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Review
. 2016 Oct 25;7:460.
doi: 10.3389/fphys.2016.00460. eCollection 2016.

Modulations of Heart Rate, ECG, and Cardio-Respiratory Coupling Observed in Polysomnography

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Free PMC article
Review

Modulations of Heart Rate, ECG, and Cardio-Respiratory Coupling Observed in Polysomnography

Thomas Penzel et al. Front Physiol. .
Free PMC article

Abstract

The cardiac component of cardio-respiratory polysomnography is covered by ECG and heart rate recordings. However, their evaluation is often underrepresented in summarizing reports. As complements to EEG, EOG, and EMG, these signals provide diagnostic information for autonomic nervous activity during sleep. This review presents major methodological developments in sleep research regarding heart rate, ECG, and cardio-respiratory couplings in a chronological (historical) sequence. It presents physiological and pathophysiological insights related to sleep medicine obtained by new technical developments. Recorded nocturnal ECG facilitates conventional heart rate variability (HRV) analysis, studies of cyclical variations of heart rate, and analysis of ECG waveform. In healthy adults, the autonomous nervous system is regulated in totally different ways during wakefulness, slow-wave sleep, and REM sleep. Analysis of beat-to-beat heart-rate variations with statistical methods enables us to estimate sleep stages based on the differences in autonomic nervous system regulation. Furthermore, up to some degree, it is possible to track transitions from wakefulness to sleep by analysis of heart-rate variations. ECG and heart rate analysis allow assessment of selected sleep disorders as well. Sleep disordered breathing can be detected reliably by studying cyclical variation of heart rate combined with respiration-modulated changes in ECG morphology (amplitude of R wave and T wave).

Keywords: ECG; autonomic function; cardiovascular regulation; heart rate; sleep apnea; sleep stages.

Figures

Figure 1
Figure 1
This figure shows cyclical fluctuations of heart rate, in beats per minute, for a patient with obstructive sleep apnea, before CPAP therapy, in the time window at the top left. The plot shows 512 s of nocturnal heart rate per line. Below this plot is the spectral analysis of this same time window. To the right, in the same type of presentation, is the heart rate of the same patient after initiation of CPAP therapy. The cyclical fluctuations of heart rate that occur during sleep apnea have been eliminated. Lower, at the bottom right, is again the spectral analysis of the heart rate. The low frequencies, characteristic for apnea—around 0.02 Hz of the heart rate variability—have disappeared. This figure originated in the Sleep Lab of the University of Marburg, Germany, and was created around 1990 from digital recordings by an Atari computer.
Figure 2
Figure 2
This figure shows the spectral analysis of the cyclical variation in heart rate with obstructive sleep apnea (OSA): left and right. This is evident in the red zones at frequencies between 0 and 0.04 Hz, which belong to the very low frequency (VLF) band. The central area shows only normal respiration, evidenced by the bright strip in the frequency range around 0.2 Hz, which belongs to the high frequency (HF) band. IBI stands for “interbeat interval” and shows the inverse heart rate. This figure originated at the Computers in Cardiology Competition (taken from Penzel et al., 2002).
Figure 3
Figure 3
Example of variation of heart rate (15-min mean) due to sleep stage, circadian timing, and sleep deprivation in a young male subject recorded for a period of altogether 56 h (middle panel). The recording consists of a Baseline sleep recording at night of 8 h, followed by a period of 40 h of sustained wakefulness inducing sleep deprivation, and finished with a Recovery sleep recording at night. For Baseline sleep and Recovery sleep periods 1-min mean and 5-min moving average values of heart rate are plotted and aligned to the sleep stage distribution (Hypnogram, 30 s resolution) in addition (upper and lower panel). It can be seen that heart rate is modulated mostly by sleep stages resulting in quite stable values during NREM sleep (sleep stages S1, S2, S3, S4) and highly variable values during REM sleep (marked with red color bars) as well as during wakefulness (marked with gray color bars). In addition changes in heart rate in part occur due to sleep stage changes accompanied by body movements (MT). In addition throughout sleep a global trend for longer RR intervals (→ lower heart rate) in the morning hours due to circadian modulation could be observed. During Recovery sleep this effect is more pronounced maybe because of the modified sleep profile due to the rebound character of sleep after 40 h of wakefulness. During the 40 h period of sustained wakefulness starting at 08:00 h in the morning and finishing in the late evening the following day it can be clearly seen that heart rate is modulated in a sinusoidal fashion by the circadian system. Although no sleep is present, the RR interval maximum (→ lowest heart rate) occurs in the morning hours after ~20 h of wakefulness. In addition fluctuations of heart rate can be observed throughout the entire 40 h period caused by a limited amount of activity and different cognitive tasks. MT, Movement Time; Wake, Wake stage; REM, Rapid Eye Movement sleep stage; S1, None REM (NREM) sleep stage 1; S2, NREM sleep stage 2; S3, NREM sleep stage 3; S4, NREM sleep stage 4.
Figure 4
Figure 4
Occurrences of heartbeats (•), as a function of the respiratory phase (0° for initiation of inhalation; 180° for beginning of exhalation), as taken from a typical subject during deep sleep. The heart-rate trend (magenta plot) shows respiratory sinus arrhythmia (RSA)—accelerated heartbeat during inhalation and retarded heartbeat during exhalation. The intensity of the RSA is determined by the amplitude of sinus modulation.
Figure 5
Figure 5
This figure shows simultaneous occurrence of respiratory sinus arrhythmia (magenta plot) and cardiorespiratory phase synchronization (blue circles). During synchronization, heartbeats occur more frequently during particular respiratory phases: here, three heartbeats take place during one respiratory cycle (dots in the blue circles; based on Bartsch et al., 2012).
Figure 6
Figure 6
The amplitude of respiratory sinus arrhythmia is distinctly a function of respiratory rate, and is most pronounced at ~5 respiratory cycles per minute (black squares). In contrast, the mean duration of episodes with phase synchronization exhibits no dependency on respiratory rate (red circles; based on Bartsch et al., 2012).
Figure 7
Figure 7
This figure shows examples of cardiorespiratory coordination during and after apnea events. The upper plot shows a so-called coordigram where the cardiorespiratory coordination is characterized by red horizontal strips. The black bars below display the detected episodes of coordination. For comparison, the second color-coded plot is the related synchrogram where again red horizontal strips characterize cardiorespiratory phase synchronization. As in the plot above, the black bars at the bottom display the detected periods of phase synchronization. The third plot shows the associated alterations of beat-to-beat intervals, with the characteristic cyclical variations that are triggered by apnea events. The fourth plot shows the associated signal for abdominal respiratory movement, with the characteristic pattern of consecutive obstructive apnea events (marked by horizontal red bars).
Figure 8
Figure 8
This figure depicts the spectrogram of heart rate for a patient with heart failure and Cheyne-Stokes breathing. The study took place in 2014 at the Interdisciplinary Sleep Medicine Center, Charité Universitätsmedizin Berlin, with application of the M1 device that records ECG, heart rate, respiration calculated by EDR, snoring, and body position. The plot results from an analysis of heart-rate variability: top signal, with marking corresponding to the dominance of high-frequency coupling (HFC), low-frequency coupling (LFC), and very low-frequency coupling (vLFC). The figure also shows an approximation of sleep stages: second signal block from the top with marking of REM, stable non-REM (shown as Stb. NR), unstable non-REM (shown as Uns. NR), and wake stages (shown as Wake). The plots at the bottom show the spectrograms of cardiorespiratory coupling (see main text), indicators for body position (up for upright, left, prone, right, and supine), the intensity of actigraphy (Act), and snoring events (Snore). This evaluation distinctly reveals impaired sleep.

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