Sequential hemodynamic and oxygen transport responses in hypovolemia, anemia, and hypoxia

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Abstract
Sequential cardiorespiratory measurements were made in 30 mongrel dogs during controlled hypovolemia, normovolemic anemia and hypoxia. The responses to each of these 3 types of O2 deprivation were studied both as a function of time and the rate of O2 delivery (normalized cardiac output .times. 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 were differences in the hemodynamic responses to the 3 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. O2 consumption (.ovrhdot.VO2) remained relatively constant until the preterminal stage. At this time O2 delivery had fallen from .apprx. 27 to < 10 ml .cntdot. min-1 .cntdot. kg-1, blood volume was < 50%, hematocrit was < 8% and arterial O2 tension was < 30 Torr at an average fractional inspired O2 concentration of 8%, for the hypovolemic, anemic and hypoxic groups, respectively. Then .ovrhdot.VO2 dropped precipitously and death rapidly occurred. .ovrhdot.VO2 represents a physiological marker of impending death in the face of progressively diminishing O2 delivery.

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