The effect of carbon dioxide on the pulmonary circulation.

At present there is experimental and clinical evidence to support the view that alteration in alveolar oxygen tension has a direct effect on pulmonary circulation. Animal experimentation (1-4) and hemodynamic studies in human subjects (5-8) indicate that pulmonary vascular resistance increases and blood flow is thereby reduced in hypoxic areas of the lung. This is apparently a mechanism by which the body decreases perfusion of poorly ventilated lung and thus maintains efficient respiration. The effect of changes in alveolar carbon dioxide tension on pulmonary hemodynamics is less well understood. Von Euler and Liljestrand (1) showed in cats that pulmonary hypertension ensued when the concentration of carbon dioxide in the inspired air was increased to 6.5 per cent. Variable responses of the pulmonary vascular dynamics have been reported by Nisell (9, 10), who studied the effect of carbon dioxide on the isolated cat lung. Stroud and Rahn ( 11 ) reported that pulmonary vascular resistance did not change when animals were ventilated with mixtures containing 5 per cent carbon dioxide. Weil, Salisbury and State (12), in an open chest dog preparation, observed that carbon dioxide can cause pulmonary vasomotion. Borst, Whittenberger, Berglund and McGregor (13), using dogs, found a redistribution of blood away from the lung ventilated with 5 per cent carbon dioxide and air mixture and concluded that local vasoconstriction occurred. In 20 patients with congenital heart disease, Shephard (14) found that 5 per cent carbon dioxide given during catheterization produced moderate but consistent degrees of pulmonary hypertension.