Cerebrovascular and Cardiovascular Responses to Graded Tilt in Patients With Autonomic Failure

Bondar, Roberta L.; Dunphy, Paul T.; Moradshahi, Peyman; Kassam, M.; Blaber, Andrew P.; Stein, Flo; Freeman, Roy

doi:10.1161/01.str.28.9.1677

Cited by 41 publications

(27 citation statements)

References 20 publications

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“…TCD is used to evaluate cerebrovascular dynamics, including its autoregulation, 32,33 in patients with sympathetic failure as well. 34,35 The diameter of the MCA remains constant over an Ϸ30 mm Hg range of blood pressure, with V mean reflecting changes in cerebral blood flow. 36 This requirement is considered to be fulfilled in upright healthy subjects given the relatively small changes in arterial pressure at brain level.…”

Section: Discussionmentioning

confidence: 99%

Orthostatic Tolerance, Cerebral Oxygenation, and Blood Velocity in Humans With Sympathetic Failure

Harms

Colier

Wieling

et al. 2000

Stroke

102

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Section: Discussionmentioning

confidence: 99%

Orthostatic Tolerance, Cerebral Oxygenation, and Blood Velocity in Humans With Sympathetic Failure

Harms

Colier

Wieling

et al. 2000

Stroke

102

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“…insulin-dependent diabetics and people with pure autonomic failure), an orthostatic challenge typically leads to inappropriate circulatory adjustments (Rayman et al 1986;Bondar et al 1997;Wieling et al 1998). In these cases, blood pressure was observed to fall and remain low during an orthostatic challenge (Bondar et al 1997;Wieling et al 1998). The fact that paraplegics are able to maintain their blood pressure suggests that other mechanisms are used to defend against orthostatic hypotension.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular responses to an orthostatic challenge and electrical-stimulation-induced leg muscle contractions in individuals with paraplegia

et al. 1999

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The purpose of this study was to investigate the cardiovascular and haemodynamic responses that occur during moderate orthostatic challenge in people with paraplegia, and the effect of electrical stimulation (ES)-induced leg muscle contractions on their responses to orthostatic challenge. Eight males with complete spinal lesions between the 5th and 12th thoracic vertebrae (PARA) and eight able-bodied individuals (AB) volunteered for this study. Changes in heart rate (fc), stroke volume (SV), cardiac output (Qc), mean arterial pressure (MAP), total peripheral resistance (TPR), limb volumes and indices of neural modulation of fc, [parasympathetic (PNS) and sympathetic (SNS) nervous system indicators] were assessed during: (1) supine rest (REST), (2) REST with lower-body negative pressure at -30 torr (LBNP -30, where 1 torr = 133.32 N/m2), and (3) for PARA only, LBNP -30 with ES-induced leg muscle contractions (LBNP + ES). LBNP -30 elicited a decrease in SV (by 23% and 22%), Qc (by 15% and 18%) and the PNS indicator, but an increase in fc (by 10% and 9%), TPR (by 23% and 17%) and calf volume (by 1.51% and 4.04%) in both PARA and AB subjects, respectively. The SNS indicator was increased in the AB group only. Compared to LBNP -30, LBNP + ES increased SV (by 20%) and Qc (by 16%), and decreased TPR (by 12%) in the PARA group. MAP was unchanged from REST during all trials, for both groups. The orthostatic challenge induced by LBNP -30 elicited similar cardiovascular adaptations in PARA and AB subjects. ES-induced muscle contractions during LBNP -30 augmented the cardiovascular responses exhibited by the PARA group, probably via reactivation of the skeletal muscle pump and improved venous return.

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“…This is particularly evident in individuals suffering from autonomic failure, such as multiple system atrophy and pure autonomic failure. 21,[77][78][79] The mechanisms underlying this tolerance to hypotension are unclear, but since the ultimate cause of symptoms in these individuals is known to be due to cerebral hypoperfusion, it is likely that there is a shift in cerebral autoregulation in these individuals, whereby cerebral blood flow is maintained despite low perfusion pressures. [77][78][79] Patients with SCI who demonstrate postural hypotension also seem to have altered cerebral haemodynamics, since many of them are able to tolerate profound hypotension and remain asymptomatic, and indeed, symptoms were only reported during documented orthostatic hypotension in approximately 60% of cases.…”

Section: Orthostatic Hypotension and Symptoms Of Cerebral Hypoperfusimentioning

confidence: 99%

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

2005

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Motor and sensory deficits are well-known consequences of spinal cord injury (SCI). During the last decade, a significant number of experimental and clinical studies have focused on the investigation of autonomic dysfunction and cardiovascular control following SCI. Numerous clinical reports have suggested that unstable blood pressure control in individuals with SCI could be responsible for their increased cardiovascular mortality. The aim of this review is to outline the incidence and pathophysiological mechanisms underlying the orthostatic hypotension that commonly occurs following SCI. We describe the clinical abnormalities of blood pressure control following SCI, with particular emphasis upon orthostatic hypotension. Possible mechanisms underlying orthostatic hypotension in SCI, such as changes in sympathetic activity, altered baroreflex function, the lack of skeletal muscle pumping activity, cardiovascular deconditioning and altered salt and water balance will be discussed. Possible alterations in cerebral autoregulation following SCI, and the impact of these changes upon cerebral perfusion are also examined. Finally, the management of orthostatic hypotension will be considered.

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Cerebrovascular and Cardiovascular Responses to Graded Tilt in Patients With Autonomic Failure

Cited by 41 publications

References 20 publications

Orthostatic Tolerance, Cerebral Oxygenation, and Blood Velocity in Humans With Sympathetic Failure

Orthostatic Tolerance, Cerebral Oxygenation, and Blood Velocity in Humans With Sympathetic Failure

Cardiovascular responses to an orthostatic challenge and electrical-stimulation-induced leg muscle contractions in individuals with paraplegia

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

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