Detrimental Effects of Hydralazine in Patients with Chronic Air-Flow Obstruction and Pulmonary Hypertension

The acute effects of intravenously administered hydralazine on pulmonary hemodynamics and ejection radionuclide angiography were evaluated in 9 patients with chronic airflow obstruction (forced expiratory volume in one second, 1.2 +/- 0.8 L, mean +/- SD), pulmonary hypertension (mean pulmonary artery pressure (PAP), 29 +/- 13 mmHg), and sleep hypoxemia (maximal sleep desaturation, 20 +/- 16%). The effect of hydralazine was measured during both normoxia and hypoxia and compared with the effect of hyperoxia. Hydralazine increased cardiac index from 3.7 +/- 0.2 to 4.5 +/- 0.8 L/min/m2 (mean +/- SE, p less than 0.05, n = 9), but there were no significant changes in PAP (29 +/- 4 to 32 +/- 4 mmHg), mean pulmonary vascular resistance index (PVRI) (390 +/- 80 to 360 +/- 80 dyn.s.cm.-5.m2), mean right ventricular stroke work index (12.7 +/- 2.7 to 15.0 +/- 2.2 g.m/m2), and mean pulmonary capillary wedge pressure (12 +/- 1 to 12 +/- 2 mmHg). Mean right ventricular ejection fraction and mean right ventricular end diastolic volume also were not changed after treatment with hydralazine. Hyperoxia was used to assess the reversibility of pulmonary hypertension and to compare this with hydralazine. Hyperoxia increased arterial oxygen saturation (SaO2) from 91 +/- 1 to 96 +/- 1% and decreased the cardiac index from 3.8 +/- 0.1 to 3.1 +/- 0.2 L/min/m2 (p less than 0.02, n = 6) but, as with hydralazine, there was no significant change in PAP (28 +/- 6 to 25 +/- 6 mmHg) and PVRI (350 +/- 120 to 360 +/- 80 dyn.s.cm-5).m2).(ABSTRACT TRUNCATED AT 250 WORDS)