Cardiopulmonary Disorders of Pregnancy
Stephen Martin
Ernest M. Graham
CARDIAC DISORDERS
Cardiac diseases complicate 1% to 4% of pregnancies in women without preexisting cardiac abnormalities. Pregnancy is associated with major alterations in circulatory physiology, and cardiovascular disease remains a major cause of nonobstetric maternal morbidity in the United States.
Hemodynamic Changes During Pregnancy
Profound hemodynamic alterations occur during pregnancy, labor, delivery, and the postpartum period. These changes begin during the first 5 to 8 weeks of pregnancy and peak in the late second trimester. Normal pregnancy is associated with fatigue, dyspnea, decreased exercise capacity, peripheral edema, and jugular venous distention. Most pregnant women have audible physiologic systolic murmurs created by augmented blood flow and a physiologic third heart sound (S3) that reflects the volumeexpanded state. The enormous changes in the cardiovascular system during pregnancy carry many implications for management of pregnant patients with cardiac disease.
Blood volume increases 40% to 50% during normal pregnancy, in part due to estrogen-mediated activation of the renin-aldosterone axis leading to sodium and water retention. The rise in blood volume is greater than the increase in red blood cell mass (20% to 30%), contributing to the fall in hemoglobin concentration causing physiologic anemia in pregnancy. Peak dilution occurs at 24 to 26 weeks.
Cardiac output increases 30% to 50% above baseline by 20 to 26 weeks’ gestation, peaks at the end of the second trimester, and then plateaus until delivery. The change in cardiac output is mediated by the following: (a) increased preload due to the rise in blood volume, (b) reduced afterload due to a fall in systemic vascular resistance, and (c) a rise in maternal heart rate of 10 to 15 beats per minute. Stroke volume increases during the first and second trimesters but declines in the third trimester due to caval compression by the gravid uterus. Cardiac output in twin pregnancies is 20% above that of singleton pregnancies. Blood pressure typically falls slightly during the first two trimesters of pregnancy because of reduction in peripheral vascular resistance related to increased progesterone production.
Labor and delivery: During labor and delivery, hemodynamic fluctuations can be profound. Each uterine contraction results in the displacement of 300 to 500 mL of blood into the general circulation. Stroke volume increases, causing a rise in cardiac output of an additional 50% with each contraction. Mean systemic pressure also rises due to maternal pain and anxiety. Blood loss during delivery can further alter the hemodynamic state.
Postpartum: Immediately postpartum, uterine involution leads to autotransfusion, which increases cardiac output dramatically. In addition, there is a relief of vena
caval compression after delivery. Increased venous return augments cardiac output and prompts brisk diuresis. The cardiovascular system returns to the prepregnant baseline within 3 to 4 weeks postpartum.
Cardiac Disease in Pregnancy
Signs and symptoms of cardiac disease overlap common symptoms and findings in pregnancy including fatigue, shortness of breath, orthopnea, palpitations, edema, systolic flow murmur, and a third heart sound.
Evaluation of cardiac disease includes a thorough history and physical examination. Noninvasive testing includes an electrocardiogram (ECG), chest radiograph, and an echocardiogram. The ECG may reveal a leftward shift of the electrical axis, especially during the third trimester when the diaphragm is pushed upward by the uterus. Ventricular extrasystoles are a common finding. Routine chest radiographs are used to assess cardiomegaly and pulmonary vascular prominence. Echocardiographic evaluation of ventricular function and structural anomalies is invaluable for diagnosis of cardiac disease in pregnancy. Many changes including mild valvular regurgitation and chamber enlargement are normal findings on echocardiogram during pregnancy.
Management of Patients with Known Cardiac Disease
Before conception: Whenever possible, women with preexisting cardiac lesions should receive preconception counseling regarding maternal and fetal risks during pregnancy and long-term maternal morbidity and mortality. The New York Heart Association (NYHA) functional class (Table 15-1) is used as a predictor of outcome. Women with NYHA class III and IV face a mortality rate of 7% and morbidity over 30%. These women should be strongly cautioned against pregnancy. A risk index using four risk factors has been shown to accurately predict a woman’s chance of having adverse cardiac or neonatal complications: (a) a prior cardiac event, (b) cyanosis or poor functional class, (c) left heart obstruction, and (d) systemic ventricular dysfunction. With two or more risk factors, the chance of cardiac event approaches 75%.
After conception: Pregnant patients with significant history require cardiac assessment as early as possible. If the pregnancy poses a serious threat to maternal health, the patient should be counseled about the option of pregnancy termination. Patients need close monitoring and follow-up by both a perinatologist and cardiologist, with attention to signs or symptoms of worsening congestive heart failure (CHF) throughout the pregnancy. Each visit should include the following: (a) cardiac examination and cardiac review of systems; (b) documentation of weight, blood pressure, and pulse; and (c) evaluation of peripheral edema.
During pregnancy: The most common cardiac complications of pregnancy include arrhythmia and CHF. If symptoms worsen, hospitalization, bed rest, diuresis, or correction of an underlying arrhythmia may be required. Sometimes, surgical correction during pregnancy becomes necessary. When possible, procedures should be performed during the early second trimester to avoid the period of fetal organogenesis and before more significant hemodynamic changes of pregnancy occur. Pregnancy is also a time of hypercoagulability, and anticoagulation should be started if appropriately indicated.
TABLE 15-1 New York Heart Association (NYHA) Functional Classification | ||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||
Antibiotic Prophylaxis for Endocarditis
American College of Obstetricians and Gynecologists (ACOG) has endorsed the 2007 American Heart Association (AHA) guidelines for prevention of infective endocarditis (IE) which represent a marked change from prior AHA guidelines. Antibiotic prophylaxis is no longer recommended, as IE is more likely to result from frequent random bacteremia with daily activities than from bacteremia caused by specific dental, gastrointestinal (GI), or genitourinary (GU) procedures. Prophylaxis is now based on the risk of adverse outcome with the procedure, and it is not recommended for GU procedures, except in high-risk patients with GU infections, to prevent wound infection and sepsis. Antibiotic prophylaxis for IE is not recommended for vaginal delivery or hysterectomy (see Chapter 27).
Specific Cardiac Conditions
Cardiomyopathy
Cardiomyopathy can be genetic, idiopathic, or caused by myocarditis or toxins and manifests during pregnancy with signs and symptoms of CHF. These include chest pain, dyspnea, paroxysmal nocturnal dyspnea, and cough. Echocardiography demonstrates chamber enlargement and reduced ventricular function. The heart becomes uniformly dilated, filling pressures increase, and cardiac output decreases. Eventually, heart failure develops and is often refractory to treatment. The 5-year survival rate is approximately 50%; therefore, careful preconception counseling is important, even if the patient is asymptomatic.
Hypertrophic cardiomyopathy with or without left ventricular outflow tract obstruction is an autosomal dominant disorder with a variable phenotype and incidence of 0.1% to 0.5% in pregnancy. Most women with hypertrophic cardiomyopathy do well in pregnancy, and complications are uncommon with prior prepregnancy risk stratification via NYHA functional class and multidisciplinary specialist management. Risk is increased in patients that are symptomatic or if there is significant left ventricular outflow obstruction. The potential exists for poor tolerance of the circulatory overload of pregnancy. Major complications include pulmonary edema secondary to diastolic dysfunction, dysrhythmias secondary to myofibrillar disarray, functional class decline, obstetric complications, and poor fetal outcomes. During pregnancy, beta-blockers should be continued and the judicious use of diuretics may be required to treat symptoms of dyspnea.
Peripartum cardiomyopathy is an idiopathic dilated cardiomyopathy that typically develops in the last month of pregnancy or within 5 months of delivery and is characterized by left ventricular systolic dysfunction with ejection fraction (EF) <45%. Incidence is 1 in 1,300 to 1 in 15,000. Risk factors include advanced maternal age; multiparity; multiple gestations; black race; obesity; malnutrition; gestational hypertension (HTN); preeclampsia; poor antenatal care; breast-feeding; cesarean section; low socioeconomic status; family history; and abuse of tobacco, alcohol, or cocaine. The most common clinical complaints are dyspnea, cough, orthopnea, paroxysmal nocturnal dyspnea, and hemoptysis. Workup and diagnosis are completed with ECG, echocardiography, and lab studies such as brain natriuretic peptide.
Of the patients who survive, approximately 50% recover normal left heart function. The mortality rate is 25% to 50%; half of those die within the first month of presentation, and the majority dies within 3 months postpartum. Prognosis is related to left ventricular dysfunction at presentation. Death results from progressive CHF, thromboembolic events, and arrhythmias.
Medical management includes fluid and salt restriction, digoxin, diuretics, vasodilators, and anticoagulants; bed rest can predispose to thromboembolism. Cardiac transplantation may be required in advanced unresolving disease. For patients diagnosed antenatally, invasive cardiac monitoring should be considered during labor and until at least 24 hours postpartum. Supplemental oxygen and regional analgesia for pain control should be administered and a passive second stage of labor facilitated by operative vaginal delivery. Cesarean section is reserved for obstetric indications. Intensive care unit monitoring should continue immediately postpartum, including detection and management of possible autotransfusion-induced pulmonary edema.
Valvular Disease
Mitral valve prolapse (MVP) is the most common congenital heart defect in women. It rarely has implications for maternal or fetal outcomes. It is the most common cause of mitral regurgitation (MR) in women.
MR is usually well tolerated during pregnancy. The fall in systemic vasoresistance improves cardiac output in pregnancy. Medical management includes diuretics in the rare event of pulmonary congestion or vasodilators for systemic HTN. Acute, severe worsening of MR can result from ruptured chordae and must be repaired surgically. Women with severe MR before pregnancy should undergo operative repair before conception. Patients with advanced disease may require central monitoring during labor.
Aortic regurgitation (AR): AR may be encountered in women with rheumatic heart disease, a congenitally bicuspid or deformed aortic valve, IE, or connective tissue disease. AR is generally well tolerated during pregnancy. Medical management includes diuretics and vasodilators. Ideally, women with severe AR should undergo operative repair before conception; as in MR, surgery during pregnancy should be considered only for control of refractory NYHA functional class III or IV symptoms.
Aortic stenosis (AS): The most common etiology of AS in pregnant women is a congenitally bicuspid valve. Mild AS with normal left ventricular function is usually well tolerated during pregnancy. Asymptomatic severe stenosis can be managed conservatively with bed rest, oxygen, and beta-blockade. Moderate to severe AS markedly increases the medical risk of pregnancy; patients are advised to delay conception until correction is performed. Symptoms, such as dyspnea, angina pectoris, or syncope, usually become apparent late in the second trimester or early
in the third trimester. Women with bicuspid aortic valves are also at increased risk for aortic dissection and should be followed carefully. Aortic root enlargement >40 mm or an increase in aortic root size during pregnancy are risk factors for dissection. Beta-blockers may be indicated in these patients.
Severe symptomatic AS can be managed by percutaneous aortic balloon valvuloplasty prior to labor and delivery but not without significant risk to both mother and fetus. If presenting early in pregnancy, termination should be discussed before surgical correction of severe AS (EF <40%). Spinal and epidural anesthesia are discouraged because of their vasodilatory effects. This disorder is characterized by a fixed afterload, thus adequate end-diastolic volume, and therefore adequate filling pressure, are necessary to maintain cardiac output. Consequently, great care must be taken to prevent hypotension, tachycardia, and hypoperfusion caused by blood loss, regional anesthesia, or other medications. Patients should be hydrated adequately and placed in the left lateral position to maximize venous return. As with mitral stenosis, hemodynamic monitoring with a pulmonary arterial catheter should be considered during labor and delivery.
Pulmonic stenosis (PS) frequently accompanies other congenital cardiac anomalies, but as an isolated lesion, PS rarely complicates pregnancy. Patients with cyanotic congenital cardiac disease tolerate pregnancy less well than those with acyanotic lesions. Echocardiogram-guided percutaneous valvotomy is a potential treatment option.
Mitral stenosis (MS) in women of childbearing age is usually due to rheumatic fever. Patients with moderate to severe MS often experience hemodynamic deterioration during the third trimester and/or during labor and delivery. Increased blood volumes and 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. Mild to moderate MS can be managed with judicious diuresis and beta-blockade, although aggressive diuresis should be avoided so as to preserve uteroplacental perfusion. Cardioselective betablockers such as metoprolol and atenolol are used to treat or prevent tachycardia, optimizing diastolic filling while preventing deleterious effects of epinephrine blockade on myometrial activity. These patients should be comanaged with a cardiologist. Patients with severe MS who develop NYHA functional class III to IV symptoms during pregnancy should undergo percutaneous balloon valvotomy.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
