Chapter 16 Cardiac Disease and Pregnancy
Cardiac disease complicates approximately 1% to 2% of all pregnancies and is a leading cause of maternal death.1,2 Historically, rheumatic valvular heart disease, particularly mitral stenosis, has been the predominant cause of heart disease in pregnancy, and in developing countries this is still the case. However, in the United States and other developed nations, corrected or palliated congenital heart disease is becoming more common. In this chapter the management of pregnant patients with cardiac disease is reviewed briefly.
PHYSIOLOGIC CHANGES DURING PREGNANCY
Pregnancy and labor impose a huge metabolic burden on the mother; the result is profound alterations in maternal physiology, particularly of the cardiovascular system.2–4 These physiologic changes begin about week 6, become maximal early in the third trimester (about week 30), and thereafter remain relatively stable until labor.
Cardiovascular Changes
Circulating volume increases by about 40%. Plasma volume increases slightly more than red cell volume, resulting in mild anemia. Cardiac output also increases by about 40% through a combination of increased preload (increased blood volume), reduced afterload (systemic vasodilation), increased heart rate (10 to 15 beats/min), and a slight increase in contractility. Blood pressure falls by 10% to 15%. Near term, uterine blood flow is 600 to 700 ml/min (10% to 15% of cardiac output). From about week 20, when the mother is in the supine position, the enlarged uterus is capable of compressing the inferior vena cava (causing maternal hypotension) and the aorta (causing reduced placental blood flow).
Pregnancy is a state of hypercoagulability during which there are increased levels of certain coagulation factors (II, VII, X) and a reduction in anticoagulant factors (e.g., protein S). This is of particular importance for mothers at increased risk for thromboembolism, such as those with mechanical heart valves, atrial fibrillation, or cyanotic heart disease.
Respiratory Changes
Displacement of the diaphragm by the enlarging uterus decreases functional residual capacity by approximately 20%. Minute ventilation increases by about 40%, resulting in mild respiratory alkalosis, which is compensated for by renal bicarbonate loss. In late pregnancy, the normal value for arterial carbon dioxide tension is about 4 kPa (30 mmHg). Edema of the upper airway and larynx may occur, particularly in the presence of preeclampsia.
Renal and Gastrointestinal Changes
Glomerular filtration rate and creatinine clearance increase, resulting in a mild reduction in serum creatinine and urea. Thus, levels of these substances at the upper limit of “normal” represent significant renal dysfunction. Pregnancy is associated with relaxation of the lower esophageal sphincter which, together with the expanding uterus, renders the mother at increased risk for gastroesophageal reflux.
Labor
Cardiac output rises throughout labor, particularly during uterine contractions. Contractions cause the expulsion of blood from the uteroplacental capacitance vessels, resulting in an autotransfusion of 300 to 500 ml of blood. Cardiac output remains elevated by 10% to 20% above predelivery levels for 24 to 48 hours after delivery, then slowly declines to prepregnancy levels over the next 10 to 14 days. Uterine contractions are associated with acute increases in heart rate and blood pressure. These hemodynamic effects are exacerbated by maternal pain and anxiety and minimized by epidural analgesia. Maternal blood loss averages 300 to 400 ml in a normal vaginal delivery and 500 to 800 ml in a cesarean section.
CARDIAC DISEASE DURING PREGNANCY
A number of kinds of cardiac lesions are associated with increased risk for adverse outcome during pregnancy (Table 16-1).5–8 In general, regurgitant valvular lesions are better tolerated than stenotic lesions. With a stenotic lesion, in which cardiac output is relatively fixed, the vasodilatation and increased preload associated with pregnancy can result in hypotension and pulmonary edema. In contrast, vasodilatation and increased preload in the setting of a regurgitant lesion tend to encourage forward flow. However, any valve lesion causing New York Heart Association (NYHA) class III or IV symptoms prior to pregnancy is unlikely to be compatible with progress to term. Some conditions, notably Eisenmenger syndrome and severe cyanotic heart disease, are associated with such a high maternal and fetal mortality rate that pregnancy is inadvisable.
Table 16-1 Cardiac Lesions Associated With High Maternal and Fetal Risk During Pregnancy
| Cyanotic heart disease |
| Severe aortic stenosis with or without symptoms |
| Mitral stenosis with NYHA functional class II to class IV symptoms |
| Mitral or aortic regurgitation with NYHA functional class III to class IV symptoms |
| Valvular heart disease resulting in severe pulmonary hypertension (pulmonary artery pressure > 75% systemic pressure) |
| Left ventricular dysfunction (ejection fraction < 40%) |
| Mechanical prosthetic valve requiring anticoagulation |
| Aortic regurgitation in Marfan syndrome |
From Siu SC, Sermer M, Harrison DA, et al: Risk and predictors for pregnancy-related complications in women with heart disease. Circulation 96:2789-2794, 1997; and from Bonow RO, Carabello B, de Leon AC, et al: ACC/AHA guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [Committee on Management of Patients With Valvular Heart Disease]. J Am Coll Cardiol 32:1486-1588, 1998. NYHA, New York Heart Association.
Mitral Stenosis
Rheumatic mitral stenosis (see Chapter 10) is the valve lesion that most commonly complicates pregnancy. The increased circulating volume and heart rate that occur during pregnancy can cause pulmonary congestion or frank pulmonary edema. The development of rapid atrial fibrillation can precipitate acute cardiac decompensation.
Mild or Moderate Mitral Stenosis
With the careful use of diuretics for relief of pulmonary congestion and β blockers for control of heart rate, mild or moderate mitral stenosis during pregnancy can usually be managed medically. A cardioselective β blocker such as metoprolol may have less effect on placental blood flow than a nonselective agent. Rapid atrial fibrillation should be aggressively treated. In most circumstances, vaginal delivery is possible. A carefully managed epidural and an assisted delivery reduce the need for pushing during labor, helping to avoid large increases in left atrial pressure. Furosemide is often given at delivery.
Severe Mitral Stenosis
Patients with severe mitral stenosis should be considered for percutaneous valvuloplasty or, if the mitral anatomy is unsuitable, for mitral valve surgery prior to conception. Patients who develop persistent heart failure during pregnancy should be considered for percutaneous valvuloplasty during the second trimester,9 or if the mitral anatomy is unsuitable (see Chapter 10), for open mitral valve surgery. Excellent results can usually be obtained with percutaneous valvuloplasty, and complications are rare.
Aortic Stenosis
Aortic stenosis (see Chapter 10) is an uncommon problem in pregnancy. Patients with known severe aortic stenosis should undergo valve replacement prior to conception—preferably involving a homograft or tissue valve, thus eliminating the need for warfarin.
Severe aortic stenosis presents a very high risk for maternal and fetal mortality. If symptoms related to aortic stenosis are present in the first trimester, termination of the pregnancy should be considered. If the pregnancy proceeds, intervention in the form of percutaneous valvuloplasty or valve replacement will be required during the second trimester. In contrast to percutaneous mitral valvuloplasty, aortic valvuloplasty is associated with a high rate of procedural complications (particularly aortic regurgitation) and provides only limited benefit. Patients with bicuspid aortic valve are at increased risk for aortic dissection during pregnancy.
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