scholarly journals Cerebral hemodynamics: a mathematical model including autoregulation, baroreflex and extracranial peripheral circulation

2021 ◽  
Author(s):  
Francisco Ambrosio Garcia ◽  
Deusdedit Lineu Spavieri Junior ◽  
Andreas Linninger
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cerebral Autoregulation ◽  
Peripheral Circulation ◽  
Flow Regulation ◽  
Pressure Waves ◽  
Vascular Bed ◽  
Blood Flow Regulation

Increasing evidence supports that cerebral autoregulation and mean arterial pressure regulation via baroreflex contribute to cerebral blood flow regulation. It is unclear whether the extracranial vascular bed of the head and neck helps reestablishing cerebral blood flow during changes in mean arterial pressure. Current computational models of cerebral blood flow regulation do not address the relationships between the intracranial and extracranial blood flow dynamics. We present a model of cerebral autoregulation, extracranial peripheral circulation and baroreflex control of heart rate and of peripheral vasculature that was included to the model of intracranial dynamics proposed by Linninger et al. (2009), which incorporates the fully coupled blood, cerebrospinal fluid and brain parenchyma systems. Autoregulation was modelled as being pressure-mediated at the arteries and arterioles and flow-mediated at the microcirculation. During simulations of a bout of acute hypotension, cerebral blood flow returns rapidly to baseline levels with a very small overshoot, whereas the blood flow to the peripheral circulation of the head and neck suffers a prolonged suppression in accordance with experimental evidence. The inclusion of baroreflex regulation at the extracranial vascular bed had a negligible effect on cerebral blood flow regulation during dynamic changes in mean arterial pressure. Moreover, the results suggest that the extracranial blood flow carries only modest information about cerebral blood flow in dynamic situations in which cerebral autoregulation is preserved and mean arterial pressure suffers alterations. This information is likely higher when the autoregulation is impaired. Steady-state cerebral blood flow in the model is kept within normal ranges despite variations in mean arterial pressure from 50 to 175 mmHg. By inputting aortic pressure waves from individuals with increasing arterial rigidity, increasing arterial systolic and pulse pressures, the model predicts the generation of intracranial pressure waves with accordingly increasing peaks and amplitudes.

A lumped parameter model of cerebral blood flow control combining cerebral autoregulation and neurovascular coupling

2012 ◽  
Vol 303 (9) ◽  
pp. H1143-H1153 ◽  
Author(s):  
Bart Spronck ◽  
Esther G. H. J. Martens ◽  
Erik D. Gommer ◽  
Frans N. van de Vosse
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Control ◽  
Cerebral Autoregulation ◽  
Neurovascular Coupling ◽  
Flow Regulation ◽  
Lumped Parameter Model ◽  
Blood Flow Regulation ◽  
Lumped Parameter ◽  
Blood Flow Control

Cerebral blood flow regulation is based on a variety of different mechanisms, of which the relative regulatory role remains largely unknown. The cerebral regulatory system expresses two regulatory properties: cerebral autoregulation and neurovascular coupling. Since partly the same mechanisms play a role in cerebral autoregulation and neurovascular coupling, this study aimed to develop a physiologically based mathematical model of cerebral blood flow regulation combining these properties. A lumped parameter model of the P2 segment of the posterior cerebral artery and its distal vessels was constructed. Blood flow regulation is exerted at the arteriolar level by vascular smooth muscle and implements myogenic, shear stress based, neurogenic, and metabolic mechanisms. In eight healthy subjects, cerebral autoregulation and neurovascular coupling were challenged by squat-stand maneuvers and visual stimulation using a checkerboard pattern, respectively. Cerebral blood flow velocity was measured using transcranial Doppler, whereas blood pressure was measured by finger volume clamping. In seven subjects, the model proposed fits autoregulation and neurovascular coupling measurement data well. Myogenic regulation is found to dominate the autoregulatory response. Neurogenic regulation, although only implemented as a first-order mechanism, describes neurovascular coupling responses to a great extent. It is concluded that our single, integrated model of cerebral blood flow control may be used to identify the main mechanisms affecting cerebral blood flow regulation in individual subjects.

Relationship of cerebral blood flow regulation to acute mountain sickness.

1989 ◽  
Vol 8 (3) ◽  
pp. 143-148 ◽  
Author(s):  
S M Otis ◽  
M E Rossman ◽  
P A Schneider ◽  
M P Rush ◽  
E B Ringelstein
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Mountain Sickness ◽  
Flow Regulation ◽  
Blood Flow Regulation ◽  
Mountain Sickness ◽  
Relationship Of

Direct Cerebral Vasodilatory Effects of Sevoflurane and Isoflurane 

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
End Tidal

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P<0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.

Abstract TP446: Independent Measures of Cerebral Blood Flow in Asymptomatic Carotid Artery Disease.

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Randolph S Marshall ◽  
MaryKay Pavol ◽  
Ken Cheung ◽  
Isabelle Strom ◽  
Kevin Slane ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Function Analysis ◽  
Flow Regulation ◽  
Critical Element ◽  
Mean Flow ◽  
Blood Flow Regulation ◽  
Hemodynamic State ◽  
Transfer Function Analysis

Background: Cerebral blood flow (CBF) regulation is a critical element in cerebrovascular pathophysiology, particularly in large vessel disease. Different methods to assess hemodynamics may represent different aspects of blood flow regulation, however, uniquely affecting outcomes and management. We examined 4 different blood-flow related measures in patients with high-grade unilateral carotid disease, assessing asymmetry between the occluded vs non-occluded side, and the correlations among the measures. Methods: Thirty-three patients (age 50-93, 19M) with unilateral 80-100% ICA occlusion but no stroke underwent: 1) quantitative resting CBF using continuous arterial spin labeling (CASL) MRI, 2) mean flow velocity (MFV) in both middle cerebral arteries (MCAs) by transcranial Doppler, 3). Vasomotor reactivity (VMR) in response to 2 minutes of 5% CO2 inhalation, and 4) Dynamic cerebral autoregulation (DCA) using continuous insonation of both MCAs for 10 minutes at depth 56mm with a standard head frame. Phase shift (PS) between spontaneous oscillations in blood pressure (measured with finger photoplethysmography) and MCA MFV at frequencies .06-.12 Hz was calculated for each hemisphere using transfer function analysis. Lower PS indicated worse autoregulation. Paired T-tests and Pearson correlations were used to look for side-to-side differences within each measure, and correlations between measures (SPSS v.22). Results: CASL CBF (p=.001), MFV (p<.001), VMR (p=.008), and DCA (p=.047) all showed significantly lower values on the occluded side. The 4 measures were independent of each other on correlation analysis, even when controlling for age and anterior circle of Willis collateral (correlation coefficients all <0.40, p-values >0.09). Conclusions: These 4 measures showed high sensitivity to the occluded carotid artery, but appear to represent independent aspects of cerebral blood flow (CASL: resting gray matter CBF; MFV: whole-hemisphere CBF; VMR: cerebrovascular reserve, and DCA: homeostatic blood flow regulation) suggesting that any given measure only partially characterizes hemodynamic state. Further investigation will use these 4 measures to predict outcomes including vascular cognitive impairment.

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

1985 ◽  
Vol 63 (6) ◽  
pp. 937-943 ◽  
Author(s):  
David J. Boarini ◽  
Neal F. Kassell ◽  
James A. Sprowell ◽  
Julie J. Olin ◽  
Hans C. Coester
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Hypotension ◽  
Content Type ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Fine Print

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

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