Of the four categories of shock, only distributive shock states following intravascular volume resuscitation are associated with an increased cardiac output but decreased vasomotor tone.4 Thus, cardiac output, stroke work, Do2, and Sv̄o2 are decreased in cardiogenic, hypovolemic, and obstructive shock but may be normal or even increased in distributive shock. However, in all conditions, HR increases associated with an increased sympathetic tone. Cardiogenic shock represents primary cardiac failure. It can be due to impaired contractility (myocardial ischemia/infarction, electrolyte imbalance, hypoxemia, hypothermia, endocrinologic diseases, metabolic poisoning, β-blockers), pump function (valvulopathy, ventriculoseptal defect, dyssrythmias), or diastolic compliance (fibrosis, infiltrative cardiomyopathies, hypertrophy). The specific cardinal findings of cardiogenic shock are increased back pressure to cardiac filling (right atrial pressure [Pra] and pulmonary artery occlusion pressure [Ppao]) and upstream edema (peripheral and pulmonary). Hypovolemic shock represents a decrease in effective circulating blood volume and venous return. It can be due to primary intravascular volume loss (hemorrhage, capillary leak), secondary intravascular volume loss (third-space loss, insensible loss through skin with burns, diarrhea, vomiting), and increased unstressed vascular volume (loss of sympathetic tone, spinal cord injury, vasodilating drugs). The specific findings of hypovolemic shock are decreased filling pressures. Obstructive shock represents a blockage of blood flow. It may be due to right ventricular (RV) outflow obstruction (pulmonary embolism, hyperinflation), tamponade (pericardial effusion, hyperinflation), or left ventricular (LV) outflow obstruction (aortic stenosis, dissecting aortic aneurysm). The specific findings of obstructive shock are often more subtle but include decreased LV diastolic compliance (small LV volume with increased Ppao) and signs of cor pulmonale (Pra greater than Ppao, tricuspid regurgitation). Distributive shock represents loss of normal sympathetic responsiveness resulting in decreased vasomotor tone. In the nonresuscitated subject, this presents as hypovolemic shock,,14 but with fluid resuscitation BP does not increase despite an increase in cardiac output. It can be due to loss of vascular responsiveness (sepsis, spinal shock, vasodilating drugs, metabolic poisons). The specific findings of distributive shock are an increased cardiac output, Do2, and Sv̄o2 despite persistent hypotension. Hemodynamic monitoring can aid in determining circulatory shock etiology.