阻塞性睡眠呼吸暂停低通气综合征患者睡眠时的呼吸中枢反应性与夜间低氧血症的关系

Abstract

目的探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者夜间低氧血症与呼吸中枢反应性的关系.方法应用动态脉搏容积血氧饱和度(SpO2)仪定量分析了24例白天二氧化碳分压(PaCO2)≥45 mm Hg(高CO2组,1 mm Hg=0.133 kPa)及39例PaCO2＜45 mm Hg(等CO2组)的OSAHS患者夜间低氧血症的严重程度.进一步应用重复呼吸法测定了其中15例患者(等CO2组11例,高CO2组4例)睡眠状态下呼吸中枢的低氧及高CO2反应性.结果 63例患者的睡眠呼吸暂停低通气指数(AHI)平均为(54±21)次/h;夜间动态SaO2监测发现高CO2组与等CO2组比较,每小时氧减饱和4%以上的次数(ODI4)为(43±23)次/h vs (29±18)次/h;SaO2＜90%的时间占总睡眠时间的百分数(SIT90)为(39±32)% vs( 15±18)% ,高CO2组均较等CO2组高; 而睡眠时的最低SaO2(LSaO2)为(56±18)% vs (66±16)%,平均SaO2(MSaO2)为(86±12)% vs(93±5)%,均较等CO2组低(P＜0.01),提示其夜间缺氧程度更重.在清醒状态下,高CO2组及等CO2组患者的高CO2反应(ΔP0.1/ΔPaCO2)、低氧反应(ΔP0.1/ΔSaO2)、口腔阻断压(P0.1)差异均无显著性(P＞0.1).进入非快动眼睡眠(NREM)及快动眼睡眠(REM)后,高CO2组患者的P0.1与等CO2组患者相同,但低氧及高CO2反应性均显著低于后者(P均＜0.05).在4例高CO2组患者中,2例高CO2反应在NREM及REM睡眠期均消失,1例在REM睡眠期近于消失;3例的低氧反应在NREM近于消失,在REM睡眠期消失.结论白天存在CO2潴留的OSAHS患者夜间睡眠时呼吸中枢的化学反应性减低甚至消失,是其夜间低氧血症较重的机制之一.

It is assumed that the reduced ventilatory control during sleep may be related to the nocturnal hypoxia in patients with obstructive sleep apnea hypopnea syndrome (OSAHS) and daytime CO(2) retention.Oxygen desaturation index (ODI(4)), sleep time spent when SaO(2) was below 90% (SIT(90)), the lowest SaO(2) (LSaO(2)) and the mean SaO(2) (MSaO(2)) during sleep were measured in 24 OSAHS patients with daytime PaCO(2) > or = 45 mm Hg and 39 with PaCO(2) < 45 mm Hg. Hypoxic (DeltaP(0.1)/DeltaSaO(2)) and hypercapnic (DeltaP(0.1)/DeltaPaCO(2)) responsiveness were measured in 11 eucapnic and 4 hypercapnic patients during wakefulness, NREM and REM sleep stages.Compared with the eucapnic patients, all the hypercapnic patients had more severe hypoxia during sleep (P < 0.05). Although both groups had similar chemical responsiveness during wakefulness, the hypercapnic patients had lower DeltaP(0.1)/DeltaSaO(2) and DeltaP(0.1)/DeltaPaCO(2) during both REM and NREM sleep (P < 0.05).The depressed chemical responsiveness during sleep plays an important role in the development of nocturnal hypoxia in OSAHS patients with daytime CO(2) retention.