Comparison of the effects of nitric oxide, nitroprusside, and nifedipine on hemodynamics and right ventricular contractility in patients with chronicpulmonary hypertension

Study objectives: The effects of inhaled nitric oxide (NO) on hemodynamics and right ventricular (RV) contractility were compared with those of nitrop russide and nifedipine in 14 patients with severe chronic pulmonary hyperte nsion. Study design: Micromanometer and balloon-tipped right heart catheterization were performed. Inhaled NO, IV nitroprusside, and sublingual nifedipine we re administered sequentially while patients breathed > 90% oxygen. Setting: Cardiac catheterization laboratory in a tertiary care teaching hos pital. Patients: Fourteen patients with severe pulmonary hypertension unrel ated to left ventricular dysfunction, Measurements and results: During NO inhalation, mean systemic arterial pres sure (MAP) was unchanged, but pulmonary artery (PA) pressure ([mean +/- SEM ] 49 +/- 2 mm Hg vs 44 +/- 2 mm Hg; p < 0.01), pulmonary vascular resistanc e (PVR; 829 +/- 68 vs 869 +/- 64 dyne . s . cm(-5); p < 0.01) and RV end-di astolic pressure (RVEDP; 12 +/- 1 vs 10 +/- 1 mm Hg; p < 0.01) decreased. S troke volume index (SVI; 31 +/- 2 vs 35 +/- 3 mL/m(2); p < 0.05) increased, and the first derivative of RV pressure at 15 mm Hg developed pressure (RV +dP/dt at DP15) was unchanged. During nitroprusside administration, MAP de creased (105 +/- 5 vs 76 +/- 5 mm Hg; p < 0.01), PA was unchanged (48 +/- 2 vs 45 +/- 3 mm Hg; p not significant), and PVR decreased (791 +/- 53 vs 66 5 +/- 53 dyne.s.cm(-5); p < 0.01). RV +dP/dt at DP15 increased (425 +/- 22 vs 465 +/- 29 mm Hg/s; p < 0.05), but SVI was unchanged, Nifedipine decreas ed MAP (103 +/- 5 vs 94 +/- 5 mm Hg; p < 0.01), PA and PVR were unchanged, RVEDP increased (12 +/- 1 vs 14 +/- 2 mm Hg; p < 0.01), and RV +dP/dt at DP 15 decreased (432 +/- 90 vs 389 +/- 21 mm Hg/s; p < 0.05). Conclusions: Inhaled NO is a selective pulmonary vasodilator in patients wi th chronic pulmonary hypertension that improves cardiac performance without altering RV contractility, Nitroprusside caused a similar degree of pulmon ary vasodilation, In contrast to inhaled NO, nitroprusside caused systemic hypotension associated with an increase in RV contractility. Acute administ ration of nifedipine did not cause pulmonary vasodilation, but RVEDP increa sed and RV contractility decreased.