Bonsignore G
Istituto di Medicina Generale e Pneumologia, Università degli Studi di Palermo, Italy.
Ann Ital Med Int. 1991 Jan-Mar;6(1 Pt 2):137-47.
Respiratory function undergoes sleep-associated changes which in normal subjects leave it unaffected. However in some cases they may be more marked than usual or may be superimposed on a pre-existing disease, thus giving rise to sleep-related ventilation disorders. These include obstructive sleep apnea syndrome (OSAS), nocturnal desaturation events of chronic obstructive pulmonary disease (COPD) and restrictive syndromes, as well as nocturnal asthmatic attacks. OSAS is a condition characterized by the frequent recurrence of interruptions of oronasal flow (greater than 10 s.) due to upper airway occlusion induced by a reduction in pharyngeal muscle tone. This phenomenon, particularly prominent in REM sleep, results in oxyhemoglobin desaturation and marked cardiovascular consequences (arrhythmias, increases in pulmonary and systemic arterial pressure), as well as symptoms (loud intermittent snoring, daytime sleepiness, intellectual deterioration etc.). Obesity is often associated with OSAS or may lead to a sleep-related hypoventilation syndrome. Treatment is based on weight loss, surgery of upper airway abnormalities, if present, and on splinting of the upper airway by the application of nasal continuous positive airway pressure. In COPD and restrictive disorders, nocturnal hypoxemia is mainly due to REM-associated loss of respiratory muscle tone, as well as in the sleep-related exaggeration of functional defects due to COPD (low chemoreceptor sensitivity, high closing volume etc.). Treatment is based on oxygen administration, provided that possible side-effects are carefully monitored. Nocturnal asthma is due to circadian changes in hormonal secretion (catecholamines, cortisol), as well as supine posture, reduced muco-ciliary clearance, gastro-esophageal reflux etc. Sleep itself plays some role through a depressed arousal reaction in slow wave sleep, resulting in more marked and prolonged attacks in this stage. Slow-release theophylline or beta-mimetic medications, as well as new chromones and antimuscarinic drugs are therapeutic alternatives.
呼吸功能会经历与睡眠相关的变化，在正常受试者中这些变化不会对其产生影响。然而，在某些情况下，这些变化可能比平常更明显，或者可能叠加在已有的疾病之上，从而引发与睡眠相关的通气障碍。这些障碍包括阻塞性睡眠呼吸暂停综合征（OSAS）、慢性阻塞性肺疾病（COPD）和限制性综合征的夜间低氧血症事件，以及夜间哮喘发作。OSAS是一种由于咽部肌肉张力降低导致上气道阻塞，引起口鼻气流频繁中断（大于10秒）反复发作的病症。这种现象在快速眼动睡眠中尤为突出，会导致氧合血红蛋白饱和度降低以及明显的心血管后果（心律失常、肺和体循环动脉压升高），还有一些症状（大声间歇性打鼾、白天嗜睡、智力衰退等）。肥胖常常与OSAS相关，或者可能导致与睡眠相关的通气不足综合征。治疗方法包括减肥、对上气道异常进行手术（如果存在），以及通过应用鼻持续气道正压通气对上气道进行夹板固定。在COPD和限制性疾病中，夜间低氧血症主要是由于与快速眼动相关的呼吸肌张力丧失，以及COPD导致的功能缺陷在睡眠中加剧（化学感受器敏感性低、闭合气量高等）。治疗基于吸氧，前提是要仔细监测可能的副作用。夜间哮喘是由于激素分泌的昼夜变化（儿茶酚胺、皮质醇），以及仰卧姿势、黏液纤毛清除功能降低、胃食管反流等原因引起的。睡眠本身也通过慢波睡眠中唤醒反应的抑制发挥一定作用，导致在此阶段发作更明显且持续时间更长。缓释茶碱或β-激动剂药物，以及新型色酮类和抗胆碱能药物是治疗选择。
