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肥胖低通气综合征作为睡眠期间一系列呼吸紊乱情况。

Obesity hypoventilation syndrome as a spectrum of respiratory disturbances during sleep.

作者信息

Berger K I, Ayappa I, Chatr-Amontri B, Marfatia A, Sorkin I B, Rapoport D M, Goldring R M

机构信息

Department of Medicine, New York University School of Medicine, New York, NY 10016, USA.

出版信息

Chest. 2001 Oct;120(4):1231-8. doi: 10.1378/chest.120.4.1231.

Abstract

OBJECTIVE

To identify the spectrum of respiratory disturbances during sleep in patients with obesity hypoventilation syndrome (OHS) and to examine the response of hypercapnia to treatment of the specific ventilatory sleep disturbances.

DESIGNS AND METHODS

Twenty-three patients with chronic awake hypercapnia (mean [+/- SD] PaCO(2), 55 +/- 6 mm Hg) and a respiratory sleep disorder were retrospectively identified. Nocturnal polysomnography testing was performed, and flow limitation (FL) was identified from the inspiratory flow-time contour. Obstructive hypoventilation was inferred from sustained FL coupled with O(2) desaturation that was corrected with treatment of the upper airway obstruction. Central hypoventilation was inferred from sustained O(2) desaturation that persisted after the correction of the upper airway obstruction. Treatment was initiated, and follow-up awake PaCO(2) measurements were obtained (follow-up range, 4 days to 7 years).

RESULTS

A variable number of obstructive sleep apneas/hypopneas (ie, obstructive sleep apnea-hypopnea syndrome [OSAHS]) were noted (range, 9 to 167 events per hour of sleep). Of 23 patients, 11 demonstrated upper airway obstruction alone (apnea-hypopnea/FL) and 12 demonstrated central sleep hypoventilation syndrome (SHVS) in addition to a variable number of OSAHS. Treatment aimed at correcting the specific ventilatory abnormalities resulted in correction of the chronic hypercapnia in all compliant patients (compliant patients: pretreatment, 57 +/- 6 mm Hg vs post-treatment, 41 +/- 4 mm Hg [p < 0.001]; noncompliant patients: pretreatment, 52 +/- 6 mm Hg vs post-treatment, 51 +/- 3 mm Hg; [difference not significant]).

CONCLUSIONS

This study demonstrates that OHS encompasses a variety of distinct pathophysiologic disturbances that cannot be distinguished clinically at presentation. Sustained obstructive hypoventilation due to partial upper airway obstruction was demonstrated as an additional mechanism for OHS that is not easily classified as SHVS or OSAHS.

摘要

目的

识别肥胖低通气综合征(OHS)患者睡眠期间的呼吸紊乱谱,并研究高碳酸血症对特定通气性睡眠紊乱治疗的反应。

设计与方法

回顾性纳入23例慢性清醒时高碳酸血症(平均[±标准差]PaCO₂,55±6 mmHg)且患有呼吸睡眠障碍的患者。进行夜间多导睡眠图测试,并从吸气流量-时间曲线识别气流受限(FL)。阻塞性通气不足是由持续的气流受限以及通过治疗上气道阻塞得以纠正的氧饱和度下降推断得出。中枢性通气不足是由上气道阻塞纠正后仍持续的氧饱和度下降推断得出。开始治疗,并获取随访时清醒状态下的PaCO₂测量值(随访时间范围为4天至7年)。

结果

记录到数量不等的阻塞性睡眠呼吸暂停/低通气(即阻塞性睡眠呼吸暂停低通气综合征[OSAHS])(范围为每小时睡眠中9至167次事件)。23例患者中,11例仅表现为上气道阻塞(呼吸暂停低通气/气流受限),12例除了数量不等的OSAHS外,还表现为中枢性睡眠通气不足综合征(SHVS)。针对纠正特定通气异常的治疗使所有依从患者的慢性高碳酸血症得到纠正(依从患者:治疗前,57±6 mmHg vs治疗后,41±4 mmHg [p<0.001];不依从患者:治疗前,52±6 mmHg vs治疗后,51±3 mmHg;[差异无统计学意义])。

结论

本研究表明,OHS包含多种不同的病理生理紊乱,在疾病表现时无法通过临床进行区分。部分上气道阻塞导致的持续性阻塞性通气不足被证明是OHS的另一种机制,这种机制不易归类为SHVS或OSAHS。

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