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Advanced Perioperative
Crisis Management
i

A DVA N C E D PERI OP ERATI VE CRI SI S

M ANAGEM ENT
ADVANCED PERIOPERATIVE CRISIS
MANAGEMENT

EDITED BY

Matthew D. McEvoy, MD
V I C E - ​C H A I R F O R E D U C A T I O N A L A F F A I R S

DIRECTOR OF CIPHER (CENTER FOR INNOVATION IN PERIOPERATIVE HEALTH,

EDUCATION, AND RESEARCH)

DEPARTMENT OF ANESTHESIOLOGY

VANDERBILT UNIVERSITY MEDICAL CENTER

PROFESSOR OF ANESTHESIOLOGY

VANDERBILT UNIVERSITY SCHOOL OF MEDICINE

NASHVILLE, TN

Cory M. Furse, MD, MPH, FAAP

ASSOCIATE PROFESSOR OF ANESTHESIOLOGY

DEPARTMENT OF ANESTHESIA AND PERIOPERATIVE MEDICINE

MEDICAL UNIVERSITY OF SOUTH CAROLINA

CHARLESTON, SC

1
iv

1
Oxford University Press is a department of the University of Oxford. It furthers
the University’s objective of excellence in research, scholarship, and education
by publishing worldwide. Oxford is a registered trade mark of Oxford University
Press in the UK and certain other countries.

Published in the United States of America by Oxford University Press

198 Madison Avenue, New York, NY 10016, United States of America.

© Oxford University Press 2017

All rights reserved. No part of this publication may be reproduced, stored in

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address above.

You must not circulate this work in any other form

and you must impose this same condition on any acquirer.

CIP data is on file at the Library of Congress

ISBN 978–​0–​19–​022645–​9

This material is not intended to be, and should not be considered, a substitute for medical or
other professional advice. Treatment for the conditions described in this material is highly dependent on
the individual circumstances. And, while this material is designed to offer accurate information with respect
to the subject matter covered and to be current as of the time it was written, research and knowledge about
medical and health issues is constantly evolving and dose schedules for medications are being revised continually,
with new side effects recognized and accounted for regularly. Readers must therefore always check
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for any liability, loss or risk that may be claimed or incurred as a consequence of the use
and/or application of any of the contents of this material.

1 3 5 7 9 8 6 4 2
Printed by Sheridan Books, Inc., United States of America
v

Matt:

To all of my colleagues, mentors, and friends who have

shaped my career and aided in creating the content and
experiences of this book over many years—​thank you.
Even more so to my amazing wife, Amy, our wonderful
5 ‘arrows’, and my parents, all of whom put up with my
crazy schedule and mentor me daily—​thank you. Finally,
Soli Deo Gloria.

Cory:

To my parents and grandparents for your acceptance, love

and support, thank you. Thanks also to my friends, my
family, und meinen lieben Schwiegereltern. To my sons
Sven and Oliver, and my loving and lovely wife Berrit-Ich
dreh mich um dich.
vi

CONTENTS

Preface  xi 12. HYPOVOLEMIC SHOCK   102

Contributors  xiii Paul David Weyker, Christopher Allen-​John Webb
and Tricia E. Brentjens

PART I. CRISIS RESOURCE MANAGEMENT: 13. OBSTRUCTIVE SHOCK   112

NONTECHNICAL SKILLS OF TEAM PERFORMANCE Julia Sobol and Jack Louro

1. A CRITICAL THINKING APPROACH TO THE UNSTABLE

PATIENT  3 PART IV. PULMONARY CRISES
Mark E. Nunnally, Arna Banerjee and Matthew D. McEvoy
14. INTRODUCTION TO PULMONARY URGENCIES AND
2. TEAMWORK AND CRISIS RESOURCE MANAGEMENT   6 EMERGENCIES  121

Scott C. Watkins, Christopher L. Cropsey and Cory M. Furse John D. Mitchell and Marek Brzezinski

3. COGNITIVE AIDS IN CURRENT PRACTICE   9 15. DIFFICULT AIRWAY   126

Christopher L. Cropsey, Scott C. Watkins,
and Matthew D. McEvoy
PART II. CARDI AC CRISES
4. INTRODUCTION TO PERIOPERATIVE CARDIAC
URGENCIES AND EMERGENCIES   15
Jason B. O’Neal and Andrew Shaw
5. MYOCARDIAL ISCHEMIA   23
Jeremy Bennett and Kara Siegrist
6. AORTIC DISRUPTION   30
Adam J. Kingeter and Bantayehu Sileshi
7. CARDIAC DYSRHYTHMIAS   35
Mark Henry and Robert J. Deegan
8. SEVERE VALVULAR DISEASE   53
Yafen Liang and Andrew Shaw
Romina G. Ilic
16. LARYNGOSPASM   134
Cory M. Furse and Matthew D. McEvoy
17. ASPIRATION PNEUMONITIS   139
Agnieszka Trzcinka
18. PHYSIOLOGIC AIRFLOW DISRUPTION:
BRONCHOSPASM, OBSTRUCTIVE
LUNG DISEASE, ASTHMA, AND STATUS
ASTHMATICUS  143
Kinza Sentissi and Stephanie Yacoubian
19. MECHANICAL AIRFLOW DISRUPTION   150
Alissa Sodickson and James Hardy
20. DISRUPTION OF DIFFUSION: INFLAMMATION   156
Shahzad Shaefi and Aaron Mittel
21. DISRUPTION OF DIFFUSION: AIRSPACE DISEASES   164
Nayema Khan and John Pawlowski

PART III. SHOCK 22. PNEUMOTHORAX   171

Jennifer Oliver and K. Annette Mizuguchi
9. INTRODUCTION TO SHOCK   67
Babar Fiza and Vivek Moitra 23. HYPOXIA DURING ANESTHESIA: MACHINE AND
MONITOR ISSUES   176
10. CARDIOGENIC SHOCK   75 Natacha Zamor
Martin Chen and Muoi Trinh
24. AIRWAY FIRE   182
11. DISTRIBUTIVE SHOCK   84 Ju-​Mei Ng
Angela Lee and Gebhard Wagener

vii
vi
PART V. METABOLIC AND ENDOCRINE CRISES
25. INTRODUCTION TO METABOLIC AND ENDOCRINE
DISEASES  189
Stephen F. Dierdorf
SECTION A. METABOLIC DISTURBANCES   191
26. MALIGNANT HYPERTHERMIA   193
Christopher L. Heine
27. PORPHYRIA   200
Stephen F. Dierdorf
28. UNDIAGNOSED PHEOCHROMOCYTOMA   205
Andrew F. Stasic
29. PERIOPERATIVE ADRENAL CRISIS   211
Jing Tao and Jeffrey J. Schwartz
30. CUSHING’S DISEASE   217
Doris M. Hardacker
SECTION B. ENDOCRINE DISTURBANCES   223
31. DIABETIC KETOACIDOSIS   225
Anne Newcomer and Michael Gropper
32. HYPERGLYCEMIC HYPEROSMOLAR STATE   232
Shamsuddin Akhtar
33. HYPOGLYCEMIA   238
Doris M. Hardacker
34. THYROTOXICOSIS   242
Nichole D. Horn
35. MYXEDEMA COMA   247
Jacquelyn E. Allison and Julie D. Dunlap
36. ACUTE LIVER FAILURE   252
Cynthia Wang and Michelle Y. Braunfeld
SECTION C. ELECTROLYTE DISTURBANCES   259
37. HYPERKALEMIA/​HYPOKALEMIA   261
Stephen F. Dierdorf
38. HYPONATREMIA/​HYPERNATREMIA   268
Brian N. Egan
39. HYPOCALCEMIA/​HYPERCALCEMIA   274
Stephen F. Dierdorf
viii
40. HYPOMAGNESEMIA/​HYPERMAGNESEMIA   280
Aali Shah
PART VI. OBSTETRIC CRISES
41. INTRODUCTION TO PERIPARTUM URGENCIES AND
EMERGENCIES FOR THE ANESTHESIA PROVIDER   289
Rachel M. Kacmar
SECTION A. MATERNAL COLLAPSE   293
42. OBSTETRIC LIFE SUPPORT: PULSELESS ELECTRICAL
ACTIVITY/​ASYSTOLE AND PULSELESS VENTRICULAR
TACHYCARDIA/​FIBRILLATION   295
Nathaniel N. Hsu and Richard C. Month
43. PERIMORTEM CESAREAN DELIVERY FOR MATERNAL
CARDIAC ARREST   303
Benjamin Cobb and Steven Lipman
44. STAT CAESAREAN DELIVERY: PREPARATION,
PLANNING, AND TEAM PERFORMANCE   308
Michael G. Richardson
SECTION B. CARDIAC CRISES   317
45. HIGH OR TOTAL SPINAL/​EPIDURAL   319
Feyce Peralta
46. PERIPARTUM CARDIOMYOPATHY   323
Emily J. Baird
47. PERIPARTUM EMBOLISM   332
Elizabeth M. S. Lange and Paloma Toledo
48. SYSTEMIC INFLAMMATORY RESPONSE SYNDROME
AND SEPSIS IN THE PREGNANT PATIENT   340
Daria M. Moaveni
49. SEVERE PREECLAMPSIA   347
Uma Sasso and Emily McQuaid-​Hanson
50. SEVERE PERIPARTUM HEMORRHAGE   354
Joy L. Hawkins
51. VALVULAR DISEASE: SPECIFIC CONSIDERATIONS FOR
MANAGEMENT DURING LABOR AND DELIVERY   363
Shobana Chandrasekhar and C. LaToya Mason
52. VESSELS: CORONARY ARTERY DISEASE IN
PREGNANCY AND PERIPARTUM ACUTE CORONARY
SYNDROME  371
Eleni Kotsis, Jamie M. Zorn and Grace Lim
53. VOLTAGE DISTURBANCES DURING PREGNANCY   378
Heather C. Nixon
C ontents
ix
SECTION C. PULMONARY/​A IRWAY CRISES   385
54. DIFFICULT AIRWAY: SPECIAL CONSIDERATIONS
IN PREGNANCY   387
Rania Elkhateb and Jill M. Mhyre
55. ASTHMA AND PREGNANCY   395
Grant C. Lynde
SECTION D. NEUROLOGIC CRISES   401
56. STROKE/​SUBARACHNOID HEMORRHAGE AND
PREGNANCY  403
Cristina Wood
57. POST–​DURAL PUNCTURE HEADACHE   412
Philip Rubin
SECTION E. METABOLIC/​E NDOCRINE CRISES   419
58. DIABETIC EMERGENCIES IN PREGNANCY   421
Maribeth Guletz and Rebecca Minehart
SECTION F. TOXINS   429
59. MAGNESIUM TOXICITY   431
Anthony T. Chau
60. LOCAL ANESTHETIC SYSTEMIC TOXICITY IN
PREGNANCY  436
Brian F. S. Allen
PART VII. NEUROLOGIC CRISES
61. INTRODUCTION TO ACUTE NEUROLOGIC EVENTS IN
THE PERIOPERATIVE PERIOD   445
Lorri A. Lee
SECTION A. CEREBRAL ORIGIN   447
62. DELIRIUM   449
Bret D. Alvis and Christopher G. Hughes
63. NONTRAUMATIC INTRACRANIAL
HEMORRHAGE  456
Deepak Sharma and Julia Metzner
64. ACUTE STROKE   463
Laurel E. Moore
65. POSTOPERATIVE VISUAL LOSS   470
Lorri A. Lee
66. SEIZURES AND STATUS EPILEPTICUS   478
Neha Aggarwala and Pirjo H. Manninen
Contents ix
67. TRAUMATIC BRAIN INJURY: TRAUMATIC SUBDURAL
HEMORRHAGE/​EPIDURAL HEMORRHAGE   483
Sheena M. Weaver
68. REFRACTORY INTRACRANIAL HYPERTENSION   492
Letha Matthews and John Barwise
69. CEREBRAL SALT WASTING   499
Mark A. Henry and Avinash B. Kumar
70. ACUTE LOSS OF INTRAOPERATIVE EVOKED POTENTIAL
SIGNALS  504
Leslie Jameson
SECTION B. SPINAL CORD, PERIPHERAL NERVOUS
SYSTEM, AND NEUROMUSCULAR JUNCTION ORIGIN   511
71. AUTONOMIC DYSREFLEXIA   513
Koffi Kla
72. NEUROGENIC SHOCK   517
Arnoley S. Abcejo and Jeffrey J. Pasternak
73. MUSCLE WEAKNESS   522
L. Jane Easdown
74. NERVE INJURIES FROM POSITIONING
AND REGIONAL BLOCKS   529
Rajnish K. Gupta and Alexandria N. Nickless
SECTION C. SYSTEMIC ORIGIN   537
75. HEPATIC ENCEPHALOPATHY   539
Bret Alvis and Amy Robertson
PART VIII. PEDIATRIC CRISES
76. INTRODUCTION TO PEDIATRIC CRISES   547
Scott C. Watkins
SECTION A. CARDIAC CRISES   553
77. EMERGENCY NONCARDIAC SURGERY IN THE
CONGENITAL HEART DISEASE PATIENT   555
Marc Hassid and Amanda T. Redding
SECTION B. PULMONARY CRISES   561
78. EPIGLOTTITIS, CROUP, AND STRIDOR   563
Michel Sabbagh and John J. Freely Jr.
79. ACUTE SEVERE ASTHMA AND BRONCHOSPASM   566
Amanda T. Redding and Marc Hassid
80. POST-​TONSILLECTOMY BLEEDING   571
Michelle Sher Rovner
x
81. DROWNING AND NEAR DROWNING   577
Alison M. Jeziorski
SECTION C. NEUROLOGIC CRISES   583
82. SEIZURES AND STATUS EPILEPTICUS   585
Pravin Taneja
SECTION D. OTHER CRISES   597
83. PYLORIC STENOSIS   599
John J. Freely Jr. and Michel Sabbagh
84. SICKLE CELL DISEASE   606
Andrew Franklin
85. HEMOPHILIA (PRESENTATION IN EMERGENCY
SURGERY)  615
J. Matthew Kynes
PART IX. TOXINS
86. INTRODUCTION TO PERIOPERATIVE CRISIS
MANAGEMENT: TOXINS   623
William R. Hand
SECTION A. SPECIFIC TOXICITIES   625
87. LOCAL ANESTHESIA SYSTEMIC TOXICITY   627
Joel Barton and Gavin Martin
x C ontents
88. BETA BLOCKER/​CALCIUM CHANNEL BLOCKER
OVERDOSE  635
Christopher L. Cropsey and Patrick B. Knight
89. COCAINE INTOXICATION AND HYPERTENSIVE
EMERGENCY  642
Jagan Ramamoorthy and Noreen E. Murphy
90. COAGULATION SYSTEM: EMERGENCY SURGERY IN
THE PATIENT TAKING WARFARIN OR LOW MOLECULAR
WEIGHT HEPARIN   650
Shannon Kilkelly
91. COAGULATION SYSTEM: DIRECT ORAL
ANTICOAGULANTS  655
Christina F. Burger, Melissa L. Bellomy
and Joseph J. Schlesinger
92. OPIOID AND BENZODIAZEPINE OVERDOSE   661
Brad Eastman and Larry Field
93. ALCOHOL WITHDRAWAL   667
Tracy McGrane
94. SEROTONIN TOXICITY   674
Patrick E. Britell and Charles M. Andrews
95. ANTICHOLINERGIC OVERDOSE   679
Philip Fanapour, Peggy White and Brenda G. Fahy
96. INSULIN OVERDOSE   687
Richard J. Novak
Index  693
xi
PREFACE
This book has grown out of decades of experience by the
overall group of authors in practicing simulation and teach-
ing concepts of perioperative crisis resource management at
our institutions, at national meetings, and in our residency
and fellowship training programs. The purpose of this book
is to fill a gap between two areas of valuable work that exist
in the perioperative emergency space; namely, between the
books that consist largely of steps of diagnosing a problem
followed by a list of immediate and subsequent treatment
steps and those reference books or review articles that form
the compendium works, including a review of all of the basic
science behind a topic. As such, the goal of this volume is
to be an up-​to-​date, high-​yield, clinically relevant resource
for understanding the epidemiology, pathophysiology, and
proper assessment and management of a wide variety of peri-
operative emergencies. Our target audience is anesthesiolo-
gists, nurse anesthetists, surgeons, recovery and critical care
nurses, and anyone else practicing within the perioperative
arena. Additionally, the case vignettes and discussion ques-
tions (all of which are able to be answered from the chapter
text) are intended to be used by educators both in the clini-
cal teaching setting and in a flipped classroom model.
But why is such a book needed? It is becoming increas-
ingly recognized that perioperative emergencies, including
full cardiac arrest, are different from out-​of-​hospital cardiac
arrest and even different from in-​hospital cardiac and res-
piratory arrest in medical patients. The problems that one
encounters and rates of survival to discharge are signifi-
cantly different in surgical and obstetrical patients. Part of
this is likely explained by the simple differences between
traditional advanced cardiac life support (ACLS) and what
has recently been called anesthesia advanced circulatory life
support (A-​ACLS).4 In traditional ACLS, there is little to
nothing known about the patient and their past medical
history by the team of first responders, the event is normally
not witnessed, the cause is typically a rhythm disturbance
and often due to coronary ischemia, and the focus is on
restoring circulation and oxygenation that may have been
absent for a long period of time. Conversely, in periopera-
tive advanced life support, or A-​ACLS, the event is almost
always witnessed, the first responders almost always know
an extensive amount about the patient, their medical his-
tory, and the events leading to the unstable or pulseless
state, the causes are quite variable, and while the focus is
also on restoring circulation and oxygenation, the interrup-
tion in either of these is frequently very brief.
However, what is similar between perioperative emer-
gencies and all others is that all care teams struggle with
poor adherence to management guidelines. As such, much
work remains to be done in training teams in crisis resource
management principles, including the use of cognitive aids,
which have been shown to greatly increase adherence to
published guidelines during urgent and emergent events.
Accordingly, while the bulk of this book concerns under-
standing the pathophysiology and management of spe-
cific diagnoses, there are three introductory chapters that
review (1) a critical thinking approach to the unstable or
pulseless patient, (2) crisis resource management principles
to improve team performance, and (3) the importance of
cognitive aids in adhering to guidelines during periopera-
tive emergencies.
The remainder of the book is structured based on the
critical thinking approach detailed in ­chapter 1. It is divided
into six major areas of instability: cardiac, pulmonary, neu-
rologic disorders, metabolic/​endocrine, and toxin-​related
disorders, as well as a section dedicated to shock states. As
the discussion in these sections focuses on the general adult
patient, we have also included sections related to specific
emergencies for obstetrical and pediatric patients, as well
as changes to any management algorithms specific to these
patient populations.
Matthew D. McEvoy and Cory M. Furse
xi
xi
CONTRIBUTORS
Arnoley S. Abcejo, MD
Resident in Anesthesiology
Department of Anesthesiology
Mayo Clinic College of Medicine
Rochester, MN
Neha Aggarwala, B.Med, FANZCA
Department of Anesthesia
Toronto Western Hospital,
University Health Network
University of Toronto
Toronto, Canada
Shamsuddin Akhtar, MD
Associate Professor
Department of Anesthesiology and Pharmacology
Yale University School of Medicine
New Haven, CT
Brian F. S. Allen, MD
Assistant Professor of Anesthesiology
Department of Anesthesiology
Vanderbilt University Medical Center
Nashville, TN
Jacquelyn E. Allison, MD
Associate Professor of Clinical Anesthesia
Indiana University School of Medicine
Indianapolis, IN
Bret D. Alvis, MD
Assistant Professor of Anesthesiology
and Critical Care Medicine
Department of Anesthesiology
Division of Critical Care Medicine
Vanderbilt University School of Medicine
Nashville, TN
Charles M. Andrews, MD, FACEP
Assistant Professor
Department of Neurosurgery
Department of Medicine, Division
of Emergency Medicine
Medical University of South Carolina
Charleston, SC
Emily J. Baird, MD, PhD
Assistant Professor
Assistant Program Director
Department of Anesthesiology
and Perioperative Medicine
Oregon Health and Science University
Portland, OR
Arna Banerjee, MD
Associate Professor of Anesthesiology
Assistant Dean for Simulation in
Medical Education
Department of Anesthesiology
Vanderbilt University Medical Center
Nashville, TN
Joel Barton, MD
Assistant Professor
Department of Anesthesia and Perioperative Medicine
Medical University of South Carolina
Charleston, SC
John Barwise, MB, ChB
Associate Professor of Clinical Anesthesiology
and Neurological Surgery
Division of Anesthesiology Critical Care Medicine
Vanderbilt University Medical Center
Nashville, TN
xiii
xvi

Melissa L. Bellomy, MD Anthony T. Chau, BSc (Pharm), ACPR, MD, FRCPC

Resident Physician Department of Anesthesiology, Perioperative and Pain
Department of Anesthesiology Medicine
Vanderbilt University Division of Obstetric Anesthesia
Nashville, TN Brigham and Women’s Hospital
Harvard Medical School
Jeremy Bennett, MD Boston, MA
Assistant Professor Department of Anesthesiology, Pharmacology, and
Cardiothoracic Anesthesia Therapeutics
Vanderbilt University Medical Center University of British Columbia
Nashville, TN Vancouver, Canada

Michelle Y. Braunfeld, MD Martin Chen, MD, MPH

Clinical Professor of Anesthesiology Assistant Professor of Anesthesiology
University of California, Los Angeles Department of Anesthesiology
David Geffen School of Medicine Columbia University Medical Center
Los Angeles, CA New York, NY

Tricia E. Brentjens, MD Benjamin Cobb, MD

Associate Professor of Anesthesiology Fellow
Columbia University Medical Center Department of Anesthesia
Division of Critical Care Anesthesia Stanford University School of Medicine
Director of Liver Transplant Anesthesia Stanford, CA
Columbia University College of Physicians and Surgeons
New York, NY Christopher L. Cropsey, MD
Assistant Professor of Anesthesiology
Patrick E. Britell, MD Department of Anesthesiology
Department of Anesthesiology Division of Critical Care Medicine
Department of Neurosurgery Vanderbilt University Medical Center
Medical University of South Carolina Nashville, TN
Charleston, SC
Robert J. Deegan, MB, PhD, FFARCSI
Marek Brzezinski, MD, PhD Professor of Anesthesiology
Professor Director of Intraoperative Echocardiography
Department of Anesthesia and Perioperative Care Department of Anesthesiology
University of California, San Francisco Vanderbilt University Medical Center
San Francisco, CA Nashville, TN

Christina F. Burger, PharmD, BCPS Stephen F. Dierdorf, MD

Clinical Pharmacist Professor of Clinical Anesthesiology
VA Tennessee Valley Healthcare System Medical University of South Carolina
Assistant Professor of Clinical Pharmacy Charleston, SC
University of Tennessee College of Pharmacy
Nashville, TN Julie D. Dunlap, MD
Assistant Professor of Clinical Anesthesia
Shobana Chandrasekhar, MD Indiana University School of Medicine
Associate Professor Indianapolis, IN
Department of Anesthesiology
Division of Obstetric and Gynecologic Anesthesiology
Baylor College of Medicine
Houston, TX

xiv C ontributors
xv

L. Jane Easdown, MD, MHPE John J. Freely Jr., MD

Associate Professor Department of Anesthesiology
Division of Neuroanesthesiology Greenville Hospital System
Vanderbilt University Medical Center Greenville, SC
Nashville, TN
Michael Gropper, MD
Brad Eastman, DO Professor and Chair
Assistant Professor Department of Anesthesiology
Department of Anesthesia and Perioperative Medicine University of California San Francisco
Medical University of South Carolina San Francisco, CA
Charleston, SC
Maribeth Guletz, MD
Brian N. Egan, MD Clinical Fellow in Anesthesia
Assistant Professor of Anesthesia Harvard Medical School
Indiana University School of Medicine Anesthesia Resident
Indianapolis, IN Department of Anesthesia, Critical Care,
and Pain Medicine
Rania Elkhateb, MD Massachusetts General Hospital
Lecturer of Anesthesia Boston, MA
Cairo University
Giza, Egypt Rajnish K. Gupta, MD
Associate Professor of Anesthesiology
Brenda G. Fahy, MD, MCCM Division of Multispecialty Adult Anesthesiology
Professor of Anesthesiology Vanderbilt University Medical Center
Department of Anesthesiology Nashville, TN
University of Florida
Gainesville, FL William R. Hand, MD
Associate Professor
Philip Fanapour, DO Department of Anesthesia and Perioperative Medicine
Critical Care Medicine Fellow Medical University of South Carolina
Department of Anesthesiology Charleston, SC
University of Florida
Gainesville, FL Doris M. Hardacker, MD
Associate Professor of Clinical Anesthesia
Larry Field, MD Indiana University School of Medicine
Associate Professor Indianapolis, IN
Department of Anesthesia and Perioperative Medicine
Medical University of South Carolina James Hardy, MBBS, BSc
Charleston, SC Staff Anesthesiologist
Northern California Anesthesia Physicians
Babar Fiza California Pacific Medical Center
Clinical Lecturer San Francisco, CA
Department of Anesthesiology
University of Michigan Marc Hassid, MD
Ann Arbor, MI Assistant Professor
Department of Anesthesia and Perioperative Medicine
Andrew Franklin, MD, MBA Medical University of South Carolina
Monroe Carell Jr. Children’s Hospital at Vanderbilt Charleston, SC
Nashville, TN

Contributors xv
xvi

Joy L. Hawkins, MD Leslie Jameson, MD

Professor of Anesthesiology Associate Professor
Director of Obstetric Anesthesia Department of Anesthesiology
University of Colorado School of Medicine University of Colorado School of Medicine
Aurora, CO Aurora, CO

Christopher L. Heine, MD Alison M. Jeziorski, MD, MBA

Assistant Professor of Anesthesia and Perioperative Medicine Assistant Professor
Medical University of South Carolina Department of Anesthesia and Perioperative Medicine
Charleston, SC Medical University of South Carolina
Charleston, SC
Mark Henry, MD Rachel M. Kacmar, MD
Cardiothoracic Anesthesiology Fellow Assistant Professor
Department of Anesthesiology Department of Anesthesiology
Vanderbilt University Medical Center University of Colorado School of Medicine
Nashville, TN Aurora, CO
Mark A. Henry, MD Nayema Khan, MD
Fellow in Critical Care Medicine Department of Anesthesia
Department of Anesthesiology Critical Care and Pain Medicine
Division of Critical Care Beth Israel Deaconess Medical Center
Vanderbilt University Boston, MA
Nashville, TN
Shannon Kilkelly, DO
Nichole D. Horn, MD Assistant Professor
Assistant Professor of Anesthesia Department of Anesthesiology
Indiana University School of Medicine Vanderbilt University Medical Center
Indianapolis, IN Nashville, TN
Adam J. Kingeter, MD
Nathaniel N. Hsu, MD
Department of Anesthesiology
Department of Anesthesiology and Critical Care
Vanderbilt University Medical Center
University of Pennsylvania
Nashville, TN
Philadelphia, PA
Koffi Kla, MD
Christopher G. Hughes, MD Assistant Professor of Clinical Anesthesiology
Associate Professor of Anesthesiology Department of Anesthesiology
and Critical Care Medicine Vanderbilt University Medical Center
Department of Anesthesiology Nashville, TN
Division of Critical Care Medicine
Vanderbilt University School of Medicine Patrick B. Knight, MD
Nashville, TN Department of Anesthesiology
Vanderbilt University Medical Center
Romina G. Ilic, MD Nashville, TN
Staff Anesthesiologist
Eleni Kotsis, DO
Beth Israel Deaconess Medical Center
Obstetric Anesthesiology Fellow
Clinical Instructor
Department of Anesthesiology
Harvard Medical School
University of Pittsburgh School of Medicine
Department of Anesthesia, Critical Care
Magee-​Womens Hospital of the University of Pittsburgh
and Pain Medicine
Medical Center
Beth Israel Deaconess Medical Center
Pittsburgh, PA
Boston, MA

xvi C ontributors
xvi

Avinash B. Kumar, MD, FCCM, FCCP Jack Louro, MD

Associate Professor Assistant Professor of Clinical Anesthesiology
Associate Fellowship Director University of Miami Health System
Department of Anesthesiology Miami, FL
Division of Critical Care
Vanderbilt University Grant C. Lynde, MD, MBA
Nashville, TN Associate Professor of Anesthesiology
Chief, Division of Practice and Process Improvement
James M. Kynes, MD Department of Anesthesiology
Assistant Professor of Anesthesiology Emory University
Department of Anesthesiology Atlanta, GA
Vanderbilt University Medical Center
Nashville, TN Pirjo H. Manninen, MD, FRCPC
Department of Anesthesia
Elizabeth M. S. Lange, MD Toronto Western Hospital
Department of Anesthesiology Toronto, Canada
Northwestern University, Feinberg School of Medicine
Gavin Martin, MB, ChB
Chicago, IL
Professor of Anesthesiology and Division Chief
Angela Lee, MD Division of Orthopaedics, Plastics, and Regional
Fellow Anesthesiology
Department of Anesthesiology Department of Anesthesiology
Columbia University College of Physicians and Surgeons Duke University Medical Center
New York, NY Durham, NC

C. LaToya Mason, MD
Lorri A. Lee, MD
Associate Professor
Professor
Department of Anesthesiology
Departments of Anesthesiology and Neurological Surgery
Division of Obstetric and Gynecologic Anesthesiology
Vanderbilt University Medical Center
Baylor College of Medicine
Nashville, TN
Houston, TX
Yafen Liang, MD Letha Matthews, MBBS
Assistant Professor of Anesthesiology Associate Professor of Clinical Anesthesiology
Division of Cardiothoracic Anesthesiology Division of Multispecialty Anesthesiology
Vanderbilt University Medical Center Clinical Director
Nashville, TN Division of Neuroanesthesiology
Vanderbilt University Medical Center
Grace Lim, MD
Nashville, TN
Assistant Professor
Department of Anesthesiology Tracy McGrane, MD, MPH
University of Pittsburgh School of Medicine Assistant Professor
Magee-​Womens Hospital of the University of Pittsburgh Vanderbilt University Medical Center
Medical Center Nashville, TN
Pittsburgh, PA
Emily McQuaid-​Hanson
Steven Lipman, MD Obstetric Anesthesiology Fellow
Clinical Associate Professor Department of Anesthesiology
Department of Anesthesia Massachusetts General Hospital
Stanford University School of Medicine Boston, MA
Stanford, CA

Contributors xvii
xvi

Julia Metzner, MD Vivek Moitra, MD, FCCM

Departments of Anesthesiology and Pain Medicine and Associate Professor
Neurological Surgery Department of Anesthesiology
University of Washington Columbia University College of Physicians
Seattle, WA and Surgeons
New York, NY
Jill M. Mhyre, MD
Associate Professor Richard C. Month, MD
Department of Anesthesiology Assistant Professor of Clinical Anesthesiology
University of Arkansas for Medical Sciences Department of Anesthesiology and Critical Care
Fayetteville, AR University of Pennsylvania
Philadelphia, PA
Rebecca Minehart, MD, MSHPEd
Assistant Professor in Anesthesia Laurel E. Moore, MD
Harvard Medical School Associate Professor
Assistant Residency Program Director Department of Anesthesiology
Obstetric Anesthesia Fellowship Program Director University of Michigan Health System
Department of Anesthesia, Critical Care, and Pain Ann Arbor, MI
Medicine
Massachusetts General Hospital Noreen E. Murphy, MD
Boston, MA Anesthesiology Resident
University of Wisconsin Hospital and Clinics
John D. Mitchell, MD Madison, WI
Residency Program Director
Department of Anesthesia, Critical Care, and Pain Medicine Anne Newcomer, MD
Beth Israel Deaconess Medical Center Clinical Fellow
Associate Professor of Anesthesia Department of Anesthesiology
Harvard Medical School University of California San Francisco
Boston, MA San Francisco, CA

Aaron Mittel, MD Ju-​Mei Ng, FANZCA

Clinical Fellow in Anesthesia Assistant Professor
Department of Anesthesia, Critical Care and Pain Medicine Harvard Medical School
Beth Israel Deaconess Medical Center Staff Anesthesiologist
Harvard Medical School Department of Anesthesiology, Perioperative
Boston, MA and Pain Medicine
Brigham Women’s Hospital
K. Annette Mizuguchi, MD, PhD, MMSc Boston, MA
Associate Clinical Professor
Department of Anesthesiology Alexandria N. Nickless, DO
University of California Staff Anesthesiologist
San Diego, California Allegheny Health Network
Pittsburgh, PA
Daria M. Moaveni, MD
Assistant Professor of Clinical Anesthesiology Heather C. Nixon, MD
Department of Anesthesiology, Perioperative Medicine, Department of Anesthesiology
and Pain Management University of Illinois Hospital and Health
University of Miami, Miller School of Medicine Sciences System
Jackson Memorial Hospital Chicago, IL
Miami, FL

xviii C ontributors
xi

Richard J. Novak, MD Amanda T. Redding, MD

Adjunct Clinical Associate Professor of Anesthesia Assistant Professor
Department of Anesthesia, Perioperative and Department of Anesthesia and Perioperative Medicine
Pain Medicine Medical University of South Carolina
Stanford University Charleston, SC
Stanford, CA
Michael G. Richardson, MD
Mark E. Nunnally, MD Associate Professor of Anesthesiology
Director, Adult Critical Care Services Vanderbilt University School of Medicine
Department of Anesthesiology, Perioperative Care, and Nashville, TN
Pain Medicine
NYU Langone Medical Center Amy Robertson, MD
New York, NY Assistant Professor of Anesthesiology
Vanderbilt University School of Medicine
Jason B. O’Neal, MD Nashville, TN
Cardiothoracic Anesthesiology Fellow
Department of Anesthesiology Michelle Sher Rovner, MD
Vanderbilt University Medical Center Assistant Professor
Nashville, TN Department of Anesthesia and Perioperative
Medicine
Jennifer Oliver, DO, MPH Medical University of South Carolina
Brigham and Women’s Hospital Charleston, SC
Boston, MA
Philip Rubin, MD
Jeffrey J. Pasternak, MD Assistant Professor of Anesthesiology
Associate Professor of Anesthesiology Yale School of Medicine
Mayo Clinic College of Medicine New Haven, CT
Rochester, MN
Michael Sabbagh, MD, MBA, FAAP
John Pawlowski, MD, PhD Assistant Professor
Director Department of Anesthesia and Perioperative Medicine
Department of Anesthesia, Critical Care, and Pain Medical University of South Carolina
Medicine Charleston, SC
Division of Thoracic Anesthesia
Beth Israel Deaconess Medical Center Uma Sasso, MD
Assistant Professor Assistant Professor
Harvard Medical School Department of Anesthesiology
Boston, MA Ohio State University
Columbus, OH
Feyce Peralta, MD
Assistant Professor of Anesthesiology Joseph J. Schlesinger, MD
Northwestern University Assistant Professor of Anesthesiology Critical Care
Chicago, IL Medicine
Vanderbilt University Medical Center
Jagan Ramamoorthy, MD Staff Physician
Assistant Professor of Anesthesiology Anesthesiology Service—​Surgical Critical Care
University of Wisconsin Hospital and Clinics VA Tennessee Valley Healthcare System
Madison, WI Nashville, TN

Contributors xix
x

Jeffrey J. Schwartz, MD Julia Sobol, MD

Associate Professor Assistant Professor of Anesthesiology
Department of Anesthesiology Columbia University Medical Center
Yale University School of Medicine NewYork-​Presbyterian Hospital
New Haven, CT New York, NY

Kinza Sentissi, MD Alissa Sodickson, MD

Resident Staff Anesthesiologist
Department of Anesthesiology Department of Anesthesiology, Perioperative
Brigham and Women’s Hospital and Pain Medicine
Boston, MA Brigham and Women’s Hospital
Boston, MA
Shahzad Shaefi, MD
Instructor in Anaesthesia Andrew F. Stasic, MD
Department of Anesthesia, Critical Care and Pain Associate Professor of Clinical Anesthesia
Medicine Indiana University School of Medicine
Beth Israel Deaconess Medical Center Indianapolis, IN
Harvard Medical School
Boston, MA Jing Tao, MD
Assistant Professor
Aali Shah, MD Department of Anesthesiology
Assistant Professor of Clinical Anesthesia Yale University School of Medicine
Indiana University School of Medicine New Haven, CT
Indianapolis, IN
Paloma Toledo, MD, MPH
Deepak Sharma, MBBS, MD, DM Center for Healthcare Studies
Departments of Anesthesiology & Pain Medicine Northwestern University, Feinberg School of Medicine
and Neurological Surgery Chicago, IL
University of Washington
Muoi Trinh, MD, MPH
Seattle, WA
Assistant Professor of Anesthesiology
Andrew Shaw, MB, FRCA, FFICM, FCCM Department of Anesthesiology
Professor and Executive Vice Chair Icahn School of Medicine at Mount Sinai
Department of Anesthesiology New York, NY
Vanderbilt University School of Medicine
Nashville, TN Agnieszka Trzcinka, MD
Instructor of Anesthesia
Kara Siegrist, MD Department of Anesthesiology, Perioperative
Anesthesiology Resident and Pain Medicine
Vanderbilt University Medical Center Brigham and Women’s Hospital
Nashville, TN Harvard Medical School
Boston, MA
Bantayehu Sileshi, MD
Department of Anesthesiology Gebhard Wagener, MD
Vanderbilt University Medical Center Associate Professor
Nashville, TN Department of Anesthesiology
Columbia University College of Physicians and Surgeons
New York, NY

xx C ontributors
xxi

Cynthia Wang, MD Peggy White, MD

Assistant Professor Assistant Professor of Anesthesiology
Department of Anesthesiology and Pain Department of Anesthesiology
Management University of Florida
University of Texas Southwestern Medical Center Gainesville, FL
Dallas, TX
Cristina Wood, MD, MS
Scott C. Watkins, MD Assistant Professor
Assistant Professor of Anesthesiology Department of Anesthesiology
Department of Anesthesiology University of Colorado School of Medicine
Division of Pediatric Anesthesia Aurora, CO
Vanderbilt University Medical Center
Nashville, TN Stephanie Yacoubian, MD
Staff Anesthesiologist
Sheena M. Weaver, MD Department of Anesthesiology, Perioperative
Assistant Professor of Clinical and Pain Medicine
Anesthesiology Brigham and Women’s Hospital
Department of Anesthesiology Boston, MA
Division of Critical Care Medicine
Vanderbilt University Medical Center Natacha Zamor, MD
Nashville, TN Staff Anesthesiologist
Signature Healthcare
Christopher Allen-​John Webb, MD Brockton, MA
Clinical Instructor of Anesthesiology
Regional Anesthesiology Fellow Jamie M. Zorn, MD
Department of Anesthesiology, Perioperative, Obstetric Anesthesiology Fellow
and Pain Medicine Department of Anesthesiology
Stanford University University of Pittsburgh School of Medicine
Stanford, CA Magee-​Womens Hospital of the University of Pittsburgh
Medical Center
Paul David Weyker, MD Pittsburgh, PA
Critical Care Fellow
Department of Anesthesia and
Perioperative Care
University of California, San Francisco
San Francisco, CA

Contributors xxi
xxi

A DVA N C E D PERI OP ERATI VE CRI SI S

M ANAGEM ENT
1

PA R T I .

CRISIS RESOURCE MANAGEMENT

N O N T E C H N I C A L S K I L L S O F T EAM PERFORMANCE
3
1.
A CRITICAL THINKING APPROACH TO THE UNSTABLE PATIENT
Mark E. Nunnally, Arna Banerjee, and Matthew D. McEvoy
INTRODUC TI O N
Several factors unfairly shape the medical community’s
approach to crisis. First, almost all assertions about ade-
quacy of care are influenced by hindsight bias.1,2 Second,
there is a common misperception that choices are obvious
in real time, and that there are simple routes to success and
failure.3 Such factors underscore the truth that clinicians do
not think enough about how to think about crises.
Cardiac arrest under anesthesia is rare, and outcomes
are better in the perioperative arena than in other settings,
particularly out of hospital arrest. Modern estimates of inci-
dence range from 5.64 to 7.1 per 10,000.5 Encountering
a rare event interrupts routine care and can lead to errors
in patient care and result in injury to the patients or sen-
tinel events.6 With such a low frequency, it becomes
challenging to maintain competence in these areas, and
practitioners must master skills in crisis management inde-
pendent of direct practice. This chapter focuses on two such
approaches. The first is learning to recognize deterioration
early enough to reverse it and avoid arrest. The second is
practicing simulated crises.
Recognizing crisis and taking evasive action are diffi-
cult skills. The rareness of cardiac arrest is confounded by
the multiple sources of failure, further rarefying infrequent
events. However, the practice of anesthesiology deals with
rare complications routinely. Difficult mask ventilation
combined with difficult laryngoscopy might occur at a fre-
quency of 4 in 1000,7 while malignant hyperthermia occurs
in about 0.18 in100,000.8 In order to be prepared for res-
cue, low-​frequency events need to be regarded as routine.
IS THIS A PRO BLEM?
Even the astute and experienced clinician can make errors
during crisis situations,9 as shown by closed claims analy-
sis and simulated studies.10 To attain expertise, clinicians
need to be exposed to these rare challenging situations,
deliberately practice managing these situations, and reflect
on their performance.11 Although emphasis is placed on
medical knowledge and learning technical skills, critical
incident reporting and observational studies show that
nontechnical skills such as dynamic decision-​making and
teamwork are a major determinant of success in crisis man-
agement.12 To manage a crisis a clinician must first detect
the problem and then take necessary steps to correct it. This
involves a constant loop of observation and recognition of
the crisis, dynamic decision-​making, and therapeutic action
followed by reevaluation.
Strategies used in Cockpit/​Crew Resource Management
(CRM) have been adopted by the healthcare industry to aid
in this process and promote safety. These include the use of
checklists and cognitive aids, established protocols for cri-
sis management, and formal training in dynamic decision-​
making, resource management, and teamwork. Studies
have shown that acquisition of these skills requires specific
education.13 Simulation-​based curricula have been devel-
oped to integrate these strategies and teach these skills.14-​
16
Teamwork training programs have also been developed,
of which TeamSTEPPS, Veterans Affairs Medical team
training program, and CRM are a few. The Effective
Management of Anesthetic Crises course is a standard-
ized 2.5-​day simulation-​based course and is a component
of training for Fellowship of Australian and New Zealand
College of Anesthetists.17
There is growing knowledge that to successfully manage
a crisis a clinician requires both technical and nontechnical
skills. Nontechnical skills complement technical skills and
contribute to safe and efficient task performance. They do
not relate to medical knowledge and can be broadly divided
into two categories—​cognitive skills (resource utilization,
planning, decision-​making, situation awareness) and inter-
personal skills (team work, leadership, communication).18
Simulation-​based curricula have been developed and used
effectively to teach and practice these skills.19
Human factors literature shows that cognitive functions
can fail during stress. Cognitive aids (posters, flowcharts,
3
4
checklists, mnemonics) can aid clinicians during crisis situ-
ations and help them recall key actions.20 Simulated train-
ing sessions may be helpful in educating clinicians on the
use and implementation of these aids.21 Mnemonics and
protocols have also been developed to aid specifically dur-
ing crisis.22
But, does this training translate into clinical practice?
Studies have shown that first-​year residents perform better
than third-​year residents after simulation-​based education
in critical care medicine.23 In a review of a small number
of studies using simulation-​based learning, authors found
that CRM skills learned in the simulation center are
transferred to the clinical setting and this improves clini-
cal outcome and may even show a decrease in mortality.24
Simulation-​trained residents also responded to cardiac
arrest events with greater compliance to American Heart
Association protocols than more experienced team leaders
not trained with simulation.25 More studies are required
to see whether simulation-​based CRM training improves
patient outcome.
P RINC IP L ES FO R D EVELO PI N G A CRI T IC AL
THINK ING A PPROACH
Crisis rarely occurs out of the blue, but it seems that way in
real time. The evolution of arrest is often presaged by subtle
abnormalities. Although these abnormalities take time to
evolve, often they are not clinically apparent until shortly
before crisis, and they do not cross a detectable threshold
until late in their evolution.26 Combinations of more subtle
signs may be apparent earlier, but detection of these requires
expertise and is confounded by fixation bias,27 when there is
a natural tendency to focus on one feature to the exclusion
of others. This is one reason why someone new to a crisis
situation may see things those involved in the process over
time will not.
How does a clinician best recognize and treat insta-
bility? Traditionally this emphasizes vital signs, which
offer reasonable sensitivity but poor specificity until cri-
sis is imminent. A systolic blood pressure of 95 mmHg in
an adult could be benign or a marker of pending arrest.
Another approach is to look at markers of perfusion as a
way to assess the adequacy of the circulation. Urine out-
put, serum lactate, assessment of tissue oxygenation, as with
near-​infrared spectroscopy (NIRS) or other tissue-​specific
probes, or central or mixed-​venous hemoglobin oxygen
saturations are indirect variables for the assessment of the
circulation. Finally, understanding that experts may uncon-
sciously recognize patterns, any sense that something is not
4 P art I . C risis R esource M anagement
quite right may be the best way for experts to see an arrest
before it happens—​this likely means that there is a deep
level of pattern recognition/​perturbation to which one
should pay attention in routine processes of care, always
asking why a patient may be deviating from responding to
ongoing management as expected.
When crisis, or pending crisis, is recognized, clinicians
must act quickly and decisively. Creating and narrowing a
differential diagnosis and formulating a stepwise approach
to management lets a clinician take decisive action in the
short space of time before arrest occurs. A classic strat-
egy, promoted by Lawrence D. H. Wood, involves asking
three crucial questions of the patient’s circulation.28 The
first question asks whether the cardiac output is too high
or too low. This question splits the differential diagnoses
into high-​and low-​cardiac output shock states. The second
asks whether the heart is too full or too empty. Intravenous
fluid resuscitation is frequently a solution to intraopera-
tive shock, but there are times when resuscitation might be
harmful. The final question addresses “what doesn’t fit?”
Rarely is crisis the result of a single random event. Shock
can unmask other problems. An astute clinician should
always be thinking of concomitant problems or alternative
explanations.
S OME PR AC T IC AL S T E PS
As noted above, persistent vigilance and practice are two
key components to being prepared when a perioperative
crisis occurs. A mental model that may help when such an
event does occur should, as noted above, start with circula-
tion. While there are a number of major categories in which
emergencies can occur (as denoted in the sections of this
book), the final common pathway for all crises involves the
circulatory system. As such, starting with an evaluation of
hemodynamics and then moving to other systems is logi-
cal, particularly for the novice, but also for the expert—​any
of whom can be prone to mental errors under stress. Thus,
when a patient becomes unstable, we suggest that clinicians
as the following questions:
1. Is there a pulse? [If no, start CPR and follow
appropriate ACLS management guidelines, with noted
alterations based on specific diagnosis (e.g., LAST)]
2. Is the origin of the instability:
a. Pump—​need for inotropic support?
b. Pipes—​need for increased/​reduced afterload?
5
c. Preload—​need for additional preload/​volume?
d. Voltage—​arrhythmia causing disturbance?
e. Vessels—​coronary ischemia/​infarction?
f. Valves—​severe valvular disease causing problem?
3. If answers to all of the above are “no,” then the issue is
not directly of cardiac origin and the clinician can move
to sequentially assessing other organ systems:
a. Pulmonary—​oxygenation, ventilation, mechanics,
airway control?
b. Neurologic—​global or focal issue? peripheral or
central?
c. Metabolic/​Endocrine—​past medical history? recent
lab values?
d. Toxins—​medication administration history, and so
forth.
4. Keep in mind that cardiac instability is always the
final common pathway and that this sequence should
be iteratively pursued until a definitive diagnosis
is reached, the problem averted, and the patient is
stabilized.
As you approach subsequent chapters in this text, we
encourage continued use of this paradigm to consider how
to place each specific diagnosis and treatment within one’s
overall mental model for approaching the unstable patient.
R EF ERENCES
1. Caplan RA, Posner KL, Cheney FW. Effect of outcome
on physician judgments of appropriateness of care. JAMA.
1991;265(15):1957–​60.
2. Einav S, Kaufman N, Sela HY. Maternal cardiac arrest and perimor-
tem caesarean delivery: evidence or expert-​based? Resuscitation.
2012;83(10):1191–​1200.
3. Wears RL, Cook RI. The illusion of explanation. Acad. Emerg. Med.
2004;11(10):1064–​5.
4. Nunnally ME, O’Connor MF, Kordylewski H, Westlake B, Dutton
RP. The incidence and risk factors for perioperative cardiac arrest
observed in the national anesthesia clinical outcomes registry.
Anesth. Analg. 2015;120(2):364–​70.
5. Kazaure HS, Roman SA, Rosenthal RA, Sosa JA. Cardiac arrest
among surgical patients: an analysis of incidence, patient charac-
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148(1):14–​21.
6. Joint Commission on Accreditation of Healthcare Organizations.
Sentinel event statistics—​June 30, 2005. http://​www.jcaho.org/
accredited+organizations/ ​ s entinel/ ​ s entinel+event+statistics.
htm2005. Accessed May 5, 2006.
7. Kheterpal S, Healy D, Aziz MF, et al. Incidence, predictors, and
outcome of difficult mask ventilation combined with difficult
A Critical Thinking A pproach to the Unstable Patient
laryngoscopy: a report from the Multicenter Perioperative Outcomes
Group. Journal of the American Society of Anesthesiologists.
2013;119(6):1360–​9.
8. Lu Z, Rosenberg H, Brady JE, Li G. Prevalence of malignant hyper-
thermia diagnosis in New York State ambulatory surgery center dis-
charge records 2002 to 2011. Anesth. Analg. 2016;122(2):449–​53.
9. Metzner J, Posner KL, Lam MS, Domino KB. Closed claims’
analysis. Best Practice and Research Clinical Anaesthesiology.
2011;25(2):263–​76.
10. DeAnda A, Gaba D. Role of experience in the response to simulated
critical incidents. Anesth. Analg. 1991;72(3):308–​15.
11. Ericsson KA. Deliberate practice and the acquisition and main-
tenance of expert performance in medicine and related domains.
Acad. Med. 2004;79(10):S70–​S81.
12. Gaba DM, Fish KJ, Howard SK, Burden A. Crisis Management in
Anesthesiology. 2nd ed. Philadelphia, PA: Elsevier Saunders; 2014.
13. Blackwood J, Duff JP, Nettel-​Aguirre A, Djogovic D, Joynt C.
Does teaching crisis resource management skills improve resuscita-
tion performance in pediatric residents? Pediatr. Crit. Care Med.
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14. Holzman RS, Cooper JB, Gaba DM, Philip JH, Small SD, Feinstein
D. Anesthesia crisis resource management: real-​life simulation train-
ing in operating room crises. J. Clin. Anesth. 1995;7(8):675–​87.
15. Gaba DM, DeAnda A. A comprehensive anesthesia simulation envi-
ronment: re-​creating the operating room for research and training.
Anesthesiology. 1988;69(3):387–​94.
16. Gaba DM, Howard SK, Fish KJ, Smith BE, Sowb YA. Simulation-​
based training in anesthesia crisis resource management (ACRM): a
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17. Weller J, Morris R, Watterson L, et al. Effective management of anaes-
thetic crises: development and evaluation of a college-​accredited
simulation-​based course for anaesthesia education in Australia and
New Zealand. Simulation in Healthcare. 2006;1(4):209–​14.
18. Flin R, Patey R, Glavin R, Maran N. Anaesthetists’ non-​technical
skills. Br. J. Anaesth. 2010;105(1):38–​44.
19. Yee B, Naik VN, Joo HS, et al. Nontechnical skills in anesthesia
crisis management with repeated exposure to simulation-​ based
education. Journal of the American Society of Anesthesiologists.
2005;103(2):241–​8.
20. Gaba DM. Perioperative cognitive aids in anesthesia: what, who,
how, and why bother? Anesth. Analg. 2013;117(5):1033–​6.
21. Goldhaber-​Fiebert SN, Howard SK. Implementing emergency man-
uals: can cognitive aids help translate best practices for patient care
during acute events? Anesth. Analg. 2013;117(5):1149–​61.
22. Runciman W, Merry A. Crises in clinical care: an approach to man-
agement. Quality and Safety in Health Care. 2005;14(3):156–​63.
23. Singer BD, Corbridge TC, Schroedl CJ, et al. First-​year residents
outperform third-​year residents after simulation-​based education in
critical care medicine. Simulation in Healthcare. 2013;8(2):67.
24. Boet S, Bould MD, Fung L, et al. Transfer of learning and patient
outcome in simulated crisis resource management: a system-
atic review. Canadian Journal of Anesthesia/​ Journal canadien
d’anesthésie. 2014;61(6):571–​82.
25. Wayne DB, Didwania A, Feinglass J, Fudala MJ, Barsuk JH,
McGaghie WC. Simulation-​based education improves quality of
care during cardiac arrest team responses at an academic teaching
hospital: a case-​control study. Chest. 2008;133(1):56–​61.
26. Cook R, Rasmussen J. “Going solid”: a model of system dynamics
and consequences for patient safety. Quality and Safety in Health
Care. 2005;14(2):130–​4.
27. Jermias J. Cognitive dissonance and resistance to change: the influ-
ence of commitment confirmation and feedback on judgment
usefulness of accounting systems. Accounting, Organizations and
Society. 2001;26(2):141–​60.
28. Wood LDH. The pathophysiology of the circulation in critical ill-
ness. In: Hall J, Schmidt G, Wood LDH, eds., Principles of Critical
Care. 3rd ed. New York: McGraw Hill; 2005:231–​48.
5
6
2.
TEAMWORK AND CRISIS RESOURCE MANAGEMENT
Scott C. Watkins, Christopher L. Cropsey, and Cory M. Furse
INTRODUC TIO N
A healthcare team can be thought of as a distinct set of two
or more clinicians working together with specific, indi-
vidual roles and tasks toward a common goal.1,2 Teamwork
can be thought of as the dynamic behaviors, cognitions,
attitudes, and skills that allow a team to perform its stated
goal.1 Nearly two decades ago, the report To Err Is Human
from the Institute of Medicine (IOM) identified team-
work as a key target for improving the quality and safety of
patient care.1,3 Although much progress has been made in
the years since the seminal IOM report was issued, team-
work remains as critical as ever to the safe delivery of health-
care. This may reflect a concurrent shift in the delivery of
medicine from “solo” practitioners to teams of healthcare
providers.
Long before the IOM report, the field of anesthesiology
recognized the importance of human error, and not deficits
in medical knowledge and skills, in relation to anesthetic
morbidity, including breakdowns in key teamwork com-
ponents such as lapses in preparation, vigilance, and the
application of existing knowledge.4 Thus, it should be no
surprise that anesthesiologists were the first to adapt “cri-
sis” resource management (CRM) to healthcare.5 Over the
last 25 years, CRM has become synonymous with a style
of team performance epitomized by healthcare providers in
high acuity, time-​pressured environments such as acute care
practice.
EVOL UTION O F CRI SI S RESO URCE
M A NAGEM EN T
In the 1970s, investigation into a series of commercial air-
line crashes highlighted “failures of interpersonal commu-
nications, decision making, and leadership” as the leading
contributors of “human error” in airline disasters.6 The term
“cockpit” resource management (CRM) was first used by
the NASA psychologist John K. Lauber.6 Lauber initially
6
used the term in the early 1970s, but it was not until the
above referenced crash investigations that CRM reached a
tipping point in aviation safety.6,7 In the ensuing years, the
general approach was implemented by all major commer-
cial airlines and evolved from “cockpit” to “crew” resource
management to emphasize the role of all aircrew members
in safe operation and level the pilot-​centric hierarchical cul-
ture.6,7 Commercial airline disasters are now extremely rare,
forcing aviation safety experts to turn to direct observations
of crew behaviors and surveys of crew attitudes to measure
the continued success of CRM.
The same errors in human performance identified in
the airline crashes of the 1970s are increasingly being rec-
ognized as contributors to medical errors and disasters
in healthcare. When one considers the major advances in
medical knowledge, therapeutics, and technology over
the last few decades, it is no surprise that human error has
emerged as one of the leading contributors to medical mis-
haps. Consider a few of the major advances within the field
of anesthesiology over the last few decades: the advent of
safer volatile anesthetics accompanied by widespread use of
depth of anesthesia monitors, routine use of pulse oximetry
and end-​tidal carbon dioxide sensors, improved hemody-
namic monitoring, and the proliferation of airway devices
making lost airways a rare occurrence. Along with these
technological advances, or possibly as a result of them, there
has been a shift toward a culture of safety within the prac-
tice of anesthesia. Thus, parallels between the evolution of
aviation safety and the safety of anesthesia are easy to draw.
ANE S T H E S IA C R IS IS R E S OU R C E
MANAGE ME NT
David Gaba, one of the pioneers of CRM and the patient
safety movement in anesthesia, describes CRM as “the
articulation of principles of individual and crew behav-
ior in ordinary and crisis situations that focuses on skills
of dynamic decision-​making, interpersonal behavior, and
7

evenly among team members so that no one member of the

KEY COMPONENTS OF CRISIS RESOURCE
BOX 2.1 team becomes task overloaded.
MANAGEMENT It is important that the team and/​or its leader know the
environment, that is, know what resources are available and
Call for Help
where to obtain those resources. Resources might include
Designate a Team Leader an expert clinician, a piece of equipment, transportation
for mobilizing the patient to another location, and so forth.
Establish Clear Roles
The assignment of team roles should be based on the indi-
Distribute the Workload vidual skill and knowledge required to fulfill those roles;
thus it is helpful if a team leader is familiar with his/​her
Know the Environment
team members.
Communicate Effectively It is important that the team leader and team members
communicate effectively using closed-​loop communication
Anticipate and Plan
in which statements, orders, and questions are read back for
Mobilize Resources Early confirmation and clarity. When possible, the team leader
and followers should communicate with each other using
Allocate Attention Wisely
first names and avoid making statements into thin air, so
Use all Available Information that it is clear at whom each statement is directed. The team
leader should remain receptive to the questions or concerns
Use Cognitive Aids
of all team members throughout the crisis.
SOURCE: Adapted from Goldhaber-​Fiebert SN, Anesthesia & Analgesia. 2013.
8
During a crisis, teams should be proactive in their
thoughts and actions, that is, anticipate and plan, in order
to stay two steps ahead of the crisis and to ensure that every
team management.”5 Gaba and colleagues have taught member of the team has a clear understanding of the prob-
and studied CRM for nearly 3 decades. Their guide to lem, the plan, and future actions. For example, when draw-
CRM includes nearly a dozen key points that any high-​ ing up the first dose of epinephrine in a cardiac arrest, the
functioning team of experts should consider when manag- team member responsible for medications should anticipate
ing a crisis (see Box 2.1).8 the potential need for a second or third dose and should
The first, and possibly the most important, step in CRM draw up those medications ahead of time. Teams should
is calling for help. One should call for help sooner rather than anticipate the need for and mobilize resources early, as there
later, mobilizing more help than might be needed and ensur- is less harm in calling for resources and not using them than
ing that the correct type of help is obtained,; for example in the in needing a resource and not having it when the difference
event of a difficult or lost airway, it is best to call for help before between a good and a bad outcome may be measured in
cardiac arrest occurs and to seek help from those with skills in seconds. For example, when managing a difficult airway, it
advanced airway management. Calling for a second opinion or is best to call for difficult airway equipment or a surgeon
help from a colleague or another expert is a useful tool when skilled in cricothyrotomy before one gets into a “can’t intu-
faced with a clinical dilemma or when one becomes fixated on bate, can’t ventilate” situation.
a problem in which a solution is not readily apparent. Teams need to allocate attention wisely in order to
The order in which the remaining key components of avoid fixation on one problem/​task at the expense of miss-
CRM are carried out is less important, but one might argue ing other problems such as a change in patient condition
that the second step should be designating a team leader. or at the expense of critical tasks such as the performance
Designating oneself as the team leader may be hard for of continuous chest compressions. Team leaders may wish
some, especially more junior, clinicians to do. It is impor- to assign a team member to monitor for changes in con-
tant that the leader maintain a global perspective, remain dition. Teams will want to use all available information
hands-​off as much as possible, be capable of directing other sources to ensure that no critical piece of the clinical puz-
members of the team, and be open and receptive to feed- zle is missed and to ensure that the team does not spend
back and input from team members. The best team leader too much time or fixate on one single piece of the puzzle.
may not be the senior-​most clinician in the room. The team For example, if following intubation no end-​tidal CO2 is
leader should establish clear roles for the remaining mem- present it is probably best to look for other confirmation
bers of the team and ensure that the workload is distributed signs of endotracheal intubation or remove the tube and

Teamwork and Crisis R esource M anagement 7

8
mask ventilate than it is to spend time troubleshooting
a “faulty” CO2 monitor. Finally, teams should consider
using any and all available cognitive aids, such as emer-
gency manuals, checklists, or smartphone applications,
during a crisis to facilitate information retrieval and aid
clinical decision-​making.
There is clear evidence that breakdowns in teamwork
lead to increased patient morbidity.9 Unfortunately, the
evidence for how we mitigate breakdowns in teamwork is
less clear. The rarity of bad outcomes, especially in the prac-
tice of anesthesia, makes it difficult to use clinical outcomes
to measure teamwork and CRM. Thus, the evidence for
teamwork and CRM consist primarily of observational and
survey data.1,9 As a result, interventions to improve team-
work and CRM in healthcare have struggled to achieve the
widespread adoption as seen in other industries.
However, the core principles that have been dis-
cussed in this chapter are widely accepted as the govern-
ing principles of best practice for delivery of high-​quality
care during urgent and emergent situations throughout
the perioperative period. The reader should keep these
in mind as specific diagnoses are considered throughout
the rest of the book, as proper adherence to CRM is the
vehicle through which specific care for a particular condi-
tion (e.g., severe anaphylaxis or local anesthetic toxicity)
should be delivered.
8 P art I . C risis R esource M anagement
R E F E R E NC E S
1. Weaver SJ, Rosen MA, DiazGranados D, et al. Does teamwork
improve performance in the operating room? A multilevel evalu-
ation. Joint Commission Journal on Quality and Patient Safety.
2010;36(3):133–​42.
2. Salas E, Dickinson TL, Converse SA, Tannenbaum SI. Toward an
understanding of team performance and training. In: Salas RWSE,
ed., Teams: Their Training and Performance. Norwood, NJ: Ablex;
1992:3–​29.
3. Kohn LT, Corrigan JM, Donaldson MS. To Err Is Human: Building
a Safer Health System. Vol 6. Washington, DC: National Academies
Press; 2000.
4. Olsson G, Hallen B. Cardiac arrest during anaesthesia: a com-
puter aided study in 250 543 anaesthetics. Acta Anaesthesiologica
Scandinavica. 1988;32(8):653–​64.
5. Gaba D. Crisis resource management and teamwork training in
anaesthesia. British Journal of Anaesthesia. 2010;105(1):3–​6.
6. Helmreich RL, Merritt AC, Wilhelm JA. The evolution of crew
resource management training in commercial aviation. International
Journal of Aviation Psychology. 1999;9(1):19–​32.
7. Gordon S, Mendenhall P, O’Connor BB. Beyond the Checklist:
What Else Health Care Can Learn from Aviation Teamwork and
Safety. Ithaca: Cornell University Press; 2012.
8. Goldhaber-​ Fiebert SN, Howard SK. Implementing emergency
manuals: can cognitive aids help translate best practices for patient
care during acute events? Anesthesia and Analgesia. 2013;117(5):
1149–​61.
9. Manser T. Teamwork and patient safety in dynamic domains
of healthcare: a review of the literature. Acta Anaesthesiologica
Scandinavica. 2009;53(2):143–​51.
9
3.
COGNITIVE AIDS IN CURRENT PRACTICE
Christopher L. Cropsey, Scott C. Watkins, and Matthew D. McEvoy
INTRODUC TI O N
As noted in the prior chapter, use of a cognitive aid (CA)
is now considered to be a core component of managing
perioperative crisis events. Interestingly, the earliest known
description of a perioperative CA comes from a 1924 arti-
cle by Babcock in which he describes posting a checklist for
managing emergencies on the wall of the operative theater.1
Despite this early advocacy, the use of such aids in medicine
are only now gaining widespread acceptance. Along the
way, other professions made cognitive aids an important
part of their daily performance. In The Checklist Manifesto:
How to Get Things Right, Atul Gawande describes the cre-
ation of flight checklists in the 1930s in response to the
increasing complexity of newer generation airplanes.2
Almost a century later, it has become clear that the cogni-
tive demands posed by the complexity of the current peri-
operative environment, which is further increased during a
crisis situation, have exceeded the limits of human cognitive
processing. For this reason, CAs are experiencing a renais-
sance, with some clinicians calling for CAs to be integrated
into all aspects of clinical care in order to improve patient
care, and a number of CAs dedicated to the management
of perioperative patients have been developed and are read-
ily available to all clinicians (See Table 3.1).3 This chapter
describes the various types of CAs, their implementation in
clinical practice, and directions for future advances.
TY P ES OF CO G N I TI VE AI D S
Modern CAs can be classified in several different ways,
one of which is the medium on which they are provided.
Historically CAs were printed on paper, but with the
proliferation of electronic handheld devices (i.e., smart-
phones and tablets), novel modes of delivery have received
increased attention. There are advantages and drawbacks to
both. Paper is attractive due to the ease of printing and low
cost, and unlike software that must be developed for a spe-
cific device or operating system, paper is universal. In addi-
tion, paper requires little maintenance with no batteries to
charge or software to upgrade and thus no risk of a paper
checklist “crashing” in the midst of a crisis due to either
hardware or software limitations. These are important con-
siderations for those that practice in extreme environments
where reliable access to either electricity or the Internet is
limited.
Electronic formats do offer some significant advantages
over paper. Electronic devices are able to store increasing
amounts of information on smaller devices, while the infor-
mation contents of paper CA are limited by the amount of
information that can be physically contained on a card or
inside a book. Electronic devices are able to move beyond
a simple checklist and provide audiovisual prompts to users
as well as dynamic decision support in the form of active
feedback and recommendations based on the actions of the
user and the outcome of the patient. This dynamic process
is difficult, if not impossible, to replicate using paper and
opens up the possibilities of increasing levels of real-​time
support for clinicians—​especially as technology and artifi-
cial intelligence improve.4 Finally, some electronic formats,
for example, mobile and Web-​based applications, offer the
ability to push automatic updates to users as new recom-
mendations and guidelines become available, thus ensur-
ing that clinicians are practicing with the most current
information.
DE S IGN AND IMPLE ME NTAT ION
Although one may assume that providing a CA of any
sort would automatically enhance outcomes, this is likely
not true, as CAs are merely tools that remain dependent
on human users for their effectiveness. Improving human
performance is a complex task that requires a change of
human behavior. Aspects of a CA’s design and usability may
9
10
TA B L E 3 . 1 P E R I OP E RAT IV E CO G N IT IVE A ID S A N D RE L ATE D RE S O U RCE S
Emergency Manuals Implementation Collaborative (EMIC)
http://​www.emergencymanuals.org/​
Society for Pediatric Anesthesia
http://​www.pedsanesthesia.org/​wp-​content/​uploads/​2015/​02/​
Critical_​Event_​Checklists.pdf
Stanford Emergency Manual
http://​emergencymanual.stanford.edu/​
Ariadne Labs OR Crisis Checklists
https://​www.ariadnelabs.org/​
Checklist for Treatment of Local Anesthetic Systemic Toxicity (LAST)
https://​www.asra.com/​
Malignant Hyperthermia resources:
Malignant Hyperthermia Association of the United States (MHAUS)
http://​www.mhaus.org/​healthcare-​professionals
European Malignant Hyperthermia Group (EMHG)
https://​emhg.org/​nc/​home/​
The Anaesthetic Crisis Manual
http://​theacm.com.au/​
play an important role in its overall effectiveness through
its impact on user behavior. Once a CA is used, there is no
guarantee that it will be used correctly; this may be further
compounded by poor design, such as small text or unclear
instructions leading to confusion or even error in following
a particular algorithm. At the most basic level, many anes-
thesia providers will simply choose to not use an available
CA, especially if it is perceived to be difficult to use; this has
been reported both anecdotally and experimentally.5,6 This
highlights the importance of proper implementation of
CAs into clinical practice being dependent on their usabil-
ity and ultimate effectiveness. Users will be unlikely to use a
CA if it is not immediately available or if they are unaware
it is available at all. Furthermore, unfamiliarity with the
content of a given CA can lead to inappropriate use. For
example, the user may select a checklist for the wrong crisis
or fail to switch to a different checklist if the original diag-
nosis is revised.7
Although popular perception may be that “anyone can
read a checklist,” in reality these should be viewed more as
medical devices, which require adequate training to use
effectively and may be most effective when used by a clinician
trained in their use. This has led to some debate about the
most appropriate user of the CA. Traditionally, checklists
were employed directly by the team leader. However, newer
research suggests that other methods of use may be more
10
Tools and resources for implementing CAs into local practice. Links to
other resources.
Emergency manual dedicated to the perioperative care of the pediatric
patient. Developed by a panel of experts in pediatric anesthesia. Free
download. Available in multiple languages. There is also a mobile
application available for free download.
Emergency manual dedicated to the perioperative management of adult
patients. Includes information for 25 perioperative crises and Crisis
Resource Management resources. Free download.
Crisis checklist with information on 12 of the most common operating
room crises. Free download. Also includes resources for implementation.
Resources for the management of LAST based on expert consensus of
the American Society for Regional Anesthesia and Pain Medicine. Paper
checklist available for free download. Links to mobile applications included.
Websites includes extensive resources for the management of MH including
CAs for purchase and information on preparing one’s practice for MH crises.
A quick reference handbook with a collection of 22 life-​threatening anesthetic
crises. Both paper and electronic formats available for purchase.
effective. One such model, referred to as a “leader-​reader”
model, uses a dedicated “reader” to physically interface
with the CA while providing prompts to the team leader.
The purported advantage of this is that it frees the leader
from the additional cognitive load of using the CA itself.
This paradigm has been shown to improve performance
in simulations of local anesthetic toxicity and obstetric
emergencies.8,9 Those interested in implementing CA into
local clinical practice should refer to the many resources on
implementation available online. (See Table 3.1).
C ONT E NT
Regardless of design, format, or method of implementation,
a CA must contain valid and reliable information, prefer-
ably based on the latest evidence-​based guidelines. The con-
tent of CAs designed for perioperative crises are frequently
based on a mixture of evidence-​based guidelines (advanced
cardiac life support), expert consensus (local anesthetic sys-
temic toxicity, malignant hyperthermia), and the authors’
opinion. Therefore, CA users should thoroughly assess the
information contained in CA before basing clinical deci-
sions on the contents of a CA. Evidence-​based guidelines
are frequently updated with new and different recommen-
dations, so CAs based on these recommendations also need
P art I . C risis R esource M anagement
1
to be updated. Therefore, one should ensure that the most
up-​to-​date CA is available and used. With the recognition
of the important role teamwork and communication play
in clinical practice, many CAs now include both technical
(i.e., medical) and nontechnical (i.e., teamwork, communi-
cation) information.
FUTUR E DI RECTI O N S
Ultimately, despite a number of ongoing questions, it
would appear that cognitive aids—​when properly design
and used—​have the ability to improve the management of
crisis situations.10–​14 There is evidence that attitudes toward
their use are changing; the age-​old stigma that a CA was
a “crutch” or a “cheat sheet” is giving way to the recogni-
tion that modern crisis situations are too complex to rely
on memory alone.15 Nonetheless, a number of outstand-
ing issues remain. There is a paucity of data on how to best
design a CA, and few studies have commented on usability
testing.16 Furthermore, much of the evidence for their use
is in the form of simulation assessment. Additional inves-
tigation is now needed to demonstrate an improvement
in actual patient outcomes (the so-​called T2 and T3 level
testing as described by Goldhaber-​Feibert et al.6) As these
hurdles are overcome, it is expected that CAs will continue
to gain wider use in the management of perioperative crises.
As the reader considers the specific diagnoses through-
out the bulk of this book, they should consider how cogni-
tive aids containing the management steps described could
be of benefit in the event of them managing these partic-
ular emergencies in the clinical setting. Readers are again
directed to a number of existing resources for many of the
events in this book as shown in Table 3.1.
R EF ERENCES
1. Babcock WW. Resuscitation during anesthesia. Anesth Analg.
1924;3:208–​13.
2. Gawande A. The Checklist Manifesto: How to Get Things Right.
1st ed. New York, NY: Metropolitan Books; 2010.
Cognitive Aids in C urrent P ractice
3. Augoustides JGT, Atkins J, Kofke WA. Much ado about checklists:
who says I need them and who moved my cheese? Anesth Analg.
2013;117(5):1037–​8. doi:10.1213/​ANE.0b013e31829e443a.
4. Morell RC, Cooper JB. APSF sponsors workshop on imple-
menting emergency manuals. Anesth Patient Saf Found Newsl.
2016;30(3):68–​71.
5. Watkins SC, Anders S, Clebone A, et al. Paper or plastic? Simulation
based evaluation of two versions of a cognitive aid for managing
pediatric peri-​operative critical events by anesthesia trainees: evalu-
ation of the society for pediatric anesthesia emergency checklist.
J Clin Monit Comput. 2016 Jun;30(3):275–​83.
6. Goldhaber-​ Fiebert SN, Howard SK. Implementing emergency
manuals: can cognitive aids help translate best practices for patient
care during acute events? Anesth Analg. 2013;117(5):1149–​61.
doi:10.1213/​ANE.0b013e318298867a.
7. Borshoff D. The limitations of crisis checklists: Anesth Analg.
2014;118(6):1387–​8. doi:10.1213/​ANE.0000000000000183.
8. Burden AR, Carr ZJ, Staman GW, Littman JJ, Torjman MC. Does
every code need a “reader?” Improvement of rare event manage-
ment with a cognitive aid “reader” during a simulated emergency:
a pilot study. Simul Healthc J Soc Simul Healthc. 2012;7(1):1–​9.
doi:10.1097/​SIH.0b013e31822c0f20.
9. McEvoy MD, Hand WR, Stoll WD, Furse CM, Nietert PJ.
Adherence to guidelines for the management of local anesthetic
systemic toxicity is improved by an electronic decision support
tool and designated “reader.” Regional anesthesia and pain medi-
cine 2014 Aug;39(4):299–​305. PMID: 24956454 PMC ID: PMC
4068273.
10. Harrison TK, Manser T, Howard SK, Gaba DM. Use of cognitive aids
in a simulated anesthetic crisis. Anesth Analg. 2006;103(3):551–​6.
doi:10.1213/​01.ane.0000229718.02478.c4.
11. Low D, Clark N, Soar J, et al. A randomised control trial to deter-
mine if use of the iResus© application on a smart phone improves
the performance of an advanced life support provider in a simulated
medical emergency. Anaesthesia. 2011;66(4):255–​62. doi:10.1111/​
j.1365-​2044.2011.06649.x.
12. Ziewacz JE, Arriaga AF, Bader AM, et al. Crisis checklists for the
operating room: development and pilot testing. J Am Coll Surg.
2011;213(2):212–​7.e10. doi:10.1016/​j.jamcollsurg.2011.04.031.
13. Field LC, McEvoy MD, Smalley JC, et al. Use of an electronic deci-
sion support tool improves management of simulated in-​hospital
cardiac arrest. Resuscitation. 2014;85(1):138–​ 42. doi:10.1016/​
j.resuscitation.2013.09.013.
14. Arriaga AF, Bader AM, Wong JM, et al. Simulation-​based trial of
surgical-​crisis checklists. N Engl J Med. 2013;368(3):246–​ 53.
doi:10.1056/​NEJMsa1204720.
15. Krombach JW, Edwards WA, Marks JD, Radke OC. Checklists and
other cognitive aids for emergency and routine anesthesia care: a sur-
vey on the perception of anesthesia providers from a large academic
US institution. Anesthesiol Pain Med. 2015;5(4). doi:10.5812/​
aamp.26300v2.
16. Marshall S. The use of cognitive aids during emergencies in anesthe-
sia: a review of the literature. Anesth Analg. 2013;117(5):1162–​71.
doi:10.1213/​ANE.0b013e31829c397b.
11
12
13

PA R T I I .

CARDIAC CRISES
14
15
4.
INTRODUCTION TO PERIOPERATIVE CARDIAC URGENCIES
AND EMERGENCIES
Jason B. O’Neal and Andrew Shaw
C
ardiac arrest in the perioperative period is unique
from cardiac arrest in other scenarios, given that
the event is typically witnessed and real-​time vital
signs are often being monitored. This enables the respond-
ing physician to quickly formulate a focused differential
diagnosis and develop a suitable treatment plan. In order
to establish the correct diagnosis, one must have an ade-
quate understanding of normal cardiac physiology and of
cardiovascular pathology and the ways in which this may
adversely affect cardiac function.
The heart consists of four chambers—​two atria and
two ventricles. The right and left sides of the heart each
have an atrium and ventricle. It is the difference in mean
peripheral to mean central venous pressure that delivers
blood to the right side of the heart, which then pumps
blood into the lungs, allowing gas exchange across the
alveolar-​capillary membrane. Oxygenated blood then
drains to the left side of the heart, which pumps blood
around the systemic circulation to all organs of the body.
Forward flow from the right to the left side of the heart,
across the pulmonary circulation, is ensured by two pairs
of unidirectional valves—​mitral and aortic on the left, and
tricuspid and pulmonic on the right. Adequate blood flow
to the heart itself is necessary for the heart to function
properly. Blood is supplied via the left anterior descend-
ing (LAD), right coronary (RCA), and left circumflex
(LCx) arteries. The left ventricle (LV) receives blood
predominantly during diastole, while the right ventricle
(RV) is perfused throughout both diastole and systole.
The conduction system in the heart coordinates electro-
mechanical coupling as follows: The sinoatrial (SA) node
triggers a depolarization wave that spreads across the right
and left atria and, after a brief delay, the atrioventricular
(AV) node conducts this signal forward to both ventricles
through the bundle of His.
This description may be a simplified overview of how the
heart functions, but it does provide a convenient conceptual
framework for consideration of the individual components
affecting myocardial performance. Anesthesiologists com-
monly discuss preload, afterload, contractility, heart rate,
and rhythm as the most important components for ade-
quate cardiac output. Insults to any of these parameters can
be detrimental to the heart. For our purposes, and in what
follows, we identify, describe, and understand these terms
and use their definitions to assist in formulating a succinct,
direct approach to an unstable patient in the perioperative
period: Pumps, Pipes, and Preload, Vessels, Voltage, and
Valves.
The right side of the heart pumps blood to the lungs,
while the left heart pumps blood throughout the body.
When one or both of these Pumps fail, the patient may
become unstable very rapidly. Heart failure may be cat-
egorized into chronic, acute, or acute on chronic subtypes,
with an overall incidence of 1% to 6% in patients undergo-
ing major surgery.1 This incidence is even higher in patients
with preexisting heart conditions, at up to 25% quoted
in the literature.1 Patients with chronic heart failure must
have detailed anesthetic plans prior to undergoing surgery
if morbidity is to be avoided. Fluid balance is a critical part
of this plan, and fluid shifts in the wrong direction can eas-
ily drive a patient with chronic heart failure into the acute
category, leading to cardiogenic shock. Several other causes
of cardiogenic shock exist, of which the more common
include cardiomyopathy, myocardial infarction (MI), and
massive pulmonary embolism (PE). Although LV failure is
the cause of most instances of cardiogenic shock, the RV
must not be overlooked, as the treatment of LV and RV fail-
ure is different.2 Acute trauma to the heart either from an
extrinsic process prior to surgery or possibly an iatrogenic
cause (i.e., surgical misadventure) must also be considered
when evaluating pump failure.
Pipes, or peripheral blood vessels, are natural exten-
sions from the heart, but any disruption in their nor-
mal function also places excessive strain on the heart in
15
16
addition to its typical workload. Conditions such as sep-
sis, anaphylaxis, or medication-​induced vasodilation ren-
der blood vessels ineffective at maintaining sufficient tone
to guarantee adequate perfusion to end organs.3 Cardiac
dysfunction in sepsis is common and may manifest as
impaired fluid responsiveness, decreased contractility,
and ventricular dilation. Anaphylaxis in the periopera-
tive setting may be as high as 1 in 383 cases,4 although
the exact mortality rate is not known.5 Angiotensin-​
converting enzyme inhibitors may contribute to hypo-
tension during anesthesia and have been reported as
possible contributors to cardiac arrest intraoperatively.6
All of these conditions are indicators of increased risk
when caring for a patient undergoing surgery.
In order for the heart to perfuse organs throughout
the body, adequate blood volume must be available to the
heart to pump. Several definitions for Preload exist, but
for our purposes the left ventricular end diastolic volume
(LVEDV) will serve as preload. Preload is affected by
venous pressure as well as venous return. Hypovolemia
due to blood loss, inadequate fluid deficit replacement,
or medication effect can dramatically decrease preload,
leading to hemodynamic instability. Estimating pre-
load is both critical and difficult, and may be achieved
using transesophageal echocardiography (TEE), pulmo-
nary artery occlusion pressure, central venous pressure,
pulse pressure variation, and many other measurements.
Although the reliability of some methods for assessing
preload continues to be questioned,7–​9 the anesthesiolo-
gist should be familiar with these techniques and pos-
sess the ability to obtain measurements and interpret the
results in order to rule out a diagnosis of hypovolemia
and evaluate preload status. Most of these measurement
techniques assess response to a fluid challenge rather than
an actual value for the volume of blood in the left ven-
tricle at end diastole, and this fact should not be forgot-
ten at the bedside when fluid administration decisions
are being made.
In addition to the pipes, the other Vessels we discuss
are the coronary arteries, which supply blood directly to
the heart. Disruption in blood flow through the coro-
naries due to hypotension or hypoperfusion impedes the
myocardium from receiving adequate oxygen and thereby
produces an inability to supply enough energy for the
heart to meet demand to perfuse the body. Blockages due
to plaque buildup or rupture, lack of blood flow from
hypotension, or tachycardia increasing oxygen demand
can all cause ischemia to occur as a result of myocardial
oxygen supply/​demand mismatch. Detection of ischemic
16
changes with TEE and/​or electrocardiography (ECG)
may be of great importance when confronted with an
unstable patient in the perioperative period. The detection
of myocardial ischemia using leads II, V4, and V5 periop-
eratively has a sensitivity of 96%.10 The use of continuous
ECG in the operating room (OR) is now considered the
minimal standard of care, and it may often demonstrate
the first signs of ischemia intraoperatively. More recently,
there has been a suggestion that detection of troponin
leaks in patients with suspected ischemia in the periopera-
tive period might be advantageous,11 although the useful-
ness of this test in the OR may be limited due to timing
of detection, which currently must be post hoc, by defini-
tion. Echocardiography is superior to ECG for detecting
ischemia and may also assist with making a diagnosis of
MI in patients with cardiac arrest.12
The conduction of electrical activity through the heart
constitutes the Voltage component of our aide memoire
for differential diagnosis of cardiac arrest in the OR. The
conduction system regulates the rate and also the rhythm
of the heart. The anesthesiologist must determine whether
disturbances in either the rate or rhythm are contributing to
the patient’s instability. If the patient is hemodynamically
unstable, algorithms directed at whether or not the patient
has a pulse are used first. Pulseless dysrhythmias include
asystole, pulseless electrical activity, ventricular fibrillation,
and ventricular tachycardia. Pulsatile rhythms may include
symptomatic bradycardia and narrow versus wide complex
tachycardias. Identifying the correct rhythm is crucial, as
the treatment is reliant on the rhythm, but diagnosis of the
underlying cause of the dysrhythmia should not be forgot-
ten. The potential causes are discussed in detail later in this
chapter.
Valves promote unidirectional blood flow between
the atrium to the ventricle and from the ventricle out
of the heart. In cases where a valve is diseased or injured,
blood flow may become bidirectional, obstructed, or both.
Understanding the physiologic changes with a stenotic ver-
sus regurgitant valve and the appropriate intervention are of
the utmost importance when treating an unstable patient.
An anesthesiologist’s ability to evaluate valves using TEE is
integral for patients with diseased valves and during surgical
interventions on valves.13
Outside of these six components, other causes of car-
diac collapse must be considered. Some of these include
aortic dissection, drug overdose, toxin exposure, hyperten-
sive crisis, disseminated intravascular coagulopathy, and
sickle cell crisis. The diagnosis and treatment for all of the
aforementioned conditions is elaborated in the remainder
P art I I . C ardiac C rises
17

BRADYCARDIA
inadequate for clinical situation or
Heart rate < 60 and/or rapidly falling
Note: heart rates between 40 and 60 are common in adults under general anesthesia

- Check surgical field/ anesthetic: Hypervagal vs hypovolemia?

- Check oximeter, capnometry, skin and field blood color R/O hypoxia!
- Could this be auto-PEEP? Specific
- Check ST segment and T-wave algorithm
Y
- Could this be gas/air embolism? thrombo/fat embolism? in addition
- Could this be high spinal? to below
- Could this be local anesthetic toxicity?
- Could this be hyperkalemia?
- Monitor ECG (identify rhythm), blood pressure, oximetry, capnography

Signs or symptoms of poor perfusion caused by the bradycardia?

(e.g. acute altered mental status, ongoing chest pain, or other signs of shock)

If severe hypotension, persistent

poor perfusion, or low ET CO2
Perfusion? (<15mm Hg): start CPR
Adequate
Blood pressure?
Observe/Monitor - Administer Oxygen, Assist
- Search for contributing ventilation, Intravenous fluids wide
causes Poor open, and secure the airway
- Consider expert AVOID hyperventilation!
consultation
- Consider atropine 0.5 mg IV while
awaiting pacer. May repeat to a total
dose of 3 mg. If ineffective, begin
Differential Diagnosis of transcutaneous pacing
Bradycardia
- Consider IV bolus epinephrine 10 to
Hypoxia 100 mcg. If response, consider
Hypervagal epinephrine (0.05 to 0.10 mcg/kg/min)
Hypovolemia or dopamine (2 to 10 mcg/kg/min)
Hyperkalemia/Hypokalemia infusion while awaiting pacer or if pacing
Hydrogen lon (acidemia) is ineffective.
Hypothermia
Hypoglycemia - Prepare for transcutaneous pacing:
Malignant Hyperthermia use without delay for high-degree block
(type II second-degree block or third-
Tamponade degree AV block). Esophageal pacing
Tension pneumothorax appropriate with narrow QRS
Trauma
Thrombosis/embolus, pulmonary - Consider CVL, arterial line
Thrombosis, coronary
QT prolongation - Prepare for transvenous pacing
Toxins - Treat contributing causes
Pulmonary hyperTension - Consider expert consultation
Figure 4.1 Bradycardia algorithm.

of this chapter, but for now we consider some of the dif-
ferences between the American Heart Association (AHA)
Advanced Cardiac Life Support (ACLS) and a more
anesthesia-​centric ACLS approach.
Outside of the perioperative setting, ACLS is often ini-
tiated on a person suffering an unwitnessed and unmoni-
tored cardiac arrest. As was previously mentioned, in the
OR when a patient suffers cardiac arrest several monitors
relaying real-​time vital signs are available both before and
during the inciting event. This can be viewed as an advan-
tage when formulating a differential diagnosis and making a
more directed treatment plan. An ECG provides a rhythm
for the anesthesiologist to analyze. Pulse oximetry gives the
anesthesiologist oxygen saturation throughout the arrest.
More advanced monitoring such as TEE, arterial cannu-
lation, and pulmonary artery catheterization can provide
clues when evaluating the patient for PE, MI, hypovolemia,
and many other causes of cardiac collapse. End-​tidal carbon
dioxide may assist with diagnosis and also help to evalu-
ate the effectiveness of chest compressions during cardio-
pulmonary resuscitation. In addition, access to the various
treatment options is readily available, enabling the anesthe-
siologist to give medications intravenously and/​or deliver
shocks in a shorter time period than in the field. Given
these advantages, one would assume an anesthesiologist
would act quickly when presented with an unstable patient.
This is not always the case, as sometimes clinicians may fail
to recognize early signs and symptoms of imminent cardiac

I ntroduction to P erioperative C ardiac Urgencies and E mergencies 17

18

Tachycardia

- Give O2
- Monitor EKG, blood pressure, oximeter, capnometry
- Could this be:
-light anesthesia? A: Assess Airway
-hypovolemia? B: Hypoventilation
-hyperthermia? C: Cardiac output/preload
-early hypoxia or hypercapnea? D: Drugs (anaphylaxis/MH)
-auto-PEEP?
- Perform Echo or TEE if possible

- Perform Immediate
- Verity or obtain IV access Synchronized Cardioversion
N Altered mental status? Y
- Obtain 12 lead EKG/rhythm strip - Verity or obtain IV access
Chest pain?
- Measure QRS - Consider expert consultation
Hypotension?
Narrow - If patient becomes pulseless, see
Comprehensive algorithm
Narrow QRS Wide (>0.12 sec)
Is the rhythm regular?
N Wide QRS
Y Is the rhythm regular?

- Regular
- Consider vagal maneuvers
- Give adenosine 6 mg IV push
- II no response, give adenosine
12 mg IV push
Convert?
N channel blocker
Y choloride 1 gm IV
- Likely re-entrant SVT
- Observe for recurrence
- Treat recurrence with
adenosine or longer acting AV
node blockers (e.g, beta
blocker or dilltiazem
- Irregular Y N
- atrial fibrillation vs atrial flutter
vs MAT
- Regular - Irregular
- low ejection fraction or severe
hypotension: load Amiodarone - if Ventricular - If atrial fibrillation with
150 mg IV over 10 min tachycardia or aberrancy, see irregular
uncertain rhythm narrow complex
- normal EF and acceptable BP- give Amiodarone tachycardia
beta blocker or calcium 150 mg IV over min
- If Torsades-de-Pointes,
and Calcium
give Magnesium
sulfate 2 g IV over 5
- Amio minutes (esp if patient
- If rhythm does Not convert, likely alternative
had baseline prolonged
atrial flutter, EAT, or junctional Lidocaine 1-1.5 QT interval). Consider
tachycardia mg/kg IV Q 3-5
repeat dose.
- Flate control with beta blocker or min x3
calcium channel blocker, consider - Prepare for - If pre-excited atrial
infusion synchronized fibrillation (AF+WPW),
-Reevaluate and treat possible cardioversion consider amiodarone
underlying causes 150 mg IV over 10
- If SVT with
aberrancy, give min and expert
adenosine 6 or 12 consultation
mg IV push,

Reconsider A, B, C, D
from above

Figure 4.2 Tachycardia algorithm.

failure. And this may lead to failure to rescue a patient suf-
fering from a severe adverse event.14
The likely underlying causes of cardiac arrest in the
perioperative setting differ from those outside of the
OR. In addition to the H’s and T’s listed in the AHA
ACLS,15 Moitra et al.14 rightfully suggest Hypervagal,
Malignant Hyperthermia, QT prolongation, and
Pulmonary hyperTension to be included in the anesthe-
siologist’s differential diagnosis list. Patients are exposed
to multiple different medications and anesthetic agents
perioperatively, and these compound or even ultimately
cause cardiac arrest. Although anaphylaxis may also
occur outside of the OR, several medications adminis-
tered to patients, particularly nondepolarizing muscle
relaxants and antibiotics, must be considered in the peri-
operative setting. Volatile agents and succinylcholine
may trigger malignant hyperthermia in the anesthetized
patient. Conditions such as hypovolemia or gas embo-
lism are much less likely to occur outside of the OR, but
should be on the differential depending on the operation

18 P art I I . C ardiac C rises

19

LV Shock
Afterload Reduction
Hypotensive? N SVR > 1600 Fenoldopam
Perform Echo/ or narrow pulse Nitroprusside
TEE in intubated patient pressure Nesiritide
ACEi
Y

Decrease
PEEP pRBC
CVP < 12 mmHg Y
Hct < 27-32?
or SPV/PPV >12%
Check CVP
and N Plasma
SPV or PPV Expander
CVP > 22
R/O tamponade
low SvO2 or ScvO2
R/O tension PTX
SPV/PPV>15%**
CVP 12-22
SPV/PPV < 12%

Vasopressin
SVR < 800 Norepinephrine
or Epi ± Dobutamine
wide pulse pressure Phenylephrine
MAINTAIN SVR < 800
Check SVR and
pulse pressure
Dobutamine
SVR > 1000
Epinephrine
or
IABP
narrow pulse pressure
VAD
Figure 4.3 LV Shock algorithm.

RV Shock
Hypotensive?
Perform Echo/
TEE in intubated patient

Give O2
Decrease PEEP

pRBC
Y
Hypovolemic?
Fluid Responsive? Hct < 27-32?
e.g, CVP < 12-16? Y Plasma
N Expanders
N

CVP > 20 R/O tamponade?

SVO2 or ScvO2 <65%** R/O tension pneumothorax?

Known or Suspected
Increased PVR? ? Decreased
coronary perfusion? Diminished
RV contractility?
Y
Y
Give O2 Y
consider Milrinone ± Vasopressin Phenylephrine
iNO Norepinephrine
Vasopressin Dobutamine
Note: these Milrinone
medications may Epinephrine
increase PVR
Figure 4.4 RV Shock algorithm.
20

Adequate Prepare for DL,

Prepare for DL N Y
Mask await next
Prepare LMA Ventilation? scheduled pause

Preform DL during
CPR
DL during pause
T = 20 sec
ETT Y
Done!
Success?

N Y
ETT
Success?
Request 20 sec pause
Done!
N

ETT Y Resume CPR

Done!
Success?

N Change operator,
(change tools)
LMA in mask ventilation
await scheduled
ROSC?
pause
+ carotid pulse
or
Ventilation Y + Aline/pleth Plan
Adequate? or Y Intubation
step-up in capnograph
N

Continue CPR
Change Tools/Operator N
LMA out/DL during CPR
Done...
Note:
ETT Y Change from 30:2
Done!
Success? preintubation
to
N 8-10 breaths/minute
asynchronous
Request 20 sec pause postintubation

ETT Y
Done!
Success?
Alternative
N

Invasive Airway

Figure 4.5 Airway algorithm.

and information available from continuous intraopera-
tive monitors.
Unlike the conventional AHA ACLS approach, the
treatments for different cardiac arrest scenarios in the peri-
operative period are not evidence based, but instead are sug-
gested protocols derived from clinical experience. Cardiac
arrest in the OR is still a rare occurrence, with estimates of
up to only 19.7 out of 10,000 anesthetics.16 This makes it
difficult to conduct studies and provide evidence behind
the appropriate treatment of the various causes for cardiac
arrest perioperatively. Anesthesia-​centric ACLS algorithms
modify the accepted AHA ACLS algorithms (see Figures
4.1, 4.2, 4.3, 4.4, 4.5, and 4.6,).14 The remaining chapters
in this section on cardiac crises focus on some of the major
causes of severe cardiac instability and arrest in the OR and
provides details on using our monitoring systems to make
a diagnosis and treat the underlying cause of cardiac arrest
both swiftly and correctly in the perioperative setting.

20 P art I I . C ardiac C rises

21

Comprehensive Algorithm

- Check surgical field/anesthetic: Hypervagal vs hypovolemia?

- Check EKG, oximeter, capnometry, skin and field blood color, quick-check circuit
- Start CPR, call for help, defibrillator
- Hold surgery, discontinue anesthesia, ventilate with 100% O2, IVs wide open
- Check ST segment and T-wave
- Could this be gas/air embolism? thrombo/fat embolism?
- Could this be local anesthetic toxicity?
- Could this be hyperkalemia?

- Confirm EKG cardiac arrest: A-line tracing, pulse, plethysmograph, capnometer

- Start CPR Titrate to ET CO2 of > 20mm Hg, Diastolic BP > 40mm Hg
- Establish airway, Avoid Hyperventilation!
- Perform Echocardiography ASAP

Shockable Check rhythm Not Shockable

Shockable?
VF/VT Asystole/PEA

- Give 1 Shock: 200-360 J Biphasic - Continue CPR

1 - Resume CPR immediately
- If VT: Calcium chloride 1 gram IV
- Epinephrine 1 mg IV, repeat Q 3-5 min
May replace 1 dose of EPi with 40 Units

Check capnometer for CO2.

2 Vaso IV
- Consider Calcium choloride if hyperkalemia
is in the differential
No
If present hold CPR and check rhythm - If PEA:
Shockable rythm? Could this be hypovolermia?
Could this be tamponade?
Y
Could this be tension pneumothorax?
Could this be auto-PEEP?
- Continue CPR while defibrillator is charging Could this be an embolism?
- Give 1 Shock: 200-360 J Biphasic
- Resume CPR immediately
- Eplnephrine 1 mg IV Repeat Q 3-5 min No
- May replace 1 dose of EPi with 40 U Vaso IV Check rhythm
Shockable?

Shockable
Check rhythm No - If Asystole, go to Box 2
Shockable? - If not pulse, go to Box 2
- If pulse present, begin Go to Box 1
Shockable post-resuscitation care Shockable

- Continue CPR while defibrillator is charging

- Give 1 shock: 200-360 J Biphasic
- Resume CPR immediately
- Consider anti-arryhthmics
- Amiodarone 300 mg IV or
- Lidocaine 1-1.5 mg/kg IV Q 3-5 min x3
- Consider Magnesium sulfate 2 grams IV
for? Torsades-de-pointes (esp in patients
with baseline prolonged QT)

Figure 4.6 Comprehensive algorithm.

R EF ERENCES 4. Savic LC, Kaura V, Yusaf M, et al.; Anaesthetic Audit and Research
Matrix Yorkshire. Incidence of suspected perioperative anaphylaxis: a
multicenter snapshot study. J Allergy Clin Immunol Pract. 2015 Feb
1. Weissman PF, et al. Perioperative heart failure in noncardiac surgery.
13. pii: S2213-​2198(15)00018-​5. doi: 10.1016/​j.jaip.2014.12.016.
UpToDate. 2012 March 28. Accessed March 3, 2015.
[Epub ahead of print].
2. Reynolds HR, Hochman JS. Cardiogenic shock: current con-
5. Dewachter P, Mouton-​Faivre C, Emala CW. Anaphylaxis and
cepts and improving outcomes. Circulation. 2008;117(5):686–​97.
anesthesia: controversies and new insights. Anesthesiology. 2009;
doi: 10.1161/​CIRCULATIONAHA.106.613596.
111(5):1141–​50. doi: 10.1097/​ALN.0b013e3181bbd443.
3. Zanotti-​Cavazzoni SL, Hollenberg SM. Cardiac dysfunction in
6. Goodman SM, Krauser D, Mackenzie CR, Memtsoudis S. Cardiac
severe sepsis and septic shock. Curr Opin Crit Care. 2009;15(5):
arrest during total hip arthroplasty in a patient on an angiotensin
392–​7. doi: 10.1097/​MCC.0b013e3283307a4e.

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2
receptor antagonist. HSS J. 2012;8(2):175–​ 83. doi: 10.1007/​
s11420-​011-​9225-​0. Epub 2012 May 11.
7. Mohsenin V. Assessment of preload and fluid responsiveness in
intensive care unit. How good are we? J Crit Care. 2015 Jan 8. pii:
S0883-​9441(15)00006-​4. doi: 10.1016/​j.jcrc.2015.01.004. [Epub
ahead of print].
8. Sasai T, Tokioka H, Fukushima T, et al. Reliability of central venous
pressure to assess left ventricular preload for fluid resuscitation in
patients with septic shock. J Intensive Care. 2014;2(1):58. doi:
10.1186/​s40560-​014-​0058-​z. eCollection 2014.
9. Levitov A, Marik PE. Echocardiographic assessment of preload
responsiveness in critically ill patients. Cardiol Res Pract. 2012;
2012:819696. doi: 10.1155/​2012/​819696. Epub 2011 Sep 12.
10. London MJ, Hollenberg M, Wong MG, et al. Intraoperative myo-
cardial ischemia: localization by continuous 12-​lead electrocardiog-
raphy. Anesthesiology. 1988;69(2):232–​41.
11. Biccard BM. Detection and management of perioperative myocar-
dial ischemia. Curr Opin Anaesthesiol. 2014;27(3):336–​43. doi:
10.1097/​ACO.0000000000000071.
22
12. Memtsoudis SG, Rosenberger P, Loffler M, et al. The usefulness
of transesophageal echocardiography during intraoperative car-
diac arrest in noncardiac surgery. Anesth Analg. 2006;102(6):
1653–​7.
13. Lee MS, Naqvi TZ. A practical guide to the use of echocardiogra-
phy in assisting structural heart disease interventions. Cardiol Clin.
2013; 31(3):441–​54. doi: 10.1016/​j.ccl.2013.04.004. Epub 2013
Jun 17.
14. Moitra VK, Gabrielli A, Maccioli GA, O’Connor MF. Anesthesia
advanced circulatory life support. Can J Anaesth. 2012;59(6):
586–​603. doi: 10.1007/​s12630-​012-​9699-​3. Epub 2012 Apr 21.
15. Field JM, Hazinski MF, Sayre MR, et al. Part 1: executive sum-
mary: 2010 American Heart Association Guidelines for Cardio­
pulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2010;122(18 Suppl 3):S640–​ 56. doi: 10.1161/​
CIRCULATIONAHA.110.970889.
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diac arrest. Anesthesiology. 2014;120(4):829–​38. doi: 10.1097/​
ALN.0000000000000153.
P art I I . C ardiac C rises
23

5.

MYOCARDIAL ISCHEMIA
Jeremy Bennett and Kara Siegrist

C L INICA L CASE dominant circulation, the LCx supplies the AVN and SAN
blood supply. The LAD supplies the anterior wall of the
A 57-​year-​old male with a past medical history of hyperten- heart and anterior two-​thirds of the interventricular septum
sion, hyperlipidemia, diabetes mellitus, and coronary artery via septal perforators and diagonal branches. Venous blood
disease presents for right carotid endarterectomy for 75%–​ returns to the right atrium via the coronary sinus, which
99% occlusion of the vessel. Anesthetic plan is for general empties the left ventricle and significant portions of the right
endotracheal anesthesia with arterial line placement and ventricle. Additional venous drainage is performed via the
peripheral intravenous access. anterior cardiac veins, which drain directly into the right
atrium, with a small portion of blood being returned directly
into the left heart via the thebesian veins.
PATHOP HY SI O LO G Y O F D I SEASE STAT E

MECHANISM
ANATOMY

The myocardium is supplied by the right coronary artery
(RCA) and left main coronary artery (LMCA) arising from
the right and left sinus of Valsalva respectively, as demon-
strated in Figure 5.1. The LMCA is a relatively short vessel
that divides into the left anterior descending (LAD) branch
and the left circumflex (LCx) branch. Occasionally a third
vessel arises from the LMCA known as the ramus interme-
dius, which supplies the high lateral wall of the left ventricle.
Coronary dominance is determined by arterial contribution of
the posterior descending artery (PDA), with the RCA demon-
strating dominance in 85%–​90% of people. In the other 15%
of patients the LCx supplies the PDA, with a small portion of
patients having codominance due to contributions from both
the RCA and LCx to the inferior septal perforator branches.
Myocardial ischemia occurs when the myocardial oxygen
supply is not adequate to meet oxygen demand. Myocardial
oxygen demand is determined by three factors: wall tension,
heart rate, and contractility. Heart rate both affects myocar-
dial oxygen consumption and decreases diastolic perfusion
time, thus tachycardia can have multiple negative effects on
myocardial oxygen balance. Wall tension is determined by
the Law of Laplace:
T = PR/​2h
Where T = wall tension, P = intraventricular pressure,
R = ventricular radius, and h = ventricular wall thickness.
Wall tension is affected by preload and afterload, with
increases in both resulting in increased wall tension.

V E N T R I C U L A R B L O O D S U P P LY
The RCA supplies the inferior (posterior) wall of the left ven-
tricle, the anterior and posterior walls of the right ventricle,
and the posterior third of the interventricular septum via the
PDA. Additionally, the atrioventricular node (AVN) is sup-
plied in 90% of patients via the conus branch, and the sino-
atrial node (SAN) in 60% of patients. The LCx runs through
the atrioventricular groove and supplies the lateral wall of the
left ventricle via obtuse marginal arteries. In patients with left
Myocardial Oxygen Supply
Myocardial oxygen supply is determined by coronary blood
flow autoregulation, coronary flow reserve, and arterial oxy-
gen content.
Coronary Blood Flow
Coronary blood flow (CBF) is composed of coronary
perfusion pressure (CPP) and coronary vascular resistance

23
24

Pulmonary
veins 120

Aortic pressure
Superior

(mm Hg)
Circumflex vena cava
100
branch of left
coronary artery Area of 80
Great sinus node
cardiac
Inferior 100
vein
vena cava
Coronary 80

Phasic coronary blood flow

sinus 60 Left
Right 40 coronary
coronary 20 artery

(mL/min)
artery
0

Posterior descending 15
branch of night
coronary artery 10
POSTERIOR VIEW
5 Right
coronary artery
0
Left atrium
Superior
vena cava
0.2 0.4 0.6 0.8 1
Aorta Left coronary Time (sec)
Right atrial artery
appendage Circumflex Figure 5.2 Pressure tracings of left and right ventricular blood flows as
branch compared to aortic systolic and diastolic pressures. The left ventricle
Right
coronary primarily receives blood flow during diastole due to reduced systolic
Descending
artery coronary blood during ventricular contraction. In contrast, the right
branch
ventricle receives coronary blood flow during both systole and diastole.
Anterior Great SOURCE: Reprinted with permission from Koeppen & Statton: Berne and Levy Physiology,
coronary cardiac 6th ed.
veins vein
Pulmonary
artery endocardium of the heart is most susceptible to auto-
regulatory failure and reduction in blood flow because of
ANTERIOR VIEW
transmural variations in autoregulation. Subendocardial
Figure 5.1 Anatomy of coronary arterial and venous circulation. autoregulation has been demonstrated to be stable in
Reprinted with permission from Koeppen & Statton: Berne and Levy normal animals at mean arterial pressures (MAPs) of 40
Physiology, 6th ed.
mmHg.2,3 Pressures below this result in autoregulatory
failure and subendocardial ischemia. Due to alterations in
to flow. Normal coronary blood flow is approximately 5% autoregulation with coronary artery disease (CAD), fail-
of total cardiac output, or roughly 250 cc/​min. Coronary ure to maintain vascular patency and CBF begins to occur
perfusion pressure equals aortic diastolic pressure minus at higher MAP.
left ventricular end diastolic pressure (CPP = AoDBP
–​LVEDP). Resistance to flow is dependent on coronary Coronary Vascular Reserve
vascular tone and patency of the vessels. During systole, par- The difference between autoregulated flow and maximal
ticularly in the left ventricle, subendocardial pressures reach coronary artery blood flow is the coronary vascular reserve.
systemic pressure, resulting in transmitted pressure across Reduction in cross-​sectional area of a blood vessel results
the blood vessel. This results in near absence of effective for- in vasodilation to maintain metabolic needs. Reduction
ward flow in the left ventricle with dependence on diastole in pressure across a stenotic lesion occurs and can result
for forward blood flow, whereas the right ventricle receives in significant changes to CBF, as flow is proportional to
arterial flow in both systole and diastole (Figure 5.2). radius to the fourth power (Poiseuille’s law). While the
Coronary blood flow is maintained relatively con- blood supply is maintained, however, the vascular reserve is
stant over a range of pressures, with maximal vasodila- decreased. As the effective coronary intraluminal opening is
tion occurring at lowest pressures. This is accomplished reduced, autoregulation may be maximal and coronary vas-
by adjustments in vascular diameter related to myogenic cular reserve is negated. Increases in heart rate may result in
and metabolic demands, known as autoregulation.1 The autoregulatory failure at higher MAP, resulting in increased

24 P art I I . C ardiac C rises

25
susceptibility to subendocardial or transmural ischemia in
patients with CAD.
Arterial Oxygen Delivery
Arterial oxygen delivery is determined by oxygen content
and CBF. Arterial oxygen content is determined by the
equation:
CaO2 = 1.34 × Hg × oxygen saturation × (0.0031 × PaO2)
There are four primary determinants of coronary blood
flow: perfusion pressure, myocardial compression, metabo-
lism, and neurohumoral control. At rest, coronary extrac-
tion of oxygen is at near maximal capacity, around 80%,
giving the heart the highest arterial-​venous O2 difference of
any organ. Thus, in times of increased demand, the heart
compensates by increasing flow via coronary vasodilation
mediated by autoregulatory mechanisms. Vasodilation
occurs by chemical and neural mediators including hypoxia,
hypercarbia, acidosis, adenosine, nitric oxide prostaglan-
dins, and vagally mediated dilation.4,5
Myocardial infarctions (MIs) are defined by myocar-
dial cell death secondary to prolonged ischemia and can be
caused by factors that increase myocardial oxygen demand
or decrease oxygen supply. Myocardial oxygen supply is
decreased by coronary occlusion (platelet aggregation and
thrombus formation at the site of plaque rupture, vaso-
spasm, etc.), hypotension, tachycardia (less diastolic coro-
nary perfusion time for left ventricle), and hypoxemia.
There is a significant debate over the exact mechanism
of perioperative MI. For most MIs that lead to a patient
requiring cardiac revascularization, most ischemia results
from atherosclerotic plaque rupture and thrombus forma-
tion, causing a transient or prolonged obstruction to flow
through coronary arteries.6 Plaques that accumulate slowly
over time can generally be compensated for by vessel dila-
tion and creation of collateral blood vessels. However, most
perioperative ischemia is believed to result from stable ath-
erosclerotic plaque that, in the setting of increased myocar-
dial oxygen demand, result in a supply-​demand mismatch
(type 2 MI). s In patients with sufficient collateralization,
complete total occlusion of a coronary artery may result in
little to no impairment of blood supply.7 However, acute
problems can arise if plaque rupture occurs with thrombus
formation and acute occlusion occurs before effective col-
lateralization has occurred.
Acute coronary syndromes result due to sudden
decreases in CBF. The left ventricle is perfused mostly
during diastole due to compression of the coronary arter-
ies during systole. Tachycardia reduces effective CBF
Myocardial Ischemia
due to reduced diastolic filling time as well as increases
in myocardial oxygen demand. Because of this, the left
ventricular subendocardium does not receive blood flow
during systole, and therefore is more vulnerable than
other endocardial layers to ischemia.8 The right ventricle
is not able to generate as high pressures as the left ven-
tricle, thus is perfused both during systole and diastole
and depends mostly on mean arterial pressure for its per-
fusion gradient.
ANGINA PECTORIS AND
M YO C A R D I A L I N FA R C T I O N
Angina pectoris is most often described as precordial chest
pain, often precipitated by physical exertion and stress, and
is often relieved by rest or nitrates. Angina can be classi-
fied as chronic stable angina or acute unstable angina.
Regardless of type, it is often due to atherosclerotic heart
disease with reduction in CBF to areas of the heart. Angina
can also occur in patients without CAD, such as in aortic
stenosis, severe left ventricular hypertrophy, vasospasm,
marked anemia, markedly elevated metabolic requirement,
or paroxysmal tachycardias. Patients often report a sense
of chest tightness, squeezing, burning, or choking rather
than sharp pain. The location is traditionally described as
behind or to the left of the sternum and may radiate down
the left arm, though presentation is markedly variable,
with women expressing “typical symptoms” only about
63%–70% of the time.9
Angina pectoris can be classified as chronic stable or
unstable angina. Chronic stable angina is chest pain that
is stable in presentation, meaning the degree of exertion
and stress that precipitate angina remains relatively stable
over time. These patients likely have CAD, but of a degree
that collateralization may have occurred or the degree of
stenosis does not represent a significant reduction in blood
flow. Patients with unstable angina are considered to have
ischemia that is acute in nature or present with a sudden
change and/​or worsening of chronic stable angina pain.
Unstable angina is considered part of the acute coronary
syndrome.
Acute coronary syndrome comprises unstable angina,
non ST-​elevation MI (NSTEMI), and ST-​elevation MI
(STEMI). Acute coronary syndrome can be diagnosed by
three presentations: (1) rest angina that last for 20 min-
utes or more, (2) new-​onset angina that limits activity, or
(3) an increase in angina beyond normal “chronic” pre-
sentation. Unstable angina and NSTEMI differ based on
whether the degree of myocardial ischemia results in tissue
damage and enzyme leak. Myocardial infarctions can be
25
26

broken down into two broad categories: non-​ST eleva-

tion MI (NSTEMI) and ST-​elevation MI (STEMI). The
NSTEMI/​unstable angina as defined by the American
College of Cardiology is the clinical syndrome associated
with increased risk of cardiac death and subsequent MI10
and demonstrates ST depression or T wave inversion on the
electrocardiogram (ECG) with positive cardiac biomarkers
(CK, CKMB, troponin I). Changes in the ECG need not be
present for diagnosis, especially if anginal equivalent is pres-
ent with positive biomarkers. The NSTEMIs are most com-
monly caused by erosion of an intraluminal atheromatous
plaque with subsequent cascade of inflammatory mediators
and thrombogenesis leading to decreased coronary blood
flow to the subendocardium.1 Other less common causes of
NSTEMIs include dynamic obstruction or spasm of a coro-
nary artery, also known as Prinzmetal’s angina; severe nar-
rowing without spasm or thrombus, such as instent stenosis
after percutaneous coronary intervention; coronary artery
dissection; or extrinsic compression.1
The STEMI is the syndrome of ST segment elevation
on the electrocardiogram with myocardial necrosis char-
acterized by increased cardiac enzymes due to transmural
myocardial infarction.1 New-​onset left bundle branch block
is also defined as the equivalent of a STEMI. Changes in
ECG may be delayed and can affect diagnosis and treatment
of patients with NSTEMI and STEMI. Bundle branch and
paced rhythms can affect initial management, particularly
in the acute setting.1,13
BOX 5.1 REVISED CARDIAC RISK INDEX
1. History of ischemic heart disease
2. History of congestive heart failure
3. History of cerebrovascular disease (stroke or transient
ischemic attack)
4. History of diabetes requiring preoperative insulin use
5. Chronic kidney disease (creatinine > 2 mg/​dL)
6. Undergoing suprainguinal vascular, intraperitoneal, or
intrathoracic surgery
Risk for cardiac death, nonfatal myocardial infarction, and nonfatal cardiac arrest:
0 predictors = 0.4%, 1 predictor = 0.9%, 2 predictors = 6.6%, ≥ 3 predictors = > 11%
intraperitoneal, or intrathoracic surgeries. Depending on
the number of positive predictors (0–​≥3) the risk for peri-
operative cardiac complications is estimated at 0.4%, 0.9%,
6.6%, and >11%, respectively.14 The RCRI is a useful tool
for assessing cardiac risk in stable patients presenting for
noncardiac surgery.
AS S E S S ME NT OF T H E PAT IE NT : PR E S E N T I N G
S IGNS AND S YMPT OMS

Myocardial infarction under general anesthesia can be dif-

RISK ficult to diagnose, because the patient is unable to commu-
Ischemic heart disease has both modifiable and nonmodifi- nicate typical symptoms such as chest pain or shortness of
able risk factors. The nonmodifiable factors include increas- breath. Hemodynamic instability may ensue following a
ing age, male gender, family history of ischemic heart myocardial infarction and may be a clue to the diagnosis.
disease. Modifiable risk factors include smoking, hyperlip- Regional wall motion abnormalities on transesophageal or
idemia, hypertension, obesity, diabetes mellitus. transthoracic echocardiogram are the most sensitive indi-
The type of surgery can also influence the risk of myo- cator of ischemia, followed by ECG changes and hemody-
cardial infarction in the perioperative time period. High-​ namic fluctuation.
15

risk surgeries include aortic and major vascular procedures.

Intermediate-​risk surgeries include carotid endarterectomy,
TRANSESOPHAGEAL ECHOCARDIOGRAPHY
head and neck surgery, intraperitoneal procedures, intra-
thoracic procedures, orthopedic procedures, and urologic Transesophageal echocardiography allows monitoring of
procedures. ventricular volume, global myocardial function, regional
The Revised Cardiac Risk Index (RCRI) provides risk wall motion abnormalities, valve assessment, and aortic
stratification for perioperative cardiac adverse events based pathology assessment. A full exam will demonstrate wall
on a multivariate analysis of comorbidities as listed on motion as either normokinetic, hypokinetic, akinetic,
Box 5.1. These include coronary artery disease, congestive or dyskinetic while assessing for additional factors and
heart failure, cerebrovascular disease, insulin-​dependent pathology. The transgastric midpapillary short axis view
diabetes mellitus, renal insufficiency (creatinine > 2 mg/​dL), is a preferred view for monitoring wall motion and isch-
and high-​risk surgeries including suprainguinal vascular, emic changes, since it provides a representation of all three

26 P art I I . C ardiac C rises

Another random document with
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indeed, they are allowed to play upon nature’s green carpet, and the
privilege might well be extended without injury to the park.
PLAYS AND PLAYERS OF THE DAY.
By Morris Bacheller.
 FRANCIS WILSON.

Of the two great divisions of the drama, tragedy is today surprisingly

similar to what it was in the days of the ancient Greeks, while
comedy has in the mean time been the subject of a remarkable
evolution. That evolution has proceeded with especial rapidity within
recent years. To find the best and noblest exemplifications of tragedy
we have to go back two centuries to the master works of
Shakespeare. A few exceptional comedies there are of Sheridan’s or
Goldsmith’s, whose popularity has not diminished with the lapse of
time, though many generations have come and gone since they
were penned. But they may be counted upon the fingers of a single
hand, and only serve to emphasize the rarity of comedies that can
hold the boards for more than a few seasons.
The development of comedy, and especially of its more farcical
branches, is, indeed, the chief feature of recent dramatic history.
Attribute it to a reaction from the increased tension of modern
business life, or assign what sociological cause you will, the fact
remains that the general demand is for plays whose aim and object
is to amuse. It cannot be maintained that this tendency is restricted
to the less educated class of theater goers. On the contrary, it is at
houses that are especially frequented by people of wealth and
fashion that the supremacy of comedy is most assured. Melodrama
is still the most drawing card in the theaters patronized by the lower
million.
The advance of comedy has been multiform. Farces of greater
ingenuity and more sustained brilliance of workmanship are written
by the playwrights of today than by their forerunners. They are
interpreted upon the boards by more finished artists, and with a
stage setting that constantly becomes more complete and costly.
The comedian has a higher professional and even social standing
now than a generation ago, and he may secure a much greater
degree of renown, with its financial accompaniment of ample
earnings. And all this arises from the workings of the old law of
supply and demand. Every art that can contribute to the
embellishment of its presentation becomes the handmaid of comedy.
Music is pressed into its service, and the result is that characteristic
phase of latter day theatricals, the burletta.
There was a time, and not so very long ago, when the
predecessors of Francis Wilson and De Wolf Hopper were set down
as “low comedians,” and relegated to an artistic rank slightly superior
to that of the circus clown. Every one knows the contrast in the
position of the modern apostles of Momus. Attend the theaters, read
the newspapers, listen to the comment of the club rooms, and you
will speedily be convinced that they are the theatrical lions of the
hour, that among all the constellations of the dramatic firmament
their planet is in the ascendant. Nor is there anything in this state of
affairs to justify the pessimistic philosopher in an outcry against the
alleged decadence of the stage. The popular taste for comedy is
neither a degraded nor a perverted one, and the success of its
leading exponents has been won upon their merits.
The comic star rises to the zenith by an ascent as difficult and
laborious as that which leads to high rank in any other profession.
Ars est celare artem, and the apparently easy spontaneity with which
he develops the humor of a stage situation is the fruit of
conscientious study and persistent practice. There are no more
painstaking actors than the two typical burlesquers who as the
Regent of Siam and the Merry Monarch have during the recent
months reigned successively at the Broadway Theater, New York.
Francis Wilson, who recently succeeded his brother potentate, has
worked his way up from the lowest rounds of the theatrical ladder.
His first appearance was with Sandford’s minstrel company in a
sketch called “The Brians,” which was played in Philadelphia. Young
as he was—only a boy in his teens—Wilson made something of a
hit. This was enough to secure him plenty of remunerative
engagements with minstrel troupes, as a member of which he
traveled all over the country. He was ambitious, however, for work of
a higher order, and to secure a foothold upon the legitimate stage he
undertook a minor part in a company that appeared at the Chestnut
Street Theater, in Philadelphia. Here again his talents declined to
conceal themselves under a bushel. In the role of Lamp, a broken
down actor in “Wild Oats,” he carried with him upon the stage an old
foil, the last relic of better days, and from this seemingly unpromising
article he managed to extract so much quiet humor that the audience
was convulsed and the star of the piece entered a formal complaint
at this interference with his supremacy.
 DE WOLF HOPPER.

The following years saw the young actor steadily advancing in his
art, but experiencing various ups and downs of fortune, which wound
up with the “stranding” of his company, Mitchell’s Pleasure Party, in
San Francisco. Next he reappeared in Philadelphia—let us hope that
he was not obliged to reach it on foot—as a member of the McCaull
troupe, with which he played in his first comic opera, “The Queen’s
Lace Handkerchief.”
From this point his career has been one of uncheckered
prosperity. He was speedily recognized as a comic opera star of no
ordinary luster. In such standard parts as that of Cadeaux in Erminie
he achieved a reputation and a popularity that finally led him to
organize a company of his own, with which he has even eclipsed his
previous successes in “The Oolah” and “The Merry Monarch.”
De Wolf Hopper’s popularity has been won still more rapidly than
that of his brother comedian. He is the youngest of our successful
actors, as well as one of the most original in his methods, but he has
been upon the boards long enough to gain a thorough dramatic
training and a varied experience. It was his enthusiasm for private
theatricals, and his success in them, that led him upon the
professional stage—in spite of the fact that he had been educated
for the law. He was only twenty when, in 1880, he appeared as the
leading spirit of the Criterion Comedy Company, which had a fair
measure of prosperity, presenting such standard plays as “Caste”
and “Our Boys.” When it disbanded he was successively with
Edward Harrigan in “The Blackbird,” and at the Madison Square
Theater under the management of Daniel Frohman. At this latter
house, in the parts of Pittacus Green in “Hazel Kirke,” and Oliver
Hathaway in “May Blossom,” he gained the approbation of
metropolitan theater goers to a degree that was greatly enhanced
during the next five years, which he passed as a member of the
McCaull opera company. His last season with that organization was
marked by a success as Casimir in “Clover” that showed an advance
upon anything he had previously done. “Wang,” which was so
notably well received at the Broadway Theater during the past
summer, was his first independent venture.
 MODJESKA AS ROSALIND.

There are those who cherish the idea that the continued success
of actors like Messrs. Wilson and Hopper is largely due to the
prestige of their reputation and the indulgence shown by the public
toward established favorites. They tell us that it matters little what
may be the merits of the piece or its staging, the star is sure to have
a following sufficient to fill the box office with a golden stream. He
might almost as well dispense with the libretto altogether, they say,
for as soon as he opens his lips to speak the audience roars with
laughter.
 MODJESKA AS PORTIA.

So far as it denies the necessity for care and labor, thought and
skill, in the preparation and presentation of a farce, this theory is
fundamentally mistaken. It has again and again been proved that no
names upon the playbill, however eminent, can make a poor play
successful. The theater going public may not be infallible, but it is too
discriminating to accept an unpalatable article because it bears a title
of repute. The later popularity of “The Oolah” has obliterated
recollection of the fact that on its first night its reception was not
enthusiastic. The critics thought and said that Wilson had made a
mistake. But the comedian set himself at work to improve the piece,
cutting here, adding there, and interlining and changing until in a
hundred small but yet not unimportant points it was a different and a
better play. This is merely a single example of those expenditures of
thought and care that escape the hasty critic, and many similar
incidents might be cited. For instance, the remarkably flexible voice
of which De Wolf Hopper makes such effective use has received
almost as careful training as a prima donna’s.

MADAME HELENA MODJESKA.

It would hardly be fair to the theatrical situation of the day to

picture it only as a regime of farce comedy. The burlesque is indeed
the most characteristic phase of the fin de siècle dramatic
development, but it is not by any means sole monarch of the stage.
The avenue that leads to the applause of the world of culture is still
open to interpreters of the art that can call forth tears as well as
laughter.
 MODJESKA AS JULIE DE MORTIMER.

No better proof of this can be given than the marked favor with
which Madame Modjeska has been everywhere received during her
comparatively brief career upon the American stage. It is true that
she had already gained a wide reputation in Europe when she
abandoned her profession and came to the New World with her
husband, Count Bozenta. They had in view the establishment of a
colony of their Polish fellow countrymen in Southern California. The
scheme was probably somewhat Utopian. At any rate it was
abandoned, and the countess, under her earlier name of Modjeska,
fitted herself for the English speaking stage.
San Francisco was the scene of her debut, and “Adrienne
Lecouvreur” the play. She has since acted in all the leading cities of
America, besides making two visits to London. Her repertory
includes a wide range of pieces of the highest intellectual order. As a
delineator of Shaksperian heroines she is unsurpassed, and her
appearances with Edwin Booth in the great dramatic classics have
been among the most notable events of recent seasons. The
intensity of her Juliet, the grace and dignity of her Portia, the pathos
of her Ophelia, and the Arcadian naïveté of her Rosalind have borne
witness to her rare endowment of histrionic talent. Among other
plays in which she has taken the leading part are “Camille,” “Mary
Stuart,” “Juanna,” “Frou-Frou,” “Odette,” and “Richelieu.” In the last
named, which she played in conjunction with Booth, she scored one
of her most notable successes as Julie de Mortimer.
Long as she has been upon the stage of two continents, Madame
Modjeska’s impersonations of Juliet or Beatrice have all the fresh
charm of youth. With exceptional skill in the portrayal of strong
emotion she combines a lightness of touch and a graceful refinement
that are peculiarly characteristic. The fact that she has never
succeeded in removing from her English speech the last faint trace
of a foreign accent, is to many of her parts rather an added interest
than a blemish.
MODJESKA AS OPHELIA.
 A DAUGHTER OF THE DESERT.
By Thomas Winthrop Hall.
A tired horse ambled slowly up to the solitary adobe house, or rather
hut, that meets the sight of the dusty traveler who journeys between
a certain station on the Southern Pacific railroad and the famous
Indian station at San Carlos. One hundred miles of dusty road that
wound over a naked, sandy plain sparsely dotted with hideous
cactus, a stretch of the desert on either side, and on the horizon
walls of gray mountains treeless as the desert itself—these were the
uncheerful surroundings of McCoy’s ranch. Worse than a prison,
more remote than a Siberian mine, lonelier than the grave, here two
human souls, father and daughter, had lived for more than twelve
years, and during that twelve years they had been away from that
adobe oasis, the girl at least, not one single day, and the father
never longer than it would take him to ride over to the mountains for
a short hunt. It was a watering station on the stage road. An artesian
well had been sunk there in the early days. Like every other work of
man it had to have its human slaves, and from the day the last
adobe had been laid these slaves had been McCoy and his daughter
Sis. The latter was a child of six when she was lifted out of the ox
wagon at the door of the house. She was now a girl of eighteen.
What a life hers had been! One unvarying monotony of cooking
and of washing, of chopping wood and feeding the horses and of
looking anxiously one day up the road for the stage to come down
and the next day down the road for the stage to come up so that she
might have dinner (a pretentious name for a meal that consisted
always of bacon, eggs, coffee and hot bread) prepared for the stage
driver and what unfortunate companions in misery he might be
transporting to or from the agency. These, alas, gulped down their
food as hastily as possible and hastened away at once, only too
anxious to get the thing over with. That was all she saw of them.
Once in a while she caught sight of a muffled figure in an ambulance
that stopped for water for its thirsty mules and knew that it was a
woman because it did not get out and swear at the heat and dust, an
officer’s wife probably—ah! how she longed to speak to her. The
rough freighters often camped there. This was the sum total of the
girl’s experience with beings of her kind save one.
That was the man who sat carelessly erect on the tired horse that
ambled up to the adobe house. Lieutenant Jack Harding was he, of
Uncle Sam’s —th regiment of cavalry. And what a man he was, to be
sure! Handsome as a Greek god, stalwart as a Norse warrior,
reckless, brave, accomplished, as gentle as a girl until aroused, then
as wild and defiant as an Apache, he was a Bayard in the eyes of
most women and a demi-god in the estimation of poor Sis. He had
stopped over night at the watering station six times in four years. Sis
dreamed of his coming months before he appeared, and dreamed,
too, of his going months after he went. She worshiped him from the
moment she first saw him. That was all. She had read many books,
for her father had taught her to read, and Jack Harding served in turn
as the hero of each novel she became possessed of, and, of course,
(O dear little trait of woman’s nature) she as the heroine.
Lieutenant Jack jumped from his horse as lightly as though a ride
of fifty miles were a mere bagatelle, and walked smilingly up to the
door. Just as he reached it Sis came bashfully to the doorway.
“Hello, Sis,” said the lieutenant cheerfully.
“O——,” replied Sis. She never could talk to him.
“Dad home?”
“Nope.”
“Hunting?”
“Yep.”
“Well, I’ve come to make my party call for the last time I was here.
Got anything to eat?”
“Only bacon and eggs.”
 “Good enough for a prince—if the prince is as hungry as I am. All
right, get them ready. I’ll go and take care of Noche. Come, Noche—
want some water, old girl?” He led off the horse, and Sis turned from
the doorway to the kitchen. As she did so she stepped just for one
moment into a little room that, were she a lady, she would call her
boudoir, though it was but little larger than a good sized piano box,
and looked searchingly at her own face in a bit of broken looking
glass. What did she see? No thing of beauty, I assure you. This girl
had not been dowered by God with that divine gift that makes every
woman who possesses it a queen. Far from it. But so ignorant of the
world was she, so much an utter stranger to the appearance of
others of her sex, that she did not know that she was remarkably
homely. Freckle faced, pug nosed, red haired, rough and worn with
work, she was in appearance positively ugly. She had often asked
her father whether or not she was good looking, and he had
invariably replied “Yes.” But he always said it in such a way that poor
Sis began at last to suspect that she was not really as beautiful as
the heroines of Scott’s novels (she knew the descriptions of them by
heart.) Still it might be, and she hoped—a thing that a woman does
almost as easily as she forgives.
The supper was eaten in the usual wondering silence on her part
and the running fire of nonsense on the part of the lieutenant. He
accused her of being in love with “Peg-leg,” the mule driver, and was
cheerfully unconscious of the fact that his words tortured her heart
until she almost broke down and cried before him. He told her all the
news of the post and the latest jokes on the officers in an endeavor
—a vain one—to make her laugh. People who have lived ten years
in a desert do not laugh. At last it was over, and she cleared away
and washed the dishes. He smoked his pipe the while, wondering
how in the world she came to be so homely, wondering how she
managed to exist in such a place, and coming to a mental conclusion
as to how long he himself could stand such a life before committing
suicide. Then he went out and took a stroll on the sandy desert. Old
McCoy was not in sight, and though it was moonlight it was hardly
probable that he would return that night. He congratulated himself,
too, that Sis had not been brought up to the ideas of good society,
else he would have to make his bed in the hay that night and leave
the house, double barred and locked, to Sis. He even thoughtlessly
muttered to himself, “What a wonderful protection a homely face is!”
Then he went back to the kitchen to talk to Sis a while before going
to bed. As he entered a sight met his astonished eyes that almost
made him burst with laughter. It was nothing more nor less than Sis
arrayed in a gown that would have been an absurdity in caricature.
Green satin trimmed with red ribbons and a red sash, formless,
shapeless, it was her pitiful attempt to appear beautiful. Her great
hands hung from the sleeves like baskets from the branches of an
apple tree. Her red face and hair looked redder still by the contrast
with the gaudy colors of the dress, and she stood in the habitual
slouching attitude so characteristic of her. Yet there was something
in her gray eyes that told him it was a supreme moment in her life—
the wearing of this dress—and he did not laugh. Indeed, for a
moment he almost felt sad. He tried to sit down as unconcernedly as
possible, and busied himself filling his pipe. He did not dare to look
at her. He hoped she would do something or say something, but she
did not. She stood there silent, intense, looking at him so earnestly
that it was but too manifest that she was trying to read his thoughts.
He must do something.
“Where did you get that dress, Sis?” he said as quietly as he
could.
“Dad gave it to me,” she answered. “He always promised me a
satin dress, and so last Christmas he sent and got the satin. I made
it. This is the first time I have worn it before any one.”
She spoke as though the words were choking her. She seemed to
be nerving herself for something unusual. She was.
“Tell me,” she cried, almost fiercely, “tell me honestly, am I
beautiful?”
He tried not to do it. He felt like a cur, a second afterwards, for
having done it. But he could not help it, do what he could to control
himself. He laughed aloud.
“O don’t—don’t—don’t——” she almost screamed. Then she fell
on the floor in a green and red heap and wept. Jack had seen
women weep before (a number of them had wept at different times
when he had come to say “good by”), but never before had he seen
such a torrent of tears as this. There was no stemming it, though he
tried very hard. It seemed an age before it ceased, and then it
seemed another age that she sat there motionless with her face in
her hands as though she was trying to hide it. He felt horribly
nervous. It took him sixteen matches, as he afterwards said, to
smoke one pipe. Finally she broke the silence. Her voice was calm
enough as she asked:
“What is a beautiful woman like?”
He did not answer in words. It was just a little hard to speak at all.
He unbuttoned his blouse and took from the inside pocket a
photograph and handed it to her. She held it fiercely in her two great
rough hands and gazed at it steadily for a long time. Poor woman,
she learned what beauty was, and she learned of the love of this
man whom she worshiped. Then she got up, handed back the
photograph to its owner and walked silently and slowly from the
room.
It was hard for Jack Harding to sleep that night. He got into a fitful
slumber along towards morning, and he had not been sleeping for an
hour when he found himself standing awake in the middle of the
room feeling for his revolver in the gray light of the early dawn.
“Nothing but a shot could wake me like that,” he said to himself,
and hastily pulling on his clothes and taking his revolver in his hand
he went through the house. The fire had been built and breakfast,
already cooked, was waiting for him. “I guess Sis didn’t sleep much
either,” he thought. He knocked at her door but received no answer.
“Milking the cow, I guess,” he thought, but there was beginning to be
a horrible dread in his heart. He ran hastily out of the house, and
there—there under his own window lay Sis, again a green and red
heap, but there was red on the dress now that was not ribbon. She
had shot herself in the breast. He ran to her and picked her up. He
carried her into the house and swore at himself for never having had
the energy to study a little surgery in all the long years of his army
idleness. Presently she revived a little and he heard her murmur
faintly: “Tell dad good by—tell him I can’t help him any longer.”
“Oh, Sis!” he pleaded, “why did you do this?”
“Because you laughed at me,” she answered.
“But I did not mean it. You are beautiful, Sis, indeed you are very
beautiful.”
“Oh no, I’m not,” she said. “I know what beauty is now.”
He could say nothing for a time. He hardly knew why he said what
he did when he spoke.
“Sis,” he asked her gently, “tell me, why did you want to be
beautiful?”
“Because—because I loved you,” she answered slowly and with a
sob.
And when her father got home that afternoon and walked gayly
into the little adobe house, he found them still together, one dead—
one weeping.
 A BRIEF BURLESQUE.
As Performed Upon the Modern Stage.

She—You love me?

He— Aye, I do indeed,

How can I prove it?

She— Is there need?

He—Nay, not for some, but you are cold—

Ah, would our life were that of old
That I might prove by feat of arms
My wish to shield you from all harms—
As knight of thine I could not fail!

She—There’s safety in a coat of mail.

He—True, so there is; but take the case

Of Orpheus—give to me his place.
For Orpheus left this world above,
At Pluto’s throne he showed his love—

She—But that’s mythology, you know—

He—To Pluto I would go to show—

She—Ah, thanks; but is it just to trace

Comparisons between his Grace
Of the Inferno and mon père?
You’d hardly find the latter there,
But in that room with door ajar
You’ll see him deep in his cigar;
Which after dinner smoke, I find,