Under normal circumstances, O 2 transport (TO 2 = cardiac output x arterial O 2 content) is regulated to provide sufficient O 2 to meet the demands of oxidative phosphorylation, quantified as the O 2 consumption (VO 2). When metabolic demands increase, TO 2 is augmented and in addition, the fractional extraction of the delivered O 2 by the tissues, the O 2ER, also increases, to levels as high as 0.80 at maximum VO 2. If TO 2 is decreased, at least in the experimental animal, VO 2 can be maintained initially by an increase in O 2ER, but eventually this mechanism is exhausted, VO 2 begins to fall, and the body invokes anaerobic means of energy generation to maintain cell integrity. In normal man, this critical level of TO 2 (TO 2crit) has not been determined, but in experimental animals it has been found once the O 2ER exceeds 0.50. Patients with sepsis and the adult respiratory distress syndrome have a very high mortality and usually die as a result of multiple organ failure. They have in addition, an apparent abnormality in their ability to extract and utilize the delivered O 2. Despite a TO 2 which is often higher than normal, patients with sepsis commonly have a lactic acidosis and when TO 2 is reduced, both groups of patients are usually unable to increase their O 2ER above the normal resting value of 0.33.(ABSTRACT TRUNCATED AT 250 WORDS)
Download full-text PDF |
Source |
---|
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!