Cardiac disease in pregnancy

A 32-year-old woman with a mechanical mitral valve presents at 8 weeks gestation, on long-term warfarin. She has read that warfarin causes birth defects and asks whether she should stop it. Her question contains the entire topic: pregnancy is a haemodynamic and thrombotic challenge, every cardiac lesion has its own risk class and its own management, and every anticoagulation choice is a trade-off between maternal and fetal harm. The decisions — mWHO classification, anticoagulation strategy, planned delivery and postpartum surveillance — are the decisions this topic rehearses.^[1][4]

Overview and definition

Cardiac disease complicates roughly 1 to 4 per cent of pregnancies and is the leading indirect cause of maternal mortality in many high-income settings. Two trends drive the modern epidemiology: older maternal age, and the survival into reproductive age of women with complex repaired congenital heart disease.^[1][5]

Pregnancy is a unique haemodynamic challenge:^[1][13]

• Cardiac output rises 30 to 50 per cent, peaking in the second trimester and again in labour (where a single contraction can raise cardiac output by a further 50 to 80 per cent).
• Blood volume rises 30 to 50 per cent, with a parallel rise in red cell mass that is smaller than the plasma rise — producing the physiological anaemia of pregnancy.
• Systemic vascular resistance falls through nitric oxide-mediated vasodilation.
• A postpartum haemodynamic surge in the first 24 to 48 hours after delivery — autotransfusion from the uterine vein, mobilisation of extravascular fluid — is the window where decompensation is commonest.^[1][5]

Two principles frame the topic. First, the risk of pregnancy is determined by the lesion, the functional class and the haemodynamic state, not by the presence of "heart disease". Second, the answer to almost every cardiac question in pregnancy is multidisciplinary — obstetric, cardiology, anaesthetic, and where relevant, cardiac surgery.^[1]

References17ShowHide

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