Time-frequency dynamics in neurally mediated syncope
- 1 October 1992
- journal article
- research article
- Published by Springer Nature in Clinical Autonomic Research
- Vol. 2 (5) , 317-326
- https://doi.org/10.1007/bf01824302
Abstract
In this study, the responses during syncope were determined by noninvasive beat-to-beat analysis during passive orthostasis. Twenty patients with recurrent unexplained syncope (13 men and seven women) and ten healthy age-matched control subjects were studied during 80° head-up tilt for 25 min. Time-frequency mapping of R-R intervals, systolic and diastolic pressures and respiration was used to determine the responses to tilt. The spectral estimation was based on a modified Wigner distribution and the frequency content was evaluated on a beat-to-beat basis. Ten patients developed syncope (tiltpositive group) during tilt, while the remaining ten were asymptomatic (tilt-negative group). Control subjects reacted to tilt by the immediate shortening of R-R intervals to a plateau with an accompanying moderate increase in diastolic pressure. In the tilt-negative group the responses to tilt were similar, but of greater amplitude. In contrast, in the tilt-positive group, R-R intervals gradually and continuously decreased with tilt while systolic and diastolic pressures increased until shortly before syncope, when an abrupt fall in blood pressure followed by R-R intervals lengthening occurred. Furthermore, the R-R intervals fluctuations at both respiratory and nonrespiratory frequencies were the highest at rest as well as during tilt in the tilt-positive group. Nonrespiratory fluctuations in blood pressure increased more during tilt in both tilt-positive and negative groups compared to the control group. The nonrespiratory fluctuations in R-R intervals and blood pressure reached a maximum at syncope, simultaneously with hypotension and bradycardia. Time-frequency mapping has demonstrated that an elevated parasympathetic tone at rest which persists during orthostasis identifies patients prone to vasodepressor syncope. The counteracting sympathetic activation is not sustained and results in hypotension followed by cardioinhibition and loss of consciousness.Keywords
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