Cardiovascular conditions are the leading cause of maternal mortality in the United States, accounting for approximately 25% of all pregnancy-related deaths.^1–4 In fact, cardiovascular disease (CVD) has been increasing as a cause of pregnancy-related mortality relative to prior years, while the proportion of deaths attributable to other common causes, such as hemorrhage and hypertensive disorders, has declined. African-American women are disproportionately represented among pregnancy-related deaths from cardiovascular causes.³

The number of pregnant women with CVD is likely to continue to rise in the future. Advances in healthcare allow the majority of children with congenital heart disease to reach reproductive age. While pregnancy was previously considered prohibitively high risk for many women with complex cardiac lesions, current consensus guidelines include very few conditions among those for which pregnancy is contraindicated (Table 22-1).⁵ In addition to women with congenital heart disease, pregnancy rates among women of advanced maternal age and other risk factors for CVD are increasing.

A multidisciplinary approach, with collaboration between an obstetrician, maternal-fetal medicine specialist, cardiologist, anesthesiologist, neonatologist, and in some cases cardiothoracic surgeon, is critical for the care of a pregnant woman with CVD. This chapter focuses on the role of the OB/GYN Hospitalist in confronting the challenge of CVD in pregnant patients, which requires the following:

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  Foundational knowledge of cardiac physiology and the hemodynamic changes of pregnancy and labor

  
  
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  Early identification of cardiac disease

Significant physiologic changes occur in the cardiac and respiratory systems starting in early pregnancy, and they reverse in the weeks following delivery (Table 22-2). These changes are usually well tolerated by pregnant patients, but they often lead to the onset of new symptoms and can alter physical examination findings and restrict accurate interpretation of diagnostic tests. Further, hemodynamic changes in pregnancy can overwhelm previously compensated cardiac disease.

ANTEPARTUM

Increase in Blood Volume

Blood volume increases starting around 6 to 8 weeks of gestation and reaches its peak at around 32 weeks. Maternal blood volume increases by approximately 40% in singleton pregnancies and nearly 70% in twin pregnancies.^6,7 Red cell mass increases by 20% to 30% due to the increased production of erythrocytes. The disproportionate increase in blood volume relative to red blood cell mass results in physiologic hemodilution and a decrease in hematocrit.⁸

Decrease in Systemic Vascular Resistance and Blood Pressure

Systemic vascular resistance begins to decrease around 5 weeks of gestation, reaches a nadir at approximately 24 weeks gestation, and then begins to increase again.⁹ This is due to the vasodilatory effect of progesterone as well as the creation of a low resistance circuit by the placenta, which is balanced in late pregnancy by the increase in blood volume.

Blood pressure begins to decrease at 7 weeks gestation, mainly due to a decrease in systemic vascular resistance. Blood pressures reach their lowest point at around 24 to 32 weeks gestational age and then gradually rise to prepregnancy levels.^10,11

Of note, position significantly affects blood pressure. While sitting or standing, systolic pressures remain stable throughout pregnancy, while diastolic pressures decrease by approximately 10 mmHg. In the left lateral recumbent position, systolic pressure decreases by 5 to 10 mmHg, while diastolic pressure decreases by 10 to 15 mmHg.

Increase in Cardiac Output

Cardiac output is the product of the stroke volume (the amount of blood pumped from the left ventricle with each heartbeat) and the heart rate. Cardiac output increases by 30% to 50% during pregnancy, with half of the increase occurring by 8 weeks gestation.¹² Twin gestations have an even larger rise in cardiac output.¹³

The increase in cardiac output is due to increases in both heart rate and stroke volume. Stroke volume rises as a result of increased preload and contractility. It rises early and declines slightly at term.^12,14 The heart rate increases starting around 5 weeks of gestation, reaching a maximal increase of 15 to 20 beats per minute by 32 weeks, which is sustained for the duration of pregnancy.^12,15

Position has a large impact on cardiac output. Movement from the left lateral recumbent to the supine position results in a decrease of 25% to 30% due to compression of the vena cava.¹⁶ Some women will experience position-related symptomatic hypotension in the second half of pregnancy, known as supine hypotension syndrome, with lightheadedness and nausea.¹⁷

The percentage of uterine blood flow increases from approximately 2% of the cardiac output in the nonpregnant patient to 17% at term when the uterus receives 450 to 800 mL/min.¹⁸

INTRAPARTUM

Labor is characterized by an increase in cardiac output due to pain, anxiety, and contractions. In the first stage of labor, cardiac output increases by 12% to 31%.^19,20 Contractions result in a return of 300 to 500 mL of blood back into the circulation, leading to an increase in stroke volume. Pain and anxiety increase cardiac output through a rise in the heart rate. The second stage of labor is characterized by an additional increase in cardiac output and large fluctuations in central venous pressure. During Valsalva, increased intrathoracic pressure leads to decreased preload, which results in reduced stroke volume and cardiac output. In response, blood vessels constrict to maintain blood pressure, and heart rate increases; however, cardiac output remains low.

Women with significant cardiovascular compromise are at risk of decompensation during labor. These risks can be minimized with adequate pain control and avoidance of Valsalva with an assisted second stage of labor.

POSTPARTUM

The immediate postpartum period is characterized by blood loss from delivery, while autotransfusion from the return into circulation of blood from the uterus and release of aorto-caval compression by the gravid uterus collectively increase the intravascular volume. Despite delivery-related blood loss, cardiac output normally increases by as much as 60% to 80% immediately following delivery, though this may vary significantly in the event of cesarean section (C-section) or hemorrhage.^19–21 Cardiac output usually remains elevated by approximately 50% for an hour after delivery.²⁰

Due to the autotransfusion and other volume shifts that occur in the immediate postpartum period, women with cardiac compromise are at greatest risk of developing pulmonary edema, which may be fulminant, during this period. Volume status and heart rate generally return to prepregnancy levels over the first 10 days postpartum. Cardiac output, systemic vascular resistance, and other cardiac indices return to prepregnancy levels more gradually for up to 12 to 24 weeks postpartum.¹⁴

Pregnancy is a state of cardiovascular stress. Women with preexisting or new onset cardiac disease present with either heart failure symptoms, arrhythmias, or both. Heart failure usually manifests as shortness of breath, dyspnea upon exertion, orthopnea, fatigue, swelling, and weight gain. Arrhythmia presents with palpitations, dizziness, and syncope, with or without heart failure symptoms.

A brief description of each commonly encountered cardiac condition by the obstetric hospitalist (Box 22-1) is provided; however, an in-depth discussion of the clinical course and management of each of them is beyond the scope of this chapter.

PERIPARTUM CARDIOMYOPATHY

Peripartum cardiomyopathy is a dilated cardiomyopathy presenting in the last month of pregnancy or within five months postpartum, resulting in depressed left ventricular systolic function. The exact etiology remains unknown. Diagnosis is made by an echocardiogram showing ejection fraction <45% or fractional shortening <30%. Additional criteria include absence of an identifiable cause for heart failure and absence of recognizable heart disease prior to the last month of pregnancy.²² Of note, approximately 20% of cases of peripartum cardiomyopathy present in the second or early third trimester. Patients with early onset disease have a similar presentation and natural course as those with onset of disease near term.²³

Following delivery, approximately 50% of patients with peripartum cardiomyopathy will experience normalization of left ventricular ejection fraction, while the remainder will have persistently compromised cardiac function.^23,24 Of women with normalization of cardiac function, approximately 20% will experience recurrence in subsequent pregnancy. Women with persistent left ventricular dysfunction have an even greater risk of recurrence and significant risk of death in subsequent pregnancies.²⁵ For this reason, pregnancy is contraindicated for women with persistent left ventricular dysfunction following delivery.

MYOCARDIAL INFARCTION/CORONARY ARTERY DISEASE

Pregnant women generally present with either chest pain or pressure with accompanying chest pain. Cardiac ischemia should always be considered in the differential. Electrocardiography (EKG) and cardiac enzymes are required to make the diagnosis. It is interesting to note that a relatively large percentage of myocardial infarctions in pregnancy are due to coronary artery dissection rather than the conventional cause, atherosclerotic coronary artery disease.

VALVULAR HEART DISEASE

Valvular heart disease may be congenital or acquired. Mitral valve stenosis remains the most common valvular lesion in women of childbearing age, followed by mitral regurgitation, aortic stenosis, and aortic regurgitation.

To decrease the risk of decompensation, goals for managing patients with valvular heart disease include detecting and controlling arrhythmias and carefully managing fluid balances, pain, and anesthesia-related blood pressure changes. Each type of lesion also carries its own specific risks and associated goals (Table 22-3).

Mitral Stenosis

Nearly all cases of mitral stenosis are the result of rheumatic heart disease.²⁶ Other causes include congenital mitral stenosis, systemic lupus erythematosus (SLE), and rheumatoid arthritis.

Mitral stenosis restricts blood flow from the left atrium to the left ventricle during diastole. Patients with mitral stenosis may experience decompensation during pregnancy as a result of increased plasma volume and increased heart rate. The increase in plasma volume can result in dilation of the left atrium and elevated left atrial pressure. An elevated heart rate results in decreased diastolic filling time, which can further increase left atrial pressure. This can lead to increased pulmonary vein pressure and resultant heart failure symptoms. Left atrial dilation may also provoke tachyarrhythmias, including atrial fibrillation, which can lead to further decompensation. In addition, patients with arrhythmias have an increased risk of venous thromboembolism (VTE).

Mitral Regurgitation

The most common cause of mitral regurgitation is mitral valve prolapse, which is seen in approximately 50% of cases. Other causes include ischemic heart disease, dilated cardiomyopathy, rheumatic fever, and Marfan syndrome.

Mitral regurgitation is characterized by a mitral valve that does not close properly during systole, leading to leakage of blood from the left ventricle into the left atrium. Pregnant patients generally tolerate mitral regurgitation well, as the decreased systemic vascular resistance that is normal in pregnancy favors forward blood flow. However, women with severe mitral regurgitation may experience left atrial enlargement and consequent arrhythmia or congestive heart failure.

Aortic Stenosis