Shock has traditionally been viewed as a perfusion deficit: "That state in which the supply of blood to the tissues of the body is inadequate to meet the body's metabolic demands."1 This definition, although appropriate to cardiogenic and hypovolemic shock, is inadequate for septic shock. The manifestations of septic shock do not relate to a perfusion deficit but to the inability of the body to effectively use existing metabolic substrate.2
The septic response is a host-related phenomenon independent of the type of invasive organism.3 Identical clinical manifestations can be seen with a diverse variety of organisms. In fact, there have been patients with the clinical picture of advanced sepsis in whom no organism was detected.4 Regardless of the stimulus, certain metabolic abnormalities appear that may progress to cause the death of the host.2,5 Approaching the pathophysiology of sepsis and septic shock from the point of