Pregnancy and Heart Disease

Pregnancy and Heart Disease

Anjli Maroo, Russell Raymond

Cardiac diseases complicate 1% to 4% of pregnancies in women without preexisting cardiac abnormalities. A working knowledge of the normal physiology of pregnancy is often helpful in the management of patients with heart disease. Patients with preexisting cardiac lesions should be counseled in advance about the risk of pregnancy. Women who develop cardiac disorders during pregnancy should be followed closely and counseled about future cardiac risks. Familiarity with the treatment of commonly encountered cardiac diseases during pregnancy is becoming increasingly important for internists and cardiologists as they join the team of obstetricians and anesthesiologists in the care of these complicated patients.

NORMAL PHYSIOLOGIC CHANGES DURING PREGNANCY

Major hemodynamic changes occur during pregnancy, during labor and delivery, and in the postpartum period (Table 1). These changes begin to take place in the first 5 to 8 weeks of gestation and reach their peak late in the second trimester. In patients with preexisting cardiac disease, cardiac decompensation often coincides with this peak.

Table 1 Normal Hemodynamic Changes During Pregnancy

Blood volume increases 40 to 50% during normal pregnancy. The rise in blood volume is greater than the increase in red blood cell mass, contributing to the fall in hemoglobin concentration, otherwise known as the anemia of pregnancy. Similarly, cardiac output rises 30% to 50% above baseline, peaking by the end of the second trimester and reaching a plateau until delivery. The increase in cardiac output is achieved by three factors: an increase in preload due to greater blood volume, reduced afterload due to a fall in systemic vascular resistance, and a rise in the maternal heart rate by 10 to 15 beats per minute. Stroke volume increases during the first and second trimesters but declines in the third trimester due to compression of the inferior vena cava by the uterus. Blood pressure typically falls about 10 mm Hg below baseline by the end of the second trimester due to reduction in systemic vascular resistance and to addition of new blood vessels in the uterus and placenta.

During labor and delivery, hemodynamic fluctuations can be profound. Each uterine contraction displaces 300 to 500 mL of blood into the general circulation. Stroke volume increases, with a resultant rise in cardiac output by an additional 50% with each contraction. Thus, it is possible for the cardiac output during labor and delivery to be 75% above baseline. Mean arterial pressure also rises, in part due to maternal pain and anxiety. Blood loss during delivery (300-400 mL for a vaginal delivery and 500-800 mL for a cesarian section) can contribute to hemodynamic stress.

The hemodynamic changes during the postpartum state are equally dramatic. Relief of inferior vena caval compression results in an increase in venous return, which in turn augments cardiac output and causes a brisk autodiuresis. The hemodynamic changes return to the prepregnant baseline within 2 to 4 weeks following vaginal delivery and within 4 to 6 weeks after cesarean section.

These marked hemodynamic changes during pregnancy account for the development of several signs and symptoms during normal pregnancy that can mimic signs and symptoms of heart disease. Normal pregnancy is typically associated with fatigue, dyspnea, and decreased exercise capacity. Pregnant women usually have mild peripheral edema and jugular venous distension. Most pregnant women have audible physiologic systolic murmurs created by augmented blood flow. A physiologic third heart sound (S₃), reflecting increased blood volume, can sometimes be auscultated. Signs and symptoms that are abnormal during pregnancy include exertional chest pain, paroxysmal nocturnal dyspnea, orthopnea, sustained atrial or ventricular arrhythmias, pulmonary edema, severe obstructive systolic murmurs, diastolic murmurs, and an S₄ gallop.

Noninvasive testing of the heart may include an electrocardiogram, a chest radiograph, plasma Brain natriuretic peptide (BNP) testing, and an echocardiogram. The electrocardiogram may reveal a leftward shift of the electrical axis, especially during the third trimester when the diaphragm is pushed upward by the uterus. Routine chest radiographs should be avoided, especially in the first trimester. BNP is typically low during normal pregnancy (usually <20 pg/mL); elevations in BNP are a useful guide in managing early cardiac dysfunction and the hypertensive disorders of pregnancy. Echocardiography is an invaluable tool for the diagnosis and evaluation of suspected cardiac disease in the pregnant patient. Normal changes attributable to pregnancy include increased left ventricular mass and dimensions.

ASSESSMENT OF RISK IN PATIENTS WITH PREEXISTING CARDIAC DISEASE

Maternal and Fetal Outcomes

Ideally, women with known preexisting cardiac lesions should discuss the impact of their heart condition on pregnancy well in advance of their pregnancy. They should discuss contraception, the maternal and fetal risks of pregnancy, and the potential long-term maternal morbidity and mortality with their physicians. Combined input from maternal-fetal medicine specialists, the patient’s obstetrician, and a cardiologist may be a great asset in managing the pregnancy.

Certain preexisting cardiac conditions carry extremely high maternal risk. Pregnancy in these patients is not advised; it is important for women with these conditions to understand the implications of pregnancy on their health. For example, women with NYHA functional class III and IV heart failure face a mortality rate upwards of 7% and a morbidity rate of more than 30% during pregnancy.

A validated cardiac risk score has been shown to predict a woman’s chance of having adverse cardiac complications during pregnancy (Table 2).^1,² Each risk factor was given a value of one point. The maternal cardiac event rates for 0, 1, and greater than 1 points are 5%, 27%, and 75%, respectively.

Table 2 Predictors of Maternal Risk for Cardiac Complications ²

Criteria	Example	Points*
Prior cardiac events	heart failure, transient ischemic attack, stroke before present pregnancy	1
Prior arrhythmia	symptomatic sustained tachyarrhythmia or bradyarrhythmia requiring treatment	1
NYHA III/IV or cyanosis		1
Valvular and outflow tract obstruction	aortic valve area <1.5 cm², mitral valve area <2 cm², or left ventricular outflow tract peak gradient > 30 mm Hg	1
Myocardial dysfunction	LVEF <40% or restrictive cardiomyopathy or hypertrophic cardiomyopathy	1

LVEF, left ventricular ejection fraction; NYHA, New York Heart Association.

* Maternal cardiac event rate for 0,1, and >1 points is 5%, 27%, and 75%, respectively.

Specific Congenital or Acquired Cardiac Lesions

Specific congenital or acquired cardiac lesions can be classified as low, intermediate, or high risk during pregnancy (Box 1).

Box 1
Maternal Cardiac Lesions and Risk of Cardiac Complications During Pregnancy

Low-Risk Lesions

Young women with uncomplicated secundum-type atrial septal defect (ASD) or isolated ventricular septal defect (VSD) usually tolerate pregnancy well. Patent ductus arteriosus (PDA) is not associated with additional maternal risk for cardiac complications if the shunt is small to moderate and if pulmonary artery pressures are normal. Once these shunts are repaired, the risk during pregnancy is minimal. It is unusual for women with such left-to-right shunts to develop pulmonary hypertension during the childbearing years; however, the presence of pulmonary hypertension with a left-to-right shunt increases the risk of complications during pregnancy substantially.

Chronic mitral regurgitation most commonly is the result of myxomatous degeneration or rheumatic heart disease and usually is well tolerated during pregnancy. However, new-onset atrial fibrillation or severe hypertension can precipitate hemodynamic deterioration. Acute mitral regurgitation (e.g., from rupture of chordae tendineae) can produce flash pulmonary edema and life-threatening cardiac decompensation. Women with severe mitral regurgitation and signs of cardiac decompensation before pregnancy are advised to undergo operative repair before conception. If valve repair is not possible, the decision to undergo valve replacement before conception should be carefully assessed on an individual basis, taking into account the patient’s age, clinical status, and plans for future childbearing. Mitral valve prolapse in isolation rarely causes any difficulties during pregnancy.

Aortic regurgitation may be encountered in women with rheumatic heart disease, a congenitally bicuspid or deformed aortic valve, infective endocarditis, or connective tissue disease. Aortic regurgitation generally is well tolerated during pregnancy. Ideally, women with severe aortic regurgitation and signs of cardiac decompensation should undergo operative repair before conception. As with the mitral valve, the decision to undergo valve replacement befoer conception requires careful consideration. Women with bicuspid aortic valves, with or without aortic regurgitation, are at increased risk for aortic dissection and should be followed carefully for signs and symptoms of this complication. Young women who are discovered to have a biscupid aortic valve should be screened for concomitant aortic coarctation.

Congestive heart failure from either mitral or aortic regurgitation can be treated with digoxin, diuretics, and vasodilators such as hydralazine. Angiotensin-converting enzyme (ACE) inhibitors are teratogenic and therefore contraindicated. Beta blockers are generally safe during pregnancy, although fetal bradycardia and growth retardation have been reported.

Moderate-Risk Lesions

Mitral Stenosis

Mitral stenosis in women of childbearing age is most often rheumatic in origin. Patients with moderate to severe mitral stenosis often experience hemodynamic deterioration during the third trimester or during labor and delivery. The physiologic increase in blood volume and rise in heart rate lead to an elevation of left atrial pressure, resulting in pulmonary edema. Additional displacement of blood volume into the systemic circulation during contractions makes labor particularly hazardous.

The development of atrial fibrillation in the pregnant patient with mitral stenosis can result in rapid decompensation. Digoxin and beta blockers can be used to reduce heart rate, and diuretics can be used to gently reduce the blood volume and left atrial pressure. With atrial fibrillation and hemodynamic deterioration, electrocardioversion can be performed safely. The development of atrial fibrillation increases the risk of stroke, necessitating the initiation of anticoagulation (see “Medication Guidelines During Pregnancy,” later).

Mild mitral stenosis can often be managed with careful medical therapy during pregnancy. In contrast, patients with moderate to severe mitral stenosis should be referred to a cardiologist. Severe mitral stenosis is associated with a high likelihood of maternal complications (including pulmonary edema and arrhythmias) or fetal complications (including premature birth, low birth weight, respiratory distress, and fetal or neonatal death), approaching 80% of pregnancies.³ These women can require correction via operative repair or replacement or via percutaneous mitral balloon valvotomy before conception. If severe mitral stenosis is discovered during pregnancy, medical therapy with diuretics and digoxin is preferred. If symptoms cannot be controlled with medical therapies, percutaneous valvotomy can be performed in the second or third trimesters to prevent fetal radiation exposure during the first trimester. Treatment options for patients with mitral stenosis are summarized in Figure 1.

Figure 1 Management strategy for patients with mitral stenosis before and during pregnancy.

Algorithm for the management of mitral stenosis in the pregnant patient. MS, mitral stenosis; PBMV, percutaneous balloon mitral valvuloplasty.

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Jul 18, 2017 | Posted by admin in GENERAL SURGERY | Comments Off

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