Hyperventilation, cerebral perfusion, and syncope

2014 ◽  
Vol 116 (7) ◽  
pp. 844-851 ◽  
Author(s):  
R. V. Immink ◽  
F. C. Pott ◽  
N. H. Secher ◽  
J. J. van Lieshout
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion ◽  
Brain Perfusion ◽  
Cerebral Hypoperfusion ◽  
Cerebral Control ◽  
Partial Pressures ◽  
Transient Loss ◽  
Global Cerebral Blood Flow ◽  
Postural Reduction

This review summarizes evidence in humans for an association between hyperventilation (HV)-induced hypocapnia and a reduction in cerebral perfusion leading to syncope defined as transient loss of consciousness (TLOC). The cerebral vasculature is sensitive to changes in both the arterial carbon dioxide (PaCO2) and oxygen (PaO2) partial pressures so that hypercapnia/hypoxia increases and hypocapnia/hyperoxia reduces global cerebral blood flow. Cerebral hypoperfusion and TLOC have been associated with hypocapnia related to HV. Notwithstanding pronounced cerebrovascular effects of PaCO2 the contribution of a low PaCO2 to the early postural reduction in middle cerebral artery blood velocity is transient. HV together with postural stress does not reduce cerebral perfusion to such an extent that TLOC develops. However when HV is combined with cardiovascular stressors like cold immersion or reduced cardiac output brain perfusion becomes jeopardized. Whether, in patients with cardiovascular disease and/or defect, cerebral blood flow cerebral control HV-induced hypocapnia elicits cerebral hypoperfusion, leading to TLOC, remains to be established.

scholarly journals Total Cerebral Blood Flow and Total Brain Perfusion in the General Population: The Rotterdam Scan Study

2007 ◽  
Vol 28 (2) ◽  
pp. 412-419 ◽  
Author(s):  
Meike W Vernooij ◽  
Aad van der Lugt ◽  
Mohammad Arfan Ikram ◽  
Piotr A Wielopolski ◽  
Henri A Vrooman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
General Population ◽  
Cerebral Perfusion ◽  
Brain Volume ◽  
Measurement Techniques ◽  
White Matter Lesions ◽  
Brain Perfusion ◽  
Linear Regression Models ◽  
Total Brain

Reduced cerebral perfusion may contribute to the development of cerebrovascular and neurodegenerative diseases. Little is known on cerebral perfusion in the general population, as most measurement techniques are too invasive for application in large groups of healthy individuals. Total cerebral blood flow (tCBF) can be noninvasively measured by magnetic resonance imaging (MRI) but is highly correlated with brain volume. We calculated total brain perfusion by dividing tCBF by brain volume, and we investigated determinants of total brain perfusion in comparison with tCBF. Secondly, we studied whether persons with a low tCBF or low total brain perfusion have a larger volume of white matter lesions (WML). This study is based on 892 persons aged 60 to 91 years from the Rotterdam Study, a population-based cohort study. We performed two-dimensional (2D) phase-contrast MRI for tCBF measurement. Brain volume and WML volume were quantitatively assessed. Cardiovascular determinants were assessed by interview and physical examination. We assessed associations between cardiovascular determinants and flow measures with linear regression models, adjusted for age and sex. Associations between tCBF or total brain perfusion and WML volume were assessed using general linear models. We found that determinants of tCBF and total brain perfusion differed largely due to the large influence of brain volume on tCBF values. Persons with low total brain perfusion had a significantly larger WML volume compared with those with high total brain perfusion. Prospective studies are required to unravel whether hypoperfusion contributes to WML formation or that tissue damage, manifested by WML, leads to brain hypoperfusion.

Effect of Ketanserin on Global Cerebral Blood Flow and Middle Cerebral Artery Flow Velocity

1995 ◽  
Vol 80 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Andreas Weyland ◽  
Heidrun Stephan ◽  
Frank Grune ◽  
Wolfgang Weyland ◽  
Hans Sonntag
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Global Cerebral Blood Flow ◽  
Artery Flow

scholarly journals Effect of acute hypoxia on regional cerebral blood flow: effect of sympathetic nerve activity

2014 ◽  
Vol 116 (9) ◽  
pp. 1189-1196 ◽  
Author(s):  
Nia C. S. Lewis ◽  
Laura Messinger ◽  
Brad Monteleone ◽  
Philip N. Ainslie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sympathetic Nerve ◽  
Regional Difference ◽  
Sympathetic Nerve Activity ◽  
Acute Hypoxia ◽  
Adrenergic Blockade ◽  
Percentage Increase ◽  
Nerve Activity ◽  
Global Cerebral Blood Flow

We examined 1) whether global cerebral blood flow (CBF) would increase across a 6-h bout of normobaric poikilocapnic hypoxia and be mediated by a larger increase in blood flow in the vertebral artery (VA) than in the internal carotid artery (ICA); and 2) whether additional increases in global CBF would be evident following an α1-adrenergic blockade via further dilation of the ICA and VA. In 11 young normotensive individuals, ultrasound measures of ICA and VA flow were obtained in normoxia (baseline) and following 60, 210, and 330 min of hypoxia (FiO2 = 0.11). Ninety minutes prior to final assessment, participants received an α1-adrenoreceptor blocker (prazosin, 1 mg/20 kg body mass) or placebo. Compared with baseline, following 60, 220, and 330 min of hypoxia, global CBF [(ICAFlow + VAFlow) ∗ 2] increased by 160 ± 52 ml/min (+28%; P = 0.05), 134 ± 23 ml/min (+23%; P = 0.02), and 113 ± 51 (+19%; P = 0.27), respectively. Compared with baseline, ICAFlow increased by 23% following 60 min of hypoxia ( P = 0.06), after which it progressively declined. The percentage increase in VA flow was consistently larger than ICA flow during hypoxia by ∼20% ( P = 0.002). Compared with baseline, ICA and VA diameters increased during hypoxia by ∼9% and ∼12%, respectively ( P ≤ 0.05), and were correlated with reductions in SaO2. Flow and diameters were unaltered following α1 blockade ( P ≥ 0.10). In conclusion, elevations in global CBF during acute hypoxia are partly mediated via greater increases in VA flow compared with ICA flow; this regional difference was unaltered following α1 blockade, indicating that a heightened sympathetic nerve activity with hypoxia does not constrain further dilation of larger extracranial blood vessels.

MRI-based measurements of whole-brain global cerebral blood flow: Comparison and validation at 1.5T and 3T

2018 ◽  
Vol 48 (5) ◽  
pp. 1273-1280 ◽  
Author(s):  
Chun-Ming Chen ◽  
Yen-Chih Huang ◽  
Cheng-Ting Shih ◽  
Yung-Fang Chen ◽  
Shin-Lei Peng
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Whole Brain ◽  
Global Cerebral Blood Flow

scholarly journals Determinants of Cerebrovascular Reserve in Patients with Significant Carotid Stenosis

2020 ◽  
Author(s):  
Joseph P Archie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Carotid Stenosis ◽  
Vascular Resistance ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Systemic Arterial Pressure ◽  
Patient Specific ◽  
Flow Reserve

AbstractIntroductionIn patients with 70% to 99% diameter carotid artery stenosis cerebral blood flow reserve may be protective of future ischemic cerebral events. Reserve cerebral blood flow is created by brain auto-regulation. Both cerebral blood flow reserve and cerebrovascular reactivity can be measured non-invasively. However, the factors and variables that determine the availability and magnitude and of reserve blood flow remain poorly understood. The availability of reserve cerebral blood flow is a predictor of stroke risk. The aim of this study is to employ a hemodynamic model to predict the variables and functional relationships that determine cerebral blood flow reserve in patients with significant carotid stenosis.MethodsA basic one-dimensional, three-unit (carotid, collateral and brain) energy conservation fluid mechanics blood flow model is employed. It has two distinct but adjacent blood flow components with normal cerebral blood flow at the interface. In the brain auto-regulated blood flow component cerebral blood flow is maintained normal by reserve flow. In the brain pressure dependent blood flow component cerebral blood flow is below normal because cerebral perfusion pressure is below the lower threshold value for auto-regulation. Patient specific values of collateral vascular resistance are determined from a model solution using clinically measured systemic and carotid arterial stump pressures. Collateral vascular resistance curves illustrate the model solutions for reserve and actual cerebral blood flow as a function of percent diameter carotid artery stenosis and mean systemic arterial pressure. The threshold cerebral perfusion pressure value for auto-regulation is assumed to be 50 mmHg. Normal auto-regulated regional cerebral blood flow is assumed to be 50 ml/min/100g. Cerebral blood flow and reserve blood flow solutions are given for systemic arterial pressures of 80, 90, 100, 110 and 120 mmHg and for three patient specific collateral vascular resistance values, Rw = 1.0 (mean patient value), Rw = 0.5 (lower 1 SD) and Rd = 3.0 (upper 1 SD).ResultsReserve cerebral blood flow is only available when a patients cerebral perfusion pressure is in the normal auto-regulatory range. Both actual and reserve cerebral blood flows are primarily from the carotid circulation when carotid stenosis is less than 60% diameter. Between 60% and 75% stenosis the remaining carotid blood flow reserve is utilized and at higher degrees of stenosis all reserve flow is from the collateral circulation. The primary independent variables that determine actual and reserve cerebral blood flow are mean systemic arterial pressure, degree of carotid stenosis and patient specific collateral vascular resistance. Approximate 16% of patients have collateral vascular resistance greater than 5.0 and are predicted to be at high risk of cerebral ischemia or infarction with progression to severe carotid stenosis or occlusion. The approximate 50% of patients with a collateral vascular resistance less than 1.0 are predicted to have adequate cerebral blood flow with progression to carotid occlusion, and most maintain some reserve. Clinically measured values of cerebral blood flow reserve or cerebrovascular reactivity are predicted to be unreliable without consideration of systemic arterial pressure and degree of carotid stenosis. Reserve cerebral blood flow values measured in patients with only moderate 60% to 70% carotid stenosis are in general too high and variable to be of clinical value, but are most reliable when measured near 80% diameter stenosis and considered as percent of the maximum reserve blood flow. Patient specific measured reserve blood flow values can be inserted into the model to calculate the collateral vascular resistance.ConclusionsPredicting cerebral blood flow reserve in patients with significant carotid stenosis is complex and multifactorial. A simple cerebrovascular model predicts that patient specific collateral vascular resistance is an excellent predictor of reserve cerebral blood flow in patients with significant carotid stenosis. Cerebral blood flow reserve measurements are of limited value without accounting for systemic pressure and actual percent carotid stenosis. Asymptomatic patients with severe carotid artery stenosis and a collateral vascular resistance greater than 1.0 are at increased risk of cerebral ischemia and may benefit from carotid endarterectomy.

Cerebral Blood Flow of the Neonatal Brain after Hypoxic-Ischemic Injury

2021 ◽  
Author(s):  
Luis Octavio Tierradentro-García ◽  
Sandra Saade-Lemus ◽  
Colbey Freeman ◽  
Matthew Kirschen ◽  
Hao Huang ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Near Infrared ◽  
Imaging Modality ◽  
Brain Perfusion ◽  
Correlation Spectroscopy ◽  
Therapeutic Interventions ◽  
Routine Practice ◽  
Diffuse Correlation Spectroscopy ◽  
Positron Emission

Objective Hypoxic-ischemic encephalopathy (HIE) in infants can have long-term adverse neurodevelopmental effects and markedly reduce quality of life. Both the initial hypoperfusion and the subsequent rapid reperfusion can cause deleterious effects in brain tissue. Cerebral blood flow (CBF) assessment in newborns with HIE can help detect abnormalities in brain perfusion to guide therapy and prognosticate patient outcomes. Study Design The review will provide an overview of the pathophysiological implications of CBF derangements in neonatal HIE, current and emerging techniques for CBF quantification, and the potential to utilize CBF as a physiologic target in managing neonates with acute HIE. Conclusion The alterations of CBF in infants during hypoxia-ischemia have been studied by using different neuroimaging techniques, including nitrous oxide and xenon clearance, transcranial Doppler ultrasonography, contrast-enhanced ultrasound, arterial spin labeling MRI, 18F-FDG positron emission tomography, near-infrared spectroscopy (NIRS), functional NIRS, and diffuse correlation spectroscopy. Consensus is lacking regarding the clinical significance of CBF estimations detected by these different modalities. Heterogeneity in the imaging modality used, regional versus global estimations of CBF, time for the scan, and variables impacting brain perfusion and cohort clinical characteristics should be considered when translating the findings described in the literature to routine practice and implementation of therapeutic interventions. Key Points

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