What is the clinical evidence from this study?

Study design: Observational. Population: Healthy (n=75). Intervention: Sleep stages and cycles (SWS vs REM) vs. Pre-sleep and between sleep stages. Primary outcome: Heart rate variability (HRV) parameters (Mean NN, SDNN, rMSSD, LF, HF, LF:HF) across sleep stages (p=<0.001).

February 21, 2020Open Access

The Inconsistent Nature of Heart Rate Variability During Sleep in Normal Children and Adolescents

Q: What are the key findings of this study?

Heart rate variability parameters varied significantly across sleep stages and cycles throughout the night, with mean NN being lowest during pre-sleep and increasing significantly across slow wave sleep cycles (p<0.001).

Key Result

Heart rate variability parameters varied significantly across sleep stages and cycles throughout the night, with mean NN being lowest during pre-sleep and increasing significantly across slow wave sleep cycles (p<0.001).

Study Design

Type

Observational (n=75)

Multicenter

Structured PICO

Does heart rate variability change significantly across different sleep stages and cycles in healthy children and adolescents?

Population

75 healthy children and adolescents aged 3.1 to 13.2 years underwent overnight polysomnography to evaluate heart rate variability across different sleep stages and cycles.

Exposure

Observation of electrocardiography during progressive cycles of slow wave sleep (SWS1, SWS2, SWS3) and rapid eye movement sleep (REM1, REM2, REM3).

Comparator

Pre-sleep baseline (3-minute segment of electrocardiography just prior to sleep onset) and comparisons between different sleep stages.

Outcome

Heart rate variability (HRV) parameters including time domain values (mean NN, SDNN, RMSSD) and frequency domain values (LF, HF, LF:HF) across sleep stages.surrogate

Heart rate variability parameters fluctuate significantly across different sleep stages and cycles in healthy children, indicating that time of night and sleep stage must be accounted for in HRV assessments.

Main Result

p-value: p=<0.001

Limitations

Vascular resistance was not measured directly during sleep.
Some high frequency (HF) power may have been excluded in very small children due to higher breathing rates (>0.4 Hz).
Analysis was restricted to children whose REM3 period preceded SWS3, reducing the sample size from 118 to 75.

Abstract

Introduction: Cardiac function is modulated by multiple factors including exogenous (circadian rhythm) and endogenous (ultradian 90-110min sleep cycle) factors. By evaluating heart rate variability (HRV) during sleep, we will better understand their influence on cardiac activity. The aim of this study was to evaluate HRV in the dark phase of the circadian rhythm during sleep in healthy children and adolescents. Methods: One three minute segment of pre-sleep electrocardiography (EEG) and three, six minute segments of electrocardiography recorded during polysomnography from 75 healthy children and adolescents were sampled during progressive cycles of slow wave sleep (SWS1, SWS2, SWS3). Three, three minute segments of rapid eye movement sleep (REM) were also assessed, with REM1 marked at the last REM period before awakening. Studies that recorded REM3 prior to SWS3 were used for assessment. HRV variables include the following time domain values: mean NN (average RR intervals over given time), SDNN (Standard Deviation of RR intervals), and RMSSD (root-mean-square of beat-to-beat differences). Frequency domain values include: low frequency (LF), high frequency (HF) and LF:HF. Results: Mixed linear effects model analysis showed a significant difference in time and frequency domain values between sleep cycles and stages. Mean NN was lowest (highest heart rate) during pre –sleep then increased significantly during SWS1 and subsequent SWS cycles. Mean NN in SWS1 was similar to all REM periods which was significantly lower than both SWS2 and SWS3. SDNN remained at pre-sleep levels until SWS3, and then significantly increased in REM1&2. There was a large drop in LF from pre-sleep to SWS1. As cycles progressed through the night, LF remains lower than awake but increases to awake like levels by REM2. RMSSD and HF were lowest in pre-sleep and increased significantly by SWS1 and remain high and stable across stages and cycles except during the REM3 period where RMSSD decreased. Conclusion: Our results demonstrate that there are considerable changes in the spectral analysis of cardiac function occurring during different sleep stages and between sleep cycles across the night. Hence, time of night and sleep stage need to be considered when reporting any HRV differences.

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