Assessment of tissue oxygenation in the critically-ill

Abstract

It is hypothesized that tissue dysoxia and O₂ 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 O₂ supply (DO₂) and O₂ demand and translates into increased anaerobic metabolism and tissue and blood lactate concentration. First-line therapeutic strategies used to avoid the development of an O₂ debt involve correction of cardiac output, haemoglobin, and O₂ 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.