Department of Pulmonary Medicine and Multidisciplinary Sleep Disorders Centre, Antwerp University Hospital and University of Antwerp, Wilrijkstraat 10, Edegem 2650, Belgium.
Respir Res. 2013 Nov 20;14(1):132. doi: 10.1186/1465-9921-14-132.
The overlap syndrome of obstructive sleep apnoea (OSA) and chronic obstructive pulmonary disease (COPD), in addition to obesity hypoventilation syndrome, represents growing health concerns, owing to the worldwide COPD and obesity epidemics and related co-morbidities. These disorders constitute the end points of a spectrum with distinct yet interrelated mechanisms that lead to a considerable health burden. The coexistence OSA and COPD seems to occur by chance, but the combination can contribute to worsened symptoms and oxygen desaturation at night, leading to disrupted sleep architecture and decreased sleep quality. Alveolar hypoventilation, ventilation-perfusion mismatch and intermittent hypercapnic events resulting from apneas and hypopneas contribute to the final clinical picture, which is quite different from the "usual" COPD. Obesity hypoventilation has emerged as a relatively common cause of chronic hypercapnic respiratory failure. Its pathophysiology results from complex interactions, among which are respiratory mechanics, ventilatory control, sleep-disordered breathing and neurohormonal disturbances, such as leptin resistance, each of which contributes to varying degrees in individual patients to the development of obesity hypoventilation. This respiratory embarrassment takes place when compensatory mechanisms like increased drive cannot be maintained or become overwhelmed. Although a unifying concept for the pathogenesis of both disorders is lacking, it seems that these patients are in a vicious cycle. This review outlines the major pathophysiological mechanisms believed to contribute to the development of these specific clinical entities. Knowledge of shared mechanisms in the overlap syndrome and obesity hypoventilation may help to identify these patients and guide therapy.
阻塞性睡眠呼吸暂停(OSA)和慢性阻塞性肺疾病(COPD)的重叠综合征,除肥胖低通气综合征外,由于全球 COPD 和肥胖症的流行以及相关的合并症,代表了日益严重的健康问题。这些疾病构成了具有不同但相互关联的机制的疾病谱的终点,导致了相当大的健康负担。OSA 和 COPD 的共存似乎是偶然发生的,但这种组合可能会导致症状恶化和夜间氧饱和度下降,从而导致睡眠结构中断和睡眠质量下降。由于呼吸暂停和低通气导致的肺泡通气不足、通气/灌注不匹配和间歇性高碳酸血症事件,导致了最终的临床特征,这与“通常”的 COPD 有很大不同。肥胖低通气已成为慢性高碳酸血症呼吸衰竭的一个相对常见的原因。其病理生理学是由复杂的相互作用引起的,其中包括呼吸力学、通气控制、睡眠呼吸障碍和神经激素紊乱,如瘦素抵抗,这些因素在个体患者中以不同程度导致肥胖低通气的发展。当不能维持或超过代偿机制(如增加驱动力)时,就会发生这种呼吸窘迫。尽管缺乏这两种疾病发病机制的统一概念,但这些患者似乎处于恶性循环中。这篇综述概述了被认为有助于这些特定临床实体发展的主要病理生理机制。对重叠综合征和肥胖低通气共享机制的认识,可能有助于识别这些患者并指导治疗。