Journal of Applied Physiology
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J Appl Physiol 89: 1317-1321, 2000;
8750-7587/00 $5.00
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Vol. 89, Issue 4, 1317-1321, October 2000

Venoarterial CO2 difference during regional ischemic or hypoxic hypoxia

Benoit Vallet1, Jean-Louis Teboul2, Stephen Cain3, and Scott Curtis4

1 Département d'Anesthésie-Réanimation 2, Centre Hospitalier Universitaire de Lille, 59800 Lille; 2 Service de Réanimation Médicale, Hôpital du Kremlin-Bicêtre, Hôpitaux de Paris, 75004 Paris, France; Departments of 3 Physiology and Biophysics and 4 Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama 35294

To test the role of blood flow in tissue hypoxia-related increased veno-arterial PCO2 difference (Delta PCO2), we decreased O2 delivery (DO2) by either decreasing flow [ischemic hypoxia (IH)] or arterial PO2 [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), hindlimb DO2 was progressively lowered every 15 min by decreasing pump-controlled flow from 60 to 10 ml · kg-1 · min-1, with arterial PO2 constant at 100 Torr. In the HH group (n = 6), hindlimb DO2 was progressively lowered every 15 min by decreasing PO2 from 100 to 15 Torr, when flow was constant at 60 ml · kg-1 · min-1. Limb DO2, O2 uptake (VO2), and Delta PCO2 were obtained every 15 min. Below the critical DO2, VO2 decreased, indicating dysoxia, and O2 extraction ratio (VO2/DO2) rose continuously and similarly in both groups, reaching a maximal value of ~90%. Delta PCO2 significantly increased in IH but never differed from baseline in HH. We conclude that absence of increased Delta PCO2 does not preclude the presence of tissue dysoxia and that decreased flow is a major determinant in increased Delta PCO2.

regional capnometry; dysoxia; oxygenation; respiratory quotient


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