The effect of cardiac output on arterial blood oxygenation

Abstract

Although classic teaching suggests that changes in cardiac output and mixed venous blood oxygen content will cause similar changes in Pa(O2), most experimental evidence indicates otherwise. The effects of changes in cardiac output on Pa(O2) are variable, ranging from essentially no effect in normal or diffusely diseased lung to a marked direct effect in regional lung collapse. The reason for this phenomenon is that a change in cardiac output itself causes a change in venous admixture or the shunt fraction in the lung. Venous admixture or shunt varies directly with cardiac output in normal or diffusely abnormal lung and indirectly with cardiac output in regional atelectasis. The net result of the cardiac output-induced changes in mixed venous blood oxygen content and venous admixture is that Pa(O2) is significantly affected by cardiac output only in the presence of regional atelectasis, where Pa(O2) is directly related to cardiac output. In the normal or diffusely diseased lung, the cardiac output-venous admixture relationship is probably due to the mechanical effects of changes in the magnitude of pulmonary blood flow and pulmonary arterial pressure. These pressure and flow changes alter the hypoxic vasoconstrictive response, which in turn results in changes of the distribution of pulmonary blood flow to areas with low ventilation-perfusion ratios or alveolar collapse. With regional atelectasis, the effects are probably due to the mechanical effects produced by differences in lung heights and pressures acting on vessels, rather than any major effect on hypoxic pulmonary vasoconstriction.