The nature of failure of pulmonary adaptation to atelectasis

The ability of the lung to decrease blood flow to an atelectatic lobe and to increase flow to normal after reinflation was investigated with a model using left lower lobe atelectasis (LLLA) in the dog. The change in the shunt fraction Q(s)/Q(t) with continuing LLLA was assumed to represent a change in blood flow to LLL. With LLLA the Q(s)/Q(t) rose from 0.112 to 0.172 and then decreased to 0.119 by the end of 2 hr at the rate of -17%/hr. Reversal of atelectasis for varying times demonstrated that the pulmonary vasoconstrictive response persisted for at least 4 hr after reinflation of LLLA. With LLL ischemia for 1 and 2 hr followed by LLLA, Q(s)/Q(t) decreased, but at a rate less than the controls, whereas after hemorrhagic shock with venous reinfusion and LLLA, the Q(s)/Q(t) did not decrease. When hemorrhagic shock was followed by arterial reinfusion, 60% had a normal response to LLLA; 40% did not. There was no difference in PVR in these two groups. Pulmonary extravascular water in both groups was the sam as in controls. Infusion of NE after 3 hr of LLA caused Q(s)/Q(t) to rise from 0.125 to 0.248, comparable to the value immediately after onset of LLLA. EPi had similar results. Catecholamines may restore blood flow to the atelectatic lobe by causing a maximum generalized pulmonary vasoconstriction or by overexpansion of the pulmonary blood volume secondary to peripheral vasoconstriction and thereby abolish any differential in pulmonary vascular resistance across the lung. The early hypoxemia of adult respiratory distress syndrome may arise not on the basis of any intrinsic lung pathology but rather as the result of a normal response of the lung to increased catecholamines.