Changes in Pulmonary Hemodynamics Produced by Isoproterenol Infusion in Emphysematous Patients

PULMONARY hypertension is a common complication of diffuse obstructive pulmonary emphysema.' While obliteration of the pulmonary vascular bed may be the principal factor that causes pulmonary hypertension, it is apparent that other factors, sueh as hypoxia, increased cardiac output, and pulmonary vasomotor tone, are important contributing elements.2 In most instances in which there is resting pulmonary hypertension, an increase in cardiac output, such as is produced by exercise, is accompanied by an increase in pulmonary artery pressure and a constant or rising pulmonary vascular resistance.3 It is the purpose of the present study to determine whether the pulmonary vascular bed in emphysematous subjects can accept an increase in blood flow without an increase in pulmonary vascular pressure or resistance. Isoproterenol was used in the present study, since it has been shown to produce pulmonarv vasodilatation when perfused into the isolated and intact dog lung4' 5 and is known to have a marked inotropic and ehronotropic myocardial action in man.