Effect of oxygen breathing on distribution of pulmonary blood flow in chronic obstructive lung disease.

Abstract

In chronic obstructive lung disease, a major functional disturbance lies in maldistribution of ventilation of the lungs. It has been postulated that, at least in some patients, compensatory regional pulmonary vasoconstriction may occur in the poorly ventilated portions of such lungs, thus reducing the range of ventilation-perfusion ratios and improving arterial oxygen tension. The evidence for this lies largely in the reduction of arterial oxygen tension or saturation that may follow the administration of pulmonary vasodilator drugs, such as tolazoline (1, 2) and aminophylline (3-5). It has been suggested that these drugs reverse pre-existing vasoconstriction in poorly ventilated regions of the lungs and that this leads to a worsening of ventilation-perfusion ratio distribution and a fall in arterial oxygen tension. Oxygen is a powerful, nonspecific, pulmonary vasodilator agent. Pain, Read, and Read (6) showed that in a group of patients with chronic lung disease oxygen breathing was sometimes associated with an increase of arterial carbon dioxide tension (Pac02 ) greater than that to be expected from any hypoventilation produced by the oxygen. It was suggested that these increases of Pa002, not due to diminished ventilation of the lungs, were also due to worsening of ventilationperfusion ratio distribution in the lungs. Analysis of the factors involved indicated that this, in turn, must reflect an increased blood flow through poorly ventilated regions of the lungs associated with oxygen breathing; that is, there was reversal of pre-existing regional compensatory vasoconstriction in some of these patients. These conclusions were based on comparisons of ventilation and Pa002 that were made when the subject was breathing air and after breathing oxygen for ten minutes. Some of the conclusions