Study objective: To evaluate whether the
discontinuation of furosemide treatment resulted in a decrease in
Paco2 and an increase in daytime and nocturnal
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
Design: Randomized, double-blind,
placebo-controlled, crossover trial.
Department of Pulmonology, Rijnstate Hospital Arnhem, the
Patients: Twenty patients with stable
COPD (10 men; median age, 70 years [range, 58 to 81 years];
FEV1 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
(Sao2) < 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
Sao2 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). Paco2 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 Paco2
in patients with COPD.