Cardiogenic shock is the leading cause of death in patients with acute ST-elevation myocardial infarction (STEMI). Characterised by a state of low cardiac output leading to end-organ hypoperfusion, cardiogenic shock complicates approximately 5–8 % of STEMIs and is associated with a mortality rate approaching 50 percent.1–3 Prompt recognition and therapeutic intervention for cardiogenic shock due to STEMI are critical for patient survival.
Aetiology
Ischaemic dysfunction of cardiac myocytes during STEMI can impair systolic and diastolic function of the right, left or both ventricles. When ischaemic injury is extensive, ventricular function can be impaired to such a degree that cardiogenic shock occurs, whereby cardiac output falls and elevated ventricular filling pressures lead to heart failure.4 The decreased cardiac output then propagates a vicious cycle of progressively worsening coronary perfusion, myocyte dysfunction, and ultimately end-organ hypoperfusion.5 This review focuses on ventricular dysfunction as the cause of shock, but cardiogenic shock can also occur from mechanical complications of STEMI such as papillary muscle, ventricular septum or free wall rupture.
Left ventricular dysfunction is implicated in the majority of cases of cardiogenic shock associated with STEMI.6 Often, the infarction involves the anterior territory of the left ventricle. Predominant right ventricular dysfunction comprises approximately 5 % of cases and is usually due to an inferior MI with proximal occlusion of the right coronary artery.7 In addition to the acute infarction, patients in cardiogenic shock often have suffered prior infarcts and tend to have severe three-vessel coronary disease, all of which leaves them prone to extensive ischaemic injury and subsequent ventricular dysfunction.4,7