Chapter 8: Cardiac Disease in Pregnancy

Comprehensive understanding of the normal physiologic adaptations to pregnancy is essential to 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.

TABLE 8-1.Expected Physiologic Changes Occurring in the Antepartum, Intrapartum, and Postpartum Periods

TABLE 8-1. Expected Physiologic Changes Occurring in the Antepartum, Intrapartum, and Postpartum Periods

Antepartum

Blood volume increases by 20%-50%
In nonpregnant females, total blood volume is ~60-70 mL/kg
Systemic vascular resistance decreases by 20%
- Accounts for majority of drop in BP
- Accommodates increase in circulating volume without increase in BP
Blood pressure (taken in sitting position)
- BP ≥140/90 abnormal at any time in gestation
- BP decreases to lowest point at 28 wk
- After 28 wk, BP increases to nonpregnant level by term
Mean arterial pressure unchanged
Heart rate increases by 10-15 beats/min
Stroke volume increases by 30%
Cardiac output increases by 30%-50%
- CO = heart rate × stroke volume. Majority of increase is from stroke volume
- Half of the expected increase occurs by 8 wk
- Peaks end of second trimester, sustained to term
- 6 L/min by term
Pulmonary capillary wedge pressure (preload to left heart) unchanged
Central venous pressure (preload to right heart) unchanged
Pulmonary vascular resistance decreases 30%
Hypercoagulable state
- Increased fibrinogen
- Platelets unchanged
- Dilutional anemia despite 30% increase in red cell mass

Intrapartum

During a contraction:
- 300-500 mL of blood enters circulation
- Heart rate increases
- Cardiac output increases by 30%
- Blood pressure increases by 10-20 mm Hg
Supine position may decrease cardiac output by 20%

Postpartum

Postpartum diuresis between days 2-5
Cardiac output increases by 50% in the immediate postpartum period
Stroke volume increases 60% in the immediate postpartum period
Reflex bradycardia occurs (15%)
These changes persist for 2 wk after delivery

TABLE 8-2.Changes in Cardiovascular Tests During Pregnancy

TABLE 8-2. Changes in Cardiovascular Tests During Pregnancy

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

COUNSELING THE PATIENT

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

TABLE 8-3.New York Heart Association Functional Classification System

TABLE 8-3. New York Heart Association Functional Classification System

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.

TABLE 8-4.Maternal Mortality Associated With Pregnancy

TABLE 8-4. Maternal Mortality Associated With Pregnancy

Group 1—Mortality <1%
Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus
Mitral stenosis—NYHA class I and II
Pulmonic/tricuspid valve disease
Corrected tetralogy of Fallot
Bioprosthetic valve
Group 2—Mortality 5%-15%
2A
- Mitral stenosis—NYHA class III and IV
- Aortic stenosis
- Coarctation of aorta without valvular involvement
- Uncorrected tetralogy of Fallot
- Previous myocardial infarction
- Marfan syndrome with normal aorta
2B
- Mitral stenosis with atrial fibrillation
- Artificial valve
Group 3—Mortality 25%-50%
Pulmonary hypertension
- Primary
- Eisenmenger syndrome
Coarctation of aorta with valvular involvement
Marfan syndrome with aortic involvement
Peripartum cardiomyopathy with persistent left ventricular dysfunction

Reproduced with permission from Belfort M, Saade G, Foley M (eds). Critical Care Obstetrics. Wiley-Blackwell; 2010.

In a recent 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.

TABLE 8-5.CARPREG Risk Score: Predictors of Maternal Cardiovascular Events

TABLE 8-5. CARPREG Risk Score: Predictors of Maternal Cardiovascular Events

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 (%)

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.¹⁵ Maternal mortality is of highest risk for patients with coronary artery disease, pulmonary hypertension, endocarditis, cardiomyopathy, and dysrhythmias.^16,17

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.¹⁸ Fetal mortality approaches 2% in pregnancies with maternal heart disease.¹⁵ 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 8-6 outlines the risks of congenital cardiac disease by maternal disorder.

TABLE 8-6.Risk of Fetal Cardiac Abnormality by Maternal Lesion

TABLE 8-6. Risk of Fetal Cardiac Abnormality by Maternal Lesion

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

22q11 deletion syndromes

Even after delivery, these patients remain at high risk for complications, with approximately 10% to 15% having at least 1 episode of heart failure, during or after pregnancy.¹⁵ 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.¹⁹

General Principles of Management

Management details for each condition are addressed separately.

Preconception Care

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.

Possible Contraindications to Pregnancy

Pulmonary arterial hypertension of any cause.^14,20
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 particularly with any residual impairment of LV function.

Antepartum Care

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.

Labor and Delivery Care

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.²¹

VALVULAR CARDIAC DISEASE

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.¹⁵ 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, are: mitral, aortic, tricuspid, and pulmonic valves. Mitral stenosis carries the greatest potential for problems during pregnancy. Table 8-7 presents a summary of relative maternal and fetal risk in patients with valvular abnormalities.²² Each valvular lesion will be addressed in the sections that follow. Table 8-8 outlines common cardiac medications and their effects on uterine blood flow and fetus.

TABLE 8-7.Classification of Valvular Heart Lesions According to Maternal and Fetal Risks

TABLE 8-7. Classification of Valvular Heart Lesions According to Maternal and Fetal Risks

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

TABLE 8-8.Cardiovascular Drugs Commonly Used in the Obstetric Intensive Care Setting and Their Effects on Uterine Blood Flow and the Fetus

TABLE 8-8. Cardiovascular Drugs Commonly Used in the Obstetric Intensive Care Setting and Their Effects on Uterine Blood Flow and the Fetus

Drug (FDA class)

Dose

Uterine blood flow (UBF)

Fetal effects

Inotropic agents

Digoxin (C)

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 (C)

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 (B)

Initiate with 1.0 μg/kg/min and titrate up to 20 μg/kg/min

No known adverse fetal effects

Epinephrine (C)

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 (C)

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 (C)

5-10 mg IV q15-30min; total dose 30 mg

Not teratogenic

Nitroglycerin (B)

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 (C)

1 mg IV q2min as needed

May ↓ by ↑ uterine tone and/or ↓ maternal BP

Not teratogenic

Readily crosses placenta

Fetal bradycardia IUGR

Labetalol (C)

10-20 mg IV followed by 20-80 mg IV q 10 min to total dose of 150 mg

Category D if used in 2nd or 3rd trimester

Atenolol (D)

5 mg IV over 5 min, repeat in 5 min to a total dose of 15 mg

Metoprolol (C)z

5 mg IV over 5 min; repeat in 10 min

Esmolol (C)

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 (C)

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 (C)

10 mg PO, repeat every 6 h

Diltiazem (C)

20 mg IV bolus over 2 min, repeat in 15 min

Vasoconstrictors

Ephedrine sulphate (C)

10-25 mg slow IV bolus, repeat q 15 min prn × 3

No effect

Not teratogenic 70% of maternal blood level in the fetus

Metaraminol (C)

Initiate with 0.1 mg/min and titrate to 2 mg/min

Mild ↓ UBF

No data available

Antidysrhythmic agents

Lidocaine (B)

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 (C)

100 mg over 30 min, then 2-6 mg/min infusion; total dose 17 mg/kg

Quinidine (C)

15 mg/kg over 60 min, then 0.02 mg/kg/min infusion

Bretylium (C)

5 mg/kg IV bolus, then 1-2 mg/min infusion

↓ UBF

Unknown

Phenytoin (D)

300 mg IV, then 100 mg every 5 min to a total of 1000 mg

No effect

Teratogenic

Fetal Hydantoin syndrome

Teratogenic

Amiodarone (D)

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

Reproduced with permission from McAnulty JH. Heart and other circulatory diseases. In: Bonica JJ, McDonald JS, eds. Principles and Practice of Obstetric Analgesia and Anesthesia. 2nd ed. Baltimore, MD: William & Wilkins; 1995;1019-1020.

Pulmonic Stenosis

Key Points

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.

Recommended Workup and Clinical Findings

Echocardiogram to evaluate severity of right outflow obstruction (>60 mm Hg consistent with severe obstruction).

Potential Complications

Right heart failure, if severe obstruction.

Medical Therapy

Generally not indicated.

Anticoagulation

Not indicated.

Anesthetic Issues

Epidural acceptable.

Labor and Delivery

Reserve cesarean for usual obstetric indications; cesarean delivery not demonstrated to improve outcome.

Tricuspid Lesions

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.

Mitral Stenosis

Key Points

Figure 8-1 is a diagram of mitral stenosis.

Most common valvular lesion 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.

FIGURE 8-1.

Pathophysiology of mitral stenosis. LV, left ventricle; PCW, pulmonary capillary wedge; RV, right ventricle.

Recommended Workup and Clinical Findings

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.

Potential Complications

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.

Key Avoids

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).

Therapy

Goals of therapy:

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.

Anticoagulation

Consider if left atrium dilated or if chronic atrial fibrillation.

Anesthetic Issues

Epidural acceptable; may help control tachycardia in labor by reducing pain.
Avoid abrupt sympathetic blockade which can decrease preload.

Labor and Delivery

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.

Mitral Insufficiency

Key Points

Figure 8-2 is a diagram of mitral insufficiency

Well tolerated in pregnancy.
Frequently due to mitral valve prolapse.
Longstanding regurgitation may lead to ventricular dysfunction and/or atrial enlargement.

FIGURE 8-2.

Pathophysiology of mitral insufficiency. LA, left atrium; LV, left ventricle; RV, right ventricle.

Recommended Workup and Clinical Findings

ECG to assess severity of regurgitation, to evaluate left atrial enlargement, and to assess ventricular function.
ECG to exclude atrial fibrillation due to enlarged left atrium.

Potential Complications

Rarely, pulmonary edema or dysrhythmias.

Key Avoids

Avoids: Mitral insufficiency, aortic insufficiency

Avoid arrhythmia (immediate treatment, if occurs).
Avoid bradycardia (increases regurgitation).
Avoid increase in systemic vascular resistance (increases regurgitation).
Avoid myocardial depressant drugs.

Medical Therapy

Necessary only in presence of ventricular dysfunction or dysrhythmias.

Anticoagulation

Consider if left atrium dilated or if chronic atrial fibrillation.

Anesthetic Issues

Epidural acceptable

Labor and Delivery

Reserve cesarean section for usual obstetric indications, cesarean delivery not demonstrated to improve outcomes.

Aortic Stenosis/Idiopathic Hypertrophic Subaortic Stenosis (IHSS)

Key Points

Figure 8-3 is a diagram of aortic stenosis.

IHSS is transmitted in autosomal dominant fashion and shares similar risks and management steps with aortic stenosis. It is characterized by hypertrophy of the ventricular septum, which can obstruct left ventricular outflow.
When isolated, stenosis is often due to bicuspid aortic valve. If multiple valves involved, it is usually rheumatic in origin.
Valve diameter normally 3 to 4 cm².
Mild disease (valve area >1.5 cm², peak gradient <50 mm Hg) tolerated well in pregnancy.
Severe disease (valve area <1 cm², peak gradient >75 mm Hg or ejection fraction <55%) is at significant risk; preconception correction recommended.
Stenotic valve leads to fixed cardiac output.
Presence of symptoms worsens outcomes. Patients with severe disease should limit activity.
Complications may develop from underperfusion or excessive flow. Consequences of underperfusion are typically more life threatening than pulmonary edema from fluid overload. Goal: pulmonary artery wedge pressures (if measured) 15 to 17 mm Hg.
Use diuretics cautiously to avoid underperfusion.

FIGURE 8-3.

Pathophysiology of aortic stenosis. LV, left ventricle.

Recommended Workup and Clinical Findings

Echocardiogram to evaluate size of aortic valve opening, gradient of flow across valve and ejection fraction.
ECG may show left ventricular hypertrophy and left atrial enlargement. Arrhythmias possible if significant left atrial enlargement is present.
Harsh systolic ejection murmur.

Potential Complications

If unable to overcome obstruction and maintain adequate cardiac output:
- Angina: due to decreased coronary perfusion
- Syncope: due to poor cerebral perfusion
- Sudden death: due to arrhythmias
- Hypervolemia may lead to pulmonary edema.

Key Avoids

Avoids: Aortic stenosis

Avoid hypotension: necessary to maintain coronary perfusion.
Avoid decreased venous return: ie, excessive blood loss, position, Valsalva.
Avoid bradycardia: cardiac output maintained by heart rate and stroke volume. If stroke volume limited by obstruction, bradycardia can worsen cardiac output.
Avoid hypervolemia: may lead to pulmonary edema.

Medical Therapy

Necessary in presence of dysrhythmias

Anticoagulation

Not indicated

Anesthetic Issues

Epidural should be used with great caution to avoid hypotension. Narcotic epidural may be acceptable.

Labor and Delivery

Reserve cesarean section for usual obstetric indications, cesarean delivery not demonstrated to improve outcomes.
Avoid exertion. Consider shortening second stage of labor.
Pulmonary edema may develop postpartum due to autotransfusion effect.

Aortic Insufficiency

Key Points

Figure 8-4 is a diagram of aortic insufficiency.

Well tolerated in pregnancy.
Significant long standing regurgitation may lead to left ventricular dysfunction.

FIGURE 8-4.

Pathophysiology of aortic insufficiency. LV, left ventricle.

Recommended Workup and Clinical Findings

Echocardiogram to assess severity of regurgitation, to evaluate left atrial enlargement, and to assess ventricular function.

Potential Complications

Complications unlikely. Risk related to underlying left ventricular dysfunction.

Key Avoids

Refer to “Avoids” for mitral insufficiency.

Medical Therapy

Necessary in presence of dysrhythmias.

Anticoagulation

Not indicated.

Anesthetic Issues

Epidural acceptable.

Labor and Delivery

Reserve cesarean section for usual obstetric indications, cesarean birth not demonstrated to improve outcomes.

Mitral Valve Prolapse

One of the most common cardiac issues during pregnancy.
Most women are asymptomatic, but may have palpitations.
Pregnancy tolerated well.
No changes in antenatal or intrapartum management recommended.

Mechanical Heart Valves

Key Points

Prevention of mechanical valve thrombosis is the primary management challenge in pregnancy. Patients with mechanical valve prostheses require lifelong anticoagulation. Warfarin is the recommended anticoagulant in the nonpregnant population.
Nonmechanical tissue valves do not significantly increase risk for thromboembolism and do not require anticoagulation unless other risk factors (ie, atrial fibrillation) are present.
Patients with any of the following are considered high risk for thrombosis:²³
- Any mechanical mitral valve.
- A mechanical aortic valve with any of the following risk factors: atrial fibrillation, previous thromboembolism, ejection fraction less than 30%, hypercoagulable state, older generation thrombogenic valves or multiple valves.
- Older, more thrombogenic valves include aortic caged-ball or tilting disc valves (ie, Lillehei Kaster, Omniscience, Starr Edwards).
- The 10-year survival for patients with mechanical valves is 70%. Pregnancy does not appear to shorten survival.²⁴

Recommended Workup and Clinical Findings

Echocardiogram to establish location and type of valve and to exclude thrombosis. Evaluation of left ventricular dysfunction is also important.
ECG to establish baseline and exclude atrial fibrillation. Findings are variable like aortic caged-ball or tilting disc valves (eg, Lillehei Kaster, Omniscience, Starr Edwards).
Auscultation can reveal a variety of findings based on the type and location of the valve. Clicking of the valve may be audible.

Potential Complications

Maternal mortality risk approximately 3%.²⁵
Valve failure may occur independent of pregnancy.
Thrombosis of the valve is primary concern.
Over- and under-anticoagulation can pose risks for mother and fetus.
Rates of pregnancy loss are increased, particularly with warfarin use.

Key Avoids

Avoids: Mechanical valves on anticoagulation

Avoid warfarin beyond 6 wk gestation to avoid development of warfarin embryopathy.
Avoid insufficient anticoagulation.
Avoid continuing anticoagulation intrapartum.
Avoid waiting too long to resume anticoagulation postpartum (4-6 h).
Avoid resuming warfarin alone postpartum. Include UFH or LMWH until therapeutic.

Medical Therapy

Anticoagulation addressed below.
Treat atrial dysrhythmias if present.

Anticoagulation

Anticoagulation decisions are tailored to patient’s risk factors and preference, as well as compliance.
The 2008 Eighth American College of Chest Physicians (ACCP) guidelines for anticoagulation are summarized below:²⁶
Daily low-dose aspirin may be added to patients at significantly increased risk for thrombosis.

Option 1: High-dose LMWH therapy throughout gestation. Start enoxaparin 1 mg/kg q 12 h. Goal anti-Xa level 4 h postinjection is ~1 (0.7-1.2) U/mL.
Option 2: High-dose UFH throughout gestation. UFH subcutaneously q 12 h. Goal anti-Xa level mid interval is 0.35-0.7 U/mL or goal mid interval aPTT ≥ 2 times control.
ption 3: Either of the above regimens through completed week 12, then change to warfarin until ~36 wk or close to delivery. Goal INR ~3 (2.5-3.5). UFH or LMWH can then be resumed until delivery.
Option 4: Coumadin throughout gestation until close to delivery. Given increase in fetal complications, this regimen should be considered only for patients at highest risk (prior thromboembolism, older generation prosthesis at mitral location).

LMWH: low-molecular-weight heparin, UFH: unfractionated heparin

Anesthetic Issues

Epidural acceptable, but must be coordinated with last dose of anticoagulant to minimize risk of epidural hematoma.
High-dose, low-molecular-weight heparin (LMWH) should be discontinued 24 hours prior to epidural placement.
If the patient is on higher doses of unfractionated heparin (UFH), document normal aPTT before placing epidural.²⁷

Labor and Delivery

Reserve cesarean delivery for usual obstetric indications, cesarean not demonstrated to improve outcomes. Operative delivery poses increased risk of bleeding related to need for anticoagulation.
Consider switch to UFH at 36 weeks or before delivery. Discontinue UFH 4 to 6 hours before delivery and resume anticoagulation 4 to 6 hours postpartum.
Start LMWH or UFH 4 to 6 hours postpartum. Start warfarin same day. Continue UFH or LMWH until warfarin therapeutic 24 to 48 hours, or minimum 72 hours.

CONGENITAL CARDIAC LESIONS

Most women with repaired congenital cardiac disease have uncomplicated pregnancies, although approximately a third display a decrease in functional class, with more than two-thirds subsequently improving post-delivery.²⁸ Approximately 1% will have a late pregnancy cardiac event, with dysrhythmias and heart failure occurring most often.²⁹

Intracardiac communications in the form of atrial and ventricular septal defects, as well as patent ductus arteriosus, allow for shunting of blood across the defect. As a result, the heart must contend with the additional demands of larger flow volumes. Over time, this can lead to ventricular dysfunction, overdistension of the atria, cardiac failure, pulmonary overload, and pulmonary hypertension. Shunts are described by the direction of flow, as well as the proportion of pulmonary to systemic flow. Flow is initially left-to-right across septal defects. As pulmonary pressures increase, however, shunting can change direction, becoming right to left, as with Eisenmenger syndrome, which is addressed later.

Atrial Septal Defect

Key Points

Secundum atrial septal defect ASD is the most common defect seen in pregnancy.
ASD size and flow can worsen in adults. Spontaneous closure is rare in adults.³⁰
Pregnancy is generally well tolerated.
Pregnancy does not change indications for closure. Patients with symptoms (paradoxical emboli, exercise intolerance, fatigue, heart failure, dysrhythmias) or pulmonary to systemic shunt flow ratios greater than 2:1 are candidates for closure of the defect.

Recommended Workup and Clinical Findings

Echocardiography to evaluate size of defect, severity of shunting, and to measure pulmonary artery pressures. Pregnancy may artifactually elevate echocardiogram estimates of pulmonary artery pressures.³¹
ECG to detect partial right bundle branch block, right axis deviation, and right ventricular hypertrophy.
Auscultation will reveal systolic ejection murmur at left sternal border and wide, fixed splitting of second heart sound.

Potential Complications

Patients with large defects and significant left-to-right shunting may develop atrial arrhythmias (atrial fibrillation) and congestive heart failure in pregnancy.
Pulmonary hypertension may be present and may lead to Eisenmenger syndrome (covered in later section; demonstrated in Fig 8-5).
Paradoxical emboli: Emboli originating in lower extremities, pelvis, or from the defect itself may travel across the defect to the brain. Unrepaired lesions have a 5% risk for venous thromboembolism.³²

FIGURE 8-5.

Pathophysiology of Eisenmenger syndrome. LA, left atrium; RA, right atrium.

Medical Therapy

Necessary in presence of dysrhythmias.

Anticoagulation

Not indicated. The role of anticoagulation for patients with a history of paradoxical emboli with unrepaired defects is unclear. Venous thromboembolic diseases (VTE) prophylaxis is recommended for patients at prolonged bed rest or perioperatively, however.

Anesthetic Issues

Epidural acceptable.

Labor and Delivery

Reserve cesarean for usual obstetric indications, cesarean delivery not demonstrated to improve outcome.

Ventricular Septal Defect (VSD)

Key Points

Common in childhood; close spontaneously or have been surgically repaired by adulthood.
Smaller VSDs (<0.5 cm) restrict flow across the lesion and carry lower risk for Eisenmenger syndrome if unrepaired. Larger lesions (>1 cm) allow for more equal flow between the left and right heart and are more frequently associated with increased pulmonary pressures and Eisenmenger syndrome in adulthood (See Fig 8-5).
Because most larger lesions have been repaired by adulthood, pregnancy is generally well tolerated.

Recommended Workup and Clinical Findings

Echocardiogram to determine size of the lesion, direction of shunt flow, to estimate pulmonary artery pressures, and to assess ventricular performance.
ECG: Although usually normal, left or right ventricular hypertrophy is occasionally noted.
Auscultation: Holosystolic thrill and murmur at left sternal border.

Potential Complications

Similar to ASD.
Congestive heart failure or dysrhythmias possible with large lesions.

Key Avoids

Avoids: ASD, VSD, and PDA

Avoid hypertension (increase in systemic vascular resistance increases left-to-right shunt).
Avoid decrease in pulmonary vascular resistance (increases left-to-right shunt).
Avoid supraventricular arrhythmias, tachycardia (may increase left-to-right shunt).
If pulmonary hypertension is present, avoid increase in pulmonary vascular resistance (metabolic acidosis, excess catecholamines, hypoxemia, nitrous oxide, hypercarbia, pharmacologic vasoconstrictors, and lung hyperinflation) and hypotension. Both may worsen right-to-left shunt and lead to Eisenmenger syndrome.

Medical Therapy

Necessary in presence of dysrhythmias.

Anticoagulation

Not indicated. Refer to comments on ASD.

Anesthetic Issues

Epidural acceptable in absence of pulmonary hypertension or Eisenmenger syndrome.

Labor and Delivery

Reserve cesarean for usual obstetric indications, as cesarean birth not demonstrated to improve outcome.
Consider air filters for all intravenous lines to decrease the risk for paradoxical embolism.³³

Patent Ductus Arteriosus (PDA)

Key Points

Most cases are diagnosed and corrected in childhood.
Uncommon lesion in pregnancy.
Small PDA usually asymptomatic and tolerated well in pregnancy.
Large PDAs are associated with risks of ventricular overload and pulmonary hypertension, similar to ASD and VSD.

Recommended Workup and Clinical Findings

Echocardiogram to evaluate diameter and length of patent ductus and to calculate pulmonary-to-systemic shunt ratio. Ratios greater than 2.2 to 1 are considered large.
ECG is usually normal, but may sometimes demonstrate left or right ventricular hypertrophy.
Auscultation: Grade 3/6 continuous systolic and diastolic murmur in infraclavicular region (Gibson murmur).

Potential Complications

Similar to ASD and VSD (See Fig 8-5).

Key Avoids

Refer to table in VSD section.

Medical Therapy

Necessary in presence of dysrhythmias.

Anticoagulation

Not indicated. Refer to comments on ASD and VSD.

Anesthetic Issues

Epidural acceptable in absence of pulmonary hypertension or Eisenmenger syndrome.

Labor and Delivery

Reserve cesarean for usual obstetric indications, as it has not been demonstrated to improve outcome.

Secondary Pulmonary Hypertension and Eisenmenger Syndrome

Key Points

Figure 8-5 is a diagram of Eisenmenger syndrome due to ASD, VSD, or PDA.

Secondary pulmonary hypertension results from excess flow into the pulmonary circulation from chronic left-to-right (systemic-to-pulmonary) shunting across an intracardiac communication (most commonly ASD, VSD, PDA).
Pulmonary pressures may exceed systemic pressures. When this happens, flow across the shunt reverses to right-to-left. The result is decreased pulmonary perfusion, hypoxemia, and worsening pulmonary hypertension as a result of hypoxemia. This reversal defines Eisenmenger syndrome.
Mortality rates are high. Pregnancy termination should be discussed with the patient if she is at a previable gestational age.
Maternal-fetal mortality is nearly 50% and occurs most often in the peripartum or recent postpartum period.³⁴

Recommended Workup and Clinical Findings

In patients with suspected secondary pulmonary hypertension (ie, pulmonary hypertension which has not arisen de novo from unknown etiologies), the following evaluation is recommended:³⁵
- Pulse oximetry (finger and toe), with and without administration of supplemental oxygen.
- ECG may show ventricular hypertrophy with associated ST-T wave changes or a right atrial abnormality.
- Chest x-ray abnormalities include dilation of the central pulmonary arteries, abrupt termination of peripheral pulmonary artery branches (pruning) and right heart enlargement.
- Complete blood count.
- Nuclear lung scintigraphy.
- Transthoracic and transesophageal echocardiography, cardiovascular magnetic resonance imaging (CMRI), or computed tomography (CT).
Cyanosis, clubbing, and poor exercise tolerance are typical findings.
Polycythemia is common.

Potential Complications

Decreased systemic vascular resistance of pregnancy tends to worsen right-to-left shunting, worsening hypoxemia and, ultimately, death in 30% to 50% of patients. Death usually occurs in the first week postpartum, most commonly due to hypoxemia, volume depletion, and thromboembolism.

Key Avoids

Avoids: Secondary pulmonary hypertension and Eisenmenger syndrome

Avoid hypotension (decrease in systemic vascular resistance causes massive right-to-left shunting, bypassing pulmonary circulation leading to severe hypoxemia and worsening pulmonary hypertension).
Avoid excessive blood loss and volume depletion (causes hypotension by decrease in venous return).
Avoid increase in pulmonary vascular resistance (ie, hypoxemia, hypercarbia, metabolic acidosis, excess catecholamines).
Avoid myocardial depressant drugs.
Avoid iron deficiency.
Avoid high altitude.
Avoid exercise.

Medical Therapy

Pulmonary artery vasodilators are recommended.³⁶

Anticoagulation

Pulmonary artery thrombosis is common in nonpregnant patients (20%-70%) and is more likely to occur in women.^37,38 Prophylactic anticoagulation should be considered in patients who choose to continue with their pregnancy.

Anesthetic Issues

Epidural is contraindicated. Narcotic-only epidural may be acceptable.

Labor and Delivery

Outcomes appear to be similar with cesarean or vaginal delivery. Mortality rates for any surgery in nonpregnant patients with Eisenmenger syndrome are high (19%).³⁹
Continuous pulse oximetry and supplemental oxygen to keep oxygen saturations greater than or equal to 90%.
Avoid even small air embolisms.

Coarctation of Aorta

Key Points

Rarely seen in pregnancy, as most are corrected in childhood.
Classic presentation in adults is hypertension.
Most commonly distal to the left subclavian artery; thus, blood pressure will measure equally in both arms. However, femoral pulses are delayed compared to brachial pulses; lower extremity pressures are lower than that noted in upper extremities.
Surgical repair is recommended for adults with “peak–to-peak” gradients greater than 20 mm Hg (the difference between the peak pressure proximal and distal to the narrowing).⁴⁰
Post-repair, patients remain at risk for complications including re-coarctation, aortic aneurysm/dissection, and hypertension.
Thirty to forty percent of patients will have bicuspid aortic valves.
Ten percent of patients will have intracranial aneurysms (versus 2% in the general population).
All patients should undergo magnetic resonance angiography of the thoracic aorta and intracranial vessels.⁴¹

Recommended Workup and Clinical Findings

Echocardiogram to identify severity of narrowing, to evaluate left ventricular function, and to exclude additional cardiac defects.
ECG is usually normal, but occasionally may show left ventricular hypertrophy.
Auscultation may be normal. Various murmurs are possible, based on presence of associated anomalies and the extent of collateral vessel development.

Potential Complications

Adults with uncorrected coarctation are likely to have hypertension and coronary artery disease and are at risk for aortic dissection and heart failure. This may be exacerbated by pregnancy.

Key Avoids

Avoids: Aortic coarctation

Avoid excessive blood loss (causes hypotension by decrease in venous return).
Avoid myocardial depressant drugs.
Avoid bradycardia.
Avoid Valsalva efforts.

Medical Therapy

Treat systemic hypertension as needed.

Anticoagulation

Not indicated.

Anesthetic Issues

Epidural should be used with great caution to avoid hypotension. Narcotic epidural may be acceptable.

Labor and Delivery

Cesarean delivery rates are higher primarily due to perceived risk of intracranial hemorrhage or aortic dissection.
Vaginal delivery may be accomplished with adequate control of pain and blood pressure fluctuations, by maintaining adequate cardiac preload, and by minimizing Valsalva efforts at delivery.

Tetralogy of Fallot

Key Points

Tetrad of findings:
- Ventricular septal defect.
- Overriding aorta.
- Right ventricular outflow obstruction.
- Right ventricular hypertrophy.
Most patients undergo intracardiac repair in first year of life.
Major long-term issues post-repair include right ventricular dysfunction/failure, tricuspid regurgitation, atrial and ventricular dysrhythmias, and sudden death.⁴²
Patients may have persistent intracardiac shunting, pulmonary hypertension, aortic root dilation, or aortic valve incompetence.
Most common cause of death is sudden cardiac arrest and heart failure. Mortality rates approximately 1% annually, 25 years post procedure.

Recommended Workup and Clinical Findings

Echocardiogram to establish cardiac anatomy, to evaluate valvular and right ventricular function, to assess pulmonary hypertension and, to measure aortic root diameter.
Electrocardiogram findings will vary, depending on the type of correction performed. It is important to establish a baseline and to exclude atrial and ventricular dysrhythmias.

Potential Complications

Spontaneous fetal loss rates are increased.
Patients with surgically corrected tetralogy of Fallot generally tolerate pregnancy well. However, patients with evidence of right ventricular dysfunction, severe pulmonary regurgitation, pulmonary hypertension, or hypoxemia are at increased risk for cardiac complications. These include dysrhythmias, cardiac failure, worsening cyanosis, pulmonary edema, and pulmonary embolism.⁴²
Patients with persistent intracardiac shunts are at additional risk. Refer to sections on VSD, ASD, and PDA.

Medical Therapy

Antidysrhythmic therapy as needed.
Patients may require diuretic therapy, β blockers, or antihypertensive medications.

Anticoagulation

Not indicated.

Anesthetic Issues

Epidural acceptable if an intracardiac shunt is not present.

Labor and Delivery

Cesarean delivery is common and typically performed due to perceived cardiac risk. However, data are lacking to demonstrate improved outcomes compared to vaginal delivery.

Marfan Syndrome

Key Points

Autosomal dominant condition with cardiac and noncardiac manifestations. Eighty percent will have cardiac manifestations of the disease.
Aneurysmal dilation and dissection of the aorta account for the majority of morbidity and mortality with Marfan syndrome.
Sixty to eighty percent of adults with Marfan syndrome will have aortic root dilation.
Risk of aortic rupture or dissection during pregnancy is roughly 10%, if aortic root diameter greater than 4 cm.⁴³ Pregnancy should be avoided if the aortic root dimension exceeds 4 cm.
Rupture and dissection may occur even with normal aortic dimension (<1%). Thus, all women with Marfan syndrome should be counseled against pregnancy; termination of pregnancy should be discussed with patients if they are at a previable gestational age.⁴⁴
Aortic root diameter greater than 4.5 cm is an indication for preconception repair, if patient desires pregnancy. The risk for dissection is decreased, but not eliminated following surgical correction.
Pregnancy may hasten rate of aortic root dilation in patients with aortic root greater than 4 cm.⁴⁵

Recommended Workup and Clinical Findings

Echocardiogram to establish size of aortic root. This should be followed serially, even if baseline diameter is normal.
Marfan syndrome is associated with other abnormalities, including: joint hypermobility, ectopia lentis, pectus excavatum, disproportionately wide arm span, scoliosis, and arachnodactyly.

Potential Complications

Aortic root dissection and rupture are the most significant risks of pregnancy.

Key Avoids

Avoids: Marfan syndrome

Avoid hypertension.
Avoid tachycardia.
Avoid Valsalva activities.

Medical Therapy

Labetalol or metoprolol is required so as to maintain maternal heart rate less than 110 beats/min after submaximal exercise and less than 90 beats/min resting.

Anticoagulation

Not indicated.

Anesthetic Issues

Epidural is acceptable and may be recommended to minimize tachycardia due to pain and to minimize urge for Valsalva efforts during delivery.

Labor and Delivery

Avoid tachycardia—consider continuous β blocker.
Assisted second stage to minimize Valsalva effort. Avoid pushing in labor.
Cesarean may benefit patients with aortic root diameter greater than 4 cm, aortic root dissection, or heart failure.⁴⁶

Peripartum Cardiomyopathy

Key Points

Criteria for diagnosis of peripartum cardiomyopathy (PPCM)
Classic:
- Development of cardiac failure in last month of pregnancy, or within 5 months postpartum.
- Absence of identifiable cause for cardiac failure.
- Absence of recognizable heart disease prior to last month of pregnancy.
Additional:
- Left ventricular systolic dysfunction: ejection fraction less than 45%, shortening fraction less than 30%, and left ventricular end-diastolic dimension greater than 2.7 cm/m² body surface area.⁴⁷
Ninety percent of cases occur in first 2 months postpartum.
Half of deaths occur in first 6 weeks postpartum.
High rate of recurrence in subsequent pregnancies, even with apparent recovery of cardiac function. Consider stress echocardiogram to evaluate cardiac function before subsequent pregnancies. Patients with incomplete recovery (ejection fraction <50%) have a high rate of decompensation and should be counseled against future pregnancies.
Recommend low salt diet (<4 g/d), fluid restriction (<2 L/d), and activity limitation.

Recommended Workup and Clinical Findings

Echocardiogram (see Key Points, above). Establish baseline and repeat every trimester, or with worsening symptoms.
ECG may show nonspecific findings, possibly atrial fibrillation.
Chest x-ray will demonstrate cardiomegaly and pulmonary edema.
Patients will typically present with shortness of breath, orthopnea, fatigue, and leg edema.
B-type natriuretic peptide (BNP) will be markedly elevated.

Potential Complications

Worsening cardiac failure and pulmonary edema. Patients with an initial ejection fraction of less than 25% are at greatest risk for requiring subsequent cardiac transplant.⁴⁸
Failure to normalize cardiac function within 6 months postpartum carries mortality rate of 85% by 5 years.
Cause of death commonly dysrhythmias, progressive cardiac failure, or thromboembolic phenomena. Atrial fibrillation is the most common dysrhythmia in patients with peripartum cardiomyopathy.⁴⁹

Key Avoids

Avoids: Cardiomyopathy

Avoid hypertension.
Avoid excessive fluid.
Avoid increasing cardiac demand.

Medical Therapy

Goals of therapy:
- Reduce preload: diuretic therapy (ie, furosemide 20-40 mg po qd).
- Reduce afterload: vasodilator therapy (ie, hydralazine, 25-100 mg po qd, amlodipine, 5-10 mg po qd; postpartum use enalapril, 5 mg bid).
- Improve contractility: digoxin, 0.25 to 0.5 mg po qd.
- Reduce myocardial oxygen requirement: Goal HR 80 to 100 beats/min (metoprolol, 25-100 mg po qd, or carvedilol, 3.25 to 25 mg po qd).
Pentoxifylline 400 mg po tid, may reduce inflammation and reduce mortality risk.^50,51

Anticoagulation

Consider in presence of significant ventricular dilation or atrial dysrhythmia. The risk for VTE associated with PPCM is highest during the first 4 weeks postpartum.⁵²

Anesthetic Issues

Epidural acceptable and will decrease both preload and afterload. Also minimizes tachycardia from pain.

Labor and Delivery

Reserve cesarean for usual obstetric indications, cesarean delivery not demonstrated to improve outcome.
Consider assisted second stage, if significant cardiac dysfunction.

Acute Myocardial Infarction

Key Points

Rare event, but risk increased by pregnancy.
3 major risk factors: age greater than 30 yrs, hypertension, diabetes.
Eighty percent occur in antepartum or postpartum period.
Findings with acute myocardial infarction (MI): atherosclerosis (40%), coronary artery dissection (27%), coronary thrombus (21%), normal coronary artery (13%-29%).^53,54
Diagnosis established with elevated troponin and/or elevated CKMB levels, plus abnormal ECG. Most associated with ST segment elevation (STEMI).

Recommended Workup and Clinical Findings

Echocardiogram to exclude unrecognized structural cardiac abnormalities and, to evaluate ventricular function.
ECG to establish diagnosis: ST segment elevation or depression, Q wave abnormalities.
Lab workup should include: troponin, CBC with platelet count, PT/INR, aPTT, electrolytes, magnesium, BUN, creatinine, blood glucose, and serum lipid profile.

Potential Complications

Cardiac arrest possible. Prepare for possibility of perimortem cesarean delivery.
Maternal mortality (in-hospital MI) 5%-7%.^55,56
Cardiac failure or dysrhythmias.

Medical Therapy

Management algorithm once acute MI suspected: (Goal is completion of MONA in <10 minutes).
- M: Morphine sulfate 2 to 4 mg IV.
- O: Oxygen via nasal cannula or mask.
- N: Nitroglycerin, 0.5 mg sublingual q 5 min × 3.
- A: Aspirin, 160 to 325 mg po (chewed).
Follow with 12-lead ECG (repeat in 5-10 minutes if MI suspected and initial ECG normal).
If ECG shows ST elevation or new left bundle branch block, treat as acute MI in consultation with cardiologist:
- β Blockers.
- IV nitroglycerin.
- IV heparin.
- Antiplatelet therapy (clopidogrel).
- Morphine IV to treat pain.
- Antithrombin therapy.
- Consider reperfusion therapy in consultation with cardiologist.
- If viable fetus, monitor fetal heart rate throughout therapy.

Anticoagulation

See above.

Anesthetic Issues

Epidural recommended to reduce afterload and to minimize pain and subsequent tachycardia.

Labor and Delivery

Expert opinion recommends postponing delivery for 2 to 3 weeks postinfarction to minimize additional cardiac demands.⁵⁴
If vaginal delivery attempted, consider assisted second stage to minimize cardiac workload.
Delivery route should be individualized. Cesarean delivery may be associated with increased mortality risk.⁵⁷
Avoid hypertension or tachycardia.
Avoid Methergine and prostaglandins as they may cause coronary vasoconstriction.

REFERENCES