无创通气治疗对慢性阻塞性肺病合并睡眠呼吸暂停患者呼吸中枢反应性的影响

目的：了解无创通气治疗对慢性阻塞性肺病（COPD）合并睡眠呼吸暂停（重叠综合征）患者呼吸中枢反应性的变化。方法：选择10例经多导生理记录仪睡眠呼吸监测确诊的睡眠呼吸暂停低通气综合征（SAHS）患者,其中5例合并COPD,平均FEV1／FVC为59％±6％,另5例为伴CO2潴留的SAHS患者,FEV1／FVC正常。两组患者的年龄、体重指数（BMI）及睡眠呼吸暂停低通气指数（AHI）匹配。分别测定10例患者在治疗前及长期家庭应用BiPAP治疗6周后呼吸中枢低氧反应性（AVE／△SaO2）及高CO2反应性（AVE／APaCO2）。结果：重叠综合征（OS）及阻塞性睡眠呼吸暂停（OSA）患者治疗前的呼吸中枢低氧反应性分别为（-0．023．±0．049）L·min^-1·％^-1及（-0.16±0．06）L·min^-1·％^-1,均低于实验室正常值（-0．35．±0．21）L·min^-1·％^-1。OS及OSA患者的高C02反应性分别为（0.54±0．16）L·min^-1·mmHg^-1及（1．3±0．62）L·min^-1·mmHg^-0,前者显著低于实验室正常值（1.26±054）L·min^-1·mmHg^-1,后者尚在正常范围内。应用BiPAP呼吸机家庭治疗6周后,OSA患者的低氧[（-0．16±0．06）L·min^-1·％^-1vs（-0．36±0.14）L·min^-1％^-1及高C02反应性[（1.3±0.62）L·min^-1·mmHg^-1 vs（1．78±0.93）L·min^-1·mmHg^-1]均显著升高,达到正常水平。OS患者的低氧反应性升高[（-0．023±0.049）L·min^-1·％^-1 vs（-0．09±0．007）L·min^-1·％^-1],但仍显著低于正常水平;高CO2反应性[（0.54±0．16）L·min^-1·mmHg^-1 vs（0．51±0.23）L·min^-1·mmHg^-1]则无显著变化。结论：重叠综合征患者呼吸中枢对低氧及高CO2刺激的反应性降低。经正压通气治疗去除睡眠呼吸紊乱后,难以在短期内恢复至正常水平,与单纯SAHS患者的改变不同,这种异常改变可能受遗传因素的影响。

Effect of noninvasive ventilation on chemoresponsiveness in patients with sleep apnea and chronic obstructive pulmonary disease

OBJECTIVE: To investigate the effect of noninvasive ventilation on respiratory control in patients with chronic obstructive pulmonary disease (COPD) combined with sleep a apnea-hypopnea syndrome (SAHS)-overlap syndrome (OS). METHODS: Ten body mass index, apnea-hypopnea index, and age-matched OSAHS patients, 5 being hypercapnic (PaCO(2) > 45 mm Hg) OSAHS patients with normal FEV(1)/FVC, and 5 being OSAHS patients with COPD and the mean FEV(1)/FVC of 59% +/- 6% underwent bi-level positive airway pressure (BiPAP) treatment. Hypoxic responses, including the ratio of the change in minute ventilation (DeltaVE) to the change in arterial oxygen saturation (DeltaSaO(2)), and hypercapnic responses (DeltaVE/DeltaPaCO(2) ratio) were tested during wakefulness before treatment and 6 weeks after the treatment. RESULTS: Before treatment, the DeltaVE/DeltaSaO(2) ratios of the OS and OSAHS patients were (-0.023 +/- 0.049) L.min(-1).%(-1) and (-0.16 +/- 0.06) L.min(-1).%(-1) respectively, both lower than the laboratory normal value [(-0.35 +/- 0.21) L.min(-1).%(-1)]. The DeltaVE/DeltaPaCO(2) ratio of the OS patients was (0.54 +/- 0.16) L.mm Hg(-1), significantly lower than the normal value [(1.26 +/- 0.54) L.mm.Hg(-1), P < 0.05]. After receiving 6 weeks of noninvasive ventilation treatment, the hypoxic response of OSAHS patients were (-0.16 +/- 0.06) L.min(-1).%(-1), significantly higher than that before treatment [(-0.36 +/- 0.14) L.min(-1).%(-1)], and hypercapnic response of the OSAHS patients was (1.30 +/- 0.62) L.min(-1).mm Hg(-1), significantly lower than that before treatment [(1.78 +/- 0.93) L.min(-1).mm Hg(-1)], both bring within the normal ranges. In the patients with OS, the hypercapnic response was unchanged [(0.54 +/- 0.16) vs (0.51 +/- 0.23) L.min(-1).mm Hg(-1)], and the hypoxic responses increased significantly but still remained at a very low level [(-0.023 +/- 0.049) vs (-0.09 +/- 0.007) L.min(-1).%(-1)] after treatment. CONCLUSION: Hypercapnic and hypoxic responses in patients with OS and in patients with OSAHS respond differently after pressure support ventilation. This indicates that depressed chemoresponsiveness in patients with OS may not be only a response to sleep-disordered breathing.