Wiegand L, Zwillich C W
Division of Pulmonary and Critical Care Medicine, Milton S. Hershey Medical Center, Pennsylvania State University Hershey.
Dis Mon. 1994 Apr;40(4):197-252. doi: 10.1016/0011-5029(94)90013-2.
The high prevalence of obstructive sleep apnea (OSA) has only recently been appreciated, in part because the symptoms and signs of chronic sleep disruption are often overlooked in spite of their debilitating consequences. They typically develop insidiously during a period of years. We now know that the lives of millions of people each year are significantly impaired by the sequelae of OSA. Many of these patients go unrecognized, with tremendous medical and economic consequences for individual patients and for society. Evidence indicates that chronic, heavy snoring may be associated with increased long-term cardiovascular and neurophysiologic morbidity. Therefore considerable interest lies in the study of the epidemiology and the natural history of these related disorders. The fundamental problem in OSA is the periodic collapse of the pharyngeal airway during sleep. The pathophysiology of this phenomenon is reviewed in some detail. During apneas caused by obstruction, airflow is impeded by the collapsed pharynx in spite of continued effort to breathe. This causes progressive asphyxia, which increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened. Hypopneas predominate in some patients and are caused by partial pharyngeal collapse. The clinical sequelae of OSA relate to the cumulative effects of exposure to periodic asphyxia and to sleep fragmentation caused by apneas and hypopneas. Some patients with frequent, brief apneas and hypopneas and normal underlying cardiopulmonary function may have considerable sleep disruption without much exposure to nocturnal hypoxia. Patients with sleep apnea often have excessive daytime sleepiness. As the disorder progresses, sleepiness becomes increasingly irresistible and dangerous, and patients develop cognitive dysfunction, inability to concentrate, memory and judgment impairment, irritability, and depression. These problems may lead to family and social problems and job loss. Cardiac and vascular morbidity in OSA may include systemic hypertension, cardiac arrhythmias, pulmonary hypertension, cor pulmonale, left ventricular dysfunction, stroke, and sudden death. The challenge for the clinician is to routinely consider the diagnosis and to incorporate several basic questions in the historical review of systems regarding daytime or inappropriate sleepiness. The diagnosis of OSA is made with polysomnography, and the decision to treat is based on an overall assessment of the severity of sleep-disordered breathing, sleep fragmentation, and associated clinical sequelae. The therapeutic options for the management of OSA are reviewed. Recognition and appropriate treatment of OSA and related disorders will often significantly enhance the patient's quality of life, overall health, productivity, and safety on the highways.
阻塞性睡眠呼吸暂停（OSA）的高患病率直到最近才受到重视，部分原因是尽管慢性睡眠中断的症状和体征会产生使人衰弱的后果，但往往被忽视。这些症状通常在数年时间里逐渐隐匿出现。我们现在知道，每年数百万患者的生活因OSA的后遗症而受到严重影响。许多这类患者未被识别，给个体患者和社会带来了巨大的医疗和经济后果。有证据表明，长期严重打鼾可能与长期心血管和神经生理发病率增加有关。因此，对这些相关疾病的流行病学和自然史的研究备受关注。OSA的根本问题是睡眠期间咽部气道的周期性塌陷。本文将详细综述这一现象的病理生理学。在由阻塞引起的呼吸暂停期间，尽管患者持续努力呼吸，但塌陷的咽部会阻碍气流。这会导致进行性窒息，进而越来越多地刺激患者对抗塌陷气道的呼吸努力，通常直到患者被唤醒。在一些患者中，呼吸浅慢较为常见，是由咽部部分塌陷引起的。OSA的临床后遗症与周期性窒息暴露以及呼吸暂停和呼吸浅慢导致的睡眠碎片化的累积效应有关。一些频繁出现短暂呼吸暂停和呼吸浅慢且基础心肺功能正常的患者，可能有相当严重的睡眠中断，但很少暴露于夜间缺氧环境。睡眠呼吸暂停患者通常白天过度嗜睡。随着病情进展，嗜睡变得越来越难以抗拒且危险，患者会出现认知功能障碍、注意力不集中、记忆力和判断力受损、易怒以及抑郁等症状。这些问题可能导致家庭和社会问题以及失业。OSA患者的心脏和血管疾病可能包括系统性高血压、心律失常、肺动脉高压、肺心病、左心室功能障碍、中风和猝死。临床医生面临的挑战是在日常工作中考虑到该诊断，并在系统回顾病史时纳入几个关于白天或不适当嗜睡的基本问题。OSA的诊断通过多导睡眠监测来进行，而治疗决策则基于对睡眠呼吸紊乱严重程度、睡眠碎片化程度以及相关临床后遗症的全面评估。本文还综述了OSA的治疗选择。识别并适当治疗OSA及相关疾病通常会显著提高患者的生活质量、整体健康状况、工作效率以及在公路上的安全性。
