Critical Care Cardiology

Cardiogenic shock begins with a primary fall in cardiac output from pump failure, which triggers compensatory sympathetic and renin-angiotensin-aldosterone activation. These responses raise systemic vascular resistance and heart rate to defend blood pressure, but the resulting rise in afterload further reduces stroke volume from the failing ventricle, and tachycardia increases myocardial oxygen demand. The consequent tissue hypoperfusion activates a systemic inflammatory response with cytokine release and, in some patients, inappropriate vasodilation resembling a mixed shock state. Left untreated, this creates a self-perpetuating spiral of falling cardiac output, rising afterload, and worsening end-organ hypoperfusion, which is why early mechanical or pharmacologic interruption of the cycle is central to management.