Obstetric Life Support Manual

Obstetric Life Support Manual
This text is a comprehensive review of normal and abnormal pregnancy physiology, the most common etiologies of
maternal medical emergencies, recognition of maternal deterioration and pending cardiopulmonary arrest, modifications to
cardiopulmonary resuscitation in pregnant and postpartum patients, special procedures that can assist in diagnosing and treating
maternal medical emergencies tailored to the setting (e.g., point-of-care ultrasound, resuscitative cesarean delivery, extracorporeal
cardiopulmonary resuscitation), treatment of trauma/stroke in pregnancy, and postpartum maternal medical emergencies. There
are streamlined algorithms and cognitive aids designed to improve a team’s ability to successfully implement techniques unique
to treating maternal medical emergencies and cardiac arrest.
• Offers a practical guide to treating complex and challenging maternal medical emergencies
• Equips the entire team responding to a maternal cardiac arrest with the current evidence-based approaches and
techniques
• Presents a thorough review, detailed algorithms, and a consolidated discussion of the practical aspects of implementation
The editors of this manual strive to use gender-inclusive language. However, in some instances, OBLS uses gender-specific
language (e.g., pregnant women) to reference a study’s findings. OBLS will periodically reassess this usage and make appropriate
adjustments.
Obstetric Life Support Manual
Etiology, prevention, and treatment of maternal
medical emergencies and cardiopulmonary
arrest in pregnant and postpartum patients
Edited by
Andrea Shields, MD, MS
Principal Investigator, Associate Professor, University of Connecticut Health Center, Farmington, Connecticut
Jacqueline Vidosh, MD
Co-Investigator, Assistant Professor, Department of Obstetrics and Gynecology
San Antonio Uniformed Services Health Education Consortium, San Antonio, Texas
Laurie Kavanagh, MPH

Program Manager, Seattle, Washington
Peter Nielsen, MD, MSS

Co-Investigator, Professor, Department of Obstetrics and Gynecology
University of Texas Health Science Center at San Antonio, San Antonio, Texas
Brook Thomson, MD
Co-Investigator, Associate Professor, Department of Obstetrics and Gynecology
University of Texas Health Science Center at San Antonio, San Antonio, Texas
Designed cover image: OBLS Logo
First edition published 2024
by CRC Press
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CRC Press is an imprint of Taylor & Francis Group, LLC
© 2024 selection and editorial matter, Andrea Shields, Jacqueline Vidosh, Laurie Kavanagh, Peter Nielsen, and Brook Thomson;
individual chapters, the contributors
This book contains information obtained from authentic and highly regarded sources. While all reasonable efforts have been made
to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liability for
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information or guidance contained in this book is intended for use by medical, scientific or healthcare professionals and is provided
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ISBN: 9781032289533 (hbk)
ISBN: 9781032289519 (pbk)
ISBN: 9781003299288 (ebk)
DOI: 10.1201/9781003299288
Typeset in Times
by Apex CoVantage, LLC
This manual is dedicated to all pregnant and postpartum people
who died from maternal cardiac arrest and Noah.
Contents
Acknowledgmentsxi
Obstetric Life Support Course Overview 1

0.1 Course Description 1
0.2 Course Objectives 1
0.3 Course Design 2
0.4 Course Prerequisites 2
0.5 Successful Course Completion Requirement 2
0.6 Course Materials 3
0.7 Manual Organization 3
0.8 Terminology 3
0.9 Highlighted Boxes 3
0.10 OBLS Algorithms, Cognitive Aids, and Checklists 3
1 Background on Maternal Cardiac Arrest 6

1.1 Introduction 6
1.2 Learning Objectives 6
1.3 Maternal Mortality 6
1.4 Epidemiology of Maternal Cardiac Arrest 8
1.5 The Role of Bias 9
1.6 Preventing Maternal Cardiac Arrest 10
1.7 Planning and Preparation 11
Chapter 1. Practice Questions 12
Chapter 1. Answers 13
Chapter 1. References 13
2 Anatomic and Physiologic Adaptations of Pregnancy 15

2.1 Introduction 15
2.3 Cardiovascular Anatomic and Physiologic Adaptations in Pregnancy 15
2.4 Respiratory Anatomic and Physiologic Adaptations in Pregnancy 16
2.5 Neurophysiologic Adaptations in Pregnancy 19
2.6 Hematologic Physiologic Adaptations in Pregnancy 20
2.7 Gastrointestinal Anatomic and Physiologic Adaptations in Pregnancy 21
2.8 Genitourinary Anatomic and Physiologic Adaptations in Pregnancy 21
2.9 Anatomic and Physiologic Impact on Medications in Pregnancy 22
2.10 Endocrine Anatomic and Physiologic Adaptations in Pregnancy 23
2.11 Immune System Adaptations in Pregnancy 23
3 Prevention of Maternal Cardiac Arrest 27

3.1 Introduction 27
3.3 Obstetric Early Warning Systems 29
3.4 Institutional Planning for Critically Ill Pregnant and Postpartum Patients 33
3.5 Communication 33
vii
viii Contents
4 Common Causes of Maternal Cardiac Arrest 37

4.1 Introduction 37
4.3 BAACC TO LIFE: Bleeding37
4.4 BAACC TO LIFE: Anesthesia40
4.5 BAACC TO LIFE: Amniotic Fluid Embolism 40
4.6 BAACC TO LIFE: Cardiovascular43
4.7 BAACC TO LIFE: Peripartum Cardiomyopathy43
4.8 BAACC to LIFE: Clot/Cerebrovascular Pulmonary Embolism 44
4.9 BAACC TO LIFE: Trauma47
4.10 BAACC TO LIFE: Overdose48
4.11 BAACC TO LIFE: Acute Lung Injury/Acute Respiratory Distress 50
4.12 BAACC TO LIFE: Ions (Glucose, K+)51
4.13 BAACC TO LIFE: Fever52
4.14 BAACC TO LIFE: Emergency Hypertension/Eclampsia 54
5 Review of Cardiopulmonary Resuscitation Modifications for Pregnant Patients

in Basic Life Support 59
5.1 Introduction 59
5.3 Review of Basic Life Support 59
5.4 Basic Life Support Changes in Pregnancy 61
5.5 Chest Compressions and Ventilation 61
5.6 Automated Chest Compression Devices 62
5.7 Defibrillation 62
5.8 Left Uterine Displacement 62
5.9 Basic Life Support in the Reproductive-Age Female with Unknown Pregnancy Status 64
5.10 Vascular Access 64
5.11 Point-of-Care Ultrasound 64
6 Review of Cardiopulmonary Resuscitation Modifications for Pregnant Patients in Advanced

Cardiac Life Support and Advanced Life Support 69
6.1 Introduction 69
6.3 Review of Advanced Cardiac Life Support 69
6.4 Interpretation of Cardiac Rhythms 72
6.5 Shockable Rhythms: Ventricular Fibrillation and Pulseless Ventricular Tachycardia 72
6.6 Refractory Ventricular Fibrillation and Ventricular Tachycardia 74
6.7 Nonshockable Rhythms: Pulseless Electrical Activity and Asystole 74
6.8 Differential Diagnosis 75
6.9 Advanced Cardiac Life Support Changes in Pregnancy 75
6.10 Obstetric Life Support Cognitive Aid 76
6.11 Airway Management: Basic 76
6.12 Airway Management: Advanced 76
6.13 Anti-Arrhythmic Drugs 78
6.14 Fetal Monitoring 78
6.15 Resuscitative Cesarean Delivery 78
6.16 Vaginal Delivery 78
Contents ix
6.17 Factors That Could Decrease the Effectiveness of Advanced Cardiac Life Support and
Cardiopulmonary Resuscitation in Pregnancy 79
6.18 Maternal Cardiac Arrest Team 79
7 Special Procedures in Obstetric Life Support 83

7.1 Introduction 83
7.3 Resuscitative Cesarean Delivery 83
7.4 OBLS in a Low-Resource Setting 89
7.5 Point-of-Care Ultrasound 89
7.6 Obesity and Maternal Cardiac Arrest 93
7.7 Extracorporeal Cardiopulmonary Resuscitation 94
7.8 Transport and Emergency Medical Staff Providers 95
8 Traumatic Maternal Cardiac Arrest 99

8.1 Introduction 99
8.3 Traumatic Cardiac Arrest Review 99
8.4 Approach to Reproductive-Age Females with Cardiac Arrest in Association with Trauma 100
Chapter 8. Reference 105
9 Postpartum Cardiac Arrest 106

9.1 Introduction 106
9.3 Causes of Postpartum Maternal Cardiac Arrest 106
9.4 Management of Postpartum Cardiac Arrest by Cause 107
10 Maternal Stroke and Acute Cerebrovascular Disease 120

10.3 Timing 123
10.4 Recognizing Warning Signs and Symptoms of Maternal Stroke 123
10.5 Out-of-Hospital Evaluation and Transport of Maternal Stroke 124
10.6 Obstetric Stroke Protocol 127
10.7 Maternal Stroke Team Composition 128
10.8 Stroke Code 129
10.9 Intracranial Hemorrhage 133
10.10 Subarachnoid Hemorrhage 133
10.11 Reversal of Coagulopathy in Intracranial Hemorrhage and Subarachnoid Hemorrhage 133
10.12 Elevated Intracranial Pressure in Intracranial Hemorrhage and Subarachnoid Hemorrhage 134
10.13 Delivery in Intracranial Hemorrhage and Subarachnoid Hemorrhage 134
10.14 Post-Stroke Care 135
10.15 Cerebral Venous Sinus Thrombosis 137
x Contents
11 Post-Arrest Care 140

11.3 Importance of Post-Arrest Care 140
11.4 Standard Post-Return of Spontaneous Circulation Checklist after Maternal Cardiac Arrest 141
11.5 Airway141
11.6 Breathing141
11.7 Circulation141
11.8 Disability142
11.9 Extracorporeal Cardiopulmonary Resuscitation 144
11.10 Etiology144
11.11 Fetus144
11.12 Gather145
11.13 Head145
11.14 When to Cease Resuscitation Efforts 146
11.15 Determination of Death and Organ Procurement 149
12 Communication during Maternal Cardiac Arrest 154

12.3 Guiding Principles of Team-Based Care 154
12.4 Maternal Cardiac Arrest Team Structure 156
12.5 Situation, Background, Assessment, and Recommendation/Request 157
12.6 Call-Outs 157
12.7 Check-Backs 158
12.8 Situation-Background-Assessment-Recommendation and Call-Outs for the Maternal Team
Entering a Maternal Cardiac Arrest Event—The 5A's 158
12.9 Communication of Maternal Cardiac Arrest and Outcomes to the Family 159
12.10 Debriefing the Team after Maternal Cardiac Arrest 161
13 Putting It All Together 165

13.2 Scenario One 165
13.3 Scenario Two 168
13.4 Scenario Three 170
13.5 Scenario Four 170
Chapter 13. Reference 172
Appendix A: Abbreviations173
Appendix B: OBLS Mnemonics175
Appendix C: Resources176
Appendix D: American Heart Association Opioid-Associated Emergency Algorithm for Healthcare Providers177
Appendix E: Post-ROSC Care Checklist IH178
Appendix F: Post-ROSC Care Checklist OH180
Appendix G: Venous Thromboembolism Prophylaxis Following Stroke181
Appendix H: Megacode Checklist OH Basic182
Appendix I: Megacode Checklist OH Advanced184
Appendix J: Megacode Checklist IH186
Appendix K: Institutional Preparedness188
Appendix L: OBLS Drug List189
Acknowledgments
Obstetric Life Support (OBLS) is made possible, and this project was funded by a generous grant from the Agency for Healthcare
Research and Quality (AHRQ), U.S. Department of Health and Human Services (HHS). The editors and authors are solely
responsible for this document’s contents, findings, and conclusions, which do not necessarily represent the views of AHRQ.
Readers should not interpret any statement in this report as an official position of AHRQ or of HHS. None of the editors or
authors has any affiliation or financial involvement that conflicts with the material presented in this report.
Thank you to our main chapter author(s) who contributed their time and expertise to the manual:
Overview: Laurie Kavanagh, Andrea Shields; Chapter 1: Lissa Melvin; Chapter 2: Peter Nielsen, Brook Thomson;
Chapter 3: Andrea Shields; Chapter 4: Andrea Shields, Jacqueline Vidosh; Chapter 5: Jacqueline Vidosh; Chapter 6:
Jacqueline Vidosh; Chapter 7: Andrea Shields; Chapter 8: Andrea Shields; Chapter 9: Jacqueline Vidosh; Chapter 10:
Eliza Miller, Kara Shetler; Chapter 11: Jacqueline Vidosh; Chapter 12: Peter Nielsen; Chapter 13: Jacqueline Vidosh.
Thank you to the other content contributors: Viviana de Assis, James Hill, Monica Lutgendorf, and Irene Stafford.
Thanks to our expert panel members who graciously contributed their time and knowledge to this project:
Elumalai Appachi, MBBS, Baylor College of Medicine Lissa Melvin, MD, Baylor College of Medicine
Julie Arafeh, RN, MSN, Clinical Concepts in Obstetrics; Eliza C. Miller, MD, Columbia University
Stanford School of Medicine, Department of Pediatrics, Charles Minard, PhD, Baylor College of Medicine
Division of Neonatal Medicine Joshua Monson, MD, Uniformed Services University
Les R. Becker, PhD, MS.MEdL, NRP, CHSE, MedStar of the Health Sciences
Institute for Innovation, MedStar Health and Vincent N. Mosesso, Jr., MD, PHP, University of
Georgetown University School of Medicine Pittsburgh School of Medicine
Utpal Bhalala, MD, Driscoll Children’s Hospital DeWayne M. Pursley, MD, MPH, Harvard Medical
Rebecca Cypher, MSN, PNNP, Maternal Fetal Faculty Physicians at Beth Israel Deaconess Medical
Solutions Center
Shad Deering, MD, Children’s Hospital of San Antonio, Jeffrey Quinlin, MD, Roy J. and Lucille A. Carver
CHRISTUS Health College of Medicine, University of Iowa
Sondie Epley, RN, University of Texas Health Science Stephen Rahm, NRP, Centre for Emergency Health
Center at San Antonio Sciences
Mary Ann Faucher, PhD, CNM, MPH, Parkland Health Carl Rose, MD, Mayo Clinic
and Hospital System P. James A. Ruiter, MD, MCFP
Afshan Hameed, MD, University of California, Irvine Cheryl K. Roth, PhD, WHNP-BC, RNC-OB, RN,
Heidi King, MS, FACHE, BCC, CMC, CPPS, Uniformed HonorHealth Scottsdale Shea & Osborn
Service University Department of Medicine Defense Brian Schaeffer, International Association of Fire Chiefs
Health Agency Amir Shamshirsaz MD, Baylor College of Medicine
Miranda Klassen, Amniotic Fluid Embolism Foundation Paloma Toledo, MD, MPH, Miller School of Medicine,
Monica Lutgendorf, MD, Uniformed Services University University of Miami
of the Health Sciences Fernando Stein, MD, Texas Children’s Hospital
David Markenson, MD, American Red Cross Carolyn Zelop, MD, American Heart Association
Thank you to Stanford University for allowing use of “Obstetric Life Support,” the American Heart Association for volun-
teering their algorithms, Laurie Kavanagh for her assistance with creating OBLS Figures 10.2, 10.6, 10.7, 12.2 and helping to
draft our algorithms, Dr. Shad Deering for his assistance in developing the megacode checklists, and Elizabeth N. Weissbrod
and Andrea McCulley for their drawings.
Many thanks to our partners—Baylor College of Medicine, the Children’s Hospital of San Antonio, and Laerdal Medical—
for collaborating with the OBLS team to create this product.
Please note that the content in this manual is copyrighted, and the OBLS name, logo, ALIVE @ 5, and BAACC TO LIFE
acronyms are all trademarked by Varda5, LLC through the US Patent and Trademark Office. Permission to reproduce or use any
of the OBLS content must be requested by email to: [email protected].
xi
Obstetric Life Support
Course Overview
0.1 COURSE DESCRIPTION

The Obstetric Life Support (OBLS) course has been created for all healthcare providers who may encounter and participate in
the management of maternal cardiopulmonary arrest or similar emergencies. Such personnel range from obstetricians and gyne-
cologists (OB/GYNs), to emergency department (ED) providers, critical care providers, nurses, midwives, anesthesia providers,
and all levels of emergency medical services (EMS) providers.
There are two broad areas of applicability of the OBLS course: in-hospital (IH) and out-of-hospital (OH). The IH applies
to providers who care for pregnant people in clinics, urgent care and ED settings, and inpatient wards. The OH applies to EMS
providers and has two arms: Advanced and Basic. Advanced OH OBLS is recommended for EMS providers who are required to
be certified in Advanced Cardiac Life Support (ACLS).
The goal of this course is to improve maternal-fetal outcomes in the setting of maternal cardiac arrest (MCA) by increasing
provider awareness and practice using the techniques specific to maternal cardiac arrest. By the end of this course, the learner
will have improved knowledge of the unique modifications to Basic Life Support (BLS) and ACLS in pregnancy and will be
better prepared to treat pregnant people in cardiac arrest.
0.2 COURSE OBJECTIVES

Upon completion of OBLS, learners should be able to do the following:
• Understand how to apply the differences in pregnancy-related changes to physiology and anatomy to the performance
of BLS and ACLS during MCA.
• Demonstrate how to recognize pending cardiopulmonary arrest in the pregnant and postpartum patient by applying
one of the early warning sign algorithms for pregnancy.
• Demonstrate effective OBLS with an emphasis on effective chest compressions with early activation of left uterine
displacement (LUD) and automated external defibrillator (AED) use as indicated.
• In the setting of cardiac arrest in reproductive-age people (pregnancy status unknown), efficiently apply point-of-care
ultrasound (POC-US), where applicable, to diagnose possible pregnancy and initiate required BLS/ACLS changes
quickly and effectively.
• Efficiently apply pregnancy-specific changes to the ACLS algorithm, with an emphasis on early resuscitative cesarean
delivery (RCD) within 5 minutes of arrest if pregnancy is suspected to be greater than 20 weeks or at the level of the
maternal umbilicus and initial round of cardiopulmonary resuscitation (CPR) is ineffective at return of spontaneous
circulation (ROSC).
• Apply unique modifications to the primary survey in a person of reproductive age undergoing trauma.
• Initiate immediate post-arrest care in the setting of ROSC, with special consideration to pregnancy/postpartum state.
• Consider extracorporeal cardiopulmonary resuscitation (ECPR) in those cases refractory to ROSC.
• Demonstrate clear and effective team communication using a TeamSTEPPSTM approach.
• Improve communication to the healthcare team and families in the setting of poor outcomes.
• Recognize proper disposition/transfer of care for a pregnant patient in cardiopulmonary arrest.
• Recognize and treat possible reversible causes of MCA.
DOI: 10.1201/9781003299288-1 1
2 Obstetric Life Support Manual
0.3 COURSE DESIGN
0.3.1 Pre-Work
Self-paced learning using the OBLS Manual for personal study. Each chapter has practice questions to reinforce the learner’s
knowledge and skills.
0.3.2 OBLS Entry Exam

Learners are required to take and pass an entry exam covering the material in this manual. OBLS used an Angoff method to
set the minimum passing scores for OH Basic, OH Advanced, and IH participants to ensure mastery of pre-work before the
in-person training. A group of subject matter experts examined each question and predicted how many minimally qualified
candidates would answer the question correctly. This method ensures that the passing grade of each of the three OBLS tracks is
verifiable and determined empirically.
0.3.3 Instructor-Led, In-Person Course

Learners will participate in small-group, simulation-based course building on the foundations of OBLS learned in the pre-work.
Instructors will lead groups in rapid-cycle deliberate practice on
• Team communication and dynamics management

• Leading and managing MCA
• Techniques such as chest compressions on a pregnant patient, LUD, and RCD
• Cardiac rhythm interpretation and vital sign management
• Application of ACLS drugs
• Debriefing for critical events
• Sharing difficult or serious news following MCA
Each scenario will take learners through situations they are going to experience when performing the OBLS Megacode. For both group
practice and graded megacode, instructors will use a detailed scoring checklist as an objective grading system to ensure that learners
have performed core concepts. Each concept is linked to a point system yielding a grade for each, and pass/fail criteria are based on
this grade. Using this checklist helps to eliminate instructor subjectivity and provides a permanent record of the learner’s performance.
0.3.4 Graded OBLS Megacode

Instructors will test each learner in how well they manage an OBLS megacode scenario. Learners may find the megacode check-
lists by which instructors will test them in Appendices H, I, and J.
0.4 COURSE PREREQUISITES

Learners must be proficient in BLS skills before taking OBLS; a basic understanding of ACLS is beneficial but not required.
The OBLS course does not review ACLS pharmacology or teach how to interpret cardiac rhythms. Learners may improve
these skills by visiting the American Heart Association at www.aha.org.
0.5 SUCCESSFUL COURSE COMPLETION REQUIREMENT

To complete OBLS, the learner must complete and pass both a competency test based on the OBLS Manual and a team leader
assessment during the in-person training megacode.
Obstetric Life Support Course Overview 3
0.6 COURSE MATERIALS

Course materials include the OBLS Manual, the OBLS student website (www.obls.org), algorithms, cognitive aids, and checklists.
0.7 MANUAL ORGANIZATION

This manual provides an overview of the physiology and anatomy of pregnant patients, with each chapter building on the pre-
vious one. The physiology and anatomy of pregnant patients are drastically different from nonpregnant patients. Consequently,
OBLS teaches how to modify BLS and ACLS in the setting of MCA. Understanding the impact of pregnancy on anatomy and
physiology empowers providers to improve care and outcomes for their patients. The manual also highlights the common causes
of MCA and introduces special procedures and effective team communication during MCA.
OBLS tools including the ALIVE @ 5TM Cognitive Aid, BAACC TO LIFETM mnemonic, and the OBLS Master Algorithm
are located following this introductory section. These aids are meant to accompany the learner throughout the course to remind
the learner that many simultaneous steps must occur within the first 5 minutes of a maternal cardiac arrest. They also trigger
a differential for causes of the arrest. This course does not include comprehensive treatment plans for each common cause of
maternal cardiac arrest. It introduces them so that learners may improve overall resuscitation efforts by developing and consid-
ering differential diagnoses early in the case management.
0.8 TERMINOLOGY
• Abbreviations and acronyms are spelled out upon their first use per chapter, followed by an abbreviation in parenthe-
ses. See Appendix A for a full list of abbreviations and acronyms.
• See Appendix B for a list of mnemonics.
• Gender-neutral language:
• In recognition of a nonbinary gender spectrum, we have incorporated gender‑neutral language where appropriate,
including using the term “patient” and the singular “they” instead of “he” or “she.”
• We continue to use gender-specific language to report most research and legal decisions.
• OBLS uses the term “resuscitative cesarean delivery” (RCD) instead of the previously common term “perimortem
cesarean delivery” as it more accurately describes the procedure including the delivery of the fetus. See Chapter 7.
0.9 HIGHLIGHTED BOXES

OBLS highlights key concepts and differences critical to the success of the OBLS techniques with the following colors:
• Key points are denoted in purple. These focus on the critical knowledge and skills and their practical applications to
successfully manage a maternal cardiac arrest.
• Case vignettes are in orange and allow the learner an opportunity to apply the concepts learned during the chapter.
• Putting it all together are in gray. These show how the OB-specific techniques work with each other to improve the
efficient application of OBLS algorithms.
0.10 OBLS ALGORITHMS, COGNITIVE AIDS, AND CHECKLISTS

These quick-reference guides aid the proper application of OBLS and develop differential diagnoses for the causes of arrest and
post-arrest care steps.
Following are algorithms, aids, and checklists with their corresponding manual location(s):
• ALIVE @ 5® Cognitive Aid (page after Introduction, and Chapter 6, Figure 6.8)
• BAACC TO LIFETM Mnemonic (page after Introduction, and Chapter 4, Figure 4.1)
• OBLS Master Algorithm (page after Introduction, and Chapter 5, Figure 5.7)
• OBLS Algorithm with Modification of CPR, pregnancy known >20 weeks and unknown (Chapter 5, Figure 5.6)
• Traumatic Maternal Cardiac Arrest Algorithm (Chapter 8, Figure 8.1)
• Post-ROSC Checklist (Appendices E and F)
• ALIVE @ 5 Maternal Cardiac Arrest Debrief Tool (Chapter 12, Figure 12.5)
• SPIKES Protocol for Sharing Difficult or Serious News (Chapter 12, Figure 12.4)
Use the aids on the following pages as references while you complete your pre-work.
• Obstetric Life Support Course Overview 5
Background on Maternal
Cardiac Arrest 1
1.1 INTRODUCTION
This chapter provides the learner with a background on maternal cardiac arrest (MCA), introduces maternal mortality trends in
the United States (U.S.), and discusses the epidemiology of MCA. It also discusses severe maternal mortality episodes and the
importance of understanding how bias impacts patient care.
1.2 LEARNING OBJECTIVES

Learner will appropriately:
• Discuss the trends in pregnancy-related mortality ratio in the U.S. compared with the global maternal mortality ratio,
including the leading causes of MCA and death.
• Describe the relationship between severe maternal morbidity (SMM) and maternal death, and the primary demo-
graphic risk factors for MCA and death.
• Discuss the potential role of implicit bias in reducing healthcare equity for all people.
• Describe current strategies being used to prevent MCA and death in the U.S.
1.3 MATERNAL MORTALITY

There has been a decreasing trend in maternal mortality for nations around the world. Although progress varies significantly by
region and country, the global maternal mortality ratio decreased from 385 deaths per 100,000 live births in 1990 to 216 deaths
per 100,000 live births in 2015.1 Unlike the worldwide trend over past decades, the U.S. has seen an increase in the pregnancy-
related mortality ratio (PRMR). This is an estimate of the number of pregnancy-related deaths for every 100,000 births. The
PRMR is often used as an indicator of a nation’s health. The Centers for Disease Control and Prevention (CDC) report that the
PRMR in the U.S. has increased from 7.2 deaths per 100,000 live births in 1987 to 17.3 deaths per 100,000 live births in 2018.2
In 2020, there were 861 reported maternal deaths in the U.S.3 According to 2017–2019 data from the Maternal Mortality Review
Committees, 80% of these deaths were determined to be preventable.4 In 2021, there were a staggering 1,201 maternal deaths in
the U.S., amounting to 33 deaths per 100,000 live births (Figure 1.1).3 This 38% increase in maternal deaths from the previous
year was largely attributed to Coronavirus Disease 2019.
Approximately 22% of maternal deaths occur antepartum, 25% on day of delivery or within 7 days after, and 53% occur
between 7 days to 1 year after pregnancy.4 Most maternal deaths within the first 7 days after delivery are due to postpartum
hemorrhage, embolism, eclampsia and hypertensive disorders.5
Maternal mortality is a complex issue at the confluence of population health, access to healthcare, gaps in clinical care and
team performance, and socioeconomic, racial, and ethnic inequalities2–9; each of these influencing health outcomes. Measuring
pregnancy-related deaths is challenging due to incomplete and sometimes inaccurate vital statistics data.10 The reasons for
increasing PRMR in the U.S. are not entirely clear and are under investigation. An improvement in identifying deaths with the
use of data linkages, changes in coding, and the addition of a pregnancy checkbox to the death certificate in 2003 may partly
6 DOI: 10.1201/9781003299288-2
1 • Background on Maternal Cardiac Arrest 7
FIGURE 1.1 Pregnancy-related mortality ratio (PRMR) trends in the United States.
FIGURE 1.2 Causes of pregnancy-related deaths in the United States (2017–2019).4
explain the increasing numbers.2,6,11 However, this improved system does not fully explain the rising trend.7 The increase in
chronic health conditions and obesity are likely contributing factors as well.2,9
The common causes of pregnancy-related deaths vary by region and patient demographics. Worldwide, hemorrhage is the
number one cause for maternal mortality.12 Causes and risk factors for pregnancy-related deaths in the U.S. have shifted over
the years. Hemorrhage, hypertensive disorders, and anesthesia-related deaths have declined since 2006, while mental health and
cardiovascular conditions have emerged as the leading cause of maternal mortality.2,6,9 Cardiac and coronary conditions were
the leading underlying cause of pregnancy-related deaths among non-Hispanic Black people, mental health conditions were the
leading underlying cause for Hispanic and non-Hispanic White people, and hemorrhage was the leading underlying cause for
non-Hispanic Asian people.32 Based on a review of pregnancy-related deaths among Al/AN people, mental health conditions and
hemorrhage were the most common underlying causes of death, accounting for 50% of deaths with a known underlying cause.2
Other causes include amniotic fluid embolism, injury, cerebrovascular accident, cancer, metabolic/endocrine, and pulmonary
conditions.4 Figure 1.2 shows common causes of pregnancy-related death in the U.S.
KEY POINTS
• The PRMR in the U.S. has increased 50%, while the global maternal mortality ratio has decreased.
• Close to 1,200 people die from pregnancy-related complications each year in the U.S., and 80% of these
deaths are preventable.
• Hemorrhage is the leading cause of maternal death worldwide, while cardiovascular and mental health
conditions, including deaths to suicide and overdose/poisoning related to substance use disorder, have
emerged as the leading causes of maternal mortality in the U.S.
1.4 EPIDEMIOLOGY OF MATERNAL CARDIAC ARREST

MCA occurs in one in 12,000 admissions for delivery in the U.S.13 It is seen as the final common pathway for many critical
illnesses and comorbidities similar to the ones that lead to maternal mortality, though with some key differences.8,13 The most
common potential etiology of cardiac arrest during hospitalization for delivery is hemorrhage followed by heart failure, AFE,
then sepsis (Figure 1.3).13 In contrast, the likelihood of MCA is highest for those diagnosed with AFE, followed by acute myocar-
dial infarction, and venous thromboembolism (VTE) (Figure 1.4).13 Heart disease, such as cardiomyopathy and cardiovascular
disease, ultimately still results in the highest number of maternal mortalities.13 Stroke is another major cause of maternal mor-
tality, accounting for 40%–70% of deaths in people with preeclampsia, most of which are due to intracerebral hemorrhage.14,15
Maternal survival to hospital discharge after cardiac arrest ranges from 40% to 60%, with survival depending on the underlying
etiology of arrest.8,13
Like data for the maternal mortality ratio, there are gaps in reporting and processing data for MCA. The variation and
inconsistencies of how information is collected make it challenging to assess the true prevalence of MCA. Researchers found
that national databases and registries in the U.S. for out-of-hospital (OH) and in-hospital (IH) cardiac arrest did not consistently
FIGURE 1.3 Proximate potential etiologies of maternal cardiac arrest during hospitalization for delivery in the United States
(1998–2011).
FIGURE 1.4 Cause-specific MCA frequency (per 1,000 women) during hospitalization for delivery in the United States (1998–2011).
FIGURE 1.5 Severe maternal morbidity iceberg.
account for pregnancy and the postpartum period.16 These examples highlight the need for a mandatory national database for
MCA.7,16 Standardization and inclusion of pregnancy and postpartum status will better allow policymakers to assess trends,
performance, and outcomes,16,17 ultimately increasing survival and quality of life.
With rising rates of obesity, chronic diseases, and cesarean sections, SMM rates also increase.18–20 Compared to MCA and
death, it is necessary to highlight that SMM cases are far more common. Maternal deaths have been described as the “tip of the
iceberg” with SMM the “rest of the iceberg”20 below the surface (Figure 1.5). For every maternal death, there are approxi-
mately 100 episodes of SMM each year.19 Many causes of SMM, including stroke and peripartum cardiomyopathy, may result
in long-term permanent disability. This underscores the importance of systematic approaches to understand and prevent severe
maternal morbidity.
KEY POINTS
• MCA is the final common pathway for many critical illnesses and comorbidities, like the ones that lead to
maternal mortality.
• Hemorrhage is the most common potential etiology of cardiac arrest during hospitalization for delivery.
• AFE is the diagnosis most frequently complicated by cardiac arrest.
• For every maternal death, there are approximately 100 episodes of severe maternal morbidity scenarios
each year.
1.5 THE ROLE OF BIAS

The lived experience of racism for specific racial and ethnic groups is a significant risk factor for maternal mortality and SMM.
In the U.S., racial and ethnic disparities have persisted for decades and remain a national issue.6,21–23 According to the CDC’s
Pregnancy-Related Mortality Surveillance System for 2016–2018, maternal mortality in the U.S. was more than three times
higher in non-Hispanic Black (Black) people and almost two times higher in American Indian/Alaska Native (AI/AN) people
when compared to non-Hispanic White (White) or Hispanic people (Figure 1.6).2 This disparity increases with maternal age.
Black and AI/AN people 30 years or older had a four to five times greater mortality compared to White, Hispanic, and Asian/
Pacific Islander (A/PI) people, with the highest risk of maternal death seen in Black people aged 40 years or older. Higher socio-
economic status and a greater level of education do not help to improve outcomes for Black people (data not available for AI/AN
people). The PRMR for Black people with a college education or higher is more than three to five times greater than their White
counterparts. And Black people with a college education or higher are two to three times as likely to die compared to White,
Hispanic, and A/PI people who have less than a high school education.21,22
FIGURE 1.6 Deaths per live births by race/ethnicity.
Health disparities exist due to a complex interaction of components that occurs on many levels. Key factors include the
patient/family (such as socioeconomic status, beliefs, biology, genetics), healthcare provider, clinical encounter, facility, com-
munity, and the healthcare system (including health insurance, distance from care, delivering hospital, and payment factors).21–24
Equally significant components contributing to healthcare disparities include social determinants of health, a deep-rooted
history of injustice and discrimination, and the role of implicit bias.23–25 Racial and ethnic disparities occur in many areas of
American life, including healthcare.
Implicit bias refers to the attitudes and stereotypes that affect our understanding, actions, and decisions in an unconscious
manner.25 These actions are contrary to our stated conscious beliefs and are involuntary. They can lead to unequal treatment of
patients based on race, ethnicity, sexual orientation, weight, language, income, and insurance status.
Implicit bias can perpetuate disparities and can directly lead to patient harm.25 In times of stress and cognitive overload,
memory is biased toward information that is consistent with stereotypes. Thus, the potential influence of implicit bias is espe-
cially pertinent in busy and stressful settings, such as in the field, emergency department (ED), or labor and delivery units.
KEY POINTS
• The lived experience of racism for specific racial and ethnic groups is a significant risk factor for maternal
mortality and SMM.
• Black people are about three times, and AI/AN people are nearly two times, as likely as White people to
die from a pregnancy-related cause.
• The highest risk of maternal death is seen in Black people 40 years of age or older.
• Implicit bias can lead to unequal treatment of patients based on race, ethnicity, sexual orientation, weight,
language, income, and insurance status.
1.6 PREVENTING MATERNAL CARDIAC ARREST

Maternal morbidity and mortality are multifaceted issues. Therefore, actions to catalyze change must occur on multiple levels.
Collaborative efforts should include the community, health facilities, patients and families, healthcare providers, and health
systems.26
Comprehensive and systematic data collection is paramount when studying maternal deaths and near-death scenarios to
understand how to prevent them. State-level maternal mortality review committees review cases of maternal deaths, outline
contributing factors, and determine strategies to help avoid poor outcomes.26 However, these valuable committees are not in all
states and data collection is not consistent. Thus, an infrastructure for systematically assessing maternal deaths is needed. In
December 2018, the U.S. Congress signed into law the Preventing Maternal Deaths Act (HR 1318). This legislation established
and supports state Maternal Mortality Review Committees to review every pregnancy-related death and develop recommenda-
tions to prevent maternal deaths through federal funding and reporting of standardized data.27
To improve maternal outcomes, healthcare providers have implemented and are using a variety of practices and strategies,
including improved education, early warning systems, team and simulation training, and the use of standardized protocols. The
Alliance for Innovation on Maternal Health (AIM)28 has provided sets of bundled guidance to provide standardized management
of obstetric emergencies to improve safety in maternity care. The California Maternal Quality Care Collaborative (CMQCC)
is an excellent example of the successful use of toolkits. These compendiums include best practice tools and articles, care
guidelines, hospital-level implementation guide, and professional education slide sets. The aim of the toolkits is to improve the
response to leading causes of preventable death among pregnant and postpartum people. The CMQCC has used data-driven,
large-scale quality improvement projects that have resulted in a 58% decrease in maternal death between 2008 to 2016 (bringing
deaths down to 5.9 per 100,000 live births) at a time when the U.S. continued to see an increase in maternal deaths.29
Outcomes are improved when patients at high risk deliver at hospitals that can appropriately care for them. Professional
organizations have developed criteria for recommended Levels of Maternal Care (LoMC) for facilities to reduce maternal mor-
bidity and mortality.18 Additionally, recommendations and systems exist for the improvement of postpartum care and addressing
critical factors, such as assistance with transitioning to a primary care physician or specialist, continued insurance coverage,
and addressing the social factors that may limit access to care.27 Last, while it is often uncomfortable for providers to accept and
confront, prejudice and stereotyping exist in healthcare and contribute to the disproportionate outcomes seen in racial and ethnic
minority individuals. In a step toward creating more significant health equity, the Alliance for Innovation on Maternal Health
created a “Reduction of Peripartum Racial/Ethnic Disparity” bundle for healthcare providers and systems. This patient safety
bundle offers insights into racial and ethnic disparities and mechanisms for safe and equitable healthcare. Recommendations
include staff-wide education on implicit bias, training on the causes of racial and ethnic disparities, best practices for shared
decision-making, and building of a culture of equity.28
KEY POINTS
• Comprehensive and systematic ways to collect data are paramount when studying maternal deaths and
near-death scenarios to understand how to prevent them.
• The Preventing Maternal Deaths Act established and supports state Maternal Mortality Review Committees
to review every pregnancy-related death and develop recommendations to prevent maternal deaths
through federal funding and reporting of standardized data.
• A variety of practices and strategies, such as improved education, early warning systems, team and sim-
ulation training, and the use of protocols, have been implemented and are being used by providers to
improve maternal outcomes.
• Safe and equitable healthcare for all includes staff-wide education on implicit bias, education on the
causes of racial and ethnic disparities, best practices for shared decision-making, and building of a culture
of equity.
1.7 PLANNING AND PREPARATION

The American Heart Association uses the Chain of Survival (Figure 1.7) to highlight the important steps that ultimately lead
to successful resuscitation, and these can be applied to both the pre- and in-hospital settings. Although there is a high risk of
maternal mortality after cardiac arrest, survival to hospital discharge for pregnant patients with IH cardiac arrest is higher
when compared to nonobstetric populations. This higher survival rate may be due to different clinical risk factors between
the two groups and/or differences in patient monitoring among hospital units.13 Alternatively, this finding may illustrate that
many arrests are reversible, representing an opportunity to optimize maternal survival with collaborative provider training and
enhanced institutional preparation.7 EMS providers play a crucial role given the potential for patient deterioration en route to
the hospital. Additionally, most postpartum deaths occur more than 7 days after delivery, a time when most patients have been
discharged from the hospital.5
It is challenging to maintain the skills and knowledge for extremely high-risk but rare events. Managing MCA demands
simultaneous coordination of appropriate interventions, teamwork, clear communication, and confidence. Team practice is
FIGURE 1.7 The American Heart Association Chain of Survival. Abbreviations: IHCA, in-hospital cardiac arrest; OHCA, out-of-hospital
cardiac arrest.
necessary to reach this goal. Research shows that simulation is a valuable tool to educate providers in managing obstetric
emergencies by improving competency in emergency decision-making, leadership skills, and individual and team performance.
Specifically, simulation improves response time to starting cardiopulmonary resuscitation (CPR) and resuscitative cesarean
delivery (RCD), airway management, better adherence to ACLS protocols, left uterine displacement (LUD), and identifying
causes of arrest.7,30 Additionally, simulation helps practitioners recognize local barriers, receive feedback, and correct mistakes
in a nonthreatening environment.31
Regardless of the complex interplay of the many factors that exist for each maternal death, MCA is the final common
pathway and represents the dividing line between survival and death.7 OBLS recommends that all practitioners be prepared to
respond and manage pregnant and postpartum patients who experience cardiac arrest.
KEY POINTS
• Survival to hospital discharge for pregnant populations with IH cardiac arrest is higher compared to non-
obstetric populations.
• Team practice through simulation can help with simultaneous coordination of knowledge, teamwork,
clear communication, and confidence when responding to an MCA.
• Simulation improves response time to starting CPR and RCD, airway management, better adherence to
ALS protocols, LUD, and identifying the causes of arrest.
CHAPTER 1. PRACTICE QUESTIONS

1. How many severe maternal morbidity cases occur for every maternal death in the U.S. each year?
A. 10
B. 50
C. 100
D. 200
2. Which racial/ethnic group has the highest risk of maternal death in the U.S.?
A. Non-Hispanic Black (Black)
B. Hispanic
C. Native American
D. White
3. According to the CDC, how many pregnancy-related deaths are preventable?

A. 10%
B. 25%
C. 50%
D. 80%
4. Since the 1980s, which cause of pregnancy-related death has been increasing over time?
A. Hemorrhage
B. Venous thromboembolism
C. Cardiovascular disease
D. Hypertensive disorders
5. Pregnancy-related deaths are most likely to occur at what point in pregnancy?

A. Antepartum (prior to delivery)
B. Peripartum (during admission for delivery and up to 6 days postpartum)
C. Late Postpartum (between 7–365 days postpartum)
D. Equally distributed throughout antepartum, peripartum, and late postpartum
CHAPTER 1. ANSWERS
1. ANSWER: C. Compared to MCA and death, severe maternal morbidity cases are far more likely to occur. Maternal
deaths have been described as the “tip of the iceberg,” and severe maternal morbidity the “rest of the iceberg.”14 In
fact, for every maternal death, there are approximately 100 episodes of severe maternal morbidity each year.
These data underscore the importance of systematic approaches to understanding and preventing severe maternal
morbidity.
2. ANSWER: A. Maternal mortality in the U.S. was more than three times higher in Black or African American people,
and more than two times higher in A/AN people, when compared to White, Hispanic, and A/PI people.
3. ANSWER: D. In the U.S., maternal deaths have increased more than 50% of maternal deaths in the last three
decades. That translates to 1,201 pregnancy-related maternal deaths in 2021. Eighty percent of these deaths are deter-
mined to be preventable.
4. ANSWER: C. Causes and risk factors for pregnancy-related deaths in the U.S. have shifted over the years.
Hemorrhage, hypertensive disorders, and anesthesia-related deaths have declined since 2006, while cardiovascular
conditions have emerged as the leading cause of maternal mortality. Collectively, cardiovascular conditions, car-
diomyopathy, and cerebrovascular accidents accounted for more than 30% of pregnancy-related deaths from 2011
to 2016.
5. ANSWER: C. Twenty-two percent of maternal deaths occur antepartum, 25% on the day of delivery or within 7 days
after, and 53% occur between 7 days to 1 year after pregnancy.
CHAPTER 1. REFERENCES
1. Alkema L, Chou D, Hogan D, et al. Global, regional, and national levels and trends in maternal mortality between 1990 and 2015,
with scenario-based projections to 2030: A systematic analysis by the UN maternal mortality estimation inter-agency group. Lancet.
2016;387:462.
2. Centers for Disease Control and Prevention. Pregnancy mortality surveillance system. Website. https://www.cdc.gov/reproductive
health/maternal-mortality/pregnancy-mortality-surveillance-system.htm. Accessed March 16, 2023.
3. Centers for Disease Control and Prevention. Maternal mortality rates in the United States, 2021. Website. https://www.cdc.gov/nchs/
data/hestat/maternal-mortality/2021/maternal-mortality-rates-2021.htm. Accessed March 17, 2023.
4. Centers for Disease Control and Prevention. Four in 5 pregnancy-related deaths in the U.S. are preventable. Website. https://www.cdc.
gov/media/releases/2022/p0919-pregnancy-related-deaths.html. Accessed March 18, 2023.
5. The Commonwealth Fund. Maternal mortality and maternity care in the United States compared with 10 other developed countries.
Website. https://www.commonwealthfund.org/publications/issue-briefs/2020/nov/maternal-mortality-maternity-care-us-compared-10-
countries. Accessed March 19, 2023.
6. Creanga A, Syverson C, Seed K, Callaghan W. Pregnancy-related mortality in the United States. 2011–2013. Obstet Gynecol.
2017;130:366. doi: 10.1097/AOG.0000000000002114.
7. Zelop CM, Einav S, Mhyre JM, Martin S. Cardiac arrest during pregnancy: Ongoing clinical conundrum. Obstet Gynecol. 2018;219(1):52.
doi: 10.1016/j.ajog.2017.12.232.
8. Zelop CM, Einav S, Mhyre JM, et al. Characteristics and outcomes of maternal cardiac arrest: A descriptive analysis of get with the
guidelines data. Resuscitation. 2018;132:17.
9. Pregnancy and Heart Disease. ACOG Practice Bulletin No. 212. American College of Obstetricians and Gynecologists. Obstet Gynecol.
2019;133(5):320–356. doi: 10.1097/AOG.0000000000003243.
10. MacDorman MF, Declercq E, Cabral H, Morton C. Recent increases in the U.S. maternal mortality rate: Disentangling trends from
measurement issues. Obstet Gynecol. 2016;128:447. doi: 10.1097/AOG.0000000000001556.
11. Davis NL, Hoyert DL, Goodman DA, et al. Contribution of maternal age and pregnancy checkbox on maternal mortality ratios in the
United States 1978–2012. Obstet Gynecol. 2017;217:352.e1. doi: 10.1016/j.ajog.2017.04.042.
12. Say L, Chou D, Gemmill A, et al. Global causes of maternal death: A WHO systematic analysis. Lancet Glob Health. 2014;2. doi:
10.1016/S2214-109X(14)70227-X.
13. Mhyre JM, Tsen LC, Einav S, et al. Cardiac arrest during hospitalization for delivery in the United States, 1998–2011. Anesthesiology.
2014. doi: 10.1097/ALN.000000000000015.
14. Hasegawa J, Ikeda T, Sekizawa A, et al. Maternal death due to stroke associated with pregnancy-induced hypertension. Circ J.
2015;79(8):1835–1840. doi: 10.1253/circj.CJ-15-0297.
15. MacKay AP, Berg CJ, Atrash H. Pregnancy-related mortality from preeclampsia and eclampsia. Obstet Gynecol. 2001;97(4). doi:
10.1016/s0029-7844(00)01223-0.
16. Shields A, Battistelli J, Thomson B. Maternal cardiac arrest: Where is our data coming from. Obstet Gynecol. 2018;131:9S.
17. Shields A, Kavanagh L, Battistelli J. Leave no woman behind: A call to standardize and expand the Get with the Guidelines® Registry.
American Journal of Obstetrics and Gynecology (2022), doi: https://doi.org/10.1016/j.ajog.2022.05.005.
18. American College of Obstetricians, Gynecologists, Society for Maternal-Fetal Medicine, Menard MK, Kilpatric S, Saade G, et al.
Levels of maternal care. Obstet Gynecol. 2015;212:259–271. doi: 10.1016/j.ajog.2014.12.030. Epub 2015 January 22.
19. The Commonwealth Fund. Severe maternal morbidity in the United States: A primer. Website. https://www.commonwealthfund.org/
publications/issue-briefs/2021/oct/severe-maternal-morbidity-united-states-primer. Accessed March 18, 2023.
20. Bryant A. Focusing on severe maternal morbidity (the rest of the iceberg). NEJM J Watch Women’s Health. Waltham; 2014. doi:
10.1056/nejm-jw.NA34784.
21. Petersen EE, Davis NL, Goodman D, et al. Racial/ethnic disparities in pregnancy related deaths—United States, 2007–2016. MMWR
Morb Wkly Rep. 2019;68:762. doi: 10.15585/mmwr.mm6835a3external icon.
22. The Council on Patient Safety in Women’s Health Care. Reduction of peripartum racial and ethnic disparities. Website. https://safe
healthcareforeverywoman.org/patient-safety-bundles/reduction-of-peripartum-racialethnic-disparities/#1472747274361-49911e4d-c2d
60f3f-74eb.
23. Warnecke RB, Oh A, Breen N, Gehlert S, et al. Approaching health disparities from a population perspective: The National Institutes of
Health Centers for Population Health and Health Disparities. Am J of Public Health. 2008;98(9):1608. doi: 10.2105/AJPH.2006.102525.
24. Institute of Medicine (US) Committee on Understanding and Eliminating Racial and Ethnic Disparities in Health Care. Unequal
treatment: Confronting racial and ethnic disparities in health care. In: Smedley BD, Stith AY, Nelson AR, ed. Unequal treatment:
Confronting racial and ethnic disparities in health care. National Academies Press; 2003.
25. Implicit Bias in Health Care. Implicit bias in health care. Website. https://www.jointcommission.org/-/media/tjc/documents/newslet
ters/quick-safety-issue-23-apr-2016-final-rev.pdf. Accessed March 18, 2023.
26. Petersen EE, Davis NL, Goodman D, et al. Vital signs: Pregnancy-related deaths, United States, 2011–2015, and strategies for preven-
tion, 13 states, 2013–2017. MMWR Morb Mortal Wkly Rep. 2019;68:423–429. doi: 10.15585/mmwr.mm6818e1.
27. Kozhimannil KB, Backes K, Hernandez E, Mendez DD, et al. Beyond the Preventing Maternal Deaths Act: Implementation and further
policy change. Health Affairs Blog. 2019. doi: 10.1377/hblog20190130.914004.
28. Alliance for Innovation on Maternal Health. Patient safety bundles. Website. https://saferbirth.org/patient-safety-bundles/#core-aim-
psbs. Accessed March 2023.
29. CA-PMSS Surveillance Report: Pregnancy-Related Deaths in California, 2008–2016. Sacramento: California Department of Public
Health, Maternal, Child and Adolescent Health Division. 2021.
30. Alimena A, Freret TS, King C, Lassey SC, Economy KE, Easter SR. Simulation to improve trainee knowledge and comfort in manag-
ing maternal cardiac arrest. AJOG Global Reports 2023;3(2). doi.org/10.1016/j.xagr.2023.100182.
31. Paige JT, Garbee DD, Brown KM, Rojas JD. Using simulation in interprofessional education. Surg Clin North Am. 2015 Aug;95(4):751–
66. doi: 10.1016/j.suc.2015.04.004.
32. Trost SL, Beauregard J, Njie F, et al. Pregnancy-Related Deaths: Data from Maternal Mortality Review Committees in 36 US States,
2017–2019. Atlanta, GA: Centers for Disease Control and Prevention, US Department of Health and Human Services; 2022.
Anatomic and Physiologic
Adaptations of Pregnancy 2
2.1 INTRODUCTION
Understanding the anatomic and physiologic adaptations during pregnancy is critical to optimizing outcomes when responding
to MCA. This chapter reviews the anatomy and physiology of the various systems in pregnancy compared to the nonpregnant
adult and sets the stage for the recommended modifications of CPR in pregnancy.

Learner will appropriately
• Describe the variations in anatomy and physiology encountered during pregnancy.

• Discuss maternal vulnerabilities that result from changes in the cardiovascular, respiratory, hematologic, gastrointes-
tinal, genitourinary, endocrinologic, and immunologic systems.
2.3 CARDIOVASCULAR ANATOMIC AND

PHYSIOLOGIC ADAPTATIONS IN PREGNANCY
The cardiovascular adaptations encountered during pregnancy are significant and varied. Throughout pregnancy, the maternal
heart rate increases by up to 20%, and maternal stroke volume increases by up to 30% by 32 weeks gestation, resulting in an
increased maternal cardiac output of over 40%. These adaptations support the rapid changes occurring throughout the body,
allowing adequate oxygen and nutrients to get to the placenta and the fetus(es). As a result, a normal grade 1–2 systolic ejection
murmur due to increased blood flow across the left and right ventricular outflow tracts may appear in up to 90% of pregnant
patients. Blood volume expands by 30% due to an increase in the plasma volume (just under a 50% increase). The red blood cell
mass increases by approximately 18%, which leads to “hemodilution of pregnancy.” The net result is that normal hemoglobin
in pregnancy is around 11% lower than that of a nonpregnant female adult. Intravascular colloid oncotic pressure and albumin
concentration both decrease (approximately 12%–18%) throughout the pregnancy as a result of hemodilution. A decline in col-
loid oncotic pressure, along with increased femoral venous pressure by uterine compression of the inferior vena cava, results in
physiologic edema.
Even though blood volume is expanding throughout pregnancy, blood pressure remains normal in the first trimester. Blood
pressure tends to decrease during the second trimester due to the decrease in systemic vascular resistance (up to 35%) in response
to hormonally mediated vasodilation and the low resistance placental circuit. Blood pressure decreases to its lowest point in the
second trimester, at times as early as 6–8 weeks gestation, with a gradual increase in the third trimester, reaching preconceptual
levels by the postpartum period.1 Measure a pregnant patient’s blood pressure as you would with a nonpregnant adult: the patient
sitting in a chair and with their arm resting at heart level.
Additional anatomic changes in the cardiovascular system have the greatest impact on CPR. The expanding uterine size
impedes blood flow through the inferior vena cava and aorta due to direct compression by the uterus on the great vessels. Once
DOI: 10.1201/9781003299288-3 15
TABLE 2.1 Anatomic and Physiologic Cardiovascular Adaptations in Pregnancy

PARAMETER VALUES IN PREGNANCY
Heart rate (HR) ↑ 20%
Stroke volume (SV) ↑ 30%
Cardiac output (CO) ↑ by more than 40%; can result in normal grade 1–2 systolic ejection murmur
Systemic vascular ↓ by more than 30%, nadir at 32 weeks
resistance (SVR)
Oncotic pressure ↓ due to hemodilution and decreased serum albumin
Uterus Palpable at the maternal umbilicus (generally corresponding to 20 weeks gestation with a single
fetus), can ↓ preload and cardiac output
Breast tissue Can be dense and enlarged, causing difficulty with hand placement and pad placement, and ↓
effectiveness of chest compressions
the uterine size reaches the umbilicus (corresponding to approximately 20 weeks in a pregnancy with a single fetus), the gravid
uterus can cause enough aortocaval compression to result in a 25% drop in cardiac output in the supine position. This can lead
to significant hypotension and can negatively impact the success of CPR.
There are several points to note:

1. Aortocaval compression occurs at the umbilicus due to the location of the bifurcation of the great vessels. As such, it is
the fundal height location in relation to the umbilicus, not strictly gestational age, that contributes to this hypotension.
2. A pregnancy with multiple fetuses (i.e., twins or triplets) often has a fundal height at or above the umbilicus prior to 20
weeks.
3. This effect may be more profound or occur more quickly as pregnancy advances.
From a clinical perspective, this compression of the inferior vena cava may keep fluids and medications from reaching the heart
quickly and is why intravenous (IV) access is recommended above the level of the diaphragm.
While the anatomic location of the heart is unchanged, maternal breast tissue often expands and may interfere with hand
placement during chest compressions. Table 2.1 summarizes the anatomic and physiologic cardiovascular changes that occur in
pregnancy.
KEY POINTS
• An increased heart rate is normal in a pregnant person.
• Measure a pregnant patient’s blood pressure as you would with a nonpregnant adult: the patient sitting
in a chair and with their arm resting at heart level.
• Pregnancy is characterized by hemodilutional anemia due to an increase in the plasma volume as com-
pared to the red blood cell mass.
• Many pregnant people experience physiologic edema due to decreased plasma oncotic pressure and an
increased femoral venous pressure.
• Once the uterine size reaches the umbilicus, cardiac output can drop by 25% in the supine position. This
may lead to significant hypotension and can compromise the success of CPR.
• Due to the expanding uterus and corresponding compression of the great vessels in supine position, place
the IV above the level of the diaphragm.
2.4 RESPIRATORY ANATOMIC AND PHYSIOLOGIC

ADAPTATIONS IN PREGNANCY
The respiratory adaptations encountered during pregnancy are substantially different from the nonpregnant state. These dif-
ferences are not only physiologic and anatomic but also influenced by maternal habitus, including the body mass index (BMI).
2 • Anatomic and Physiologic Adaptations of Pregnancy 17
During pregnancy, hormones such as progesterone, estrogen, and prostaglandin influence physiologic changes in the respiratory
system.
Estrogen increases during pregnancy and results in an increase in the number and sensitivity of central progesterone recep-
tors in the hypothalamus and medulla.2 Estrogen also enhances the effects of progesterone.3 Progesterone levels increase during
pregnancy and peak at 37 weeks gestation. Progesterone increases the sensitivity of the respiratory center to carbon dioxide,
relaxes airway smooth muscle tone (resulting in a bronchodilatory effect), and increases swelling and vascularity of mucosal sur-
faces resulting in increased nasal congestion4 and decreased internal tracheal diameter. These effects result in decreased nasal
patency and can lead to an increase in the Mallampati score.5
The Mallampati score, used by providers to assess the suspected difficulty of laryngoscopy, includes four classifications
(Figure 2.1). Class I shows full visualization of the oropharynx (little or no anticipated difficulty), ranging to class IV, which
corresponds to no visualization of the soft palate (significant anticipated difficulty). Multiple studies have shown an increase
in Mallampati score to class IV at term in over 30% of patients. Labor can negatively impact the Mallampati score due to an
increase in airway edema, leading to increased difficulty in airway management.3,5
Prostaglandins are present during all trimesters of pregnancy and increase during labor. Prostaglandin F2alpha (F2α)
increases airway resistance through bronchial smooth muscle constriction. Prostaglandins E1 and E2 have bronchodilatory
effects. It is for this reason that carboprost tromethamine, a synthetic analogue of prostaglandin F2α, commonly used to treat
postpartum hemorrhage, is contraindicated in patients with asthma. Carboprost can exacerbate asthma by increasing airway
resistance.
KEY POINTS
• Hormonal changes in pregnancy, mediated mainly through increased progesterone, can increase swelling
of the mucosal surfaces of the airway, leading to an increase in nasal congestion.
• Pregnancy negatively impacts the Mallampati score, reflecting a progressively more difficult airway as
pregnancy advances, especially in labor.
• Avoid using carboprost, a prostaglandin F2α analog, in treating postpartum hemorrhage in patients with
asthma. Carboprost increases airway resistance through bronchial smooth muscle constriction.
Anatomic changes of pregnancy also contribute to respiratory changes. As the uterus grows, it elevates the diaphragm, ulti-
mately leading to decreased functional residual capacity and total lung capacity. There is a significant increase in oxygen
demand during normal pregnancy.6 Combined with decreased functional residual capacity, this increased demand leads to
overall lower oxygen reserves, putting a pregnant person at increased risk of oxygen desaturation much more rapidly than a
nonpregnant person. The desaturation time is substantially shorter in pregnancy, at 3 minutes, compared to 9 minutes in non-
pregnant adults. Normal maternal blood gases reflect a mild respiratory alkalosis (pH = 7.4), which is higher than the non-
pregnant population (pH = 7.35–7.45). Maternal PaCO2 is also mildly decreased (28–32 mm Hg) compared to nonpregnancy
values (PaCO2 35–45 mm Hg).7 Table 2.2 compares normal arterial blood gas (ABG) values between pregnant and nonpregnant
patients. The resultant effects of these hormonal and anatomic changes are summarized in Figure 2.2 and Table 2.3.8
FIGURE 2.1 Mallampati scoring system.

TABLE 2.2 Arterial Blood Gas Values in Pregnant versus Nonpregnant Patients
STATUS pH PaCO2 PaO2 HCO3-
Pregnant 7.40–7.45 28–32 mm Hg >100 mm Hg 22 mEq/L

Nonpregnant 7.35–7.45 35–45 mm Hg 75–100 mm Hg 22–26 mEq/L
FIGURE 2.2 Flow diagram summarizing the most important effects of biochemical (left) and mechanical (right) pregnancy-induced
factors on pulmonary function, ventilatory pattern, and gas exchange.9 Abbreviations: ERV, expiratory reserve volume; FRC, functional
residual capacity; IC, inspiratory capacity, PCO2, carbon dioxide tension; PO2, oxygen tension; TLC, total lung capacity; VC, vital capacity,
AB, abdomen; RC, rib cage; ↑, increased; ↓, decreased; ≈, no change.9
TABLE 2.3 Anatomic and Physiologic Respiratory Adaptations in Pregnancy

Functional reserve capacity (FRC) ↓ by 20%
Expiratory reserve volume (ERV) ↓ by 15%–20%
Residual volume (RV) ↓ by 20%–25%
Tidal volume (TV) ↑ by 30%–40%
Minute ventilation ↑ by 50%
Diaphragm Elevated by gravid uterus resulting in ↓ FRC, ERV, RV, and total lung capacity
Progesterone ↑ sensitivity of the respiratory center to carbon dioxide, relaxes airway smooth muscle
tone (resulting in a bronchodilatory effect), and mediates hyperemia and edema of
mucosal surfaces ↓ nasal patency
The result of these normal physiologic adaptations in pregnancy is a more clinically challenging airway. Table 2.4 lists the
anatomic and physiologic changes and clinical consequences of these adaptations (gastrointestinal adaptations and impact on the
airway are also discussed later in this chapter). Providers must be aware of these adaptations and prevent avoidable complications.
For example, preoxygenation is critical prior to the intubation of a pregnant patient due to the increased risks of desaturation.
A pregnant patient who presents with respiratory distress and has PaCO2 values >42 mm Hg should be immediately evaluated
for respiratory decompensation, with a low threshold for intubation. The increase in PaCO2 levels indicates a decrease in minute
ventilation, signifying impending respiratory decompensation as respiratory fatigue results in decreased minute ventilation.
KEY POINTS
• An enlarged uterus decreases total lung capacity.
• Adaptations in the respiratory system during pregnancy lead to ↑ oxygen consumption, ↓ oxygen reserve,
and ↑ vulnerability to earlier oxygen desaturation.
• Pregnancy is characterized with mild respiratory alkalosis, and normal ABG values for PaCO2 are
28–32 mm Hg, lower than nonpregnant adults.
• Adaptations of the respiratory system are varied and result in a clinically challenging airway during
pregnancy.
• A decreased lower esophageal sphincter tone increases the risk of aspiration during pregnancy.
TABLE 2.4 Pregnancy-Related Maternal Anatomic and Physiologic Factors That May Contribute to Airway Difficulties and Adverse
Airway-Related Events10
ANATOMIC AND PHYSIOLOGIC CHANGES CLINICAL CONSEQUENCES
Airway • Weight gain in pregnancy • Difficulty with positioning
• Increased breast size • Difficulty with laryngoscope insertion
• Increased vascularity and edema of the • Increased risk of airway bleeding and potential
airway mucosa difficulty with endotracheal intubation
Respiratory • Reduced functional residual capacity • Increased rate of oxygen desaturation
Metabolic • Increased oxygen consumption secondary to • Increased rate of oxygen desaturation
increased metabolic demand
Gastrointestinal • Decreased lower esophageal sphincter tone • Increased risk of gastric regurgitation and
• Delayed gastric emptying pulmonary aspiration
2.5 NEUROPHYSIOLOGIC ADAPTATIONS IN PREGNANCY

Normal pregnancy results in several physiologic changes in the maternal nervous system. These changes can be categorized into
central nervous system (CNS) changes, peripheral/autonomic nervous system (PANS) changes, and cerebrovascular adaptations
(Table 2.5).
In the CNS, the normal hormonal changes of pregnancy have profound effects on neurotransmitters including oxytocin,
prolactin, and dopamine, all of which play critical roles in pregnancy, birth, lactation, and maternal-infant bonding. Additional
neurotransmitter changes, such as changes in the gamma-aminobutyric acid (GABA) receptor, can make the maternal brain
more susceptible to seizure activity. In addition, pregnancy changes the maternal metabolism of medications that affect the CNS,
such as anti-seizure medications, making people with epilepsy vulnerable to increased seizure activity. Of note, noneclamptic
seizures are the leading cause of sudden cardiac death in pregnant people with epilepsy.
In the PANS, normal pregnancy increases sympathetic tone, decreases parasympathetic activity, and impairs baroreceptor
activity, all factors that may affect a person’s response to acute hypertension or hypotension, contributing to cardiac arrest risk.
Preeclampsia is associated with an even greater increase in sympathetic hyperactivity, a factor that may contribute to cardiac
arrhythmias, myocardial stunning, and coronary artery and/or cerebral artery vasospasm.
Pregnancy also has important effects on the cerebral vasculature. The brain requires a constant supply of energy and has
no energy storage capacity. To address this, the cerebral vasculature dynamically adjusts to ensure constant cerebral blood
flow at a wide range of blood pressures, a process known as cerebral autoregulation. Cerebral autoregulation appears to be
enhanced during normal pregnancy but impaired during hypertensive pregnancy and in the postpartum period. In addition, the
blood–brain barrier shows increased permeability in normal and especially in hypertensive pregnancy. Last, pregnancy-related
hypercoagulability (see Chapter 10) can affect the cerebral veins and draining sinuses, leading to cerebral venous sinus throm-
bosis. These features likely contribute to increased risk of postpartum stroke, particularly in those with hypertensive disorders.
TABLE 2.5 Maternal Central Nervous System Changes

SYSTEM ANATOMIC AND PHYSIOLOGIC CHANGES CLINICAL CONSEQUENCES
Central nervous system Changes in neurotransmitter levels and Lowered seizure threshold
(brain) activity
Metabolic Changes in metabolism of anti‑seizure Increased risk of breakthrough seizures in
medications people with epilepsy
Peripheral/Autonomic Increased sympathetic activity Increased risk of vasospasm and cardiac
nervous system Decreased baroreceptor reflex arrhythmias; impaired response to acute
hypertension or hypotension
Cerebral vasculature Changes in cerebral autoregulation, especially Inability to compensate in brain for acute blood
postpartum pressure changes
Increased blood–brain barrier permeability Increased risk of ischemic or hemorrhagic stroke
Hypercoagulability Increased risk of cerebral venous thrombosis
KEY POINTS
• Normal pregnancy lowers the seizure threshold and alters maternal metabolism, increasing the risk of
seizures, particularly for those with epilepsy.
• Pregnancy causes sympathetic nervous system activation, which is exaggerated in people with
preeclampsia.
• Baroreceptor activity is altered in pregnancy; this may affect people’s response to acute hypertension or
hypotension.
• Changes in cerebral autoregulation and the blood–brain barrier may contribute to risk of pregnancy-as-
sociated stroke, especially in the postpartum period.
2.6 HEMATOLOGIC PHYSIOLOGIC ADAPTATIONS IN PREGNANCY

Significant hematologic adaptations occur during pregnancy. As previously mentioned, blood volume expands by 30% (approx
imately 1.5 L) due to a relative increase in the plasma volume compared to the red blood cell mass. It is normal to see an
increased white blood cell (WBC) count in a pregnant person,11 sometimes elevating as high as 29,000 cells per cubic milliliter
during labor. Most pregnant people have a normal platelet count throughout pregnancy (150,000–400,000 per microliter). Lower
platelet counts in pregnancy (as low as 70,000 per microliter) may be encountered due to gestational thrombocytopenia.12 This
is a benign, transient condition that improves after delivery. Table 2.6. summarizes hematologic adaptations during pregnancy.
Pregnancy also results in an increased risk of thrombosis due to its multiple effects on Virchow’s triad (hypercoagulabil-
ity, venous stasis, and vascular damage). There are significant increases in circulating estrogen and prothrombotic coagulation
factors (such as fibrinogen, von Willebrand factor, and factors II, VII, VIII, and X). In addition, there is an acquired functional
resistance to activated protein C and a 50%–60% reduction in protein S. Further derangements in coagulation hemostasis include
a reduction in plasminogen activator and an increase in plasminogen activator inhibitors.13 These changes result in a hypercoagu-
lable state. Pressure on the pelvic vessels and inferior vena cava from the enlarging uterus increases venous stasis. These changes
make a pregnant patient more susceptible to clot formation and pulmonary embolism.13
Normal values of fibrinogen in pregnancy are often higher (373–619 mg/mL) than those in nonpregnant patients (200–400
mg/dL). In the setting of active or recent bleeding, a fibrinogen level of 200–250 mg/dL may be an early indicator of significant
hemorrhage and hypofibrinogenemia, prompting further evaluation. In the setting of significant bleeding (blood loss of >1,500
mL) or hypofibrinogenemia, administer blood products containing fibrinogen (such as fresh frozen plasma [FFP] or cryoprecip-
itate [cryo]).
TABLE 2.6 Physiologic Hematologic Adaptations in Pregnancy

Fibrinogen Increases up to 600 mg/dL, average 400 mg/dL
Hemoglobin/Hematocrit Decreases: average hemoglobin 11.2 g/dL
Platelets No change: gestational thrombocytopenia can occur in 7%–12%
at term12, with platelet counts typically above 70,000
Prothrombin time/Partial thromboplastin time No change
WBC count Slightly increased: as high as 25,000–29,000 in labor
KEY POINTS
• It is normal for the WBC count to be elevated in pregnant people, and this does not necessarily suggest
infection.
• Gestational thrombocytopenia may result in platelet counts as low as 70,000 per microliter in an other-
wise normal pregnancy.
• Pregnancy causes an increased risk of developing blood clots due to hypercoagulability and venous stasis.
• A fibrinogen level of 200–250 is considered low for pregnancy and should prompt further workup for
bleeding and consideration of blood products.
2.7 GASTROINTESTINAL ANATOMIC AND

PHYSIOLOGIC ADAPTATIONS IN PREGNANCY
The gastrointestinal adaptations encountered during pregnancy result from both hormonal and anatomic causes. Increased saliva
production in the oropharynx is common.14,15 Gastric emptying is unchanged during pregnancy16 but may be prolonged after
giving opiates or sedatives (as may be seen during labor analgesia). The lower esophageal sphincter resting pressure is decreased
secondary to progesterone effect. Increased progesterone and decreased motilin mutually contribute to lower motility of the
small and large intestines. Combined with the compressive effects of the gravid uterus, this decreased intestinal motility leads
to an increase in transit time, and constipation is common in pregnancy. Mechanical factors also cause the liver to shift upward
from the abdominal cavity into the thoracic cavity. The gallbladder has decreased motility with a resultant increase in gallstone
formation during pregnancy. Uterine distension, especially during the third trimester, can contribute to the increased incidence
of hemorrhoids and urinary and renal incontinence.
The collective effect of increased saliva production, decreased lower esophageal sphincter resting pressure, and increased
transit time through the intestines poses a significant risk for vomiting and aspiration during a maternal code (Table 2.7). In
pregnancy, the airway may be obstructed and the vocal cords hard to see due to excessive oropharyngeal secretions. If possible,
suction equipment should be immediately available during intubation given that liberal suctioning may be necessary. Early intu-
bation will serve to secure the airway and protect against aspiration.
Injury to the liver during chest compressions may occur because the liver shifts upward from the abdominal cavity into
the chest cavity under the ribs and sternum. Several reports document liver lacerations following maternal resuscitation.17,18 It is
unknown if these lacerations were a consequence of vigorous chest compressions or spontaneous rupture of the liver capsule due
to pregnancy-specific causes such as preeclampsia. Changing hand placement will make chest compressions less effective and
therefore decrease the likelihood of ROSC.19 Current American Heart Association (AHA) guidelines recommend maintaining
normal hand placement and performing an ultrasound to look for evidence of liver laceration/free fluid if ROSC is achieved and
there is a suspicion for hypovolemia.
TABLE 2.7 Anatomic and Physiologic Gastrointestinal Adaptations in Pregnancy

Gallbladder ↓ motility
↑ lithogenicity of bile/gallstones
Gastric emptying Unchanged
Liver Elevated into chest by growing uterus
Lower esophageal sphincter ↓ pressure/tone
Rectum/anus ↑ hemorrhoids, incontinence
Saliva ↑ (ptyalism in up to 35%)
Small and large intestine ↓ motility/↑ transit time
↑ constipation, bloating
KEY POINTS
• There is a significant increase in the risk of vomiting and aspiration before and after a maternal code.
• Early intubation will serve to secure the airway and protect against aspiration.
• Injury to the liver during chest compressions may occur because the liver shifts upward from the abdom-
inal cavity into the chest cavity under the ribs and sternum.
2.8 GENITOURINARY ANATOMIC AND PHYSIOLOGIC

Urinary tract adaptations encountered during pregnancy predispose people to infections and alter the metabolism or clearance
of certain medications. The hormonal effect of increased progesterone, as well as compression of the ureters at the pelvic brim,
lead to caliceal and renal pelvis dilation and may be considered hydronephrosis by radiologic standards in up to 80% of patients.
The right side is affected more often due to dextrorotation of the uterus by the sigmoid colon, kinking of the ureter as it crosses
the right iliac artery, and proximity to the right ovarian vein. Ureteral dilation also occurs due to progesterone relaxation of
smooth muscle. Uterine growth may also create compression, causing the ureters to become elongated, tortuous, and displaced
laterally with advancing gestational age. Superior and anterior displacement and compression by the enlarging uterus may fur-
ther decrease bladder capacity.
The dilation of and decrease in peristalsis of the urinary collecting system, combined with intermittent vesicoureteral reflux
due to increased intravesicular and decreased intraureteral pressure through an incompetent vesicoureteral valve,20,21 lead to the
collection of up to 300 mL of static urine in the pregnant bladder. This urinary stasis can serve as a reservoir for bacteria and
lead to an increase in urinary tract infections including pyelonephritis and urosepsis. Urosepsis is a common cause of sepsis in
pregnancy and should be considered in the setting of unstable maternal status and concern for infectious etiology.
Increased renal perfusion and glomerular filtration rate (GFR) are seen in pregnancy due to increased cardiac output and
decreased systemic vascular resistance. GFR is also increased due to increased renal blood flow caused by pregnancy-related
hormones. Reduced vascular responsiveness to vasopressors such as angiotensin II, norepinephrine, and antidiuretic hormone
has also been shown.22 Renal plasma flow (RPF) increases by 80% by the end of the first trimester, with a 50% increase in GFR.
Both parameters decrease toward prepregnancy values near term with RPF returning to near preconception levels. GFR remains
significantly elevated.
The physiologic increase in GFR during pregnancy results in a decrease in serum creatinine concentration to a normal
range of 0.4–0.8 mg/dL and blood urea nitrogen to 8–10 mg/dL.23 The plasma osmolality in normal pregnancy decreases to 270
mOsmol/kg from a nonpregnant level of 275–290 mOsmol/kg. Hyponatremia is also common in pregnancy with a decrease in
plasma sodium concentration to 4–5 mEq/L below nonpregnant levels, with sodium levels remaining above 130 mEq/L.24 The
increased GFR also leads to increases in proteinuria and glucosuria in pregnancy. Urinary protein excretion rises from about
100 mg daily to about 150–200 mg daily in the third trimester, with values >300 mg per day considered an abnormal elevation.25
Glucosuria (defined as glucose in the urine) is present in 50% of pregnant people and may occur independent of serum glucose
levels.26 Hypouricemia is also present with serum uric acid reaching a nadir of 2.0–4.0 mg/dL in the second trimester before
slowly returning to baseline by term.27
The mild respiratory alkalosis that occurs in pregnancy results in a compensatory decrease in plasma bicarbonate levels
from 26 mmol/L to approximately 22 mmol/L.23 Second, the serum anion gap falls from 10.7 in the nonpregnant state to 8.5
during pregnancy.28 This is likely due to the physiologic hypoalbuminemia of pregnancy, since negatively charged albumin is
a major component of the anion gap.
Doubling of a patient’s baseline creatinine, which is normally decreased to 0.4–0.6 mg/dL in pregnancy, to a value of 1.0
mg/dL or greater, usually indicates significant renal impairment in a patient with a normal baseline creatinine.
KEY POINTS
• Pregnant people are more prone to urinary tract infections and urosepsis due to urinary stasis.
• Pregnancy is characterized by respiratory alkalosis, decreased plasma bicarbonate levels to approximately
22 mmol/L, and a decreased serum anion gap to 8.5.
• Vesicoureteral reflux may make pregnant patients more susceptible to urinary tract infections and urosepsis.
2.9 ANATOMIC AND PHYSIOLOGIC IMPACT

ON MEDICATIONS IN PREGNANCY
Common obstetric medications with renal clearance, such as magnesium sulfate, can rapidly increase to toxic levels and lead to
ventricular arrhythmias and cardiac arrest if not carefully monitored and adjusted when decreased renal clearance/renal impair-
ment is present.
Table 2.8 summarizes the resultant effects of these physiologic and anatomic changes. Medications such as digoxin, phe-
nytoin, and midazolam are protein bound and can also lead to toxic levels more easily due to the low albumin levels in preg-
nancy combined with other physiologic changes, including increased tidal volume, partially compensated respiratory alkalosis,
slowed gastrointestinal motility, and altered activity of hepatic drug-metabolizing enzymes.29 Even though pregnancy can alter
the pharmacokinetic properties of some drugs, it is still recommended to give the same medications and doses in MCA used in
nonpregnant adult cardiac arrest.30
TABLE 2.8 Anatomic and Physiologic Genitourinary and Acid-Base Adaptations in Pregnancy
Acid-base balance ↑ bicarbonate excretion23
Bladder/ureter ↑ vesicoureteral reflux
↑ frequency, nocturia, urgency, dysuria, incontinence
Glomerular filtration rate/renal plasma flow ↑ 50%23
↓ creatinine to <0.8 mg/dL
↑ excretion of glucose, protein, and amino acids23
Kidney size ↑ 1–1.5 cm,31 ↑ volume by 30%
Osmolality ↓ threshold for thirst/vasopressin release
↑ vasopressin metabolism
Hyponatremia
Ureteral dilation Resembles hydronephrosis32
KEY POINTS
• Use all medications and their doses in CPR for MCA as you would for adult CPR. Do not change them
based on the physiologic adaptations during pregnancy.
• High-risk medications with renal clearance, such as magnesium sulfate, can rapidly lead to cardiac arrest
if not carefully monitored and adjusted when renal impairment is present.
2.10 ENDOCRINE ANATOMIC AND PHYSIOLOGIC

While the endocrine system undergoes various changes in pregnancy, these adaptations are relatively gradual and generally do
not have a direct impact in a cardiac arrest scenario. Pregnancy may exacerbate some endocrine conditions, especially in the set-
ting of noncompliance, and may predispose chronically ill people to cardiac arrest (e.g., diabetic ketoacidosis and thyroid storm).
While this course does not cover the management of diabetic ketoacidosis (DKA), EMS and IH personnel caring for pregnant
people should be aware that they are susceptible to DKA at much lower, and even normal, glucose thresholds. Thyroid storm
in pregnancy may occur because of noncompliance with medications used to treat hyperthyroidism or unrecognized new-onset
hyperthyroidism. Thyroid storm may be precipitated by stressors such as labor and delivery, surgical delivery (such as cesarean
delivery), infection, and trauma. Early recognition and treatment of thyroid storm are critical to avoiding cardiovascular collapse.
Thyroid storm can also be associated with preeclampsia, most commonly with severe features, and should be considered in the
differential diagnosis of people with hypertension, especially with thyroid dysfunction.
KEY POINTS
• Pregnant patients are much more susceptible to DKA at lower and even normal glucose thresholds.
• In a pregnant patient with hyperthyroidism, early recognition of thyroid storm and appropriate treatment
will help avoid cardiovascular collapse.
2.11 IMMUNE SYSTEM ADAPTATIONS IN PREGNANCY

Alterations of the immune system during pregnancy may help explain the altered susceptibility to and severity of infectious
diseases during pregnancy. As pregnancy progresses, estrogen and progesterone levels progressively increase to supraphysi-
ologic values. Whereas innate immunity is enhanced in pregnancy, cell-mediated and humoral immunity may be moderately
suppressed, which may increase a pregnant person’s susceptibility to certain infections such as influenza. Many infectious dis-
eases will follow a similar course to that which occurs in a nonpregnant person, and the management in pregnancy will also be
TABLE 2.9 Anatomic and Physiologic Endocrinologic Adaptations in Pregnancy

PARAMETER NORMAL VALUES IN PREGNANCY
FT3 (free) 2.4–4.4 pg/mL
FT4 (free) 5.4–11.7 ng/dL
Glucose <95 mg/dL fasting, <140 mg/dL 2-hour postprandial
TSH 0.34–4.25 IU/mL
Abbreviations: FT3, free triiodothyronine; FT4, free thyroxine; TSH, thyroid-stimulating hormone.
similar. Any infection that would lead to sepsis in nonpregnant patients can affect pregnant patients with risks for morbidity and
mortality that are similar to or greater than nonpregnant patients. Although there is strong evidence for the increased severity
of certain infections among pregnant people, the evidence regarding initial susceptibility to infection in pregnancy is weaker.
Pregnancy physiologic changes may mask many of the signs and symptoms that would typically be used to identify a serious
infection early in its course. See Chapter 3 for more details on how to recognize an unstable pregnant patient and manage sepsis.
KEY POINTS
• Alterations in cell-mediated and humoral immunity in pregnancy increase a pregnant person's susceptibil-
ity to certain infections, such as influenza.
• Pregnancy physiologic changes may mask many of the signs and symptoms that would typically be used
to identify a serious infection early in its course.

1. A pregnant patient presents for their obstetric visit at 13 weeks and has a hemoglobin of 11.3%. You tell them that this
value is normal and results from an increase in which of the following?
A. Oncotic pressure relative to systemic vascular resistance
B. Glomerular filtration rate relative to blood volume
C. Plasma volume relative to red blood cell mass
D. Red blood cell mass relative to blood volume
2. Which of the following BEST reflects the normal acid-base status in pregnancy?
A. Mild respiratory acidosis
B. PaCO2 between 28 and 32 mm Hg
C. Compensatory respiratory acidosis
D. pH of 7.35
3. An increase in the Mallampati score during pregnancy leads to difficulty with airway management. During a maternal
cardiac arrest, a change in the size of which of the following MOST significantly impacts the Mallampati score?
A. Neck
B. Breasts
C. Oropharynx
D. Nasal passage
4. Which of the following normal physiologic responses results in a GREATER risk of aspiration during pregnancy?
A. Decrease in motility of the gallbladder
B. Decrease in Mallampati score
C. Increase in biliary sludge
D. Decrease in lower esophageal sphincter tone
5. Which of the following reasons accounts for people being more susceptible to urinary tract infections and urosepsis
during pregnancy?
A. Increased vesicoureteral reflux
B. Increased peristalsis of the ureters
C. Decreased intravesical pressure
D. Decreased glucosuria
CHAPTER 2. ANSWERS
1. ANSWER: C. Blood volume expands by 30% due to an increase in the plasma volume (just under a 50% increase).
The red blood cell mass increases by approximately 18%, leading to hemodilution. The net result is that normal
hemoglobin in pregnancy is around 11%, lower than that of a nonpregnant female adult. Intravascular colloid oncotic
pressure and albumin concentration (12%–18%) both decrease throughout the pregnancy as a result of hemodilution.
2. ANSWER: B. Maternal blood gases typically reflect a mild respiratory alkalosis (pH = 7.4), which is different from
the nonpregnant population (pH = 7.35–7.45). Maternal PaCO2 is also mildly decreased (28–32 mm Hg) due to an
increase in minute ventilation. This is also different in the nonpregnant population, where normal ABG values for
PaCO2 are 35–45 mm Hg.
3. ANSWER: C. An increase in oropharyngeal edema, especially during labor, significantly impacts the Mallampati
score. Multiple studies have shown an increase in Mallampati score to class IV at term in over 30% of patients, largely
due to an increase in oropharyngeal edema.
4. ANSWER: D. The collective effect of increased saliva production and transit time through the intestines, poten-
tially prolonged gastric emptying, and decreased lower esophageal sphincter resting pressure poses a significant
risk for vomiting and aspiration during a maternal code. Suction equipment should be immediately available given
that liberal suctioning may be necessary. Early intubation will serve to secure the airway and protect against
aspiration.
5. ANSWER: A. The dilation of and decrease in peristalsis of the urinary collecting system, combined with increased
vesicoureteral reflux due to increased intravesicular and decreased intraureteral pressure through an incompetent
vesicoureteral valve, lead to the collection of up to 300 mL of static urine. This urinary stasis can serve as a reservoir
for bacteria and lead to a urinary tract infection including pyelonephritis and potential for urosepsis.
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28. Akbari A, Wilkes P, Lindheimer M, Lepage N, Filler G. Reference intervals for anion gap and strong ion difference in pregnancy:
A pilot study. Hypertens Pregnancy. 2007;26(1):111.
29. Costantine MM. Physiologic and pharmacokinetic changes in pregnancy. Front Pharmacol. 2014;5(65). doi: 10.3389/fphar.2014.00065.
30. Jeejeebhoy F, Zelop C, Lipman S, Carvalho B, Joglar J, Mhyre J, Katz V, Lapinsky S, Einav S, Warnes C, Page R, Griffin R, Jain A,
Dainty K, Arafeh J, Windrim R, Koren G, Callaway C and on behalf of the American Heart Association Emergency Cardiovascular
Care Committee, Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation, Council on Cardiovascular Diseases in
the Young, and Council on Clinical Cardiology. Cardiac Arrest in Pregnancy. Circulation. 2015;132:1747–1773. https://doi.org/10.1161/
CIR.0000000000000300.
31. Bailey RR, Rolleston GL. Kidney length and ureteric dilatation in the puerperium. Obstet Gynaecol Br Commonw. 1971;78:55. doi:
10.1111/j.1471-0528.1971.tb00191.x.
32. Rasmussen PE, Nielsen FR. Hydronephrosis during pregnancy: A literature survey. Eur J Obstet Gynecol Reprod Biol. 1988;27:249.
Prevention of Maternal
Cardiac Arrest 3
3.1 INTRODUCTION
A 2022 CDC report suggested that more than 80% of maternal mortalities following MCA could have been prevented. Most of
the causes of MCA will result in demonstrable changes in symptoms and vital signs prior to the development of cardiac arrest.
This chapter reviews the following:
• How vital signs can be used with tools such as maternal early warning systems to assist with detecting the deteriorat-
ing maternal status.
• Examples of scoring systems that can be integrated into clinical practice for early detection of deteriorating maternal
status.
• Management strategies and escalation protocols that have been utilized in response to change in status.
• How to recognize the presenting symptoms and signs of the most common causes leading to maternal cardiac arrest.

• Identify specific trigger thresholds for responding to changes in the patient’s vital signs and clinical condition.
• Describe a plan for and implementation of diagnostic workup.
• Describe at least two different tools available for early recognition of unstable pregnant patients.
• Describe management strategies and escalation protocols.
3.2.1 Normal and Abnormal Maternal Vital Signs and Symptoms

Normal physiologic changes in pregnancy may mask maternal deterioration in the critically ill patient at different times in preg-
nancy. Recognizing a critically ill pregnant person requires an understanding of the normal physiologic changes in pregnancy,
which are covered in previous chapters and are reviewed here (Table 3.1). External factors that influence maternal physiology
are covered next.
Because pregnancy generally occurs in a younger and fitter population, lower baseline and mean arterial blood pressure
are common as is mild maternal tachycardia. In nonpregnant patients, vital sign changes (such as hypotension and tachycar-
dia) are some of the earliest indicators of deteriorating status. However, waiting for vital sign changes to indicate maternal
deterioration is not always reliable, as these warning signs may be masked or may not appear until the moment of impending
respiratory or cardiovascular collapse (such as maternal hypotension or tachycardia during acute blood loss). A compre-
hensive understanding of normal physiology in pregnancy and its impact on vital signs is critical to the accurate and timely
interpretation of vital signs and symptoms and recognition of maternal deterioration. Tables 3.2 and 3.3, respectively, outline
the common symptoms and conditions and the normal physiologic changes throughout pregnancy that may mask serious
conditions.
DOI: 10.1201/9781003299288-4 27
TABLE 3.1 Impact of Normal Physiologic Changes in Pregnancy on Maternal Condition

SYSTEM CHANGES EFFECT
Blood ↑ plasma volume Dilutional anemia
↑ red cell volume Greater reduction of oxygen supply to tissues
Cardiovascular ↓ peripheral vascular resistance Masks initial signs of sepsis and increased
↑ heart rate hypoperfusion
↓ arterial pressure
↑ cardiac output
Coagulation ↑ factors VII, VIII, IX, X, XII, von Willebrand and ↑ risk of thrombotic events
fibrinogen ↑ risk of disseminated intravascular coagulation
↓ protein S
↓ fibrinolytic activity
Gastrointestinal ↓ muscle tone across the digestive tract ↑ risk of bacterial translocation
Delayed gastric emptying ↑ risk of aspiration pneumonia
Diaphragm elevation by the pregnant ↑ risk of cholestasis, hyperbilirubinemia, and
womb jaundice
Changes in bile composition
↑ production of pro-inflammatory cytokines by
Kupffer cells
Genital ↓ vaginal pH ↑ risk of chorioamnionitis
↑ glycogen in vaginal epithelium
Renal Ureteropelvic dilation and Asymptomatic bacteriuria
↓ ureteral pressure due to smooth muscle Delayed identification of renal injury secondary
relaxation to sepsis
Flaccid bladder ↑ risk of pyelonephritis and urosepsis
↑ intravesical pressure due to the pregnant
uterus weight
↑ vesicoureteral reflux
↑ renal plasma flow
↑ glomerular filtration rate
↓ urea and creatinine average values
Respiratory ↑ tidal volume Impaired oxygenation
↓ residual volume Delayed physiologic response to metabolic
↑ minute ventilation by 30%–40% acidosis
↑ respiratory center stimulation
↑ respiratory rate
↓ PaCO2
TABLE 3.2 Common Changes and Symptoms in Pregnancy That May Mask Serious Conditions
MOST COMMON SYMPTOMS NORMAL PHYSIOLOGIC CHANGES SERIOUS CONDITIONS MASKED
Headache Tension, migraine, rebound, postdural Stroke, cerebral venous sinus thrombosis
puncture
Heartburn Gastroesophageal reflux Myocardial infarction, preeclampsia,
HELLP syndrome, pancreatitis
Shortness of breath Dyspnea of pregnancy, asthma Pulmonary embolism, cardiomyopathy/
heart failure
Nausea and vomiting Nausea and vomiting of pregnancy Preeclampsia, HELLP syndrome,
pancreatitis, myocardial infarction
Swollen ankles/feet Gestational edema, prior injury Preeclampsia, deep venous thrombosis,
cardiomyopathy/heart failure
Palpitations/Chest pain Anemia, anxiety, thyroid disorder Myocardial infarction, cardiac arrythmia,
cardiomyopathy/heart failure
Abbreviation: HELLP, hemolysis, elevated liver enzymes, and low platelets.

3 • Prevention of Maternal Cardiac Arrest 29
TABLE 3.3 Conditions Masked by Normal Physiologic Changes during Pregnancy

TIME IN PREGNANCY NORMAL PHYSIOLOGIC CHANGES CONDITIONS MASKED
Antepartum
• Gestational edema • Cardiomyopathy, cardiovascular disease,
• Shortness of breath cerebral edema, stroke
• Mild tachycardia
• Predisposition to asymptomatic • Pyelonephritis and/or sepsis (e.g., urinary
bacteriuria tract infection can rapidly progress in
susceptible pregnant patients, especially
those with diabetes or sickle cell disease)
Intrapartum
Fluid administration • Temporary increase in blood pressure • Predisposed to pulmonary edema with
• Dilution of coagulation factors infection, and disseminated intravascular
coagulation in hemorrhage
Labor pain • Increased blood pressure • Infection/sepsis, pulmonary embolism,
• Mild to moderate tachycardia preeclampsia, abruption
• Shortness of breath
Pain medications • Blunts pain response • Sepsis, intra-abdominal hemorrhage
• Alters mental status
Regional anesthesia • Decrease in mean arterial pressure • Intra-abdominal hemorrhage, infection
• Low-grade fever
• Blunts pain response
Hemorrhage medications • Low-grade fever • Infection/sepsis
(e.g., misoprostol)
Early postpartum
• Maternal tachycardia • Postpartum hemorrhage (may not see
• Baseline low blood pressure changes until after a quantitative blood loss
• Increased blood volume of 1,500 mL)
• Increased coagulation factors
• No clear portal of entry for genitourinary • Puerperal sepsis caused by group
infections A streptococcus
Late postpartum
• Exhaustion from lack of sleep Major depression, suicidal ideation
• Postpartum blues
KEY POINTS
• Normal physiologic changes in pregnancy may mask maternal deterioration in the critically ill patient.
• Clinical factors such as normal physiologic changes of pregnancy, fluid administration, anesthesia, and
medications may alter maternal vital signs and mask clinical deterioration until the moment of impending
respiratory or cardiovascular collapse.
3.3 OBSTETRIC EARLY WARNING SYSTEMS

There are several obstetric early warning systems (EWS) to detect changes in maternal vital signs that precede critical illness
and identify patients who may need rapid escalation of care. While most of these systems are applied to the in-hospital setting,
there are a few out-of-hospital warning systems for sepsis.1 An EWS functions as a screening and communication tool and con-
tains two essential components:
• The maternal early warning criteria

• An effective escalation policy
Current warning systems can be divided into single-parameter scoring systems and aggregate-weighted scoring systems. Single-
parameter systems evaluate individual vital sign parameters, and an evaluation is triggered if any single parameter is abnormal.
Aggregate-weighted scoring systems use a combination of maternal parameters (e.g., temperature, blood pressure, pulse, respi-
ratory rate, oxygen saturation, level of consciousness, pain level, proteinuria, discharge/lochia) to arrive at an aggregate clinical
score, which triggers an evaluation. Single-parameter systems are simpler and more specific, meaning they are more likely to
identify risk of death. In comparison, aggregate-weighted scoring systems are more complex and more sensitive. A more sensi-
tive test will detect multiple minor changes in vital signs earlier than those using a single parameter.
The increased specificity of the single-parameter systems will increase the positive predictive value (PPV) of the test. The
PPV indicates how likely it is that a patient with a positive screening test truly has the disease. In this case, a flag in an EWS
will identify a critically ill mother. Additionally, the prevalence of the disease (critical illness) in the population being tested will
affect the PPV of the test. In populations with a higher prevalence of the condition, the PPV will be higher than in lower-prev-
alence populations.
Current limitations include their relatively low PPV, with many suffering from a high false trigger rate, which can contribute
to what is known as trigger fatigue, especially in high-volume, high-acuity units.2 Systems with higher specificity, lower sensi-
tivity, and higher predictive value may be ideal for these units, to help minimize the false trigger rate. It should be noted that no
one system is universally applicable to all healthcare settings.
Facilities should choose a system that best meets their needs and balances the trade-offs between sensitivity and specificity.
Table 3.4 lists current early warning systems, and Table 3.5 outlines their predictive values.
Effective escalation algorithms consist of guidance on communication including when and how to call for help (activate the
rapid response team) and how providers will respond (come to the patient’s bedside for evaluation), guidance on initial diagnostic
evaluation and treatment, and timing of repeat observations.
TABLE 3.4 Proposed Early Warning Systems for Predicting Adverse Obstetric Outcomes3
IN-HOSPITAL OUT-OF-HOSPITAL
Confidential Enquiry into Maternal and Child Health (CEMACH) Quick Sequential Organ Failure Assessment Score (qSOFA)1
Modified Early Obstetric Warning System
CRADLE Vital Signs Alert Early Warning Red Flag Sepsis4
System
Preeclampsia Integrated Estimate of RiSk (PIERS; fullPIERS and
miniPIERS models)
Intensive Care National Audit & Research
Centre (ICNARC) Modified Early
Obstetric Warning System
Irish Maternity Early Warning System (IMEWS)
Maternal Early Warning Criteria (MEWC)
Maternal Early Warning Trigger (MEWT) tool
Modified Early Obstetric Warning System
(MEOWS)
Modified Early Warning System (MEWS)
National Early Warning System (NEWS)
Sepsis in Obstetrics Score (S.O.S.)
CMQCC Maternal Sepsis Evaluation Flow Chart
TABLE 3.5 Predictive Values of Early Warning Systems

TOOL IN-HOSPITAL OUT-OF- PARAMETER POSITIVE NEGATIVE
HOSPITAL PREDICTIVE VALUE PREDICTIVE VALUE
MEOWS X Aggregate 41%–54% 97%–98%
MEWC X Single
MEWS X 5.4%
MEWT X Aggregate 12%–95% 77%–99%
Red Flag X Aggregate
Sepsis
S.O.S. X Aggregate 98.6%
CMQCC* X Aggregate 97% 99%
*CMQCC undergoing validation trials with anticipated sensitivity and specificity values based on clinical practice data sets.5
3.3.1 Examples of Obstetric Early Warning Systems

This section introduces examples of early warning systems and how providers may implement them for prompt recognition of
the critically ill pregnant patient. Institutions adopting an EWS for identification of the critically ill pregnant patient should tailor
it to their specific needs and unique unit considerations. Reviewed are two selected examples of maternal EWS: the Maternal
Early Warning Trigger (MEWT) and the S.O.S. OBLS do not endorse any specific EWS.
KEY POINTS
• An obstetric EWS uses a combination of maternal parameters (e.g., temperature, blood pressure, pulse,
respiratory rate, oxygen saturation, level of consciousness, pain level, proteinuria, discharge/lochia) to
arrive at a clinical score, and the clinical score is used to trigger an escalation algorithm.
• An EWS is limited by a low PPV resulting in a high false alarm rate. This can contribute to trigger fatigue,
especially in high-volume, high-acuity units.
• Adoption of an EWS for identification of the critically ill pregnant patient should be specific and modified
to an institution/unit’s needs.
3.3.2 MEWT
The MEWT tool has been shown to reduce maternal morbidity in the U.S.6 It is designed to address the four most common causes
of maternal morbidity: infection-sepsis, cardiopulmonary dysfunction, hypertension, and obstetric hemorrhage. The MEWT
tool provides criteria for the assessment of vital signs and management recommendations.6 The MEWT tool contains parameters
for maternal status, or “maternal triggers,” which include changes in vital signs (temperature, oxygen saturation, heart rate, respi-
ratory rate, blood pressure), any altered mental status, and/or the presence of fetal tachycardia. The MEWT tool includes nurses’
concerns about the patient, with suggested pathways leading to expanded evaluation and an escalation algorithm. Laboratory and
radiologic evaluation are also recommended within the primary categories as part of the algorithm (Figure 3.1).
3.3.3 S.O.S.
S.O.S. is used to predict the need for an intensive care unit (ICU) admission in pregnant people presenting with signs and
symptoms concerning for sepsis.7 This validated scoring system uses physiologic and laboratory parameters to arrive at a clin-
ical score (Table 3.6). A prospective validation trial of the S.O.S. on 1,250 pregnant or postpartum people presenting to the
emergency department who met criteria for systemic inflammatory response syndrome revealed that 425 (34%) had a clinical
TABLE 3.6 S.O.S.7

VARIABLE HIGH ABNORMAL RANGE NORMAL LOW ABNORMAL RANGE
Score +4 +3 +2 +1 0 +1 +2 +3 +4
Temperature (°C) >40.9 39–40.9 38.5–38.9 36–38.4 34–35.9 32–33.9 30–31.9 <30
Systolic blood pressure >90 70–90 <70
(mm Hg)
Heart rate (beats per >179 150–179 130–179 120–129 <119
minute)
Respiratory rate (breaths >49 35–49 25–34 12–24 10–11 6–9 <5
per minute)
SpO2 (%) >92% 90%–91% 85%–89% <85%
White blood cell count (/μL) >39.9 25–39.9 17–24.9 5.7–16.9 3–5.6 1–2.9 <1
% Immature neutrophils >10% <10%
Lactic acid (mmol/L) >4 <4
Used with permission from Dr. Catherine Albright.

FIGURE 3.1 MEW T algorithm.
Used with permission from Dr. L aurence Shields.
suspicion or diagnosis of infection, with 14 (3.3%) admitted to the ICU. A score less than six had a negative predictive value of
98.6% and ruled out the need for ICU admission.7 Those with a score of six or higher were more likely to be admitted to the ICU,
admitted to a telemetry unit, and have antibiotic therapy initiated. This is one of the only validated scoring systems specific to the
detection of septic shock in pregnancy. More research is needed to determine if this scoring system reduces maternal morbidity
and mortality.
3.4 INSTITUTIONAL PLANNING FOR CRITICALLY ILL

PREGNANT AND POSTPARTUM PATIENTS
Prevention of MCA is multifactorial, and access to and compliance with prenatal and postpartum care are essential. Additionally,
all hospitals caring for obstetric patients must have a written policy in place to identify and evaluate critically ill pregnant or
postpartum patients and ensure that they have adequate resources to care for these types of patients. Designating a team to
respond to MCA ensures a unified call to action for obstetric/gynecologic providers, and the code and neonatal/pediatrics teams.
Chapter 6 reviews MCA teams (MCATs) in more detail.
Hospitals with limited resources should institute a maternal transport policy, allowing efficient transfer of patients to the
proper maternal care facility.
KEY POINTS
• All hospitals caring for obstetric patients must have a written policy in place to identify and evaluate crit-
ically ill pregnant or postpartum patients and ensure that they have adequate resources to care for these
types of patients.
• S.O.S. is the only validated scoring system for predicting ICU admission in maternal sepsis and uses phys-
iologic and laboratory parameters to arrive at a clinical score. An S.O.S. score less than 6 rules out the
need for ICU admission.
• The CMQCC two-step flow chart for diagnosis and treatment of maternal sepsis is currently undergoing
validation trials.
3.5 COMMUNICATION
Timely and accurate communication between the nurse and clinician is vital, especially with the escalation of care. There are
numerous recommendations to improve initial communication of early warning signs, proper escalation of care, and ongoing
communication about changes in the patient status to prevent delays and potential patient harm.
Chapter 12 reviews effective communication styles to address these issues. An established, supported, and transparent chain
of command policy can help to alleviate tension that may occur when escalating care.
The following clinical vignette presents how the MEWT and S.O.S. tools can be implemented for earlier recognition of a
critically ill pregnant patient.
Case Vignette
An 18-year-old multiparous person at 16 weeks gestation with a twin pregnancy presents to the ED, reporting the
presence of fever, pain with urination, and back pain. In addition, the patient describes feeling short of breath and
appears lethargic.
Admission vital signs are temperature 101.5°F, blood pressure 90/60, pulse 130, respiratory rate 30, and pulse
oximetry of 88% on room air. Chest radiographs, a complete blood count, a comprehensive metabolic panel, blood
and urine cultures, and lactic acid are ordered. After diagnosing pyelonephritis, the team gives IV fluid boluses and
2 L of oxygen by nasal cannula, orders antibiotics, and calls for an obstetric consult. They administer antibiotics
1.5 hours after the patient’s arrival at the ED. During this time they also administer 2.5 L of IV fluids.
Two hours after initial presentation to the ED, the patient reports worsening shortness of breath and chest
tightness, and passes out. The patient is unresponsive and without a pulse. The team calls a maternal code and
starts OBLS. The cardiac rhythm is noted to be pulseless electrical activity (PEA). The team palpates the uterus at the
umbilicus, continues high-quality cardiopulmonary resuscitation (CPR) and left uterine displacement, and adminis-
ters epinephrine.
After 4 minutes of CPR, the rhythm check continues to show PEA. While intubating, the team notices a frothy
ooze from the endotracheal tube. The OB/GYN performs a resuscitative cesarean delivery, and the neonatal team
provides comfort care to the nonviable neonates. After 2 more minutes of CPR, a rhythm check demonstrates ven-
tricular fibrillation, and shock is applied. The patient has return of spontaneous circulation and is sent to the ICU for
post-arrest management of presumed urosepsis with respiratory failure due to acute respiratory distress syndrome.
Care includes mechanical ventilation and high positive end-expiratory pressure.
REVIEW QUESTIONS
Q. What are abnormal vital sign parameters in pregnancy?
A. Based on MEWT, abnormal vital signs include the following:
1. Maternal heart rate >110 or <50

2. Temperature >100.4°F or <96.9°F
3. Respirations: >24 or <12
4. Blood pressure: systolic >155 or <80 or diastolic >105 or <45
5. Pulse ox: ≤93%
6. Any altered mental status
7. Fetal heart rate >160 (infection concern)
While each reporting system varies slightly, these are reflective of the generally accepted abnormal param-
eters in pregnancy.
Q. According to the MEWT tool and based on the presenting symptoms and signs, which major category
would this patient correspond to—cardiovascular, infection-sepsis, hypertension, or obstetric hemorrhage?
A. Based on the presenting vital signs, the MEWT tool would be triggered via maternal fever, abnormal
heart rate (>110), elevated respiratory rate (>24), and low pulse ox reading (<93%). Based on MEWT, the
presence of greater than two triggers should prompt immediate provider evaluation as well as activation
of the “infection-sepsis” tree.
Q. What scoring systems can be applied to the pregnant patient to screen for risk for adverse outcome or
admission to the ICU?
A. There are multiple different warning systems, and no one system is perfect. Following are the warning
systems currently available. See Tables 3.3 and 3.4 for more information.
1. MEWT 4. MEWS 7. CRADLE 10. PIERS

2. MEOWS 5. S.O.S. 8. ICNARC 11. CMQCC
3. MEWC 6. NEWS 9. CEMACH
Q. What is the treatment for a pregnant patient with suspected sepsis?

A. Following the MEWT protocol, promptly evaluate a patient with suspected sepsis. Follow with labs (com-
plete blood count, cultures, comprehensive metabolic panel, lactic acid) and prompt administration of
broad-spectrum antibiotics and IV fluids with fluid resuscitation. Ideally, antibiotics are started within the
“golden hour” of presentation. Each patient’s clinical presentation and score (based on MEWT or S.O.S.,
for instance) will prompt where the patient should be admitted (i.e., floor or ICU). Closely monitor the
patient’s response to resuscitation and treatment to ensure therapies are working and that end organ
damage/injury is avoided or contained.
Applying the MEWT to our clinical vignette, a provider would be directed to the following:
1. The major category of “infection-sepsis” based on maternal fever and four abnormal triggers (pulse
oximetry, temperature, heart rate, and respiratory rate), then to
2. The “sepsis-septic shock” category based on heart rate, then

3. Triggered to notify the rapid response team, ICU transfer, and/or consult as appropriate, then
• Obtain complete blood count, start antibiotics, and consider blood cultures
• Test for organ dysfunction (e.g., lactic acid, liver function tests, total bilirubin, creatinine, and urine
output)
4. Start fluid resuscitation.
Applying the S.O.S. system, a provider would recognize the following:
1. Preliminary S.O.S. is 9 before lab results, which would alert the provider to suspect sepsis that will
likely require ICU admission.
2. Administer broad-spectrum antibiotics within 1 hour of suspected sepsis to comply with the surviving
sepsis campaign bundle and reduce maternal morbidity and mortality.
3. Administer IV fluids and closely monitor inputs and outputs, as patients with urosepsis in pregnancy
are at increased risk of lung injury, pulmonary edema, and acute respiratory distress syndrome.

1. The priority goal of the obstetric EWS is to identify patients who may need which of the following?
A. Rapid escalation of care
B. Immediate cesarean delivery
C. The MCAT
D. CPR
2. Which of the following signs or symptoms requires an escalation of care in a patient in labor?
A. White blood cell count of 20,000/mm
B. Fetal heart rate of 160 beats per minute
C. Shortness of breath during pushing attempts
D. Altered mental status
3. Which of the following statements BEST reflect current obstetric emergency warning systems?
A. Can use same vital sign parameters as nonpregnant patients
B. Their use may decrease maternal morbidity
C. Have high positive predictive value, with low false-positive trigger rates
D. Do not require a process for escalation of care
4. A nulliparous person at 16 weeks gestation presents to the emergency department with reports of shortness of
breath and chest pain. Pulse is 120 and pulse oximeter is 90%. The patient is afebrile. Which of the following
laboratory and imaging examinations would be the BEST next step in management according to the MEWT
protocol?
A. B-type natriuretic peptide (BNP), cardiac enzymes, electrocardiogram (ECG), echo, and spiral computed
tomography
B. Lactic acid, liver function tests (LFTs), total bili, and creatinine
C. Complete blood count (CBC), disseminated intravascular coagulation (DIC) panel
D. Random glucose, hemoglobin A1c, comprehensive metabolic panel (CMP)
5. Which of the following validated EWS predicts the need for admission to the ICU from sepsis in pregnancy?
A. MEWT
B. MEOWS
C. S.O.S.
D. CEMACH Modified Early Obstetric Warning System
CHAPTER 3. ANSWERS
1. ANSWER: A. Obstetric emergency warning systems have been proposed to detect changes in maternal vital signs that
precede critical illness and identify patients who may need rapid escalation of care. Warning systems use a com-
bination of maternal parameters (such as temperature, blood pressure, pulse, respiratory rate, oxygen saturation, level
of consciousness, pain level, proteinuria, discharge/lochia) to arrive at a clinical score, and the clinical score is used to
trigger an escalation algorithm. Escalation algorithms guide the timing of repeat observations, when and how to call for
help (e.g., call the provider about the patient’s status, call the provider to the bedside, and/or activate the rapid response
team), and initial diagnostic evaluation and treatment. While patients who trigger rapid escalation of care based on an
EWS may ultimately need the MCAT, immediate cesarean delivery, or CPR, the most correct answer is A.
2. ANSWER: D. Warning systems use a combination of maternal parameters (such as temperature, blood pressure,
pulse, respiratory rate, oxygen saturation, level of consciousness, pain level, proteinuria, discharge/lochia) to arrive at
a clinical score, which then triggers an escalation algorithm. Most warning systems include any mental status change
as a significant maternal trigger that requires escalation of care. While a white blood cell count of 20,000 is abnormal
in the nonpregnant population, this may be normal for a patient in labor. Similarly, it is normal for a patient to have
shortness of breath with pushing efforts. A fetal heart rate of 160 bpm can be a sign for fetal distress (such as in the
setting of infection) however is not as concerning as maternal altered mental status. Also, as a single indicator, it
would not trigger immediate escalation of care.
3. ANSWER: B. Normal physiologic changes in pregnancy may mask maternal deterioration in the critically ill patient.
EWS use a combination of maternal parameters to arrive at a clinical score, which then triggers an escalation algo-
rithm. The MEWT tool has been shown to reduce maternal morbidity in the U.S.
4. ANSWER: A. The MEWT tool is designed to address the four most common causes of maternal morbidity: infection-
sepsis, cardiopulmonary, hypertension in pregnancy, and obstetric hemorrhage. MEWT provides criteria for the
assessment of vital signs and management recommendations. According to the MEWT algorithm, this patient has
two or more abnormal vital signs concerning for cardiovascular disease. The proposed evaluation based on the tool
and category (cardiovascular) is a BNP, cardiac enzymes, ECG, echo, and spiral computed tomography to evaluate
for some of the common etiologies of cardiovascular disease in pregnancy (e.g., pulmonary embolism, pulmonary
hypertension, pulmonary edema, myocardial infarction, cardiomyopathy/congestive heart failure, and arrhythmia).
5. ANSWER: C. The only validated scoring system for the detection of sepsis during pregnancy that will likely require
ICU admission is the S.O.S. This scoring system was developed to predict the need for ICU admission in pregnant
people presenting with signs and symptoms concerning for sepsis. The scoring system uses physiologic and laboratory
parameters to arrive at a clinical score. A score less than 6 has a negative predictive value of 98.6% and rules out the
need for ICU admission.
1. Shu E, Tall CI, Frye W, et al. Pre-hospital qSOFA as a predictor of sepsis and mortality. Am J Emerg Med. 2019 Jul;37(7):1273–1278.
doi: 10.1016/j.ajem.2018.09.025. Epub 2018 September 18.
2. Blumenthal E, Hooshvar N, McQuade M, McNulty J. A validation study of maternal early warning systems: A retrospective cohort
study. Am J Perinatol. 2019 Sep;36(11):1106–1114. doi: 10.1055/s-0039-1681097.
3. Umar A, Ameh CA, Muriithi F, Mathai M. Early warning systems in obstetrics: A systematic literature review. PLoS One.
2019;14(5):e0217864. doi: 10.1371/journal.pone.0217864.
4. Seymour CW, Cooke CR, Heckbert SR, Spertus JA, Callaway CW, Martin-Gill C, Yealy DM, Rea TD, Angus DC. Prehospital intrave-
nous access and fluid resuscitation in severe sepsis: An observational cohort study. Crit Care. 2014 September 27;18(5):533. doi: 10.1186/
s13054-014-0533-x.
5. Gibbs R, Bauer M, Olvera L, Sakowski C, Cape V, Main E. Improving Diagnosis and Treatment of Maternal Sepsis: A California
Maternal Quality Care Collaborative Quality Improvement Toolkit. 2022. Available at https://www.cmqcc.org/resources-toolkits/
toolkits/improving-diagnosis-and-treatment-maternal-sepsis-errata-712022. Accessed March 18, 2023.
6. Shields LE, Wiesner S, Klein C, Pelletreau B, Hedriana HL. Use of maternal early warning trigger tool reduces maternal morbidity. Am
J Obstet Gynecol. 2016;21(4):527.e1–527.e6. doi: 10.1016/j.ajog.2016.01.154.
7. Albright CM, Has J, Rouse L, Hughes L. Internal validation of the Sepsis in Obstetrics Score to identify risk of morbidity from sepsis
in pregnancy. Obstet Gynecol. 2017 October;13(4):747–755. doi: 10.1097/AOG.0000000000002260.
Common Causes of
Maternal Cardiac Arrest 4
4.1 INTRODUCTION
Maternal cardiac arrest (MCA) results from etiologies which are substantially different and more broadly diverse than those
etiologies associated with cardiac arrest in the nonpregnant patient. This chapter highlights some of the most common causes
of MCA, reviews presenting symptoms and signs, and introduces initial steps to prevent the progression from symptoms to full
arrest. Additionally, we review the immediately reversible causes of MCA that providers must recognize and treat quickly for
optimal recovery. Finally, we introduce the mnemonic and post-arrest aid BAACC TO LIFE to help recall the common etiolo-
gies of MCA (Figure 4.1 and Appendix D, respectively).

• Review the most common etiologies of MCA.

• Recognize the presenting symptoms and signs of the etiologies that may lead to MCA.
• Discuss the treatment of the most common etiologies leading to MCA.
• Recognize and understand treatments for the leading immediately reversible causes of MCA, including hypoglyce-
mia, high spinal, and lidocaine and magnesium sulfate toxicity.
• Describe the major causes of MCA using the mnemonic BAACC TO LIFE.
4.3 BAACC TO LIFE: BLEEDING

Maternal hemorrhage is the leading cause of maternal morbidity and mortality worldwide.1 Bleeding following delivery, known
as postpartum hemorrhage (PPH), accounts for approximately three-quarters of these cases.1 More than 50% of maternal deaths
from PPH happen within the first 24 hours of delivery.2 Delayed PPH is defined as bleeding occurring more than 24 hours
after delivery and less than 6 weeks postpartum. Uterine atony is the most common cause of PPH, occurring in approximately
70%–80% of cases.3 A uterus at term receives 500–800 mL of blood per minute; thus, uterine atony can result in rapid loss of
large amounts of blood. Other causes of maternal hemorrhage are listed in Table 4.1. Due to how common and severe PPH can
be, it is essential that all patients are closely monitored for bleeding during the first 24–48 hours after delivery.
PPH is a symptom. Once identified, providers should search for the cause (diagnosis), while simultaneously transfusing
blood products as necessary. If concerned about excessive bleeding following delivery, providers should perform a detailed
examination for, and control, the source of bleeding. Further laboratory evaluation includes a complete blood count and
coagulation studies, although providers should not wait on these results to begin medical treatment of obstetric hemorrhage.
Laboratory assessments during PPH are helpful to monitor trends, though values in acute hemorrhage often lag. As PPH is
the most common cause of uterine atony, Table 4.3 describes the treatment options for uterine atony. If medical treatment is
DOI: 10.1201/9781003299288-5 37
FIGURE 4.1 Etiologies for maternal cardiac arrest, the BAACC TO LIFE mnemonic.
TABLE 4.1 Maternal Hemorrhage: Major Causes throughout Pregnancy

TIME PERIOD MAJOR CAUSES OF HEMORRHAGE
Antepartum • Placental abnormalities (abruption, previa, accreta spectrum)
• Trauma
• Uterine rupture
• Coagulation defects (inherited, acquired)
Intrapartum or immediate postpartum • Uterine atony
(within 24 hours of delivery) • Uterine inversion
• Coagulation defects (inherited or acquired)
• Vaginal/cervical lacerations
• Episiotomy
• Retained conception products or retained placenta, placental
abnormalities (abruption, previa, accreta spectrum)
• Amniotic fluid embolism (AFE)
• Uterine rupture
• Bleeding surgical sites/pedicles
Delayed postpartum (>24 hours after • Retained products of conception/placenta
delivery, <6 weeks postpartum) • Infection
unsuccessful, proceed with tamponade balloon placement, vacuum-induced hemorrhage control, or laparotomy (surgery) with
the potential need for a hysterectomy to control the bleeding.
Pregnant people can lose up to 1,500 mL of blood before showing changes in vital signs. Thus, maternal vital sign changes
in the setting of bleeding are an ominous sign, and providers should promptly activate the massive transfusion protocol and rapid
response teams. Rapid volume repletion with IV fluid and blood products, as well as identification and correction of the source
of bleeding, will reduce the likelihood of significant maternal morbidity or mortality. Table 4.2 outlines a stage-based response
to obstetric hemorrhage.
Delayed hemorrhages (≥24 hours and <6 weeks from delivery) can also occur. Provide all postpartum patients with detailed
discharge instructions that include when to seek medical care for excessive bleeding.
4 • Common Causes of Maternal Cardiac Arrest 39
KEY POINTS
• Maternal hemorrhage is the leading cause of maternal morbidity and mortality worldwide. Postpartum
hemorrhage from uterine atony accounts for approximately three-quarters of these cases.
• Pregnant people can lose up to 1,500 mL of blood before showing vital sign changes. If vital sign changes
are present, prompt activation of the massive transfusion protocol and rapid response team is indicated.
• Time and indecision kill. Do not delay treatment during maternal hemorrhage. Ongoing hemorrhage with
or without maternal vital sign changes requires swift activation of the massive blood transfusion protocol
and rapid response team. Refractory hemorrhage requires surgery, with possible hysterectomy to control
the bleeding.
TABLE 4.2 Stage-Based Hemorrhage Management

STAGE DEFINITION ACTION
Identify Hemorrhage
Risk on Admission
Stage 0 • Active management with • Quantitative blood loss (QBL) assessment (1 g = 1 mL)
oxytocin infusion • Ongoing evaluation of vital signs
Stage 1 • Continued bleeding and blood • Notify obstetric (OB) and anesthesia providers
loss • Establish IV
• >1,000 mL vaginal or cesarean • Massage fundus
• Early vital sign changes (15%) • Administer second uterotonic
• Increased bleeding in recovery • Empty bladder
period • Type and cross for 2 units packed red blood cells (PRBC)
• Consider potential etiologies
• Cumulative QBL
Stage 2 • Continued bleeding with QBL • OB provider to bedside
<1,500 mL • Administer a third uterotonic
• Start second IV
• Administer tranexamic acid
• Uterine balloon tamponade or vacuum-induced
hemorrhage control
• Move to operating room, prepare for procedural
interventions
• B-Lynch
• Interventional radiology
• Transfuse 2 units PRBC (do not wait for lab results)
• Order STAT labs (complete blood count, comprehensive
metabolic panel, prothrombin time/partial
thromboplastin time, fibrinogen)
• Cumulative QBL
• Announce vital signs
Stage 3 • QBL ≥1,500 mL or maternal • Activate Massive Transfusion Protocol
tachycardia, hypotension, or • Transfuse 1:1:1 (PRBC:fresh frozen plasma:platelets) or
vital sign changes whole blood, if available
• Or >2 units PRBC administered • Notify second surgeon or gynecology/oncology surgeon,
• Or suspect disseminated if available
intravascular coagulation (DIC) • Consider hysterectomy if still bleeding
• Keep patient warm
• Use fluid warmer/rapid infuser
• Repeat labs every 30–60 minutes
• Postpartum intensive care unit management
Stage 4 • Cardiac arrest • Obstetric life support
TABLE 4.3 Medical Treatment of Postpartum Hemorrhage Due to Uterine Atony

MEDICATION DOSE SIDE EFFECTS CONTRAINDICATIONS
Oxytocin 10–40 units in 500–1,000 mL IV Nausea, vomiting, hyponatremia Hypersensitivity to oxytocin
continuous infusion due to antidiuretic effect,
cardiac arrhythmia
15-Methyl 250 mcg intramuscular or Nausea, vomiting, diarrhea, Asthma, history of allergy to
prostaglandin F2a intramyometrial every 15 bronchospasm prostaglandins, hypertension
minutes for 8 doses (use with caution)
Methylergonovine 200 mcg intramuscular every Hypertension, seizure, headache, Hypertension, preeclampsia,
maleate 2–4 hours abdominal pain, nausea, and cardiovascular disease
vomiting
Misoprostol 600–1,000 mcg rectal, oral, or Fever, diarrhea, nausea, Allergy to prostaglandins
sublingual, single dose vomiting, stomach cramps, gas,
constipation, headache
Tranexamic acid 1-g IV infusion or slow push over Nausea, vomiting, diarrhea, Active intravascular clotting
(TXA) 10 minutes; may repeat 1 dose allergic dermatitis, and (e.g., deep vein thrombosis or
in 30 minutes hypotension observed when IV pulmonary embolism),
injection is too rapid subarachnoid hemorrhage,
acquired defective color vision
4.4 BAACC TO LIFE: ANESTHESIA

Maternal deaths can occur from complications due to intrapartum regional and general anesthesia. In a series of maternal deaths
in Michigan between 1985 and 2003, anesthesia-related deaths contributed to 1.7% of maternal deaths.4 These cases often result
from the presence of other comorbidities, such as preeclampsia with severe features or extreme obesity, where the presence
of oropharyngeal edema complicates airway management. Risk factors for anesthesia-related maternal deaths are listed in
Table 4.4.
Providers should be aware of potential anesthetic complications, such as high spinal or lidocaine toxicity, which can occur
in pregnant people with few risk factors. These immediately reversible causes of MCA require prompt recognition and treatment.
A pregnant patient with a high spinal will frequently report feeling anxious; have difficulty breathing, nausea, and numbness
or weakness of the arms; and may develop hypotension and bradycardia. Symptoms may proceed to loss of consciousness and
respiratory arrest. Treatment for high spinal consists of supportive care with 100% oxygen application for ventilation, IV fluid
bolus, and possible intubation. Other actions include activation of the rapid response team, and administering lipid emulsion,
and peripheral vasoconstrictors (alpha 1-antagonist) such as phenylephrine for hypotension and atropine for bradycardia. Other
vasoconstrictors that may be used include ephedrine and low doses of dilute adrenaline solution.
A pregnant person with acute local anesthetic systemic toxicity during placement of the epidural or repair of a perineal
laceration may present with circumoral numbness, facial tingling, restlessness, vertigo, tinnitus, slurred speech, tonic-clonic
seizures, and cardiac arrest. Figure 4.2 reviews the treatment of acute local anesthetic systemic toxicity.
4.5 BAACC TO LIFE: AMNIOTIC FLUID EMBOLISM

AFE is a rare and catastrophic complication of pregnancy with a comparatively high mortality rate. The incidence of AFE is low,
between 1.9 and 6.1 per 100,000 births, and with a mortality rate as high as 60%. AFE is thought to be an immune-mediated
response to amniotic fluid and debris circulating in the maternal bloodstream. Though AFE typically occurs during labor or
shortly after birth, it can be associated with trauma and prolonged rupture of membranes. Consider AFE in the differential diag-
nosis of sudden cardiovascular collapse of a laboring or recently delivered person.
AFE often presents with cardiac arrest, thus the initial response should be high-quality CPR. AFE occurs in two stages.
The first stage consists of a respiratory arrest phase, and the second phase consists of a hemorrhagic phase, which quickly
develops into DIC.
TABLE 4.4 Risk Factors for Anesthesia-Related Maternal Deaths4

Airway obstruction Lived experience of anti-Black racism
Emergence and recovery from general anesthesia Obesity
Lack of clinical protocols and safety Perioperative hypoventilation
measures in delivering anesthetic care
FIGURE 4.2 Management of acute local anesthetic toxicity. (A) Sequence of symptoms and required treatments. (B) Sequence of
symptoms and program of lipid emulsion (20%) infusion. Abbreviations: ACLS, advanced cardiovascular life support; CPR, cardiopul-
monary resuscitation; ICU, intensive care unit; LA, local anesthetic.
Signs and symptoms might include the following:
• Acute-onset chest pain

• Shortness of breath
• Nausea and/or vomiting
• Tachypnea, tachycardia, and hypotension
• Patient report of feeling an impending sense of doom
• Rapid deterioration into respiratory arrest
The respiratory arrest phase includes increased levels of pulmonary vasoconstrictors and mechanical obstruction that lead
to respiratory failure and severe hypoxemia and severe acute right heart failure. These lead to hemodynamic collapse,
TABLE 4.5 Recommended Medication Doses to Treat Acute Right Ventricular Failure
AGENT DOSE
Dobutamine 2.5–5.0 mcg/kg per minute. Higher doses may compromise
right ventricular filling time caused by tachycardia
Inhaled nitric oxide 5–40 ppm. Follow methemoglobin levels every 6 hours,
and avoid abrupt discontinuation
Inhaled prostacyclin 10–50 ng/kg per minute
IV prostacyclin Start at 1–2 ng/kg per minute through a central line and
titrate to desired effect. Side effects include systemic
hypotension, nausea, vomiting, headache, jaw pain, and
diarrhea
Milrinone 0.25–0.75 mcg/kg per minute. Most common side effect is
systemic hypotension
Norepinephrine 0.05–3.3 mcg/kg per minute
Sildenafil 20 mg three times a day by mouth or through nasogastric or orogastric tube
decreased left-sided cardiac output, and late-onset left ventricular failure. These ultimately lead to cardiogenic pulmonary
edema and systemic hypotension. Please see Table 4.5 for medications that can be considered in the treatment of right heart
failure.
Airway management with immediate intubation is crucial during the respiratory arrest stage. Current recommended
treatment for the respiratory phase of AFE includes pulmonary vasodilators, prostaglandins, and sympathomimetics to
address right ventricular failure. Norepinephrine and inotropes are used to maintain hemodynamics and address left ventric-
ular failure. The hemorrhagic phase consists of activation of factor VII and platelets with DIC. Inflammation further acti-
vates the clotting cascade, and ongoing hemorrhage contributes to hemodynamic instability.5 During the hemorrhagic phase,
early and aggressive utilization of the massive transfusion protocol with goal-directed transfusion will improve the patient’s
chances of survival.
If AFE results in cardiac arrest, perform RCD as indicated (subsequent chapters review RCD in detail). While treatment for
AFE is mostly supportive, consider using the A-OK protocol6 as soon as suspicion for AFE is raised. This consists of:
• 1 mg Atropine
• 8 mg Ondansetron
• 30 mg Ketorolac
Supportive post-arrest care often occurs in the intensive care unit and consists of vasopressors, medications, and transfusion if
indicated. Successful treatment of AFE with cardiopulmonary bypass and exchange transfusions has also been described.
KEY POINTS
• AFE has a high mortality rate and is usually seen with cardiac arrest.
• AFE should be suspected in a patient with acute development of hypoxia, hypotension, and coagulopathy.
• Upon recognizing AFE, perform high-quality CPR, supportive care, and consider the A-OK protocol.
• AFE requires aggressive supportive management utilizing massive transfusion protocol, rapid intubation,
and delivery.
• Recommendations for treating the respiratory phase of AFE consist of pulmonary vasodilators, prostaglan-
dins, and sympathomimetics.
• Right ventricular failure should be treated with inotropic agents and pulmonary vasodilators.
4.6 BAACC TO LIFE: CARDIOVASCULAR

The mean age of first-time mothers has been steadily climbing for the past 50 years and is currently 26 years of age.7 Compared
to their historical counterparts, pregnant patients also tend to have more comorbidities, with cardiovascular disease currently
complicating approximately 4% of all pregnancies in the U.S.7 Cardiovascular disease is also responsible for more than a third
of U.S. maternal mortalities, with the vast majority of these due to acquired cardiovascular disease.8 This section reviews peri-
partum cardiomyopathy and acute coronary syndrome. The following red flags require prompt evaluation, hospitalization, and
consultation with cardiology and maternal-fetal medicine for acute symptoms of cardiovascular disease9:
• Shortness of breath at rest

• Severe orthopnea four or more pillows
• Orthopnea: shortness of breath when lying down
• Four or more pillows: the number of pillows needed to prop the patient to improve their breathing
• Resting heart rate ≥120 bpm
• Resting systolic blood pressure ≥160 mm Hg
• Resting respiratory rate ≥30
• Oxygen saturations ≤94% with or without personal history of cardiovascular disease
4.7 BAACC TO LIFE: PERIPARTUM CARDIOMYOPATHY

Peripartum cardiomyopathy (PPCM) is the most common cardiomyopathy diagnosed in pregnancy10 and is the leading cause of
late postpartum maternal mortality.3 PPCM is an idiopathic disorder defined as heart failure occurring during the last month of
pregnancy and up to 5 months postpartum, and more rare, 1 year postpartum.3 A person with PPCM will typically present with
increasing shortness of breath upon exertion (dyspnea on exertion), at rest (dyspnea), or while lying down (orthopnea).
Excessive weight gain and peripheral edema can be seen from fluid retention, especially with advanced disease. On physical
exam, patients can have mild tachycardia, hypertension, and hypoxia (oxygenation saturations <94% on room air). On physical
exam, bibasilar crackles of the lungs may be heard, and jugular venous distention (JVD) may be present. People with PPCM will
also have a decreased ejection fraction on echocardiogram and a B-type natriuretic peptide ≥100 pg/mL. Prompt evaluation and
treatment are important to improve maternal outcomes. Although many patients will experience recovery of cardiac function in
the first 3–6 months postpartum, some may experience irreversible cardiac dysfunction, and there is a high rate of recurrence in
subsequent pregnancies.
4.7.1 Cardiovascular: Other

Based on guidance from the American College of Obstetricians and Gynecologists, any pregnant patient presenting with chest
pain (either typical or atypical) should be evaluated for acute coronary syndrome. Typical symptoms include chest pain, shortness
of breath, radiating left arm pain, and/or palpitations. Atypical chest pain includes nausea/vomiting, epigastric, and abdominal
pain. Evaluation is like the workup for nonpregnant patients and should include an electrocardiogram and laboratory evaluation
with cardiac enzymes such as troponins. While evaluating and treating, place pregnant patients in full left lateral tilt to
improve venous return to the heart.
Obstetric Life Support otherwise recommends following the same guidelines as for nonpregnant patients: administer oxy-
gen, aspirin, nitroglycerin, and a beta-blocker (unless the patient has asthma), and use IV heparin and interventional cardiac
catheterization if there is concern for acute coronary syndrome. To reduce fetal exposure to radiation, shield the pregnant abdo-
men during the cardiac catheterization.
KEY POINTS
• When evaluating patients for acute cardiac concerns, place them in a left lateral tilt. Initial treatment is the
same as for nonpregnant adults.
• Perform interventional cardiac catheterization if there is concern for acute coronary syndrome in a
pregnant patient. Shield the abdomen to reduce fetal radiation exposure.
• A person with PPCM will typically present with increasing shortness of breath, excessive weight gain, and
ankle swelling.
4.8 BAACC TO LIFE: CLOT/CEREBROVASCULAR/

PULMONARY EMBOLISM
Pulmonary embolism (PE) is a life-threatening condition that has been associated with severe maternal morbidity and mor-
tality. Injuries to vascular structures (from an injury or surgery), increased venous stasis (from pregnancy or immobilization),
and increased hypercoagulability (due to increased circulating estrogen and increased clotting factors) all increase a pregnant
person’s chances of developing a blood clot.
Patients with PE typically present with acute-onset shortness of breath, tachycardia, and/or chest pain. Initial evaluation
consists of an electrocardiogram and chest radiography. Historically, D-dimer testing has not been clinically useful during preg-
nancy as increased D-dimer concentrations are found in a normal pregnancy, resulting in a high rate of false-positive D-dimer
tests.11 New evidence suggests that a pregnancy-adapted YEARS criteria with D-dimer testing helps to rule out pulmonary
embolism in pregnant patients.12 This algorithm uses the assessment of the following three clinical criteria for pulmonary embo-
lism (YEARS criteria):
• Clinical signs of deep vein thrombosis (DVT)

• Hemoptysis
• PE as the most likely diagnosis
In patients with clinical signs of DVT based on the YEARS criteria, a lower extremity compression ultrasound is performed
on the symptomatic leg(s). If the ultrasound is abnormal, anticoagulation is initiated. If the ultrasound is negative, a D-dimer is
sent, with further evaluation based on positive YEARS criteria and D-dimer levels.12 Table 4.6 summarizes the recommended
evaluation strategy based on YEARS criteria and D-dimer levels.
While most accurate in the first trimester, use of the YEARS criteria resulted in a reduced number of patients who had CT
angiograms of the chest, thus reducing radiation exposure during pregnancy. While further studies may be required, the preg-
nancy YEARS algorithm using D-dimers with the YEARS clinical criteria can be used to evaluate for PE in all trimesters of
pregnancy.12
If clinical suspicion is high for PE, start therapeutic anticoagulation therapy empirically with heparin or low-molecular-
weight heparin while pursuing further evaluation with either CT angiogram of the chest, or ventilation-perfusion scan. Shield the
pregnant person’s abdomen when performing a CT angiogram. Fetal anomalies, growth restriction, and pregnancy loss have not
been reported with radiation exposure of less than 50 milligray (mGy).13 The risk of carcinogenesis because of in utero exposure
TABLE 4.6 Pregnancy YEARS Evaluation12

POSITIVE YEARS CRITERIA D-DIMER LEVELS EVALUATION AND RECOMMENDATIONS
None <1,000 ng/mL PE ruled out, no anticoagulation
None ≥1,000 ng/mL Computed tomography (CT) pulmonary
angiography, with anticoagulation if
positive CT angiography
One to three <500 ng/mL PE ruled out, no anticoagulation
One to three ≥500 ng/mL CT pulmonary angiography, with
anticoagulation if positive CT angiography
to radiologic procedures is unclear, but probably rare,13 and necessary diagnostic imaging for maternal indications should not
be withheld.
Treating PE in pregnancy includes therapeutic anticoagulation consisting of unfractionated or low-molecular-weight heparin
with possible transition to warfarin in the postpartum patient. Heparin or low-molecular-weight heparin are preferred anticoag-
ulants in pregnancy as neither cross the placenta. Generally, low-molecular-weight heparin is preferred due to more predictable
anticoagulant effect and lower risk of developing heparin-induced thrombocytopenia. However, in unstable patients or where
surgical intervention is necessary, unfractionated heparin is preferred due to the ease of monitoring levels and reversibility.
If the patient is receiving unfractionated heparin, obtain a complete blood count 4–5 days after starting heparin to assess for
thrombocytopenia indicative of heparin-induced thrombocytopenia. Oral anticoagulation with non–vitamin K antagonist is not
recommended in pregnant or postpartum nursing mothers. Warfarin is also not recommended in pregnancy due to its teratogenic
potential, though it may be used in postpartum nursing mothers.
Case reports describe treatment for massive/saddle PE leading to MCA. Patients have been successfully treated with
both thrombolytic therapy and embolectomy with favorable maternal and fetal outcomes. Emerging data show improved
maternal outcomes using ECPR in this patient population and should also be considered. These patients will require a large
multidisciplinary team (such as maternal-fetal medicine, pulmonologist, and vascular or cardiothoracic surgery specialists),
and consideration should be given to transporting them to an ECPR-capable facility. These patients will often undergo RCD
and may be at higher risk for bleeding complications. Thus, consider this complication in the decision to initiate thrombo-
lytic therapy.
4.8.1 Cerebrovascular (Stroke)

While stroke is a rare cause of sudden cardiac death, it is a leading cause of severe maternal morbidity and mortality, particu-
larly in those with preeclampsia.8,14 Stroke can be either ischemic, due to blockage of a cerebral artery or vein, or hemorrhagic,
due to rupture of blood vessels in or around the brain. Importantly, ischemic and hemorrhagic strokes can present with similar
symptoms, so a rapid head CT is always needed to exclude hemorrhage. Stroke can occur at any time in pregnancy but is most
common in the first 2 weeks postpartum. All types of stroke can cause death directly due to swelling and herniation of the brain,
or indirectly as a result of poststroke complications such as aspiration or pulmonary embolism. Failure to recognize stroke signs
and symptoms and act promptly can lead to devastating consequences, since “Time Is Brain.”15 Common stroke syndromes are
reviewed in Table 4.7. A few stroke types have extremely high morbidity and mortality and are reviewed here.
Large vessel occlusion (LVO) is the occlusion of large arteries supplying blood to the brain, including the carotid, middle
cerebral, or vertebrobasilar arteries. This is most commonly caused by a blood clot embolizing from the heart. This can occur in
the setting of heart failure, arrhythmia, or so-called paradoxical embolism from a DVT in a person with a patent foramen ovale.
Treatment for LVO may include IV thrombolysis or mechanical thrombectomy. While strokes due to LVO can cause severe
disability and death, treatment has been revolutionized due to the success of thrombectomy trials.16 Pregnancy is not a contrain-
dication to thrombolysis or mechanical thrombectomy, and stroke protocols should be followed as usual, with close involvement
of the obstetrics and neurology team. Importantly, a basilar artery occlusion may present with sudden loss of consciousness and
convulsive activity and should always be considered in an unresponsive patient.
Subarachnoid hemorrhage (SAH) occurs most commonly when an artery ruptures on the surface of the brain causing
arterial hemorrhage into the subarachnoid space. This can be due to a ruptured intracranial aneurysm, or to other causes. The
TABLE 4.7 Stroke Causes, Signs, and Symptoms

STROKE CAUSE SIGNS AND SYMPTOMS
Left carotid or middle cerebral Left gaze deviation, aphasia, right hemiparesis,
artery occlusion hemiplegia
Right mouth/facial droop and right hemineglect
Right carotid or middle cerebral Right gaze deviation, left hemineglect, left
artery occlusion hemiparesis
Left mouth/facial droop and left hemiplegia
Basilar artery occlusion Headache; loss of vision; loss of consciousness,
posturing, convulsive activity
Subarachnoid hemorrhage “Thunderclap” headache, neck stiffness, vomiting, loss
of consciousness
Intracerebral hemorrhage Headache, vomiting, focal neurologic deficits
(depending on location of bleed), seizure
presenting symptom is most commonly a sudden “thunderclap” headache. SAH can result in an overwhelming sympathetic
nervous system surge, leading to neurogenic myocardial stunning and cardiac arrest.17 For this reason, we recommend that all
patients with cardiac arrest have prompt brain imaging prior to initiation of cooling protocols.
The management of SAH is complex and should be done in close consultation with neurocritical care specialists, vascular
neurologists, or neurosurgeons, in a neurocritical care unit, if possible.
Intracerebral hemorrhage (ICH) is a leading cause of death and disability in people with preeclampsia.18 Patients may present
with headache, focal neurologic deficits (similar to ischemic stroke), seizure, or loss of consciousness, and may mimic eclampsia,
making prompt brain imaging critical. Antithrombotic medications should be reversed, and immediate lowering of the blood pres-
sure (BP) to below systolic BP of 140 is recommended, as well as elevation of the head of the bed.19 Like SAH, ICH requires multi-
disciplinary management, ideally in a neurocritical care unit. Different hemorrhagic and ischemic strokes are illustrated in Figure
4.3. Table 4.7 outlines the type of stroke and the corresponding signs and symptoms teams should be aware of.
The out-of-hospital and in-hospital acute management of maternal stroke are reviewed in more detail in Chapter 10.
KEY POINTS
• PE is a frequent cause of MCA and should be suspected in the setting of acute maternal shortness of
breath, hypoxia, and tachycardia. Evaluate promptly with a computed tomography (CT) angiogram of the
chest, shielding the abdomen.
• Treat PE in pregnancy with therapeutic anticoagulation with heparin or low-molecular-weight heparin.
Consider either thrombolytics, such as recombinant tissue plasminogen activator (rtPA) or catheter/sur-
gical thrombectomy, for PE and a hemodynamically unstable patient. However, use thrombolysis with
caution in patients in cardiac arrest who are candidates for RCD or who have undergone surgery within a
2-week window.
• ECPR is emerging as a possible therapy of choice for massive PE resulting in maternal cardiac arrest. Limited
data also support the use of thrombolytics for thrombectomy in pregnant patients with massive PE.
• In acute stroke, follow “Time Is Brain” and institutional stroke protocols (Code Stroke).
• Pregnancy is not a contraindication to acute therapies for ischemic stroke such as IV thrombolysis and
mechanical thrombectomy. Multidisciplinary consultation is recommended including obstetrics and
neurology.
• SAH can cause cardiac arrest due to neurogenic myocardial stunning.
• ICH and basilar artery occlusion can both present with loss of consciousness and/or convulsions. Brain
imaging is recommended in all unresponsive patients.
FIGURE 4.3 Ischemic and hemorrhagic strokes.

From www.strokeinfo.org/stroke-facts-statistics/.
4.9 BAACC TO LIFE: TRAUMA

Trauma is damage to the body caused by an external force. This force can come in many different forms, from falls to intimate
partner violence (IPV). This section reviews causes of unintentional (such as low-speed motor vehicle collisions or falls) and
intentional (such as IPV) trauma in pregnancy, as well as commonly seen consequences of trauma that can lead to MCA (such
as tension pneumothorax and cardiac tamponade).
4.9.1 Unintentional Trauma: Motor Vehicle Collision

Even seemingly minor trauma, such as a low-speed motor vehicle collision, can lead to devastating consequences. Therefore, it
is critical to closely monitor pregnant patients following a traumatic incident.
Motor vehicle collisions are the most common cause of trauma in pregnancy, followed by falls.20 Approximately one in 12
pregnancies will be affected by some form of trauma.21 Trauma is the leading cause of nonobstetric, or indirect, mortality in
pregnant patients. Adverse pregnancy outcomes can occur even after seemingly minor trauma.
Blunt abdominal trauma, occurring during falls or motor vehicle collisions, can result in significant injuries and increase
a pregnant patient’s risk for placental abruption (where the placenta separates from the uterine wall).21 In early pregnancy, the
uterus is small and protected by the maternal pelvis. After 12 weeks of gestation, the uterus becomes an intra-abdominal organ,
and there is an increased risk for direct injury with trauma.
Placental abruption occurs when trauma to the abdomen and uterus results in shearing forces between the elastic uterine
wall and the inelastic placenta. These forces result in premature separation of the placenta and bleeding. Placental abruptions
are typically associated with abdominal pain, contractions, and vaginal bleeding. Some abruptions are concealed, with the
bleeding remaining within the uterus and without any visible vaginal bleeding. Bleeding from placental abruptions can be severe
and catastrophic, leading to hypovolemic shock, fetal death, and DIC. More insidious presentations of abruptions can occur,
especially in the setting of concealed hemorrhages, where there may be minimal changes in maternal vitals with significant
intra-abdominal bleeding that can quickly lead to hemodynamic instability, and cardiac arrest.
Evaluate patients involved in motor vehicle collisions and falls according to Advanced Trauma and Life Support protocols.22
Prompt maternal evaluation and treatment are key. Therefore, do not delay necessary diagnostic imaging and treatments due to
pregnancy. For more minor trauma, evaluate patients with fetal and contraction monitoring after the event. In patients with no
clinical evidence of abruption (no abdominal pain, vaginal bleeding, or contractions) and no evidence of abruption on ultrasound,
monitor for a minimum of 6 hours. Monitor the following patients for a minimum of 24 hours:
• Patients experiencing abdominal pain, vaginal bleeding, or four or more contractions per hour
• Patients with an ultrasound showing possible abruption
• Patients who experienced significant falls or motor vehicle collisions
4.9.2 Intentional Trauma: Assault, Intimate Partner Violence, Suicide

IPV is a serious public health issue. In the U.S., the rates of IPV are between 4% and 20% during pregnancy.23 Pregnancy is
linked to an increased risk of intimate partner homicide.24,25 Nearly half of female homicide victims are killed by a current or
former male intimate partner, and approximately 15% of female homicide victims of reproductive age (18–44 years) were preg-
nant or postpartum.26 Of those who reported violence during pregnancy, a majority report a history of abuse by the same partner
prior to pregnancy, and half report being assaulted for the first time during pregnancy.23 Prevention is paramount to halting the
cycle of IPV. Obstetric Life Support recommends universal screening for IPV of pregnant patients at the first prenatal visit and
at least once each trimester and postpartum.27 Private screening and referral to services for those experiencing IPV allow people
to leave abusive relationships. These are the first steps to breaking the cycle of violence and reducing maternal morbidity and
mortality from IPV.
4.9.3 Suicide
Suicide attempts are a significant cause of maternal cardiac arrest, both in pregnancy and within the first year postpartum.28
A 2017 study revealed that almost 5% of MCAs occurred as a result of suicide, most of these hanging, jumping, or intentionally
falling.29
These methods differ from those used by nonpregnant people, which typically involve overdose or poisoning. Another
study revealed that almost one-third of pregnancy-related deaths resulted from self-harm, although most of these occurred in
the postpartum period (2004–2012).30
Universal mental health screenings should be performed at the initiation of prenatal care, at 28 weeks, and at postpartum
visits. The American College of Obstetricians and Gynecologists advocates for increased visits in the postpartum period to
improve maternal well-being, including an early postpartum (within 1–3 weeks) and a late postpartum (up to 12 weeks) visit.
Access to appropriate mental health treatment and therapies are also important.
4.9.4 Tamponade, Cardiac

There are multiple causes of cardiac tamponade, but the most common cause is trauma to the heart (such as gunshot wounds or
blunt trauma). Other causes include pericarditis (infection of the pericardium), ruptured aortic aneurysm, myocardial infarction,
invasive cancer, or iatrogenic injury such as from cardiac catheterization or central line placement. Blood or fluid builds up
between the heart and the pericardial sac. As the sac fills, it restricts the heart’s ability to pump blood effectively, which can lead
to cardiac arrest. Patients with cardiac tamponade will often present with severe chest pain, tachycardia, muffled heart sounds,
low blood pressure, and increased jugular venous distention.
Treat cardiac tamponade with a pericardiocentesis, which drains the fluid in the sac. This releases the pressure from the
pericardial fluid. Pericardiocentesis can be performed initially with needle decompression; however, in the setting of major
trauma and a large effusion, a thoracotomy may be required. POC-US is especially helpful in this situation, as it can both diag-
nose a cardiac tamponade and help guide needle placement during pericardiocentesis.
KEY POINTS
• Trauma is the leading indirect, or nonobstetric, cause of maternal mortality.
• Minor trauma in pregnancy can lead to devastating consequences. If patients have evidence of vaginal
bleeding, contractions or abdominal pain, monitor for a minimum of 24 hours.
• Trauma from motor vehicle collision is the most common form of trauma seen in pregnancy.
• Pregnant people are at high risk for IPV and suicide.
• Pregnancy and postpartum may be associated with more violent means of suicide, such as hanging,
jumping, or intentional falling.
• Cardiac tamponade is typically associated with the classic triad of hypotension, muffled or distant heart
sounds, and jugular venous distention. Early decompression of the pericardium via needle pericardiocentesis
is recommended.
4.10 BAACC TO LIFE: OVERDOSE

Accidental and intentional overdose can occur in both in-hospital and out-of-hospital settings. In the labor and delivery suite,
anesthesia complications or iatrogenic overdoses from IV magnesium sulfate can lead to MCA. In out-of-hospital settings, opioid
overdose is the most common cause of accidental overdose leading to MCA. If suspected and treated early, these causes of MCA
are easily reversed and treated. Reversible causes and treatments of overdose leading to maternal respiratory and cardiac arrest
are reviewed in Table 4.8 and are discussed in more detail in the following sections. Of note, lidocaine toxicity was previously
reviewed in the Anesthesia section earlier in this chapter but is included in Table 4.8 as it falls into the category of a reversible
cause of MCA.
4.10.1 Overdose: Magnesium Toxicity

In pregnancy, magnesium sulfate is used for seizure prevention in preeclampsia with severe features or eclampsia, or for fetal
neuroprotection in preterm labor. Magnesium sulfate is usually given intravenously, although it can also be given intramuscularly
in the setting of a patient with eclampsia (seizures) without IV access. Magnesium toxicity may result from errors such as inap-
propriate mixing or bolusing or may occur due to decreased magnesium sulfate clearance in patients with renal insufficiency.
Conditions such as preexisting renal disease or preeclampsia can affect the kidneys’ ability to clear magnesium, which can lead
TABLE 4.8 Reversible Causes and Treatments of Overdose Leading to Maternal Respiratory and Cardiac Arrest
CAUSE OF OVERDOSE TREATMENT
Benzodiazepine overdose • Overdose within 1–2 hours: gastric lavage
• Overdose within 4 hours: activated charcoal
• Severe overdose (including respiratory or cardiac arrest):
Flumazenil 0.2 mg IV × 1, wait 30 seconds, then 0.3 mg ×1 as
required, wait 30 seconds, then 0.5 mg IV every minute as
required up to six times for maximum of 5 mg totalb
Local anesthetic systemic toxicity (see the Anesthesia section) • Lipid emulsion: bolus 1.5 mL/kg IV over 1 minute, then
continuous infusion 0.25–0.5 mL/kg/min with repeat bolus up
to two times for persistent cardiovascular collapse
• Continue infusion for approximately 10 minutes following
cardiovascular stability
• Upper limit of 10 mL/kg over the first 30 minutes of
administration
Magnesium toxicity • 10 mL of 10% calcium gluconate given intravenously over
3 minutesa
Opioid overdose • Naloxone 2 mg intranasal or 0.4 mg intramuscular, repeat
after 4 minutes if necessary
a
If not readily available, pharmacy may need to mix.
b
Patients receiving flumazenil must be closely monitored as it can cause withdrawal and seizures in patients with chronic b
enzodiazepine abuse.
to a buildup of toxic magnesium levels over time. Monitor patients receiving IV magnesium sulfate with periodic assessments
for clinical signs of magnesium toxicity. Signs of magnesium toxicity include the loss of deep tendon reflexes and decreased
respiratory rate which can lead to respiratory depression and cardiac arrest. Development of these symptoms should alert the
provider to the possibility of magnesium toxicity. Treatment includes the prompt discontinuation of magnesium sulfate while
a STAT serum magnesium level is obtained. Administer calcium gluconate if significant magnesium toxicity is suspected, and
intubate the patient if respiratory depression is present. Magnesium sulfate levels of >25 mEq/L may result in maternal cardiac
arrest. Table 4.9 reviews serum magnesium levels and the corresponding physical exam findings.
If the patient receiving IV magnesium sulfate has acute or chronic renal insufficiency, periodically monitor for clinical signs
of magnesium toxicity. Consider using serum magnesium levels in addition to lower magnesium infusion rates. Target magne-
sium levels are typically in the range of 4–6 mEq/L. Recommendations include stopping the magnesium infusion at levels of
8 mEq/L and monitoring serum magnesium values every 2 hours to ensure resolution. For levels >10 mEq/L, administer calcium
gluconate and consider intubation if respiratory depression is present.
KEY POINTS
• Magnesium toxicity—either as a medication error or unrecognized toxic buildup in patients with acute or
chronic renal insufficiency—can lead to maternal respiratory or cardiac arrest in pregnant patients with
receiving treatment for preeclampsia or preterm labor.
• Deep tendon reflexes and respiratory exam should be periodically monitored to identify and prevent
magnesium toxicity.
• Treat magnesium toxicity promptly with IV calcium gluconate and supportive care with intubation in the
setting of respiratory depression.
TABLE 4.9 Magnesium Serum Levels (mEq/L) and

Corresponding Physical Exam Findings
mEq/L FINDINGS
<7 Normal findings
7–9 Loss of deep tendon reflexes
10–24 Respiratory depression
>25 Cardiac arrest
4.10.2 Overdose: Opioids

Between 2000 and 2009, there was a fivefold increase in the rate of opioid abuse during pregnancy.31 Maternal deaths from
opioid overdose are also increasing in the postpartum period. Studies show that one in 300 people who have a cesarean delivery
become addicted to opioids.32 Cesarean delivery is the most common surgical procedure performed in the U.S., and most of
these patients are being given opioids at the time of surgery. Cesarean delivery therefore represents a common source of initial
exposure to opioids. OBLS recommends using protocols such as enhanced recovery after surgery (ERAS) to reduce or limit the
number of pills prescribed at the time of discharge from a hospitalization for delivery.
Signs and symptoms of opioid toxicity include respiratory depression, pinpoint pupils, clammy and/or cold skin, and unre-
sponsiveness. Risk factors for opioid toxicity or overdose include a history of opioid use or abuse, recent major surgery or acci-
dent, untreated mental health disorders, and socioeconomic factors associated with substance use.
The treatment for opioid overdose is naloxone, which is safe for use in pregnancy and the postpartum period. The dose for
naloxone is 2 milligrams administered intranasally or 0.4 milligrams intramuscularly. If the initial dose proves ineffective, a
second dose can be administered after 4 minutes.
4.10.3 Overdose: Other

Approximately 5% of pregnancies are complicated by at least one form of drug abuse, including benzodiazepine abuse.33,34 While
less commonly a sole cause of overdose, benzodiazepine use is seen more frequently in patients with mental health conditions,
including anxiety and post-traumatic stress disorder. Benzodiazepine abuse can have detrimental effects on both the mother and
the fetus, especially when used in conjunction with narcotics and/or alcohol.35 These combinations increase the drug’s sedative
effects, thereby increasing the patient’s risk of respiratory collapse and arrest. Presenting symptoms of benzodiazepine overdose
include excessive sedation, difficult arousal, and sluggish speech.
Signs include shallow breathing, clammy skin, bluish lips, dilated pupils, weak or rapid pulse, low blood pressure, and
depressed reflexes. Patients may also present in a coma and/or cardiopulmonary arrest. Treatment of benzodiazepine over-
dose depends on the timing of the overdose and the severity of the presentation. If the benzodiazepine overdose occurs within
1–2 hours of presentation, gastric lavage may be adequate. If the overdose occurs within 4 hours of presentation, activated
charcoal should be used. Administer flumazenil if the patient presents with a severe overdose with coma and/or cardiac arrest.
This should be carefully monitored, as flumazenil can precipitate withdrawal and/or seizures in patients who chronically abuse
benzodiazepine.
KEY POINTS
• The incidence of opioid overdose is rising in pregnant and postpartum patients.
• In the U.S., one in 300 patients who undergoes a cesarean delivery develops an opioid addiction.
• If cardiac arrest is due to opioid overdose, start high-quality CPR and consider administering naloxone.
• If cardiac arrest is due to benzodiazepine overdose, start high-quality CPR and consider flumazenil as an
antidote.
4.11 BAACC TO LIFE: ACUTE LUNG INJURY/

ACUTE RESPIRATORY DISTRESS
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are clinical syndromes of acute respiratory failure with
substantial morbidity and mortality. ALI and ARDS can be caused by lung infection, sepsis, aspiration, multiple trauma/shock,
and other insults, such as transfusion-related acute lung injury. These are reviewed in Table 4.10.
Symptoms of ALI and ARDS include shortness of breath, hypoxemia, and reduced breath sounds or bibasilar crackles.
Confirm the diagnosis with imaging studies such as chest radiography or CT scan. Do not withhold such procedures from a
pregnant patient due to concern for radiation exposure.36 Promptly evaluate for intubation any pregnant person presenting with
respiratory distress and hypoxemia (oxygen <90%) with hypercapnia (elevated PaCO2).
TABLE 4.10 Pregnancy-Associated Direct and Indirect Causes of Acute Lung Injury/Acute Respiratory Distress Syndrome
INDIRECT DIRECT
Aspiration Cesarean delivery
Intubation
Asthma Iatrogenic—secondary to administration Asthma exacerbation/attack
of Hemabate
Exacerbation due to infection/exercise/
smoking
DIC Inherited coagulopathy Retained products of
conception
AFE
Massive transfusion Multiple trauma Postpartum hemorrhage
Pancreatitis Gallstones, hypertriglyceridemia, alcoholism Pregnancy-associated pancreatitis
Pneumonia Pneumonia Pulmonary edema
Influenza Preeclampsia
Varicella Tocolysis
Coccidioidomycosis
Sepsis Pyelonephritis Chorioamnionitis
Listeria bacteremia Missed abortion
Trauma Tension pneumothorax
Hemothorax
4.11.1 BAACC TO LIFE: Acute Lung Injury: Tension Pneumothorax/Hemothorax

Early recognition of injuries such as tension pneumothorax leads to timely treatment and prevention of cardiac arrest. Tension
pneumothorax or hemothorax is typically caused by a punctured lung, typically from trauma (from fractured rib[s], gunshot
or stabbing injuries, or following chest surgery). A spontaneous pneumothorax can occur in patients with a history of tobacco
abuse or those with underlying lung disease (such as cystic fibrosis or apical blebs) and can progress in a tension pneumothorax.
Decompress a tension pneumothorax or hemothorax in the field by inserting a large-bore (14- or 16-gauge) needle into the fourth
intercostal space in the midaxillary line. Follow this with more definitive treatment with a chest tube when the patient arrives
at the hospital.
See Chapter 8 for more details on managing traumatic MCA.
KEY POINTS
• Common causes for ALI in pregnancy include sepsis, pneumonia, trauma, DIC, and massive transfusion.
• If in the field, decompress a tension pneumothorax with the lateral insertion of large-bore needle at the
fourth intercostal space in the midaxillary line. Once the patient arrives at the hospital, follow with more
definitive treatment with a chest tube.
4.12 BAACC TO LIFE: IONS (GLUCOSE, K+)

Acidosis rarely causes MCA; however, there are important factors that can increase the risk for electrolyte abnormalities to
cause cardiac arrest in pregnancy. For example, pregestational diabetes may result in an increased risk for hypoglycemia in
the first trimester, precipitated by pregnancy-related nausea and vomiting (hyperemesis gravidarum). In diabetic people with
significant nausea and vomiting, hypoglycemia can lead to mental confusion, seizures, arrhythmias, a hypoglycemic coma, and
cardiac arrest. Obtain a point-of-care glucose value for any pregnant or postpartum person in cardiac arrest. When the patient
is unconscious and/or in cardiac arrest, treat severe hypoglycemia with an IV bolus of 20–50 mL of 50% glucose solution or a
subcutaneous or intramuscular (IM) injection of glucagon 0.5–1.0 mg.
While a relatively rare cause of maternal cardiac arrest, DKA affects up to 5%–10% of pregnancies complicated by insu-
lin-dependent diabetes, most commonly in the setting of type 1 diabetes mellitus. DKA can occur in the setting of lower or nor-
mal blood glucose levels and is often precipitated by hyperemesis in early pregnancy, infections, lack of compliance with insulin,
new onset of the diagnosis in pregnancy, and prenatal steroid use. With appropriate management, maternal mortality is rare in
the setting of DKA. These patients improve rapidly with identification and correction of the underlying cause and aggressive IV
fluid hydration, insulin, electrolyte repletion, and subsequent improvements in acidosis.
As chronic comorbidities such as cardiac disease, long-standing pregestational diabetes, and renal disease increase in the
pregnant population, electrolyte abnormalities may become more common etiologies of maternal cardiac arrest. The most con-
cerning electrolyte abnormalities include hypo- and hyperkalemia, both of which may precede cardiac arrest. Manage patients
with high-risk conditions for electrolyte abnormalities (pregnant patients receiving dialysis) with a multidisciplinary team com-
posed of specialists in maternal-fetal medicine, cardiology, and nephrology. This team can coordinate care to prevent dangerous
electrolyte abnormalities from occurring during pregnancy and postpartum.
KEY POINTS
• In a pregnancy complicated by insulin-dependent diabetes, DKA may be diagnosed with low or normal
glucose values.
• Obtain a point-of-care glucose value for any pregnant or postpartum person in cardiac arrest.
• Patients with DKA improve rapidly with aggressive IV fluid hydration, insulin, electrolyte repletion, and
subsequent improvement in acidosis.
4.13 BAACC TO LIFE: FEVER

According to the CDC, infection or sepsis is responsible for approximately 12.4% of maternal deaths.8 Sepsis is the third leading
all-cause of cardiac arrest in the U.S., accounting for 13% of these events.35 Clinical signs and symptoms of sepsis in pregnancy
include the following:
• Body temperature changes (e.g., hypothermia and hyperthermia)

• Tachycardia (heart rate >120)
• Changes in white blood cell (WBC) count (e.g., high or low WBC count)
• Hypotension (systolic BP <90, diastolic BP <60, mean arterial pressure <60–65)
Recognizing sepsis in a pregnant person can be challenging due to the physiologic changes in pregnancy that may mask early
clinical signs of sepsis. For example, 25% of pregnant people who died from sepsis never develop a fever.37 WBC counts are
commonly elevated in pregnancy, and intrapartum levels may be as high as 29,000 per microliter. Lower blood pressure is com-
mon in healthy, pregnant persons due to the vasodilatory effects of progesterone, especially in the second trimester. Additionally,
infectious sources may not be obvious because the portal of entry may be the genitourinary tract, such as seen with group
A streptococcal infection.
The S.O.S.38 is the only validated scoring system for identifying patients with sepsis in pregnancy who may require admis-
sion to the intensive care unit. Please see Chapter 3 for more details on this early warning system. The dysregulated host response
to infection can affect any organ system in the body. Table 4.11 summarizes common dysfunctions seen in various organ systems
during sepsis.
Obstetric causes of infection during pregnancy include septic abortions, chorioamnionitis, endometritis, and wound infec-
tions. Nonobstetric causes include urinary tract infections, appendicitis, and pneumonia. Based on the most recent Surviving
Sepsis Campaign recommendations for adults with suspected sepsis or septic shock include obtaining blood cultures and serum
lactate. Other markers of inflammation such as C-reactive protein and procalcitonin may also be considered. Sepsis or septic
shock should be aggressively treated with broad-spectrum antibiotics (tailored toward the most likely source) and balanced crys-
talloid solutions within 1 hour of presentation with abnormal vital signs and/or documentation of clinical concern.39 Patients with
refractory hypotension or evidence of end organ hypoperfusion should be started on vasopressors such as norepinephrine, with
a search for the cause of the underlying infection, and therapies aimed at source control. In the absence of sepsis treatment data
in pregnancy, experts recommend adoption of these guidelines for treatment of sepsis in pregnancy.39
TABLE 4.11 Organ Systems Affected by Sepsis

ORGAN SYSTEM PRESENTATION
Cardiovascular Hypotension, myocardial dysfunction
Central nervous Altered mental status
Endocrine Adrenal dysfunction and increased insulin resistance
Gastrointestinal Paralytic ileus
Hepatic Hepatic failure or transaminitis
Hematologic Thrombocytopenia or DIC
Pulmonary ARDS
Urinary Oliguria, acute kidney injury
FIGURE 4.4 Initial treatment of sepsis during pregnancy.

Adapted from Society for Maternal-Fetal Medicine.40
Table 4.12 reviews appropriate antibiotic selection for sepsis in pregnancy. Importantly, group A streptococcal infections
during pregnancy or the postpartum period can rapidly progress to death within 2–8 hours of the initial presentation. Invasive
group A streptococcal infections present most commonly in the postpartum period, though they can rarely present in the intra-
partum period. Clinical signs can include disproportionate pain on exam and with abnormal vital signs. The Infectious Diseases
Society of America recommends treatment of group A streptococcal infection with high-dose penicillin and clindamycin.
TABLE 4.12 Antibiotic Selection for Sepsis in Pregnancy41

First-line agents • Penicillin 3 million units IV every 4 hours, plus
• Gentamicin 1.5 mg/kg IV, then 1 mg/kg IV every 8 hours or
5 mg/kg every 24 hours, plus
• Clindamycin 900 mg IV every 8 hours
Alternative • Vancomycin 15 mg/kg IV, then dose by pharmacy, plus
• Piperacillin-tazobactam 4.5 grams IV every 6 hours
Penicillin allergic • Vancomycin 15 mg/kg IV, then dose by pharmacy, plus
• Meropenem 500 mg IV every 6 hours
KEY POINTS
• Clinical signs and symptoms of sepsis include:
• Body temperature changes (hypothermia and hyperthermia)
• Tachycardia (heart rate >120)
• Changes in WBC count (high or low WBC count)
• Hypotension (systolic BP <90, diastolic BP <60 mean arterial pressure <60–65)
• Recognizing sepsis in a pregnant person can be challenging given that normal physiologic changes in
pregnancy may mask symptoms and signs of sepsis
• Group A streptococcal infection is an important cause of postpartum sepsis and should be treated rapidly
with high-dose penicillin and clindamycin
4.14 BAACC TO LIFE: EMERGENCY HYPERTENSION/ECLAMPSIA

Essential hypertension affects 6%–8% of all pregnancies in the U.S.42 Pregnant patients affected by hypertension have increased
risks of significant morbidity, including preeclampsia, eclampsia, pulmonary edema, and stroke.40 Presenting symptoms of pre-
eclampsia typically occur after 20 weeks gestation, and include headache, swelling, malaise, right upper quadrant abdominal
pain, nausea, and vomiting. Presenting signs of preeclampsia include persistent systolic blood pressure elevations ≥140, and/or
diastolic blood pressure elevations ≥90 in patients without preexisting hypertension, or worsening control of blood pressure in
those with preexisting hypertension with or without proteinuria. Edema is a common finding in preeclampsia and results from
fluid retention due to proteinuria and reduced intravascular oncotic pressure. Jaundice is rarely seen in preeclampsia. Laboratory
findings include elevated hemoglobin and hematocrit due to hemoconcentration, low platelets, elevated liver enzymes, elevated
serum creatinine, proteinuria, and hemolysis. The diagnosis of preeclampsia with severe features is based on both clinical and
laboratory findings and is reviewed in Table 4.13.
Preeclampsia affects 6%–8% of all first-time pregnancies in the U.S.43 The incidence is even higher in those with other
comorbidities such as chronic hypertension, a history of preeclampsia in a prior pregnancy, obesity, multiple gestation, or under-
lying renal disease. Pregnant patients affected by hypertension and other comorbidities have increased risks of significant mor-
bidity, including preeclampsia, eclampsia, pulmonary edema, and stroke.
Treat preeclampsia with severe features to prevent eclamptic seizures with a continuous IV infusion of magnesium sulfate
and blood pressure control. A patient with persistent, severe systolic blood pressure ≥160 or persistent, severe diastolic blood
TABLE 4.13 Severe Features of Preeclampsia

Acute renal insufficiency or failure (serum creatinine >1.1 mg/dL Pulmonary edema
or doubling of baseline serum creatinine)
Elevated liver enzymes (two times the upper limit), or right Systolic blood pressure ≥160 mm Hg or diastolic blood pressure
upper quadrant/epigastric pain ≥110 mm Hg
New-onset headache, vision changes, or mental status changes Thrombocytopenia (platelet count <100,000)
pressures ≥110 should be promptly treated within 15–30 minutes with antihypertensive therapy to avoid maternal stroke. Most
protocols on the acute treatment of severe hypertension in pregnancy include the following first-line agents:
• Hydralazine (IV or IM)

• Labetalol (IV)
• Nifedipine, immediate release (oral)
Short-acting oral nifedipine is the treatment of choice in a conscious patient without IV access. Labetalol is contraindicated in
patients with asthma.
The following presents treatment of generalized seizures. If eclamptic seizures occur, they are usually self-limited but
should be treated aggressively and timed, if possible, from the onset of the first seizure. Start magnesium sulfate to prevent
further seizures from occurring. In a patient without a seizure history, a seizure is most likely to be due to eclampsia, and
intravenous access should be established to administer a 6-g bolus of magnesium sulfate over 15–20 minutes, followed by a
a maintanence infusion of 2 g/hour. If the patient is already receiving a maintenance magnesium sulfate infusion of 2 g/hour
and experiences another seizure, a second 2-g bolus of magnesium sulfate is given over 15–20 minutes followed by resuming
the 2 g/hour infusion.
If another seizure occurs after a second bolus of magnesium, give an alternate therapy such as a benzodiazepine (IV
lorazepam 2–4 mg or midazolam 2.5–5 mg). Magnesium sulfate and/or benzodiazepines can also be given intramuscularly or
intraosseously in patients who present with eclamptic seizures and do not have IV access. The usual IM dose of magnesium is
10 g, divided into two 5-g doses, administered as two intramuscular injections, one into each gluteal muscle. The intraosseous
dosing is the same as the IV dosing described earlier.
For refractory seizures lasting more than 5 minutes without return to baseline (status epilepticus), benzodiazepines should
be immediately administered, airway secured, and neurology consulted emergently or a Code Stroke activated. In the prehospi-
tal setting, midazolam can be administered intramuscularly in the field at a dose of 10 mg IM for adults >40 kg. Airway should
be secured and a fingerstick glucose obtained per usual emergency medical services protocols for convulsive status epilepticus.
Eclamptic seizures are typically generalized; any focality of seizure semiology, such as forced gaze deviation, unilateral jerking,
or twitching should prompt a Code Stroke activation and immediate brain imaging, as this may indicate a structural lesion such
as an intracerebral hemorrhage.
In the out-of-hospital setting, pregnant people presenting with seizures should not be assumed to have eclampsia, as those
with epilepsy may experience “breakthrough” seizures during pregnancy due to hormonally induced neurophysiologic changes
(see Chapter 2). As soon as seizures are controlled and the patient is stabilized, OBLS recommends emergent brain imaging with
noncontrast head CT to rule out intracranial hemorrhage or ischemic stroke.
The Council on Patient Safety in Women’s Health Care’s Alliance for Innovation on Maternal Health Program has devel-
oped a bundle on unit readiness, recognition and prevention, response, and reporting of severe hypertension in pregnancy.44 Its
hypertension bundle endorses facility-wide implementation and dissemination of protocols to assist with recognition and rapid
treatment of severe-range hypertension in pregnancy (within 30 minutes from recognition) to reduce the risk of stroke and
maternal mortality.45
KEY POINTS
• Pregnant patients affected by essential hypertension have increased risks of major morbidity including
preeclampsia, eclampsia, and stroke.
• Presenting symptoms of preeclampsia include headache, swelling, malaise, and right upper quadrant
abdominal pain after 20 weeks gestation.
• Presenting signs of preeclampsia include blood pressure elevations ≥140/90 in patients without preex-
isting hypertension or worsening control of blood pressure in those with preexisting hypertension and
proteinuria after 20 weeks gestation.
• A pregnant person with persistent severe-range blood pressure ≥160/110 is at risk for stroke. Treat severe
blood pressure with antihypertensive therapy within 15–30 minutes.
• The treatment of choice for prevention of eclamptic seizures in those affected with preeclampsia with
severe features is intravenous infusion of magnesium sulfate.
• Short-acting oral nifedipine is a first-line agent for acute severe hypertension in a patient without IV
access.
• Do not give labetalol to people with asthma.

1. In OBLS, which mnemonic is used to remember etiologies of MCA?
A. SURVIVE at 5
B. 5 to be ALIVE
C. LUD for LIFE
D. BAACC TO LIFE
2. Which of the following is the MOST common cause for maternal mortality worldwide?
A. Hemorrhage
B. Venous thromboembolism
C. Cardiovascular diseases
D. Hypertension
3. A pregnant person at 40 weeks gestation has preeclampsia with severe features with acute renal insufficiency and
oliguria. While being induced and treated with IV magnesium sulfate for seizure prophylaxis, the patient becomes
inattentive, has slowed responses to stimulation, and pulse is in the 40s. Which of the following is the BEST next step
after calling the rapid response team and stopping the magnesium sulfate infusion?
A. Give an IV bolus of lactated Ringer solution
B. Begin chest compressions
C. Administer calcium gluconate
D. Re-bolus the magnesium sulfate
4. A pregnant person at 20 weeks is diagnosed in the field with a left tension pneumothorax. Emergency medical services
providers are administering bag-mask ventilation with an ETCO2 <10 mm Hg. What is the most appropriate next step?
A. Needle decompression
B. Chest tube placement in the field
C. Pericardiocentesis
D. Intubation and mechanical ventilation
5. A patient with extreme obesity who just delivered their first child 12 hours ago by cesarean delivery reports sudden
onset shortness of breath and chest pain. On exam, the patient is writhing in bed, blood pressure is 70/40 mm Hg, and
pulse is 140 beats per minute. An abdominal exam is benign. The patient becomes unconscious and pulseless. What
is the most likely etiology for the cardiac arrest?
A. Eclampsia
B. Opioid overdose
C. Intra-abdominal hemorrhage
D. Massive pulmonary embolism
CHAPTER 4. ANSWERS
1. ANSWER: D. OBLS uses the mnemonic BAACC TO LIFE to recall the potential etiologies of MCA.
2. ANSWER: A. Maternal hemorrhage is the number one cause of maternal morbidity and mortality worldwide.
Postpartum hemorrhage is the most common cause of maternal hemorrhage, occurring in 4%–6% of all pregnancies,
with greater than 50% of maternal deaths from this cause occurring within the first 24 hours of delivery. Postpartum
hemorrhage is caused by uterine atony in approximately 70%–80% of cases.
3. ANSWER: C. Patients with preeclampsia with severe features who are receiving IV magnesium sulfate are at risk for
magnesium toxicity. This risk is even greater with underlying renal insufficiency. Monitoring for magnesium toxicity
can occur by clinical exam assessing for the loss of deep tendon reflexes and decreased respiratory rate, and/or by
periodic monitoring of magnesium levels, especially in patients with underlying renal disease. Development of signs
and/or symptoms of magnesium toxicity should have prompt discontinuation of magnesium sulfate while a STAT
serum magnesium level is obtained. Calcium gluconate should be administered if significant magnesium toxicity is
suspected, as in this patient.
4. ANSWER: A. Early recognition of injuries such as tension pneumothorax can lead to more timely treatment and
prevention of cardiac arrest. Tension pneumothorax or hemothorax is most caused due to a punctured lung, typically
from trauma (such as from fractured rib, gunshot or stab injury, or following chest surgery). Decompress a tension
pneumothorax or hemothorax on the field by inserting a large-bore (14- or 16-gauge) needle into the fourth intercostal
space in the midaxillary line. Follow with more definitive treatment via chest tube when the patient arrives at the
hospital.
5. ANSWER: D. Patients with pulmonary embolism will typically present with acute-onset shortness of breath, tachy-
cardia, and chest pain. Initial evaluation should consist of an electrocardiogram and chest radiography. If clinical
suspicion is high for pulmonary embolism, start therapeutic anticoagulation therapy empirically with heparin or
low-molecular-weight heparin while pursuing further evaluation with either CT angiogram of the chest, or ventila-
tion-perfusion scan.
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Obstetric Life Support Manual

Laurie Kavanagh, MPH

Peter Nielsen, MD, MSS

Obstetric Life Support Course Overview 1

1 Background on Maternal Cardiac Arrest 6

2 Anatomic and Physiologic Adaptations of Pregnancy 15

3 Prevention of Maternal Cardiac Arrest 27

4 Common Causes of Maternal Cardiac Arrest 37

5 Review of Cardiopulmonary Resuscitation Modifications for Pregnant Patients

6 Review of Cardiopulmonary Resuscitation Modifications for Pregnant Patients in Advanced

7 Special Procedures in Obstetric Life Support 83

8 Traumatic Maternal Cardiac Arrest 99

9 Postpartum Cardiac Arrest 106

10 Maternal Stroke and Acute Cerebrovascular Disease 120

11 Post-Arrest Care 140

12 Communication during Maternal Cardiac Arrest 154

13 Putting It All Together 165

0.1 COURSE DESCRIPTION

0.2 COURSE OBJECTIVES

0.3 COURSE DESIGN

0.3.2 OBLS Entry Exam

0.3.3 Instructor-Led, In-Person Course

• Team communication and dynamics management

0.3.4 Graded OBLS Megacode

0.4 COURSE PREREQUISITES

0.5 SUCCESSFUL COURSE COMPLETION REQUIREMENT

0.6 COURSE MATERIALS

0.7 MANUAL ORGANIZATION

0.9 HIGHLIGHTED BOXES

0.10 OBLS ALGORITHMS, COGNITIVE AIDS, AND CHECKLISTS

1.2 LEARNING OBJECTIVES

1.3 MATERNAL MORTALITY

FIGURE 1.2 Causes of pregnancy-related deaths in the United States (2017–2019).4

1.4 EPIDEMIOLOGY OF MATERNAL CARDIAC ARREST

FIGURE 1.5 Severe maternal morbidity iceberg.

1.5 THE ROLE OF BIAS

FIGURE 1.6 Deaths per live births by race/ethnicity.

1.6 PREVENTING MATERNAL CARDIAC ARREST

1.7 PLANNING AND PREPARATION

CHAPTER 1. PRACTICE QUESTIONS

3. According to the CDC, how many pregnancy-related deaths are preventable?

5. Pregnancy-related deaths are most likely to occur at what point in pregnancy?

2.2 LEARNING OBJECTIVES

• Describe the variations in anatomy and physiology encountered during pregnancy.

2.3 CARDIOVASCULAR ANATOMIC AND

TABLE 2.1 Anatomic and Physiologic Cardiovascular Adaptations in Pregnancy

There are several points to note:

2.4 RESPIRATORY ANATOMIC AND PHYSIOLOGIC

FIGURE 2.1 Mallampati scoring system.

Pregnant 7.40–7.45 28–32 mm Hg >100 mm Hg 22 mEq/L

TABLE 2.3 Anatomic and Physiologic Respiratory Adaptations in Pregnancy

2.5 NEUROPHYSIOLOGIC ADAPTATIONS IN PREGNANCY

TABLE 2.5 Maternal Central Nervous System Changes

2.6 HEMATOLOGIC PHYSIOLOGIC ADAPTATIONS IN PREGNANCY

TABLE 2.6 Physiologic Hematologic Adaptations in Pregnancy

2.7 GASTROINTESTINAL ANATOMIC AND

TABLE 2.7 Anatomic and Physiologic Gastrointestinal Adaptations in Pregnancy

2.8 GENITOURINARY ANATOMIC AND PHYSIOLOGIC

2.9 ANATOMIC AND PHYSIOLOGIC IMPACT

2.10 ENDOCRINE ANATOMIC AND PHYSIOLOGIC

2.11 IMMUNE SYSTEM ADAPTATIONS IN PREGNANCY

TABLE 2.9 Anatomic and Physiologic Endocrinologic Adaptations in Pregnancy

CHAPTER 2. PRACTICE QUESTIONS

3.2 LEARNING OBJECTIVES

Obstetric Life Support Course Overview 1

1 Background on Maternal Cardiac Arrest 6

2 Anatomic and Physiologic Adaptations of Pregnancy 15

3 Prevention of Maternal Cardiac Arrest 27

4 Common Causes of Maternal Cardiac Arrest 37

7 Special Procedures in Obstetric Life Support 83

8 Traumatic Maternal Cardiac Arrest 99

9 Postpartum Cardiac Arrest 106

10 Maternal Stroke and Acute Cerebrovascular Disease 120

11 Post-Arrest Care 140

12 Communication during Maternal Cardiac Arrest 154

13 Putting It All Together 165