Hb. Hopf et al., LOW-FREQUENCY SPECTRAL POWER OF HEART-RATE-VARIABILITY IS NOT A SPECIFIC MARKER OF CARDIAC SYMPATHETIC MODULATION, Anesthesiology, 82(3), 1995, pp. 609-619
Background: Heart rate variability in the frequency domain has been pr
oposed to reflect cardiac autonomic control. Therefore, measurement of
heart rate variability may be useful to assess the effect of epidural
anesthesia on cardiac autonomic tone, Accordingly, the effects of pre
ganglionic cardiac sympathetic blockade by segmental epidural anesthes
ia were evaluated in humans on spectral power of heart rate variabilit
y, Specifically, the hypothesis that cardiac sympathetic blockade atte
nuates low-frequency spectral power, assumed to reflect cardiac sympat
hetic modulation, was tested. Methods: Ten subjects were studied while
supine and during a 15-min 40-degrees head-up tilt both before and af
ter cardiac sympathetic blockade by segmental thoracic epidural anesth
esia (sensory block: C6-T6). EGG, arterial pressure, and respiratory e
xcursion (Whitney gauge) were recorded, and a fast-Fiourier-transforma
tion was applied to 512-s data segments of heart rate derived from the
digitized ECG at the end of each intervention. Results: With cardiac
sympathetic blockade alone and the subjects supine, both low-frequency
(LF, 0.06-0.15 Hz) and high-frequency (HF, 0.15-0.80 Hz) spectral pow
er remained unchanged. During tilt, epidural anesthesia attenuated the
evoked increase in heart rate (+11 . min(-1) +/- 7 SD vs. +6 +/- 7, P
= 0.024). However, while during tilt cardiac sympathetic blockade sig
nificantly decreased the LF/HF ratio (3.68 +/- 2.52 vs. 2.85 +/- 2.15,
P = 0.041 vs. tilt before sympathetic blockade), a presumed marker of
sympathovagal interaction, absolute and fractional LF and HF power di
d not change. Conclusions: Although preganglionic cardiac sympathetic
blockade reduced the LF/HF ratio during tilt, it did not alter spectra
l power in the LF band during rest or tilt, Accordingly, low-frequency
spectral power is unlikely to specifically reflect cardiac sympatheti
c modulation in humans.