Ischemic cardiogenic shock is a complex, self-perpetuating pathological process that frequently causes death irrespective of medical therapy. Early definition of coronary anatomy is a pivotal step towards survival. Those destined to develop shock are likely to have three-vessel or left main stem disease with previously impaired left ventricular function. Early reperfusion of the occluded artery can limit infarct size, but ischemia-reperfusion injury or the ‘no-reflow’ phenomenon can preclude improvement in myocardial contractility. Emergence of shock depends upon the volume of ischemic myocardium, stroke volume, and peripheral vascular resistance. If cytokine release triggers the systemic inflammatory response, systemic vascular resistance falls and inadequate coronary perfusion pressure heralds the downward spiral. Survival depends on early recognition of shock, followed by aggressive targeted treatment of left, right, or biventricular failure. The goal is to prevent end-organ dysfunction and severe metabolic derangement by raising mean arterial pressure, which is achieved with inotropes and vasopressors, often at the expense of tachycardia, elevated myocardial oxygen consumption, and extended ischemia. The value of intra-aortic balloon counter-pulsation is now questioned in patients with advanced shock. When mean arterial pressure is <55 mmHg with serum lactate >11 mmol/l, death is likely and mechanical circulatory support becomes the only chance for survival.