Is Oxygen Consumption an Important Clinical Target?

Abstract

In the late 1960s and early 1970s a new syndrome was recognized following episodes of sepsis, ruptures of aortic aneurysm and multiple trauma. It consisted of development of progressive failures of vital organs: liver, kidneys, lungs and heart, starting from 1 to 3 days after the initial insult and culminating usually in death 14 to 21 days later, and was named multiple organ failure (MOF). The syndrome carried a mortality of greater than 80%. The exact cause and sequence of the events that arose at the time of the insult and resulted in MOF remain obscure, but hypotension, poor perfusion and relative hypoxia were thought to be important initiating events. It was in this context that the increase of arterial saturation by the addition of positive end-expiratory pressure (PEEP) became important and the physiological effects of PEEP in patients ventilated for adult respiratory distress syndrome (ARDS) were studied by Powers et al. [1]. They showed that the addition of PEEP caused changes in cardiac output and thus oxygen delivery (DO₂) and similar changes in the whole body oxygen consumption (VO₂) [1]. This work was interpreted as showing that VO₂ depended on DO₂ in patients with ARDS. The same type of apparent dependence has been found in a variety of other conditions of critical illness and has been termed “supply dependence” (Fig. 1)[2].