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

Abstract

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

Loop Diuretic Therapy in Heart Failure: The Need for Solid Evidence on a Fluid Issue

“…When given to severe chronic HF patients, loop diuretics resulted in acute fall in stroke volume index, increase in LV filling pressure and systemic vascular resistance, as well as neurohormonal activation such as elevated plasma renin activity (PRA), plasma norepinephrine levels, and plasma arginine vasopressin levels. 8 In one early study, LV filling pressure and systemic vascular resistance were elevated 20 minutes after IV furosemide administration but returned nearly back to baseline after 1 to 2 hours. 8 These hemodynamic effects were attributed to vasoconstriction mediated by the renin-angiotensin-aldosterone system (RAAS).…”

“…8 In one early study, LV filling pressure and systemic vascular resistance were elevated 20 minutes after IV furosemide administration but returned nearly back to baseline after 1 to 2 hours. 8 These hemodynamic effects were attributed to vasoconstriction mediated by the renin-angiotensin-aldosterone system (RAAS).…”

Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006: Diagnosis and management

“…An accurate and rapid diagnosis of AHF is important to the timely institution of appropriate therapy and to improve clinical outcomes (67)(68)(69), and is based on a careful evaluation of symptoms and clinical findings, supported by appropriate investigations such as electrocardigraphy, chest radiography and, if available, echocardiography and biomarkers. It is important to classify patients based on the presence or absence of congestion and signs of low cardiac output and impaired tissue perfusion to administer the appropriate therapy (70,71). Detailed information on demographics and common clinical presentations of AdHF have been reported from the Acute Decompensated Heart Failure National Registry (ADHERE) (72).…”

Natriuretic and Neurohormonal Responses to Nesiritide, Furosemide, and Combined Nesiritide and Furosemide in Patients With Stable Systolic Dysfunction

“…3,14 Neurohormonal activation due to loop diuretics can occur in a matter of minutes as a consequence of a direct stimulatory effect on the renin-angiotensin-aldosterone system (RAAS), independent of volume change. 15 This early activation of the RAAS may diminish diuretic responsiveness. Loop diuretics also produce subacute and chronic RAAS activation.…”