Hemodynamic support in septic shock

Shock, defined as an imbalance between oxygen demand and oxygen supply, results in alterations in tissue perfusion, with reduction in delivery of oxygen and other nutrients to tissues, causing cellular, and then organ, dysfunction. The ultimate goals of hemodynamic therapy in shock are to restore effective tissue perfusion and to normalize cellular metabolism. In hypovolemic, cardiogenic, and obstructive shock, hypotension occurs as the result of a decrease in cardiac output, with consequent anaerobic tissue metabolism. Septic shock, however, typically results from distributive alterations, so that alterations in tissue perfusion result from abnormal control of the microvasculature with abnormal distribution of a normal or increased cardiac output. Cellular alterations in sepsis also result from the important inflammatory response, with the involvement of many mediators, including nitric oxide. Hence the endpoints of therapy are much more difficult to define with certainty than in other forms of shock in which a reduction in blood flow is the dominant problem. The complex nature of the pathophysiology of sepsis has led to considerable confusion and controversy regarding optimal patient management. Nevertheless, it is possible to develop a basic approach to the hemodynamic support of sepsis, which will almost certainly change as our understanding of sepsis improves further. Altered tissue perfusion in septic shock