Effects of Lung Hyperinflation on Pulmonary Circulation

Abstract

Inflation of the lung affects large and small pulmonary vessels in two distinct ways. It is thought to dilate extraalveolar vessels (large arteries and veins) as perivascular pressure becomes more negative but to compress and stretch alveolar vessels (located in the alveolar wall and surrounded by alveolar pressure). Under West’s Zone II conditions, where pulmonary artery pressure (Ppa) exceeds alveolar pressure (Palv) which in turn is greater than left atrial pressure (Pla), blood flow (Q) depends on the pressure gradient Ppa-Palv with Palv being the effective downstream pressure. When Palv exceeds Pla, thin walled vessels subjected to alveolar pressure may act as Starling resistors; that is they flutter open and shut with flow like the device used by Starling in his heart-lung preparation. Permutt and Riley¹ showed that small muscular vessels could also act as Starling resistors as they collapse due to muscular tone or critical closing pressure. In chronic hypoxia the development of new muscle in normal thin walled arterioles down to 20 μm diameter and surrounded by alveoli suggests that these vessels may collapse due to muscle tone. There is also narrowing of the lumen of these vessels due to the encroachment by the new muscle. Could this affect the influence of alveolar pressure on the pulmonary circulation? Harris et al.^2,3 observed that during exercise Ppa/Q lines were displaced upwards to higher Ppa values in chronic bronchitic patients but not in normal subjects. They suggested that this might be due to raised alveolar pressure in bronchitic patients.