Relation of Postural Vasovagal Syncope to Splanchnic Hypervolemia in Adolescents

Stewart, Julian M.; McLeod, Kenneth J.; Sanyal, Sanjukta; Herzberg, Gilbert Z.; Montgomery, Leslie D.

doi:10.1161/01.cir.0000145543.88293.21

Cited by 64 publications

(67 citation statements)

References 33 publications

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“…Interestingly, the temporal loss of the cardiovagal baroreflex in fainters coincides with the loss of cerebral autoregulation that we previously reported (25) and also coincides with maximum thoracic hypovolemia and the onset of hyperpnea (39,41). Our previous data suggest that excessive thoracic hypovolemia during orthostasis results in progressive deterioration of the cardiovagal baroreflex, hyperpnea, and progressive enhancement of respiratory control of HR and blood pressure, which via pulmonary stretch sympatholytic and vagotonic reflexes contribute to the characteristic hypotension and bradycardia of vasovagal syncope.…”

Section: H533 Cardiovagal Phase Synchronization and Directionality Dusupporting

confidence: 79%

“…Phase synchronization methods succeed in demonstrating this link. Thus there is support for the proposal that cardiovagal activity is lost before fainting and superseded by hyperpnea and hyperventilation induced through thoracic hypovolemia, which in turn drives changes in HR and arterial pressure (16,39,41).…”

Section: H535 Cardiovagal Phase Synchronization and Directionality Dumentioning

confidence: 92%

“…The reasons for this are unknown but may relate to the loss of the baroreflex. We have shown in fainters that there is excessive gravitational pooling of blood within the dependent vasculature with resultant thoracic hypovolemia and impaired compensatory splanchnic vasoconstriction and venoconstriction (24,39,41). Splanchnic pooling does not necessarily provoke fainting and can occur in forms of chronic orthostatic intolerance, in which fainting typically does not occur (40).…”

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confidence: 99%

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Respiration drives phase synchronization between blood pressure and RR interval following loss of cardiovagal baroreflex during vasovagal syncope

Ocon¹,

Medow

Taneja

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Ocon AJ, Medow MS, Taneja I, Stewart JM. Respiration drives phase synchronization between blood pressure and RR interval following loss of cardiovagal baroreflex during vasovagal syncope. Am J Physiol Heart Circ Physiol 300: H527-H540, 2011. First published November 12, 2010 doi:10.1152/ajpheart.00257.2010.-Loss of the cardiovagal baroreflex (CVB), thoracic hypovolemia, and hyperpnea contribute to the nonlinear time-dependent hemodynamic instability of vasovagal syncope. We used a nonlinear phase synchronization index (PhSI) to describe the extent of coupling between cardiorespiratory parameters, systolic blood pressure (SBP) or arterial pressure (AP), RR interval (RR), and ventilation, and a directional index (DI) measuring the direction of coupling. We also examined phase differences directly. We hypothesized that AP-RR interval PhSI would be normal during early upright tilt, indicating intact CVB, but would progressively decrease as faint approached and CVB failed. Continuous measurements of AP, RR interval, respiratory plethysomography, and end-tidal CO 2 were recorded supine and during 70-degree head-up tilt in 15 control subjects and 15 fainters. Data were evaluated during five distinct times: baseline, early tilt, late tilt, faint, and recovery. During late tilt to faint, fainters exhibited a biphasic change in SBP-RR interval PhSI. Initially in fainters during late tilt, SBP-RR interval PhSI decreased (fainters, from 0.65 Ϯ 0.04 to 0.24 Ϯ 0.03 vs. control subjects, from 0.51 Ϯ 0.03 to 0.48 Ϯ 0.03; P Ͻ 0.01) but then increased at the time of faint (fainters ϭ 0.80 Ϯ 0.03 vs. control subjects ϭ 0.42 Ϯ 0.04; P Ͻ 0.001) coinciding with a change in phase difference from positive to negative. Starting in late tilt and continuing through faint, fainters exhibited increasing phase coupling between respiration and AP PhSI (fainters ϭ 0.54 Ϯ 0.06 vs. control subjects ϭ 0.27 Ϯ 0.03; P Ͻ 0.001) and between respiration and RR interval (fainters ϭ 0.54 Ϯ 0.05 vs. control subjects ϭ 0.37 Ϯ 0.04; P Ͻ 0.01). DI indicated respiratory driven AP (fainters ϭ 0.84 Ϯ 0.04 vs. control subjects ϭ 0.39 Ϯ 0.09; P Ͻ 0.01) and RR interval (fainters ϭ 0.73 Ϯ 0.10 vs. control subjects ϭ 0.23 Ϯ 0.11; P Ͻ 0.001) in fainters. The initial drop in the SBP-RR interval PhSI and directional change of phase difference at late tilt indicates loss of cardiovagal baroreflex. The subsequent increase in SBP-RR interval PhSI is due to a respiratory synchronization and drive on both AP and RR interval. Cardiovagal baroreflex is lost before syncope and supplanted by respiratory reflexes, producing hypotension and bradycardia. orthostatsis; nonlinear; fainting THE 2009 GUIDELINES FOR THE diagnosis and management of syncope define syncope as a transient loss of consciousness due to transient global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous complete recovery (22). Vasovagal syncope, also known as simple faint, often occurs in young people following prolonged orthostasis. As illustrated in Fig. 1, loss of consci...

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Section: H533 Cardiovagal Phase Synchronization and Directionality Dusupporting

confidence: 79%

Section: H535 Cardiovagal Phase Synchronization and Directionality Dumentioning

confidence: 92%

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confidence: 99%

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Respiration drives phase synchronization between blood pressure and RR interval following loss of cardiovagal baroreflex during vasovagal syncope

Ocon¹,

Medow

Taneja

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…The slow decline corresponded to a decrease in cardiac output (CO) and in central hypovolemia caused by failure of splanchnic vasoconstriction and enhanced splanchnic blood pooling (34,36). However, total peripheral resistance (TPR) was initially increased compared with control.…”

mentioning

confidence: 99%

Multiresolution wavelet analysis of time-dependent physiological responses in syncopal youths

Nowak¹,

Ocon²,

Taneja³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Our prior studies indicated that postural fainting relates to thoracic hypovolemia. A supranormal increase in initial vascular resistance was sustained by increased peripheral resistance until late during head-up tilt (HUT), whereas splanchnic resistance, cardiac output, and blood pressure (BP) decreased throughout HUT. Our aim in the present study was to investigate the alterations of baroreflex activity that occur in synchrony with the beat-to-beat time-dependent changes in heart rate (HR), BP, and total peripheral resistance (TPR). We proposed that changes of low-frequency Mayer waves reflect sympathetic baroreflex. We used DWT multiresolution analyses to measure their time dependence. We studied 22 patients, 13 to 21 yr old, 14 who fainted within 10 min of upright tilt (fainters) and 8 healthy control subjects. Multiresolution analysis was obtained of continuous BP, HR, and respirations as a function of time during 70°upright tilt at different scales corresponding to frequency bands. Wavelet power was concentrated in scales corresponding to 0.125 and 0.25 Hz. A major difference from control subjects was observed in fainters at the 0.125 Hz AP scale, which progressively decreased from early HUT. The alpha index at 0.125 Hz was increased in fainters. RR interval 0.25 Hz power decreased in fainters and controls but was markedly increased in fainters with syncope and thereafter corresponding to increased vagal tone compared with control subjects at those times only. The data imply a rapid reduction in time-dependent sympathetic baroreflex activity in fainters but not control subjects during HUT. baroreflex; syncope; variance SYNCOPE (FAINTING) IS DEFINED by a sudden transient loss of consciousness and postural tone due to cerebral hypoperfusion (8). Simple postural faint is identified with upright vasovagal syncope in which vasodilation-induced hypotension and bradycardia are relieved by recumbency (18). Upright orthostatic stress testing and specifically upright tilt table testing have been used to provoke postural fainting episodes. We recently reported on the time course of physiological changes during upright tilt using a system of fiducial points. Fiducial points allowed for the comparison of relevant physiological events across patients with simple postural fainting. The fiducial points were baseline, 1-min after head-up tilt (HUT), the onset of gradual blood pressure (BP) decline, mid decline, late decline just prior to the actual faint, and the faint itself, which was the final fiducial point comprising the rapid fall in BP and heart rate (HR) (Fig. 1). These events were consistently present in all young syncopal patients.During early tilt we demonstrated a time-dependent increase in HR coinciding with an initially stable arterial pressure (AP) and followed by a slow decrease in AP. The slow decline corresponded to a decrease in cardiac output (CO) and in central hypovolemia caused by failure of splanchnic vasoconstriction and enhanced splanchnic blood pooling (34, 36). However, total peripheral resistan...

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“…Increased calf venous pooling has been reported in subjects prone to syncope (72), while others have argued against the importance of blood pooling in the lower limb (73,74). Increased blood pooling in the splanchnic beds, possibly leading to increased central hypovolemia has also been detected in VVS patients (75). The central hypovolemia that occurs during orthostatic stress is compensated by mobilization of blood from peripheral capacitance vessel towards the central circulation, as well as by net capillary fluid absorption from tissue to blood in order to increase venous return to the heart and thus defend central blood volume (24,28,31,76).…”

Section: Pathophysiology Of Vasovagal Syncopementioning

confidence: 99%

Cardiovascular regulation in women with vasovagal syncope : With special reference to the venous system

Skoog¹

2016

Linköping University Medical Dissertations

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Relation of Postural Vasovagal Syncope to Splanchnic Hypervolemia in Adolescents

Cited by 64 publications

References 33 publications

Respiration drives phase synchronization between blood pressure and RR interval following loss of cardiovagal baroreflex during vasovagal syncope

Respiration drives phase synchronization between blood pressure and RR interval following loss of cardiovagal baroreflex during vasovagal syncope

Multiresolution wavelet analysis of time-dependent physiological responses in syncopal youths

Cardiovascular regulation in women with vasovagal syncope : With special reference to the venous system

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