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The occurrence of individual slow waves in sleep is predicted by heart rate.

ABSTRACT: The integration of near-infrared spectroscopy and electroencephalography measures presents an ideal method to study the haemodynamics of sleep. While the cortical dynamics and neuro-modulating influences affecting the transition from wakefulness to sleep is well researched, the assumption has been that individual slow waves, the hallmark of deep sleep, are spontaneously occurring cortical events. By creating event-related potentials from the NIRS recording, time-locked to the onset of thousands of individual slow waves, we show the onset of slow waves is phase-locked to an ongoing oscillation in the NIRS recording. This oscillation stems from the moment to moment fluctuations of light absorption caused by arterial pulsations driven by the heart beat. The same oscillating signal can be detected if the electrocardiogram is time-locked to the onset of the slow wave. The ongoing NIRS oscillation suggests that individual slow wave initiation is dependent on that signal, and not the other way round. However, the precise causal links remain speculative. We propose several potential mechanisms: that the heart-beat or arterial pulsation acts as a stimulus which evokes a down-state; local fluctuations in energy supply may lead to a network effect of hyperpolarization; that the arterial pulsations lead to corresponding changes in the cerebral-spinal-fluid which evokes the slow wave; or that a third neural generator, regulating heart rate and slow waves may be involved.

SUBMITTER: Mensen A

PROVIDER: S-EPMC4957222 | biostudies-other | 2016 Jul

REPOSITORIES: biostudies-other

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The occurrence of individual slow waves in sleep is predicted by heart rate.

Mensen Armand A Zhang Zhongxing Z Qi Ming M Khatami Ramin R

Scientific reports 20160722

The integration of near-infrared spectroscopy and electroencephalography measures presents an ideal method to study the haemodynamics of sleep. While the cortical dynamics and neuro-modulating influences affecting the transition from wakefulness to sleep is well researched, the assumption has been that individual slow waves, the hallmark of deep sleep, are spontaneously occurring cortical events. By creating event-related potentials from the NIRS recording, time-locked to the onset of thousands ...[more]

PMID: 27445083

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Project description:BackgroundPropofol causes significant cardiovascular depression and a slowing of neurophysiological activity. However, literature on its effect on the heart rate remains mixed, and it is not known whether cortical slow waves are related to cardiac activity in propofol anesthesia.MethodsThe authors performed a secondary analysis of electrocardiographic and electroencephalographic data collected as part of a previously published study where n = 16 healthy volunteers underwent a slow infusion of propofol up to an estimated effect-site concentration of 4 µg/ml. Heart rate, heart rate variability, and individual slow electroencephalographic waves were extracted for each subject. Timing between slow-wave start and the preceding R-wave was tested against a uniform random surrogate. Heart rate data were further examined as a post hoc analysis in n = 96 members of an American Society of Anesthesiologists Physical Status II/III older clinical population collected as part of the AlphaMax trial.ResultsThe slow propofol infusion increased the heart rate in a dose-dependent manner (mean ± SD, increase of +4.2 ± 1.5 beats/min/[μg ml-1]; P < 0.001). The effect was smaller but still significant in the older clinical population. In healthy volunteers, propofol decreased the electrocardiogram R-wave amplitude (median [25th to 75th percentile], decrease of -83 [-245 to -28] μV; P < 0.001). Heart rate variability showed a loss of high-frequency parasympathetic activity. Individual cortical slow waves were coupled to the heartbeat. Heartbeat incidence peaked about 450 ms before slow-wave onset, and mean slow-wave frequency correlated with mean heart rate.ConclusionsThe authors observed a robust increase in heart rate with increasing propofol concentrations in healthy volunteers and patients. This was likely due to decreased parasympathetic cardioinhibition. Similar to non-rapid eye movement sleep, cortical slow waves are coupled to the cardiac rhythm, perhaps due to a common brainstem generator.Editor’s perspective

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The occurrence of individual slow waves in sleep is predicted by heart rate.

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The occurrence of individual slow waves in sleep is predicted by heart rate.

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