Copyright © 1983 by the European Society of Cardiology.
© 1983, by the European Society of Cardiology
Haemodynamic effects of frusemide and its influence on repetitive rapid volume loading in acute myocardial infarction
University Department of Cardiovascular Studies and Department of Medical Cardiology, The General Infirmary, Leeds England
Received 15 November 1982; revised 10 February 1983; .
Correspondence to: Dr S. H. Taylor, Department of Medical Cardiology, The General Infirmary, Great George Street, Leeds LSI 3EX, England
Abstract
The haemodynamic effects of intravenous frusemide (1 mg/kg) were studied in 22 male patients with left ventricular failure following acute myocardial infarction. Radiographic pulmonary oedema was present in all patients and their average left heart filling pressure was 20 mmHg. Bolus injection of the drug was followed by immediate increases in systemic arterial pressure (P < 0.05) and heart rate (<0.05); these declined to pre-injection values after 60 min. Following frusemide there were progressive reductions in left heart filling pressure (P < 0.01), thermodilution cardiac output (P < 0.01) and stroke volume (P < 0.05) and a progressive increase in the derived systemic vascular resistance (P < 0.05). There was an average diuresis of 860 ml during the 90 min following the frusemide injection. The influence of frusemide on left ventricular performance was studied by comparing the circulatory effects of passive leg raising in the control period with those at 30, 60 and 90 min after the drug. In the control period this manoeuvre increased left heart filling pressure, but not heart rate, cardiac output, stroke volume or systemic vascular resistance. Ninety minutes after frusemide, but not before, passive leg raising resulted in a significant increase in cardiac output (P < 0.01) and stroke volume at a similar increment in filling pressure and a significant reduction in the systemic vascular resistance (P <0.05). These circulatory actions of intravenous frusemide are compatible with initial arteriolar constriction and venodilatation followed by depletion of blood volume with subsequent change in left ventricular pumping performance.
Key Words: Frusemide • left ventricular filling pressure • cardiac output; passive leg raising
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