Blood flow, not hypoxia, determines intramucosal PCO2.
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.
Gutierrez
Guillermo
G
Pulmonary and Critical Care Medicine Division, Department of Medicine, The George Washington University Medical Center, Washington, DC, USA. ggutierrez@mfa.gwu.edu
D000138:Acidosis / Q000378:metabolism*; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism*; D015687:Cell Hypoxia; D002986:Clinical Trials as Topic; D016638:Critical Illness; D004285:Dogs; D005753:Gastric Mucosa / Q000098:blood supply* / Q000378:metabolism*; D006801:Humans; D007413:Intestinal Mucosa / Q000098:blood supply / Q000378:metabolism; D008365:Manometry; D018482:Muscle, Skeletal / Q000098:blood supply / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D010101:Oxygen Consumption; D010313:Partial Pressure; D012039:Regional Blood Flow; D012756:Sheep; D012772:Shock, Septic / Q000378:metabolism
D002245:Carbon Dioxide; D010100:Oxygen