STUDY OBJECTIVE: To evaluate whether the discontinuation of furosemide treatment resulted in a decrease in PaCO(2) and an increase in daytime and nocturnal oxygenation. BACKGROUND: Furosemide is widely prescribed in patients with COPD for the treatment of peripheral edema. It is known that furosemide causes a metabolic alkalosis. A diminished chemoreceptor stimulation may cause a decreased alveolar ventilation. DESIGN: Randomized, double-blind, placebo-controlled, crossover trial. SETTING: Department of Pulmonology, Rijnstate Hospital Arnhem, the Netherlands. PATIENTS: Twenty patients with stable COPD (10 men; median age, 70 years [range, 58 to 81 years]; FEV(1) 35% predicted [range, 19 to 70% predicted]). Subjects were included if they had received furosemide, 40 mg/d, for the treatment of peripheral edema for at least a month and if they had a mean nocturnal arterial oxygen saturation (SaO(2)) < 92%. Patients with cardiac left and/or right ventricular dysfunction, sleep apneas, and patients receiving other diuretics, angiotensin-converting enzyme inhibitors, potassium or chloride replacement therapy, or long-term oxygen treatment were excluded. INTERVENTION: Furosemide was discontinued for 1 week and replaced by placebo treatment in the first or the second week. MEASUREMENTS AND RESULTS:Ventilation, daytime arterial blood gas levels, and nocturnal SaO(2) were measured at baseline, after 1, and after 2 weeks. Sixteen subjects completed the study. Ventilation increased from 10.4 L/min (range, 6.7 to 15.4 L/min) at baseline to 11.6 L/min (range, 8.7 to 14.0 L/min) after discontinuation of furosemide (p < 0.05). PaCO(2) decreased from 45 mm Hg (range, 35 to 64 mm Hg) to 41 mm Hg (range, 32 to 61 mm Hg; p < 0.01). Daytime and nocturnal oxygenation did not improve. CONCLUSIONS: Although it does not improve oxygenation, the discontinuation of furosemide decreases PaCO(2) in patients with COPD.
RCT Entities:
STUDY OBJECTIVE: To evaluate whether the discontinuation of furosemide treatment resulted in a decrease in PaCO(2) and an increase in daytime and nocturnal oxygenation. BACKGROUND:Furosemide is widely prescribed in patients with COPD for the treatment of peripheral edema. It is known that furosemide causes a metabolic alkalosis. A diminished chemoreceptor stimulation may cause a decreased alveolar ventilation. DESIGN: Randomized, double-blind, placebo-controlled, crossover trial. SETTING: Department of Pulmonology, Rijnstate Hospital Arnhem, the Netherlands. PATIENTS: Twenty patients with stable COPD (10 men; median age, 70 years [range, 58 to 81 years]; FEV(1) 35% predicted [range, 19 to 70% predicted]). Subjects were included if they had received furosemide, 40 mg/d, for the treatment of peripheral edema for at least a month and if they had a mean nocturnal arterial oxygen saturation (SaO(2)) < 92%. Patients with cardiac left and/or right ventricular dysfunction, sleep apneas, and patients receiving other diuretics, angiotensin-converting enzyme inhibitors, potassium or chloride replacement therapy, or long-term oxygen treatment were excluded. INTERVENTION: Furosemide was discontinued for 1 week and replaced by placebo treatment in the first or the second week. MEASUREMENTS AND RESULTS: Ventilation, daytime arterial blood gas levels, and nocturnal SaO(2) were measured at baseline, after 1, and after 2 weeks. Sixteen subjects completed the study. Ventilation increased from 10.4 L/min (range, 6.7 to 15.4 L/min) at baseline to 11.6 L/min (range, 8.7 to 14.0 L/min) after discontinuation of furosemide (p < 0.05). PaCO(2) decreased from 45 mm Hg (range, 35 to 64 mm Hg) to 41 mm Hg (range, 32 to 61 mm Hg; p < 0.01). Daytime and nocturnal oxygenation did not improve. CONCLUSIONS: Although it does not improve oxygenation, the discontinuation of furosemide decreases PaCO(2) in patients with COPD.
Authors: Claudio Terzano; Fabio Di Stefano; Vittoria Conti; Marta Di Nicola; Gregorino Paone; Angelo Petroianni; Alberto Ricci Journal: PLoS One Date: 2012-04-23 Impact factor: 3.240