Assessment of tissue oxygenation in the critically-ill

It is hypothesized that tissue dysoxia and O-2 debt are major factors in the development and the propagation of multiple organ failure in critically ill patients. Dysoxia is the result of an abnormal relationship between O-2 supply (DO2) and O-2 demand and translates into increased anaerobic metabolism and tissue and blood lactate concentration. First-line therapeutic strategies used to avoid the development of an O-2 debt involve correction of cardiac output, haemoglobin, and O-2 saturation in order to increase DO2 above its critical value. They are not sufficient, however, to ensure appropriate end-organ perfusion and oxygenation. The adequacy of cardiac output towards tissue metabolic requirements may be appreciated by venous-to-arterial and gut mucosal-to-arterial PCO2 differences. This review details these strategies and discusses their usefulness in current practice.