Previous studies had demonstrated reduced Vo2 during and immediately after surgical trauma from inadequate or maldistributed blood flow and reduced tissue perfusion. The first part of the present study, which is purely descriptive, documents greater tissue oxygen deficits in patients who subsequently develop multiple organ failure than in patients without organ failure. In lethal cases, the oxygen deficits were greater in magnitude and duration. Moreover, the very early appearance of oxygen debt suggests that reduced tissue oxygenation is the primary event, while organ failure and death are the result of this antecedent physiologic event.
In the second part of this study, prospective clinical trials demonstrated that reduction in the calculated oxygen debt was followed by reduced organ failure and decreased mortality when increased Vo2 was maintained at supranormal values. Thus, evidence suggests that reduced tissue oxygenation from maldistributed or inadequate tissue perfusion in the face of increased metabolic need is an early pathogenic mechanism that produces organ failure and death. Possible contributing influences of inadequate perfusion include (a) myocardial and metabolic depression from anesthetic agents; (b) delay or failure to keep up with fluid and blood losses; (c) uneven vasoconstriction by neural mechanisms; (d) preexisting limitations from anemia; (e) chronic cardiac, respiratory, and renal insufficiencies; (f) cytokines, eicosanoids, and other chemical mediators; and (g) inadequate cardiac and respiratory compensatory responsiveness.