Venoarterial CO2 difference during regional ischemic or hypoxic hypoxia

Abstract

To test the role of blood flow in tissue hypoxia-related increased veno-arterial Pco 2difference (ΔPco 2), we decreased O2 delivery (D˙o 2) by either decreasing flow [ischemic hypoxia (IH)] or arterial Po 2 [hypoxic hypoxia (HH)] in an in situ, vascularly isolated, innervated dog hindlimb perfused with a pump-membrane oxygenator system. Twelve anesthetized and ventilated dogs were studied, with systemic hemodynamics maintained within normal range. In the IH group ( n = 6), hindlimbD˙o 2 was progressively lowered every 15 min by decreasing pump-controlled flow from 60 to 10 ml · kg−1 · min−1, with arterial Po 2 constant at 100 Torr. In the HH group ( n = 6), hindlimbD˙o 2 was progressively lowered every 15 min by decreasing Po 2 from 100 to 15 Torr, when flow was constant at 60 ml · kg−1 · min−1. LimbD˙o 2, O2 uptake (V˙o 2), and ΔPco 2 were obtained every 15 min. Below the criticalD˙o 2,V˙o 2 decreased, indicating dysoxia, and O2 extraction ratio (V˙o 2/D˙o 2) rose continuously and similarly in both groups, reaching a maximal value of ∼90%. ΔPco 2 significantly increased in IH but never differed from baseline in HH. We conclude that absence of increased ΔPco 2 does not preclude the presence of tissue dysoxia and that decreased flow is a major determinant in increased ΔPco 2.