Professional Documents
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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
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
6000 Broken Sound Parkway NW, Suite 300, Boca Raton, FL 33487–2742
and by CRC Press
4 Park Square, Milton Park, Abingdon, Oxon, OX14 4RN
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
any errors or omissions that may be made. The publishers wish to make clear that any views or opinions expressed in this book by
individual editors, authors or contributors are personal to them and do not necessarily reflect the views/opinions of the publishers. The
information or guidance contained in this book is intended for use by medical, scientific or healthcare professionals and is provided
strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the patient’s medical history,
relevant manufacturer’s instructions and the appropriate best practice guidelines. Because of the rapid advances in medical science, any
information or advice on dosages, procedures or diagnoses should be independently verified. The reader is strongly urged to consult
the relevant national drug formulary and the drug companies’ and device or material manufacturers’ printed instructions, and their
websites, before administering or utilizing any of the drugs, devices or materials mentioned in this book. This book does not indicate
whether a particular treatment is appropriate or suitable for a particular individual. Ultimately it is the sole responsibility of the medical
professional to make his or her own professional judgements, so as to advise and treat patients appropriately. The authors and publishers
have also attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if
permission to publish in this form has not been obtained. If any copyright material has not been acknowledged please write and let us
know so we may rectify in any future reprint.
An Open Access version of this book will be made available at www.taylorfrancis.com under a Creative Commons Attribution-Non
Commercial-No Derivatives 4.0 license.
Trademark notice: Product or corporate names may be trademarks or registered trademarks and are used only for identification and
explanation without intent to infringe.
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
vii
viii Contents
Chapter 3. Answers 36
Chapter 3. References 36
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
Chapter 6. Practice Questions 81
Chapter 6. Answers 82
Chapter 6. References 82
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
• 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
0.3.1 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.
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.
0.8 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.
• 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.
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.
• 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.
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.
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.
8 Obstetric Life Support Manual
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).
1 • Background on Maternal Cardiac Arrest 9
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.
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.
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.
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.
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
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
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.
14 Obstetric Life Support Manual
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.
DOI: 10.1201/9781003299288-3 15
16 Obstetric Life Support Manual
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.
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.
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
TABLE 2.2 Arterial Blood Gas Values in Pregnant versus Nonpregnant Patients
STATUS pH PaCO2 PaO2 HCO3-
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
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.
2 • Anatomic and Physiologic Adaptations of Pregnancy 19
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
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.
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 • Anatomic and Physiologic Adaptations of Pregnancy 21
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.
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.
TABLE 2.8 Anatomic and Physiologic Genitourinary and Acid-Base Adaptations in Pregnancy
PARAMETER VALUES 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.
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.
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.
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
2 • Anatomic and Physiologic Adaptations of Pregnancy 25
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.
CHAPTER 2. REFERENCES
1. Sanghavi M, Rutherford JD. Cardiovascular physiology of pregnancy. Circulation. 2014;130:1003–1008. doi: 10.1161/
CIRCULATIONAHA.114.009029.
2. Weinberger SE, Weiss ST, Cohen WR, Weiss JW, Johnson. Pregnancy and the lung. Am Rev Respir Dis. 1980 Mar;121(3):559–81. doi:
10.1164/arrd.1980.121.3.559.
3. Boutonnet M, Faitot V, Katz A, Salomon L, Keita H. Mallampati class changes during pregnancy, labour, and after delivery: can these
be predicted? Br J Anaesth. 2010;104(1):67–70. doi: 10.1093/bja/aep356.
4. Lyons HA, Antonio R. The sensitivity of the respiratory center in pregnancy and after administration of progesterone. Trans Assoc Am
Physicians. 1959;72:173–180.
5. Pilkington S, Carli F, Dakin MJ, et al. Increase in Mallampati score during pregnancy. British Journal of Anaesthesia. 1995;74(6):
638–642. doi: 10.1093/bja/74.6.638.
6. Crapo RO. Normal cardiopulmonary physiology during pregnancy. Clin Obstet Gynecol. 1996;39(1):3–16. doi: 10.1097/00003081-
199603000-00004.
7. Arterial Blood Gas (ABG) interpretation for medical students, OSCEs and MRCP PACES. Oxford Medical Education. Website. http://
www.oxfordmedicaleducation.com/abgs/abg-interpretation/. Accessed March 11, 2023.
8. Antony KM, Racusin DA, Aagaard K, Dildy GA. Maternal Physiology. In Gabbe S, Niebyl J, Simpson J, et al. ed. Obstetrics: Normal
and Problem Pregnancies. Elsevier; 2016:46.
9. LoMauro A, Aliverti A. Respiratory physiology of pregnancy. Physiology masterclass. Breathe. 2015;11(4):297–301. doi:
10.1183/20734735.008615.
10. Bordoni L, Parsons K, Rucklidge MWM. Obstetric Airway Management. Obstetric Anesthesia Tutorial 393. ATOTW 393 (14
December 2018).
11. Abbassi-Ghanavati M, Greer L, Cunningham F. Pregnancy and laboratory studies: A reference table for clinicians. Obstet Gynecol.
2009;114(6):1326–1331. doi: 10.1097/AOG.0b013e3181c2bde8.
12. Boehlen F, Hohlfeld P, Extermann P, Perneger TV, de Moerloose P. Platelet count at term pregnancy: a reappraisal of the threshold.
Obstet Gynecol. 2000;95(1):29–33. doi: 10.1016/s0029-7844(99)00537-2.
13. Ye Y, Vattai A, Zhang X, Zhu J, Thaler CJ, Mahner S, Jeschke U, Von Schönfeldt V. Role of plasminogen activator inhibitor type 1
in pathologies of female reproductive diseases. International Journal of Molecular Sciences. 2017;18(8):1651. https://doi.org/10.3390/
ijms18081651.
14. Thaxter Nesbeth KA, Samuels LA, Nicholson Daley C, et al. Ptyalism in pregnancy—a review of epidemiology and practices. Eur J
Obstet Gynecol Reprod Biol. 2016;198:47. doi: 10.1016/j.ejogrb.2015.12.022.
15. Nazik E, Eryilmaz G. Incidence of pregnancy-related discomforts and management approaches to relieve them among pregnant women.
J Clin Nurs 2014;23:1736. doi:10.1111/jocn.12323.
16. Whitehead EM, Smith M, Dean Y, O’Sullivan G. An evaluation of gastric emptying times in pregnancy and the puerperium. Anaesthesia
1993;48:53.
26 Obstetric Life Support Manual
17. Shinohara S, Uchida Y, Kasai M, Ogawa T, Hirata S. Liver injury after cardiopulmonary resuscitation for cardiac arrest during cesarean
delivery. Int J Obstet Anesth. 2017 Feb;29:86–87. doi: 10.1016/j.ijoa.2016.09.007.
18. Cox TR, Crimmins SD, Shannon AM, Atkins KL, Tesoriero R, Malinow AM. Liver lacerations as a complication of CPR during preg-
nancy. Resuscitation. 2018 Jan;122:121–125. doi: 10.1016/j.resuscitation.2017.10.027.
19. Callaway CW, Soar J, Aibiki M, Böttiger BW, Brooks SC, Deakin CD, Donnino MW, Drajer S, Kloeck W, Morley PT, Morrison LJ,
Neumar RW, Nicholson TC, Nolan JP, Okada K, O’Neil BJ, Paiva EF, Parr MJ, Wang TL, Witt J; on behalf of the Advanced Life
Support Chapter Collaborators. Part 4: Advanced life support: 2015 International Consensus on Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care Science with Treatment Recommendations. Circulation. 2015;132(suppl 1):S84–S145. doi.org/10.1161/
CIR.0000000000000273.
20. Mattingly RF, Borkowf HI. Clinical implications of ureteral reflux in pregnancy. Clin Obstet Gynecol. 1978;21(3):863. doi:
10.1097/00003081-197809000-00022.
21. Heidrick WP, Mattingly RF, Amberg JR. Vesicoureteral reflux in pregnancy. Obstet Gynecol. 1967;29(4):571.
22. Gant NF, Chand S, Whalley PJ, MacDonald PC. The nature of pressor responsiveness to angiotensin II in human pregnancy. Obstet
Gynecol. 1974;43(6):854.
23. Cunningham F, Leveno KJ, Bloom SL, Dashe JS, Hoffman BL, Casey BM, Spong CY (Eds). Maternal physiology. Williams Obstetrics,
25e. McGraw-Hill; 2018. https://accessmedicine.mhmedical.com/content.aspx?bookid=1918§ionid=144754618. Accessed March
12, 2023.
24. Lindheimer MD, Barron WM, Davison JM. Osmoregulation of thirst and vasopressin release in pregnancy. Am J Physiol. 1989;257(2
Pt 2):F159.
25. Kattah A, Milic N, White W, Garovic V. Spot urine protein measurements in normotensive pregnancies, pregnancies with isolated
proteinuria and preeclampsia. Am J Physiol Regul Integr Comp Physiol. 2017;313:R418. doi: 10.1152/ajpregu.00508.2016.
26. Alto WA. No need for glycosuria/proteinuria screen in pregnant women. J Fam Pract. 2005;54:978.
27. Lind T, Godfrey KA, Otun H, Philips PR. Changes in serum uric acid concentrations during normal pregnancy. Br J Obstet Gynaecol.
1984;91(2):128. doi: 10.1111/j.1471-0528.1984.tb05895.x.
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.
DOI: 10.1201/9781003299288-4 27
28 Obstetric Life Support Manual
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
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.
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.
30 Obstetric Life Support Manual
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
*CMQCC undergoing validation trials with anticipated sensitivity and specificity values based on clinical practice data sets.5
3 • Prevention of Maternal Cardiac Arrest 31
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
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.
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.
34 Obstetric Life Support Manual
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:
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.
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
3 • Prevention of Maternal Cardiac Arrest 35
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.
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
36 Obstetric Life Support Manual
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.
CHAPTER 3. REFERENCES
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).
DOI: 10.1201/9781003299288-5 37
38 Obstetric Life Support Manual
FIGURE 4.1 Etiologies for maternal cardiac arrest, the BAACC TO LIFE mnemonic.
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.
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.
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,
42 Obstetric Life Support Manual
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 • Common Causes of Maternal Cardiac Arrest 43
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.
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
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.
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.
• 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
4.9.3 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
48 Obstetric Life Support Manual
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.
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.
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.
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.
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
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.
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.
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
4 • Common Causes of Maternal Cardiac Arrest 53
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.
54 Obstetric Life Support Manual
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
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:
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.
56 Obstetric Life Support Manual
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
4 • Common Causes of Maternal Cardiac Arrest 57
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.
CHAPTER 4. REFERENCES
1. 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.
2. Obstetric Hemorrhage (+AIM). Council on Patient Safety in Women’s Health Care. Website. https://saferbirth.org/wp-content/uploads/
U2-FINAL_AIM_Bundle_ObstetricHemorrhage.pdf. Accessed September 13, 2019.
3. Committee on Practice Bulletins—Obstetrics. Practice Bulletin No. 183: Postpartum hemorrhage. Obstet Gynecol. 2017;13(4):e168–
e186. doi: 10.1097/AOG.0000000000002351.
4. Mhyre JM, Riesner MN, Polley LS, Naughton NN. A series of anesthesia-related maternal deaths in Michigan, 1985–2003.
Anesthesiology. 2007;10(6):1096–1104. doi: 10.1097/01.anes.0000267592.34626.6b.
5. Saade G, Hankins GVD, Clark SL. SMFM Clinical Guideline No. 9. Amniotic fluid embolism: Diagnosis and management. Am J
Obstet Gynecol. 2016 August;215(2):B16–B24. doi: 10.1016/j.ajog.2016.03.012.
6. Shamshirsaz AA, Clark S. Amniotic fluid embolism. Obstet Gynecol Clin North Am. 2016. doi: 10.1016/j.ogc.2016.07.001.
7. Mathews T, Hamilton B. Mean age of mothers is on the rise: United States, 2000–2014. NCHS data brief. No. 232. National Center for
Health Statistics. 2016 January.
8. Centers for Disease Control and Prevention. Pregnancy mortality surveillance system. Website. www.cdc.gov/reproductivehealth/
maternal-mortality/pregnancy-mortality-surveillance-system.htm. Accessed September 17, 2019.
9. California Maternal Quality Care Collaborative (CMQCC). Improving health care response to cardiovascular disease in pregnancy
and postpartum. Website. www.cmqcc.org/resources-toolkits/toolkits/improving-health-care-response-cardiovascular-disease-
pregnancy-and2019.
10. Schaufelberger M. Cardiomyopathy and pregnancy. Heart. 2019;105:1543–1551. doi: 10.1136/heartjnl-2018-313476.
11. 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.
12. van der Pol LM, Tromeur C, Bistervels I, et al. Pregnancy-adapted YEARS algorithm for diagnosis of suspected pulmonary embolism.
N Engl J Med. 2019;380:1139–1149. doi: 10.1056/NEJMoa1813865.
13. ACOG Committee Opinion. Number 723. Guidelines for diagnostic imaging during pregnancy and lactation. Obstet Gynecol. 2017. doi:
10.1097/00006250-200510000-00052.
14. 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.
15. Saver J. Time is brain-quantified. Stroke. 2006;37(1):263–266.
16. Goyal M, Menon BK, van Zwam WH, et al. Endovascular thrombectomy after large-vessel ischaemic stroke: A meta-analysis of indi-
vidual patient data from five randomised trials. Lancet. 2016;387(10029):1723–1731.
17. Inamasu J, Nakagawa Y, Kuramae T, Nakatsukasa M, Miyatake S. Subarachnoid hemorrhage causing cardiopulmonary arrest:
Resuscitation profiles and outcomes. Neurol Med Chir (Tokyo). 2011;51(9):619–623. doi: 10.2176/nmc.51.619.
18. 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.
19. Hemphill JC, Greenberg SM, Anderson CS, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: A guideline
for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2015;46:2032–2060.
20. Mendez-Figueroa H, Dahlke JD, Vrees R, Rouse DJ. Trauma in pregnancy: An updated systematic review. Am J Obstet Gynecol. 209.
doi: 10.1016/j.ajog.2013.01.021.
21. Murphy NJ, Quinlan J. Trauma in pregnancy: Assessment, management, and prevention. Am Fam Physician. 2014;90(0):717–724.
22. Advanced Trauma Life Support. American College of Surgeons. Website. www.facs.org/quality-programs/trauma/atls. Updated 2020.
23. Lutgendorf MA. Intimate partner violence and women’s health. Obstet Gynecol. 2019;134:470–480. doi: 10.1097/AOG.0000000000003326.
58 Obstetric Life Support Manual
24. Campo M. Domestic and family violence in pregnancy and early parenthood overview and emerging interventions. Website. https://
aifs.gov.au/sites/default/files/publication-documents/cfca-resource-dv-pregnancy_0.pdf. Updated 2020.
25. Garcia-Moreno C, Jansen H, Ellsberg M, Heise L, Watts CH. Prevalence of intimate partner violence: Findings from the WHO
multi-country study on women’s health and domestic violence. Lancet. 2006;368. doi: 10.1016/S0140-6736(06)69523-8.
26. Petrosky E, Blair JM, Betz CJ, Fowler KA, Jack SP, Lyons BH. Racial and ethnic differences in homicides of adult women and the role
of intimate partner violence—United States, 2003–2014. MMWR Morb Mortal Wkly Rep. 2017. doi: 10.15585/mmwr.mm6628a1.
27. ACOG Committee Opinion 518. Intimate partner violence. Obstet Gynecol. 2012. doi: 10.1097/AOG.0b013e318249ff74.
28. Campbell J, Matoff-Stepp S, Velez ML, Cox HH, Laughon K. Pregnancy-associated deaths from homicide, suicide, and drug overdose:
Review of research and the intersection with intimate partner violence. J Womens Health (Larchmt). 2021;30(2):236–244. doi: 10.1089/
jwh.2020.8875. Epub 2020 Dec 8. PMID: 33295844; PMCID: PMC8020563.
29. Grigoriadis S, Wilton AS, Kurdyak PA, Rhodes AE, et al. Perinatal suicide in Ontario, Canada: A 15-year population-based study.
CMAJ. 2017. doi: 10.1503/cmaj.170088.
30. Metz TD, Rovner P, Hoffman MC, Allshouse AA, Beckwith KM, Binswanger IA. Maternal deaths from suicide and overdose in
Colorado, 2004–2012. Obstet Gynecol. 2016;128(6):1233–1240. doi: 10.1097/AOG.0000000000001695.
31. National Institute on Drug Abuse. Substance use while pregnant and breastfeeding. National Institutes of Health; U.S. Department
of Health and Human Services. May 4, 2022. Website. https://nida.nih.gov/publications/research-reports/substance-use-in-women/
substance-use-while-pregnant-breastfeeding. Updated 2023.
32. Bateman BT, Franklin JM, Bykov K, et al. Persistent opioid use following cesarean delivery: Patterns and predictors among opioid-
naïve women. Am J Obstet Gynecol. 2016. doi: 10.1016/j.ajog.2016.03.016.
33. Wendell AD. Overview and epidemiology of substance abuse in pregnancy. Clin Obstet Gynecol. 2013;56(1):91–96. doi: 10.1097/
GRF.0b013e31827feeb9.
34. National Institute on Drug Abuse (NIDA). Sex and gender differences in substance use. National Institutes of Health; U.S. Department
of Health and Human Services. May 4, 2022. Website. https://nida.nih.gov/publications/research-reports/substance-use-in-women/
sex-gender-differences-in-substance-use. Updated 2023.
35. 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.
36. American Committee Opinion No. 723. Guidelines for diagnostic imaging during pregnancy and lactation. American College of
Obstetricians and Gynecologists. Obstet Gynecol 2017;130:e210–6.
37. Bauer ME, Lorenz RP, Bauer ST, Rao K, Anderson FW. Maternal deaths due to sepsis in the state of Michigan, 1999–2006. Obstet
Gynecol. 2015;12(4):747–752. doi: 10.1097/AOG.0000000000001028.
38. 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.
39. Evans L, et al. Surviving sepsis campaign: International guidelines for management of sepsis and septic shock 2021. Crit Care Med.
49(11):p e1063–e1143. doi: 10.1097/CCM.0000000000005337.
40. SMFM consult series #47: Sepsis during pregnancy and the puerperium. Society for Maternal Fetal Medicine. Website. www.smfm.
org/publications/271-smfm-consult-series-47-sepsis-during-pregnancy-and-the-puerperium. Accessed September 18, 2019.
41. Barton JR, Sibai B. Severe sepsis and septic shock in pregnancy. Obstet Gynecol. 2012 September;12(3):689–706. doi: 10.1097/
AOG.0b013e318263a52d.
42. Seely E. Hypertension in pregnancy: A potential window into long-term cardiovascular risk in women. J Clin Endocrinol Metab. doi:
10.1210/jcem.84.6.5785.
43. Mayrink J, Souza RT, Feitosa FE, et al. Incidence and risk factors for preeclampsia in a cohort of healthy nulliparous pregnant women:
A nested case-control study. Sci Rep. 2019. doi: 10.1038/s41598-019-46011-3.
44. Severe Hypertension in Pregnancy (+AIM). Council on Patient Safety in Women’s Health Care. Website. https://saferbirth.org/psbs/
severe-hypertension-in-pregnancy/. Updated 2020.
45. https://saferbirth.org/wp-content/uploads/U1-FINAL_AIM_Bundle_SHP2022.pdf