Distribution function of transit times in the human pulmonary circulation

Abstract

The distribution function of pulmonary transit times (fPTT) defines contact time between blood and vascular bed, which affects gas exchange and endothelial metabolic functions. This study was undertaken to assess effects of abnormal pulmonary inflow (P̄(PA)) and outflow pressures (P(LA)) on fPTT. Three groups were studied: five patients with elevated P(LA) and passive pulmonary hypertension (LVD-Ab), eight with normal P(LA) (LVD-Nl), and six with pulmonary disease and various levels of P(PA) (PD). Empirical complex exponential functions were convoluted on right and left ventricular indicator-dilution curves to derive fPTT; mean transit time (Mo1), standard deviation (Sm2), and cube root of the third moment about Mo1 (Sm3) were calculated by standard equations. A single linear regression of Sm3 and Sm2 on Mo1 was observed for all patients, regardless of disease process. Inverse relations between Mo1, Sm2, and Sm3 and blood flow were highly significant, but dispersion volumes (DV = Mo1 x flow) were higher in patients with elevated P̄(PA). Significant linear regressions of fPTT parameters on P̄(PA), derived in LVD-Nl and LVD-Ab patients, failed to predict Mo1, Sm2, and Sm3 for the PD group, whereas linear regressions on P(LA) accurately predicted Mo1, Sm2, and Sm3 in the PD group. Relations between fPTT parameters and P(LA) were equally well fit by exponential equations in all 19 patients, consistent with an asymptotic pressure-volume relation of distensible vessels. Microvascular pressure (P(MV)), combining P(PA) and P(LA), was not a better predictor of fPTT parameters in LVD-NL and LVD-Ab patients but provided a slightly closer estimate of relative dispersion and skewness in PD patients. We conclude that, under conditions of this study, P(LA) is a major determinant of fPTT, somewhat modified by elevated P(PA) and cardiac output in patients with lung disease.