Easton P A, West P, Meatherall R C, Brewster J F, Lertzman M, Kryger M H
Sleep. 1987 Jun;10(3):224-33. doi: 10.1093/sleep/10.3.224.
The effect of a moderately intoxicating dose of ethanol on sleep was evaluated in five patients with severe emphysematous chronic obstructive pulmonary disease (COPD) (mean FEV1 0.83 L, PaO2 75 mm Hg). Mean serum ethanol before sleep was 129 mg/dl. With alcohol, total sleep time per night decreased from a mean of 293 to 238 min. Relative sleep time per stage also changed; NREM time increased, and REM time decreased greater than 50%. Alcohol caused significant O2 desaturation; group mean sleep arterial oxygen saturation (SaO2) decreased from 90.6 to 87.7% with alcohol. Although the decrease in SaO2 was not uniform across all sleep stages, no individual sleep stage accounted for the desaturation. The fall in SaO2 with alcohol was not explained by increasing apneas or hypopneas. Mean heart rate increased significantly from 71.8 to 77.1 with alcohol, with premature ventricular contractions increasing in two subjects. Excessive alcohol ingestion in severe COPD alters total sleep time and stage distribution, decreases SaO2 without significant change in apneas, and increases heart rate. Prior to sleep, patients with severe COPD should strictly limit ingestion of alcohol.
在5例重度肺气肿慢性阻塞性肺疾病(COPD)患者(平均第一秒用力呼气容积为0.83L,动脉血氧分压为75mmHg)中评估了中等中毒剂量乙醇对睡眠的影响。睡前平均血清乙醇浓度为129mg/dl。摄入乙醇后,每晚总睡眠时间从平均293分钟减少至238分钟。每个睡眠阶段的相对睡眠时间也发生了变化;非快速眼动睡眠(NREM)时间增加,快速眼动睡眠(REM)时间减少超过50%。乙醇导致明显的氧饱和度下降;饮酒后组平均睡眠动脉血氧饱和度(SaO2)从90.6%降至87.7%。尽管SaO2在所有睡眠阶段的下降并不均匀,但没有单个睡眠阶段是导致氧饱和度下降的原因。饮酒导致的SaO2下降并非由呼吸暂停或呼吸浅慢增加所致。饮酒后平均心率从71.8显著增加至77.1,两名受试者的室性早搏增加。重度COPD患者过量摄入乙醇会改变总睡眠时间和睡眠阶段分布,降低SaO2且呼吸暂停无显著变化,并增加心率。重度COPD患者在睡前应严格限制乙醇摄入。