Determinants of circulatory response to intravenous hydralazine in congestive heart failure.

To determine whether the circulatory response to hydralazine in heart failure is influenced by initial hemodynamic status or left ventricular (LV) chamber size, 28 patients with chronic LV dysfunction were studied. Hemodynamic measurements and echocardiographic LV end-diastolic dimension were correlated with the response to 20 mg of intravenous hydralazine and to a dose titrated in each patient to reduce systemic resistance by greater than or equal to 20%. Hydralazine, 20 mg, decreased systemic resistance from 23 +/- 8 to 18 +/- 8 U (p less than 0.01) and increased the cardiac index from 2.0 +/- 0.5 to 2.5 +/- 0.6 liters/min/m2 (p less than 0.01) and the stroke work index from 21 +/- 11 to 24 +/- 9 g . m/m2 (p less than 0.05). Titrating the dose to decrease systemic resistance by greater than or equal to 20% increased the cardiac index further to 2.7 +/- 0.6 liters/min/m2 and the stroke work index to 32 +/- 9 g . m/m2. The change in systemic resistance produced by 20 mg of hydralazine correlated only with initial systemic resistance (r = 0.53), suggesting that vascular response to hydralazine is a direct function of initial vascular resistance. The percentage change in stroke work index produced by 20 mg of hydralazine correlated directly with indexes of LV preload-end-diastolic wall stress (r = 0.69) and pulmonary wedge pressure (r = 0.43) and inversely with stroke work index (r = -0.49), an index of ventricular work. Similar but less close correlations were observed when the dose of hydralazine was titrated. The hemodynamic response to hydralazine did not correlate with LV end-diastolic dimension or right atrial pressure. Thus, vascular response to moderate doses of hydralazine is related to initial systemic vascular resistance. LV pump response is related to the level of initial LV pump dysfunction but not to LV chamber size or right atrial pressure.