Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Distinguish pathological peripartum heart failure from normal pregnancy symptoms and coordinate pregnancy-safe acute, chronic and future-pregnancy care.
PPCM is a diagnosis of exclusion in a high-risk physiological period. Because symptoms overlap normal pregnancy and thromboembolism, diagnosis depends on urgent clinical assessment, natriuretic peptide testing and echocardiography rather than reassurance from age or an uncomplicated pregnancy.
Care should be led by a Pregnancy Heart Team spanning cardiology, obstetric medicine, maternal-fetal medicine, anaesthesia and neonatology. Stabilisation, delivery timing and medication compatibility are considered together.
Prognosis tracks initial LV/RV severity and recovery. Persistent dysfunction requires chronic HF/device care; even complete recovery requires future-pregnancy counselling and surveillance.
Peripartum cardiomyopathy is otherwise-unexplained systolic heart failure arising late in pregnancy or postpartum. Vascular, hormonal and oxidative stresses are thought to injure a susceptible myocardium.
Pre-eclampsia and other hypertensive disorders are associated with greater risk and may add afterload and endothelial stress. They may also independently cause pulmonary oedema, so coexistence needs careful assessment.
Multiple gestation increases plasma volume, cardiac output and hormonal exposure. This greater haemodynamic burden may reveal limited myocardial reserve during late pregnancy or after delivery.
Some patients appear to share genetic or familial susceptibility with dilated cardiomyopathy. Pregnancy then acts as a physiological stressor, although no single predisposition establishes the diagnosis.
PPCM probably reflects several interacting pathways. Late-pregnancy and postpartum haemodynamic, vascular and hormonal changes may trigger or reveal systolic dysfunction in a susceptible myocardium, but no single mechanism explains every case.
Reduced myocardial contractility lowers ejection fraction, with or without ventricular dilatation. Stroke volume falls and compensatory sympathetic and neurohormonal pathways become activated.
Reduced forward output and neurohormonal sodium and water retention raise left-sided filling pressure. Pulmonary venous congestion produces orthopnoea and oedema, while annular dilatation can cause functional mitral regurgitation.
Extensive left or biventricular failure reduces maternal cardiac output. Hypotension, organ injury, malignant arrhythmia and cardiogenic shock can develop during an already vulnerable physiological period.
Severe ventricular dysfunction causes intracardiac stasis, compounded by the hypercoagulable peripartum state. Left-ventricular thrombus may embolise systemically, while concurrent venous thrombosis may cause pulmonary embolism.
Progressive exertional or resting breathlessness, orthopnoea, PND, cough, oedema, abdominal congestion and profound fatigue.
Persistent resting tachycardia, low oxygen saturation, raised JVP, gallop, pulmonary crackles, hypotension or new functional MR.
Typically late pregnancy or early postpartum, but modern definitions recognise presentation across the peripartum months; timing never replaces exclusion of another cause.
Multiple gestation, hypertensive disorders, pre-eclampsia and some ancestry/geographical settings increase risk but are not diagnostic.
Pulmonary oedema, hypoperfusion, malignant arrhythmia, embolic neurology or severe biventricular failure requires critical care and Pregnancy Heart Team activation.
Mild exertional breathlessness and dependent oedema are common. Resting hypoxia, persistent orthopnoea, raised JVP, crackles or objective ventricular dysfunction should not be attributed to normal pregnancy without urgent assessment.
Hypertension, proteinuria or other maternal-organ dysfunction support pre-eclampsia. Echocardiography may show preserved systolic function, although pre-eclampsia and peripartum cardiomyopathy can coexist.
Pleuritic pain, haemoptysis, disproportionate hypoxaemia and right-heart strain favour embolism. Pregnancy and the postpartum period increase thromboembolic risk, so assessment remains urgent.
Prominent chest pain, regional ECG change or regional wall-motion abnormality raises concern for coronary ischaemia, including spontaneous coronary artery dissection in the peripartum setting.
Symptoms or documented dysfunction predating late pregnancy, or familial and genetic clues, support pre-existing cardiomyopathy. Cardiac magnetic resonance may identify an alternative injury pattern, but myocarditis can overlap and timing alone cannot establish peripartum cardiomyopathy.
Pleuritic pain, haemoptysis or disproportionate hypoxia suggests PE; chest pain/ECG change requires ACS and SCAD assessment.
Rising left-sided filling pressure floods the lungs, while severe pump failure lowers organ perfusion. Critical illness may require ventilatory, circulatory and specialist pregnancy-heart-team support.
A dysfunctional or acutely injured ventricle can become electrically unstable. Sustained ventricular tachycardia or fibrillation can cause syncope, collapse or sudden cardiac death.
Low ventricular flow and peripartum hypercoagulability promote thrombus formation. Left-sided thrombus may cause stroke or limb ischaemia, whereas venous or right-sided thrombus may cause pulmonary embolism.
Incomplete recovery leaves ventricular dilatation and reduced systolic function. Ongoing heart-failure treatment, rhythm surveillance and sometimes device assessment may be required after pregnancy.
A subsequent pregnancy can provoke recurrent ventricular dysfunction even after apparent recovery. Persistently reduced function carries greater risk and makes pre-conception specialist counselling essential.
Resting hypoxia, orthopnoea, raised JVP or pulmonary oedema must never be normalised as late-pregnancy symptoms.
PPCM can meet the systolic-dysfunction definition without a dilated ventricle.
Haemodynamic shifts and thrombosis risk continue after delivery; birth is not the end of cardiac monitoring.
Some specialist PPCM strategies consider prolactin blockade, but MHRA advises against routine suppression and lists uncontrolled/hypertensive pregnancy and severe cardiovascular contraindications; specialist risk review is essential.
Later pregnancy can relapse even after normalisation, while persistent dysfunction confers substantially greater risk.
Reassuring severe orthopnoea or persistent tachycardia as normal pregnancy.
Starting an ACE inhibitor, ARB, ARNI, MRA or SGLT2 inhibitor before delivery.
Diagnosing PPCM without excluding PE, pre-eclampsia, ACS/SCAD and pre-existing disease.
Using bromocriptine routinely without checking MHRA contraindications, BP and anticoagulation strategy.
Discharging after symptomatic improvement without repeat echo and pre-conception follow-up.
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At 36 weeks, a patient has new orthopnoea, resting pulse 118, oxygen saturation 91% and bibasal crackles. What is the best next step?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem ·
Use the minimum effective dose: hypovolaemia, electrolyte loss and renal injury can reduce maternal and placental perfusion. Monitor weight, BP, U&E and fetal context.
Contraindicated during pregnancy. Check BP, renal function and potassium before and after initiation/titration; review hypovolaemia, renal-artery stenosis, hyperkalaemia and previous ACE-inhibitor angioedema. During breastfeeding monitor the infant for poor feeding, lethargy, pallor, inadequate weight gain and, especially when young, reduced wet nappies.