阻塞性睡眠呼吸暂停低通气综合征患者脑血管自动调节潜力分析

目的 评价阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者脑血管的自动调节能力.方法 选择济南市第四人民医院神经科自2007年2月至2009年5月就诊或住院的OSAHS患者76例,根据患者呼吸暂停低通气指数(AHI)和夜间最低血氧饱和度(LSaO2)分为轻、中、重度OSAHS组,选择同期有打鼾史的健康体检者32例作对照组,利用多导睡眠仪监测睡眠相关指标及不同时段血压,通过经颅多普勒超声(TCD)检测结合倾斜实验、屏气实验评价患者脑血管的CO2反应性和自动调节能力.结果 与对照组比较,OSAHS组患者AHI较高、LSaO2较低、微觉醒指数(MI)较高,暂停时收缩压增高,S1占睡眠时间的百分比增高、S3+4占睡眠时间的百分比降低,差异均有统计学意义(P＜0.05).与对照组和轻度OSAHS组比较,中、重度OSAHS组患者呼吸抑制指数(BHI)降低、由卧位至立位平均动脉压恢复90%所用时间(TMAP)增加;与对照组比较,OSAHS组患者血管运动反应性(VMR)降低、由卧位至立位脑血流速度(CBFV)恢复90%所用时间(TCBFV)增加,差异均有统计学意义(P＜0.05).中重度OSAHS患者卧立位时血压、平均CBFV的差异均有统计学意义(P＜0.05),立位血压和平均CBFV之间呈正相关关系(r=0.384,P=0.005).结论 OSAHS患者尤其是中重度患者脑血管调节功能受损,卒中风险可能增加.导致OSAHS患者脑血管调节受损的主要因素为夜间低氧血症、高碳酸血症、血压波动及睡眠结构紊乱.

Abstract：

Objective To evaluate the cerebral autoregulation in patients with obstructive sleep apnea-hypopnea syndrome (OASHS) using transcranial Doppler (TCD)-CO2 test and head-upright tilt test (HUTT) from the aspects of nocturnal hypoxemia/hypercapnia and sleep structure. Methods Seventy-six patients with OSAHS visiting our hospital from February 2007 to May 2009 were chosen in our study and divided into severe OSAHS group (n=26), moderate OSAHS group (n=29) and mild OSAHS group (n=21) according to the apnea-hypopnea index (AHI), and the lowest oxygen saturation (LSaO2); 32 healthy controls, having snore history, were adopted too. Polysomnography monitor was used for night-7-h sleep monitoring and blood pressure monitoring; sleep-related indicators and blood pressure at different times were analyzed. Cerebrovascular reactivity was calculated in terms of the breath-holding index (BHI) and vascular motor reactivity (VMR) by TCD-CO2 test; Changes of cerebral blood flow velocity (CBFV), blood pressure (Bp), and the time from squatting-to-tilt position for the mean arterial pressure (TMAP) and the CBFV (TCBFV) returning to ＞90% of baseline levels were detected by HUTT to assess the cerebral pressure-autoregulation. Results The AHI, microarousal index (MI) and the percentages of S1 in the non-rapid eye movement sleep period in the severe, moderate and mild OSAHS groups were all significantly higher than those in the control group (P＜0.05); the LSaO2 and the percentages of S3+4 in the non-rapid eye movement sleep period in all the OSAHS groups were significantly lower than those in the control group (P＜0.05); no significant difference in blood pressure before apnea was noted between the OSAHS groups and the control group (P＞0.05), however, the systolic blood pressure while apnea in all the OSAHS groups was significantly higher than that in the control group (P＜0.05). As compared with the controls and mild OSAHS group (1.89±0.36, 1.75±0.41), severe and moderate OSAHS groups (0.71 ±0.17, 1.12±0.23, respectively) showed significantly decreased BHI (P＜0.05); As compared with the controls (0.68±0.11), and the mild, moderate and severe OSAHS groups (0.20±0.04, 0.34±0.07 and 0.55±0.17, respectively) showed significantly decreased VMR (P＜0.05); TMAP in the moderate and severe OSAHS groups was significantly longer than that in the controls and mild OSAHS group (P＜0.05); TCBFV in the mild, moderate and severe OSAHS groups was significantly longer than that in the controls (P＜0.05). Significant difference on the levels of Bp and CBFV during tilt was noted between the moderate and severe OSAHS groups (P＜0.05); Pearson analysis showed a linkage between Bp and CBFV changes (r=0.384, P=0.005). Conclusion Cerebrovascular autoregulation is impaired in patients with OSAHS, especially in the moderate and severe groups, which may increase the risk of stroke. The major risk factors for cerebrovascular autoregulation in patients with OSAHS are night hypoxemia, hypercapnia, blood pressure fluctuation and severe sleep disorders.

Cerebral autoregulation in patients with obstructive sleep apnea-hypopnea syndrome

Objective To evaluate the cerebral autoregulation in patients with obstructive sleep apnea-hypopnea syndrome (OASHS) using transcranial Doppler (TCD)-CO2 test and head-upright tilt test (HUTT) from the aspects of nocturnal hypoxemia/hypercapnia and sleep structure. Methods Seventy-six patients with OSAHS visiting our hospital from February 2007 to May 2009 were chosen in our study and divided into severe OSAHS group (n=26), moderate OSAHS group (n=29) and mild OSAHS group (n=21) according to the apnea-hypopnea index (AHI), and the lowest oxygen saturation (LSaO2); 32 healthy controls, having snore history, were adopted too. Polysomnography monitor was used for night-7-h sleep monitoring and blood pressure monitoring; sleep-related indicators and blood pressure at different times were analyzed. Cerebrovascular reactivity was calculated in terms of the breath-holding index (BHI) and vascular motor reactivity (VMR) by TCD-CO2 test; Changes of cerebral blood flow velocity (CBFV), blood pressure (Bp), and the time from squatting-to-tilt position for the mean arterial pressure (TMAP) and the CBFV (TCBFV) returning to ＞90% of baseline levels were detected by HUTT to assess the cerebral pressure-autoregulation. Results The AHI, microarousal index (MI) and the percentages of S1 in the non-rapid eye movement sleep period in the severe, moderate and mild OSAHS groups were all significantly higher than those in the control group (P＜0.05); the LSaO2 and the percentages of S3+4 in the non-rapid eye movement sleep period in all the OSAHS groups were significantly lower than those in the control group (P＜0.05); no significant difference in blood pressure before apnea was noted between the OSAHS groups and the control group (P＞0.05), however, the systolic blood pressure while apnea in all the OSAHS groups was significantly higher than that in the control group (P＜0.05). As compared with the controls and mild OSAHS group (1.89±0.36, 1.75±0.41), severe and moderate OSAHS groups (0.71 ±0.17, 1.12±0.23, respectively) showed significantly decreased BHI (P＜0.05); As compared with the controls (0.68±0.11), and the mild, moderate and severe OSAHS groups (0.20±0.04, 0.34±0.07 and 0.55±0.17, respectively) showed significantly decreased VMR (P＜0.05); TMAP in the moderate and severe OSAHS groups was significantly longer than that in the controls and mild OSAHS group (P＜0.05); TCBFV in the mild, moderate and severe OSAHS groups was significantly longer than that in the controls (P＜0.05). Significant difference on the levels of Bp and CBFV during tilt was noted between the moderate and severe OSAHS groups (P＜0.05); Pearson analysis showed a linkage between Bp and CBFV changes (r=0.384, P=0.005). Conclusion Cerebrovascular autoregulation is impaired in patients with OSAHS, especially in the moderate and severe groups, which may increase the risk of stroke. The major risk factors for cerebrovascular autoregulation in patients with OSAHS are night hypoxemia, hypercapnia, blood pressure fluctuation and severe sleep disorders.