Posttrauma Oxygen Debt and Its Metabolic Consequences

Abstract

Oxygen is the critical carbon acceptor in the generation of energy from metabolic fuel substrates. Consequently, oxygen consumption is a closely regulated phenomenon in all animal cells and more complex higher organisms. Following injury, or during severe sepsis, oxygen consumption increases, especially when these conditions are associated with an increase in body temperature. Moreover, the host-defense response consequent on these conditions changes both the quality and the quantity of the metabolic response. Over the years, evidence has been accumulated that the host-defense response pattern can be initiated by a number of different etiologic agents. These range from sterile inflammatory mediators or tissue injury, anamestic immunologic challenges, bacterial endotoxin administration and/or sepsis, and hypovolemic ischemic shock produced either by blood loss, third space fluid dislocations from the circulatory system, or cardiac failure. In these latter conditions, oxygen delivery is restricted by a decreased flow. As a consequence, oxygen consumption decreases, falling below the oxidative requirement of various organ metabohc processes (Fig. 1). In this concept, a decrease in oxygen consumption occurring after the loss of perfusion to metabolic tissues, which reduces delivery below the baseline level of oxygen consumption, produces a deficit in oxygen consumption, which is the accumulating difference over time between the organism’s oxygen demand and the actual oxygen consumption permitted. This deficit is known as the oxygen debt (O₂ debt).