Acute Vasoconstrictor Response to Intravenous Furosemide in Patients with Chronic Congestive Heart Failure

Publisher Website
Google Scholar
Abstract
Hemodynamic and neurohumoral responses to acute diuretic therapy were measured in 15 patients with severe chronic heart failure given i.v. furosemide, 1.3 .+-. 0.6 mg/kg body wt. Left ventricular pump function deteriorated by 20 min, as indicated by a fall in stroke volume index (27 .+-. 8 to 24 .+-. 7 ml/min .cntdot. m2 body surface area, (P < 0.01) and an increase in left ventricular filling pressure (28 .+-. 7 to 33 .+-. 9 mm Hg, P < 0.01). Increases occurred in heart rate (87 .+-. 13 to 91 .+-. 16 beats/min, P < 0.01), mean arterial pressure (90 .+-. 15 to 96 .+-. 15 mm Hg, P < 0.01), systemic vascular resistance (1454 .+-. 394 to 1676 .+-. 415 dynes .cntdot. s .cntdot. cm-5, P < 0.01), plasma renin activity (9.9 .+-. 8.5 to 17.8 ng/ml .cntdot. h, P < 0.05), plasma norepinephrine level (667 .+-. 390 to 839 .+-. 368 pg/ml, P < 0.01) and plasma Arg vasopressin level (6.2 .+-. 1.3 to 8.3 .+-. 2.0 pg/ml, P < 0.01). During the next 3.5 h the patients had diuresis (2085 .+-. 1035 ml) and the expected fall in filling pressure (28 .+-. 7 to 22 .+-. 10 mm Hg, P < 0.01). Neurohumoral indicators also returned toward the control levels. I.v. furosemide, in patients with severe chronic heart failure, is associated with acute pump dysfunction temporally related to activation of the neurohumoral axis.

This publication has 1 reference indexed in Scilit: