American Journal of Emergency Medicine xxx (2015) xxx–xxx

Contents lists available at ScienceDirect

American Journal of Emergency Medicine

journal homepage: www.elsevier.com/locate/ajem

Review

The pregnant heart: cardiac emergencies during pregnancy☆,☆☆

Alyson J. McGregor, MD, MA a,⁎, Rebecca Barron, MD, MPH a, Karen Rosene-Montella, MD b
a
Department of Emergency Medicine, Warren Alpert Medical School of Brown University, Providence, RI, 02903
b
Department of Medicine, Warren Alpert Medical School of Brown University, Providence, RI, 02903

a r t i c l e i n f o a b s t r a c t

Article history: Background: Cardiovascular emergencies in pregnant patients are often considered a rare event; however, heart
Received 12 January 2015 disease as a cause of maternal mortality is steadily increasing.
Received in revised form 23 February 2015 Discussion: In this article, we review 3 common cardiovascular emergencies and the important subtle differences
Accepted 24 February 2015 in their treatment in the pregnant patient: peripartum/postpartum cardiomyopathy, acute myocardial infarction,
Available online xxxx
and cardiac resuscitation.
Conclusion: Managing these conditions in the emergency department setting requires a high index of suspicion,
knowledge of anatomical and physiologic changes associated with pregnancy, and updated management
strategies related to optimizing maternal and fetal health.
© 2015 Elsevier Inc. All rights reserved.

1. Introduction The authors include experienced emergency medicine physi-

Maternal mortality in industrialized countries is increasing, with 28
pregnancy-related deaths per 100, 000 live births in the United States in
2013, up from 17 in 2005 [1]. Women are increasingly seeking pregnan-
cy at a later age: 1 in 12 first births in the United States in 2008 was to
women aged 35 years and older compared with 1 in 100 in 1970 [2].
Postponing childbearing until the fourth and fifth decades of life has
contributed to the increased risk on the cardiovascular system that the
stress of pregnancy places. As a result, heart disease has emerged as
the leading cause of maternal mortality, with cardiomyopathy and
cardiovascular disease accounting for 26% of maternal deaths in the
United States between 2006 and 2010.
Cardiovascular emergencies in pregnancy are considered rare but
often require multidisciplinary consultants and specialized protocols
and equipment as well as an understanding of subtle differences in
the treatment of critically ill pregnant patients. These patients can be
some of the most stressful cases that clinicians encounter, as there is a
need to consider the unique physiologic and anatomical changes of
pregnancy, which ultimately affect the outcome of both the mother
and the fetus.
☆ Prior presentations: None.
☆☆ Funding sources: Sponsored by the Division of Sex and Gender in Emergency
Medicine at the Department of Emergency Medicine at Warrant Alpert Medical School
of Brown University.
⁎ Corresponding author at: Sex and Gender in Emergency Medicine Division, Sex and
Gender in Emergency Medicine Fellowship, Department of Emergency Medicine, Warren
Alpert Medical School at Brown University, 593 Eddy St, Claverick 200.1, Providence, RI,
02903. Tel.: +1 401 226 3317; fax: +1 401 444 4307.
E-mail address: amcgregormd@gmail.com (A.J. McGregor).
cians and an obstetric medicine physician with an active obstetric
medicine service at one of the nation's busiest and only level 1
trauma center in southeastern New England. With an emergency
department (ED) census of more than 110, 000 annually, a myriad
of conditions are cared for, including those specific to pregnancy.
The purpose of this review is to summarize the key epidemiology,
etiology, diagnostic, and clinical management recommendations
as well as any specialized considerations that are essential for
clinicians to consider for 3 common cardiovascular emergencies
in the pregnant patient: peripartum/postpartum cardiomyopathy,
acute myocardial infarction (AMI), and cardiac resuscitation.
2. Discussion
2.1. Peripartum/postpartum cardiomyopathy
A life-threatening disease of uncertain etiology characterized
by left ventricular (LV) systolic dysfunction found in previously
healthy pregnant women is referred to as peripartum/postpartum
cardiomyopathy (PPCM). The initial presentation of these patients
is frequently to the ED, and their evaluation, differential diagnosis,
management, and disposition are somewhat different from
other patients with heart failure (HF) [3]. Pregnant patients with
known cardiovascular conditions that can precede HF are more
likely to have knowledge of their symptomatic and cardiac func-
tional status, but PPCM occurs in patients without previous HF
symptoms, thus presenting a diagnostic and treatment dilemma
to clinicians.
2.1.1. Epidemiology
The incidence of PPCM in the United States seems to be increasing
(1:4350 in 1993 to 1:2229 in 2002) with a significantly higher incidence

http://dx.doi.org/10.1016/j.ajem.2015.02.046
0735-6757/© 2015 Elsevier Inc. All rights reserved.

Please cite this article as: McGregor AJ, et al, The pregnant heart: cardiac emergencies during pregnancy, Am J Emerg Med (2015), http://
dx.doi.org/10.1016/j.ajem.2015.02.046
2 A.J. McGregor et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx

in African American women [4,5]. Because the number of live births in
the United States is greater than 4.3 million per year, the estimated an-
nual number of new patients with PPCM in the United States is approx-
imately 1350 [6]. Advanced maternal age, tocolytic therapy, or twin
pregnancy may identify subgroups of women with higher incidence
rates [7,8]. Based on the difficulties in diagnosis, it is estimated
that many milder cases are left undetected. This is a concerning feature
because the risk and severity of PPCM in a subsequent pregnancy are
increased by 20% to 50% [9] depending on whether LV function has
returned to normal.
2.1.2. Etiology
The etiology and risk factors of PPCM are largely unknown, but
clinical and experimental data suggest inflammation, autoimmune
processes, apoptosis, viral infections, malnutrition, hormonal abnormal-
ities, stress-activated cytokines, and endothelial dysfunction as possible
pathomechanisms [10]. Data indicate that cleavage of the nursing
hormone prolactin by catepsin D results in oxidative stress on the endo-
thelium, cardiac vasculature, and cardiomyocyte function [11].
2.1.3. Diagnostic challenges
Previously healthy women will present with sudden onset symp-
toms of HF (dyspnea, weakness, and edema), which is characterized
by LV systolic dysfunction during the last month of pregnancy and the
first 5 months after delivery [12]. The diagnostic criteria for PPCM,
defined by the National Heart, Lung, and Blood Institute, include the
absence of any identifiable cause for HF without known preexisting
cardiac disease [13]. Early signs and symptoms of HF can be mistaken
for physiological changes seen with pregnancy; however, orthopnea,
persistent dyspnea, and tachypnea are not usually present in normal
pregnancy. This often leads to a delayed diagnosis requiring clinicians
to have a high index of suspicion when cardiac symptomatology
seems disproportionate to the stage of pregnancy [14].
Moreover, symptoms of HF in patients with PPCM are often
attributed to preeclampsia and pregnancy-induced hypertension
in patients with these conditions. Some degree of LV dysfunction
and both cardiogenic and noncardiogenic pulmonary edema may
occur in association with preeclampsia, making it difficult to differ-
entiate PPCM early in the course of the disease. Further complicat-
ing the diagnosis are mild cases of PPCM, which may evade clinical
attention [15], and atypical presentations as a result of thromboem-
bolic events (cerebral, peripheral, and mesenteric emboli), which
can present as stroke, transient ischemic attack, limb ischemia, or
abdominal pain [16].
An electrocardiogram (ECG) should be performed in all patients
with suspected PPCM, as it can assist in distinguishing PPCM from
other etiologies. Several studies have investigated the prevalence
of ECG abnormalities in PPCM [17-19] and found the majority pre-
sented with “abnormal” 12-lead ECGs. Specifically, the T-wave and
ST-segment abnormalities in the context of PPCM may place these
patients at similar risk for adverse outcomes to those with myocardi-
al ischemia [19].
Pregnancy is associated with approximately 2-fold higher increase
in B-type natriuretic peptide (BNP) levels compared with nonpregnant
women [20]. However, patients with PPCM commonly have an addi-
tional increase in plasma concentration of BNP or N-terminal pro-BNP
as a result of the elevated LV end-diastolic pressure due to systolic dys-
function [21]. The rise of total creatine kinase and creatine kinase-MB is
directly correlated with type of delivery, duration of labor, parity of the
mother, and birth weight [22] and may not be helpful in detecting
PPCM. Findings of cardiomegaly, pulmonary venous congestion, and
pleural effusions may be detected on chest radiographs [23]. Echocardi-
ography is the keystone in the diagnosis of PPCM and essential in de-
tecting the reduced LV ejection fraction (LVEF) as well as evaluating
the presence of LV dilatation or thrombus [16]. Cardiac magnetic reso-
nance imaging (MRI) has been used in a limited number of patients
for the assessment of cardiac function and detection of mural thrombi
or myocardial fibrosis; however, the use of gadolinium should be
avoided during pregnancy, as there are theoretical concerns for fetal
nephrogenic toxicity as it crosses the placenta [24-26].
Biomarkers specific for PPCM in relation to normal physiological
conditions in peripartum women are urgently needed for early diagno-
sis and risk stratification. The high prevalence of elevated N-terminal
pro-BNP, activated cathepsin D, and 16-kd prolactin in the serum
of PPCM patients may be helpful in determining a disease-specific
biomarker profile. To aid in early detection, a self-test has been
developed by Fett [27] and summarized in Table 1 to assist patients in
distinguishing normal-term pregnancy and postpartum signs and
symptoms. Although it has yet to be systemically validated, it can be
useful reminder for clinicians and serve as a reference point for response
to treatment [27].
2.1.4. Treatment considerations
At present, PPCM is listed as a form of dilated cardiomyopathy
(DCM) by the National Heart, Lung, and Blood Institute [28] and is treat-
ed according to the guidelines for DCM without specific recommenda-
tions for therapy targeting pregnant or lactating women [7]. Table 2
illustrates recommendations for select cardiac drug use in pregnancy
adapted from the European Society of Gynecology Guidelines on the
Management of Cardiovascular Disease During Pregnancy [29]. The fol-
lowing important drug alterations should be considered. Angiotensin-
converting enzyme (ACE) inhibitors are contraindicated in pregnancy
due to the risk of fetal renal failure. Hydralazine should be considered
the drug of choice for afterload reduction until the patient has delivered.
Spironolactone has been associated with virilization of female fetuses.
Treatment otherwise includes standard pharmacotherapy for HF with
β-blockers, vasodilators, inotropes, digoxin, and diuretics [7,30]. Small
trials have shown the addition of bromocriptine, a dopamine D2
receptor agonist that blocks prolactin, appeared to improve LVEF and
a composite clinical outcome in women with acute severe PPCM
[3,30]. In addition, pentoxifylline, in addition to conventional therapy,
improved combined clinical end points of functional status, cardiac
function, and death [31].
Patients with PPCM have an increased risk of thromboembolic com-
plications due to the hypercoaguable state associated with pregnancy as
well as the prothrombotic effects associated with HF, specifically LVEF
less than 35%, due to abnormal blood flow, blood stasis, and endothelial
dysfunction [16,32]. Anticoagulation can be considered in these
patients, but the actual risk of venous thromboembolism is unknown
[33]. Expert recommendations favor anticoagulation in patients with
very low LVEF using unfractionated or low-molecular-weight heparin,
as warfarin is contraindicated due to its fetotoxicity [29].
If maximal medical therapy fails, an LV assist device may be imple-
mented as a bridge to recovery considering a significant proportion of
patients normalize their LV function within the first 6 months postpar-
tum [34,35]. In addition, cardiac transplantation is also a viable treat-
ment option for patients who improve clinically but are unsuccessful
in weaning off the LV assist device [35]. Although investigation con-
tinues on the molecular basis of PPCM, controlled trials are also needed
for potential new treatments including apheresis, immunosuppression,
immunoadsorption, and antiviral agents [36,37].
2.1.5. Prognosis
Prognosis of affected women is poor, with reported mortality rates
averaged at 15% worldwide and full recovery in only 23% to 32% of
PPCM patients with continuous deterioration in up to 50% of cases
despite optimal medical treatment [38,39]. Complications associated
with PPCM include severe HF, cardiogenic shock, cardiopulmonary
arrest, arrhythmias, thromboembolic complications, and death [14].
Predictors of complications were LVEF less than 25%, delay of diagnosis,
and failure to prevent or diagnosis thromboembolic disease [40].

Please cite this article as: McGregor AJ, et al, The pregnant heart: cardiac emergencies during pregnancy, Am J Emerg Med (2015), http://
dx.doi.org/10.1016/j.ajem.2015.02.046
 A.J. McGregor et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx 3

Table 1
Self-test for early diagnosis of HF in peripartum cardiomyopathy

Symptom Severity

Orthopnea (difficulty breathing when lying flat) None Need to elevate head Need to elevate ≥45°
0 points 1 point 2 points
Dyspnea (shortness of breath on exertion) None Climbing ≥8 steps Walking on level
0 points 1 point 2 points
Unexplained cough None At night Day and night
0 points 1 point 2 points
Swelling (pitting edema) lower extremities None Below knee Above and below knee
0 points 1 point 2 points
Excessive weight gain during last month of pregnancy b2 lb per week 2-4 lb per week N4 lb per week
0 points 1 point 2 points
Palpitations (sensation of irregular heartbeats) None When lying down at night Day and night, any position
0 points 1 point 2 points

Total score greater than 4 points suggests a need for further evaluation.

2.1.6. Summary 2.2. Acute myocardial infarction in pregnancy

Peripartum/postpartum cardiomyopathy is a potentially life-threatening
condition whose incidence is increasing and can be associated with significant
maternal and fetal morbidity and mortality. Most patients present within the
first 4 months after delivery. Early signs and symptoms of HF, such as dyspnea
on exertion, lower extremity edema, and fatigue, are often mistaken for
pregnancy/peripartum-associated physiological discomfort. Electrocardio-
gram, chest radiograph, and significantly elevated BNP levels can assist clini-
cians in the diagnosis. Echocardiographic evaluation is recommended to
assess LVEF. Treatment is consistent with management of DCM with the ex-
ception to avoid use of teratogenic medications such as ACE inhibitors, Angio-
tensin II Receptor Blockers (ARBs), and warfarin. Early diagnosis is essential
because survival and recovery are both improved by early detection.
Acute myocardial infarction during pregnancy and the puerperium is
an uncommon but catastrophic condition that is usually not associated
with pregnancy. However, the risk of AMI appears to be 3 to 4 times
higher in pregnancy compared with nonpregnant women of reproductive
age. The prevalence of coronary artery disease (CAD) in women increases
with age and comorbidities [41]. With more women delaying childbirth,
the number of pregnant women diagnosed with AMI will likely increase.
Risk factors for CAD in pregnancy are similar to those traditional risk fac-
tors observed in the general population: diabetes, hypertension, tobacco
use, hyperlipidemia, and family history [42]. Additional myocardial in-
farction (MI) risk factors specific to pregnancy include gestational

Table 2
Select drugs for management of cardiac disease in pregnancy adapted from European Society of Cardiology Guidelines on the management of cardiovascular disease during pregnancy

Drugs Classification FDA pregnancy Placenta Transfer to Pregnancy/lactation-related adverse effects

categorya permeable breast milk

Peripartum cardiomyopathy
Digoxin Cardiac glycoside C Yes Yes Unknown
Furosemide Diuretic C Yes Yes Maternal and fetal death (animal studies),
hydronephrosis (animal studies),
potential for higher birth weight
Hydralazine Antihypertensive C Yes Yes Adverse effects on fetal growth (animal studies)
Lisinopril ACE inhibitor D Yes Unknown Adverse effects on fetal growth and survival,
oligohydramnios, prematurity, IUGR, PDA
Metoprolol β-Blocker C Yes Yes Fetal death (animal studies)
Nitrogylcerin Vasodilator C Yes Unknown None known
Spironolactone Aldosterone antagonist C Yes Yes Adverse effects on fetal growth and survival
Warfarin Anticoagulant X Yes No Adverse effects on fetal growth and survival,
bleeding abnormalities
MI
Aspirin Antiplatelet agent D Yes Yes Adverse effects on fetal growth and survival,
bleeding abnormalities,
salicylate intoxication, premature closure
of ductus arteriosus, neonatal acidosis
Clopidogrel Antiplatelet agent B Unknown Unknown None known
Heparin (unfractionated) Anticoagulant C No No Increased resorptions (animal studies)
Cardiac arrest
Amiodarone Antiarrhythmic (class III) D Yes Yes Congenital hypothyroidism/hyperthyroidism,
adverse effects on fetal growth and survival
(animal studies)
Epinephrine α-/β-agonist C Yes Unknown Teratogenic (animal studies)

Abbreviations: FDA, Food and Drug Administration; IUGR, intrauterine growth restriction; PDA, patent ductus arteriosus.
a
Food and Drug Administration pregnancy categories: A, adequate and well-controlled studies have failed to demonstrate a risk to the fetus in the first trimester of pregnancy
(and there is no evidence of risk in later trimesters); B, animal reproduction studies have failed to demonstrate a risk to the fetus, and there are no adequate and well-controlled studies in
pregnant women; C, animal reproduction studies have shown an adverse effect on the fetus, and there are no adequate and well-controlled studies in humans, but potential benefits may
warrant use of the drug in pregnant women despite potential risks; D, there is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing ex-
perience or studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks; X, studies in animals or humans have demonstrated fetal
abnormalities and/or there is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience, and the risks involved in use of the drug
in pregnant women clearly outweigh potential benefits.

Please cite this article as: McGregor AJ, et al, The pregnant heart: cardiac emergencies during pregnancy, Am J Emerg Med (2015), http://
dx.doi.org/10.1016/j.ajem.2015.02.046
4 A.J. McGregor et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
diabetes, gestational hypertension, and preeclampsia/eclampsia as well
as pregnancy itself [43].
Previous pregnancy outcome may predict future risk of ischemic
heart disease. Pregnancies complicated by preeclampsia, especially in
association with intrauterine growth restriction, preterm birth, and ges-
tational diabetes, increase the risk of future ischemic heart disease and
cardiac mortality. It is unclear whether pregnancy unmasks a common
etiology to both conditions that are characterized by metabolic
syndrome and endothelial dysfunction or if the pregnancy complication
itself confers the increased risk [44].
Increasingly recognized cause of acute coronary syndrome (ACS) in
young peripartum or postpartum females with a low atherosclerotic
risk factor burden is spontaneous coronary artery dissection (SCAD) [45].
2.2.1. Epidemiology
The incidence of AMI during pregnancy complicates less than 1 in
10 000 pregnancies [46,47], and when it does occur, it is usually not a
result of plaque rupture as up to one fourth are due to SCAD [48]. The
risk of an MI also differs by race and ethnicity, with black women having
the highest risk compared with white and Hispanic women [47]. Mater-
nal mortality from MI has been estimated to be from 19% to 37% [46]
and is greatest in the third trimester [49]. Most maternal deaths occur
at the time of infarction or within 2 weeks of infarction, usually in
association with labor and delivery. Neonatal mortality has been report-
ed to be less than that of the mother but still elevated (13%-17%) when
compared with the population at large [46,47]. Maternal survival is
generally associated with good fetal outcomes.
2.2.2. Etiology
More commonly, the cause of AMI in pregnancy is SCAD, but it may
also be caused by coronary embolism, vasospasm, thrombus due to a
hypercoagulable state, atherosclerosis, or as a complication of pre-
eclampsia [50]. The cause of SCAD is unclear and seems to be related
to an underlying vascular predisposition exacerbated by pregnancy,
such as connective tissue disorders and vasospasm [51]. When athero-
sclerosis is suspected, the normal physiology of pregnancy can exacer-
bate underlying CAD. The marked increases in blood volume, stroke
volume, and heart rate seen in pregnancy increase myocardial oxygen
demand, whereas physiological anemia and decreased diastolic blood
pressure reduce myocardial oxygen supply [42]. Although MI has been
reported in pregnant women at all stages of pregnancy and postpartum,
it occurs more commonly in the third trimester with an important dis-
tinction that cases of SCAD can occur as early as 2 weeks after concep-
tion [48,52]. There is a higher incidence of anterior wall MI with
multivessel involvement in a large proportion of patients with SCAD,
supporting a generalized rather than localized vessel wall changes in
pregnancy [53].
2.2.3. Diagnostic challenges
The diagnosis of ischemic heart disease and SCAD presenting as an
AMI can be challenging in this population and is not without risk to
the fetus. Clinical presentations include chest pain, dyspnea, HF, ventric-
ular arrhythmia, and cardiogenic shock [52]. Electrocardiography can be
helpful even in cases of SCAD, as it frequently presents with ST-segment
elevations [54]. Measuring cardiac troponin level is the preferred cardi-
ac enzyme, as it is not increased by uterine contractions, which can lead
to a significant increase in myoglobin, creatine kinase, and creatine
kinase-MB [55].
Diagnostic imaging procedures including echocardiography, chest
radiography, angiography, computed tomography and MRI may be indi-
cated and have been used safely in the pregnant patient. The criterion
standard imaging for SCAD is coronary angiography as long as measures
are taken to prevent iatrogenic propagation of the dissection. Computed
tomography with intravenous contrast is an effective diagnostic tool for
SCAD when the coronary arteries are greater than 2 mm in diameter
[56]; however, this modality delivers a relatively large dose of radiation,
Please cite this article as: McGregor AJ, et al, The pregnant heart: cardiac emergencies during pregnancy, Am J Emerg Med (2015), http://
dx.doi.org/10.1016/j.ajem.2015.02.046
which can pose teratogenic effects between the 2nd and 20th week of
embryonic age along with a risk of carcinogenesis in the fetus regardless
of the radiation dose [26]. The iodinated contrast material has also been
associated with neonatal hypothyroidism [57]. Magnetic resonance im-
aging is a good choice to minimize radiation when evaluating for perfu-
sion defects but can be problematic due to length of the study, especially
if the patient is hemodynamically compromised. There is also the con-
cern for teratogenic effects of intravenous gadolinium. Transesophageal
and intravascular echocardiography can also be considered where avail-
able. The choice should balance presumed risk to the pregnant woman
and the fetus with the need to make a diagnosis to preserve maternal
well-being.
Interpretation of diagnostic tests needs to take into account the nor-
mal physiologic changes in the heart and vascular system that occur in
pregnancy, which alters the physical, radiographic, and echocardio-
graphic examinations in both health and disease [58]. The accuracy of
exercise electrocardiography in diagnosing CAD is lower in both non-
pregnant and pregnant women compared to men, and fetal bradycardia
has been reported during maximal exercise in healthy pregnant women
[59]. If exercise stress testing is used to aid in the diagnosis of CAD in
pregnant women, a submaximal exercise protocol with fetal monitoring
is recommended [58]. Fetal radiation exposure during stress testing
with thallium 201 or technetium Tc 99m–labeled sestamibi is approxi-
mately 0.1-0.2 Gy. Because of the lack of an adequate safety profile of ra-
diopharmaceutical agents on a developing fetus, nuclear imaging is best
avoided in pregnancy especially during organogenesis [60]. In the sec-
ond and third trimesters, nuclear imaging may still pose a risk of intra-
uterine growth restriction, central nervous system abnormalities, and
malignancy [42].
Diagnostic coronary angiography may also be considered in preg-
nant patients when ACS is suspected. There are wide variations in fetal
radiation exposure with the use of fluoroscopy making dose calculations
difficult. Appropriate abdominal shielding, use of a brachial or radial ap-
proach, and lower fluoroscopy times can minimize radiation exposure.
2.2.4. Treatment considerations
The optimal medication regimen for AMI in pregnant women is un-
known. Evidence supports the use of salicylates, β-blockers, nitroglycer-
in, calcium antagonists, and heparin when needed during pregnancy
(Table 2) [29]. Heparin is often routinely administered for standard
AMI management, but it should be discontinued if SCAD is identified.
Recent recommendations by the European Society of Cardiology have
suggested the use of clopidogrel only after stenting and refraining
from the use of glycoprotein IIb/IIIa inhibitors, bivalirudin, prasugrel,
and ticagrelor in pregnancy [29]. Treatment for SCAD is considered the
same as for nonpregnant patients and focuses on reducing blood pres-
sure and pulse to decrease shear stress on the vessels along with appro-
priate consultation of vascular or cardiothoracic surgery. Glycoprotein
IIb/IIIa inhibitors and thrombolytics are contraindicated in SCAD, as
there is a potential to extend the intramural hematoma. Conservative
therapy is preferred in the management of stable SCAD patients, as
most dissected segments heal spontaneously [61]. Although the use of
guideline-recommended drug therapy seems desirable for maternal
management of AMI during pregnancy, information on fetal safety for
some of these drugs is limited [62] and may contribute to the observed
lack of standard cardiac medication regimens used and the high rate of
complications in this patient population [53].
Conservative therapies should be considered in pregnant patients to
minimize risks to mother and fetus; however, it is important to remem-
ber the crucial role that intervention can serve when medically neces-
sary. Performing angioplasty in pregnancy carries risks that are
considered similar to those in the nonpregnant patient [42]. According
to the European Society of Cardiology and American College of Cardiol-
ogy/American Heart Association (AHA) guidelines, coronary angioplas-
ty is the preferred reperfusion therapy for ST-segment MI (STEMI) and
unstable patients with non-STEMI during pregnancy [29]. Coronary
 A.J. McGregor et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
revascularization should be used to relieve significant coronary obstruc-
tion in patients with SCAD, but treatment should be restricted to severe
obstructions of proximal segments keeping in mind the risks of propa-
gating the dissection [53].
When considering thrombolytic therapy, pregnancy is considered a
relative contraindication, although evidence for this is based on case re-
ports and case series. As mentioned, thrombolysis is not recommended
if SCAD is suspected, as it will increase the risk of hemorrhage and fur-
ther progression of the dissection [47]. It is also not recommended in pa-
tients with placenta previa or abnormal placental insertion or in those
who are close to term. The risk for hemorrhagic complications increases
when thrombolytics are given at the time of delivery but has been used
successfully when remote from delivery for the treatment of hemody-
namically significant pulmonary embolism.
No studies have compared percutaneous coronary intervention with
thrombolysis in pregnant women with an AMI. Each case must be eval-
uated individually to determine whether revascularization should be
pursued and when necessary perform coronary artery bypass grafting.
2.2.5. Delivery considerations
Labor significantly increases hemodynamic requirements causing an
increased myocardial demand, which can further lead to the risk of MI.
When possible, delivery should be postponed at least 2 weeks in the
cases of maternal ACS [47,63].
2.2.6. Summary
There are several important aspects that differentiate AMI in pregnant
patients from that of nonpregnant patients. Most patients develop their
AMI by mechanisms other than atherosclerotic CAD, such as SCAD. The
diagnosis of AMI is often not suspected in this population, as signs and
symptoms include chest discomfort, dyspnea, and fatigue, which can be
mistaken for normal manifestations of pregnancy. There is frequent
contribution of the left anterior descending coronary arteries resulting
in anterior wall involvement and high incidence of LV dysfunction, HF,
cardiogenic shock, and mortality. Use of thrombolytic therapy has many
risks associated with use in this population, due to the frequency of
SCAD or normal coronary arteries, and should be considered with caution.
Use of guideline-recommended medication regimens and revasculariza-
tion should be measured and used, as the preservation of maternal perfu-
sion and oxygenation is critical to fetal health as well as maternal health.
2.3. Cardiac resuscitation in pregnancy
Maternal cardiac arrest is the most complicated arrest scenario with
2 patients and requiring specialized equipment and multiple teams
(emergency medicine, obstetrical, anesthesia, and neonatal), yet there
is a lack of science in this area of resuscitation [64]. Education and train-
ing are essential to managing a maternal cardiac arrest; however, the
current skill, knowledge, and implementation of existing guidelines
among hospital staff are often lacking [65,66].
2.3.1. Epidemiology
Maternal cardiac arrest occurs at a reported rate of approximately 14
per year, according to the National Registry of CPR [67] and complicates
1 in 30 000 pregnancies in the United States annually [68]. A typical
gravid victim of cardiac arrest is younger in age with fewer underlying
medical conditions than a nonpregnant victim; however, with the
recent trends in delayed childbearing, this demographic may change.
Advances in medical care are leading to successful pregnancies in
women with complex health conditions that are then predisposed to
catastrophic outcomes requiring cardiopulmonary resuscitation (CPR).
2.3.2. Etiology
Available data on maternal mortality indicate the major causes of
maternal cardiac arrest, in order of decreasing frequency, are venous
thromboembolism, preeclampsia, sepsis, amniotic fluid embolism,
Please cite this article as: McGregor AJ, et al, The pregnant heart: cardiac emergencies during pregnancy, Am J Emerg Med (2015), http://
dx.doi.org/10.1016/j.ajem.2015.02.046
5
Table 3
Evidence-based management of cardiac arrest during pregnancy: AHA 2010 Guidelines
Emergency management of cardiac arrest during pregnancy
• Coordinate multiple teams.
• Use usual resuscitation measures including defibrillation and ACLS medications.
• Consider the airway to be difficult.
• Obtain intravenous access above the diaphragm.
• Assign a dedicated timer to document 4 min after onset of maternal arrest.
• Perform perimortem cesarean delivery by 5 min.
• Consider expanded etiology for cause of death.
hemorrhage, trauma, iatrogenic (anesthesia, allergy, drug errors), or
congenital or acquired heart disease [69,70].
2.3.3. Special considerations
2.3.3.1. Physiologic changes effect on resuscitation. The International
Liaison Committee on Resuscitation published the most science on ma-
ternal resuscitation, which led to the AHA 2010 Guideline update in
Table 3, the first evidence-based algorithm for management of cardiac
arrest during pregnancy [71]. It includes what should be the basis for
emergency responses during maternal cardiac arrest.
High-quality CPR with some modifications in the basic and advanced
cardiovascular life support techniques and an understanding of the
physiologic changes that occur in pregnancy are essential to the suc-
cessful resuscitation of a pregnant women and survival of the fetus
[72]. Airway management is more difficult due in part to the increased
vascularity resulting in upper airway edema and a 20% reduction in
functional residual capacity with increased oxygen demand in pregnan-
cy [73]. Ventilation volumes may need to be decreased due to the ele-
vated diaphragm. Chest compressions are performed slightly higher
on the sternum if there is a gravid uterus. Compression of the inferior
vena cava (IVC) by the gravid uterus may interfere with maternal hemo-
dynamics hindering successful resuscitation of the mother [50,71]. One
of the essential techniques is to positioned the pregnant patient with a
wedge under the side so that the gravid uterus is displaced laterally, de-
creasing both aortic and IVC compression.
Pharmacologic agents are given based on electrocardiographic
rhythm and maternal response. Higher doses may be considered to ac-
count for the expanded plasma volume of pregnancy. Defibrillation is
performed according to the recommended advanced cardiac life
support (ACLS) protocol with recommendations that fetal monitors
are removed to prevent electric arcing during defibrillation [71].
2.3.3.2. Perimorteum cesarean delivery. Both resuscitation and obstetric
guidelines suggest that perimortem cesarean delivery (PMCD) be con-
sidered within 4 minutes of maternal collapse if there is no return of
spontaneous circulation (ROSC) with the delivery of the fetus within 5
minutes in women beyond 20 weeks of gestation [71,74]. Infant survival
and neurologic status appear to be inversely proportional to the time
between maternal cardiac arrest and delivery. Despite the recommen-
dation of PMCD within 5 minutes of maternal cardiac arrest, it has
been proposed that infant survival has occurred in deliveries more
than 15 minutes after maternal cardiac arrest. These finding suggest
that considering PMCD is prudent, even when there is a delay after a
cardiac arrest.
The estimated gestational age of the fetus is often difficult to obtain
in an emergency situation. A gross visual estimate of the uterus reaching
the umbilicus at 20 weeks of gestation is often helpful. In addition, bed-
side ultrasonographic estimates may assist in at least determining
roughly the size and trimester of the fetus. Documenting fetal heart
tones before PMCD is not recommended, as it is time consuming and
may negatively impact outcome.
It is important for the clinicians to realize that the delivery of the
fetus is recommended to facilitate maternal resuscitation. One retro-
spective cohort from the Netherlands reported that PMCD was mainly
6 A.J. McGregor et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx

Table 4
Summary recommendations

PPCM • Maintain a high index of suspicion for PPCM in patients whose “normal pregnancy” symptoms of weakness, edema, and dyspnea seem exaggerated.
• Examine the ECG for T-wave and ST-segment abnormalities.
• Suspect PPCM with markedly elevated BNP levels.
• Obtain echocardiography to determine reduced LVEF.
• Avoid the use of teratogenic drugs, such as ACE inhibitors, in the management of HF due to PPCM.
• Consider anticoagulation with heparin in patients with very low LVEF.
AMI • Consider alternative etiologies of AMI, such as SCAD, embolism, vasospasm, and thrombus in pregnant patients
• Recognize that SCAD can present as a STEMI pattern on the ECG.
• Obtain a troponin, as it is the preferred cardiac marker in pregnancy.
• Consider additional diagnostic testing if suspecting SCAD such as angiography, CT, or MRI keeping in mind the potential risks to the fetus.
• Avoid the use of thrombolysis in the management of AMI in pregnant patients, particularly if SCAD is suspected.
Cardiac resuscitation • Assume the pregnant patient has a difficult airway.
• Displace the uterus laterally or place the pregnant patient in the left lateral decubitus position during CPR to relieve compression of the IVC and aorta.
• Consider performing PMCD within 4 min of cardiac arrest if there is no ROSC in pregnant patients beyond 20 wk of gestation.

Abbreviation: CT, computed tomography.

considered for fetal viability; however, after the completion of a training
course on the importance of PMCD for maternal benefit, the frequency
of performed PMCD significantly increased [64]. The indications for
the procedure are for maternal well-being regardless of the fetal status.
2.3.3.3. Therapeutic hypothermia. Previous trials of therapeutic hypother-
mia (TH) for survivors of cardiac arrest have excluded pregnant patients
[75,76]. Pregnancy has traditionally been cited as a contraindication for
treatment with TH due to the theoretical increased risk of impaired coagu-
lation in the bleeding or post-PMCD patient, until the most recent 2010
AHA guidelines where it was recommended on a case-by-case basis
[71,75]. As of December 2012, there have been 2 documented cases of suc-
cessful resuscitation of a pregnant patient and fetus with TH [77]. The over-
all success of TH in the nonpregnant population, combined with its
successful application described in these case reports, suggests that TH
can be offered to pregnant women with ROSC after resuscitation [77].
2.3.3.4. Summary. Various obstetric and nonobstetric causes can lead to
cardiac arrest in pregnant women. Whatever the cause, an understand-
ing of basic resuscitation principles and the specific challenges that cli-
nicians face when cardiac arrest occurs in pregnancy is essential to
optimize the chances of survival for both the mother and the fetus. In
general, consider difficult airway management techniques and perform
ACLS with special attention to displacing the gravid uterus laterally.
Early intervention with PMCD is strongly supported in the course of a
cardiopulmonary arrest at advanced gestational age, as the delivery is
considered a resuscitative intervention to improve maternal outcome.
3. Conclusion
The normal changes that occur during pregnancy are demanding on
the cardiovascular system. A high index of suspicion, timely diagnosis,
and effective management of cardiovascular emergencies in pregnancy
are crucial. Despite the fact that cardiac disease in pregnancy encom-
passes a large spectrum of pathologic conditions, their management is
very similar to that of nonpregnant patients. Critical differences are
summarized in Table 4 and include avoiding use of ACE inhibitors during
decompensated HF and using percutaneous coronary intervention in-
stead of thrombolysis when institutionally available. Although there are
important subtle differences in cardiac conditions, such as PPCM, AMI,
and cardiac resuscitation in the pregnant patient, the overall emergency
management guidelines remain the same keeping in mind the critical no-
tion that survival of the fetus depends on the health of the mother.
References
[1] World Health Organization. Maternal mortality in 1990-2013. United States of
America: WHO, UNICEF, UNFPA, The World Bank, and United Nations Population Di-
vision Maternal Mortality Estimation Inter-Agency Group; 2013.
[2] Mathews TJ, Hamilton HE. Delayed childbearing: more women are having their first
child later in life. NCHS Data Brief; 2009 1–8.
[3] Yamac H, Bultmann I, Sliwa K, Hilfiker-Kleiner D. Prolactin: a new therapeutic target
in peripartum cardiomyopathy. Heart 2010;96:1352–7.
[4] Sliwa K, Hilfiker-Kleiner D, Mebazaa A, Petrie MC, Maggioni AP, Regitz-Zagrosek V,
et al. EURObservational Research Programme: a worldwide registry on peripartum
cardiomyopathy (PPCM) in conjunction with the Heart Failure Association of the
European Society of Cardiology Working Group on PPCM. Eur J Heart Fail 2014;16:
583–91.
[5] Mielniczuk LM, Williams K, Davis DR, Tang AS, Lemery R, Green MS, et al. Frequency
of peripartum cardiomyopathy. Am J Cardiol 2006;97:1765–8.
[6] Martin JA, Hamilton BE, Sutton PD, Ventura SJ, Mathews TJ, Kirmeyer S, et al. Births:
final data for 2007. Natl Vital Stat Rep 2010;58:1–85.
[7] Sliwa K, Fett J, Elkayam U. Peripartum cardiomyopathy. Lancet 2006;368:687–93.
[8] Elkayam U. Clinical characteristics of peripartum cardiomyopathy in the United
States: diagnosis, prognosis, and management. J Am Coll Cardiol 2011;58:659–70.
[9] Sliwa K, Forster O, Libhaber E, Fett JD, Sundstrom JB, Hilfiker-Kleiner D, et al. Peripar-
tum cardiomyopathy: inflammatory markers as predictors of outcome in 100 pro-
spectively studied patients. Eur Heart J 2006;27:441–6.
[10] Hilfiker-Kleiner D, Sliwa K. Pathophysiology and epidemiology of peripartum car-
diomyopathy. Nat Rev Cardiol 2014;11:364–70.
[11] Halkein J, Tabruyn SP, Ricke-Hoch M, Haghikia A, Nguyen NQ, Scherr M, et al.
MicroRNA-146a is a therapeutic target and biomarker for peripartum cardiomyopa-
thy. J Clin Invest 2013;123:2143–54.
[12] Selle T, Renger I, Labidi S, Bultmann I, Hilfiker-Kleiner D. Reviewing peripartum car-
diomyopathy: current state of knowledge. Futur Cardiol 2009;5:175–89.
[13] Pearson GD, Veille JC, Rahimtoola S, Hsia J, Oakley CM, Hosenpud JD, et al. Peripar-
tum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare
Diseases (National Institutes of Health) workshop recommendations and review.
JAMA 2000;283:1183–8.
[14] Goland S, Modi K, Bitar F, Janmohamed M, Mirocha JM, Czer LS, et al. Clinical profile and
predictors of complications in peripartum cardiomyopathy. J Card Fail 2009;15:645–50.
[15] Gunderson EP, Croen LA, Chiang V, Yoshida CK, Walton D, Go AS. Epidemiology of
peripartum cardiomyopathy: incidence, predictors, and outcomes. Obstet Gynecol
2011;118:583–91.
[16] Sliwa K, Hilfiker-Kleiner D, Petrie MC, Mebazaa A, Pieske B, Buchmann E, et al. Cur-
rent state of knowledge on aetiology, diagnosis, management, and therapy of peri-
partum cardiomyopathy: a position statement from the Heart Failure Association
of the European Society of Cardiology Working Group on peripartum cardiomyopa-
thy. Eur J Heart Fail 2010;12:767–78.
[17] Desai D, Moodley J, Naidoo D. Peripartum cardiomyopathy: experiences at King Ed-
ward VIII Hospital, Durban, South Africa and a review of the literature. Trop Dr 1995;
25:118–23.
[18] Diao M, Diop IB, Kane A, Camara S, Kane A, Sarr M, et al. Electrocardiographic record-
ing of long duration (Holter) of 24 hours during idiopathic cardiomyopathy of the
peripartum. Arch Mal Coeur Vaiss 2004;97:25–30.
[19] Tibazarwa K, Lee G, Mayosi B, Carrington M, Stewart S, Sliwa K. The 12-lead ECG in
peripartum cardiomyopathy. Cardiovasc J Afr 2012;23:322–9.
[20] Hameed AB, Chan K, Ghamsary M, Elkayam U. Longitudinal changes in the B-type
natriuretic peptide levels in normal pregnancy and postpartum. Clin Cardiol 2009;
32:E60–2.
[21] Forster O, Hilfiker-Kleiner D, Ansari AA, Sundstrom JB, Libhaber E, Tshani W, et al. Rever-
sal of IFN-gamma, oxLDL and prolactin serum levels correlate with clinical improve-
ment in patients with peripartum cardiomyopathy. Eur J Heart Fail 2008;10:861–8.
[22] Chemnitz G, Nevermann L, Schmidt E, Schmidt FW, Lobers J. Creatine kinase (EC-
No.2.7.3.2) and creatine kinase isoenzymes during pregnancy and labor and in the
cord blood. Clin Biochem 1979;12:277–81.
[23] Witlin AG, Mabie WC, Sibai BM. Peripartum cardiomyopathy: a longitudinal echo-
cardiographic study. Am J Obstet Gynecol 1997;177:1129–32.
[24] Ntusi NB, Chin A. Characterisation of peripartum cardiomyopathy by cardiac mag-
netic resonance imaging. Eur Radiol 2009;19:1324–5 [author reply 6–7].
[25] Leurent G, Baruteau AE, Larralde A, Ollivier R, Schleich JM, Boulmier D, et al. Contri-
bution of cardiac MRI in the comprehension of peripartum cardiomyopathy patho-
genesis. Int J Cardiol 2009;132:e91–3.

Please cite this article as: McGregor AJ, et al, The pregnant heart: cardiac emergencies during pregnancy, Am J Emerg Med (2015), http://
dx.doi.org/10.1016/j.ajem.2015.02.046
 A.J. McGregor et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
[26] Chen MM, Coakley FV, Kaimal A, Laros Jr RK. Guidelines for computed tomography
and magnetic resonance imaging use during pregnancy and lactation. Obstet
Gynecol 2008;112:333–40.
[27] Fett JD. Validation of a self-test for early diagnosis of heart failure in peripartum car-
diomyopathy. Crit Pathw Cardiol 2011;10:44–5.
[28] National Heart, Lung, and Blood Institute. Other names for cardiomyopathy; 2011.
[29] European Society of G, Association for European Paediatric C, German Society for
Gender M, Regitz-Zagrosek V, Blomstrom Lundqvist C, Borghi C, et al. ESC Guidelines
on the management of cardiovascular diseases during pregnancy: the Task Force on
the Management of Cardiovascular Diseases during Pregnancy of the European
Society of Cardiology (ESC). Eur Heart J 2011;32:3147–97.
[30] Sliwa K, Blauwet L, Tibazarwa K, Libhaber E, Smedema JP, Becker A, et al. Evaluation
of bromocriptine in the treatment of acute severe peripartum cardiomyopathy: a
proof-of-concept pilot study. Circulation 2010;121:1465–73.
[31] Sliwa K, Woodiwiss A, Candy G, Badenhorst D, Libhaber C, Norton G, et al. Effects of
pentoxifylline on cytokine profiles and left ventricular performance in patients with
decompensated congestive heart failure secondary to idiopathic dilated cardiomy-
opathy. Am J Cardiol 2002;90:1118–22.
[32] Capriola M. Peripartum cardiomyopathy: a review. Int J Womens Health 2013;5:
1–8.
[33] Corriveau S, Cooray M, Douketis J. To thin or not to thin: a case of peripartum cardio-
myopathy. Can J Cardiol 2014;30:835e1–2.
[34] Rasmusson KD, Stehlik J, Brown RN, Renlund DG, Wagoner LE, Torre-Amione G, et al.
Long-term outcomes of cardiac transplantation for peri-partum cardiomyopathy: a
multiinstitutional analysis. J Heart Lung Transplant 2007;26:1097–104.
[35] Zimmerman H, Bose R, Smith R, Copeland JG. Treatment of peripartum cardiomyop-
athy with mechanical assist devices and cardiac transplantation. Ann Thorac Surg
2010;89:1211–7.
[36] Staudt A, Schaper F, Stangl V, Plagemann A, Bohm M, Merkel K, et al.
Immunohistological changes in dilated cardiomyopathy induced by immunoadsorption
therapy and subsequent immunoglobulin substitution. Circulation 2001;103:2681–6.
[37] Cooper Jr LT. The natural history and role of immunoadsorption in dilated cardiomy-
opathy. J Clin Apher 2005;20:256–60.
[38] Brar SS, Khan SS, Sandhu GK, Jorgensen MB, Parikh N, Hsu JW, et al. Incidence, mor-
tality, and racial differences in peripartum cardiomyopathy. Am J Cardiol 2007;100:
302–4.
[39] Modi KA, Illum S, Jariatul K, Caldito G, Reddy PC. Poor outcome of indigent patients
with peripartum cardiomyopathy in the United States. Am J Obstet Gynecol 2009;
201:171e1–5.
[40] Amos AM, Jaber WA, Russell SD. Improved outcomes in peripartum cardiomyopathy
with contemporary. Am Heart J 2006;152:509–13.
[41] Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, Borden WB, et al. Heart dis-
ease and stroke statistics—2012 update: a report from the American Heart Associa-
tion. Circulation 2012;125:e2-220.
[42] Kealey A. Coronary artery disease and myocardial infarction in pregnancy: a review
of epidemiology, diagnosis, and medical and surgical management. Can J Cardiol
2010;26:185–9.
[43] Ladner HE, Danielsen B, Gilbert WM. Acute myocardial infarction in pregnancy and
the puerperium: a population-based study. Obstet Gynecol 2005;105:480–4.
[44] James AH, Jamison MG, Biswas MS, Brancazio LR, Swamy GK, Myers ER. Acute myo-
cardial infarction in pregnancy: a United States population-based study. Circulation
2006;113:1564–71.
[45] Tokura M, Taguchi I, Kageyama M, Nasuno T, Nishiyama Y, Koshiji N, et al.
Clinical features of spontaneous coronary artery dissection. J Cardiol 2014;63:119–22.
[46] Badui E, Enciso R. Acute myocardial infarction during pregnancy and puerperium: a
review. Angiology 1996;47:739–56.
[47] Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy.
Ann Intern Med 1996;125:751–62.
[48] Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. J Am Coll
Cardiol 2008;52:171–80.
[49] Chaithiraphan V, Gowda RM, Khan IA, Reimers CD. Peripartum acute myocardial
infarction: management perspective. Am J Ther 2003;10:75–7.
[50] Ueland K, Novy MJ, Peterson EN, Metcalfe J. Maternal cardiovascular dynamics. IV.
The influence of gestational age on the maternal cardiovascular response to posture
and exercise. Am J Obstet Gynecol 1969;104:856–64.
[51] Hampole CV, Philip F, Shafii A, Pettersson G, Anesi GL, Patel JB, et al. Spontaneous
coronary artery dissection in Ehlers-Danlos syndrome. Ann Thorac Surg 2011;92:
1883–4.
Please cite this article as: McGregor AJ, et al, The pregnant heart: cardiac emergencies during pregnancy, Am J Emerg Med (2015), http://
dx.doi.org/10.1016/j.ajem.2015.02.046
7
[52] Vijayaraghavan R, Verma S, Gupta N, Saw J. Pregnancy-related spontaneous coro-
nary artery dissection. Circulation 2014;130:1915–20.
[53] Elkayam U, Jalnapurkar S, Barakkat MN, Khatri N, Kealey AJ, Mehra A, et al.
Pregnancy-associated acute myocardial infarction: a review of contemporary expe-
rience in 150 cases between 2006 and 2011. Circulation 2014;129:1695–702.
[54] Tweet MS, Hayes SN, Pitta SR, Simari RD, Lerman A, Lennon RJ, et al. Clinical features,
management, and prognosis of spontaneous coronary artery dissection. Circulation
2012;126:579–88.
[55] Shade Jr GH, Ross G, Bever FN, Uddin Z, Devireddy L, Gardin JM. Troponin I in the di-
agnosis of acute myocardial infarction in pregnancy, labor, and post partum. Am J
Obstet Gynecol 2002;187:1719–20.
[56] Saw J. Spontaneous coronary artery dissection. Can J Cardiol 2013;29:1027–33.
[57] Gynecology ACoOa. Committee on Obstetric Practice: Guidelines for Diagnostic Im-
aging During Pregnancy. Committee Opinion; 2004[Nmber 299].
[58] Ain DL, Narula J, Sengupta PP. Cardiovascular imaging and diagnostic procedures in
pregnancy. Cardiol Clin 2012;30:331–41.
[59] Carpenter MW, Sady SP, Hoegsberg B, Sady MA, Haydon B, Cullinane EM, et al. Fetal
heart rate response to maternal exertion. JAMA 1988;259:3006–9.
[60] Baggish AL, Boucher CA. Radiopharmaceutical agents for myocardial perfusion imag-
ing. Circulation 2008;118:1668–74.
[61] Saw J, Ricci D, Starovoytov A, Fox R, Buller CE. Spontaneous coronary artery dissec-
tion: prevalence of predisposing conditions including fibromuscular dysplasia in a
tertiary center cohort. J Am Coll Cardiol Intv 2013;6:44–52.
[62] Frishman WH, Elkayam U, Aronow WS. Cardiovascular drugs in pregnancy. Cardiol
Clin 2012;30:463–91.
[63] Hankins GD, Wendel Jr GD, Leveno KJ, Stoneham J. Myocardial infarction during
pregnancy: a review. Obstet Gynecol 1985;65:139–46.
[64] Jeejeebhoy FM, Zelop CM, Windrim R, Carvalho JC, Dorian P, Morrison LJ. Manage-
ment of cardiac arrest in pregnancy: a systematic review. Resuscitation 2011;82:
801–9.
[65] Einav S, Matot I, Berkenstadt H, Bromiker R, Weiniger CF. A survey of labour ward
clinicians' knowledge of maternal cardiac arrest and resuscitation. Int J Obstet
Anesth 2008;17:238–42.
[66] Lipman SS, Daniels KI, Carvalho B, Arafeh J, Harney K, Puck A, et al. Deficits in the
provision of cardiopulmonary resuscitation during simulated obstetric crises. Am J
Obstet Gynecol 2010;203:179e1–5.
[67] Brady WJ, Gurka KK, Mehring B, Peberdy MA, O'Connor RE. American Heart
Association's Get with the Guidelines I. In-hospital cardiac arrest: impact of moni-
toring and witnessed event on patient survival and neurologic status at hospital dis-
charge. Resuscitation 2011;82:845–52.
[68] Farinelli CK, Hameed AB. Cardiopulmonary resuscitation in pregnancy. Cardiol Clin
2012;30:453–61.
[69] Luppi CJ. Cardiopulmonary resuscitation: pregnant women are different. AACN Clin
Issues 1997;8:574–85.
[70] Mallampalli A, Powner DJ, Gardner MO. Cardiopulmonary resuscitation and somatic
support of the pregnant patient. Crit Care Clin 2004;20:747–61.
[71] Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, et al. Part
12: cardiac arrest in special situations: 2010 American Heart Association Guidelines
for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation
2010;122:S829–61.
[72] Kim S, You JS, Lee HS, Lee JH, Park YS, Chung SP, et al. Quality of chest compressions
performed by inexperienced rescuers in simulated cardiac arrest associated with
pregnancy. Resuscitation 2013;84:98–102.
[73] King SE, Gabbott DA. Maternal cardiac arrest—rarely occurs, rarely researched. Re-
suscitation 2011;82:795–6.
[74] Soar J, Perkins GD, Abbas G, Alfonzo A, Barelli A, Bierens JJ, et al. European Resusci-
tation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special
circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypother-
mia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, elec-
trocution. Resuscitation 2010;81:1400–33.
[75] Holzer M. Targeted temperature management for comatose survivors of cardiac ar-
rest. N Engl J Med 2010;363:1256–64.
[76] Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, et al. Treatment
of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N
Engl J Med 2002;346:557–63.
[77] Chauhan A, Musunuru H, Donnino M, McCurdy MT, Chauhan V, Walsh M. The use of
therapeutic hypothermia after cardiac arrest in a pregnant patient. Ann Emerg Med
2012;60:786–9.