had previous coronary stenting, however, are controversial. Some publications recommend that aspirin should not be stopped routinely in the perioperative period at all, while a recent systematic review and metanalysis suggests that aspirin has no significant effect on overall survival, cardiovascular mortality, or arterial ischemic events, while reducing venous thromboembolic events at the expense of increased risk of major bleeding. C. Timing of elective surgery in the setting of previous PCI presents a special challenge. Management decisions should be made in consultation with the patient’s cardiologist and surgeon. 1. Balloon angioplasty without stent placement. The ACC/AHA recommend that elective noncardiac surgery should be delayed 14 days after balloon angioplasty. Aspirin therapy should be continued in the perioperative period. 2. Bare-metal coronary stents (BMS). Current recommendations are to delay elective noncardiac surgery for 30 days following PCI with BMS. This time period allows for the completion of thienopyridine therapy and the endothelialization of the stent. The risk of ischemic events is greatest within 30 days of PCI, significantly lower at 30 to 90 days, and lowest after 90 days. Aspirin therapy should be continued perioperatively. 3. Drug-eluting stents (DES). Thrombosis of DES can occur months after placement and is often related to the omission of dual antiplatelet therapy (DAPT) perioperatively. The current consensus recommendation is to defer elective surgery for at least 3 months, and optimally 6 months, following placement. Aspirin therapy should be continued perioperatively. Elective noncardiac surgery after DES implantation may be considered after 3 to 6 months if the risk of further delay is greater than the expected risks of ischemia and stent thrombosis. 4. Should a noncardiac surgical procedure be required within the time frame recommended for DAPT following PCI, consider continuing the therapy throughout the perioperative period. If bleeding risk necessitates the discontinuation of thienopyridine therapy, continue aspirin therapy and restart thienopyridines as soon as possible. D. Supplemental oxygen should be provided to all patients who have a significant risk of ischemia. E. Monitoring is discussed in Chapter 15. F. Anesthetic technique. There are no convincing data to support the superiority of one particular anesthetic technique over another in the management of patients at risk for perioperative cardiac events; the anesthetic technique should be decided upon based on patient and surgical factors. The use of MAC, local, or neuraxial combination can be more hemodynamically stable compared to general anesthesia but presents challenges with regard to anticoagulation status, level of consciousness, and pain control (tachycardia and hypertension). For major open abdominal aortic surgery, it has been shown that epidural anesthesia with general anesthesia improved pain control while reducing postoperative respiratory failure and MI; however, there was no observed difference in mortality. 73 V. Ischemic Heart Disease CAD afflicts an estimated 30% of patients undergoing surgery in the United States. CAD increases in prevalence with age. Other risk factors include hypercholesterolemia, male gender, hypertension, cigarette smoking, diabetes mellitus, obesity, and family history of premature development of ischemic heart disease. CAD is a risk factor for perioperative cardiac complications, including MI, unstable angina, congestive heart failure (CHF), and serious dysrhythmias. A. Pathophysiology. Myocardial ischemia occurs when oxygen demand exceeds oxygen delivery. B. Supply. The myocardium is supplied via coronary arteries. Myocardial oxygen supply depends on coronary artery diameter, LV diastolic pressure, aortic diastolic pressure, and arterial oxygen content. 1. Coronary blood flow is dependent on the aortic root-to-downstream coronary pressure gradient. Most coronary blood flow occurs during diastole. Coronary artery blood flow in normal individuals is controlled primarily through local mediators. The coronary arteries of patients with significant CAD may be maximally dilated at rest. 2. Heart rate is inversely proportional to the length of diastole. Faster heart rates decrease the duration of maximal coronary perfusion. 3. Blood oxygen content is determined by hemoglobin concentration, oxygen saturation, and dissolved oxygen content. Increasing inspired oxygen fraction and/or hemoglobin concentration increases blood oxygen content. C. Demand. Myocardial oxygen consumption (MVO2) is increased by increases in ventricular wall tension and heart rate (velocity of shortening) and, to a lesser degree, contractility. 1. Ventricular wall tension is modeled by Laplace law: wall tension is directly proportional to the ventricular transmural pressure and the ventricular radius and inversely proportional to the ventricular wall thickness. Changes in these parameters affect oxygen demand. 2. Heart rate. Tachycardia is well tolerated in normal hearts. Atherosclerotic coronary arteries may not adequately dilate to meet increased demands of faster heart rates. 3. Contractility increases with the increased chronotropy, myocardial stretch, calcium, and catecholamines. Increasing contractility increases oxygen consumption. D. Supply and demand balance. Atherosclerosis is the most common etiology for supply-demand imbalances. Conditions such as aortic stenosis, systemic hypertension, and hypertrophic cardiomyopathy, which are characterized by marked ventricular hypertrophy and high intraventricular pressures, may also increase MVO2. These conditions may create imbalances, even in the setting of normal coronary arteries. The goal of treatment is to improve the myocardial oxygen supply-demand balance. 1. Increase supply a. Increase coronary perfusion pressure with the administration of volume or α-adrenergic agonists to increase aortic root diastolic pressure. b. Increase coronary blood flow with nitrates to dilate coronary arteries. c. Increase oxygen content by raising hemoglobin concentration or oxygen partial pressure. 2. Decrease demand a. Decrease heart rate either directly with β-adrenergic antagonists or indirectly by treating underlying causes of tachycardia (eg, pain, anxiety). b. Decrease ventricular size (decrease wall tension) by decreasing preload with nitrates, calcium channel antagonists, or diuretics. Occasionally, increasing inotropy may decrease demand by decreasing ventricular size and wall tension. c. Decreasing contractility may decrease MVO2 if ventricular size and wall tension do not increase excessively. Calcium channel blockers and volatile anesthetics decrease contractility. d. Intra-aortic balloon counter pulsation increases coronary perfusion pressure by augmenting diastolic pressure. It also reduces resistance to LV ejection, thereby reducing LV size and wall tension. 74 VI. Valvular Heart Disease A. Aortic stenosis 1. The etiology is usually progressive calcification and narrowing of a tricuspid or bicuspid valve. Severity is defined by valve area and mean gradient (mild, greater than 1.5 cm2 or less than 25 mm Hg; moderate, between 1.0 and 1.5 cm2 or between 25 and 40 mm Hg; and severe, less than 1.0 cm2 or greater than 40 mm Hg, respectively). 2. Symptoms of angina, syncope, or heart failure develop late in the disease process. In the absence of surgical intervention, the average survival is 2 to 3 years following the onset of symptoms. 3. Pathophysiology. The ventricle becomes hypertrophied and stiff in response to the increased pressure load. Coordinated atrial contraction becomes critical to maintaining adequate ventricular filling and stroke volume. The ventricle is susceptible to ischemia due to increased muscle mass and decreased coronary perfusion in the setting of increased intraventricular pressure. 4. Anesthetic considerations. Aortic stenosis is the only valvular lesion associated with an increased risk of perioperative ischemia, MI, and death. a. Normal sinus rhythm and adequate volume status should be maintained. b. Avoid systemic hypotension. Hypotension should be treated immediately and aggressively with an α-agonist such as phenylephrine to maintain adequate coronary perfusion pressure. c. Avoid tachycardia. Tachycardia results in increased oxygen demand along with a shorter period of diastole leading to decreased coronary perfusion and reduced cardiac output. Severe bradycardia can lead to reduced cardiac output and should be avoided as well. Cardiac pacing capabilities should be considered to treat severe bradycardia. Supraventricular tachydysrhythmias should be treated aggressively with direct current cardioversion. d. Nitrates and peripheral vasodilators should be administered with extreme caution. e. The treatment of ischemia in these patients is directed at increasing oxygen delivery by raising coronary perfusion pressure and decreasing oxygen consumption (by increasing blood pressure and lowering heart rate). B. Aortic regurgitation 1. Etiologies include rheumatic heart disease, endocarditis, trauma, collagen vascular diseases, and processes that dilate the aortic root (eg, aneurysm, Marfan syndrome, and syphilis). 2. Pathophysiology a. Acute aortic regurgitation may cause sudden LV volume overload with increased LV end-- diastolic pressure and pulmonary capillary occlusion pressure. Manifestations include decreased cardiac output, CHF, tachycardia, and vasoconstriction. b. Chronic aortic regurgitation leads to LV dilation and eccentric hypertrophy. Symptoms may be minimal until late in the disease process when left-sided heart failure occurs. 3. Anesthetic considerations a. Maintain a normal to slightly increased heart rate to minimize regurgitation and maintain aortic diastolic and coronary artery perfusion pressure. b. Maintain adequate volume status. c. Improve forward flow and decrease LV end-diastolic pressure and ventricular wall tension with vasodilators. d. Avoid peripheral arterial vasoconstrictors, which may worsen regurgitation. e. Consider pacing. These patients have an increased incidence of conduction abnormalities. f. Intra-aortic balloon counter pulsation is generally contraindicated in the setting of aortic regurgitation. C. Mitral stenosis 1. The etiology is almost always rheumatic. 2. Pathophysiology a. Increased left atrial pressure and volume overload increase left atrial size and may cause atrial fibrillation and pulmonary edema. b. Elevated left atrial pressure increases pulmonary venous pressure and pulmonary vascular resistance. In turn, right ventricular pressure is increased for a given cardiac output. Chronic pulmonary hypertension produces pulmonary vascular remodeling. Pulmonary hypertension may lead to tricuspid regurgitation, RV failure, and decreased cardiac output. 3. Anesthetic considerations a. Avoid tachycardia. Tachycardia is poorly tolerated because of decreased diastolic filling time leading to decreased cardiac output and increases in left atrial pressure. Control ventricular response pharmacologically or consider cardioversion for patients with atrial fibrillation. Continue digoxin, calcium channel blockers, and β-adrenergic blockers perioperatively. b. Avoid pulmonary hypertension. Hypoxia, hypercarbia, acidosis, atelectasis, and sympathomimetics increase pulmonary vascular resistance. Oxygen, hypocarbia, alkalosis, nitrates, prostaglandin E1, and inhaled nitric oxide decrease pulmonary vascular resistance. 75  c. Hypotension may indicate RV failure. Inotropes and agents that decrease pulmonary hypertension may be useful (eg, dobutamine, milrinone, nitrates, prostaglandin E1, and inhaled nitric oxide). d. Pulmonary artery catheter may assist in the perioperative evaluation of volume status, intracardiac pressures, and cardiac output. e. Premedication should be adequate to prevent anxiety and tachycardia. Exercise caution in patients with hypotension, pulmonary hypertension, or low cardiac output. D. Mitral regurgitation 1. Etiologies include mitral valve prolapse, ischemic heart disease, endocarditis, and post-MI papillary muscle rupture. 2. Pathophysiology. Mitral regurgitation allows blood to be ejected into the LA during systole. The amount of regurgitant flow depends on the ventricular-atrial pressure gradient, size of the mitral orifice, and duration of systole. a. Acute mitral regurgitation usually occurs in the setting of MI. Acute volume overload of the left side of the heart leads to LV dysfunction with increased ventricular wall tension. b. Chronic mitral regurgitation causes gradual left atrial and LV overload and dilation with compensatory eccentric hypertrophy. c. Measurement of ejection fraction does not accurately reflect forward flow, because the incompetent valve permits immediate bidirectional ejection with systole. 3. Anesthetic considerations a. Relative tachycardia is desirable to decrease ventricular filling time and ventricular volume. b. Afterload reduction is beneficial. Increased systemic vascular resistance will increase regurgitation. c. Maintain preload. 76 VII. Congestive Heart Failure Heart failure results from impairment of ventricular systolic or diastolic function. Heart failure manifests as dyspnea, fatigue, decreased exercise tolerance, and pulmonary or peripheral edema. Heart failure can be classified into two categories: (1) heart failure with reduced ejection fraction (HFrEF) that is associated with variable degrees of LV enlargement and depressed ventricular ejection and (2) heart failure with preserved ejection fraction (HFpEF) in which diastolic dysfunction is pronounced. A. Etiologies include ischemic cardiomyopathy; hypertension; valvular heart disease; endocrine and metabolic causes such as diabetes, thyroid disease, and acromegaly; toxic cardiomyopathies due to alcohol, cocaine, or chemotherapy; nutritional causes such as carnitine deficiency; infective causes such as viral myocarditis, human immunodeficiency virus (HIV) infection, and Chagas disease; iron overload states; amyloidosis; sarcoidosis; and catecholamine-induced takotsubo. B. Pathophysiology of heart failure is the culmination of progressive changes in myocyte architecture that result in changes in ventricular shape, chamber size, ventricular wall thickness, and stiffness that lead to reduced myocardial function and cardiac output. C. Anesthetic considerations. Hemodynamic goals aim to preserve cardiac output and minimize myocardial work. Medical management should be optimized preoperatively. 1. Maintain preload but with caution. Patients with impaired LV function depend on preload to maintain cardiac output; however, they are at risk of pulmonary edema with fluid overload. 2. Avoid tachycardia to minimize myocardial work and preserve ventricular filling during diastole. 3. Aggressively treat arrhythmias as they may lead to reduction in cardiac output. In a failing ventricle, left ventricular end-diastolic volume (LVEDV) is heavily dependent on atrial contraction. The absence of coordinated atrial contractions (such as in atrial fibrillation) can lead to significant compromise of ventricular preload. 4. Preserve contractility. Patients with heart failure may rely on increased sympathetic tone to maintain cardiac output. As a result, they may become profoundly hypotensive following induction or even after analgesic or anxiolytic therapy. Inotropic support may be required. 5. Afterload reduction is favorable as it reduces myocardial work. If vasopressors are needed, they should be used with caution. D. Anesthetic considerations for durable left ventricular assist devices (LVADs) Approximately 20% to 30% of patients with durable LVADs will present for noncardiac surgery. The two most commonly implanted LVADs are the HeartMate 3 (Abbott, Abbott Park, IL) and the HeartWare HVAD (Medtronic, Dublin, Ireland). These are both considered continuous centrifugal flow assist devices and are FDA approved for bridge to transplant or destination therapy that is a final intervention for patients who are poor heart transplant candidates. Hemodynamic goals should focus on maintaining adequate preload and preserved afterload. Patients with LVADs may not be good candidates for regional techniques due to anticoagulation but should be considered for local or MAC techniques when indicated. 1. Preoperative considerations a. Perform a system controller history review and contact the institutional or patient’s LVAD care team. The team can help in interpretation of any alarms or faults the device may have as well as any previous interventions required. b. Review pertinent laboratory studies and physical examination to assess for other sequelae of end-stage heart failure (progression of kidney or liver disease). c. Discuss any current home inotropic medications, anticoagulation, and/or presence of CIEDs. Most LVAD patients will have had a CIED placed prior to LVAD implantation due to their reduced EF and risk for sudden cardiac death. 2. Intraoperative considerations a. Ensure reliable AC power and/or backup battery power for the LVAD b. Monitor with standard ASA monitors, and consider the use of an invasive arterial line if unable to obtain NIBP or if clinically indicated. A pulmonary artery catheter for monitoring pulmonary artery pressure and central venous pressure should be considered depending on procedure type and patient status. We can also consider the use of cerebral oximetry for monitoring of cerebral perfusion. Transesophageal echocardiography is not mandatory but should be available to assist in troubleshooting hemodynamic events. c. Induction of anesthesia should be focused on adequate preoxygenation, avoidance of significant reductions in afterload, maintaining heart rate and rhythm, and optimizing fluid balance. d. Patient can be positioned in the usual fashion including prone and lateral as long as close attention is paid to the driveline of the LVAD. e. Administer surgical site infection prophylaxis with antibiotics in the usual fashion; however, close attention should be paid to proper sterile technique around the driveline site. f. Target mean arterial pressure goals 65 to 80 mm Hg, to be maintained with either volume resuscitation or afterload support (vasopressin preferred due to reduced effect on PVR). If continued hemodynamic instability is observed, consider increasing LVAD pump speed. g. Maintenance of right ventricular function and reducing pulmonary artery pressure is crucial. Preventing hypoxia, hypercarbia, acidosis, and immediate correction of arrhythmias is imperative. For additional reduction in pulmonary artery pressure, consider the use of pulmonary vasodilators such as inhaled epoprostenol, nitric oxide, or milrinone. h. If mechanically ventilating, strategy is aimed at mitigating hypoxia and hypercarbia with an avoidance of excessive positive end-expiratory pressure (PEEP) or high tidal volumes, which can result in a hemodynamically significant reduction in preload. i. Intraoperative challenges specific to LVAD patients include 1. Suction events a. Occurs when the IVS is shifted toward the inflow cannula located in the LV leading to obstruction of the inflow cannula and hypotension, arrythmias, and pump flow reductions. This can result from hypovolemia, increased PVR, and/or increased LVAD pump speeds. Treatment depends on the etiology but can include fluid bolus or transfusion, vasopressor therapy (phenylephrine or vasopressin bolus), and lowering LVAD pump speed. 2. Power failure a. This can occur when there is a disconnection of the driveline from the system controller or when the system is unplugged from AC power with inadequate backup battery. The best way to avoid this is to secure alternative AC power sources and ensuring backup batteries are charged. 3. LVAD pump thrombosis a. This critical event rarely occurs intraoperatively but can lead to complete pump failure and hemodynamic collapse. This occurs when thrombus forms inside the LVAD pump due to inadequate anticoagulation, acute 77  increases in afterload, or dramatic reductions in pump speeds. Signs of pump thrombosis include sudden increases in pump power without resultant increases in pump flow and speed. Treatment usually involves replacement of the LVAD. 3. Postoperative considerations a. Recovery of LVAD patients can be performed in the postanesthesia care unit (PACU) but may require intensive care unit (ICU)–level care depending on the intraoperative course. b. Attention should be paid to any preoperative programming changes of a patient’s CIED; it is advised to reverse these changes in the postoperative period prior to discharge. c. Reinitiate anticoagulation therapy in coordination with the surgical team. 78 VIII. Hypertrophic Cardiomyopathy Hypertrophic cardiomyopathy is a cardiac disorder characterized by asymmetric LV hypertrophy and impaired relaxation in diastole. Although most patients with hypertrophic cardiomyopathy do not have an increased LV outflow tract gradient at rest, many of them develop dynamic outflow tract obstruction with decreased filling and increased contractility. Under these conditions, as flow accelerates through the narrowed LV outflow tract, it creates drag, which pulls the anterior leaflet of the mitral valve toward the septum. This systolic anterior motion (SAM) of the anterior mitral leaflet leads to further outflow obstruction and mitral regurgitation. A. Anesthetic considerations. Factors that worsen the outflow obstruction include decreased arterial pressure, decreased intraventricular volume, increased contractility, and increased heart rate. 1. Maintain normal volume status. 2. Avoid tachycardia. Continue β-adrenergic and calcium channel blocker therapy for heart rate control. 3. Maintain normal sinus rhythm. Consider cardioversion for supraventricular tachycardia. 4. Avoid hypotension. Correct vasodilation with α-adrenergic agonists to avoid tachycardia and marked changes in contractility. Use nitrates and peripheral dilators with extreme caution. 5. Use inotropes with caution. Increased inotropy may exacerbate the outflow obstruction. 79 IX. Congenital Heart Disease With improvement in the survival of congenital heart disease (CHD) patients, anesthesiologists are encountering them with greater frequency as adults in noncardiac surgical settings. Depending on the underlying lesion, an adult with a history of CHD (ACHD) may have an uncorrected lesion or may have undergone a reparative or palliative procedure in the past. As the medical and surgical management of these conditions continues to evolve, different patients with the same original congenital defect may present having undergone significantly different procedures and, as a result, may differ in their anatomy and physiology. Transferring patient care to institutions with extensive experience in managing these disorders should be considered. A. General considerations 1. A thorough understanding of the patient’s cardiac anatomy, physiology, and functional status along with the physiologic stresses associated with the surgical procedure is essential. 2. Myocardial dysfunction may be present as a long-term consequence of the physiology of the original lesion or the subsequent reparative or palliative procedure. It may also be a consequence of chronic hypoxemia. 3. Dysrhythmias are common and may be due to the pathophysiology of the cardiovascular defect or scarring from prior surgery. Intra-atrial reentrant tachycardia and ventricular tachycardia are commonly encountered in this patient population. 4. Cyanotic patients are often polycythemic and at risk for stroke and thrombosis. Intravenous hydration is important. Hemodilution may be considered in the instance of a preoperative hematocrit greater than 60%. Abnormal hemostasis, usually mild in severity, has been noted in patients with cyanotic CHD. 5. Systemic air emboli are a constant danger in the presence of bidirectional or right-to-left shunts. Intravenous lines must be purged of air bubbles, and air filters should be used. 6. Infective endocarditis prophylaxis. Some CHD patients require antibiotic prophylaxis for infective endocarditis with certain procedures. See Chapter 8. 7. A complete discussion of the specific lesions common in ACHD patients is beyond the scope of this chapter. For a more thorough treatment of the subject, plea