Incorporating a parenchymal thermal diffusion cerebral blood flow probe in bedside assessment of cerebral autoregulation and vasoreactivity in patients with severe traumatic brain injury

2011 ◽  
Vol 114 (1) ◽  
pp. 62-70 ◽  
Author(s):  
Guy Rosenthal ◽  
Rene O. Sanchez-Mejia ◽  
Nicolas Phan ◽  
J. Claude Hemphill ◽  
Christine Martin ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
White Matter ◽  
Thermal Diffusion ◽  
Cerebral Autoregulation ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Severe Tbi ◽  
Cerebral Vascular Resistance

Object Cerebral autoregulation may be altered after traumatic brain injury (TBI). Recent evidence suggests that patients' autoregulatory status following severe TBI may influence cerebral perfusion pressure management. The authors evaluated the utility of incorporating a recently upgraded parenchymal thermal diffusion probe for the measurement of cerebral blood flow (CBF) in the neurointensive care unit for assessing cerebral autoregulation and vasoreactivity at bedside. Methods The authors evaluated 20 patients with severe TBI admitted to San Francisco General Hospital who underwent advanced neuromonitoring. Patients had a parenchymal thermal diffusion probe placed for continuous bedside monitoring of local CBF (locCBF) in addition to the standard intracranial pressure and brain tissue oxygen tension (PbtO2) monitoring. The CBF probes were placed in the white matter using a separate cranial bolt. A pressure challenge, whereby mean arterial pressure (MAP) was increased by about 10 mm Hg, was performed in all patients to assess autoregulation. Cerebral CO2 vasoreactivity was assessed with a hyperventilation challenge. Local cerebral vascular resistance (locCVR) was calculated by dividing cerebral perfusion pressure by locCBF. Local cerebral vascular resistance normalized to baseline (locCVRnormalized) was also calculated for the MAP and hyperventilation challenges. Results In all cases, bedside measurement of locCBF using a cranial bolt in patients with severe TBI resulted in correct placement in the white matter with a low rate of complications. Mean locCBF decreased substantially with hyperventilation challenge (−7 ± 8 ml/100 g/min, p = 0.0002) and increased slightly with MAP challenge (1 ± 7 ml/100 g/min, p = 0.17). Measurements of locCBF following MAP and hyperventilation challenges can be used to calculate locCVR. In 83% of cases, locCVR increased during a hyperventilation challenge (mean change +3.5 ± 3.8 mm Hg/ml/100 g/min, p = 0.0002), indicating preserved cerebral CO2 vasoreactivity. In contrast, we observed a more variable response of locCVR to MAP challenge, with increased locCVR in only 53% of cases during a MAP challenge (mean change −0.17 ± 3.9 mm Hg/ml/100 g/min, p = 0.64) indicating that in many cases autoregulation was impaired following severe TBI. Conclusions Use of the Hemedex thermal diffusion probe appears to be a safe and feasible method that enables continuous monitoring of CBF at the bedside. Cerebral autoregulation and CO2 vasoreactivity can be assessed in patients with severe TBI using the CBF probe by calculating locCVR in response to MAP and hyperventilation challenges. Determining whether CVR increases or decreases with a MAP challenge (locCVRnormalized) may be a simple provocative test to determine patients' autoregulatory status following severe TBI and helping to optimize CPP management.

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 Metabolism and Blood Flow Following Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Metabolism ◽  
Elevated Intracranial Pressure ◽  
Metabolic Demand ◽  
Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

Effects of graded hypotension on cerebral blood flow, blood volume, and mean transit time in dogs

1992 ◽  
Vol 262 (6) ◽  
pp. H1908-H1914 ◽  
Author(s):  
M. Ferrari ◽  
D. A. Wilson ◽  
D. F. Hanley ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion Pressure ◽  
Blood Volume ◽  
Transit Time ◽  
Cerebral Perfusion ◽  
Pressure Range ◽  
Cerebral Blood Volume ◽  
Perfusion Pressure ◽  
Mean Transit Time

This study tested the hypothesis that cerebral blood flow (CBF) is maintained by vasodilation, which manifests itself as a progressive increase in mean transit time (MTT) and cerebral blood volume (CBV) when cerebral perfusion pressure is reduced. Cerebral perfusion pressure was decreased in 10 pentobarbital-anesthetized dogs by controlled hemorrhage. Microsphere-determined CBF was autoregulated in all tested cerebral regions over the 40- to 130-mmHg cerebral perfusion pressure range but decreased by 50% at approximately 30 mmHg. MTT and CBV progressively and proportionately increased in the right parietal cerebral cortex over the 40- to 130-mmHg cerebral perfusion pressure range. Total hemoglobin content (Hb1), measured in the same area by an optical method, increased in parallel with the increases in CBV computed as the (CBF.MTT) product. At 30 mmHg cerebral perfusion pressure, CBV and Hb were still increased and MTT was disproportionately lengthened (690% of control). We conclude that within the autoregulatory range, CBF constancy is maintained by both increased CBV and MTT. Outside the autoregulatory range, substantial prolongation of the MTT occurs. When CBV is maximal, further reductions in cerebral perfusion pressure produce disproportionate increases in MTT that signal the loss of cerebral vascular dilatory hemodynamic reserve.

scholarly journals Cerebral Blood Flow in Patients with Intracranial Pressure Elevation due to Traumatic Brain Edema

1976 ◽  
Vol 3 (1) ◽  
pp. 35-37 ◽  
Author(s):  
W. A. Tweed ◽  
Jørn Overgaard
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Brain Edema ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Monitoring And Control ◽  
Intracranial Pressure Elevation ◽  
Flow Through ◽  
And Control

SUMMARY:The object of this study was to determine if traumatic brain edema (BE) and increased intracranial pressure (ICP) reduce cerebral blood flow (CBF). Two groups of patients were studied, one with slight BE and ICP less than 20 mm Hg., the other with pronounced BE and ICP over 20 mm Hg. Although ICP was higher and cerebral perfusion pressure lower in pro-nounced edema there was only a small and non-significant reduction in CBF and no difference in cerebro-vascular resistance. Since traumatic BE does not increase resistance to blood flow through the brain, cerebral perfusion can be maintained if an adequate perfusion pressure is established. This in turn, demands the monitoring and control of ICP.

Neuropsychiatric lupus or not? Cerebral hypoperfusion by perfusion-weighted MRI in normal-appearing white matter in primary neuropsychiatric lupus erythematosus

2017 ◽  
Vol 77 (3) ◽  
pp. 441-448 ◽  
Author(s):  
Efrosini Papadaki ◽  
Antonis Fanouriakis ◽  
Eleftherios Kavroulakis ◽  
Dimitra Karageorgou ◽  
Prodromos Sidiropoulos ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
White Matter ◽  
Lupus Erythematosus ◽  
Cerebral Perfusion ◽  
Dynamic Susceptibility ◽  
Neuropsychiatric Lupus ◽  
Normal Appearing White Matter ◽  
Conventional Mri ◽  
Dsc Mri

ObjectivesCerebral perfusion abnormalities have been reported in systemic lupus erythematosus (SLE) but their value in distinguishing lupus from non-lupus-related neuropsychiatric events remains elusive. We examined whether dynamic susceptibility contrast-enhanced perfusion MRI (DSC-MRI), a minimally invasive and widely available method of cerebral perfusion assessment, may assist neuropsychiatric SLE (NPSLE) diagnosis.MethodsIn total, 76patients with SLE (37 primary NPSLE, 16 secondary NPSLE, 23 non-NPSLE) and 31 healthy controls underwent conventional MRI (cMRI) and DSC-MRI. Attribution of NPSLE to lupus or not was based on multidisciplinary assessment including cMRI results and response to treatment. Cerebral blood volume and flow were estimated in 18 normal-appearing white and deep grey matter areas.ResultsThe most common manifestations were mood disorder, cognitive disorder and headache. Patients with primary NPSLE had lower cerebral blood flow and volume in several normal-appearing white matter areas compared with controls (P<0.0001) and lower cerebral blood flow in the semioval centre bilaterally, compared with non-NPSLE and patients with secondary NPSLE (P<0.001). A cut-off for cerebral blood flow of 0.77 in the left semioval centre discriminated primary NPSLE from non-NPSLE/secondary NPSLE with 80% sensitivity and 67%–69% specificity. Blood flow values in the left semioval centre showed substantially higher sensitivity than cMRI (81% vs 19%–24%) for diagnosing primary NPSLE with the combination of the two modalities yielding 94%–100% specificity in discriminating primary from secondary NPSLE.ConclusionPrimary NPSLE is characterised by significant hypoperfusion in cerebral white matter that appears normal on cMRI. The combination of DSC-MRI-measured blood flow in the brain semioval centre with conventional MRI may improve NPSLE diagnosis.

CONTINUOUS COMPUTERIZED TRACKING DEFINES RELATIONSHIP BETWEEN CEREBRAL BLOOD FLOW, CEREBRAL PERFUSION PRESSURE AND TIME

1995 ◽  
Vol 23 (Supplement) ◽  
pp. A79
Author(s):  
George Chovanes ◽  
Michael Pasquale ◽  
Mark Cipolle ◽  
Rafael Richards ◽  
Michael Rhodes
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure
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