Effect of low-dose atropine on heart rate fluctuations during orthostatic load: a spectral analysis

Weise, F.; Baltrusch, Kyle M.; Heydenreich, F.

doi:10.1016/0165-1838(89)90171-9

Cited by 30 publications

(13 citation statements)

References 17 publications

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“…The present finding corroborates the data previously obtained in steady-state conditions using small bolus doses of atropine [1,21,31,44]. It is likely that atropine, at a low dose, activated the vagus within a physiological range, which enabled the vagal tone to be modulated [28].…”

Section: Discussionsupporting

confidence: 94%

“…This study aimed to use the smoothed pseudo-Wigner-Ville transformation (SPWVT) to perform an instant time-/frequency-domain analysis of the continuous (fast) changes in vagal activity occurring during an infusion of atropine. In addition, this procedure allows estimation of RSA during the short initial "paradoxical" vagomimetic period, resulting from a low dose of atropine which is observed prior to the vagolytic effect associated with higher doses of the drug [1,21,31,44,45]. This study was carried out using healthy volunteers following beta-adrenoceptor blockade and during controlled respiration.…”

Section: Introductionmentioning

confidence: 99%

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Relationship between pulse interval and respiratory sinus arrhythmia: a time- and frequency-domain analysis of the effects of atropine

Médigue

Girard

Laude

et al. 2001

Pflügers Arch - Eur J Physiol

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Respiratory sinus arrhythmia (RSA) estimation is commonly used as a non-invasive index of cardiac vagal tone. To test this relationship, vagal tone was augmented or blocked using atropine. The study was carried out using 14 healthy volunteers, following beta-adrenoceptor blockade (10 mg bisoprolol per os) and during controlled respiration (0.25 Hz) in order to limit the confounding effects of cardiac sympathetic tone and respiration pattern changes. Atropine was slowly infused intravenously over a 30-min period up to a vagolytic cumulative dose of 0.04 mg/kg. The instant vagal tone was compared to the instant RSA value obtained from a time-/frequency-domain analysis of pulse interval (PI). RSA and PI varied in the same direction with an initial increase corresponding to the early vagomimetic effect of atropine followed by a decrease during the vagolytic phase. The comparative percentage fluctuations of RSA and PI over this large vagal tone range indicate that RSA is more sensitive (about twofold) than PI in reflecting fluctuations around the set point. This dissociated behaviour of PI and heart rate variability could be important to our understanding of the circulatory changes that result from fluctuations in vagal inputs to the sinus node.

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Relationship between pulse interval and respiratory sinus arrhythmia: a time- and frequency-domain analysis of the effects of atropine

Médigue

Girard

Laude

et al. 2001

Pflügers Arch - Eur J Physiol

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“…A leftward shift of the LF peak was found in healthy humans during HUT or exercise [16,17], whereas a rightward shift was detected in post-exercise recovery and after vagal stimulation with very low doses of atropine [16,18]. It is difficult to relate these observations to our results, since neither the patients nor the controls with poor orthostatic tolerance showed any clear sign of enhanced sympathetic activation or decreased vagal activity.…”

Section: Discussioncontrasting

confidence: 79%

Cross-spectral analysis of cardiovascular parameters whilst supine may identify subjects with poor orthostatic tolerance

et al. 2003

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An easy and low-cost method for identification of subjects prone to orthostatic vasovagal syncope would be of clinical benefit. An orthostatic test with 60 degrees head-up tilt and progressive lower-body negative pressure was performed on 79 patients with histories of unexplained syncope and 26 control subjects. The test was stopped at the onset of presyncope and time to presyncope was taken as a measure of orthostatic tolerance. Spectral and cross-spectral analysis was performed on the supine time series of the R-R interval (ECG) and systolic pressure (Finapres) recorded before the beginning of the test. According to reference values, 38 patients and 11 controls were classified as having poor orthostatic tolerance (PPT and CPT respectively), whereas 41 patients and 15 controls displayed normal orthostatic tolerance (PNT and CNT respectively). The central frequency of the low-frequency (LF approximately equal to 0.1 Hz.) oscillations in PNT and CNT was significantly higher than that in PPT and CPT. In addition, it was significantly linearly correlated with the time of presyncope. Using our test of orthostatic tolerance as a comparison, the LF central frequency allows the classification of subjects with poor or normal tolerance with 80% sensitivity and 82% specificity. These results suggest that the LF central frequency in the supine position may provide a useful index in the diagnosis of orthostatic intolerance.

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“…Similar changes have also been seen during exercise [34]. Following exercise or after vagal stimulation with low doses of atropine, the frequency increased [34,35]. Decreases also occur in diabetic and other neuropathies, anesthesia, and hemorrhage [19,32,36].…”

Section: Autonomic Function In Subjects During Orthostatic Stressmentioning

confidence: 71%

Spectral and cross-spectral autoregressive analysis of cardiovascular variables in subjects with different degrees of orthostatic tolerance

Gulli

Wight

Hainsworth

et al. 2001

Clinical Autonomic Research

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The mechanisms leading to vasovagal syncope are still unclear. A simple discriminating test for the identification of syncopeprone subjects is not presently available. Fifty-two subjects had a stepwise orthostatic test with 60 ~ tilt and -20 and -40 mm Hg lower-body negative pressure before the appearance of impending syncope symptoms. Spectral and cross-spectral analyses of heart period and systolic pressure time series were performed to estimate the power of the high-frequency (= 0.25 Hz) and low-frequency (= 0.1 Hz) oscillations, the coherence between heart period and systolic pressure, and the mean low-frequency and high-frequency central frequency, phase shift, and transfer fimction at maximal coherence. According to time to presyncope, the 52 subjects were divided into two groups: 25 with normal orthostatic tolerance, and 27 with poor orthostatic tolerance. In the supine positions, the mean central low-frequency was significantly lower in poortolerance group than in normal-tolerance group, discriminating poor from normal orthostatic tolerance with 80% specificity and 83% sensitivity, and was significantly correlated to time to presyncope. In the 2 to 3 minutes preceding syncope, subjects with poor orthostatic tolerance had less tachycardia, lower low-frequency power of systolic pressure, higher respiratory frequency, and a less negative phase shift in highfrequency range. In presyncope, sympathetic activation is reduced in subjects with poor orthostatic tolerance. In addition, the higher breathing frequency and the smaller negativity of phase shift in high-frequency range, which may indicate an inadequate engagement of the baroreflex, suggest a causal role of respiration in the development of syncope. Supine central values of low frequency may be proposed as a valuable clinical index of orthostatic intolerance. Received April 20, 2000; accepted as revised February 22, 2001Vasovagal, or neurocardiogenic, syncope is a sudden onset ofhypotension often associated with bradycardia and sometimes asystole, and leads to a short period of loss of consciousness that is usually followed by a rapid and complete recovery. Although the actual trigger mechanisms for the attack are still debated, it is now well established that there is an inappropriate change in autonomic nervous activity consisting of sympathetic withdrawal and often an increase in vagal efferent discharge [1,2]. Vasodilatation is the dominant syncope-initiating effect because prevention of bradycardia by administration of atropine or by cardiac pacing does not usually prevent the hypotension [3,4].Vasovagal attacks are associated with decreased cardiac filling and can be reproduced in a laboratory by applying a sufficiently severe orthostatic stress. Sometimes, a period of passive head-up tilting alone can induce the attacks [5], but often it is necessary to increase the stress by combining it with a vasodilator, such as isoproterenol [6] or nitrate [7], or by combining head-up tilting with suction applied to the lower body [8]. However, it may not alw...

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Effect of low-dose atropine on heart rate fluctuations during orthostatic load: a spectral analysis

Cited by 30 publications

References 17 publications

Relationship between pulse interval and respiratory sinus arrhythmia: a time- and frequency-domain analysis of the effects of atropine

Relationship between pulse interval and respiratory sinus arrhythmia: a time- and frequency-domain analysis of the effects of atropine

Cross-spectral analysis of cardiovascular parameters whilst supine may identify subjects with poor orthostatic tolerance

Spectral and cross-spectral autoregressive analysis of cardiovascular variables in subjects with different degrees of orthostatic tolerance

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