Holmedahl Nils Henrik, Øverland Britt, Fondenes Ove, Ellingsen Ivar, Hardie Jon Andrew
LHL-klinikkene, Glittre, Glittreklinikken, postboks 104 Åneby, 1485, Hakadal, Norway,
Sleep Breath. 2015 Mar;19(1):307-14. doi: 10.1007/s11325-014-1020-y. Epub 2014 Jun 17.
PURPOSE/BACKGROUND: The purpose of this study is to explore the effect of a moderate dose of alcohol on sleep architecture and respiration in chronic obstructive pulmonary disease (COPD). Alcohol depresses both hypercapnic and hypoxic ventilatory drives in awake, normal individuals and reduces the amount of rapid eye movement (REM) sleep and oxygen saturation (SpO2) in sleeping COPD subjects.
Prospectively designed, open-label interventional study in a pulmonary rehabilitation hospital. Twenty-six (nine males) stable inpatients, median forced expiratory volume first second (FEV1) 40.5 % of predicted, median age 65 years, investigated by polysomnography including transcutaneous measurement of carbon dioxide pressure increase (ΔPtcCO2) in randomized order of either control sleep or intervention with 0.5 g of ethanol/kilogram bodyweight, taken orally immediately before lights off.
Alcohol induced a mean increase (95 % confidence interval, [CI]) in the mean ΔPtcCO2 of 0.10 kPa (0.002-0.206, P = 0.047) and a mean decrease (CI) in the REM-sleep percentage of total sleep time (REM % of TST) of 3.1 % (0.2-6.0), (P = 0.020). Six subjects with apnea/hypopnea index (AHI) ≥15 had fewer apneas/hypopneas during alcohol versus control sleep (mean reduction of AHI 11 (1-20), P = 0.046). Alcohol-sleep changes in SpO2, but not in ΔPtcCO2, correlated with daytime arterial pressures of carbon dioxide (PaCO2) and oxygen (PaO2).
Occasional use of a moderate, bedtime dose of alcohol has only minor respiratory depressant effects on the majority of COPD subjects, and in a minority even slightly improves respiration during sleep. However, caution is appropriate as this study is small and higher doses of alcohol may result in major respiratory depressive and additional negative health effects.
目的/背景：本研究旨在探讨中等剂量酒精对慢性阻塞性肺疾病（COPD）患者睡眠结构和呼吸的影响。酒精会抑制清醒的正常个体的高碳酸血症和低氧通气驱动，并减少COPD睡眠受试者的快速眼动（REM）睡眠时间和血氧饱和度（SpO2）。
在一家肺康复医院进行前瞻性设计的开放标签干预研究。26名（9名男性）病情稳定的住院患者，第一秒用力呼气量（FEV1）中位数为预测值的40.5%，年龄中位数为65岁，通过多导睡眠图进行研究，包括经皮测量二氧化碳压力升高（ΔPtcCO2），按照随机顺序进行对照睡眠或在熄灯前立即口服0.5克乙醇/千克体重进行干预。
酒精导致平均ΔPtcCO2平均增加（95%置信区间，[CI]）0.10 kPa（0.002 - 0.206，P = 0.047），总睡眠时间中REM睡眠百分比（REM % of TST）平均降低（CI）3.1%（0.2 - 6.0），（P = 0.020）。6名呼吸暂停/低通气指数（AHI）≥15的受试者在饮酒睡眠期间的呼吸暂停/低通气次数少于对照睡眠（AHI平均降低11次（1 - 20），P = 0.046）。酒精引起的SpO2睡眠变化与日间动脉二氧化碳分压（PaCO2）和氧分压（PaO2）相关，但与ΔPtcCO2无关。
偶尔在睡前使用中等剂量酒精对大多数COPD受试者只有轻微的呼吸抑制作用，少数人甚至在睡眠期间呼吸略有改善。然而，由于本研究规模较小，且更高剂量的酒精可能导致严重的呼吸抑制和其他负面健康影响，因此仍需谨慎。
