njit-etd2003-081 - New Jersey Institute of Technology

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In 1985, Akselrod et al. studied beat-to-beat variability of blood pressure, as well
as heart rate, in response to respiration [11]. They concluded that blood pressure
fluctuations at the respiratory frequency result almost entirely from the direct effect of
centrally mediated heart rate fluctuations. Lower frequency fluctuations in blood
pressure were associated with variability in vasomotor activity. Madwed et al.
specifically investigated the low frequency oscillations in arterial blood pressure and
heart rate using a simple computer model [12], but later applied their techniques to
evaluate low frequency oscillations in arterial pressure during induced hemorrhage in
dogs [13]. During hemorrhage, they found that the low frequency oscillations were
dominant over the higher frequency respiratory related fluctuations, in contrast with the
baseline condition. Lipsitz et al. studied the spectral characteristics of heart rate
variability in response to postural tilt [14]. They found that total heart rate variability
increases upon tilting in the young, while heart rate variability remained unchanged for
older subjects during tilt. Malliani et al. studied cardiovascular neural regulation in the
frequency domain, and found that the ratio of high frequency to low frequency power in
heart rate variability is reflective of sympatho-vagal balance [15]. They concluded that
functional states accompanied by an increased sympathetic activity are characterized by
a shift in the balance of heart rate spectral power towards low frequency, and the
opposite occurs during increased vagal activity, where the balance shifts towards high
frequency spectral power in heart rate. Sleight et al. investigated the physiology and
pathophysiology of heart rate and blood pressure variability in humans, finding that
spectral analysis of cardiovascular variability is more a measure of baroreflex gain than
of specific sympathetic or parasympathetic tone, or the balance between them [16].