Supply dependency of oxygen uptake in ARDS: myth or reality?
Several reports state that oxygen uptake changed in direct correlation with changes in total oxygen delivery to the tissues in the adult respiratory distress syndrome (ARDS). Oxygen uptake appeared to be limited by oxygen delivery even at normally adequate levels so that uptake was abnormally dependent on supply. These reports are discussed with respect to whether or not such a result could have been due to errors in measurement or to mathematical coupling by relating two quantities that shared a common variable. Having rejected that proposition, animal experiments are cited in which abnormal oxygen supply dependency was produced by microembolization. The accompanying loss of reactive hyperemia and inability to extract oxygen were consistent with a progressive loss of recruitable capillaries. Evidence is presented that the potential for embolization in ARDS is greatly enhanced by activation of the complement and arachidonic acid cascades as well as by the xanthine oxidase system. The resultant use of molecular oxygen by non-ATP producing oxidase systems might also account for the increase of supply dependent oxygen demand in ARDS.
D000818:Animals; D001775:Blood Circulation; D002302:Cardiac Output; D003167:Complement Activation; D004617:Embolism / Q000503:physiopathology; D005609:Free Radicals; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D008833:Microcirculation / Q000503:physiopathology; D010100:Oxygen / Q000097:blood / Q000378:metabolism; D010101:Oxygen Consumption; D012039:Regional Blood Flow; D012128:Respiratory Distress Syndrome / Q000378:metabolism / Q000503:physiopathology*
D005609:Free Radicals; D010100:Oxygen