Kittivoravitkul Prapun, Kaw Roop, Hatipoğlu Umur, Wang Lu, Aboussouan Loutfi S
1 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Phramongkutklao Hospital, Bangkok, Thailand; and.
2 Department of Hospital Medicine, Medicine Institute.
Ann Am Thorac Soc. 2016 Feb;13(2):259-64. doi: 10.1513/AnnalsATS.201508-563OC.
The progression from obesity and obstructive sleep apnea to obesity with hypoventilation and daytime hypercapnia may relate to features of sleep-disordered breathing events that affect loading and unloading of carbon dioxide.
To determine whether the wake Pco2 increases over time in untreated obstructive sleep apnea, and whether that increase is explained by changes in sleep-disordered breathing event duration, interevent duration, or postevent ventilation amplitude.
We selected 14 adults who had two polysomnographic studies more than 1 year apart because of untreated or suboptimally treated moderate to severe obstructive sleep apnea. Demographic and polysomnographic data were reviewed for both sets of studies, including the evening wake end-tidal CO2, the ratio of mean event to mean interevent duration (subsuming apneas and hypopneas), and the ratio of mean post- to preevent breath amplitude.
The mean (SD) wake end-tidal Pco2 increased between studies from 35.9 (4.2) to 39.5 (3.9) mm Hg (P < 0.005). The wake end-tidal CO2 correlated inversely with the post- to pre-event breath amplitude and positively with the ratio of mean event to mean interevent duration and with body mass index. However, those three variables were not significantly changed between the two studies. The wake end-tidal CO2 did not correlate with the apnea-hypopnea index or age. There was a significant increase in bicarbonate level between studies (median, 24.0-26.5 mmol/L; P = 0.01).
In our study cohort, wake end-tidal CO2 correlated with body mass index and features of sleep apnea that influence the balance of loading and unloading of CO2. However, those features remained fixed over time, even as the wake Pco2 and bicarbonate levels increased with untreated sleep apnea.
从肥胖和阻塞性睡眠呼吸暂停发展到肥胖伴通气不足和日间高碳酸血症，可能与影响二氧化碳加载和卸载的睡眠呼吸紊乱事件特征有关。
确定在未经治疗的阻塞性睡眠呼吸暂停患者中，清醒时的二氧化碳分压（Pco2）是否随时间增加，以及这种增加是否可由睡眠呼吸紊乱事件持续时间、事件间隔时间或事件后通气幅度的变化来解释。
我们选取了14名成年人，他们因未经治疗或治疗不充分的中度至重度阻塞性睡眠呼吸暂停，相隔1年以上进行了两次多导睡眠图研究。对两组研究的人口统计学和多导睡眠图数据进行了回顾，包括夜间清醒时的呼气末二氧化碳、平均事件与平均事件间隔持续时间之比（包括呼吸暂停和呼吸不足），以及平均事件后与事件前呼吸幅度之比。
两次研究之间，清醒时呼气末平均Pco2从35.9（4.2）mmHg升高至39.5（3.9）mmHg（P < 0.005）。清醒时呼气末二氧化碳与事件后与事件前呼吸幅度呈负相关，与平均事件与平均事件间隔持续时间之比以及体重指数呈正相关。然而，这三个变量在两次研究之间没有显著变化。清醒时呼气末二氧化碳与呼吸暂停低通气指数或年龄无关。两次研究之间碳酸氢盐水平有显著升高（中位数，24.0 - 26.5 mmol/L；P = 0.01）。
在我们的研究队列中，清醒时呼气末二氧化碳与体重指数以及影响二氧化碳加载和卸载平衡的睡眠呼吸暂停特征相关。然而，即使清醒时Pco2和碳酸氢盐水平随着未经治疗的睡眠呼吸暂停而升高，这些特征随时间保持不变。
