Hemodynamic effects of nifedipine on secondary pulmonary hypertension in man.
We evaluated the hemodynamic effects of the calcium antagonist nifedipine in 13 consecutive patients admitted to the intensive care unit with secondary pulmonary hypertension. Etiology of secondary pulmonary hypertension was: chronic obstructive pulmonary disease (n = 9), pulmonary emboli (n = 2), pulmonary fibrosis (n = 2). We obtained the resting hemodynamic parameters before, and 60, 120, 180 minutes after the sublingual administration of nifedipine 20 mg. All patients had normal pulmonary artery wedge pressure before nifedipine. After 60 minutes, systolic pulmonary artery pressure fell from 72.3 +/- 7 to 57.3 +/- 5.4 mm Hg (p less than 0.005) and mean pulmonary artery pressure from 44.6 +/- 4.0 to 33.6 +/- 3.2 mm Hg (p less than 0.001). Cardiac output rose from 6.36 +/- 0.56 to 7.65 +/- 0.64 l/min (p less than 0.005). The pulmonary vascular resistance fell from 431 +/- 58 to 238 +/- 36 dynes. sec. cm-5 (p less than 0.001). Heart rate, mean systemic arterial pressure, pulmonary artery wedge pressure, total systemic vascular resistance and arterial partial pressure of O2 (PaO2) remained unchanged. In this heterogenous population we were unable to reproduce the results of other authors, showing a correlation between PaO2 and fall of pulmonary vascular resistance. These findings confirm the pulmonary vasodilating effect of nifedipine in patients with secondary pulmonary hypertension.
D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy*; D009543:Nifedipine / Q000627:therapeutic use*; D010100:Oxygen / Q000097:blood; D011669:Pulmonary Wedge Pressure / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects
D009543:Nifedipine; D010100:Oxygen