Sequential hemodynamic and oxygen transport responses in hypovolemia, anemia, and hypoxia.
Sequential cardiorespiratory measurements were made in 30 mongrel dogs during controlled hypovolemia, normovolemic anemia, and hypoxia. The responses to each of these three types of O2 deprivation were studied both as a function of time and of the rate of O2 delivery (normalized cardiac output x arterial O2 content). With progressively decreasing O2 delivery, compensations appeared, reached a maximum, and fell before the final circulatory deterioration. O2 extraction increased in each experiment, but there was differences in the hemodynamic responses to the three types of O2 deprivation; e.g., cardiac output increased in the anemic dogs, and there were greater increases in systemic and pulmonary resistances after hemorrhage. The striking finding was that O2 consumption (VO2) remained relatively constant until the preterminal stage. At this time O2 delivery had fallen from about 27 to less than 10 ml . min-1 . kg-1, blood volume was less than 50%, hematocrit was less than 8%, and arterial O2 tension was less than 30 Torr at an average fractional inspired O2 concentration of 8%, for the hypovolemic, anemic, and hypoxic groups, respectively. Then VO2 dropped precipitously and death rapidly occurred. These results suggest that VO2 represents a physiological marker of impending death in the face of progressively diminishing O2 delivery.
D000740:Anemia / Q000503:physiopathology*; D000818:Animals; D001810:Blood Volume; D004285:Dogs; D005260:Female; D006439:Hemodynamics; D006470:Hemorrhage / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D010100:Oxygen / Q000097:blood*; D012119:Respiration; D012769:Shock / Q000503:physiopathology*; D013997:Time Factors
D010100:Oxygen