Lethal endotoxin shock. Oxygen deficit, lactic acid levels, and other metabolic changes

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Abstract
Progressive stagnant hypoxia secondary to inadequate tissue perfusion has been suggested as the final common pathway of all lethal shock syndromes. These studies tested this hypothesis by determining the oxygen deficit during lethal endotoxemic shock and correlating oxygen deficit with metabolic and hemodynamic measurements. Lactic acid and "excess lactate" rose to modest levels shortly after onset of shock but did not parallel the progressive increase in oxygen deficit. Thus, the degree of bacteriemia was not a reliable guide to the extent of hypoxia during endotoxin shock. It is postulated that endotoxin interferes with basic cellular metabolic processes, in addition to producing hemodynamic changes leading to decreased cardiac output, vasoconstriction, and shock, and that stagnant hypoxia alone is not the final pathway of lethal endotoxin shock.