It is hypothesized that tissue dysoxia and O-2 debt are major factors in th
e development and the propagation of multiple organ failure in critically i
ll patients. Dysoxia is the result of an abnormal relationship between O-2
supply (DO2) and O-2 demand and translates into increased anaerobic metabol
ism and tissue and blood lactate concentration. First-line therapeutic stra
tegies used to avoid the development of an O-2 debt involve correction of c
ardiac output, haemoglobin, and O-2 saturation in order to increase DO2 abo
ve its critical value. They are not sufficient, however, to ensure appropri
ate end-organ perfusion and oxygenation. The adequacy of cardiac output tow
ards tissue metabolic requirements may be appreciated by venous-to-arterial
and gut mucosal-to-arterial PCO2 differences. This review details these st
rategies and discusses their usefulness in current practice.