Effect of O2 affinity on arterial PO2 in animals with central vascular shunts.

Abstract

Central vascular or intracardiac shunts result in venous admixture and reduced saturation of systemic arterial blood. This is pronounced in most species of amphibians and reptiles and may occur as congenital defects in homeotherms. A two-compartment model is useful to analyze the effects of shunt on O2 transport. The PO2 of a mixture of pulmonary (ideal) and mixed venous (shunt) blood will be a function of the resulting O2 saturation, analogous to the principle of the "mixing method" in vitro. Furthermore, for a given saturation, the PO2 of systemic arterial blood (PaO2) should be inversely related to the O2 affinity of the mixed blood. The present study tested this two-compartment model of shunt in animals with normally occurring right-to-left shunts (amphibians and reptiles) and with dogs having artificial shunts. The O2 dissociation curves (ODC) of the blood were manipulated by varying body temperature and blood pH. For any level of saturation of systemic arterial blood, the PaO2 was found to increase with factors that shifted the ODC to the right. This experimental support of mathematical models of shunting and PaO2 suggests that animals with intracardiac or central vascular shunts are benefited by low-O2-affinity blood, a condition that is common in amphibians and reptiles. For an individual ectothermic vertebrate, an increase in O2 demand due to increased body temperature would, because of decreased O2 affinity, be accompanied and perhaps facilitated by an increase in PaO2 if saturation remained constant.