A mathematical model of tissue-blood carbon dioxide exchange during hypoxia.

Abstract

A two-compartment mass transport model of tissue CO(2) exchange is developed to examine the relative contributions of blood flow and cellular hypoxia (dysoxia) to increases in tissue and venous blood CO(2) concentration. The model assumes perfectly mixed homogeneous conditions, steady-state equilibrium, and CO(2) production occurring exclusively at the tissues. The behavior of the model is compared with published data derived from an isolated dog hindlimb preparation subjected to either reductions in blood flow (ischemic hypoxia) or decreases in arterial PO(2) (hypoxic hypoxia). The results of the model corroborate the experimental finding of greater venous and tissue CO(2) concentrations with ischemic hypoxia than with hypoxic hypoxia. The model also predicts increases in tissue CO(2) concentration under conditions of adequate O(2) supply if CO(2) transfer from tissue to blood becomes impaired. Consequently, from a theoretical perspective, it appears that increases in the tissue or venous blood CO(2) concentration are neither sensitive nor specific markers of tissue dysoxia. The results of the model support the notion that changes in tissue and venous blood CO(2) concentration during dysoxia reflect primarily alterations in vascular perfusion and not scarcity in cellular energy supply.