Cardiac disease in pregnancy

Published on 09/03/2015 by admin

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Chapter 48 Cardiac disease in pregnancy

Michael Flynn

Incidence. Fewer than 1% of all pregnancies are affected by maternal cardiac disease.

Pathophysiology of cardiovascular changes in pregnancy

Intravascular volume

This is increased by 50% by early mid-trimester and peaks at 32–34 weeks gestation. In a woman with limited cardiac output secondary to cardiovascular disease, volume overload is poorly tolerated and congestive cardiac failure a risk.

Decreased peripheral resistance in pregnancy

This is important in the woman with potential right-to-left shunts, as the shunts tend to increase with lowered vascular resistance.

Cardiac output

• Cardiac output rises early in pregnancy, and is unrelated to rise in plasma volume.
• In labour, the cardiac output rises progressively from the first stage to an additional 50% in the late second stage, with an increase of over 7 L/minute. This great change, plus the dramatic shifts of fluid that occur at delivery, is poorly tolerated in women whose cardiac output depends on adequate preload (pulmonary hypertension) or those with fixed cardiac output (mitral stenosis).
• Epidural anaesthesia and general anaesthesia produce dramatic changes in cardiac output.

Maternal mortality risks in cardiovascular disease

Mortality is most likely in conditions where pulmonary blood flow cannot be raised secondary to obstruction. Maternal mortality risk may be classified into the following three groups.

Low risk (mortality <1 %)

• uncomplicated atrial septal defect, ventricular septal defect or patent ductus arteriosus
• mitral stenosis
• tricuspid incompetence
• corrected tetralogy of Fallot
• bioprosthetic valve

Medium risk (mortality <15%)

• mitral stenosis with atrial fibrillation
• artificial valve
• previous myocardial infarction
• aortic stenosis
• uncorrected tetralogy
• uncomplicated coarctation of aorta or Marfan’s syndrome

High risk (mortality <50%)

• pulmonary hypertension
• Eisenmenger’s syndrome
• complicated coarctation
• Marfan’s syndrome with aortic dilatation
• peripartum cardiomyopathy

Fetal risks in maternal cardiovascular disease

Family history

• The presence of a congenital cardiac anomaly in either parent or sibling increases the risk of cardiac anomaly in the offspring to about 2%–4%, or twice that of the normal population. The risk rises to 10%–12% in mothers with defects, including atrial septal defect, ventricular septal defect, patent ductus arteriosus and tetralogy of Fallot. These have multivariant inheritance.
• Idiopathic hypertrophic subaortic stenosis is an autosomal dominant condition.
• Environmental risk factors include rubella virus and alcohol.

In women with cyanotic heart disease

The maternal haematocrit appears to correlate with perinatal outcome; a haematocrit of >65% is associated with poor outcome.

Management of cardiovascular disease in pregnancy

History

• The commonest symptom of heart disease is breathlessness on exertion, although this is unreliable in pregnancy.
• Syncope can occur with normal pregnancy, aortic stenosis, hypertrophic obstructive cardiomyopathy, tetralogy of Fallot and dysrhythmias.
• A history of rheumatic fever or previous investigation for a murmur are important.

Physical examination

• In normal pregnancy it is common for premature atrial and ventricular ectopics, oedema, loud first heart sound and third heart sounds to be present.
• An ejection systolic murmur may be present in up to 90% of women.

Investigations

• Chest X-ray in normal pregnancy shows slight cardiomegaly and increased pulmonary vascular markings.
• Electrocardiograph in normal pregnancy shows inversion in T waves, Q wave in lead III.
• Echocardiography is required to identify structural abnormalities.

Counselling

• Ideally, cardiovascular disease is identified and investigated before pregnancy, with the maternal risks evaluated and appropriate contraception advised.
• If termination of pregnancy is indicated, prostaglandin termination should be used with caution. Possible indications for termination include Eisenmenger’s syndrome, primary pulmonary hypertension and pulmonary veno-occlusive disease.
• Risk factors for congestive cardiac failure need to be monitored and managed appropriately. Risks include infections, hypertension, obesity, multiple pregnancy, anaemia, arrhythmia and hyperthyroidism.

Endocarditis and pregnancy

• The efficacy of antibiotic prophylaxis against infective endocarditis in pregnancy has not been proven, although it is accepted that benefits override the possible risks.
• Women at risk include those with prosthetic heart valves, most congenital malformations, rheumatic mitral stenosis, hypertrophic cardiomyopathy, mitral valve prolapse with regurgitation, or past history of subacute bacterial endocarditis.
• A regimen may include intravenous (amoxy)ampicillin 1–2 g every 8 hours, together with gentamicin 1.5 mg/kg when labour commences and continuing for 24 hours.

Antenatal management

• Attend a combined obstetric and cardiac clinic.
• Ensure adequate rest.
• Watch for risks of congestive cardiac failure.
• Initiate anticoagulation therapy for patients with pulmonary hypertension, artificial valves or atrial fibrillation.

Labour

• Aim for spontaneous vaginal delivery at term, as induction of labour is associated with an increased risk of sepsis and caesarean section.
• Maintain a strict fluid balance.
• Adequate analgesia is essential, although epidural should be used with caution, especially in hypertrophic obstructive cardiomyopathy, aortic stenosis and Eisenmenger’s syndrome.
• Avoid aortocaval compression.
• Shorten the second stage.
• If possible, avoid delivery in the lithotomy position.
• Avoid ergometrine.
• If possible, avoid caesarean section in the presence of cardiac failure.
• Oxygen supplementation is recommended.
• Avoid sympathomimetic drugs.
• Prevent endocarditis with intravenous antibiotics.
• Discuss with the woman the use of intensive monitoring and intensive care in labour.

Postpartum

• Maintain a strict fluid balance to predict cardiac failure associated with the major fluid shifts after delivery of the placenta.
• Continued oxygen postpartum is advised.

Congenital heart disease

Atrial septal defect

This is the commonest congenital anomaly, usually asymptomatic but occasionally associated with atrial fibrillation. Hypervolaemia in pregnancy can cause worsening in left-to-right shunting. This increases the burden on the right ventricle, which in turn may result in cardiac failure. Most patients tolerate pregnancy, labour and delivery well. In labour, general management includes the use of prophylactic antibiotics and avoidance of fluid overload, and the use of lumbar epidural is usually well-tolerated.

Ventricular septal defect

There is a risk of cardiac failure, arrhythmias and aortic regurgitation with large defects. If uncomplicated, the pregnancy, labour and delivery are tolerated well. The management is as for atrial septal defect.

Patent ductus arteriosus

While usually asymptomatic and well-tolerated in pregnancy, labour and delivery, the possibility of high-pressure, high-flow left-to-right shunting with large lesions may worsen prognosis.

Eisenmenger’s syndrome

This is a syndrome arising from conditions of congenital left-to-right shunt, in which progressive pulmonary hypertension leads to shunt reversal or bidirectional shunting. In the antepartum period, reduced vascular resistance causes an increase in right-to-left shunting. This leads to a reduction in pulmonary perfusion, with hypoxia and deterioration of the fetal/maternal condition.

Hypotension in the woman with Eisenmenger’s syndrome reduces right ventricular filling pressure and lowers perfusion in pulmonary beds. Therefore, reduction in blood pressure with haemorrhage or anaesthesia can lead to sudden death.

Management

• If corrected in childhood with no residual damage, there are usually no complications. If not, then pulmonary hypertension could decompensate during pregnancy.
• Advise the patient about the risks of continuing pregnancy.
• Avoid caesarean section and epidural anaesthesia.
• Initiate anticoagulation therapy.
• Avoid ergometrine and procedures that produce a sudden rise in venous return.

Coarctation of the aorta

The commonest site is at the origin of the left subclavian artery and can be associated with abnormal aorta, ventricular septal defect, patent ductus arteriosus and intracranial aneurysm in the circle of Willis.

Maternal mortality risk is dependent on whether there are associated vascular or cardiac lesions and on the increased risk of pre-eclampsia. There is a risk of dissection of aorta with hyperdynamic pregnancy state, and management involves treating hypertension aggressively.

Tetralogy of Fallot

This cyanotic heart condition consists of ventricular septal defect, overriding aorta, right ventricular hypertrophy and pulmonary stenosis. If uncorrected, the maternal mortality rises to 4%–15%.

Pulmonary hypertension

There is high maternal mortality during pregnancy or immediately postpartum. Avoid fluid overload, pulmonary congestion, heart failure and hypotension. It can lead to hypoxia and sudden cardiac death.

Acquired cardiac lesions

Rheumatic heart disease

This is the commonest heart disease in pregnancy.

Risks

• reduced ability to increase cardiac output in those with significant mitral stenosis
• endocarditis with mitral regurgitation
• sudden death with aortic stenosis
• pulmonary oedema with severe aortic regurgitation

Acute rheumatic fever

• is very uncommon in pregnancy
• presents with non-specific malaise, joint pains, anaemia, rash
• diagnosis includes raised antistreptolysin-O titre, electrocardiograph with prolonged PR and QT intervals, erythrocyte sedimentation rate >80 mm/hour (normal pregnancy <60 mm/hour)

Mitral stenosis

• This is the commonest rheumatic valvular lesion in pregnancy. The main problem is that ventricular diastolic filling against a valvular obstruction can cause a relatively fixed cardiac output and therefore risks acute cardiac failure and pulmonary oedema, and occasionally atrial fibrillation.
• Clinical symptoms include increasing shortness of breath and fatigue.
• On examination, there are signs of cardiac failure, atrial fibrillation, and the early diastolic rumbling murmur is heard.
• Atrial fibrillation is associated with a risk of thromboembolism, and requires anticoagulation therapy.

Management

• Cardiac output in mitral stenosis depends on adequate diastolic filling time and left ventricular preload. Therefore, tachycardia (from infections or blood loss) and fluid overload must be carefully avoided.
• Labour is a vulnerable time. Intrapartum fluctuations of cardiac output can be minimised with the use of epidural anaesthesia and a careful watch postpartum for fluid shifts.
• Antibiotic prophylaxis is indicated to avoid endocarditis.
• Immediately after delivery of the baby, there is a sharp rise in left atrial pressure, which may precipitate cardiac failure.

Mitral insufficiency

This may be secondary to rheumatic fever. However, the more common lesion is mitral valve prolapse. It is usually well tolerated in pregnancy, except for the risks of atrial fibrillation and endocarditis (therefore, require antibiotic prophylaxis in labour).

Aortic stenosis

• There is a higher maternal mortality in rheumatic compared with congenital aortic stenosis.
• It is not considered haemodynamically significant until the orifice is less than a third of normal size.
• In severe aortic stenosis, there is relatively fixed cardiac output, resulting in inadequate coronary artery and cerebral perfusion causing angina, syncope and sudden death. The times of greatest risk are delivery and pregnancy termination.
• It is very important to maintain adequate cardiac output. If hypotension occurs with blood loss, epidural or inferior vena caval occlusion, sudden death can occur.
• Surgical correction of the disease before conception greatly improves prognosis.

Aortic insufficiency

This is usually well tolerated in pregnancy, as tachycardia results in less time for regurgitation. Endocarditis prophylaxis is indicated in labour.

Cardiomyopathy

Hypertrophic obstructive cardiomyopathy

• This is a subaortic stenosis, with pathological appearances of hypertrophy and disorganisation of cardiac muscle.
• The woman presents with chest pain, syncope and arrhythmia.
• Diagnosis is made on echocardiography.
• The pregnancy is often well tolerated, and outcome is dependent on the severity of left ventricular outflow tract obstruction.
• Management includes beta-blocker if indicated, avoiding hypotension because of the risk of obstruction of left ventricular outflow tract, which occurs in aortocaval compression, and antepartum/postpartum haemorrhage.

Peripartum cardiomyopathy

• This rare cardiomyopathy may develop in the last month of pregnancy or the first 6 months postpartum, with a peak incidence in the second postpartum month.
• It is more common in older multiparous patients who breastfeed and have a history of hypertension, pre-eclampsia or multiple pregnancy with poor nutrition.
• Investigations include chest X-ray with non-specific cardiomegaly, electrocardiography, showing non-specific changes or widespread abnormalities or arrhythmias, and echocardiography with a grossly dilated heart.
• Management includes anticardiac failure therapy, anticoagulation, and aiming for a vaginal delivery. Treat with diuretics and beta-blockers, decrease sodium intake, and use angiotensin-converting enzyme (ACE) inhibitors when delivered.
• The major cause of mortality is thromboembolism.
• Counsel the patient regarding the recurrence rate in future pregnancies. If the heart returns to a normal size within 12 months, there is less than a 15% mortality in the next pregnancy. If cardiomegaly persists until the next pregnancy, there is a 40%–80% associated mortality.

Marfan’s syndrome

This is an autosomal dominant disorder characterised by a generalised weakness of connective tissue. It is associated with mitral or aortic regurgitation and dangerous weaknesses in the aortic root and aortic wall.

Maternal risks

• These include vascular aneurysms, especially rupture or dissection of the aorta or splenic artery, and abnormal aortic valve or aortic dilatation.
• Initial echocardiography evaluation includes the diameter of the aortic root. If the aortic root is <40 mm, the maternal mortality is <5%, but if the dilatation is >40 mm, the mortality reaches 50%.

Management

• Treat hypertension aggressively.
• Use beta-blocker medication if aortic dilatations are present, even without hypertension, as this reduces the pulsatile pressure and decreases the force of contraction of the heart, thereby reducing the rate of progress of aortic dilatation.
• Perform a caesarean section if there is evidence of aortic disease.

Myocardial infarction

The overall mortality in pregnancy is 35%, but mortality increases as pregnancy progresses. In young women, myocardial infarction in the puerperium is often associated with pre-eclampsia, possibly from dissection of coronary arteries.

Management

• Management is similar to that for non-pregnant patients.
• Delivery within 2 weeks of the infarction raises mortality.
• Labour must be intensively monitored.
• Continuous oxygen and epidural anaesthesia is indicated.
• Management includes elective shortening of the second stage with instrumental delivery.
• Ergometrine is contraindicated, as it may cause coronary artery spasm.

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