Author + information
- Received October 17, 1997
- Revision received January 27, 1998
- Accepted January 28, 1998
- Published online May 1, 1998.
- Sophia Abdel Kafi, MDA,
- Christian Mélot, MD, PhDA,
- Jean-Luc Vachiéry, MDA,
- Serge Brimioulle, MD, PhDA and
- Robert Naeije, MD, PhDA,* ()
- ↵*Dr. Robert Naeije, Department of Intensive Care, Erasme University Hospital, Route de Lennik 808, 1070 Brussels, Belgium.
Objectives. This study sought to determine the site of increased pulmonary vascular resistance (PVR) in primary pulmonary hypertension by standard 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 mean 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 μg/kg body weight per min, in 11 patients with primary pulmonary hypertension. Reversibility of pulmonary hypertension was assessed by the inhalation of 20 ppm nitric oxide (NO), and, in 6 patients, by an infusion of prostacyclin.
Results. At baseline, Ppa was 52 ± 3 mm Hg (mean value ± SE), Q 2.2 ± 0.2 liters/min per m2, and Pc′ 29 ± 3 mm Hg. Dobutamine did not affect Pc′ and allowed the calculation of an averaged extrapolated pressure intercept of Ppa/Q plots of 34 mm Hg. Inhaled NO had no effect. Prostacyclin decreased Pc′ and PVR. Exercise increased Pc′ to 40 ± 3 mm Hg but did not affect PVR.
Conclusions. These findings are compatible with a major increase of resistance and reactivity at the periphery of the pulmonary arterial tree.
- Received October 17, 1997.
- Revision received January 27, 1998.
- Accepted January 28, 1998.
- The American College of Cardiology