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Am J Physiol Regul Integr Comp Physiol (November 16, 2006). doi:10.1152/ajpregu.00642.2006
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Submitted on September 12, 2006
Accepted on November 4, 2006

Cardiac changes during arousals from non-REM sleep in healthy volunteers

Eugene Nalivaiko1*, Peter G Catcheside2, Amanda Adams2, Amy S Jordan2, Danny J Eckert2, and R Doug McEvoy3

1 Human Physiology, Flinders University, Adelaide, South Australia, Australia
2 Adelaide Institute for Sleep Health, Repatriation General Hospital, Adelaide, South Australia, Australia
3 Repatriation General Hospital, Adelaide Institute for Sleep Health, Adelaide, South Australia, Australia

* To whom correspondence should be addressed. E-mail: eugene.nalivaiko{at}flinders.edu.au.

Our aim was to evaluate cardiac changes evoked by spontaneous and sound-induced arousals from sleep. Cardiac responses to spontaneous and auditory-induced arousals were recorded during overnight sleep studies in 28 young healthy subjects (14 males, 14 females) during non-REM sleep. Computerised analysis was applied to assess beat-to-beat changes in heart rate, atrio-ventricular conductance and ventricular repolarisation from 30 s prior to 60 s after the auditory tone. During both types of arousals, the most consistent change was the increase in the heart rate (in 62% of spontaneous and in 89% of sound-induced arousals). This was accompanied by an increase or no change in PR interval and by a decrease or no change in QT interval. The magnitude of all cardiac changes was significantly higher for tone-induced vs. spontaneous arousals (mean±SD for heart rate: +9±8 vs. +13±9 beats per min; for PR prolongation: 14±16 vs. 24±22 ms; for QT shortening: -12±6 vs. -20±9 ms). The prevalence of transient tachycardia and PR prolongation was also significantly higher for tone-induced vs. spontaneous arousals (tachycardia: 85% vs. 57% of arousals, p<0.001; PR prolongation: 51% vs. 25% of arousals, p<0.001). All cardiac responses were short-lasting (10-15 s). We conclude that cardiac pacemaker region, conducting system and ventricular myocardium may be under independent neural control. Prolongation of atrio-ventricular delay may serve to increase ventricular filling during arousal from sleep. Whether prolonged atrio-ventricular conductance associated with increased sympathetic outflow to the ventricular myocardium contributes to arrhythmogenesis during sudden arousal from sleep remains to be evaluated.




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[Abstract] [Full Text] [PDF]




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