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阻塞性睡眠呼吸暂停中的呼吸暂停期血流动力学反应

Peri-apneic hemodynamic reactions in obstructive sleep apnea.

作者信息

Muraja-Murro Anu, Nieminen Outi, Julkunen Petro, Töyräs Juha, Laitinen Tomi, Mervaala Esa

机构信息

Department of Clinical Neurophysiology, Kuopio University Hospital, P.O. Box 100, FIN-70029 KYS, Kuopio, Finland; Institute of Clinical Medicine, University of Eastern Finland, P.O. Box 1627, FIN-70211 KYS, Kuopio, Finland.

Department of Clinical Neurophysiology, Kuopio University Hospital, P.O. Box 100, FIN-70029 KYS, Kuopio, Finland; Institute of Clinical Medicine, University of Eastern Finland, P.O. Box 1627, FIN-70211 KYS, Kuopio, Finland.

出版信息

Pathophysiology. 2017 Sep;24(3):197-203. doi: 10.1016/j.pathophys.2017.05.003. Epub 2017 May 31.

DOI:10.1016/j.pathophys.2017.05.003
PMID:28601366
Abstract

Obstructive sleep apnea (OSA) increases cardiovascular morbidity and mortality. Little is known on acute peri-apneic hemodynamic alterations due to apneas. We assessed these rapid changes and how duration of apnea might contribute to them. Eight patients with severe OSA were studied with polysomnography including continuous blood pressure monitoring. Peri-apneic hemodynamic alterations, heart rate, blood pressure, stroke volume, cardiac output and peripheral resistance, were assessed in short (<20s) and long (>27s) apneas. Systolic and diastolic blood pressure along with heart rate elevated significantly in both apneas. These changes occurred within first 10 beats immediately after apnea. In contrast to short apneas long apneas caused sudden increase of 0.7l in cardiac output. Acute and pronounced peri-apneic hemodynamic alterations were seen during both short and long apneas. These described rapid hemodynamic changes might escape autoregulatory mechanisms of several organs, thus making OSA patients vulnerable to acute cardiovascular events.

摘要

阻塞性睡眠呼吸暂停(OSA)会增加心血管疾病的发病率和死亡率。对于因呼吸暂停导致的急性呼吸暂停周围血流动力学改变,我们知之甚少。我们评估了这些快速变化以及呼吸暂停持续时间可能对其产生的影响。对8例重度OSA患者进行了多导睡眠图检查,包括连续血压监测。在短(<20秒)和长(>27秒)呼吸暂停期间,评估呼吸暂停周围的血流动力学改变、心率、血压、每搏输出量、心输出量和外周阻力。两种呼吸暂停时收缩压和舒张压以及心率均显著升高。这些变化发生在呼吸暂停后的前10次心跳内。与短呼吸暂停不同,长呼吸暂停导致心输出量突然增加0.7升。在短呼吸暂停和长呼吸暂停期间均观察到急性且明显的呼吸暂停周围血流动力学改变。这些所描述的快速血流动力学变化可能会逃过多个器官的自动调节机制,从而使OSA患者易发生急性心血管事件。

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