Brijker Folkert, Heijdra Yvonne F, van den Elshout Frank J J, Folgering Hans Th M
Department of Pulmonary Diseases, Rijnstate Hospital Arnhem, The Netherlands.
Chest. 2002 Feb;121(2):377-82. doi: 10.1378/chest.121.2.377.
To evaluate whether the discontinuation of furosemide treatment resulted in a decrease in PaCO(2) and an increase in daytime and nocturnal oxygenation.
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.
Randomized, double-blind, placebo-controlled, crossover trial.
Department of Pulmonology, Rijnstate Hospital Arnhem, the Netherlands.
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.
Furosemide was discontinued for 1 week and replaced by placebo treatment in the first or the second week.
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.
Although it does not improve oxygenation, the discontinuation of furosemide decreases PaCO(2) in patients with COPD.
评估停用呋塞米治疗是否会导致动脉血二氧化碳分压（PaCO₂）降低以及日间和夜间氧合增加。
呋塞米在慢性阻塞性肺疾病（COPD）患者中被广泛用于治疗外周水肿。已知呋塞米会导致代谢性碱中毒。化学感受器刺激减弱可能会导致肺泡通气减少。
随机、双盲、安慰剂对照、交叉试验。
荷兰阿纳姆里恩斯塔特医院肺病科。
20例稳定期COPD患者（10名男性；年龄中位数70岁[范围58至81岁]；第1秒用力呼气容积（FEV₁）为预测值的35%[范围19%至70%预测值]）。如果受试者接受过40毫克/天的呋塞米治疗外周水肿至少一个月且夜间动脉血氧饱和度（SaO₂）平均<92%，则纳入研究。排除有心脏左和/或右心室功能障碍、睡眠呼吸暂停的患者，以及正在接受其他利尿剂、血管紧张素转换酶抑制剂、钾或氯替代疗法或长期氧疗的患者。
呋塞米停用1周，并在第一周或第二周用安慰剂治疗替代。
在基线、1周后和2周后测量通气、日间动脉血气水平和夜间SaO₂。16名受试者完成了研究。停用呋塞米后，通气量从基线时的10.4升/分钟（范围6.7至15.4升/分钟）增加到11.6升/分钟（范围8.7至14.0升/分钟）（p<0.05）。PaCO₂从45毫米汞柱（范围35至64毫米汞柱）降至41毫米汞柱（范围32至61毫米汞柱；p<0.01）。日间和夜间氧合没有改善。
虽然停用呋塞米不能改善氧合，但可降低COPD患者的PaCO₂。
