Differences in Mechanism Between Syncope Resulting from Rapid Onset Acceleration and Orthostatic Stress

Self, David A.; White, Curtis D.; Shaffstall, Robert M.; Mtinangi, B. L.; Croft, Jennifer S.

doi:10.21236/ada333371

Cited by 17 publications

(20 citation statements)

References 2 publications

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“…Little is known quantitatively about this process in humans. Approximately 80% of the blood pooled in the lower limb is contained in the upper leg (thighs, buttocks) (Ludbrook, 1966;Self et al 1996) with less pooling in the calf and foot (Buckey et al 1988); additionally, there is some modest pooling in the abdominal and pelvic regions (Sjostrand, 1952;Wolthuis et al 1975;Inamura et al 1996;Halliwill et al 1998). The blood pooled in the veins of the feet and calf is arterial in origin, in that it arises as a result of decreased venous drainage of that region.…”

Section: Regulation Of Blood Pressure and Venous Capacitance In Healtmentioning

confidence: 99%

Pathophysiological basis of orthostatic hypotension in autonomic failure

Smit

Halliwill²,

Low

et al. 1999

The Journal of Physiology

321

209

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Patients with autonomic failure may be seriously incapacitated in activities of daily living due to orthostatic hypotension. Their low blood pressure is ascribed to a defective increase in arterial resistance and an excessive venous pooling upon standing. Effective pharmacological treatment is now available, but may aggravate supine hypertension and have other undesirable effects. Additionally, pharmacological treatment is less successful for hypotension with physical exercise or in warm surroundings (Bannister & Mathias, 1992). Non-pharmacological measures are regarded as a cornerstone in the treatment of orthostatic hypotension. These measures consist of chronic expansion of the extracellular volume or reducing the vascular volume in which pooling occurs (Bannister & Mathias, 1992). The latter includes protective measures like physical countermanoeuvres which can be applied by those patients with no major additional neurological and musculo-skeletal disorders, and external support garments which can be recommended to all patients. We reasoned that selection and use of appropriate protective measures would be facilitated by understanding the fundamental physiological mechanisms that prevent excessive orthostatic pooling in healthy subjects, why these mechanisms fail in patients with autonomic failure, and how these protective measures work. Therefore we reviewed the literature and summarized the available data about the amount and location of venous pooling in patients with autonomic failure and the effectiveness of physical countermanoeuvres and external support garments.

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Section: Regulation Of Blood Pressure and Venous Capacitance In Healtmentioning

confidence: 99%

Pathophysiological basis of orthostatic hypotension in autonomic failure

Smit

Halliwill²,

Low

et al. 1999

The Journal of Physiology

321

209

View full text Add to dashboard Cite

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“…The observation contrasts with head-up tilt studies showing prevention of neurally mediated presyncope with NET inhibition (17). The discrepancy may be explained by fundamental pathophysiological differences between neurally mediated syncope and G-LOC (19). Neurally mediated syncope is characterized by sudden sympathetic withdrawal.…”

Section: Discussionmentioning

confidence: 62%

“…NET inhibition prevents neurally mediated presyncope during head-up tilt testing, which is characterized by sympathetic withdrawal (17). In contrast, G-LOC occurs when the hydrostatic pressure gradient overwhelms sympathetically mediated adaptations in blood pressure control (19).Given the importance of NET for blood pressure control at rest and during orthostatic stress on one hand, and the differences between orthostatic and hypergravitational stress on the other, we used selective pharmacological inhibition of NET to further elucidate the role of NET for hemodynamic adaptations to hypergravitational stress elicited by centrifugation. …”

mentioning

confidence: 99%

“…In this setting, the ability of the cardiovascular system to maintain cerebral perfusion determines gravity (G) tolerance. Once the physiological challenge imposed by hypergravitation overwhelms the adjustment mechanisms, gravitation-induced loss of consciousness (G-LOC) ensues (19). Sympathetic nervous system activation, which is modulated by the vestibular system (23), is a crucial mechanism to maintain cerebral perfusion pressure (3,24).…”

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confidence: 99%

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confidence: 99%

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Norepinephrine transporter inhibition alters the hemodynamic response to hypergravitation

Strempel

Schroeder²,

Hemmersbach³

et al. 2008

Journal of Applied Physiology

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transporter inhibition alters the hemodynamic response to hypergravitation. J Appl Physiol 104: 756-760, 2008. First published January 10, 2008 doi:10.1152/japplphysiol.01128.2007.-Sympathetically mediated tachycardia and vasoconstriction maintain blood pressure during hypergravitational stress, thereby preventing gravitation-induced loss of consciousness. Norepinephrine transporter (NET) inhibition prevents neurally mediated (pre)syncope during gravitational stress imposed by head-up tilt testing. Thus it seems reasonable that NET inhibition could increase tolerance to hypergravitational stress. We performed a double-blind, randomized, placebo-controlled crossover study in 11 healthy men (26 Ϯ 1 yr, body mass index 24 Ϯ 1 kg/m 2 ), who ingested the selective NET inhibitor reboxetine (4 mg) or matching placebo 25, 13, and 1 h before testing on separate days. We monitored heart rate, blood pressure, and thoracic impedance in three different body positions (supine, seated, standing) and during a graded centrifuge run (incremental steps of 0.5 g for 3 min each, up to a maximal vertical acceleration load of 3 g). NET inhibition increased supine blood pressure and heart rate. With placebo, blood pressure increased in the seated position and was well maintained during standing. However, with NET inhibition, blood pressure decreased in the seated and standing position. During hypergravitation, blood pressure increased in a graded fashion with placebo. With NET inhibition, the increase in blood pressure during hypergravitation was profoundly diminished. Conversely, the tachycardic responses to sitting, standing, and hypergravitation all were greatly increased with NET inhibition. In contrast to our expectation, short-term NET inhibition did not improve tolerance to hypergravitation. Redistribution of sympathetic activity to the heart or changes in baroreflex responses could explain the excessive tachycardia that we observed. norepinephrine reuptake transporter; cardiovascular regulation; autonomic nervous system; human HYPERGRAVITATION INDUCED BY rapid flight maneuvers or centrifugation challenges the cardiovascular system through increased venous pooling and plasma extravasation into the dependent parts of the body. In addition, hypergravitation elicits considerable psychological stress and engages the vestibular system (1, 23). In this setting, the ability of the cardiovascular system to maintain cerebral perfusion determines gravity (G) tolerance. Once the physiological challenge imposed by hypergravitation overwhelms the adjustment mechanisms, gravitation-induced loss of consciousness (G-LOC) ensues (19). Sympathetic nervous system activation, which is modulated by the vestibular system (23), is a crucial mechanism to maintain cerebral perfusion pressure (3, 24). Sympathetic cardiovascular responses are mediated by norepinephrine acting on adrenergic receptors (6). The synaptic norepinephrine concentration is regulated through norepinephrine release and norepinephrine re-uptake by the neuronal norepinephrine transp...

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