HEART DISEASE AND PREGNANCY



Marked changes in normal circulatory physi­ology occur during pregnancy. The cardiac output rises by the end of the first trimester, peaking at a level in the twentieth to twenty-fourth week that is maintained until after delivery. Increases in stroke volume, heart rate (10 beats per minute) and blood volume and decreases in systolic blood pressure and the systemic and pulmonary vascular resistances result. Oxygen consumption and minute venti­lation increase. Easy fatigability, decreased ex­ercise tolerance, dyspnea, peripheral edema, a third heart sound, and a midsystolic murmur may be normal in pregnancy. The mechanical pressure of a gravid uterus on the inferior vena cava may decrease venous return and reduce cardiac out­put. The hemodynamic stresses of pregnancy can exacerbate any pre-existing cardiac abnormality.

Most rheumatic valvular disease in young women involves mitral stenosis. Mitral stenosis is aggravated by the increased cardiac output and heart rate required during pregnancy. The inci­dence of heart failure increases as pregnancy pro­gresses. These patients have an increased risk of complications from atrial fibrillation, emboli, or endocarditis during pregnancy. Nevertheless, most of these patients can be managed carefully through a relatively uneventful pregnancy. Right ventricular failure may increase the peripheral edema, venous stasis, and risk of pulmonary em­bolism.

Women with significant mitral or aortic val­vular disease who desire children may require surgical correction of the lesion before concep­tion. Cardiac surgical intervention during preg­nancy carries an increased risk for both mother and fetus. If a valve is inserted, one should con­sider a porcine valve so that anticoagulation may be avoided. Warfarin crosses the placenta but he­parin does not. Warfarin may produce fetal de­velopmental abnormalities if administered in the first trimester. The use of heparin versus warfarin during various stages of pregnancy is controver­sial, but it is clear that warfarin should be replaced by heparin during the last two to three weeks of pregnancy. Heparin is discontinued and if nec­essary protamine administered upon the onset of labor. Patients given warfarin should not breast feed, since it is excreted in breast milk. Patients with prosthetic valves probably should receive peripartum endocarditis prophylaxis.

Survival to reproductive age in patients with congenital heart disease has become more com­mon since the advent of surgical intervention. The risk of pregnancy in patients after surgical cor­rection of congenital heart lesions depends on the completeness of their repair and residual defects such as left ventricular dysfunction or pulmonary hypertension. Patients with uncomplicated car­diac lesions such as ostium secundum atrial sep­tal defects usually tolerate pregnancy without any problem. Patients with uncorrected cyanotic heart disease such as tetralogy of Fallot may have dif­ficulty carrying a pregnancy to term. The infants often have low birth weights. Adverse hemody­namics may result in increased right-to-left shunt and increasing maternal cyanosis, increasing the risk to both mother and child. In patients with severe pulmonary vascular obstruction (for ex­ample, Eisenmenger’s syndrome), the fixed re­sistance allows little circulatory reserve, and fluc­tuations in systemic vascular resistance, cardiac output, and blood volume are very poorly toler­ated, especially during labor and the puerperium. Severe aortic stenosis also limits cardiac reserve, and the risk of exertional syncope may increase during pregnancy. Patients with Marfan’s syn­drome are at markedly increased risk of aortic dis­section during pregnancy. Women with coarcta­tion of the aorta also have an increased risk of aortic dissection during pregnancy. Women with persistent cardiomegaly following peripartum cardiomyopathy are at high risk during subse­quent pregnancies.

Maternal and fetal complications and mortality are directly related to functional class, and ther­apy should be optimized throughout pregnancy. Heart failure should be treated by decreased ac­tivity, decreased salt intake, and administration of digitalis and diuretics. If heart failure is re­fractory to medical therapy, termination of preg­nancy should be considered. Patients with heart failure may need to be hospitalized during the final weeks of pregnancy. Serious arrhythmias are managed with conventional therapy. Chest x-rays and cardiac catheterization should be avoided if possible because of the radiation risks to the fetus. Factors that may exacerbate heart failure should be eliminated. Most women with heart disease should undergo a spontaneous term vaginal de­livery, although Caesarean section may be nec­essary in selected seriously ill patients.