scholarly journals Impact of Systemic Arterial Pressure, Collateral Vascular Resistance and Degree of Carotid Stenosis on Cerebral Blood Flow, Reserve Blood Flow, Critical Carotid Stenosis, Cerebral Ischemia and Carotid Hemodynamics

2021 ◽  
Author(s):  
Joseph P Archie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Carotid Artery ◽  
Arterial Pressure ◽  
Carotid Stenosis ◽  
Vascular Resistance ◽  
Systemic Arterial Pressure ◽  
Patient Specific ◽  
Carotid Blood Flow

AbstractIntroductionCarotid artery stenosis related stroke is a major health care concern. Current risk management strategies for patients with asymptomatic carotid stenosis include ultrasound surveillance and occasionally an estimate of cerebral blood flow reserve. Other patient specific hemodynamic variables may be predictive of ischemic stroke risk. This study, based on a cerebral blood flow hemodynamic model, aims to investigate the impact of systemic arterial pressure, collateral vascular resistance and degree of carotid stenosis on cerebral ischemic risk, cerebrovascular blood flow reserve, critical carotid artery stenosis, carotid artery blood flow and carotid stenosis hemodynamics.MethodsThis study uses a three-component (carotid, collateral, brain) energy conservation cerebrovascular fluid mechanics model in combination with the Lassen cerebral blood flow autoregulation model that predicts cerebral blood flow in patients with carotid stenosis. It is a two-phase model, zone A when regional cerebral blood flow is autoregulated at normal values and zone B when cerebral blood flow is below normal and dependent on collateral perfusion pressure. The model solution with carotid artery occlusion defines collateral vascular resistance, with patient specific values calculated from clinical pressure measurements. In addition to cerebral blood flow the model predicts critical stenosis values and carotid and collateral blood flows as a function of systemic arterial pressure and percent diameter stenosis. Carotid stenosis blood flow velocities and energy dissipation are predicted from carotid blood flow solutions.ResultsThe model defines patient specific collateral vascular resistance, cerebral vascular resistance and critical carotid stenosis. It predicts carotid vascular resistance to be non-linearly proportional to area carotid stenosis. Solutions include reserve cerebral blood flow, the carotid and collateral components of cerebral blood flow, criteria for cerebral ischemia and carotid stenosis hemodynamics. Critical carotid stenosis is determined by mean systemic arterial pressure and the Lassen autoregulation threshold cerebral perfusion pressure. Critical stenosis values range from 61% to 76% diameter stenosis when mean systemic arterial pressures are 80mmHg to 120mmHg and the cerebral autoregulation pressure threshold is 50mmHg. When carotid stenosis is less than critical, cerebral blood flow is maintained normal and the ratios of carotid blood flow to collateral blood flow are inversely proportional to the carotid to collateral vascular resistance ratios. At stenosis greater than the critical, carotid blood flow is not adequate to maintain normal cerebral blood flow, cerebral blood flow is primarily collateral flow, all reserve blood flow is collateral and prevention of cerebral ischemia requires adequate collateral flow. Patient specific collateral vascular resistance values less than 1.0 predict normal cerebral blood flow at moderate to severe stenosis. Values greater than 1.0 predicts cerebral ischemia to be dependent on the magnitude of collateral vascular resistance. Systemic arterial pressure is a major determinant of carotid stenosis hemodynamics. Carotid blood flow velocities increase with carotid stenosis and have progressively higher variance depending on collateral blood flow as predicted by collateral vascular resistance. Turbulent flow energy dissipation intensity is similarly inversely proportional to collateral vascular resistance at severe carotid stenosis.ConclusionsCerebral, collateral and carotid blood flow solutions are determined by systemic arterial pressure, collateral vascular resistance and degree of stenosis. Critical carotid stenosis, systemic arterial pressure and collateral vascular resistance are primary determinants of cerebral ischemic risk in patients with significant carotid stenosis.

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.

scholarly journals A hemodynamic model to predict regional cerebral blood flow and blood flow reserve in patients with carotid stenosis

2020 ◽  
Author(s):  
joseph p archie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Carotid Stenosis ◽  
Vascular Resistance ◽  
Regional Cerebral Blood Flow ◽  
Patient Specific ◽  
Regional Cerebral Blood ◽  
Flow Curves ◽  
Flow Reserve

Joseph P Archie Jr, PhD, MD Abstract Purpose. Patients with 50% or greater diameter stenosis are at risk for ischemic stroke due to embolization and/or reduced cerebral blood flow. The hemodynamics of progressive carotid stenosis on cerebral blood flow and blood flow reserve has not been adequately measured or predicted. This information is needed for stroke risk stratification in patients with carotid stenosis. The aim of this hemodynamic model study is to predict the contribution of carotid and collateral blood flows to regional cerebral blood flow and cerebral blood flow reserve in patients with moderate to severe carotid stenosis. Methods. A one-dimensional three-parameter fluid mechanics model for the carotid, collateral and brain vascular systems is used to predict regional cerebral blood flow and blood flow reserve as a function of percent diameter carotid stenosis. The model is based on the principal of conservation of energy as employed by Bernoulli to describe fluid flow on a streamline. When applied to the human cerebrovascular system there are three vascular resistance components; carotid, collateral and brain. Carotid artery vascular resistance is assumed to be a function of fractional percent carotid artery area stenosis. This is not a complex modern computational fluid mechanics study. The model blood flow algebraic equations have simple solutions, one of which gives patient specific collateral resistance values. The solutions are given as patient specific cerebral blood flows and flow reserve as a function of percent diameter stenosis. Established normal clinical values of regional cerebral blood flow, cerebral blood flow auto-regulation and the lower threshold of cerebral perfusion pressure for cerebral auto-regulation are used. Carotid vascular resistance is assumed to be proportional to percent area carotid stenosis. Theoretical solutions use mean systemic arterial pressure of 100mmHg and key clinical values of patient collateral vascular resistance. Clinical solutions use patient measured systemic arterial pressures and carotid stump pressures. The solutions are given as patient specific cerebral blood flow and reserve cerebral blood flow curves over the range of diameter carotid stenosis. Results. Normal regional cerebral blood flow of 50ml/min/100g is predicted to be maintained up to 65% diameter carotid stenosis as reserve blood flow is reduced. With further progression of carotid stenosis to occlusion approximately half of patients are predicted to develop some reduction in cerebral blood flow. However, only about 20% of patients have a decrease in cerebral blood flow below the 30ml/min/100g threshold for cerebral ischemic symptoms. Approximately 10% of patients are predicted to develop regional cerebral blood flow less than the 18ml/min/100g threshold for irreversible ischemic injury. The model predicts critical carotid artery stenosis to be between 65% and 71% diameter depending on mean systemic arterial pressure. With higher degrees of stenosis carotid artery blood flow cannot maintain normal cerebral flow without the contribution of collateral flow. The predicted magnitude of carotid energy dissipation between 60% and 90% stenosis is consistent with observed cervical bruit intensity. Predicted patient specific cerebral blood flow reserve is adequate to prevent significant cerebral ischemia in the majority of patients. Conclusions. Patient specific collateral vascular resistance blood flow curves predict regional cerebral blood flow and blood flow reserve as a function of the degree of diameter carotid artery stenosis. The carotid component of cerebral blood flow is predicted to maintain normal cerebral blood flow up to a critical carotid diameter stenosis of 65% to 71%. Collateral blood flow is necessary to maintain normal cerebral flow at higher degrees of carotid stenosis. The clinical model predicts that many patients do not have sufficient collateral flow to prevent a decrease in cerebral flow should carotid stenosis progress to high grade or occlusion. However, only about 10% of patients are predicted to develop irreversible regional cerebral ischemic injury. Estimated carotid stenosis energy dissipation magnitudes agree with observed cervical bruit intensity. Correlation of predicted cerebral reserve blood flow curves with clinically measured cerebrovascular reactivity/reserve has the potential to predict the probability of future cerebral ischemia in asymptomatic patients with 60% to 80% stenosis.

Cerebral circulatory responses of near-term ovine fetuses during sustained fetal placental embolization

1997 ◽  
Vol 273 (4) ◽  
pp. H2001-H2008 ◽  
Author(s):  
Robert Gagnon ◽  
Tasha Lamb ◽  
Bryan Richardson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Vascular Resistance ◽  
External Carotid Artery ◽  
External Carotid ◽  
Carotid Blood Flow ◽  
Arterial Blood ◽  
Pregnant Sheep ◽  
Flow Waveforms

To test the hypothesis that, in response to an increase in placental vascular resistance and progressive fetal asphyxia, the changes in external carotid blood flow waveforms are directly related to changes in external carotid vascular resistance, we embolized the fetal side of the placenta in pregnant sheep and measured cerebral and external carotid artery circulatory changes in relation to changes in external carotid artery flow waveforms. Chronically catheterized fetal sheep at 0.85 of gestation were embolized ( n = 11) in the descending aorta for 6 h, until fetal arterial pH fell to ∼6.90. Fetuses became rapidly hypoxemic ( P < 0.0001) and developed a mixed respiratory and metabolic acidosis ( P< 0.0001 for [Formula: see text], pH, and base excess). There was a transient 40% increase in external carotid blood flow at pH ∼7.25 and a parallel 32% increase in fetal arterial blood pressure (both P < 0.01), whereas the external vascular resistance remained unaltered. Cerebral blood flow increased by 130% ( P < 0.0001), and cerebral vascular resistance decreased by 125% ( P < 0.0001) throughout the study. The external carotid resistance index (RI) decreased by 32% ( P < 0.0001) at the time external carotid vascular resistance remained unchanged. This fall in external carotid RI was due almost entirely to a 110% increase in external carotid fundamental impedance ( P < 0.001). We conclude that the poor relationship between the changes in external carotid vascular resistance and RI indicated that other hemodynamic factors such as vascular impedance to pulsatile flow must be measured for correct interpretation of changes in flow waveform shape under hypoxic conditions. In addition, changes in external carotid blood flow were not proportional to changes in cerebral blood flow in this model.

scholarly journals Skeletal muscle blood flow responses to hypoperfusion at rest and during rhythmic exercise in humans

2009 ◽  
Vol 107 (2) ◽  
pp. 429-437 ◽  
Author(s):  
Darren P. Casey ◽  
Michael J. Joyner
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Brachial Artery ◽  
Muscle Blood Flow ◽  
Systemic Arterial Pressure ◽  
Collateral Flow ◽  
Elastic Recoil ◽  
Balloon Inflation ◽  
Acute Increase

We evaluated the contribution of changes in systemic arterial pressure and local vasodilation to blood flow restoration in contracting human muscles during acute hypoperfusion. Healthy subjects ( n = 10) performed rhythmic forearm exercise (10% and 20% of maximum) while a balloon in the brachial artery located above the elbow was inflated. Each trial included 3 min of rest, exercise, exercise with balloon inflation, and exercise after balloon deflation. Forearm blood flow (FBF) was measured using Doppler ultrasound. Blood pressure on both sides of the balloon was measured using a brachial artery catheter (distal pressure), and Finometer for proximal (systemic) arterial pressure. Balloon inflation during exercise reduced distal arterial pressure, and FBF fell 37–41%. There was also a surprising acute increase in forearm vascular resistance (distal pressure/FBF). This was followed by recovery of distal arterial pressure and forearm vasodilation that caused a marked (∼75%) restoration of flow that was not associated with significant changes in systemic arterial pressure. During validation trials ( n = 6) at rest and with exercise both balloon and brachial artery diameters were stable when the balloon was inflated. Our findings indicate that at these exercise intensities 1) the restoration of FBF during exercise with hypoperfusion relied primarily on local dilator responses in conjunction with restoration of distal perfusion pressure likely as a result of increased collateral flow around the elbow, and 2) a loss of pulsatile flow and elastic recoil in the forearm may have contributed to the acute increase in vascular resistance seen at the onset of hypoperfusion.

Hyperthermia-induced vasoconstriction of the carotid artery, a possible causative factor of heatstroke

2004 ◽  
Vol 96 (5) ◽  
pp. 1875-1878 ◽  
Author(s):  
Seham Mustafa ◽  
O. Thulesius ◽  
H. N. Ismael
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Carotid Artery ◽  
Brain Damage ◽  
Experimental Studies ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Electrical Field ◽  
Basal Tone

Clinical and experimental studies indicate that hyperthermia can cause heatstroke with cerebral ischemia and brain damage. However, no study has examined the direct effects of heating carotid artery smooth muscle and tested the hypothesis that hyperthermia induces arterial vasoconstriction and, thereby, decreases cerebral blood flow. We recorded isometric tension of rabbit carotid artery strips in organ baths during stepwise temperature elevation. The heating responses were tested at basal tone, in norepinephrine- and KCl-precontracted vessels, and after electrical field stimulation. Stepwise heating from 37°C to 47°C induced reproducible graded contraction proportional to temperature. The responses could be elicited at basal tone and in precontracted vessels. Heating decreased the contractile responses to norepinephrine and electrical field stimulation but increased contraction to KCl. These responses were not eliminated by pretreatment with the neuronal blocker tetrodotoxin. Our results demonstrate that heating carotid artery preparations above 37°C (normothermia) induced a reversible graded vasoconstriction proportional to temperature. In vivo this reaction may lead to a decrease in cerebral blood flow and cerebral ischemia with brain damage as in heatstroke. The heating-induced contraction is not mediated by a neurogenic process but is due to altered transcellular Ca2+ transport. Cooling, in particular of the neck area, therefore, should be used in the treatment of heatstroke.

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