Severe sepsis (acute organ dysfunction secondary to infection) and septic shock (severe sepsis plus hypotension not reversed with fluid resuscitation) are major health care problems, affecting millions of individuals around the world each year, killing one in four patients (and often more), and increasing in incidence. 1 Sepsis represents a continuum from an inciting infectious event and host-pathogen interaction to the hemodynamic consequences caused by the relationship among proinflammatory, anti-inflammatory, and apoptotic mediators and is associated with circulatory insufficiency from hypovolemia, myocardial depression, increased metabolic rate, and vasoregulatory perfusion abnormalities eventually leading to an imbalance between tissue oxygen supply and demand, causing global tissue hypoxia. 2 Studies have shown a tendency for increased oxygen consumption (VO2) with an increased tissue oxygen extraction during initial hypodynamic or normodynamic circulation. 3 Later in the hyperdynamic circulation, when cardiac output and systemic oxygen delivery (DO2) are augmented therapeutically to 50% to 80% above normal values, an associated elevation of global VO2 may be seen. 3 In nonsurvivors, oxygen extraction may be impaired at supranormal values of DO2 in the presence of peripheral tissue hypoxia. 4 The presence of elevated blood lactate concentrations suggests tissue hypoxia and indicates continued impairment of Vo2 with supranormal DO2. 3 Autopsy data on patients have failed to reveal the cause of death in patients with sepsis. Necrosis