Shock, which is characterized by multisystem end-organ hypoperfusion and tissue hypoxia, is a frequent problem requiring ICU admission. A variety of clinical indicators of shock exist, including reduced mean arterial pressure, tachycardia, tachypnea, cool extremities, altered mental status, oliguria, and lactic acidosis. Although hypotension is usually observed in shock, there is not a specific blood pressure threshold that is used to define it. Shock can result from decreased cardiac output, decreased systemic vascular resistance, or both. The three main categories of shock are hypovolemic, cardiogenic, and high cardiac output/low systemic vascular resistance. Clinical evaluation can be useful to assess the adequacy of cardiac output, with narrow pulse pressure, cool extremities, and delayed capillary refill suggestive of reduced cardiac output. Indicators of high cardiac output (e.g., widened pulse pressure, warm extremities, and rapid capillary refill) associated with shock suggest reduced systemic vascular resistance. Reduced cardiac output can be due to intravascular volume depletion (e.g., hemorrhage) or cardiac dysfunction. Intravascular volume depletion can be assessed through changes in right atrial pressure with spontaneous respirations or changes in pulse pressure during positive pressure mechanical ventilation. Reduced systemic vascular resistance is often caused by sepsis, but high cardiac output hypotension is also seen in pancreatitis, liver failure, burns, anaphylaxis, peripheral arteriovenous shunts, and thyrotoxicosis. Early resuscitation of septic and cardiogenic shock may improve survival; objective assessments such as echocardiography and/or invasive vascular monitoring should be used to complement clinical evaluation and minimize end-organ damage. The approach to the pt in shock is outlined in Fig. 4-1.