General MedicineTier 1Disease (DEADMAN)

Hypotension or shock - cardiogenic

Description

Shock from primary cardiac pump failure - reduced cardiac output despite adequate/increased filling pressures
Causes: acute MI (commonest), acute decompensated heart failure, arrhythmia, acute valvular failure (papillary muscle rupture, endocarditis), myocarditis, cardiac tamponade (technically obstructive, often grouped here), massive PE (obstructive)

Epidemiology

Complicates ~5-10% of STEMI presentations; remains high-mortality despite revascularisation advances
Risk factors: large infarct territory, prior LV dysfunction, mechanical complications, delayed presentation

Aetiopathogenesis

Myocardial dysfunction -> reduced stroke volume -> reduced cardiac output -> compensatory but maladaptive vasoconstriction and fluid retention -> worsening congestion and further myocardial strain
Mechanical complications (VSD, papillary muscle/free wall rupture) cause abrupt haemodynamic collapse days post-infarct
Right ventricular infarction - preload-dependent shock, worsened by nitrates/diuretics

Diagnosis

Clinical: hypotension, cold/clammy peripheries, oliguria, pulmonary oedema (or clear lungs if RV-predominant), raised JVP
ECG (STEMI, arrhythmia), echocardiography (LV function, mechanical complication, tamponade, RV involvement), troponin, lactate
Invasive haemodynamic monitoring in complex/refractory cases

Management

1. Treat the cause

Urgent revascularisation (PCI) for MI-related cardiogenic shock - the single most important intervention
Mechanical complications - urgent surgical repair
RV infarction - avoid nitrates/diuretics, give fluids to maintain preload

2. Haemodynamic support

Inotropes (dobutamine, milrinone) to improve contractility; vasopressors (noradrenaline) if hypotensive despite inotropy
Mechanical circulatory support (intra-aortic balloon pump, Impella, VA-ECMO) for refractory shock as a bridge to recovery/transplant/decision
Cautious fluid management - avoid over-resuscitation worsening pulmonary oedema, except RV-predominant shock

3. Rhythm/mechanical

Treat arrhythmia driving shock (cardioversion, pacing)
Pericardiocentesis for tamponade

Associations

Multi-organ failure (cardiorenal syndrome, hepatic congestion), arrhythmia, mechanical complications post-MI
High short-term mortality despite modern revascularisation and mechanical support

Natural history & complications

Mortality remains substantial (30-50%) even with contemporary PCI and mechanical support
Early revascularisation is the strongest modifiable determinant of survival in MI-related shock
Survivors often have significant residual LV dysfunction requiring long-term heart failure management

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