Key result
Sound-induced arousals from non-REM sleep resulted in a significantly higher prevalence of transient tachycardia (85% vs 57%, P<0.001) compared to spontaneous arousals.
Why the study?
Do sound-induced arousals evoke different cardiac changes compared to spontaneous arousals during non-REM sleep in healthy volunteers?
Observational (n=28)
Do sound-induced arousals evoke different cardiac changes compared to spontaneous arousals during non-REM sleep in healthy volunteers?
Sound-induced arousals from non-REM sleep elicit more pronounced transient tachycardia, PR prolongation, and QT shortening than spontaneous arousals in healthy volunteers.
Answers are grounded in this paper and cite their sources.
Arousals from NREM sleep trigger acute cardiac responses in healthy adults; leaves open whether these extend to CV risk prediction in sleep-disordered populations.
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-rapid eye movement sleep. Computerized analysis was applied to assess beat-to-beat changes in heart rate, atrio-ventricular conductance, and ventricular repolarization from 30 s before 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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Nalivaiko et al. (2006) conducted an observational in Healthy volunteers (n=28). Sound-induced arousals vs. Spontaneous arousals was evaluated on Prevalence of transient tachycardia (p=<0.001). Sound-induced arousals from non-REM sleep resulted in a significantly higher prevalence of transient tachycardia (85% vs 57%, P<0.001) compared to spontaneous arousals.
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