Abstract
This clinical case report presents synchronous physiological data from an individual in whom a spontaneous vasovagal reaction occurred without syncope. The physiological data are presented for three main phases: Baseline (0–200 s), vasovagal reaction (200–600 s), and recovery period (600–1200 s). The first physiological changes occurred at around 200 s, with a decrease in blood pressure, peak in heart rate and vastus lateralis tissue oxygenation, and a drop in alpha power. The vasovagal reaction was associated with a progressive decrease in blood pressure, heart rate and cerebral oxygenation, whilst the mean middle cerebral artery blood flow velocity and blood oxygen saturation remained unchanged. Heart rate variability parameters indicated significant parasympathetic activation with a decrease in sympathetic tone and increased baroreflex sensitivity. The total blood volume and tissue oxygenation index (TOI) dropped in the brain but slightly increased in the vastus lateralis, suggesting cerebral hypoperfusion with blood volume pooling in the lower body part. Cerebral hypoperfusion during the vasovagal reaction was associated with electroencephalography (EEG) flattening (i.e., decreased power in beta and theta activity) followed by an EEG high-amplitude “slow” phase (i.e., increased power in theta activity). The subject developed signs and symptoms of pre-syncope with EEG flattening and slowing during prolonged periods of symptomatic hypotension, but did not lose consciousness.
Highlights
Vasovagal reactions include arterial vasodilation and bradycardia as mechanisms that may precipitate a syncopal response (Lewis, 1932); defined as a transient loss of consciousness caused by cerebral hypoperfusion followed by spontaneous recovery (Freeman et al, 2011)
Two detection and emission probes were located on the forehead and on the vastus lateralis in order to measure tissue oxygenation index (TOI), defined as the ratio of oxy-hemoglobin to change of total hemoglobin concentration, and relative concentration of total hemoglobin in cerebral and muscular areas
EEG alpha power substantially decreased before the symptomatic vasovagal reaction (Figure 3B) in the frontal, central and posterior brain regions
Summary
Vasovagal reactions include arterial vasodilation and bradycardia as mechanisms that may precipitate a syncopal response (Lewis, 1932); defined as a transient loss of consciousness caused by cerebral hypoperfusion followed by spontaneous recovery (Freeman et al, 2011). The EEG signal shows EEG slowing during vasovagal reaction without and with syncope (loss of consciousness). This case study reports continuous physiological changes with simultaneous EEG results during a spontaneous and unexpected vasovagal reaction without loss of consciousness, which occurred in a young individual participating in a clinical trial. The subject remained conscious during vasovagal reaction but showed decreased postural tone and auditory impairment The study he was participating in was approved by the ethical committee of Zürich, Switzerland (201800006). Two detection and emission probes were located on the forehead and on the vastus lateralis in order to measure tissue oxygenation index (TOI), defined as the ratio of oxy-hemoglobin to change of total hemoglobin concentration, and relative concentration of total hemoglobin (tHb, normalized tissue hemoglobin index) in cerebral and muscular areas
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