The effect of sleep loss on breathing in chronic obstructive pulmonary disease.
The effect of sleep loss on breathing in chronic obstructive pulmonary disease.
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睡眠不足对慢性阻塞性肺疾病呼吸的影响。
DOI：
10.1378/chest.91.1.29
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发表时间：
1987
期刊：
影响因子：
9.6
通讯作者：
Thomas V. Burke
中科院分区：
文献类型：
--
作者：
Barbara Phillips;Barbara Phillips;Kevin R. Cooper;Kevin R. Cooper;Thomas V. Burke;Thomas V. Burke
我们以前已经证明，一个晚上的睡眠剥夺导致肺功能和呼吸反应性显着恶化吸入二氧化碳在正常人。由于即使是肺功能的轻微下降，在慢性气流受限患者中也可能具有临床意义，因此我们进行了本研究，以评估睡眠不足对慢性阻塞性肺疾病（COPD）患者呼吸的影响。入选本研究的标准是一秒钟用力呼气量与用力肺活量（FEV 1/FVC）的比值小于60%，在测试的两周内没有因肺部疾病住院，在测试的三个月内两次肺功能测试稳定（小于30%的变化），并且没有哮喘史。我们研究了15名男性（平均年龄，57 +/- 3岁）在连续两个上午。以随机方式对患者进行了睡眠剥夺和非睡眠剥夺的研究。患者住院进行研究，以便监测和强制睡眠剥夺，药物，吸烟和饮食。我们发现，睡眠剥夺后，FEV 1（1.06 +/- 0.11至1.00 +/- 0.09 L; p <0.05）和FVC（2.56 +/- 0.20至2.43 +/- 0.17 L; p <0.05）下降幅度较小，但具有统计学显著性福尔斯。最大自主通气量（MVV）和对二氧化碳的反应也发生了类似幅度的变化，但无统计学意义。动脉血氧分压（PaO 2）和二氧化碳分压（PaCO 2）不受影响。口腔最大呼气压略有增加，但口腔最大吸气压（MIP）下降。我们的结论是，睡眠不足与重度COPD患者的FEV 1和FVC的小但显著的福尔斯下降相关，以及MVV、每分钟通气量和MIP的相似幅度的变化。尽管COPD加重时经常伴随的睡眠丧失可能是肺储备的轻微额外压力，但稳定的慢性气流阻塞患者一夜的睡眠丧失不会产生重大的临床后果。
We have previously shown that one night of sleep deprivation results in significant deterioration of spirometric performance and ventilatory responsiveness to inhaled carbon dioxide in normal people. Since even a small decrease in pulmonary function may be clinically important in patients with chronic limitation of airflow, we undertook the present study to assess the effects of sleep loss on breathing in patients with chronic obstructive pulmonary disease (COPD). Criteria for inclusion in this study were a ratio of the forced expiratory volume in one second over the forced vital capacity (FEV1/FVC) of less than 60 percent, no hospital admission for pulmonary disease within two weeks of testing, stable (less than 30 percent variation) in tests of pulmonary function on two occasions within three months of testing, and no history of asthma. We studied 15 men (mean age, 57 +/- 3 years) on two consecutive mornings. Patients were studied with and without sleep deprivation in a randomized fashion. Patients were hospitalized for the study so that sleep deprivation, medications, smoking, and diet could be monitored and enforced. We found small but statistically significant falls in FEV1 (1.06 +/- 0.11 to 1.00 +/- 0.09 L; p less than 0.05) and in FVC (2.56 +/- 0.20 to 2.43 +/- 0.17 L; p less than 0.05) following sleep deprivation. Changes of similar magnitude which were not statistically significant occurred in maximal voluntary ventilation (MVV) and response to carbon dioxide. The arterial oxygen (PaO2) and carbon dioxide (PaCO2) tensions were not affected. Maximal expiratory pressure at the mouth increased slightly, but there was a fall in maximal inspiratory pressure (MIP) at the mouth. We conclude that sleep loss is associated with small but significant falls in FEV1 and FVC, as well as changes of similar magnitude in MVV, minute ventilation, and MIP in patients with severe COPD. Although the sleep loss which frequently accompanies exacerbations of COPD may be a slight additional stress of pulmonary reserve, a single night's loss of sleep in the patient with stable chronic airflow obstruction does not have major clinical consequences.