Simultaneous Cerebrovascular and Cardiovascular Responses During Presyncope

Bondar, Roberta L.; Kassam, M.; Stein, Flo; Dunphy, Paul T.; Fortney, S M; Riedesel, Marvin L.

doi:10.1161/01.str.26.10.1794

Cited by 85 publications

(83 citation statements)

References 27 publications

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“…Altered cerebrovascular control unrelated to changes in PET CO 2 has been reported during LBNP following bed rest (44) and parabolic flight (38). 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.…”

Section: Discussionmentioning

confidence: 98%

“…CFV MCA has been found to decrease with upright tilt (13,17,27,38) and lower body negative pressure (LBNP) (6,22). Concomitant with this decrease in CBF is a drop in PET CO 2 (6,17,22,27,38).…”

Section: Discussionmentioning

confidence: 99%

“…Concomitant with this decrease in CBF is a drop in PET CO 2 (6,17,22,27,38). Because it is well known that a decrease in Pa CO 2 results in an increase in CVR (30), we investigated the possibility that the hypocapnia associated with orthostatic stress might be the cause of the cerebral hypoperfusion during 10 min of HUT.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

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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“…27 Conversely, stellate ganglion blockade did not change vertebral CBF in patients with headache. 28 Recently, we and others have shown that during LBNP, 10,11 head-up tilt, 12,13 and cold pressor tests, 29 all of which enhance sympathetic nerve activity, CBF velocity decreased in the absence of systemic hypotension. These data suggest the presence of cerebral vasoconstriction, associated with the augmented sympathetic activity.…”

Section: Steady-state Autoregulationmentioning

confidence: 95%

“…Different methods may assess different aspects of CBF. Recently, with the advent of transcranial Doppler technology for the measurement of CBF velocity with high-temporal resolution, we 10,11 and others 12,13 have observed that in humans, CBF velocity in the middle cerebral artery (MCA) decreased substantially during lower body negative pressure (LBNP) and head-up tilt in the absence of systemic hypotension. These findings suggest the presence of cerebral vasoconstriction associated with the augmented sympathetic nerve activity during orthostatic stress.…”

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confidence: 99%

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

et al. 2002

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Background-The purpose of the present study was to determine the role of autonomic neural control of dynamic cerebral autoregulation in humans. Methods and Results-We measured arterial pressure and cerebral blood flow (CBF) velocity in 12 healthy subjects (aged 29Ϯ6 years) before and after ganglion blockade with trimethaphan. CBF velocity was measured in the middle cerebral artery using transcranial Doppler. The magnitude of spontaneous changes in mean blood pressure and CBF velocity were quantified by spectral analysis. The transfer function gain, phase, and coherence between these variables were estimated to quantify dynamic cerebral autoregulation. After ganglion blockade, systolic and pulse pressure decreased significantly by 13% and 26%, respectively. CBF velocity decreased by 6% (PϽ0.05). In the very low frequency range (0.02 to 0.07 Hz), mean blood pressure variability decreased significantly (by 82%), while CBF velocity variability persisted. Thus, transfer function gain increased by 81%. In addition, the phase lead of CBF velocity to arterial pressure diminished. These changes in transfer function gain and phase persisted despite restoration of arterial pressure by infusion of phenylephrine and normalization of mean blood pressure variability by oscillatory lower body negative pressure. Conclusions-These data suggest that dynamic cerebral autoregulation is altered by ganglion blockade. We speculate that autonomic neural control of the cerebral circulation is tonically active and likely plays a significant role in the regulation of beat-to

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Cerebral Blood‐Flow Regulation During Hemorrhage

Rickards

2015

Comprehensive Physiology

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Massive uncontrolled blood loss can occur under a variety of conditions including trauma, as a complication of childbirth or surgery, ruptured ulcers, clotting disorders, and hemorrhagic fevers. Across the continuum of hemorrhage, loss of blood volume is a significant challenge to the maintenance of cerebral perfusion. During the initial stages of hemorrhage, reflex mechanisms are activated to protect cerebral perfusion, but persistent blood loss will eventually reduce global cerebral blood flow and the delivery of metabolic substrates, leading to generalized cerebral ischemia, hypoxia, and ultimately, neuronal cell death. Cerebral blood flow is controlled by various regulatory mechanisms, including prevailing arterial pressure, intracranial pressure, arterial blood gases, neural activity, and metabolic demand. Hemorrhage represents a unique physiological stress to the brain, as it influences each of these regulatory mechanisms, resulting in complex interplay that ultimately challenges the ability of the brain to maintain adequate perfusion. Early studies of actual hemorrhage in humans employed blood loss protocols up to 1000 mL, but did not include any measurements of cerebral blood flow. As ethical considerations necessarily constrain the use of human volunteers for massive blood loss studies that induce irreversible shock, most of what is known about cerebral blood-flow responses to hemorrhage has been determined from animal models. Limitations of species differences regarding regulatory mechanisms, anatomy, and the effect of anesthesia, however, must be considered. Advances in monitoring technologies, and a recent renewed interest in understanding cerebral blood-flow regulation in humans, however, is rapidly accelerating knowledge in this field.

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Simultaneous Cerebrovascular and Cardiovascular Responses During Presyncope

Cited by 85 publications

References 27 publications

Cerebral blood flow during orthostasis: role of arterial CO₂

Cerebral blood flow during orthostasis: role of arterial CO₂

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

Cerebral Blood‐Flow Regulation During Hemorrhage

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Simultaneous Cerebrovascular and Cardiovascular Responses During Presyncope

Cited by 85 publications

References 27 publications

Cerebral blood flow during orthostasis: role of arterial CO2

Cerebral blood flow during orthostasis: role of arterial CO2

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

Cerebral Blood‐Flow Regulation During Hemorrhage

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Product

Resources

About

Cerebral blood flow during orthostasis: role of arterial CO₂

Cerebral blood flow during orthostasis: role of arterial CO₂