• Grant N Willson, Ronald R Grunstein, Turkka Kirjavainen, Iven H Young, Amanda J Piper, Colin E Sullivan, and Ian Wilcox.
• Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Missenden Road, Camperdown, Sydney, NSW 2050, Australia. gnw@med.usyd.edu.au
• J Sleep Res. 2007 Dec 1;16(4):421-7.

AbstractThis 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.

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