Intravenous furosemide rapidly reduced average left ventricular filling pressure from 20.4 to 14.8 mm Hg within 5-15 minutes, an effect primarily vascular in origin and preceding diuresis.
Observational (n=20)
Does intravenous furosemide improve left ventricular filling pressure and venous capacitance in patients with left ventricular failure after acute myocardial infarction?
Intravenous furosemide provides immediate relief of pulmonary congestion through vascular mechanisms (increased venous capacitance) before its diuretic effects begin.
Absolute Event Rate: 14.8% vs 20.4%
Abstract Furosemide, 0.5 to 1.0 mg per kilogram intravenously, was given to 20 patients with left ventricular failure after acute myocardial infarction. Within five to 15 minutes, average left ventricular filling pressure fell from 20.4 to 14.8 mm Hg, accompanied by a 52 per cent increase in mean calf venous capacitance. During the same period there was no physiologically important change in either urine output or heart rate, blood pressure and cardiac output. Peak increase in urine flow (from mean of 0.82 to 4.0 ml per minute) occurred at 30 minutes, and peak natriuretic effect at 60 minutes. Thus, the action of furosemide in the treatment of pulmonary congestion is immediate and is not related to its diuretic properties. Rather, the prompt fall in left ventricular filling pressure probably is primarily vascular in origin, since marked changes in venous capacitance accompany this phenomenon, which is only later supplemented by the increase in urine output and electrolyte excretion. (N Engl J Med 288:1087...
Dikshit et al. (Thu,) conducted a observational in Left ventricular failure after acute myocardial infarction (n=20). Furosemide was evaluated on Left ventricular filling pressure. Intravenous furosemide rapidly reduced average left ventricular filling pressure from 20.4 to 14.8 mm Hg within 5-15 minutes, an effect primarily vascular in origin and preceding diuresis.
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