Inotropes and vasopressors play a key role in the management of shock. The goal of therapy is to restore end-organ perfusion by augmenting cardiac output (CO) and vascular tone. Clinical trial data have thus far failed to identify precise hemodynamic end points associated with better outcomes; in any event, such end points are highly likely to be determined on an individualized basis, reflecting patients’ chronic arterial blood pressure, baseline cardiac function, and other pathophysiologic factors (e.g., end-stage renal failure, cardiac ischemia).1 Inotropes enhance cardiac contractility and CO; vasopressors raise blood pressure. The impact of these drugs in restoring hemodynamic parameters to “normal” values has principally been used to evaluate their effectiveness, with clinical practice guided by extrapolation from animal studies and pharmacologic trials.2 However, these drugs have important extra-cardiovascular effects on metabolic, neurohormonal, and autonomic regulation that are also injurious. This review discusses the mechanisms and evidence base for inotropes and vasopressors in various types of shock. This review contains 3 figures, and 39 references. Keywords: inotropes, vasopressors, catecholamines, monitoring, shock states, cardiogenic, hemorrhagic, septic, neurogenic