Variations in pulmonary gas exchange due to changes in pulmonary artery pressure and flow

Abstract

Effective gas exchange in the lung is achieved by an adequate matching of ventilation to perfusion. In a normal, erect lung, the distribution of ventilation and perfusion is such that several alveolar-capillary units can be observed. At the apex of the lung, alveoli that are hyperventilated with respect to their perfusion can be found. These alveolar-capillary units contribute to an arterial-alveolar Pco, difference, and their magnitude can be assessed by a calculation of the alveolar dead space to alveolar tidal volume ratio. At the bottom of the erect lung, alveoli that are hyperperfused with respect to their ventilation are present, and they contribute to decrease the arterial oxygen tension, and to generate an alveolararterial PO2 gradient. Their magnitude can be calculated by the venous admixture, or shunt equation. Anatomical arteriovenous shunts in the pulmonary circulation will affect gas exchange in the same manner. The largest bulk of the alveolar-capillary units show a ventilation that is commensurate with their perfusion. There can be another possible combination of ventilation-to-perfusion relationships, i.e., units with neither ventilation nor perfusion. They would not contribute to either the alveolar dead space to alveolar tidal volume ration, or the venous admixture, and the lung functions as though these units were not present. The effect of alterations in the ventilationto-perfusion relationship upon pulmonary gas exchange have been studied theoretically [9, 17, 181, in experimental animals [7, 13, 15, 23, 25, 281, and in patients [ 1, 3, 4, 8, 12, 16, 191. Less is known, however, concerning the effects of passive hemodynamic changes in the pulmonary circulation upon gas exchange. In previous experiments, we observed a positive, linear relationship between cardiac output and venous admixture in animals under controlled ventilation [7]. In order to provide additional information concerning the specific influence of passive hemodynamic alterations upon pulmonary gas exchange, a series of experiments were performed on isolated, perfused dog lungs.