Oxygen consumption in septic shock: collective review.

That a decline in oxygen consumption (VO2) might herald onset of septic shock prior to hemodynamic collapse is suggested by previous observations in humans and animals in which VO2 appeared to be suppressed in systemic sepsis, despite normal or supranormal cardiac output, and in cellular and mitochondrial preparations exposed to endotoxin, despite adequate flow of perfusate. That a supranormal VO2 might be one of the best predictors of ultimate survival is suggested by data collected from humans during various stages of septic shock. To evaluate VO2 as an early indicator of sepsis, the effect of endotoxemia was observed in 20 rhesus monkeys divided into groups according to hypodynamic, normodynamic, and hyperdynamic blood flow states; the effect of sepsis was observed in seven preterminal septic humans during the final hours of their lives. VO2 was measured using a new device that evaluates expired gases by means of a relatively simple feedback-controlled gas replenishment technique. In neither the primates nor the humans was it possible to demonstrate a flow-independent depression of VO2. VO2 was distinctly elevated in each of the humans over some interval during the final day of life. These observations, plus an in-depth review of the literature, suggest that other variables, particularly peripheral vascular resistance, systemic and regional blood flow, and oxygen extraction fraction attempt to accommodate in an effort to sustain VO2. Probability of survival in sepsis appears to be enhanced by VO2 and cardiac output that are supranormal; yet even when VO2 is elevated, death can ensue within minutes to hours. Significant decline in VO2 is a grave prognostic sign, almost always preceded by a relatively easily detected hemodynamic change. Systemic VO2 appears to represent neither a specific early indicator of sepsis nor a certain prognosticator of survival outcome; it might provide useful information regarding adequacy of resuscitation.