Kaluza C L, Krachman S L, D'Alonzo G E
Sleep Disorders Center, Temple University Medical School and Hospital, Philadelphia, Pa., USA.
J Am Osteopath Assoc. 1995 Jul;95(7):420-6.
Obstructive sleep apnea is a multisystemic disorder with pathologic sequelae that become apparent after a number of years. Patients with obstructive sleep apnea generally present with hypersomnolence, and diagnosis is eventually established through observation of the patient during sleep. Patients with obstructive sleep apnea snore loudly and experience nocturnal oxygen desaturation and repetitive disruptions from sleep that eventually lead to daytime hypersomnolence. Numerous complex interactive pathophysiologic events occur during each obstructive episode, and it is important for the clinician to be aware of the cardiopulmonary, neurologic, and anatomic abnormalities associated with this condition. The anatomic configuration of the pharynx and the physiologic response to occlusion of the upper airway have a major role in the pathogenesis of this disorder. Alveolar ventilation during an apneic episode is immediately reduced to zero, and the metabolic demands for oxygen must be met by oxygen stores within the body. With repetitive episodes of obstruction, the oxygen stores within the lungs are diminished and the rate of arterial oxyhemoglobin desaturation increases. During apneic episodes, the systemic blood pressure increases while heart rate and cardiac output decrease. Bradydysrhythmias have been noted with the obstructive apneic episodes, and ventricular dysrhythmias are associated with episodes of severe oxyhemoglobin desaturation. Coexisting cardiopulmonary or neuromuscular disease in patients with obstructive sleep apnea contributes to the development of hypoventilation, serious gas exchange derangement, and general cardiovascular instability.
阻塞性睡眠呼吸暂停是一种多系统疾病，其病理后遗症在数年后才会显现出来。阻塞性睡眠呼吸暂停患者通常表现为嗜睡，最终通过对患者睡眠期间的观察来确诊。阻塞性睡眠呼吸暂停患者会大声打鼾，夜间出现氧饱和度下降以及睡眠反复中断，最终导致日间嗜睡。在每次阻塞发作期间会发生许多复杂的相互作用的病理生理事件，临床医生了解与该疾病相关的心肺、神经和解剖学异常情况很重要。咽部的解剖结构和对上气道阻塞的生理反应在该疾病的发病机制中起主要作用。呼吸暂停发作期间肺泡通气立即降至零，身体内的氧储备必须满足对氧气的代谢需求。随着阻塞的反复发生，肺内的氧储备减少，动脉血氧血红蛋白饱和度下降的速率增加。在呼吸暂停发作期间，全身血压升高，而心率和心输出量降低。阻塞性呼吸暂停发作时会出现心动过缓，室性心律失常与严重的血氧血红蛋白饱和度下降发作有关。阻塞性睡眠呼吸暂停患者并存心肺或神经肌肉疾病会导致通气不足、严重的气体交换紊乱和全身心血管不稳定的发生。
