慢性阻塞性肺疾病合并睡眠呼吸暂停（重叠综合征）患者夜间呼吸中枢驱动

Overlap syndrome is defined as patients with coexistent of obstructive sleep apnea (OSA) and chronic obstructivepulmonary disease (COPD). It has been previously reported that both COPD and OSA are independent risk of sleep related hypoventilation, consequently patients with overlap syndrome are usually assumed to have a higher mortality rate and more severe hypoxia or respiratory failure compared with either condition alone. Our previous study showed nocturnal oxygen desaturation associated with COPD was due to sleep related reduction in neural respiratory drive, whereas hypopnea in patients with OSA is characterized with an increase in upper airway resistance associated with increased neural respiratory drive. The mechanisms underlying sleep related hypoventilation inpatients with overlap syndromeare still unclear. In this project, we are going to investigate the underlying mechanisms of sleep related hypoventilation and respiratory failure in patients with overlap syndrome by assessment of neural respiratory drive and upper airway resistance with diaphragm EMG and the ratio of diaphragm EMG to airflow. This study will help us to understand the mechanism underlying sleep related respiratory failure and could lead to new treatment for patients with overlap syndrome.

重叠综合征是指慢性阻塞性肺疾病（COPD）与阻塞性睡眠呼吸暂停（OSA）同时并存。由于二者均可导致缺氧，一些学者推测重叠综合征患者较单纯OSA或COPD更容易出现夜间低氧血症和呼吸衰竭,死亡率也更高。我们前期的研究发现单纯COPD患者夜间低氧血症主要是由于呼吸中枢驱动下降所致；而OSA患者睡眠低通气主要与上气道阻力增高伴随呼吸中枢驱动代偿性增加有关。重叠综合征患者睡眠低通气和呼吸衰竭的机理尚不清楚。这一研究以课题组发展的具有自主知识产权的技术为基础，记录膈肌肌电反映呼吸中枢驱动，以我们最近建立的膈肌肌电与气流的比值这一指标评价上气道阻力，探讨重叠综合征患者睡眠相关的低通气及呼吸衰竭发生机制，为合理治疗重叠综合征寻找新方法。

重叠综合征是指慢性阻塞性肺疾病（COPD）与阻塞性睡眠呼吸暂停（OSA）同时并存。由于二者均可导致缺氧，一些学者推测重叠综合征（OS）患者较单纯OSA或COPD更容易出现夜间低氧血症和呼吸衰竭,死亡率也更高。我们前期的研究发现单纯COPD患者夜间低氧血症主要是由于呼吸中枢驱动下降所致；而OSA患者睡眠低通气主要与上气道阻力增高伴随呼吸中枢驱动代偿性增加有关。重叠综合征患者睡眠低通气和呼吸衰竭的机理尚不清楚。这一研究以课题组发展的具有自主知识产权的技术为基础，记录膈肌肌电反映呼吸中枢驱动，以我们最近建立的膈肌肌电与气流的比值这一指标评价上气道阻力，探讨了重叠综合征患者睡眠相关低通气的发生机制。本研究结果显示对比单纯COPD组(8.6±2.0 to 6.5±1.5 L/min, p<0.001)，从清醒期到Ⅱ期睡眠OS组的分钟通气量下降幅度相似(8.3±2.0 to 6.1±1.8 L/min, P<0.001)。COPD患者进入睡眠后呼吸中枢驱动出现明显下降(29.5±13.3% to 23.0 ±8.9% of maximal, p<0.01)，而OS患者睡眠前后呼吸中枢驱动变化不明显。无论是单纯COPD患者还是健康受试者的膈肌肌电与气流的比值睡眠前后都变化不大，但在OSA患者及OS患者中出现明显变化 (p<0.05)。该研究结果提示OS患者夜间低通气的主要原因是由于上气道阻力增加而非呼吸中枢驱动下降有关。这一研究为OS患者在选择不同治疗方式时提供了理论依据。