Cerebral Autoregulatory Responses to Head-Up Tilt in Normal Subjects and Patients With Recurrent Vasovagal Syncope

Carey, Brian J.; Manktelow, Bradley N; Panerai, Ronney B.; Potter, John F.

doi:10.1161/hc3301.094908

Cited by 112 publications

(110 citation statements)

References 36 publications

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“…At the intracranial level, the postural change is considered to produce a decrease in cerebral perfusion pressure, which, together with the hyperventilation-induced hypocapnia induced by the hypotensive stimulus (45), may result in cerebral hypoperfusion, which, in turn, accounts for the reduction in V MCA and TOI (9,26,28,39,42), also observed in the present study.…”

Section: Hutsupporting

confidence: 79%

Inconsistent detection of changes in cerebral blood volume by near infrared spectroscopy in standard clinical tests

Canova

Roatta

Bosone³

et al. 2011

Journal of Applied Physiology

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The attractive possibility of near infrared spectroscopy (NIRS) to noninvasively assess cerebral blood volume and oxygenation is challenged by the possible interference from extracranial tissues. However, to what extent this may affect cerebral NIRS monitoring during standard clinical tests is ignored. To address this issue, 29 healthy subjects underwent a randomized sequence of three maneuvers that differently affect intra- and extracranial circulation: Valsalva maneuver (VM), hyperventilation (HV), and head-up tilt (HUT). Putative intracranial (“i”) and extracranial (“e”) NIRS signals were collected from the forehead and from the cheek, respectively, and acquired together with cutaneous plethysmography at the forehead (PPG), cerebral blood velocity from the middle cerebral artery, and arterial blood pressure. Extracranial contribution to cerebral NIRS monitoring was investigated by comparing Beer-Lambert (BL) and spatially resolved spectroscopy (SRS) blood volume indicators [the total hemoglobin concentration (tHb) and the total hemoglobin index, (THI)] and by correlating their changes with changes in extracranial circulation. While THIe and tHbe generally provided concordant indications, tHbi and THIi exhibited opposite-sign changes in a high percentage of cases (VM: 46%; HV: 31%; HUT: 40%). Moreover, tHbi was correlated with THIi only during HV ( P < 0.05), not during VM and HUT, while it correlated with PPG in all three maneuvers ( P < 0.01). These results evidence that extracranial circulation may markedly affect BL parameters in a high percentage of cases, even during standard clinical tests. Surface plethysmography at the forehead is suggested as complementary monitoring helpful in the interpretation of cerebral NIRS parameters.

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Section: Hutsupporting

confidence: 79%

Inconsistent detection of changes in cerebral blood volume by near infrared spectroscopy in standard clinical tests

Canova

Roatta

Bosone³

et al. 2011

Journal of Applied Physiology

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“…In addition, a paradoxical cerebral vasoconstriction in healthy (5,6,22,38) and orthostatically intolerant (13,14) individuals has been reported during postural stress and LBNP. However, our previous work (38), as well as that of others (8,21), showed that cerebral autoregulation remains intact during HUT in healthy subjects, suggesting that decreases in perfusion pressure were unlikely to be the cause of the decrease in cerebral flow. Similarly, analysis of transfer function gain between CFV and blood pressure found no change in gains during tilt in these subjects (data not shown).…”

Section: Discussionmentioning

confidence: 83%

Cerebral blood flow during orthostasis: role of arterial CO₂

Serrador

Hughson²,

Kowalchuk³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Reductions in end-tidal PCO2 (PETCO 2 ) during upright posture have been suggested to be the result of hyperventilation and the cause of decreases in cerebral blood flow (CBF). The goal of this study was to determine whether decreases in PETCO 2 reflected decreases in arterial PCO2 (PaCO 2 ) and their relation to increases in alveolar ventilation (V A) and decreases in CBF. Fifteen healthy subjects (10 women and 5 men) were subjected to a 10-min head-up tilt (HUT) protocol. PaCO 2 , V A, and cerebral flow velocity (CFV) in the middle and anterior cerebral arteries were examined. In 12 subjects who completed the protocol, reductions in PETCO 2 and PaCO 2 (Ϫ1.7 Ϯ 0.5 and Ϫ1.1 Ϯ 0.4 mmHg, P Ͻ 0.05) during minute 1 of HUT were associated with a significant increase in V A (ϩ0.7 Ϯ 0.3 l/min, P Ͻ 0.05). However, further decreases in Pa CO 2 (Ϫ0.5 Ϯ 0.5 mmHg, P Ͻ 0.05), from minute 1 to the last minute of HUT, occurred even though V A did not change significantly (Ϫ0.2 Ϯ 0.3 l/min, P ϭ not significant). Similarly, CFV in the middle and anterior cerebral arteries decreased (Ϫ7 Ϯ 2 and Ϫ8 Ϯ 2%, P Ͻ 0.05) from minute 1 to the last minute of HUT, despite minimal changes in PaCO 2 . These data suggest that decreases in PET CO 2 and PaCO 2 during upright posture are not solely due to increased V A but could be due to ventilation-perfusion mismatch or a redistribution of CO2 stores. Furthermore, the reduction in PaCO 2 did not fully explain the decrease in CFV throughout HUT. These data suggest that factors in addition to a reduction in PaCO 2 play a role in the CBF response to orthostatic stress. transcranial Doppler; cerebral vasoconstriction; head-up tilt IT HAS BEEN WIDELY NOTED that orthostatic stress in humans decreases end-tidal PCO 2 (PET CO 2 ) or arterial PCO 2 (Pa CO 2 ) (1,4,17,27,36,38,41). Because Pa CO 2 is known to be critical in control of cerebral blood flow (CBF) (30), decreased Pa CO 2 during tilt could play a role in orthostatic intolerance through inappropriate cerebral vasoconstriction. It has been hypothesized that hyperventilation in the upright posture reduces Pa CO 2 , compromising CBF and leading to syncope (27).One inherent problem with this previous work is the use of PET CO 2 to represent Pa CO 2 . Previous work has found that although, in the supine position, PET CO 2 is closely matched to Pa CO 2 (i.e., ϳ0.8 mmHg greater), the assumption of the upright posture resulted in the PET CO 2 being ϳ2.9 mmHg lower than Pa CO 2 (4).No studies have directly measured alveolar ventilation (V A) and CBF during head-up tilt (HUT) and characterized their association to Pa CO 2 . On the basis of our previous findings that decreases in PET CO 2 did not relate to changes in minute ventilation (V E) (36), we hypothesized that Pa CO 2 decreases would be attenuated compared with PET CO 2 and would not be the predominant factor in reduced CBF during HUT. METHODS Subjects.Fifteen subjects [10 women and 5 men, averaging 25.3 yr of age (range 21-32 yr), 64.3 Ϯ 20.5 (SD) kg body wt, 174 Ϯ 9 cm] with no history of card...

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“…CrCP is the ABP at which cerebral blood flow approaches zero 27 and reflects closing forces acting on the vessel, namely ICP and WT. 23 Therefore, CrCP is an important parameter during any conditions where WT or ICP may change (such as syncope, 28 the Valsalva maneuver, 29 or plateau waves of ICP 22 ). The difference between the 'opening' force ABP and 'closing' force of CrCP is the force that keeps vessels open and has been denoted the 'closing margin'.…”

Section: Icp-dependent Cerebroprotection: Vascular Wt and The Cushingmentioning

confidence: 99%

Cerebral haemodynamics during experimental intracranial hypertension

Donnelly

Czosnyka

Harland

et al. 2016

J Cereb Blood Flow Metab

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Intracranial hypertension is a common final pathway in many acute neurological conditions. However, the cerebral haemodynamic response to acute intracranial hypertension is poorly understood. We assessed cerebral haemodynamics (arterial blood pressure, intracranial pressure, laser Doppler flowmetry, basilar artery Doppler flow velocity, and vascular wall tension) in 27 basilar artery-dependent rabbits during experimental (artificial CSF infusion) intracranial hypertension. From baseline ($9 mmHg; SE 1.5) to moderate intracranial pressure ($41 mmHg; SE 2.2), mean flow velocity remained unchanged (47 to 45 cm/s; p ¼ 0.38), arterial blood pressure increased (88.8 to 94.2 mmHg; p < 0.01), whereas laser Doppler flowmetry and wall tension decreased (laser Doppler flowmetry 100 to 39.1% p < 0.001; wall tension 19.3 to 9.8 mmHg, p < 0.001). From moderate to high intracranial pressure ($75 mmHg; SE 3.7), both mean flow velocity and laser Doppler flowmetry decreased (45 to 31.3 cm/s p < 0.001, laser Doppler flowmetry 39.1 to 13.3%, p < 0.001), arterial blood pressure increased still further (94.2 to 114.5 mmHg; p < 0.001), while wall tension was unchanged (9.7 to 9.6 mmHg; p ¼ 0.35).This animal model of acute intracranial hypertension demonstrated two intracranial pressuredependent cerebroprotective mechanisms: with moderate increases in intracranial pressure, wall tension decreased, and arterial blood pressure increased, while with severe increases in intracranial pressure, an arterial blood pressure increase predominated. Clinical monitoring of such phenomena could help individualise the management of neurocritical patients.

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Cerebral Autoregulatory Responses to Head-Up Tilt in Normal Subjects and Patients With Recurrent Vasovagal Syncope

Cited by 112 publications

References 36 publications

Inconsistent detection of changes in cerebral blood volume by near infrared spectroscopy in standard clinical tests

Inconsistent detection of changes in cerebral blood volume by near infrared spectroscopy in standard clinical tests

Cerebral blood flow during orthostasis: role of arterial CO₂

Cerebral haemodynamics during experimental intracranial hypertension

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Cerebral Autoregulatory Responses to Head-Up Tilt in Normal Subjects and Patients With Recurrent Vasovagal Syncope

Cited by 112 publications

References 36 publications

Inconsistent detection of changes in cerebral blood volume by near infrared spectroscopy in standard clinical tests

Inconsistent detection of changes in cerebral blood volume by near infrared spectroscopy in standard clinical tests

Cerebral blood flow during orthostasis: role of arterial CO2

Cerebral haemodynamics during experimental intracranial hypertension

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Cerebral blood flow during orthostasis: role of arterial CO₂