Published ahead of print on December 4, 2003, doi:10.1164/rccm.200305-702OC Am. J. Respir. Crit. Care Med., Volume 169, Number 4, February 2004, 525-533 A more recent version of this article appeared on February 15, 2004
Submitted on May 31, 2003 A Mathematical Model of Tissue-Blood Carbon Dioxide Exchange During HypoxiaGuillermo Gutierrez1*1 Pulmonary and Critical Care Medicine, The George Washington University, Washington, D.C., USA * To whom correspondence should be addressed. E-mail: ggutierrez{at}mfa.gwu.edu.
A two compartment mass transport model of tissue CO2 exchange is developed to examine the relative contributions of blood flow and cellular hypoxia (dysoxia) to increases in tissue and venous blood CO2 concentration. The model assumes perfectly mixed homogeneous conditions, steady state equilibrium and CO2 production occurring exclusively at the tissues. The behavior of the model is compared to published data derived from an isolated dog hindlimb preparation subjected either to reductions in blood flow (ischemic hypoxia) or to decreases in arterial PO2 (hypoxic hypoxia). The results of the model corroborate the experimental finding of greater venous and tissue CO2 concentrations with ischemic hypoxia than with hypoxic hypoxia. The model also predicts increases in CO2 concentration under conditions of adequate O2 supply, should CO2 transfer from tissue to blood become impaired. Consequently, from a theoretical perspective, it appears that increases in tissue or venous blood CO2 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 CO2 concentration during dysoxia reflect primarily alterations in vascular perfusion and not scarcity in cellular energy supply. Key words: CO2 production, oxygen delivery, oxygen consumption, tissue oxygenation, venous PCO2
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