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阻塞性睡眠呼吸暂停综合征中的高碳酸血症。对“匹克威克综合征”的重新评估。

Hypercapnia in the obstructive sleep apnea syndrome. A reevaluation of the "Pickwickian syndrome".

作者信息

Rapoport D M, Garay S M, Epstein H, Goldring R M

出版信息

Chest. 1986 May;89(5):627-35. doi: 10.1378/chest.89.5.627.

Abstract

The mechanisms of hypercapnia in eight patients with the "Pickwickian" syndrome and obstructive sleep apnea (OSAS) were evaluated pretherapy and posttherapy (tracheostomy in seven patients and chronic nocturnal use of nasal CPAP in one). Four patients (correctors) became eucapnic within two weeks of therapy. Four others (noncorrectors) remained hypercapnic. Neither residual apneas, changes in pulmonary function, change in anatomic dead space, nor changes in ventilatory chemoresponsiveness differentiated the two groups, nor did the last three factors account for return to eucapnia in the correctors. The results indicated two separate mechanisms exist for chronic hypercapnia in OSAS: a critical balance between the ventilation during the time spent awake and hypoventilation due to apneas, a mechanism removed by treatment for obstructive apnea; and sustained hypoventilation independent of the apnea phenomenon and therefore not correctible. The subset of patients with the second mechanism appears to represent the true "Pickwickian" syndrome and can be identified before therapy by measuring a low level of ventilation in the sustained awake state.

摘要

对8例患有“匹克威克综合征”和阻塞性睡眠呼吸暂停(OSAS)的患者在治疗前和治疗后(7例行气管造口术,1例长期夜间使用鼻持续气道正压通气)评估了高碳酸血症的机制。4例患者(纠正者)在治疗后两周内恢复正常碳酸血症。另外4例(未纠正者)仍为高碳酸血症。残余呼吸暂停、肺功能变化、解剖无效腔改变或通气化学反应性改变均不能区分这两组患者,后三个因素也不能解释纠正者恢复正常碳酸血症的原因。结果表明,OSAS慢性高碳酸血症存在两种不同机制:清醒时通气与呼吸暂停导致的通气不足之间的关键平衡,这是一种因阻塞性呼吸暂停治疗而消除的机制;以及与呼吸暂停现象无关的持续性通气不足,因此无法纠正。具有第二种机制的患者亚组似乎代表了真正的“匹克威克综合征”,并且可以在治疗前通过测量持续清醒状态下的低通气水平来识别。

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