Pathophysiological Mechanisms Underlying Vasovagal Syncope in Young Subjects

Wieling, Wouter; Smit, Adrianus A. J.; C.E, CATHERINE; STEENWIJK, DE JONG-DE VOS; JOHANNNES, J; LIESHOUT, VAN; Karemaker, John M.

doi:10.1111/j.1540-8159.1997.tb03622.x

Cited by 21 publications

(48 citation statements)

References 28 publications

(5 reference statements)

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“…Stroke volumes found in the present study were signi®cantly smaller during HUT compared with SUP, as found in previous studies (Rowell, 1993;Wieling et al, 1997). This is caused by blood pooling in the legs and splanchnic area during standing (Rowell, 1993), resulting in a diminished venous return.…”

Section: Circulatory Responsessupporting

confidence: 87%

“…This is caused by blood pooling in the legs and splanchnic area during standing (Rowell, 1993), resulting in a diminished venous return. The signi®cantly higher HR found in the present as well as in other studies (Wang et al, 1996;Wieling et al, 1997) partly compensates for this smaller stroke volume in an attempt to maintain cardiac output. The signi®cantly higher HR found in the present as well as in other studies (Wang et al, 1996;Wieling et al, 1997) partly compensates for this smaller stroke volume in an attempt to maintain cardiac output.…”

Section: Circulatory Responsessupporting

confidence: 78%

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Reproducibility of the alterations in circulation and cerebral oxygenation from supine rest to head‐up tilt

Houtman

Colier

Hopman

et al. 1999

Clinical Physiology

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Cardiovascular stability, as affected by several diseases, may be assessed by head-up tilt testing. Follow-up studies are essential in both evaluating interventions and assessing progression. However, data on the reproducibility of the changes in circulatory status and cerebral oxygenation provoked by head-up tilt testing are fundamental to follow-up studies. The aim of this study was, therefore, to assess the reproducibility of the alterations in stroke volume (SV), mean arterial pressure (MAP), as well as oxygenated ([O2Hb]) and deoxygenated haemoglobin ([HHb]) concentration in cerebral tissue from supine rest (SUP) to head-up tilt (HUT). SV was calculated by Modelflow, a pulse contour method, from the finger arterial pressure wave measured by Portapres, the portable version of Finapres. [O2Hb] and [HHb] were measured using near-infrared spectroscopy (NIRS). Ten healthy individuals visited the laboratory on two different days. On both days, they underwent 10 min SUP followed by 10 min 70 degrees HUT twice. SV decreased, which was (in part) compensated for by an increased heart rate, while MAP increased slightly during HUT compared with SUP. Although [HHb] increased during HUT, no presyncope symptoms were experienced. The circulatory variables (SV, HR and MAP) as well as [HHb] showed an acceptably small systematic and random error as well as reproducibility error compared with the observed difference between HUT and SUP and were similar between and within visits. Therefore, it is concluded that MAP measured by Portapres and SV calculated by Modelflow as well as HHb measured by NIRS seem to be reproducible and may therefore be used in follow-up studies.

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Section: Circulatory Responsessupporting

confidence: 87%

Section: Circulatory Responsessupporting

confidence: 78%

Reproducibility of the alterations in circulation and cerebral oxygenation from supine rest to head‐up tilt

Houtman

Colier

Hopman

et al. 1999

Clinical Physiology

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“…While VVS can occur in young and ostensibly healthy people 5 , it is important to validate our findings in populations more susceptible to VVS.…”

Section: Discussionmentioning

confidence: 80%

“…1,5 VVS accounts for >77% of reported syncope episodes and occurs more frequently in young individuals. 2 The incidence of VVS displays a daily pattern with a broad peak in the morning (6:00-12:00).…”

mentioning

confidence: 99%

Endogenous Circadian Rhythm in Vasovagal Response to Head-Up Tilt

Scheer

Laker

et al. 2011

Circulation

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Background The incidence of syncope exhibits a daily pattern with more occurrences in the morning, possibly due to influences from the endogenous circadian system and/or the daily pattern of behavioral/emotional stimuli. This study tested the hypothesis that the circadian system modulates cardiovascular responses to postural stress, leading to increased susceptibility to syncope at specific times of day. Methods and Results Twelve subjects underwent a 13-day in-laboratory protocol, in which subjects’ sleep-wake cycles were adjusted to 20 hours for 12 cycles. A 15-minute title-table test (60° head-up) was performed ~4.5 hours after scheduled awakening in each cycle so that twelve tests in each subject were distributed evenly across the circadian cycle. Out of 144 tests, signs/symptoms of presyncope were observed in 21 tests in 6 subjects. These presyncope events displayed a clear circadian rhythm (P=0.028) with 17 cases (81%) in the circadian phase range corresponding to ~22:30-10:30 (4.25 times of the probability from the other half of the circadian cycle). Significant circadian rhythms were also observed in hemodynamic and autonomic function markers (blood pressure, heart rate, epinephrine, norepinephrine, and indices of cardiac vagal tone) that may underlie the circadian rhythm of presyncope susceptibility. Conclusion The circadian system affects cardiovascular responses to postural stressors resulting in greater susceptibility to presyncope during the biological night. This finding suggests that night-shift workers and people with disrupted sleep at night may have great risk of syncope due to their exposure to postural stressors during the biological night.

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“…19,20 This is caused by blood pooling in the legs and splanchnic area with the body upright, 19 resulting in a diminished venous return and, consequently, a decreased stroke volume via the Frank-Starling mechanism. The signi®cantly higher HR, found in the present as well as in other studies, 20,21 partly compensates this smaller stroke volume and reduces the decrease in cardiac output. Cardiac output and MAP were unaltered in AB during head-up tilt most likely due to a sympathetic nervous system-induced increase in total peripheral resistance.…”

Section: Circulatory Responsesmentioning

confidence: 99%

Systemic circulation and cerebral oxygenation during head-up tilt in spinal cord injured individuals

et al. 2000

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Objective: To compare tilt-induced alterations in cardiovascular homeostasis and cerebral oxygenation of spinal cord-injured (SCI) to able-bodied (AB) individuals. Design: Subjects underwent 10 min supine rest followed by 10 min 708 head-up tilt. The last 5 min of supine rest and head-up tilt were analyzed, provided a steady state existed. Subjects: SCI individuals (n=11), with lesions between C4 and T4, and AB individuals (n=10), all males and balanced for age and weight. Conclusion: SCI demonstrated a greater decrease of MAP and stroke volume with a similar decrease in cerebral oxygenation compared to AB. This suggests that although systemic circulation was less well regulated in SCI compared with AB, cerebral circulation in SCI was maintained as in AB.

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Pathophysiological Mechanisms Underlying Vasovagal Syncope in Young Subjects

Cited by 21 publications

References 28 publications

Reproducibility of the alterations in circulation and cerebral oxygenation from supine rest to head‐up tilt

Reproducibility of the alterations in circulation and cerebral oxygenation from supine rest to head‐up tilt

Endogenous Circadian Rhythm in Vasovagal Response to Head-Up Tilt

Systemic circulation and cerebral oxygenation during head-up tilt in spinal cord injured individuals

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