Identifying critical DO2 with compensatory reserve during simulated hemorrhage in humans.

Abstract

Based on previous experiments in nonhuman primates, we hypothesized that DO2 crit in humans is 5-6ml O2 ·kg-1 min-1 . We measured the compensatory reserve (CRM) and calculated oxygen delivery (DO2 ) in 166 healthy, normotensive, nonsmoking subjects (97 males, 69 females) during progressive central hypovolemia induced by lower body negative pressure as a model of ongoing hemorrhage. Subjects were classified as having either high tolerance (HT; N=111) or low tolerance (LT; N=55) to central hypovolemia. HT and LT groups were matched for age, weight, BMI, and vital signs, DO2 and CRM at baseline. The CRM-DO2 relationship was best fitted to a logarithmic model in HT subjects (amalgamated R2 =0.971) and a second-order polynomial model in the LT group (amalgamated R2 =0.991). Average DO2 crit for the entire subject cohort was estimated at 5.3ml O2 ·kg-1 min-1 , but was ~14% lower in HT compared with LT subjects. The reduction in DO2 from 40% CRM to 20% CRM was 2-fold greater in the LT compared with the HT group. Average DO2 crit in humans is 5.3ml O2 ·kg-1 min-1 , but is ~14% lower in HT compared with LT subjects. The CRM-DO2 relationship is curvilinear in humans, and different when comparing HT and LT individuals. The threshold for an emergent monitoring signal should be recalibrated from 30% to 40% CRM given that the decline in DO2 from 40% CRM to 20% CRM for LT subjects is located on the steepest part of the CRM-DO2 relationship.