To understand the sequence of hemodynamic events elicited by active (stand-up) and passive (head-up tilt, HUT) changes in posture, we monitored heart rate and arterial blood pressure continuously in ten healthy volunteers at rest, during rapid tilts (7s' HUTover 2 secs), slow tilts (75" HUToverSOsecs), andstand tests. A marked initial transient dmp in mean arterial pressure (MAP) and increase in heart rate (HR) seen during rapid tilt, RZ and stand-up, SU, were absent during slow tilt, SZ While the magnitudes of transient heart rate peak and blood pressure minimum for RT and SU, respectively, were different, their relative timing was well preserved. We attribute the fiming to the response of homeostatic repex mechanisms. No statistically significant difference could be detected when comparing steady-state values of MAP and HR for SU and HUT 140 seconds afer the onset of the respective stress. IntroductionCardiovascular adaptation to the upright posture depends on the proper interplay of the hemodynamic system and the reflex mechanisms that maintain blood pressure homeostasis. Failure of one of the subsystems to adapt to the gravitation-induced shifts in blood volume often results in a collection of clinical symptoms termed orthostatic intolerance (01).Clinically, 01 is diagnosed on the basis of a drop in arterial blood pressure or an excessive increase in heart rate measured a certain time after the assumption of the upright posture. However, little is learned about the mechanisms underlying 0 1 by making a single isolated measurements of MAP and HR at a certain time after onset of gravitational stress. Research done in our laboratory aims at using the information contained in the transient response of hemodynamic variables to gravitational stress to identify mechanisms underlying cardiovascular maladaptation to the upright posture. To achieve this goal, it is necessary to understand better the transient hemodynamic events elicited by an active change in posture and passive changes in posture. Specifically, we are interested in quantifying the degree of similarity between the hemodynamic responses seen during stand up, rapid, and slow head-up tilt. 2. MethodsWe recruited ten healthy volunteers (5 males. 5 females) to participate in this study. The mean age was 28.7f1.2 years, the mean height was 172.8f4.0 cm, and the mean weight was 70.6f4.5 kg'. Participants regularly engaged in light to moderate physical activity and had no sign of cardiovascular disease. Each volunteer gave written, informed consent prior to participation in the study. Each participant was instrumented with a standard clinical ECG monitor and a non-invasive blood pressure monitoring device (FINAPRES). ECG and the arterial pressure waveforms were recorded throughout the duration of the experiment. After instrumentation, subjects rested on a tilt table with foot support and subsequently underwent a series of six changes in posture: two stand-ups, two rapid HUTs (75" HUT over 2 secs), and two slow HUTs (75' HUT over 50 secs) each lasting ...
To understand the association of heart rate control with rapid eye movement, we studied heart rate and eye movement continuously during sleep in 10 IntroductionNormal sleep is characterized by cycles of non-rapideye-movement followed by rapid-eye-movement (REM) sleep, with typically 5-6 cycles of durations approximately 90 minutes over the course of the night. While heart rate during sleep has been studied in the past for both rapid eye movement (REM) sleep and non-REM sleep [1][2][3][4], there remains a lack of consensus whether the rapid eye movement during sleep elicit consistent heart rate response, partly due to the difficulty in extracting eye movements from noisy electrooculogram (EOG) signals. We characterized the association of heart rate control with rapid eye movement by studying heart rate and eye movement continuously during sleep in 10 young, healthy subjects. MethodsWe studied 10 young healthy subjects, who did not suffer from any sleep disorder. Subjects had regular sleep habits. None of the subjects were taking any medication.The study took place over 3 nights in a sound-proof, airconditioned (22-24Celcius) sleep room. Polysomnographic recordings included EOG, electroencephalogram (EEG), chin electromyogram (EMG) and ECG. Subjects went to bed at their regular bedtime and got up spontaneously. The first and second nights were used for habituation, and the data obtained on the third night was used for analysis.The HR was obtained from ECG recordings during sleep. Sleep stages were scored using standard Rechtschaffen Kales criteria [5]. Eye electrodes are attached on the upper-outer edge of the right eye and lower-outer edge of the left eye, with a common electrode on the left mastoid. If both eyes move in the same direction, the polarity of the both eye potentials will be opposite, and vise versa. In order to avoid detecting transmitted EEG potentials from frontal lobes, two signals that have the same polarity are omitted. EOG data were digitized with a sampling rate of 64Hz. Each eye movement was extracted from EOG recordings using semi-automated algorithm followed by physician's confirmation (Fig. 1).We computed the detrended fluctuations analysis (DFA) exponents [6][7][8][9] of HRV during non-REM sleep and REM sleep. Exponents are calculated from linear fits to log-log plots of F(n) versus n in the regime 70 < n < 300. We chose this fitting range to be above the regime of short-range correlations related to breathing and below the n values where statistical errors become too large due to the finite length of the sleep stages.We analyzed instantaneous heart rate before and after the onset of the rapid eye movements. The maximum HR of moving 10 second window average between the onset and 30 second after the onset of rapid eye movements are compared with the 30 seconds average HR before the onset.
Recently, it has come to be accepted that the result of the tilt test is specific to neurally mediated syncope (vasovagal syncope). Only rarely is a case of paroxysmal atrial fibrillation without any organic diseases in childhood reported. A case reported here of a 14‐year‐old boy with neurally mediated syncope; which was complicated by paroxysmal atrial fibrillation, and which was diagnosed by performing the tilt test. Atrial fibrillation can be induced by the extraordinary stimulation of the vagal nerve during syncope. In a child, neurally mediated syncope complicated with paroxysmal atrial fibrillation has not been previously reported.
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