Abstract
Reduced cardiac output is a crucial determinant in hypovolemic, cardiogenic and obstructive types of acute circulatory failure, but cardiac output is considered less meaningful in septic shock where the primary defect is thought to be peripheral. In septic states, oxygen transport values are typically elevated, and the altered oxygen extraction (ratio of oxygen uptake over oxygen supply) limits the ability of the tissues to increase their oxygen uptake in relation to high oxygen needs. To correct tissue hypoxia, oxygen consumption should be increased to a level where oxygen uptake equals oxygen demand and lactic acidosis resolves. For a given level of oxygen demand, the best option is to improve oxygen extraction so that oxygen consumption will be higher for the same level of oxygen transport. This, however, is very difficult. Another approach can consist of further increasing oxygen transport to meet the elevated oxygen demand. Whenever possible, the metabolic needs of the tissues should be restrained.
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