Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Risk-stratify cardiovascular disease before and during pregnancy, recognise maternal emergencies and coordinate care through a Pregnancy Heart Team.
Maternal cardiovascular assessment balances maternal autonomy, fetal considerations and the harm of delayed treatment. The Pregnancy Heart Team core includes obstetrics, cardiology, anaesthesia, midwifery and specialist nursing, with genetics, surgery and intensive care added as needed.
Risk is dynamic. A woman who was stable before pregnancy may deteriorate with rising cardiac output, anaemia, hypertension, arrhythmia, thrombosis or postpartum autotransfusion. A written delivery and postpartum plan prevents fragmented decisions.
Congenital lesions, valve disease and aortopathy may become clinically important as pregnancy increases flow and wall stress. Previous repair does not exclude residual obstruction, regurgitation or aortic risk.
Cardiomyopathy, severe ventricular dysfunction and pulmonary arterial hypertension confer limited haemodynamic reserve. Pregnancy can expose or aggravate failure even when symptoms were modest beforehand.
Hypertensive disorders, peripartum cardiomyopathy and venous thromboembolism arise during pregnancy or postpartum. Placental dysfunction, myocardial vulnerability and pregnancy-related hypercoagulability contribute in differing proportions.
Anaemia, infection, arrhythmia and fluid imbalance can unmask previously compensated disease. Risk is especially dynamic around delivery and the early postpartum redistribution of blood and extracellular fluid.
Pregnancy expands plasma volume and increases heart rate and cardiac output while systemic vascular resistance usually falls. The larger circulating load raises demands on valves, ventricles and great vessels.
Stenotic valves cannot accommodate higher flow without rising gradients, while impaired ventricles may not handle increased preload. Filling pressures rise, producing systemic or pulmonary congestion.
Hypercoagulability and venous stasis increase thromboembolic risk. Hypertension and pregnancy-related vascular changes may add shear stress in susceptible aortas and worsen ventricular afterload.
Labour changes preload and sympathetic tone; after delivery, uterine autotransfusion and mobilisation of extracellular fluid can abruptly increase cardiac filling. Decompensation may therefore occur after an apparently stable birth.
Orthopnoea, paroxysmal nocturnal dyspnoea, hypoxaemia, pulmonary crepitations, raised JVP or a persistent resting tachycardia is not explained by normal pregnancy.
Sustained palpitations with presyncope/syncope, structural disease or an abnormal ECG needs urgent rhythm assessment.
Abrupt severe chest/back pain, pulse deficit or neurological signs in an aortopathy is an emergency.
New HF toward the end of pregnancy or in the months after delivery with LV systolic dysfunction after exclusion of another cause.
Pulmonary arterial hypertension/Eisenmenger, severe ventricular dysfunction, previous peripartum cardiomyopathy with residual dysfunction and high-risk aortopathy are mWHO 2.0 class IV contexts.
Mild exertional breathlessness and dependent oedema can occur normally. Orthopnoea, hypoxaemia, pulmonary crepitations, raised jugular venous pressure or persistent resting tachycardia instead suggest cardiovascular pathology.
Acute dyspnoea, pleuritic pain, hypoxaemia, syncope or disproportionate tachycardia should prompt PE assessment. Unilateral leg symptoms and right-heart strain support thromboembolism rather than isolated left-heart failure.
New hypertension with proteinuria or maternal organ dysfunction can cause headache, pulmonary oedema and cardiac strain. Blood pressure, urine findings, platelets and liver or renal abnormalities help distinguish it.
New heart failure late in pregnancy or after delivery with left-ventricular systolic dysfunction suggests this diagnosis after other causes are excluded. Echocardiography separates it from uncomplicated physiological breathlessness.
Persistent chest pain, ischaemic ECG or troponin change suggests myocardial injury; abrupt severe chest or back pain, pulse disparity or neurological signs raises concern for dissection.
Volume expansion and limited cardiac reserve may cause pulmonary oedema, systemic congestion or low output. Risk can peak during delivery or postpartum fluid mobilisation rather than during antenatal review.
Chamber stretch, scar and physiological adrenergic drive may trigger sustained arrhythmia. Pregnancy-related hypercoagulability also increases venous or intracardiac thrombosis, pulmonary embolism and stroke risk.
In susceptible aortopathy, increased wall stress and hypertension may precipitate rapid dilatation or dissection. Sudden chest or back pain demands urgent definitive assessment.
Maternal hypoxaemia, low cardiac output or severe vascular disease can reduce placental perfusion. Consequences may include impaired fetal growth, prematurity or fetal loss, depending on lesion severity and maternal stability.
Autotransfusion and mobilisation of extracellular fluid can precipitate pulmonary oedema after an apparently stable delivery.
For many cardiac conditions a planned vaginal birth with good analgesia and an assisted second stage is haemodynamically preferable; indication, not diagnosis alone, determines caesarean delivery.
Pregnancy changes modality choice and technique but rarely justifies leaving a dangerous PE or dissection undiagnosed.
Valve gradients increase with pregnancy cardiac output, so integrate valve area, symptoms and ventricular response.
Hypertensive disorders, gestational diabetes and preterm delivery should trigger long-term risk-factor follow-up.
Calling orthopnoea, hypoxaemia or syncope normal pregnancy symptoms.
Continuing an ACE inhibitor or ARB into pregnancy without urgent medication review.
Using a DOAC for a mechanical valve or VTE treatment during pregnancy.
Choosing caesarean delivery solely because heart disease is present.
Ending cardiac observation immediately after birth despite postpartum fluid shifts.
Your practice draft is saved in this browser.
Under the 2025 ESC framework, which group should be managed by a Pregnancy Heart Team from pre-pregnancy onward?
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 · Content changes
Avoid or use specialist caution with asthma, bradycardia, heart block or decompensated heart failure; monitor maternal BP/heart rate and fetal growth.
Use a modified-release product; headache, flushing and hypotension. Avoid grapefruit and account for CYP3A4 interactions; do not use short-acting nifedipine for uncontrolled rapid BP reduction.