Cardiac Disease in Pregnancy

Cardiac disease complicates 1–3% of pregnancies but is a leading cause of indirect (non-obstetric) maternal mortality. The exam wants you to integrate cardiology with the haemodynamic stress of pregnancy: know the NYHA-based prognosis, the three "danger windows," the lesions that forbid pregnancy outright, and the drug list that is safe versus banned.

Why pregnancy stresses the heart

Pregnancy is a high-output, low-resistance state. The diseased heart that copes at rest decompensates when these changes peak.

Parameter	Direction of change	Magnitude	Timing of peak
Blood volume	↑	+40–50%	30–34 weeks
Plasma volume	↑ (> RBC mass)	+45%	→ physiological anaemia
Cardiac output	↑	+30–50%	begins 5 wks, plateaus ~28–32 wks
Heart rate	↑	+10–20 bpm	progressive
Stroke volume	↑	early rise	falls late term
Systemic vascular resistance	↓	−20–30%	mid-pregnancy nadir
Colloid osmotic pressure	↓	predisposes to pulmonary oedema	term

Cardiac output rises further in labour (each uterine contraction auto-transfuses ~300–500 mL) and peaks immediately postpartum due to relief of caval compression and uterine involution emptying blood into the systemic circulation.

High-yield: There are three periods of maximal cardiac risk — (1) 28–32 weeks (CO/blood volume peak), (2) second stage of labour (bearing-down effort), and (3) immediately postpartum / first 24–72 h (auto-transfusion + fluid shifts). The single "most dangerous period" classically quoted is 32 weeks (around 28–32 wks).

Classification of risk

NYHA functional classification (clinical, prognostic)

Class	Symptoms	Outcome
I	No limitation; ordinary activity asymptomatic	Excellent; pregnancy usually well tolerated
II	Slight limitation; symptoms on ordinary activity	Good with monitoring
III	Marked limitation; symptoms on less-than-ordinary activity	High risk; consider termination/intensive care
IV	Symptoms at rest	Pregnancy contraindicated; very high mortality

High-yield: NYHA Class I and II generally have good maternal outcomes; Class III and IV carry markedly increased mortality. The classification is functional — it is assessed clinically, not by echo. Maternal mortality is concentrated in Classes III–IV.

WHO (mWHO) risk classification

The modified WHO classification is the modern lesion-based tool the exam increasingly references.

• mWHO I – minimal risk (small/repaired lesions, mild PS, mild MVP).
• mWHO II – small increase (unoperated ASD/VSD, repaired tetralogy).
• mWHO II–III – moderate (mild LV dysfunction, HCM, native/tissue valve disease not in IV).
• mWHO III – significantly increased risk; expert care, frequent cardiology review (mechanical valve, systemic RV, Fontan, cyanotic heart disease).
• mWHO IV – pregnancy contraindicated; if it occurs, discuss termination.

High-yield (mWHO IV — pregnancy contraindicated): Pulmonary arterial hypertension of any cause / Eisenmenger syndrome, severe systemic ventricular dysfunction (LVEF < 30% or NYHA III–IV), previous peripartum cardiomyopathy with any residual LV impairment, severe symptomatic mitral stenosis, severe symptomatic aortic stenosis, Marfan with aorta > 45 mm, bicuspid aortic valve with aorta > 50 mm, native severe coarctation.

Spectrum of lesions: rheumatic vs congenital

Historically rheumatic heart disease dominated pregnancy cardiac disease in India; with falling rheumatic incidence and more women with surgically corrected congenital lesions surviving to reproductive age, congenital heart disease is now the commonest in the West. In India, rheumatic mitral stenosis remains the single most common and most dangerous acquired valvular lesion in pregnancy.

Feature	Mitral stenosis (rheumatic)	Regurgitant / left-to-right shunt lesions
Example	MS, the prototype	MR, AR, VSD, ASD, PDA
Tolerance of pregnancy	Poorly tolerated	Generally well tolerated
Why	Fixed orifice; tachycardia + ↑volume → ↑LA pressure → pulmonary oedema	↓SVR of pregnancy reduces regurgitant/shunt fraction
Feared event	Acute pulmonary oedema, AF with fast ventricular rate	Less acute decompensation

High-yield: Stenotic lesions (especially mitral stenosis) tolerate pregnancy badly; regurgitant lesions tolerate it well. This is because the fall in SVR worsens fixed-orifice stenosis but unloads regurgitation. The dangerous moment in MS is tachycardia (shortens diastole → less LV filling → pulmonary oedema) — hence beta-blockers are central.

Mitral stenosis — practical points

• Symptoms worsen as volume peaks (28–32 wks) and in labour.
• Atrial fibrillation with rapid ventricular rate is the classic precipitant of acute decompensation.
• Management: rate control with beta-blockers (metoprolol; labetalol), diuretics for congestion, restrict activity, treat anaemia and infection.
• For severe symptomatic MS refractory to medical therapy → percutaneous balloon mitral valvotomy (PBMV), ideally in the second trimester with abdominal shielding. PBMV is the procedure of choice over open surgery in pregnancy.

Eisenmenger syndrome (the classic catch)

A pre-existing left-to-right shunt (VSD/ASD/PDA) develops pulmonary vascular obstructive disease → pulmonary hypertension → reversal to right-to-left shunt with cyanosis.

• Pregnancy is absolutely contraindicated; maternal mortality 30–50%.
• The fall in SVR worsens the right-to-left shunt → profound hypoxaemia.
• Death typically occurs peripartum or in the first postpartum week.
• If a patient presents already pregnant → counsel for termination.

High-yield: Eisenmenger syndrome = absolute contraindication to pregnancy. Other absolute contraindications: primary pulmonary hypertension, severe symptomatic aortic stenosis, Marfan with dilated aortic root (> 45 mm), severe LV dysfunction (EF < 30%), and prior PPCM with residual dysfunction.

Peripartum cardiomyopathy (PPCM)

A favourite NEET PG topic — a dilated cardiomyopathy unique to the peripartum window.

Definition / diagnostic criteria (4 classic criteria):

1. Heart failure developing in the last month of pregnancy or within 5 months postpartum.
2. Absence of an identifiable cause of heart failure.
3. Absence of recognisable heart disease before the last month of pregnancy.
4. LV systolic dysfunction with LVEF < 45% (± LV dilation, fractional shortening < 30%).

High-yield: PPCM presents most commonly in the first month postpartum, NOT antenatally. The timing window "last month of pregnancy to 5 months postpartum" and EF < 45% are the examined numbers. It is a diagnosis of exclusion.

Risk factors: multiparity, multiple gestation, advanced maternal age, pre-eclampsia/hypertension, African descent, twin pregnancy, prolonged tocolysis.

Clinical features: dyspnoea, orthopnoea, oedema, fatigue (overlaps with normal late pregnancy — high index of suspicion needed). Risk of mural thrombus and embolism.

Management:

• Standard heart-failure therapy: diuretics, beta-blockers, hydralazine + nitrates (antenatally) and ACE inhibitors / ARBs postpartum (ACEi contraindicated antenatally).
• Anticoagulation for very low EF (< 30–35%) due to thromboembolic risk.
• Bromocriptine (blocks prolactin) is an emerging adjunct.
• Diuretics, salt restriction.

Prognosis: Outcome hinges on LV recovery. If LV size/function does NOT normalise, a subsequent pregnancy is contraindicated (high recurrence and mortality). Even with recovery, recurrence risk persists.

High-yield: Prior PPCM with persistent LV dysfunction → future pregnancy contraindicated (mWHO IV). If EF fully recovers, future pregnancy is still high-risk but conditionally possible.

Clinical features & the mimicry problem

Normal pregnancy mimics heart disease: dyspnoea, fatigue, dependent oedema, a hyperdynamic apex, physiological systolic ejection murmur, third heart sound, and venous hum/mammary souffle are all normal.

Finding	Normal in pregnancy	Pathological — needs work-up
Systolic ejection (flow) murmur	Yes (very common)	—
Soft S3	Yes	—
Diastolic murmur	No	Always pathological
Loud (≥ grade 3/6) or harsh systolic murmur	—	Suspicious
Cyanosis, clubbing	No	Pathological
Fixed split S2, parasternal heave	No	Pathological

High-yield: A diastolic murmur in pregnancy is always pathological and mandates echocardiography. Likewise cyanosis, clubbing, or a loud thrill.

Diagnosis & investigation of choice

• Echocardiography = investigation of choice (safe, no radiation; quantifies lesion severity, EF, chamber size, pulmonary pressures). It is also used to diagnose PPCM and to guide PBMV.
• ECG: may show normal pregnancy changes (left-axis shift, small Q/inverted T in III); useful for arrhythmia.
• Chest X-ray: only with abdominal shielding if essential.
• BNP/NT-proBNP: normally only mildly elevated in pregnancy; a markedly raised value suggests cardiac decompensation.

Management — stepwise antenatal approach

Booking → risk-stratify (NYHA + mWHO + echo) → joint cardiac-obstetric clinic → optimise medical therapy → plan delivery → intensive peripartum monitoring → postpartum vigilance.

1. Pre-conception counselling — the ideal; assess mWHO class, correct lesions before pregnancy, review teratogenic drugs (warfarin, ACEi).
2. Antenatal — frequent visits, treat anaemia/infection/arrhythmia aggressively (they precipitate failure), limit weight gain and activity, influenza vaccination, restrict excessive exertion.
3. Anticoagulation for mechanical valves — the classic dilemma (see below).
4. Mode of delivery — vaginal delivery is preferred in most cardiac disease (lower haemodynamic stress, less blood loss, fewer infections than caesarean). Caesarean reserved for obstetric indications and specific lesions (severe AS, Marfan with dilated aorta, Eisenmenger, recent/acute decompensation).
5. Second stage — shorten/assist with forceps or vacuum to avoid Valsalva straining; epidural analgesia reduces pain-driven tachycardia and afterload.
6. Infective endocarditis prophylaxis — not routinely recommended for uncomplicated vaginal/caesarean delivery; reserved for highest-risk lesions per current guidelines.
7. Postpartum — most dangerous immediate period; monitor in HDU for 24–72 h, cautious fluid balance, watch for pulmonary oedema. Avoid ergometrine for routine third-stage management in cardiac patients.

High-yield: Vaginal delivery with a shortened, assisted second stage and epidural is the preferred mode in most cardiac disease. Ergometrine is avoided (causes intense vasoconstriction and a sudden rise in venous return/BP). Oxytocin is given as a slow infusion (bolus causes hypotension and tachycardia).

Drugs in cardiac disease of pregnancy

Drug / class	Status in pregnancy	Note
Beta-blockers (metoprolol, labetalol)	Safe / preferred	Rate control in MS, PPCM, arrhythmia; atenolol best avoided (IUGR)
Heparin (LMWH/UFH)	Safe (does not cross placenta)	Anticoagulant of choice in 1st trimester & near term
Hydralazine, methyldopa, nifedipine	Safe	BP control
Digoxin	Safe	Rate control / failure
Furosemide (diuretics)	Use cautiously	For pulmonary congestion
Adenosine	Safe	DOC for acute SVT
Warfarin	Teratogenic (1st trimester); fetal warfarin syndrome, fetal bleeding	Best avoided 6–12 wks & near term
ACE inhibitors / ARBs	Contraindicated	Fetal renal dysgenesis, oligohydramnios, skull defects
Amiodarone	Avoid	Fetal hypothyroidism, IUGR
Ergometrine	Avoid in cardiac patients	Vasoconstriction, BP/venous-return surge

High-yield (banned/teratogenic): ACE inhibitors, ARBs, warfarin (1st trimester), amiodarone, atenolol are the cardiac drugs to mark as contraindicated/avoid. DOC for acute SVT in pregnancy = adenosine. Safe rate control = beta-blockers + digoxin.

Mechanical prosthetic valve anticoagulation (classic dilemma)

• Warfarin gives the best maternal valve protection but is teratogenic (especially weeks 6–12) and risks fetal intracranial bleed.
• LMWH/UFH is fetus-safe but carries higher maternal valve thrombosis risk.
• Common scheme: heparin in the first trimester and near term; warfarin in the second trimester (or warfarin throughout if daily dose is low, e.g. ≤ 5 mg). Switch to heparin before delivery.

Complications

• Acute pulmonary oedema / congestive cardiac failure — peak at 28–32 wks, in labour, and postpartum.
• Atrial fibrillation / other arrhythmias — especially with MS; precipitate decompensation and thromboembolism.
• Infective endocarditis.
• Thromboembolism — valve thrombosis, mural thrombus (PPCM), pulmonary embolism.
• Maternal death — cardiac disease is a leading indirect cause of maternal mortality.
• Fetal: IUGR, prematurity, fetal loss (especially cyanotic/Eisenmenger), and recurrence of congenital heart disease in offspring (counsel ~3–5%, higher with maternal CHD).

Key differentials

• Physiological dyspnoea of pregnancy vs early heart failure — orthopnoea, PND, raised JVP, basal crepitations and a diastolic murmur favour pathology.
• PPCM vs pre-eclampsia/pulmonary oedema of pre-eclampsia vs amniotic fluid embolism vs pre-existing dilated cardiomyopathy — overlapping breathlessness; echo + timing + proteinuria/BP differentiate.
• Pulmonary embolism vs cardiac decompensation — both cause acute dyspnoea postpartum.
• Anaemic high-output state vs structural disease.

Recently asked / exam angle

• "Most dangerous period for a cardiac patient in pregnancy?" → around 32 weeks (28–32 wks) when blood volume/CO peak; the immediate postpartum is the other classic answer.
• "Absolute contraindication to pregnancy among cardiac lesions?" → Eisenmenger syndrome / pulmonary arterial hypertension.
• PPCM single-best-answer stems: timing (last month → 5 months postpartum), EF cut-off (< 45%), it is a diagnosis of exclusion, and future pregnancy contraindicated if LV does not recover.
• "Which valvular lesion tolerates pregnancy worst?" → Mitral stenosis (stenotic > regurgitant).
• "Procedure for severe symptomatic MS in pregnancy?" → PBMV in the second trimester.
• Drug catches: ACEi/ARB and warfarin contraindicated; adenosine = DOC for SVT; ergometrine avoided; atenolol avoided (IUGR).
• NYHA is a functional (clinical) classification, with Class III–IV carrying the high mortality.
• Preferred delivery: vaginal with assisted shortened second stage + epidural, not elective caesarean.

Rapid revision

1. Blood volume rises ~40–50%, peaking at 30–34 weeks; cardiac output peaks immediately postpartum.
2. Three danger windows: 28–32 wks, second stage of labour, immediate postpartum.
3. NYHA I–II = good prognosis; III–IV = high mortality (functional classification).
4. Mitral stenosis is the worst-tolerated lesion; stenotic > regurgitant in danger.
5. In MS, tachycardia and AF precipitate pulmonary oedema → control rate with beta-blockers.
6. Severe symptomatic MS in pregnancy → PBMV in 2nd trimester.
7. Eisenmenger syndrome / pulmonary hypertension = absolute contraindication (mortality 30–50%).
8. PPCM: heart failure last month → 5 months postpartum, no other cause, EF < 45%, diagnosis of exclusion; commonest in first postpartum month.
9. Prior PPCM with persistent LV dysfunction → future pregnancy contraindicated.
10. A diastolic murmur in pregnancy is always pathological → echocardiography (investigation of choice).
11. Banned drugs: ACEi/ARB, warfarin (1st trimester), amiodarone, atenolol; adenosine = DOC for SVT; heparin is the safe anticoagulant.
12. Delivery: vaginal, assisted shortened second stage + epidural; avoid ergometrine; oxytocin as slow infusion.