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

Peri-apneic hemodynamic reactions in obstructive sleep apnea.

Author information

1
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. Electronic address: anu.muraja-murro@kuh.fi.
2
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.
3
Department of Clinical Neurophysiology, Kuopio University Hospital, P.O. Box 100, FIN-70029 KYS, Kuopio, Finland; Department of Applied Physics, University of Eastern Finland, P.O. Box 1627, FIN-70211 KYS, Kuopio, Finland.
4
Department of Clinical Physiology and Nuclear Medicine, 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.

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.

KEYWORDS:

Cardiovascular morbidity; Hemodynamic changes; Sleep apnea

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