Physiological and clinical significance of the pressure difference in alveolar-arterial gas and problems in its determination

Abstract

A∼aD show the differences between the mean partial pressure of alveolar O2, CO2 and N2 gases and arterial ones. These will be explained in three parts, A) physiological significances, B) clinical significances, and C) problems in the measurements, with special reference to the concept of the alveolar gas and its actual condition. A) Physiological significances. The uneven distribution of ventilation causes A-aDO2, a-ADCO2 and a-ADN2, while that of perfusion causes only a-ADCO2. It was confirmed that A-aDO2 and a-ADCO2 were chiefly reflective of the group of alveoli with low ventilation-perfusion-ratio and its perfusion fraction was higher than the ventilation fraction, and that a-ADCO2 was chiefly reflective of the alveolar group with high ventilation-perfusion-ratio and its ventilation fraction was higher than that of perfusion fraction. Moreover, it was mentioned as the problems to evaluate that A-aDO2 increased according to the anatomical shunts and the trouble of diffusion through alveolar membranes, a-ADCO2 was caused by the uneven distributions of both ventilation and perfusion, and in the pulmonary embolism only by the macroembolus, and that they were easily false positive in the case with the dead space hyperventilation in the air ways. B) Clinical significances. In many obstructive lung diseases studied, the alveolar dead space ventilation ratio was correlative with the a-ADCO2 (r=0.927) and was roughly correlative with the A-aDO2 (r= 0.528). When the ventilation-perfusion-ratio was over 4.0, the ventilation equivalence (not only) for O2 but also for CO2 increased, therefore in cardiopulmonary diseases with a-ADCO2, the alveolar ventilations calculated from the alveolar air equation substituting values of arterial carbon dioxide tensions were influenced to be underestimated as to the a-ADCO2, consequently the net volume i.e. the real space of air was not revealed. The shunt like effects were exponentially correlative with the A-aDO2 (physiol. (QS)/(QT) = 1.5e0.047(A-aDO2)). The carbon QT monoxide diffusing capacity reduced in both cases with the increased A-aDO2 and with the increased a-ADCO2. Neither the A-aDO2 nor the a-ADCO2 correlated with the FEV1/VC. The total pulmonary vascular resistance correlated roughly with the A-aDO2 and the a-ADCO2 respectively (r=0.522, r=0.660). The A-aDO2 had negative correlation with the arterial oxygen tensions (r=-0.765), while the a-ADCO2 were roughly correlative with the arterial carbon dioxide tensions (r= 0.643).