Blood flow, not hypoxia, determines intramucosal PCO(2)

Monitoring tissue hypoxia in critically ill patients is a challenging task. Tissue PCO(2 )has long been proposed as a marker of tissue hypoxia, although there is considerable controversy on whether the rise in CO(2 )with hypoxia is caused by anaerobic metabolism and excess CO(2 )production or by the accumulation of aerobically produced CO(2 )in the setting of blood flow stagnation. The prevention of increases in intestinal PCO(2 )in aggressively resuscitated septic animals supports the notion that tissue CO(2 )accumulation is a function of decreases in blood flow, not of tissue hypoxia.