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睡眠呼吸暂停与左心室功能障碍患者的通气控制:阻塞性与中枢性睡眠呼吸暂停的比较

Ventilatory control in patients with sleep apnoea and left ventricular dysfunction: comparison of obstructive and central sleep apnoea.

作者信息

Wilcox I, McNamara S G, Dodd M J, Sullivan C E

机构信息

Dept of Medicine, University of Sydney, Royal Prince Alfred Hospital, NSW, Australia.

出版信息

Eur Respir J. 1998 Jan;11(1):7-13. doi: 10.1183/09031936.98.11010007.

DOI:10.1183/09031936.98.11010007
PMID:9543263
Abstract

Sleep apnoea is common in patients with heart failure. While most patients have central sleep apnoea (CSA), a minority have obstructive sleep apnoea (OSA). The pathophysiology of CSA is not well understood. We hypothesized that central chemosensitivity would be an important pathophysiological factor in patients with CSA, and not in OSA. The aim of this study was to compare ventilatory responses between patients with CSA and those with OSA. Acute ventilatory responses to eucapnic hypoxia and hyperoxic hypercapnia were measured during wakefulness in 34 patients (33 males and one female, aged 59+/-8 yrs (mean+/-SD)), with stable medically-treated left ventricular dysfunction (LVD) and sleep apnoea (18 OSA and 16 CSA). Patients with CSA had a decreased awake end-tidal carbon dioxide tension (4.1+/-0.5 kPa), increased ventilatory response to carbon dioxide (0.65+/-0.43 L.min.(-1).kPa PCO2(-1)), and eucapnic hypoxic responses in the normal range (0.6+/-0.4 L.min(-1)/% fall in arterial oxygen saturation (Sa,O2)). In contrast, patients with OSA had normal end-tidal carbon dioxide tension (4.9+/-0.5 kPa), and normal ventilatory responses to hypercapnia (0.29+/-0.16 L.min(-1).kPa PCO2(-1)) and hypoxia (0.5+/-0.5 L-min(-1)/% fall in Sa,O2). These findings suggest that augmented chemosensitivity to hypercapnia may be an important factor in the pathophysiology of central sleep apnoea in patients with heart failure.

摘要

睡眠呼吸暂停在心力衰竭患者中很常见。虽然大多数患者患有中枢性睡眠呼吸暂停(CSA),但少数患者患有阻塞性睡眠呼吸暂停(OSA)。CSA的病理生理学尚未完全了解。我们假设中枢化学敏感性是CSA患者而非OSA患者的重要病理生理因素。本研究的目的是比较CSA患者和OSA患者的通气反应。在34例(33例男性和1例女性,年龄59±8岁(均值±标准差))患有稳定的药物治疗的左心室功能障碍(LVD)和睡眠呼吸暂停(18例OSA和16例CSA)的患者清醒状态下,测量了对等碳酸血气缺氧和高氧高碳酸血症的急性通气反应。CSA患者清醒时的呼气末二氧化碳分压降低(4.1±0.5 kPa),对二氧化碳的通气反应增加(0.65±0.43 L·min⁻¹·kPa⁻¹ PCO₂),等碳酸血气缺氧反应在正常范围内(0.6±0.4 L·min⁻¹/动脉血氧饱和度(SaO₂)下降百分比)。相比之下,OSA患者的呼气末二氧化碳分压正常(4.9±0.5 kPa),对高碳酸血症(0.29±0.16 L·min⁻¹·kPa⁻¹ PCO₂)和缺氧(0.

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