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

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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 b

Department of Emergency Medicine, Warren Alpert Medical School of Brown University, Providence, RI, 02903 Department of Medicine, Warren Alpert Medical School of Brown University, Providence, RI, 02903

a r t i c l e

i n f o

Article history: Received 12 January 2015 Received in revised form 23 February 2015 Accepted 24 February 2015 Available online xxxx

a b s t r a c t Background: Cardiovascular emergencies in pregnant patients are often considered a rare event; however, heart disease as a cause of maternal mortality is steadily increasing. Discussion: In this article, we review 3 common cardiovascular emergencies and the important subtle differences in their treatment in the pregnant patient: peripartum/postpartum cardiomyopathy, acute myocardial infarction, 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 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 pregnancy 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: [email protected] (A.J. McGregor).

The authors include experienced emergency medicine physicians 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 functional 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

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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

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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 annual number of new patients with PPCM in the United States is approximately 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 abnormalities, 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 endothelium, cardiac vasculature, and cardiomyocyte function [11]. 2.1.3. Diagnostic challenges Previously healthy women will present with sudden onset symptoms 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 differentiate PPCM early in the course of the disease. Further complicating the diagnosis are mild cases of PPCM, which may evade clinical attention [15], and atypical presentations as a result of thromboembolic 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 presented 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 myocardial 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 additional increase in plasma concentration of BNP or N-terminal pro-BNP as a result of the elevated LV end-diastolic pressure due to systolic dysfunction [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]. Echocardiography is the keystone in the diagnosis of PPCM and essential in detecting the reduced LV ejection fraction (LVEF) as well as evaluating the presence of LV dilatation or thrombus [16]. Cardiac magnetic resonance 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 diagnosis 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 treated according to the guidelines for DCM without specific recommendations 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 following important drug alterations should be considered. Angiotensinconverting 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 complications 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 implemented as a bridge to recovery considering a significant proportion of patients normalize their LV function within the first 6 months postpartum [34,35]. In addition, cardiac transplantation is also a viable treatment option for patients who improve clinically but are unsuccessful in weaning off the LV assist device [35]. Although investigation continues 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

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

Severity

Orthopnea (difficulty breathing when lying flat)

None 0 points None 0 points None 0 points None 0 points b2 lb per week 0 points None 0 points

Dyspnea (shortness of breath on exertion) Unexplained cough Swelling (pitting edema) lower extremities Excessive weight gain during last month of pregnancy Palpitations (sensation of irregular heartbeats)

Need to elevate head 1 point Climbing ≥8 steps 1 point At night 1 point Below knee 1 point 2-4 lb per week 1 point When lying down at night 1 point

Need to elevate ≥45° 2 points Walking on level 2 points Day and night 2 points Above and below knee 2 points N4 lb per week 2 points Day and night, any position 2 points

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

2.1.6. Summary 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. Electrocardiogram, chest radiograph, and significantly elevated BNP levels can assist clinicians in the diagnosis. Echocardiographic evaluation is recommended to assess LVEF. Treatment is consistent with management of DCM with the exception to avoid use of teratogenic medications such as ACE inhibitors, Angiotensin II Receptor Blockers (ARBs), and warfarin. Early diagnosis is essential because survival and recovery are both improved by early detection.

2.2. Acute myocardial infarction in pregnancy 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 factors observed in the general population: diabetes, hypertension, tobacco use, hyperlipidemia, and family history [42]. Additional myocardial infarction (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 categorya

Placenta permeable

Transfer to breast milk

Pregnancy/lactation-related adverse effects

Peripartum cardiomyopathy Digoxin Furosemide

Cardiac glycoside Diuretic

C C

Yes Yes

Yes Yes

Hydralazine Lisinopril

Antihypertensive ACE inhibitor

C D

Yes Yes

Yes Unknown

Metoprolol Nitrogylcerin Spironolactone Warfarin

β-Blocker Vasodilator Aldosterone antagonist Anticoagulant

C C C X

Yes Yes Yes Yes

Yes Unknown Yes No

Unknown Maternal and fetal death (animal studies), hydronephrosis (animal studies), potential for higher birth weight Adverse effects on fetal growth (animal studies) Adverse effects on fetal growth and survival, oligohydramnios, prematurity, IUGR, PDA Fetal death (animal studies) None known Adverse effects on fetal growth and survival Adverse effects on fetal growth and survival, bleeding abnormalities

MI Aspirin

Antiplatelet agent

D

Yes

Yes

Clopidogrel Heparin (unfractionated) Cardiac arrest Amiodarone

Antiplatelet agent Anticoagulant

B C

Unknown No

Unknown No

Antiarrhythmic (class III)

D

Yes

Yes

Epinephrine

α-/β-agonist

C

Yes

Unknown

Adverse effects on fetal growth and survival, bleeding abnormalities, salicylate intoxication, premature closure of ductus arteriosus, neonatal acidosis None known Increased resorptions (animal studies) Congenital hypothyroidism/hyperthyroidism, adverse effects on fetal growth and survival (animal studies) 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 experience 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.

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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 gestational 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]. Maternal 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 reported 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 preeclampsia [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 atherosclerosis is suspected, the normal physiology of pregnancy can exacerbate 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 distinction that cases of SCAD can occur as early as 2 weeks after conception [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, ventricular 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 cardiac 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 indicated 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,

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 imaging is a good choice to minimize radiation when evaluating for perfusion defects but can be problematic due to length of the study, especially if the patient is hemodynamically compromised. There is also the concern for teratogenic effects of intravenous gadolinium. Transesophageal and intravascular echocardiography can also be considered where available. 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 normal physiologic changes in the heart and vascular system that occur in pregnancy, which alters the physical, radiographic, and echocardiographic examinations in both health and disease [58]. The accuracy of exercise electrocardiography in diagnosing CAD is lower in both nonpregnant 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 approximately 0.1-0.2 Gy. Because of the lack of an adequate safety profile of radiopharmaceutical agents on a developing fetus, nuclear imaging is best avoided in pregnancy especially during organogenesis [60]. In the second and third trimesters, nuclear imaging may still pose a risk of intrauterine growth restriction, central nervous system abnormalities, and malignancy [42]. Diagnostic coronary angiography may also be considered in pregnant 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 approach, and lower fluoroscopy times can minimize radiation exposure. 2.2.4. Treatment considerations The optimal medication regimen for AMI in pregnant women is unknown. Evidence supports the use of salicylates, β-blockers, nitroglycerin, 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 pressure and pulse to decrease shear stress on the vessels along with appropriate 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 remember the crucial role that intervention can serve when medically necessary. 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 Cardiology/American Heart Association (AHA) guidelines, coronary angioplasty is the preferred reperfusion therapy for ST-segment MI (STEMI) and unstable patients with non-STEMI during pregnancy [29]. Coronary

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

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revascularization should be used to relieve significant coronary obstruction in patients with SCAD, but treatment should be restricted to severe obstructions of proximal segments keeping in mind the risks of propagating the dissection [53]. When considering thrombolytic therapy, pregnancy is considered a relative contraindication, although evidence for this is based on case reports and case series. As mentioned, thrombolysis is not recommended if SCAD is suspected, as it will increase the risk of hemorrhage and further progression of the dissection [47]. It is also not recommended in patients 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 hemodynamically significant pulmonary embolism. No studies have compared percutaneous coronary intervention with thrombolysis in pregnant women with an AMI. Each case must be evaluated 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 revascularization should be measured and used, as the preservation of maternal perfusion 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 training 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,

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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 maternal 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 successful 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 pregnancy [73]. Ventilation volumes may need to be decreased due to the elevated 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 hemodynamics 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, decreasing both aortic and IVC compression. Pharmacologic agents are given based on electrocardiographic rhythm and maternal response. Higher doses may be considered to account 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 considered 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 recommendation 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, bedside 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 retrospective cohort from the Netherlands reported that PMCD was mainly

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

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Table 4 Summary recommendations • • • • • • AMI • • • • • Cardiac resuscitation • • •

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. 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. 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 hypothermia (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 coagulation 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 successful resuscitation of a pregnant patient and fetus with TH [77]. The overall 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 understanding of basic resuscitation principles and the specific challenges that clinicians 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 encompasses 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 instead 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 notion 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 Division Maternal Mortality Estimation Inter-Agency Group; 2013.

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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