PARTITIONING OF PULMONARY VASCULAR-RESISTANCE IN PRIMARY PULMONARY-HYPERTENSION

Objectives. This study sought to determine the site of increased pulmo nary vascular resistance (PVR) in primary pulmonary hypertension by st andard bedside hemodynamic evaluation. Background. The measurement of pulmonary vascular pressures at several levels of flow (Q) allows the discrimination between active and passive, flow-dependent changes in m ean pulmonary artery pressure (Ppa), and may detect the presence of an increased pulmonary vascular closing pressure. The determination of a capillary pressure (Pc') from the analysis of a Ppa decay curve after balloon occlusion allows the partitioning of PVR in an arterial and a (capillary + venous) segment. These approaches have not been reported in primary pulmonary hypertension. Methods. Ppa and Pc' were measured at baseline and after an increase in Q induced either by exercise or by an infusion of dobutamine, at a dosage up to 8 mu g/kg body weight per min, in 11 patients with primary pulmonary hypertension. Reversibi lity of pulmonary hypertension was assessed by the inhalation of 20 pp m nitric oxide (NO), and, in 6 patients, by an infusion of prostacycli n. clin. Results. At baseline, Ppa was 52 +/- 3 mm Hg (mean value +/- SE), Q 2.2 +/- 0.2 liters/min per m(2), and Pc' 29 +/- 3 mm Hg. Dobuta mine did not affect Pc' and allowed the calculation of an averaged ext rapolated pressure intercept of Ppa/Q plots of 34 mm Hg. Inhaled NO ha d no effect. Prostacyclin decreased Pc' and PVR. Exercise increased Pc ' to 40 +/- 3 mm Hg but did not affect PVR. Conclusions. These finding s are compatible with a major increase of resistance and reactivity at the periphery of the pulmonary arterial tree. (C) 1998 by the America n College of Cardiology.