Cardiogenic shock is a relatively specific clinical syndrome characterized by decreased cardiac output, elevated left ventricular filling pressure, and arterial hypotension with vital organ hypoperfusion. It most commonly occurs as the consequence of extensive left ventricular damage due to myocardial infarction. The prognosis of patients with cardiogenic shock is very poor, because by definition there are no readily correctable metabolic, hemodynamic, humoral, or infectious problems whose treatment may lead to improved circulatory function. Pharmacologic support of the patient with cardiogenic shock plays a major role in clinical management. Diuretics, inotropic agents, and vasodilator drugs all have a place in the management of selected patients with low output states and cardiogenic shock following myocardial infarction. Diuretics such as furosemide may be used to relieve symptoms of pulmonary congestion, but are not effective in reversing hypotension or vital organ hypoperfusion; in advanced shock states with acute renal failure, they may be totally ineffective. The most commonly employed and effective inotropic agents are the sympathomimetic amines dopamine and dobutamine, which have complex effects on important variables in cardiogenic shock, including the heart's inotropic and chronotropic states, myocardial oxygen requirements, left ventricular filling pressure, and peripheral vascular tone. All inotropic agents have the capacity to intensify myocardial ischemia because they may increase myocardial oxygen requirements in the face of limited arterial blood flow; isoproterenol, epinephrine, and norepinephrine appear to be particularly troublesome in this regard. Vasodilator agents (phentolamine, nitroprusside, and nitroglycerin) have also been used to alter left ventricular loading conditions in patients otherwise supported by inotropic drugs, and may be particularly useful in the management of "mechanical" complications of infarction such as mitral regurgitation and interventricular septal rupture. The use of these drugs, just as that of inotropic agents, must be tailored to specific hemodynamic abnormalities documented in individual patients.