Spectral analysis of heart rate variability during quiet sleep in normal human fetuses between 36 and 40 weeks of gestation

Abstract

Respiratory sinus arrhythmia (RSA) is a clinical manifestation of the parasympathetic nervous system which can be identified in the high-frequency region of the heart rate variability (HRV) power spectrum. The purpose of this study was to determine the relative contribution of RSA to overall HRV for human fetuses in quiet sleep. The study population consisted of 13 normal human fetuses between 36 and 40 weeks of gestation for whom data were collected during spontaneous breathing and normally occurring apneic periods. Fetal breathing was monitored continuously using real-time sonography. The fetal electrocardiogram was captured transabdominally in 3-min blocks at a rate of 833 Hz and fetal R-waves were extracted from the raw signal using adaptive signal processing techniques. Fetal behavioral state was determined at the beginning and end of each 3-min data collection period. The fetal R-wave interbeat intervals (IBIs) were converted to equally-spaced, time-based data, and linear detrending of the time series was accomplished by subtracting the mean heart period from each weighted IBI. Total power (TP, 0.0–2.5 Hz) was divided into RSA (0.4–1.0 Hz), high-frequency (HF, 0.2–2.5 Hz), low-frequency (LF, 0.04–0.2 Hz), and very-low-frequency (VLF 0.0–0.04 Hz) regions, and the power densities were summed to determine the absolute power for each frequency component. A total of 81 3 min blocks (mean per subject 6.3, range 2–14) were available for analysis. Eleven (85%) of 13 fetuses demonstrated at HF peak during fetal breathing, and RSA accounted for approximately 20% of the TP. Although HF amplitude was reduced in the absence of fetal respiratory activity, RSA did not invariably disappear during periods of apnea, as the HF peak was recognized in seven (54%) fetuses when no respiratory activity was observed. Total power was approximately evenly distributed between the VLF, LF, and HF regions, and this distribution was independent of whether the fetus was breathing or not. However, the absolute power was significantly greater ( P < 0.05) during breathing as compared to non-breathing for TP and for the VLF, LF, HF, and RSA components. We conclude that RSA is common in normal human fetuses and is a significant factor contributing to HRV.