Cerebral Hemodynamics of Syncope

McHenry, Lawrence C.; Fazekas, Joseph F.; Sullivan, John

doi:10.1097/00000441-196102000-00004

Cited by 59 publications

(31 citation statements)

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“…This reduction in estimated mitochondrial oxygen tension was attributed to an elevated CMRO 2 by ∼8%, a decreased CBF by ∼15%, and an O 2 extraction that was only increased by ∼7%. Such a minimal increase in O 2 extraction is in stark contrast to experimental evidence during presyncope (291), reduced CBF with indomethacin (257), and theoretical estimations (165) (see Cerebral metabolism); a discrepancy that is left to speculation. Perhaps these estimation of cerebral mitochondrial oxygen tension are confounded by the assumption of constant O 2 diffusibility [indeed a currently valid assumption (241,364,473)], or by the negation of potential cerebral oxygen stores via glycogen (57) or neuroglobin (60).…”

Section: Effects Of Cerebral Blood Flow Metabolism and Oxygenationmentioning

confidence: 66%

“…Therefore, cerebral oxygen extraction can be described as being inversely proportional to CBF when metabolism is held constant, and directly proportional to metabolism when CBF is held constant. Experimental data indicate that O EF can increase upward of 70% to 80% in extreme conditions (291). While, according to theoretical considerations, the critical reduction in CBF where increases in O EF no longer suffice to maintain a constant CMRO 2 is ∼50% to 60% (165,255).…”

Section: Metabolic Regulation Of Cerebral Blood Flow Cerebral Metabolismmentioning

confidence: 97%

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Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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Section: Effects Of Cerebral Blood Flow Metabolism and Oxygenationmentioning

confidence: 66%

Section: Metabolic Regulation Of Cerebral Blood Flow Cerebral Metabolismmentioning

confidence: 97%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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“…The brain compensates for reductions in cerebral blood flow by increasing oxygen extraction (determined via assessment of cerebral arterial-venous oxygen difference) (25,31). Reducing the cerebral blood flow reserve (by indomethacin) prior to exposure to maximal LBNP does not change tolerance, sug- gesting that increases in oxygen extraction would compensate for the decrease in oxygen delivery (25); oxygen extraction was not assessed during LBNP to directly test this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

The role of cerebral oxygenation and regional cerebral blood flow on tolerance to central hypovolemia

Kay

Rickards

2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Kay VL, Rickards CA. The role of cerebral oxygenation and regional cerebral blood flow on tolerance to central hypovolemia. Am J Physiol Regul Integr Comp Physiol 310: R375-R383, 2016. First published December 16, 2015 doi:10.1152/ajpregu.00367.2015Tolerance to central hypovolemia is highly variable, and accumulating evidence suggests that protection of anterior cerebral blood flow (CBF) is not an underlying mechanism. We hypothesized that individuals with high tolerance to central hypovolemia would exhibit protection of cerebral oxygenation (ScO2), and prolonged preservation of CBF in the posterior vs. anterior cerebral circulation. Eighteen subjects (7 male/11 female) completed a presyncope-limited lower body negative pressure (LBNP) protocol (3 mmHg/min onset rate). ScO2 (via near-infrared spectroscopy), middle cerebral artery velocity (MCAv), posterior cerebral artery velocity (PCAv) (both via transcranial Doppler ultrasound), and arterial pressure (via finger photoplethysmography) were measured continuously. Subjects who completed Ն70 mmHg LBNP were classified as high tolerant (HT; n ϭ 7) and low tolerant (LT; n ϭ 11) if they completed Յ60 mmHg LBNP. The minimum difference in LBNP tolerance between groups was 193 s (LT ϭ 1,243 Ϯ 185 s vs. HT ϭ 1,996 Ϯ 212 s; P Ͻ 0.001; Cohen's d ϭ 3.8). Despite similar reductions in mean MCAv in both groups, ScO2 decreased in LT subjects from Ϫ15 mmHg LBNP (P ϭ 0.002; Cohen's dϭ1.8), but was maintained at baseline values until Ϫ75 mmHg LBNP in HT subjects (P Ͻ 0.001; Cohen's d ϭ 2.2); ScO2 was lower at Ϫ30 and Ϫ45 mmHg LBNP in LT subjects (P Յ 0.02; Cohen's d Ն 1.1). Similarly, mean PCAv decreased below baseline from Ϫ30 mmHg LBNP in LT subjects (P ϭ 0.004; Cohen's d ϭ 1.0), but remained unchanged from baseline in HT subjects until Ϫ75 mmHg (P ϭ 0.006; Cohen's d ϭ 2.0); PCAv was lower at Ϫ30 and Ϫ45 mmHg LBNP in LT subjects (P Յ 0.01; Cohen's d Ն 0.94). Individuals with higher tolerance to central hypovolemia exhibit prolonged preservation of CBF in the posterior cerebral circulation and sustained cerebral tissue oxygenation, both associated with a delay in the onset of presyncope.posterior cerebral artery; middle cerebral artery; lower body negative pressure HEMORRHAGE DUE TO TRAUMA IS one of the leading causes of morbidity and mortality worldwide in both the civilian and military settings (1, 2, 13, 22, 32). A major factor contributing to death and disability from severe blood loss is poor tissue perfusion and oxygenation of the vital organs (1, 13, 22). Prolonged cerebral hypoperfusion can lead to neuronal cell death, and if the patient survives, long-term cognitive impairment and physical disability (32). Understanding cerebral hemodynamic responses to blood loss is an essential target for improving survival to hemorrhagic injury, and developing effective therapeutic interventions (35). As there is considerable variability in survival time following hemorrhagic injuries (40), as well as tolerance to simulated hemorrhage (7,15,24,26), it is crucial to determine the rol...

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“…15 When autoregulatory capacity is finally exceeded, CBF decreases more rapidly and OEF increases dramatically. 16 The CBV is more variable in the autoregulatory range. 9 The cerebral rate for oxygen metabolism (CMRO 2 ) remains unchanged over the initial and late decreased levels of CPP.…”

Section: Pathophysiology Of Chronic Cerebrovascular Diseasementioning

confidence: 99%

The Acetazolamide Challenge: Techniques and Applications in the Evaluation of Chronic Cerebral Ischemia

Vagal¹,

Leach²,

Fernández-Ulloa³

et al. 2009

AJNR Am J Neuroradiol

154

116

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SUMMARY:The acetazolamide (ACZ) challenge test is a useful clinical tool and a reliable predictor of critically reduced perfusion. In patients with chronic steno-occlusive disease, the ability to maintain normal cerebral blood flow by reducing vascular resistance secondary to autoregulatory vasodilation is compromised. Identification of the presence and degree of autoregulatory vasodilation (reflecting the cerebrovascular reserve) is a significant prognostic factor in patients with chronic cerebrovascular disease. The pharmacologic challenge of a vasodilatory stimulus such as ACZ can also be used to optimize the treatment strategies for these patients. The pathophysiology, methods, and clinical applications of the ACZ challenge test are discussed in this article. Viability of the cerebral parenchyma is dependent on the ability of the brain vasculature to provide adequate levels of cerebral blood flow (CBF). In patients with chronic stenoocclusive disease, the ability to maintain normal CBF by reducing vascular resistance is compromised. Identification of the degree of autoregulatory vasodilation reflects cerebrovascular reserve (CVR), which is a significant prognostic factor in chronic cerebrovascular disease.1-5 Flow reserve can be assessed with the use of paired blood flow measurements, with the initial measurement obtained at baseline and the second, after a vasodilatory stimulus, such as acetazolamide (ACZ). 6 Pathophysiology of Chronic Cerebrovascular DiseaseChronic cerebral hypoperfusion is usually the result of occlusion or stenosis of large arteries in the neck or the circle of Willis. Clinical symptoms and manifestations of brain ischemia in patients with chronic cerebrovascular disease (CVD) develop as a consequence of 2 main mechanisms: embolic events from atherosclerotic plaques resulting in local compromise of blood flow and systemic hemodynamic alterations that further reduce an already compromised cerebral perfusion state. 7The hemodynamic changes due to a decline in cerebral perfusion pressure have been studied by many investigators. 6,[8][9][10][11] Chronic CBF restriction causes a progressive decrease in cerebral perfusion pressure (CPP). Initially, decreases of CPP cause varying degrees of autoregulatory vasodilation of small distal arterioles.12 Powers 10 and Powers et al 11 proposed a 2-stage classification of hemodynamic impairment in patients with CVD. In stage I (autoregulatory vasodilation), autoregulation reduces cerebral vascular resistance. CBF and oxygen extraction fraction (OEF) are not significantly changed. Increases of cerebral blood volume (CBV) and mean transit time (MTT) are 2 parameters that reflect this initial phase of compensatory autoregulatory vasodilation. Further decreases of CPP beyond cerebral autoregulatory vasodilation capacity eventually result in stage II (autoregulatory failure), characterized by decreases of CBF and increases of OEF. When the CBF decreases, neurons increase the fraction of oxygen extracted from the blood to maintain normal neurologic function. ...

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Cerebral Hemodynamics of Syncope

Cited by 59 publications

References 0 publications

Cerebral Vascular Control and Metabolism in Heat Stress

Cerebral Vascular Control and Metabolism in Heat Stress

The role of cerebral oxygenation and regional cerebral blood flow on tolerance to central hypovolemia

The Acetazolamide Challenge: Techniques and Applications in the Evaluation of Chronic Cerebral Ischemia

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