Willson Grant N, Grunstein Ronald R, Kirjavainen Turkka, Young Iven H, Piper Amanda J, Sullivan Colin E, Wilcox Ian
Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Missenden Road, Camperdown, Sydney, NSW 2050, Australia.
J Sleep Res. 2007 Dec;16(4):421-7. doi: 10.1111/j.1365-2869.2007.00616.x.
This study examined the influence of electroencephalographic (EEG) arousal on the magnitude and morphology of the pressor response to Cheyne-Stokes respiration (CSR) in subjects with congestive heart failure (CHF). Thirteen subjects with stable CHF (left ventricular ejection fraction, 26 +/- 7%) and CSR (apnea-hypopnea index 52 +/- 15 h(-1)) underwent overnight polysomnography with beat-to-beat measurement of systemic arterial blood pressure (BP). CSR events were divided into those with or without an EEG arousal defined according to the criteria of the American Sleep Disorders Association. The pressor response was quantified in terms of the delta BP change (difference between the minimum BP during apnea and maximum BP during hyperpnea). Changes in the morphology of the pressor response were assessed by subdividing individual respiratory events into six periods (three during apnea: A1, A2, A3; and three during hyperpnea: H1, H2, H3). Considerable fluctuations in BP and heart rate (HR) were observed across the CSR cycle (delta mean BP 20.2 +/- 6.5 mmHg). The presence of an EEG arousal did not alter the amplitude of fluctuations in BP. Mean blood pressure (MBP) increased 21.0 +/- 7.5 mmHg with arousal versus 19.3 +/- 5.8 mmHg without arousal (NS). A repeated measures ANOVA showed no significant interaction between the presence of arousal and the proportional change in mean BP across the six periods, indicating that an EEG arousal had no effect on the morphology of MBP change during CSR [F(5,60) = 1.44, P = 0.22]. This study showed that EEG-defined arousal does not amplify the pressor response to CSR in CHF.
本研究探讨了脑电图(EEG)觉醒对充血性心力衰竭(CHF)患者对潮式呼吸(CSR)的升压反应幅度和形态的影响。13例稳定型CHF患者(左心室射血分数为26±7%)伴有CSR(呼吸暂停低通气指数为52±15次/小时),接受了整夜多导睡眠监测,并逐搏测量体循环动脉血压(BP)。根据美国睡眠障碍协会的标准,将CSR事件分为伴有或不伴有EEG觉醒的事件。通过收缩压变化量(呼吸暂停期间的最低血压与呼吸增强期间的最高血压之差)来量化升压反应。通过将个体呼吸事件细分为六个阶段(呼吸暂停期间三个:A1、A2、A3;呼吸增强期间三个:H1、H2、H3)来评估升压反应形态的变化。在整个CSR周期中观察到血压和心率(HR)有相当大波动(平均收缩压变化量为20.2±6.5mmHg)。EEG觉醒的存在并未改变血压波动幅度。有觉醒时平均血压(MBP)升高21.0±7.5mmHg,无觉醒时为19.3±5.8mmHg(无显著性差异)。重复测量方差分析显示,觉醒的存在与六个阶段平均血压的比例变化之间无显著交互作用,表明EEG觉醒对CSR期间MBP变化的形态无影响[F(5,60)=1.44,P=0.22]。本研究表明,EEG定义的觉醒不会增强CHF患者对CSR的升压反应。