Abstract
Monitoring tissue hypoxia in critically ill patients is a challenging task. Tissue PCO2 has long been proposed as a marker of tissue hypoxia, although there is considerable controversy on whether the rise in CO2 with hypoxia is caused by anaerobic metabolism and excess CO2 production or by the accumulation of aerobically produced CO2 in the setting of blood flow stagnation. The prevention of increases in intestinal PCO2 in aggressively resuscitated septic animals supports the notion that tissue CO2 accumulation is a function of decreases in blood flow, not of tissue hypoxia.
Highlights
A reliable and practical method to detect the onset of tissue hypoxia in critically ill patients would be an invaluable tool in guiding the timing and aggressiveness of resuscitation efforts
Numerous clinical and experimental studies show a strong correlation between increases in tissue PCO2 and poor patient outcome, gastric tonometry or sublingual tonometry have encountered variable clinical acceptance
Technical difficulties certainly have dampened the initial enthusiasm for PCO2 tonometry, but a more challenging obstacle to the widespread use of this technology has been an inadequate understanding of the mechanism(s) that result in tissue CO2 accumulation
Summary
A reliable and practical method to detect the onset of tissue hypoxia in critically ill patients would be an invaluable tool in guiding the timing and aggressiveness of resuscitation efforts. Enthusiastic acceptance of the ‘supranormal’ O2 delivery concept, produced by the infusion of fluid volume, inotropic agents and blood products [5], has been tempered by studies finding no efficacy [6], or even increased mortality [7], with this approach. Measuring tissue PCO2 with a gastric tonometer [10] or a sublingual tonometer [11,12] has been proposed as a physiologically sound method of detecting decreases in organ perfusion.
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