Effect of intrapulmonary hematocrit maldistribution on O2, CO2, and inert gas exchange.

The potential effect of intrapulmonary variations in hematocrit on gas exchange has been studied in theoretical models of the lung containing maldistribution of both hematocrit (Hct) and ventilation-perfusion (VA/Q) ratio. Hematocrit inequality enhanced gas exchange when units of low VA/Q were given a low Hct, arterial PO2 rising by as much as 14 Torr and PCO2 falling by up to 2 Torr depending on the particular distributions of Hct and VA/Q, whereas gas exchange was depressed when units of low VA/Q had a high Hct. After measuring inert gas solubilities in both dog and human blood of different Hct, the effect of Hct inequality on inert gas exchange was similarly assessed. Solubility was found to increase with HCT for less soluble gases. Because of this, conditions for enhancement of inert and O2 exchange by HCt inequality coincided, and it was found that in general the effects on O2 and inert gas transfer were quantitatively internally consistent. Even when Hct inequality was extreme, the resulting perturbation of inert gas concentrations was sufficiently small that the main features of the recovered VA/Q distributions were unaltered.