Cardiovascular disease in pregnancy

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

Key points

Assess known CVD before conception using mWHO 2.0 plus lesion-specific and individual factors.
Women with mWHO 2.0 class II-III or higher should be evaluated and managed by a Pregnancy Heart Team from pre-pregnancy through postpartum care.
mWHO 2.0 class IV indicates extremely high maternal and fetal risk; provide expert shared decision-making and discuss alternatives to pregnancy, not coercive care.
Normal pregnancy increases plasma volume, heart rate and cardiac output; these changes can unmask valve disease, cardiomyopathy, pulmonary hypertension or aortopathy.
Use ECG and echocardiography freely when indicated; do not withhold essential chest imaging or CT solely because of pregnancy.
ACE inhibitors and ARBs should be avoided when planning pregnancy and are contraindicated during pregnancy; DOACs are not used for pregnancy anticoagulation.
Haemodynamic risk often peaks around delivery and the early postpartum fluid shift, so the plan must extend beyond birth.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Pre-existing structural disease

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.

Pre-existing myocardial or pulmonary vascular disease

Cardiomyopathy, severe ventricular dysfunction and pulmonary arterial hypertension confer limited haemodynamic reserve. Pregnancy can expose or aggravate failure even when symptoms were modest beforehand.

Pregnancy-associated cardiovascular disease

Hypertensive disorders, peripartum cardiomyopathy and venous thromboembolism arise during pregnancy or postpartum. Placental dysfunction, myocardial vulnerability and pregnancy-related hypercoagulability contribute in differing proportions.

Physiological stressors

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.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Circulatory adaptation
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.
2
Limited reserve becomes apparent
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.
3
Vascular and thrombotic stress
Hypercoagulability and venous stasis increase thromboembolic risk. Hypertension and pregnancy-related vascular changes may add shear stress in susceptible aortas and worsen ventricular afterload.
4
Delivery and postpartum shift
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.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Concerning breathlessness

Orthopnoea, paroxysmal nocturnal dyspnoea, hypoxaemia, pulmonary crepitations, raised JVP or a persistent resting tachycardia is not explained by normal pregnancy.

Arrhythmic symptoms

Sustained palpitations with presyncope/syncope, structural disease or an abnormal ECG needs urgent rhythm assessment.

Aortic syndromeRed flag

Abrupt severe chest/back pain, pulse deficit or neurological signs in an aortopathy is an emergency.

Peripartum cardiomyopathy

New HF toward the end of pregnancy or in the months after delivery with LV systolic dysfunction after exclusion of another cause.

Very-high-risk substrate

Pulmonary arterial hypertension/Eisenmenger, severe ventricular dysfunction, previous peripartum cardiomyopathy with residual dysfunction and high-risk aortopathy are mWHO 2.0 class IV contexts.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
12-lead ECG and rhythm monitoringFirst step
Why
Assess chest pain, syncope, palpitations or known arrhythmia.
Interpretation and limitations
Minor axis/interval changes can occur in pregnancy, but pathological ST-T changes, significant conduction disease or sustained arrhythmia require evaluation.
02
Transthoracic echocardiography
Why
Assess ventricular function, valves, pulmonary pressure and aortic dimensions without radiation.
Interpretation and limitations
Compare with pre-pregnancy measurements and interpret flow-dependent valve gradients in the context of increased cardiac output.
03
FBC, renal/liver profile, troponin and BNP/NT-proBNP
Why
Identify anaemia, pre-eclampsia organ involvement, myocardial injury and heart failure.
Interpretation and limitations
Use indication and trends; troponin elevation is not a normal pregnancy finding.
04
Chest radiograph, CT or MRI
Why
Diagnose pulmonary oedema, PE or aortic disease when clinically required.
Interpretation and limitations
Use the lowest reasonable radiation and avoid gadolinium unless essential, but diagnostic delay can be more dangerous than fetal exposure.
05
mWHO 2.0 and lesion-specific assessment
Why
Predict maternal risk and determine level/site of care.
Interpretation and limitations
Integrate anatomy, ventricular function, symptoms, prior events, aortic size and comorbidity; the class does not replace individual counselling.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Physiological pregnancy symptoms

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.

Pulmonary embolism

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.

Pre-eclampsia

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.

Peripartum cardiomyopathy

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.

Acute coronary or aortic syndrome

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.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01FirstPre-pregnancy cardiovascular reviewFirst stepKnown or suspected CVD, prior cardiotoxic therapy or important family/genetic cardiac history.

1Define diagnosis, functional status, ventricular/valve/aortic state, rhythm and previous pregnancy outcomes.
2Assign mWHO 2.0 risk and refer class II-III or higher to a Pregnancy Heart Team.
3Review every medicine for pregnancy and breastfeeding safety; replace ACE inhibitors/ARBs and plan anticoagulation where relevant.
4Discuss maternal and fetal risks, inheritance, contraception, timing and alternatives using shared decision-making.

02NextAntenatal and delivery planPregnancy in a woman with significant CVD.

1Set surveillance frequency, target blood pressure, rhythm/echo monitoring and fetal assessment according to risk.
2Optimise anaemia, hypertension, volume status and disease-specific treatment without withholding necessary maternal therapy.
3Write a multidisciplinary plan covering place, timing and mode of delivery, anaesthesia, monitoring and antithrombotic timing.
4Plan enhanced observation in the early postpartum period and restart or modify long-term cardiac medicines safely.

03EscalationAcute cardiovascular symptomsEscalationChest pain, pulmonary oedema, syncope, sustained arrhythmia, shock or suspected aortic syndrome/PE.

1Activate maternal emergency care and assess ABCDE with continuous maternal monitoring and fetal assessment when viable.
2DefinitiveUse ECG, biomarkers, urgent echo and definitive chest/aortic/PE imaging according to the suspected diagnosis.
3Treat the maternal emergency using disease-specific national resuscitation and cardiology guidance with obstetric/anaesthetic input.
4Transfer to a specialist centre and decide delivery timing only after stabilisation unless immediate delivery is itself required for resuscitation.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

NICE first-line antihypertensive option in pregnancy when suitable.

Labetalol

For hypertension in pregnancy, start 100 mg orally twice daily; increase at weekly intervals as needed, up to 100 to 400 mg three times daily, maximum 2.4 g/day.

Avoid or use specialist caution with asthma, bradycardia, heart block or decompensated heart failure; monitor maternal BP/heart rate and fetal growth.

NICE alternative when labetalol is unsuitable.

Nifedipine modified release

A typical starting dose is 10 mg orally every 12 hours, titrated to a maximum 40 mg every 12 hours for the referenced MR product.

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.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Maternal heart failure

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.

Arrhythmia and thromboembolism

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.

Aortic complication

In susceptible aortopathy, increased wall stress and hypertension may precipitate rapid dilatation or dissection. Sudden chest or back pain demands urgent definitive assessment.

Placental and fetal compromise

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.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Pregnancy Heart Team review frequency based on mWHO 2.0 class and lesion-specific risk.
At each review assess symptoms, oxygen saturation, blood pressure, heart rate/rhythm, volume status and medicine adherence.
Use serial echo for ventricular, valve or aortic disease and biomarkers when they are part of the disease-specific plan.
Monitor fetal growth and placental wellbeing when maternal disease or medicines can affect perfusion/growth.
Continue surveillance through the early postpartum haemodynamic shift and arrange long-term cardiovascular follow-up after adverse pregnancy outcomes.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Postpartum is not low risk

Autotransfusion and mobilisation of extracellular fluid can precipitate pulmonary oedema after an apparently stable delivery.

Vaginal delivery often wins

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.

Imaging should answer a question

Pregnancy changes modality choice and technique but rarely justifies leaving a dangerous PE or dissection undiagnosed.

Flow raises gradients

Valve gradients increase with pregnancy cardiac output, so integrate valve area, symptoms and ventricular response.

Adverse pregnancy outcomes predict later CVD

Hypertensive disorders, gestational diabetes and preterm delivery should trigger long-term risk-factor follow-up.

11Common pitfallsFrequent interpretation and management errors.

01
Calling orthopnoea, hypoxaemia or syncope normal pregnancy symptoms.
02
Continuing an ACE inhibitor or ARB into pregnancy without urgent medication review.
03
Using a DOAC for a mechanical valve or VTE treatment during pregnancy.
04
Choosing caesarean delivery solely because heart disease is present.
05
Ending cardiac observation immediately after birth despite postpartum fluid shifts.