Obstetric Critical Care Masterclass

M9Cardiac critical care, dysrhythmias, acute coronary syndromes and arrest

Module 9 of 22 · sources reviewed 2026-08-12

Sources reviewed Mon Aug 10 2026 00:00:00 GMT+0000 (Coordinated Universal Time) · version 2026.08.12

Clinical overview

Cardiovascular disease in pregnancy ranges from previously known valve or congenital disease to first-presentation peripartum cardiomyopathy (PPCM), arrhythmia, pulmonary hypertension, aortic catastrophe or pregnancy-associated acute coronary syndrome. The postpartum period is especially dangerous: venous return and afterload change, extracellular fluid mobilises, and the symptoms of heart failure can be mistaken for normal postnatal fatigue or infection.

The initial critical-care questions are physiological. Is the patient congested or underfilled? Is perfusion failing? Is the left ventricle, right ventricle, valve, rhythm, coronary circulation or aorta the dominant problem? Is pregnancy or delivery worsening the mechanism? Treat instability immediately while ECG, POCUS/formal echocardiography, biomarkers and imaging refine the diagnosis.

Core knowledge

Acute heart failure phenotypes

Acute heart failure is a syndrome, not one fluid state. Patients may be wet or dry, perfused or hypoperfused. Pulmonary oedema with hypertension requires oxygen/positive pressure, afterload control and diuresis where appropriate; cardiogenic shock requires maintenance of perfusion pressure, support of forward flow and treatment of the cause. Giving routine fluid to all hypotensive cardiac patients can be fatal.

Pregnancy-specific causes include:

  • PPCM, usually presenting toward the end of pregnancy or in the months after birth with otherwise unexplained LV systolic dysfunction, commonly LVEF below 45%;
  • decompensated rheumatic/other valve disease;
  • congenital disease and aortopathy;
  • pulmonary arterial hypertension and acute RV failure;
  • pre-eclamptic pulmonary oedema from afterload, permeability and fluid factors;
  • myocardial ischaemia/infarction, including spontaneous coronary artery dissection (SCAD);
  • myocarditis, stress cardiomyopathy, tachycardia-mediated failure and severe anaemia; and
  • iatrogenic fluid or tocolytic effects.

Echocardiography defines ventricular and valve function, pulmonary-pressure probability and pericardium. Chest radiography, ECG, troponin, natriuretic peptides and definitive imaging are used according to the question. A biomarker is not a diagnosis; trends and imaging matter.

Cardiogenic shock

Cardiogenic shock is inadequate output from pump failure. Look for cool peripheries, altered mentation, oliguria, rising lactate, pulmonary congestion, elevated venous pressure and impaired ventricular function. Some patients are hypotensive; others maintain pressure at the cost of severe vasoconstriction.

Support oxygenation and ventilation, but recognise that positive pressure can reduce preload and worsen RV failure or profound hypovolaemia. Use norepinephrine when perfusion pressure is inadequate, then add/select inotropy for persistent low output under critical-care/cardiology guidance. Treat arrhythmia, ischaemia, valve obstruction/regurgitation, hypertension or myocarditis. Refer early for mechanical circulatory support/ECMO when deterioration is potentially reversible and conventional support is failing.

PPCM treatment follows heart-failure physiology with pregnancy/lactation medication constraints. ACE inhibitors, angiotensin-receptor blockers, ARNIs and mineralocorticoid antagonists require pregnancy-specific review and are generally avoided antenatally; appropriate postpartum regimens depend on breastfeeding and specialist guidance. Bromocriptine is specialist therapy in selected PPCM protocols and requires consideration of thrombosis and anticoagulation; it is not a universal ICU prescription.

Pulmonary hypertension and right-heart failure

Severe pulmonary hypertension carries very high maternal risk. Acute rises in pulmonary vascular resistance—from hypoxaemia, hypercapnia, acidosis, pain, pulmonary embolism or high airway pressures—can precipitate RV failure. Maintain oxygenation, avoid severe acidosis, preserve systemic pressure for RV coronary perfusion and avoid both underfilling and excessive volume. Intubation and delivery are high-risk transitions requiring expert planning. Pulmonary vasodilators and mechanical support are tertiary specialist therapies.

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