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

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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 FEV_1/FVC 为59%±6%,另5例为伴 CO_2潴留的 SAHS 患者,FEV_1/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(ΔVE/ΔSaO_2)及高 CO_2反应性(ΔVE/ΔPaCO_2)。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CO_2反应性分别为(0.54±0.16)L·min~(-1)·mm Hg~(-1)及(1.3±0.62)L·min~(-1)·mm Hg~(-1),前者显著低于实验室正常值(1.26±0.54)L·min~(-1)·min Hg~(-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)·%~(-1)vs(-0.36±0.14)L·min~(-1)·%~(-1)]及高 CO_2反应性[(1.3±0.62)L·min~(-1)·mm Hg~(-1)vs(1.78±0.93)L·min~(-1)·mm Hg~(-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 CO_2反应性[(0.54±0.16)L·min~(-1)·mm Hg~(-1)vs(0.51±0.23)L·min~(-1)·mm Hg~(-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 CO_2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。 Objective To investigate the changes of respiratory reactivity in patients with chronic obstructive pulmonary disease (COPD) complicated with sleep apnea (overlap syndrome) by noninvasive ventilation. Methods Ten patients with sleep apnea-hypopnea syndrome (SAHS) confirmed by polysomnography sleep apnea-hypopnea syndrome were selected. Among them, 5 patients had COPD with an average FEV 1 / FVC of 59% ± 6% and the other 5 patients had CO 2 Preserved SAHS patients, FEV_1 / FVC normal. The age, body mass index (BMI), and sleep apnea-hypopnea index (AHI) matched for both groups. Respiratory hypoxemia (ΔVE / ΔSaO_2) and high CO_2 reactivity (ΔVE / ΔPaCO_2) were measured in 10 patients before and after long-term treatment with BiPAP. Results The respiratory center hypoxia reactivity before treatment in patients with overlap syndrome (OS) and obstructive sleep apnea (OSA) were (-0.023 ± 0.049) L · min -1 (-1) and (-0.16 ± 0.06) L · min -1 (-1) ·% -1 were lower than the normal value of laboratory (-0.35 ± 0.21) L · min -1 (-1) . The high CO 2 reactivity in patients with OS and OSA was (0.54 ± 0.16) L · min -1 · mm Hg -1 and 1.3 ± 0.62 L · min -1 · mm Hg ~ (-1), the former was significantly lower than the normal laboratory (1.26 ± 0.54) L · min -1 (-1) · min Hg -1, which was still in the normal range. After 6 weeks of treatment with BiPAP ventilator family therapy, the hypoxemia in OSA patients [(-0.16 ± 0.06) L · min -1 (-1) vs (-0.36 ± 0.14) L · min -1 (-1) ·% -1] and high CO 2 reactivity [(1.3 ± 0.62) L · min -1 · mm Hg -1 vs -1.78 ± 0.93 L · min -1 ) · Mm Hg ~ (-1)] were significantly increased, reaching the normal level. The hypoxemic reactivity of patients with OS increased (-0.023 ± 0.049) L · min -1 (-1) vs (-0.09 ± 0.007) L · min -1 (%) -1)], but still lower than the normal level. High CO 2 reactivity [(0.54 ± 0.16) L · min -1 · mm Hg -1 vs 0.51 ± 0.23 L · min ~ -1) · mm Hg -1], no significant change was observed. Conclusions The respiratory center of patients with overlapping syndrome has a decreased responsiveness to hypoxia and hyper-CO 2 stimulation. After positive pressure ventilation treatment to remove sleep disordered breathing, it is difficult to return to normal levels in a short period of time, which is different from the changes in patients with simple SAHS. The abnormal changes may be affected by genetic factors.
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