Adv Cardiol. 2011;46:171-195. doi: 10.1159/000325109. Epub 2011 Oct 13.
Obstructive sleep apnea (OSA) is characterized by repetitive episodes of complete or partial obstruction of the upper airway during sleep that lead to an increase in airway resistance and respiratory effort. This may produce oxygen desaturation, hypercapnia and central nervous system arousal that restore airflow. OSA is associated with hemodynamic changes that are related to alterations in the activity of the autonomic nervous system. During the course of an apnea, the heart rate may slow down, increase or remain stable. The blood pressure decreases at the start of the apnea and increases at its terminal portion. When ventilation resumes, heart rate, blood pressure and ventilation reach a peak accompanied by an abrupt reduction in left ventricular stroke volume. During the early phase of apnea, sympathetic nerve activity (SNA) is suppressed; it then increases constantly and reaches a peak at the end of apnea and on arousal. As soon as ventilation resumes, there is an abrupt inhibition of SNA in the peripheral blood vessels. The resumption of ventilation occurs in the context of peripheral vasoconstriction and increased peripheral resistance. This situation persists for several seconds after the SNA has ceased, due to the kinetics of norepinephrine uptake, release and washout at the neurovascular junction. Hypoxemia, hypercapnia, lung inflation and blood pressure are important factors that may modulate these autonomic changes. The alterations in the autonomic nervous system are carried over into wakefulness and may contribute to the development of the cardiovascular disorders associated with OSA, including sympathovagal imbalance accompanied with changes in the baroreflex and chemoreflex. The hemodynamic and autonomic dysfunction associated with OSA is improved following treatment with continuous positive airway pressure.
阻塞性睡眠呼吸暂停（OSA）的特征是睡眠期间上气道反复出现完全或部分阻塞，导致气道阻力增加和呼吸努力增强。这可能会导致氧饱和度下降、高碳酸血症以及恢复气流的中枢神经系统觉醒。OSA与自主神经系统活动改变相关的血流动力学变化有关。在呼吸暂停过程中，心率可能减慢、加快或保持稳定。呼吸暂停开始时血压下降，结束时血压升高。通气恢复时，心率、血压和通气量达到峰值，同时左心室每搏输出量突然减少。在呼吸暂停早期，交感神经活动（SNA）受到抑制；随后持续增加，在呼吸暂停结束和觉醒时达到峰值。通气一恢复，外周血管中的SNA就会突然受到抑制。通气恢复发生在外周血管收缩和外周阻力增加的情况下。由于去甲肾上腺素在神经血管交界处的摄取、释放和清除动力学，这种情况在SNA停止后会持续数秒。低氧血症、高碳酸血症、肺膨胀和血压是可能调节这些自主神经变化的重要因素。自主神经系统的改变会延续到清醒状态，并可能导致与OSA相关的心血管疾病的发展，包括伴有压力反射和化学反射变化的交感迷走神经失衡。持续气道正压通气治疗后，与OSA相关的血流动力学和自主神经功能障碍会得到改善。
