Cardiac disease complicates approximately 4% of all pregnancies in the United States; however, these patients are at a disproportionate increase in risk for maternal deaths (10%-25%).1,2 Congenital cardiac lesions are 3 times more common than acquired, adult-onset abnormalities in pregnant patients. Intensive care unit (ICU) admissions due to maternal cardiac disease comprise up to 15% of obstetric ICU admissions, yet these patients account for up to 50% of all maternal deaths in the ICU.3-9 The incidence of an acute coronary event is increasing during pregnancy due to older maternal age at child-bearing along with higher rates of hypertension and obesity in women.10 Pregnant cardiac patients are at risk of developing cardiac decompensation and adverse pregnancy outcomes based on the type of cardiac lesion. Pregnancy can have a negative influence on systolic and diastolic function in women with structural heart disease, which can persist 6 months after pregnancy.11 Further complicating the issue, common complaints of normal pregnancy such as dyspnea, fatigue, palpitations, orthopnea, and pedal edema mimic symptoms of worsening cardiac disease and can create challenges for the clinician when evaluating a pregnant patient with cardiac disease.
In this chapter, we will review valvular, congenital, and acquired cardiac lesions and their impact on pregnancy management. Each section will address the concerns specific to the relevant abnormality, including key points in antepartum management, as well as anesthetic and delivery issues.
Comprehensive understanding of the normal physiologic adaptations to pregnancy is essential for successful management of patients with cardiac disease. Conditions which may be asymptomatic while nonpregnant can deteriorate in the pregnant state. Table 8-1 outlines key physiologic changes in a normal singleton gestation. Multiple gestations can be expected to have even more dramatic physiologic changes. Table 8-2 provides an overview of changes in cardiovascular evaluations during pregnancy.
Antepartum
Intrapartum
Postpartum
|
| Cardiovascular exam | Findings in pregnancy |
|---|---|
| Chest x-ray | Apparent cardiomegaly Enlarged left atrium Increased vascular markings |
| Electrocardiography | Right axis deviation Right bundle branch block ST-segment depression of 1 mm on left precordial leads Q waves in lead III T-wave inversion in leads III, V2, and V3 |
| Echocardiography | Trivial tricuspid regurgitation Pulmonary regurgitation Increased left atrial size Increased left ventricular end-diastolic dimensions by 6%-10% Mitral regurgitation Pericardial effusion |
Establishing baseline cardiac function is essential for pregnant cardiac patients. Functional status for patients with cardiac disease is commonly classified according to the New York Heart Association (NYHA) classification system as outlined in Table 8-3. Patients with NYHA class I or II have less risk of complications compared to those in class III or IV.12 Table 8-4 classifies various cardiac abnormalities according to maternal death risk estimates; however, the patient’s particular history is not included in these estimates.13
| Class I | No limitations of physical activity. Ordinary physical activity does not precipitate cardiovascular symptoms such as dyspnea, angina, fatigue, or palpitations. |
| Class II | Slight limitation of physical activity. Ordinary physical activity will precipitate cardiovascular symptoms. Patients are comfortable at rest. |
| Class III | Less than ordinary physical activity precipitates symptoms that markedly limit activity. Patients are comfortable at rest. |
| Class IV | Patients have discomfort with any physical activity. Symptoms are present at rest. |
Group 1—Mortality <1%
Group 2—Mortality 5%-15% 2A
2B
Group 3—Mortality 25%-50%
|
In a large multicenter prospective study of almost 600 pregnancies complicated by maternal cardiac disease, the authors created a risk score to predict the likelihood of a maternal cardiovascular event in the presence of specific predictors for maternal complications.14 Table 8-5 outlines risk prediction according to CARPREG Risk Score.
New York Heart Association (NYHA) functional class>II Cyanosis (room air saturation <90%) Prior cardiovascular event Systolic ventricular ejection fraction <40% Left heart obstruction For each CARPREG predictor that is present, a point is assigned Risk Estimation of Maternal Cardiovascular Complications | |
| No. of predictors | Risk of cardiac event in pregnancy (%) |
| 0 | 5 |
| 1 | 27 |
| >1 | 75 |
More recently, the modified World Health Organization (mWHO) score has been shown to better predict cardiac complications than other risk scores with better adjustment to all subgroups of patients and for congenital heart disease15,16 and is recommended as the method to assess maternal risk. This risk score also includes contraindications for pregnancy not incorporated in the CARPREG score. Table 8-6 outlines the risk prediction according to the mWHO risk score.17
| Risk class | Risk of pregnancy by medical condition | Maternal risk factors |
|---|---|---|
| I | No detectable increased risk of maternal mortality and no/mild increase in morbidity. | Uncomplicated, small/mild pulmonary stenosis, PDA, mitral valve prolapse Successfully repaired simple lesions (ASD, VSD, PDA, anomalous pulmonary venous drainage) Atrial or ventricular ectopic beats, isolated |
| II | Small increased risk of maternal mortality or moderate increase in morbidity. | Unoperated atrial or ventricular septal defect Repaired tetralogy of Fallot Most arrhythmias |
| II-III | Moderate increase in maternal morbidity and mortality risk. | Mild left ventricular impairment Hypertrophic cardiomyopathy Native or tissue valvular heart disease not considered WHO I or IV Marfan syndrome without aortic dilatation Aorta <45 mm in aortic disease associated with bicuspid aortic valve Repaired coarctation |
| III | Significantly increased risk of maternal mortality or severe morbidity. Expert counseling required. If pregnancy is decided upon, intensive specialist cardiac and obstetric monitoring needed throughout pregnancy, childbirth, and the puerperium. | Mechanical valve Systemic right ventricle Fontan circulation Cyanotic heart disease (unrepaired) Other complex congenital heart disease Aortic dilatation 40-45 mm in Marfan syndrome Aortic dilatation 45-50 mm in aortic disease associated with bicuspid aortic valve |
| IV | Extremely high risk of maternal mortality or severe morbidity; pregnancy contraindicated. If pregnancy occurs, termination should be discussed. If pregnancy continues, care as for class III. | Pulmonary arterial hypertension of any cause Severe systemic ventricular dysfunction (LVEF <30%, NYHA III-IV) Previous peripartum cardiomyopathy with any residual impairment of left ventricular function Severe mitral stenosis, severe symptomatic aortic stenosis Marfan syndrome with aorta dilated >45 mm Aortic dilation >50 mm in aortic disease associated with bicuspid aortic valve Native severe coarctation |
The most commonly encountered cardiac events are pulmonary edema and dysrhythmias. One large, multinational study of over 1300 patients with cardiac disease showed that the most common obstetrical complications are gestational hypertension and preeclampsia.18 Maternal mortality is of highest risk for patients with coronary artery disease, pulmonary hypertension, endocarditis, cardiomyopathy, and dysrhythmias.19,20
Neonatal complications are more likely to occur in patients with NYHA class greater than II, those who require anticoagulation during pregnancy, history of smoking, multiple gestation, and left heart obstruction. These complications include small for gestational age infants, delivery before 34 weeks’ gestation, and neonatal death.21 Fetal mortality approaches 2% in pregnancies with maternal heart disease.18 Structural cardiac anomalies (excluding autosomal dominant disorders) occur in 2% to 18% of fetuses born to patients with a history of congenital cardiac disease. Therefore, fetal echocardiography is recommended for all pregnant patients with structural cardiac defects. Table 8-7 outlines the risks of congenital cardiac disease by maternal disorder.
| Maternal lesion | Risk if mother is affected (%) |
|---|---|
| Tetralogy of Fallot | 2-4.5 |
| Aortic coarctation | 4-14.1 |
| Atrial septal defect | 4.6-11 |
| Ventricular septal defect | 6-15.6 |
| Pulmonary stenosis | 5.3-6.5 |
| Aortic stenosis | 8-17.9 |
| Persistent ductus arteriosus | 4.1 |
| Marfan syndrome | 50 |
| 22q11 deletion syndromes | 50 |
Even after delivery, these patients remain at high risk for complications, with approximately 10% to 15% having at least one episode of heart failure, during or after pregnancy.18 In one study of 100 patients, postpartum complications were seen in about 4% of NYHA I/II patients and in 27% of NYHA III/IV patients.22
Management details for each condition are addressed separately.
Baseline evaluation of cardiac function.
Counseling regarding pregnancy risk for mother and fetus.
Consultation with cardiologist and maternal fetal medicine specialist, if possible.
Review current medications to determine appropriateness of their use during pregnancy.
Routine preconception care as for all patients: assessment of immunization status, screening for genetic diseases as indicated, supplemental folic acid.
Pulmonary arterial hypertension of any cause.14,23
Marfan syndrome, with dilated aortic root greater than 40 mm.
Aortic dilation greater than 50 mm in aortic disease associated with bicuspid aortic valve.
Severe left heart obstructive lesions (severe mitral stenosis, severe symptomatic aortic stenosis [AS] or native severe coarctation).
Severe systemic left ventricular (LV) dysfunction (LV ejection fraction <30%, NYHA III-IV).
Previous peripartum cardiomyopathy (PPCM) particularly with any residual impairment of LV function.
A team approach to antepartum care is recommended and should include maternal fetal medicine, cardiology, and anesthesia as indicated, particularly for patients with congenital cardiac disease.
Patients should be evaluated regularly for signs and symptoms of cardiac decompensation.
Fetal echocardiogram between 20 and 24 weeks’ gestation is indicated in the presence of maternal congenital heart disease.
Periodic ultrasound to assess fetal growth.
Antepartum fetal surveillance starting at 30 to 34 weeks if concerns for fetal growth restriction or maternal complications.
Attention to fluid intake and output. Maintain all IV fluids on pumps.
Avoid supine positioning.
Supplemental oxygen.
Cesarean delivery is not routinely recommended in the setting of maternal cardiac disease.
Endocarditis prophylaxis is no longer recommended for any genitourinary procedures, even in patients with the highest risk lesions.24
Valvular abnormalities may be congenital or acquired. However, the majority of lesions are acquired secondary to rheumatic fever, which accounts for 90% of cardiac disorders in pregnancy worldwide. Heart failure is the most common complication; patients with valvular heart disease have a higher mortality rate than those with congenital heart disease.18 The degree of risk for development of complications (particularly dysrhythmias and pulmonary edema) depends on the specific valve lesion, number of valves involved, and the degree of valvular obstruction, particularly of the mitral and aortic valves. The frequency of affected valves, in decreasing order, is: mitral, aortic, tricuspid, and pulmonic valves. Mitral stenosis carries the greatest potential for problems during pregnancy. Table 8-8 presents a summary of relative maternal and fetal risk in patients with valvular abnormalities.25 Each valvular lesion will be addressed in the sections that follow. Table 8-9 outlines common cardiac medications and their effects on uterine blood flow and fetus.
| Low maternal and fetal risks | High maternal and fetal risks | High maternal risks |
|---|---|---|
| Asymptomatic aortic stenosis with a low mean outflow gradient (<50 mm Hg), normal LV systolic function | Severe aortic stenosis with or without symptoms | Ejection fraction <40% |
| Aortic regurgitation, NYHA class I or II with normal LV function | Aortic regurgitation, NYHA class III or IV | Previous heart failure |
| Mitral regurgitation, NYHA class I or II, normal LV function | Mitral stenosis, NYHA class II, III, or IV | Previous stroke or transient ischemic attack |
| Mitral valve prolapse with none to moderate mitral regurgitation, normal LV function | Mitral regurgitation, NYHA class III or IV | |
| Mild to moderate mitral stenosis, no pulmonary hypertension | Aortic or mitral valve disease with pulmonary hypertension | |
| Mild to moderate pulmonary valve stenosis | Aortic or mitral valve disease with LV dysfunction Maternal cyanosis NYHA class III or IV |
| Drug | Dose | Uterine blood flow (UBF) | Fetal effects |
|---|---|---|---|
| Inotropic agents | |||
| Digoxin | Loading dose 0.5 mg IV over 5 min, then 0.25 mg IV q6h × 2 Maintenance 0.125-0.375 mg IV/PO qd | No change | Placental transfer Higher maternal maintenance dose required for fetal effect Not teratogenic |
| Dopamine | Initiate with 5 μg/kg/min and titrate by 5-10 μg/kg/min to max 50 μg/kg/min | Directly ↓ UBF May ↑ UBF with improved maternal hemodynamics | No known adverse fetal effects |
| Dobutamine | Initiate with 1.0 μg/kg/min and titrate up to 20 μg/kg/min | No known adverse fetal effects | |
| Epinephrine | Endotracheal, 0.5-1.0 mg q5min; IV 0.5 mg bolus and follow with 2-10 μg/kg/min infusion | Not teratogenic | |
| Vasodilators | |||
| Nitroprusside | Initiate with 0.3 μg/kg/min and titrate to 10 μg/kg/min | ↑ UBF unless significant ↓ in maternal BP | No known adverse fetal effects Potential for fetal cyanide toxicity Avoid prolonged use |
| Hydralazine | 5-10 mg IV q15-30min; total dose 30 mg | Not teratogenic | |
| Nitroglycerin | 0.4-0.8 mg sublingual 1-2 in of dermal paste, IV infusion 10 μg/min, titrate up by 10-20 μg/min prn | Not teratogenic | |
| β Blockers | |||
| Propranolol | 1 mg IV q2min as needed | May ↓ by ↑ uterine tone and/or ↓ maternal BP | Not teratogenic Readily crosses placenta Fetal bradycardia, fetal growth restriction |
| Labetalol | 10-20 mg IV followed by 20-80 mg IV q10 min to total dose of 150 mg | Same as propranolol
Same as propranalol | |
| Atenolol | 5 mg IV over 5 min, repeat in 5 min to a total dose of 15 mg | ||
| Metoprolol | 5 mg IV over 5 min; repeat in 10 min | ||
| Esmolol | 500 ug/kg IV over 1 min with infusion rate of 50-200 μg/kg/min | No known adverse fetal effects Rapid metabolism (1/2 life 11 min) also occurs in the fetus | |
| Calcium channel blockers | |||
| Verapamil | 2.5-5 mg IV bolus over 2 min, repeat in 5 min and then q30 min prn to a max dose 20 mg | Mild ↓ UBF | Not teratogenic |
| Nifedipine | 10 mg PO, repeat every 6 h | ||
| Diltiazem | 20 mg IV bolus over 2 min, repeat in 15 min | ||
| Vasoconstrictors | |||
| Ephedrine sulfate | 10-25 mg slow IV bolus, repeat q15 min prn × 3 | No effect | Not teratogenic 70% of maternal blood level in the fetus |
| Metaraminol | Initiate with 0.1 mg/min and titrate to 2 mg/min | Mild ↓ UBF | No data available |
| Antidysrhythmic agents | |||
| Lidocaine | 1 mg/kg bolus; repeat 1/2 bolus at 10 min as needed × 4; infusion at 1-4 mg/min; total dose 3 mg/kg | No effect | Not teratogenic Rapidly crosses placenta |
| Procainamide | 100 mg over 30 min, then 2-6 mg/min infusion; total dose 17 mg/kg | ||
| Quinidine | 15 mg/kg over 60 min, then 0.02 mg/kg/min infusion | ||
| Bretylium | 5 mg/kg IV bolus, then 1-2 mg/min infusion | ↓ UBF | Unknown |
| Phenytoin | 300 mg IV, then 100 mg every 5 min to a total of 1000 mg | No effect | Teratogenic |
| Fetal hydantoin syndrome | |||
| Teratogenic | |||
| Amiodarone | 5 mg/kg IV over 3 min, then 10 mg/kg/day | Transient bradycardia | |
| Prolonged QT | |||
| AV node blocking agents | |||
| Adenosine | 6 mg IV bolus over 1-3 s, followed by 20 mL saline bolus; may repeat at 12 mg in 1-2 min × 2 | ↑ or ↓ UBF | No known adverse fetal effects |
| Verapamil | As stated above | ||
| β-Blockers | As stated above | ||
| Digoxin | As stated above | ||
Isolated lesions most commonly are acquired, as a result of endocarditis, in intravenous drug abusers.
Well tolerated in pregnancy, with minimal risk of right heart failure.
Echocardiogram to evaluate severity of right outflow obstruction (>60 mm Hg consistent with severe obstruction).
Right heart failure, if severe obstruction.
Generally not indicated.
Not indicated.
Epidural acceptable.
Reserve cesarean for usual obstetric indications; cesarean delivery not demonstrated to improve outcome.
Isolated lesions most commonly a result of endocarditis in intravenous drug abusers.
Well tolerated in pregnancy, with minimal risk of right heart failure.
Rarely clinically significant in pregnancy.
Figure 8-1 is a diagram of mitral stenosis.
Most common valvular lesion in pregnancy and responsible for most of the morbidity and mortality of rheumatic heart disease in pregnancy.
Stenosis of the mitral valve impedes flow of blood from left atrium to left ventricle.
Elevated left atrial pressures necessary to maintain adequate left ventricular filling across restricted opening.
Patients with moderate or severe stenosis are most likely to develop cardiac complications.
Patients may be asymptomatic until physiologic changes of pregnancy unmask the lesion.
Symptomatic patients may undergo balloon valvulotomy during pregnancy.
Echocardiogram to establish severity of stenosis and size of left atrium.
Symptoms unusual until valve area less than 2 cm2.
Moderate mitral stenosis: 1 to 1.5 cm2 valve area.
Severe mitral stenosis: less than 1 cm2 valve area.
Electrocardiogram (ECG) to exclude atrial fibrillation from enlarged left atrium. ECG (and echocardiogram) may also show left atrial enlargement; right ventricular hypertrophy and right atrial enlargement in cases of pulmonary hypertension.
Auscultation: loud first heart sound, an opening snap, and rumbling diastolic murmur.
Pulmonary edema, atrial fibrillation, and supraventricular tachycardia are the most common maternal complications.
Sixty percent develop their initial episode of pulmonary edema at a mean gestational age of 30 weeks.
Thromboembolism can develop as a result of left atrial dilation. May present as a stroke.
Box 8-1 presents key avoids in case of mitral stenosis.
Box 8-1 Avoids: Mitral stenosis
Avoid tachycardia (decreases diastolic ventricular filling time).
Avoid fluid overload (may cause atrial fibrillation, pulmonary edema, and right ventricular failure).
Avoid decrease in systemic vascular resistance/hypotension (decrease in cardiac output).
Avoid increase in pulmonary vascular resistance (hypoxia).
Prevent tachycardia: pain management, β blockers. Goal: HR less than 100 beats/min.
Maintain left ventricular filling (preload) to overcome obstruction. Inadequate preload may not be able to overcome obstruction, may lead to inadequate left ventricular filling and decreased cardiac output.
Diuretics to treat pulmonary edema, as needed.
Digoxin to treat atrial fibrillation, as needed.
Consider if left atrium dilated or if chronic atrial fibrillation.
Epidural acceptable; may help control tachycardia in labor by reducing pain.
Avoid abrupt sympathetic blockade which can decrease preload.
Tocolytic agents that cause tachycardia are contraindicated for premature labor (eg, terbutaline).
Hemodynamic monitoring for severe mitral stenosis.
Consider assisted second stage of labor.
Reserve cesarean for usual obstetric indications; cesarean delivery not demonstrated to improve outcome.
Figure 8-2 is a diagram of mitral insufficiency
FIGURE 8-2
Pathophysiology of mitral insufficiency. LA, left atrium; LV, left ventricle; RV, right ventricle.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
