Evaluate and manage a patient with cardiac disease in pregnancy

In one line

Cardiac disease is the single most important non-obstetric cause of maternal death in South Africa, and the registrar's task is to risk-stratify before the haemodynamic load of pregnancy unmasks the lesion — using the modified WHO (mWHO) classification to decide who may proceed, who needs a pregnancy heart team, and who should be counselled against pregnancy altogether.

This chapter assumes the groundwork in the physiology of pregnancy and the murmur work-up taught at Intermediate; the consultant layer is classifying the lesion by how it fails under load, the named anticoagulation and PPCM regimens and exactly how they differ, the trial appraisal, and the judgement calls at the extremes of viability and at delivery.

Assessment

The Final candidate is expected to move beyond "murmur in pregnancy" to a structured risk assessment. Physiological pregnancy raises cardiac output ~40–50%, drops systemic vascular resistance and adds a hypercoagulable, volume-loaded state that peaks late in the second trimester, again at delivery and — dangerously — in the first 48 hours postpartum as the autotransfusion of uterine blood returns. A fixed-output lesion (severe mitral stenosis, pulmonary hypertension) cannot accommodate this and decompensates.

Classify the lesion by how it fails under load

The Intermediate list of "valve lesions and congenital defects" is assumed. Decompensation is predictable from the haemodynamic category, because pregnancy's three insults — a 40–50% rise in cardiac output, a fall in SVR, and the autotransfusion/diuresis of the early puerperium — each punish a different physiology. Sorting every patient into one of these categories sets the management:

• Fixed-output / inflow-obstructed lesions (severe mitral stenosis, severe aortic stenosis, pulmonary hypertension). These cannot raise stroke volume to meet the demand, so the body raises heart rate instead — and tachycardia is the enemy. In mitral stenosis the shortened diastole collapses transvalvular filling; in aortic stenosis the shortened diastole starves coronary perfusion of a hypertrophied ventricle; in pulmonary hypertension any fall in preload or rise in pulmonary resistance precipitates acute RV failure and a fatal low-output spiral. Management is therefore to rate-control, preserve preload and sinus rhythm, and guard against the fall in SVR (so regional anaesthesia must be incremental, never a single-shot spinal). Pulmonary arterial hypertension consequently sits in mWHO IV.
• Volume-overload / regurgitant lesions (mitral regurgitation, aortic regurgitation, most left-to-right shunts). The fall in SVR is protective — it reduces regurgitant fraction and afterload — so these are generally well tolerated, and the danger window is the postpartum SVR rebound and volume shift, not the antenatal period. These women usually reach term on surveillance and afterload-friendly drugs rather than intervention.
• Cyanotic / shunt lesions where SVR is load-bearing (Eisenmenger, uncorrected cyanotic CHD, systemic-RV physiology). Here the falling SVR worsens right-to-left shunting and deepens hypoxaemia, and the hypercoagulable state threatens paradoxical embolism. Management is to maintain afterload, give meticulous thromboprophylaxis, and avoid air in lines; Eisenmenger carries some of the highest maternal mortality of any lesion and belongs in the "advise against pregnancy" group.
• Aortopathy (Marfan, Loeys-Dietz, bicuspid-valve aortopathy, Turner syndrome). The lesion is the wall, not the valve: oestrogen-driven medial change plus the hyperdynamic circulation raise dissection risk, which clusters in the third trimester and early puerperium. Management is beta-blockade throughout, trimester-by-trimester aortic imaging, and mode-of-delivery decided by root diameter (see Management). Aortic dissection complicates roughly 3–5% of Marfan pregnancies.
• Pump-failure lesions (dilated/peripartum cardiomyopathy, severe LV impairment). A ventricle already at the limit of its Frank-Starling reserve cannot absorb a 50% output rise. The EF threshold drives everything (EF <30% is mWHO IV), and PPCM is its own diagnostic and therapeutic problem (below).

History. Establish the lesion, prior cardiac events, current NYHA functional class, exercise tolerance and arrhythmia. In the SA setting, actively seek rheumatic fever history and a previous diagnosis of peripartum cardiomyopathy (PPCM) — recurrence risk is substantial and worse if LV function has not normalised. SA maternal cardiac deaths are driven overwhelmingly by rheumatic disease (chiefly mitral stenosis) plus PPCM, the opposite mix to high-income registries dominated by congenital disease — so the index of suspicion for a tight, undiagnosed mitral valve in a late-booking patient must be high.

Examination. Distinguish the benign flow murmur of pregnancy from pathology. Red flags mandating echocardiography: a diastolic murmur, a loud or radiating systolic murmur, fixed splitting, signs of failure (raised JVP, basal crepitations, hepatomegaly), cyanosis or clubbing, and resting tachycardia disproportionate to gestation. Any woman presenting in pregnancy or up to ~6 months postpartum with dyspnoea or heart-failure symptoms should be "red-flagged" — orthopnoea and paroxysmal nocturnal dyspnoea are never physiological.

The atypical and subtle presentations that catch the unwary

The masked case is more dangerous than the classic one. Several traps recur:

• Decompensation that mimics normal late pregnancy. Ankle oedema, exertional breathlessness, a soft systolic flow murmur and a third heart sound are all physiological in the third trimester — which is exactly why a tight mitral stenosis or an early cardiomyopathy hides. The discriminators are orthopnoea, PND, a resting tachycardia that does not settle, a diastolic murmur, and a raised JVP — none of which are physiological. Treat new functional-class deterioration as cardiac until proven otherwise.
• PPCM presenting as something else. Because it strikes a young, previously well woman, PPCM is misattributed to chest infection, pulmonary embolism, "anxiety" or pre-eclampsia. The postpartum woman re-presenting with breathlessness, a cough (sometimes pink frothy sputum mistaken for infection) and fatigue needs an echo, not a course of antibiotics.
• The first presentation is the emergency. In a poorly resourced antenatal pathway, the lesion is often unmasked by acute pulmonary oedema in labour or by new atrial fibrillation — the "first contact" is a crisis, and the diagnosis is made retrospectively on the post-stabilisation echo.
• Functional class can lag the lesion. A woman may report NYHA I–II yet have severe stenosis because she has unconsciously limited her activity. Objective exercise tolerance and the echo, not the self-reported class alone, define risk.

Investigations. ECG and transthoracic echocardiography are the workhorses — echo defines lesion, valve area/gradients, LV ejection fraction and pulmonary pressures. NT-proBNP is useful: a level rising or >128 pg/mL around 20 weeks independently predicts adverse events. Chest radiography (shielded) is justified where failure is suspected. The output of assessment is a mWHO class, which drives everything downstream.

Reading the investigations like a consultant — where the numbers mislead

• Echocardiographic severity thresholds carry the diagnosis. Severe mitral stenosis is a valve area ≲1.0 cm²; the pregnant patient with an area in the 1.0–1.5 cm² range may look stable at booking and decompensate at 24–28 weeks as output peaks, so the gradient at rest in early pregnancy under-reads the risk — exercise or the natural haemodynamic stress test of advancing gestation reveals it. For aortic stenosis, a mean gradient is flow-dependent: the high-output pregnant state inflates the gradient, so do not over-call severity, but equally a "moderate" gradient in a symptomatic woman is severe physiology.
• NT-proBNP interprets in trend, not as a single value. Pregnancy modestly raises BNP/NT-proBNP versus the non-pregnant state, so a mildly raised level is not automatically failure; a level that rises serially or sits high around 20 weeks is the signal that predicts events, and a normal level is a useful negative. It does not distinguish lesion type.
• The ECG is for rhythm and strain, not diagnosis. New AF in a woman with a diastolic murmur is mitral stenosis until proven otherwise; right-axis deviation and RV strain point to pulmonary hypertension or a shunt.
• Pulse oximetry and the hyperoxia response matter in suspected shunt/cyanotic disease — resting desaturation, or a fall on exertion, reframes the risk entirely.
• What echo cannot give you is the trajectory. A reassuring booking echo does not license complacency; the assessment is repeated across gestation because the lesion's tolerance is being continuously tested by a rising load.

The differentials and mimics that change management

Several conditions masquerade as, or coexist with, cardiac disease, and getting the call wrong sends treatment in the wrong direction:

• Pulmonary oedema of pre-eclampsia vs cardiogenic pulmonary oedema. Both flood the lungs and both restrict fluids, but the pre-eclamptic needs delivery and magnesium while the mitral-stenotic needs rate control and (sometimes) valvuloplasty — and a woman can have both. The echo and the BP context separate them; the cross-link to pre-eclampsia-early-onset-severe is deliberate because the fluid discipline is shared.
• Pulmonary embolism vs PPCM vs an acute valve lesion in the breathless postpartum woman — the work-up (echo, troponin, D-dimer is unhelpful in pregnancy, CTPA where indicated) must distinguish them because anticoagulation, inotropes and bromocriptine are not interchangeable treatments.
• Amniotic-fluid embolism can present as sudden cardiorespiratory collapse with RV failure and mimic massive PE or an arrhythmic cardiac arrest.
• Thyrotoxic high-output state, severe anaemia and sepsis all produce a hyperdynamic circulation, tachycardia and a flow murmur that can be mistaken for structural disease — and conversely can tip a borderline lesion into failure, so they are treated as well as, not instead of, looking for the structural problem.

Management

Immediate (the decompensated woman). Treat acute pulmonary oedema with sitting position, oxygen, IV furosemide, and nitrates if BP allows; avoid fluid overload. New atrial fibrillation in mitral stenosis is an emergency — rate-control with a beta-blocker (the loss of atrial kick and tachycardia collapse the diastolic filling time across a stenotic valve). DC cardiovert if haemodynamically unstable; cardioversion is safe in pregnancy. Severe haemodynamic compromise in mWHO IV may demand termination discussion or early delivery as a life-saving manoeuvre.

Ongoing (antenatal). Refer to a combined cardiac–obstetric clinic (in SA these are established at Charlotte Maxeke Johannesburg, Groote Schuur and Tygerberg) — joint care matches Western outcomes even in low-resource cohorts. Optimise drugs to pregnancy-compatible agents: beta-blockers (labetalol, bisoprolol — avoid atenolol for growth restriction), furosemide, hydralazine/nifedipine, methyldopa. Stop ACE inhibitors, ARBs, and mineralocorticoid-receptor antagonists (fetotoxic) and switch before or as soon as pregnancy is recognised. Severe symptomatic mitral stenosis refractory to medical therapy is best treated by percutaneous balloon mitral valvuloplasty, ideally in the second trimester with abdominal shielding — surgery on cardiopulmonary bypass carries high fetal loss and is reserved for failure of percutaneous options.

Subtype-specific antenatal management — the consultant decisions

• Severe mitral stenosis. Medical control first: a beta-blocker (bisoprolol/metoprolol) to lengthen diastole, cautious diuretic for congestion, and rhythm control. When symptoms persist despite optimal medical therapy (typically NYHA III–IV or pulmonary hypertension), percutaneous balloon mitral valvuloplasty (PBMV) in the second trimester is the procedure of choice. Suitability is judged on echocardiographic morphology — the Wilkins score (leaflet mobility, leaflet thickening, subvalvular thickening, calcification; lower scores predict success) — with PBMV favoured for pliable, non-calcified valves with no more than mild mitral regurgitation. Procedural success is a post-procedure valve area ≥1.5 cm² (or ≥50% increase) without inducing significant regurgitation; in experienced hands it can be done under transthoracic-echo guidance with minimal or no fluoroscopy, sparing the fetus radiation. Open commissurotomy/replacement on bypass is the fallback because fetal loss on cardiopulmonary bypass is high.
• Pulmonary arterial hypertension (mWHO IV). The honest counsel is against pregnancy and for early termination if it occurs, because maternal mortality remains of the order of ~9% in contemporary registry data and historically much higher. For a woman who declines termination or presents late, care is in a PH-expert centre: PAH-targeted therapy is rationalised to the agents acceptable in pregnancy — prostacyclins (e.g. epoprostenol, inhaled iloprost), phosphodiesterase-5 inhibitors (sildenafil), and calcium-channel blockers only in proven vasoreactive disease — while endothelin-receptor antagonists (bosentan, macitentan) and riociguat are contraindicated (teratogenic) and must be stopped. The peripartum and first postpartum week are the lethal window; delivery is planned in a centre with the ability to manage acute RV failure.
• Aortopathy. Beta-blockade throughout to blunt the rate of aortic-wall stress, trimester-by-trimester (and early-postpartum) echocardiographic surveillance of the root, and strict BP control. Threshold for pre-pregnancy repair and for delivery planning is root diameter: the European threshold for "avoid/repair before pregnancy" in Marfan is ~45 mm (lower with adverse family history or rapid growth, and lower still in Loeys-Dietz and vascular Ehlers-Danlos). Mode of delivery is diameter-driven (see below).
• Mechanical valve. The whole antenatal plan turns on the anticoagulation strategy (below) and on getting the woman onto a delivery pathway that is never on warfarin at birth.
• Left-to-right shunts and regurgitant lesions. Usually managed expectantly to term with afterload-friendly antihypertensives and surveillance; the priority is recognising the minority who develop failure or arrhythmia.

Mechanical-valve anticoagulation — the named regimens and exactly how they differ

Mechanical valve anticoagulation turns on naming the options, quantifying the trade-off, and applying the dose threshold. The fundamental tension: warfarin gives the best valve protection but crosses the placenta and causes a dose-related embryopathy (nasal/skeletal, in the 6–12-week window) and fetal loss; LMWH does not cross the placenta (no embryopathy) but, if not rigorously anti-Xa-monitored, carries a materially higher valve-thrombosis risk. The registry teaching figures make the trade-off concrete: valve thrombosis is lowest on warfarin throughout (roughly 4% or less), intermediate with a first-trimester heparin substitution then warfarin (~9%), and unacceptably high on heparin throughout pregnancy (of the order of one-third) — while fetal loss runs the opposite way. The named strategies:

• Regimen 1 — warfarin throughout to ~36 weeks (then switch to heparin for delivery). Lowest maternal valve-thrombosis risk; highest embryopathy/fetal-loss risk. Reserved for the low-dose-warfarin patient.
• Regimen 2 — LMWH (dose-adjusted, anti-Xa-targeted) for the first trimester, then warfarin in T2/T3 to ~36 weeks. Avoids the embryopathy window at the cost of a higher valve-thrombosis risk in the heparin phase — which is why the LMWH must be dose-adjusted to peak anti-Xa levels (with trough levels increasingly used too), not given as a fixed prophylactic dose.
• Regimen 3 — dose-adjusted LMWH throughout. Eliminates embryopathy entirely but carries the highest thrombotic risk if monitoring lapses; used when warfarin is refused or contraindicated, and only with disciplined anti-Xa surveillance.

The ESC-favoured, dose-stratified rule resolves which regimen a given woman gets:

• If warfarin dose ≤5 mg/day maintains a therapeutic INR, continue warfarin through the second and third trimesters until ~36 weeks (the low dose carries a lower embryopathy risk, so its valve protection wins the trade-off).
• If >5 mg/day is needed, substitute dose-adjusted LMWH in the first trimester (peak anti-Xa monitored), then warfarin in T2/T3 — accepting the small thrombosis penalty of the heparin window to avoid the higher embryopathy of high-dose warfarin.
• Before planned delivery, switch from warfarin to LMWH and then to IV unfractionated heparin, stopped peripartum; warfarin must not be on board for vaginal birth (fetal intracranial haemorrhage risk in an anticoagulated fetus). Restart anticoagulation postpartum once haemostasis is secure.

The SA caveat is access and adherence: reliable anti-Xa monitoring (NHLS), INR access and clinic follow-up are not uniform across district facilities, so the regimen chosen must be the one that can actually be monitored where the woman lives — a theoretically optimal LMWH plan that cannot be anti-Xa-checked is more dangerous than a simpler, monitorable warfarin plan. This is a referral-to-a-heart-team decision, not a district one.

Peripartum cardiomyopathy — subtype-specific therapy

PPCM is managed as heart failure with reduced ejection fraction plus a disease-specific adjunct. Standard heart-failure therapy applies, with the pregnancy-versus-postpartum drug split as the only complication:

• Antenatally (if PPCM presents before delivery): beta-blocker, diuretic for congestion, hydralazine/nitrate for afterload (because ACE-inhibitors/ARBs/MRAs are fetotoxic and deferred until after delivery), and delivery planning.
• Postnatally: add an ACE-inhibitor/ARB and a mineralocorticoid-receptor antagonist as in standard HFrEF; these are compatible with breastfeeding in the usual agents.
• Bromocriptine is the disease-specific adjunct, targeting the cardiotoxic 16-kDa prolactin fragment (mechanism below). It is given with mandatory anticoagulation because of thrombotic risk, and suppresses lactation — a real counselling cost.
• Anticoagulation because of the markedly raised thromboembolic risk in a dilated, akinetic ventricle (LV thrombus), especially with very low EF.
• Advanced therapies — wearable cardioverter-defibrillator for the recovery window (sudden-death risk while EF is depressed but may recover, so permanent ICD is deferred), inotropes/mechanical support (levosimendan, ECMO, LVAD) and transplant in refractory shock — belong at a tertiary cardiac centre.

Peripartum (delivery plan)

Vaginal delivery is preferred for most — it has lower haemorrhage, infection and thrombosis risk than caesarean. Plan early-epidural assisted second stage to blunt the Valsalva/cardiac-output surge. Caesarean is reserved for obstetric indication or specific lesions (severe aortic stenosis, aortopathy, failed anticoagulation switch). Avoid ergometrine for PPH (vasoconstriction/coronary spasm) — use oxytocin by slow infusion; this builds on the PPH drills and is extended in postpartum-haemorrhage. The first 48 hours postpartum require continued monitoring.

A few delivery-plan refinements matter:

• The mode-of-delivery decision is lesion-specific, not blanket. Most lesions: assisted vaginal delivery with a planned, instrument-shortened second stage. Aortopathy is graded by root diameter — vaginal delivery is acceptable below ~40 mm, regional anaesthesia with an expedited/assisted second stage or caesarean is reasonable at 40–45 mm, and caesarean is favoured above ~45 mm or with rapid growth. Severe aortic stenosis, Eisenmenger and acutely decompensated lesions generally argue for a planned caesarean in a controlled, monitored setting.
• The oxytocic matters. Oxytocin causes vasodilatation and a reflex tachycardia if bolused — give it as a slow, low-dose infusion, never a rapid IV bolus, in fixed-output lesions. Ergometrine is avoided (coronary vasospasm, afterload spike); a carboprost decision is individualised because it can raise pulmonary pressures. The principle: prevent PPH actively but with the gentlest haemodynamic footprint.
• Anaesthesia is part of the cardiac plan. Incremental epidural (not single-shot spinal) preserves SVR in fixed-output and shunt lesions; the anaesthetist is a named member of the team, and invasive monitoring (arterial line, sometimes central access) is planned in advance for the high-risk lesion.
• Fluid balance and the autotransfusion. The immediate postpartum autotransfusion of ~500 mL of uterine blood plus aortocaval decompression can tip a fixed-output or failing ventricle into pulmonary oedema — this, not the delivery itself, is often the lethal moment, so monitored HDU-level care continues through the first 24–48 hours.

Long-term. Reliable contraception is integral. mWHO III–IV women should avoid further pregnancy until counselled — long-acting reversible contraception (progestogen implant, IUS) is first-line; oestrogen is thrombogenic and contraindicated in many lesions. Initiate before discharge where possible — the postpartum contraception groundwork is assumed and extended in contraception-in-high-risk-women, with the progestogen-only rationale in progesterone-in-obstetrics-gynaecology.

Postnatal, follow-up, recurrence and counselling

• The danger does not end at delivery. Many cardiac deaths — PPCM especially — present after discharge, so a structured postnatal cardiac review (symptoms, echo where indicated) is planned, not left to the woman to seek.
• PPCM follow-up and recurrence counselling. Echocardiographic recovery is tracked to 6–12 months. The subsequent-pregnancy risk turns on whether the EF has fully normalised: women whose LV function has not recovered face a substantial risk of relapse and death in a future pregnancy and should be counselled firmly against it; even those who recover carry a real recurrence risk and need pre-pregnancy counselling and surveillance. Heart-failure therapy is continued and de-escalated only on objective recovery, not on symptoms alone.
• Mechanical-valve and PAH women need their long-term anticoagulation/targeted therapy resumed and their contraception locked in before discharge — a gap here is how the next high-risk pregnancy happens.
• Contraception is a cardiac prescription. mWHO III–IV: progestogen-only LARC (implant or IUS) first; avoid oestrogen (thrombogenic, and dangerous in cyanotic, PAH, mechanical-valve and cardiomyopathy patients). Where future pregnancy is contraindicated, discuss permanent contraception, but weigh the anaesthetic/haemodynamic risk of the sterilisation procedure itself.
• Pre-pregnancy counselling is the highest-leverage intervention. The whole risk equation is best handled before conception — optimise the lesion, switch teratogenic drugs, fix a valve electively, and give an honest mWHO-anchored estimate of maternal risk — which is why every high-risk cardiac woman of reproductive age should leave a cardiology contact with a documented pregnancy plan.

The evidence & the controversy

The mWHO classification is the only prospectively validated maternal cardiac risk tool and anchors the 2018 ESC guideline. Its weakness is that it is largely lesion-based and expert-derived; CARPREG II (a 10-variable weighted score) out-discriminated mWHO, CARPREG I and ZAHARA with a C-statistic of 0.78 (95% CI 0.73–0.83), so pragmatic practice runs mWHO and an individualised score plus functional/biomarker assessment together rather than treating any one as definitive. The SA caveat is crucial: the ROPAC validation found mWHO discriminates far less well in emerging-country cohorts (cardiac-event rate 36.3% vs 12.8% in advanced settings), so a "low" mWHO class in a district patient with rheumatic disease and late booking should not be over-reassuring.

The anticoagulation evidence resists a clean answer — and that is the point. No randomised trial settles mechanical-valve anticoagulation in pregnancy; the evidence is registry and cohort. The ROPAC mechanical-valve cohort quantified the trade-off that drives the dose-stratified rule (only ~58% event-free pregnancy with a live birth; valve thrombosis concentrated in first-trimester heparin switches; warfarin protecting the valve at the fetus's expense). Cohort data give the often-quoted gradient of valve-thrombosis risk — lowest on warfarin throughout, intermediate on first-trimester-heparin-then-warfarin, and highest on heparin throughout — which is why guidelines anchor the 5 mg warfarin threshold rather than a one-size rule. The unresolved controversy is whether well-monitored modern LMWH (rigorous peak-and-trough anti-Xa) narrows the thrombosis gap enough to make embryopathy-free regimens the default; in SA, where that monitoring is not uniformly available, the pragmatic answer leans on what can be measured locally.

PAH and aortopathy define the "advise against pregnancy" end. PAH carried the worst lesion-specific mortality (~9%) in the ROPAC 10-year cohort, with the postpartum week as the danger window; this — not optimism about modern targeted therapy — underpins the mWHO IV counsel against pregnancy. For aortopathy the controversy is the exact diameter threshold (the European 45 mm versus more conservative 40 mm positions, modified by family history and growth rate), and dissection still occurs below threshold, so the diameter is a guide, not a guarantee.

PPCM is where SA practice and the literature are most live. It causes roughly a third of cardiac maternal deaths in our Saving Mothers data, presents predominantly postpartum with acute symptoms, and disproportionately affects young women — making it the lesion most often missed in a busy labour ward. The pathophysiological model — oxidative cleavage of prolactin into a cardiotoxic 16-kDa fragment — underpins bromocriptine therapy (e.g. 2.5 mg daily for ≥1 week in uncomplicated cases; longer regimens for EF <25% or shock), which must be given with anticoagulation because of thrombotic risk. Most PPCM recovers — the IPAC cohort showed 72% regained an LVEF ≥50% by 12 months — but a baseline LVEF <30% marks the high-risk group (1-year event-free survival 82% vs 99%), and these women must be counselled that a subsequent pregnancy carries real risk of relapse and death if LV function has not fully normalised. The bromocriptine evidence is suggestive rather than definitive — the South African open-label RCT (n=63) had no placebo arm, and the larger EORP PPCM registry (van der Meer 2024) found the bromocriptine-treated group reached the composite endpoint of death/readmission/persistent severe LV dysfunction less often than standard care (22.0% vs 33.3%, P=0.044), but the benefit was driven by less persistent severe LV dysfunction with no mortality difference (and, reassuringly, no excess thromboembolism). So bromocriptine is an adjunct to standard heart-failure therapy (beta-blocker, diuretic, ACE-inhibitor/ARB after delivery) with mandatory anticoagulation — not a substitute, and not a proven mortality-reducer.

Landmark trials & key evidence

The studies that anchor management in this area, with the effect sizes that define them.

Worked viva — how to structure the answer

Examiners give a stem like "a 27-year-old at 30 weeks, known rheumatic mitral stenosis, presents breathless with new fast atrial fibrillation and bibasal crepitations." A high-scoring answer runs:

1. Frame it — "This is acute decompensation of a fixed-output lesion: new AF in mitral stenosis has lost atrial kick and shortened diastole, collapsing filling across a stenotic valve — a cardiac emergency, not just 'AF in pregnancy'."
2. Resuscitate and make safe — sit her up, oxygen, IV furosemide for the oedema; rate-control the AF with a beta-blocker (the killer here is the tachycardia); DC cardiovert if she is haemodynamically unstable (safe in pregnancy); anticoagulate; continuous monitoring; senior obstetric, cardiology and anaesthetic alert.
3. Classify and risk-stratify — name the lesion, get an urgent echo (valve area, gradient, pulmonary pressures, LV function), assign an mWHO class, and state where she is cared for: a combined cardiac–obstetric unit, transferring if she is not in one.
4. Decide the lesion-specific plan — "If she remains symptomatic despite medical control, the definitive antenatal option is balloon mitral valvuloplasty in this trimester, suitability judged on the Wilkins score; bypass surgery is the fallback because of fetal loss."
5. Plan delivery — assisted vaginal delivery with an epidural and a shortened second stage; oxytocin by slow infusion, not bolus; avoid ergometrine; HDU monitoring through the first 24–48 hours for the autotransfusion load.
6. Justify from evidence — mWHO as the anchor (with the ROPAC caveat that it under-predicts in SA), CARPREG II as the individual score, and the postpartum window as the danger period.
7. Close the loop — postnatal cardiac review, progestogen-only LARC (avoid oestrogen), and pre-pregnancy counselling and valve optimisation before any future pregnancy.

Exam traps & red flags

• Calling decompensation "anxiety" or "deconditioning." Orthopnoea, PND and a diastolic murmur are pathological — investigate, don't reassure.
• Forgetting the postpartum danger window. Many cardiac deaths (especially PPCM) present after delivery; discharge is not the all-clear, and the autotransfusion of the early puerperium can drown a fixed-output ventricle.
• Defaulting to caesarean "because of the heart." Vaginal delivery is safer for most; choose mode for obstetric/lesion indication, with a planned assisted second stage — but know the aortopathy diameter thresholds that do tip toward caesarean.
• Mismanaging mitral stenosis in AF — tachycardia is the killer; rate-control and anticoagulate, don't just push fluids.
• Single-shot spinal in a fixed-output lesion — the abrupt fall in SVR can be fatal; use an incremental epidural.
• Continuing ACE-inhibitors/ARBs/spironolactone in a known cardiac patient who conceives — fetotoxic; switch immediately. Conversely, withholding them postpartum in PPCM denies proven HFrEF therapy.
• Leaving warfarin on board for delivery, or choosing an LMWH regimen that cannot be anti-Xa-monitored where the woman lives — both end in disaster.
• Continuing endothelin-receptor antagonists or riociguat in a PAH patient who conceives — teratogenic; stop and switch to a pregnancy-acceptable agent in an expert centre.
• Ergometrine for PPH in a cardiac patient — coronary vasospasm and afterload spike; use oxytocin infusion (slow, not bolus).
• Bromocriptine without anticoagulation — the prothrombotic risk is the reason anticoagulation is mandatory; and remember it suppresses lactation.
• Missing mWHO IV. Pulmonary arterial hypertension and severe LV impairment carry up to ~40–100% event rates — the correct counsel is against pregnancy and for effective contraception, not optimistic surveillance.

Evidence anchors

• 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy — European Heart Journal 2018
• What is new in the 2018 ESC guidelines (mWHO, pregnancy heart team, bromocriptine) — PMC, 2019
• Modified WHO Classification of Maternal Cardiovascular Risk — event rates per class
• CARPREG II Study — Pregnancy Outcomes in Women With Heart Disease (Silversides et al.) — JACC 2018; PMID 29793631
• ROPAC — Global cardiac risk assessment / mWHO validation (van Hagen et al.) — Eur J Heart Fail 2016; PMID 27006109
• ROPAC — 10-year outcomes in women with cardiovascular disease (Roos-Hesselink et al.) — Eur Heart J 2019
• ROPAC — Pregnancy in women with a mechanical heart valve (van Hagen et al.) — Circulation 2015; PMID 26100109
• IPAC — Clinical outcomes for peripartum cardiomyopathy in North America (McNamara et al.) — JACC 2015
• Bromocriptine for the treatment of peripartum cardiomyopathy: a multicentre randomised study (Hilfiker-Kleiner, Sliwa et al.) — Eur Heart J 2017
• EORP PPCM registry — bromocriptine treatment and outcomes in peripartum cardiomyopathy (van der Meer et al.) — Eur Heart J 2024
• 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension (PAH drugs acceptable/contraindicated in pregnancy) — Eur Heart J 2022
• Cardiovascular disease in pregnancy: the South African perspective — Cardiovasc J Afr
• Cardiac disease in pregnancy: when to raise the 'red flag' (Saving Mothers data, red flags) — SAMJ 2018
• Pregnancy in women with cardiac disease — Charlotte Maxeke Johannesburg one-year review (Soma-Pillay et al.) — Cardiovasc J Afr 2021; DOI 10.5830/CVJA-2020-062
• NDoH Saving Mothers (NCCEMD) reports — cardiac disease as leading non-obstetric cause of maternal death in SA (no stable open URL)
• South African Medicines Formulary (SAMF) — pregnancy-compatible cardiac drug dosing