Alterations in Ventilation-Perfusion Relationships in the Lung after Breathing Inert Dust or Bronchoconstrictor Aerosols and after Short Periods of Voluntary Hyperventilation

Abstract

Aerosols of carbachol, and clouds of calcium carbonate dust were administered to normal subjects, and both disturbed the evenness of alveolar ventilation as measured by the single-breath oxygen test. Following carbachol aerosol there was an increase in alveolar-arterial difference in oxygen tension (A-aD), no change in the ratio of physiological dead space to tidal volume (VD/VT), and a decrease in anatomical dead space. After breathing dust clouds, A-aD increased, and so did VD/VT, but there was no change in anatomical dead space. Both A-aD and physiological dead space returned to control values sooner than did the single-breath oxygen test. The possibility that this indicates a local redistribution of pulmonary capillary blood flow in response to the acute disturbance of distribution of alveolar ventilation is discussed. After a brief period of voluntary hyperventilation in the sitting position there was an increase in physiological dead space and in V D/VT, that persisted for 60 min., but only a small and non significant decrease in A-aD. When a fall in Pco2 was prevented by addition of carbon dioxide to the inspired gas during hyperventilation, there was no significant alteration in VD/VT or A-aD. Subjects who hyperventilated, breathing air in the supine position showed hardly any change in VD/VT and no alteration in A-aD. It is postulated that hypocapnia during hyperventilation may lead to a fall in pulmonary arterial pressure and a decreased blood flow to the upper zones of the lung; the possible mechanisms are discussed.