Interaction among autoregulation, CO2 reactivity, and intracranial pressure: a mathematical model

1998 ◽  
Vol 274 (5) ◽  
pp. H1715-H1728 ◽  
Author(s):  
Mauro Ursino ◽  
Carlo Alberto Lodi
Keyword(s):  
Mathematical Model ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Nonlinear Interaction ◽  
Cerebral Blood Volume ◽  
Cerebral Hemodynamics ◽  
Pial Arteries ◽  
Arterial Circulation ◽  
Neurosurgical Patients

The relationships among cerebral blood flow, cerebral blood volume, intracranial pressure (ICP), and the action of cerebrovascular regulatory mechanisms (autoregulation and CO2 reactivity) were investigated by means of a mathematical model. The model incorporates the cerebrospinal fluid (CSF) circulation, the intracranial pressure-volume relationship, and cerebral hemodynamics. The latter is based on the following main assumptions: the middle cerebral arteries behave passively following transmural pressure changes; the pial arterial circulation includes two segments (large and small pial arteries) subject to different autoregulation mechanisms; and the venous cerebrovascular bed behaves as a Starling resistor. A new aspect of the model exists in the description of CO2 reactivity in the pial arterial circulation and in the analysis of its nonlinear interaction with autoregulation. Simulation results, obtained at constant ICP using various combinations of mean arterial pressure and CO2 pressure, substantially support data on cerebral blood flow and velocity reported in the physiological literature concerning both the separate effects of CO2 and autoregulation and their nonlinear interaction. Simulations performed in dynamic conditions with varying ICP underline the existence of a significant correlation between ICP dynamics and cerebral hemodynamics in response to CO2 changes. This correlation may significantly increase in pathological subjects with poor intracranial compliance and reduced CSF outflow. In perspective, the model can be used to study ICP and blood velocity time patterns in neurosurgical patients in order to gain a deeper insight into the pathophysiological mechanisms leading to intracranial hypertension and secondary brain damage.

scholarly journals Effects of Midazolam on Cerebral Hemodynamics and Cerebral Vasomotor Responsiveness to Carbon Dioxide

1983 ◽  
Vol 3 (2) ◽  
pp. 246-249 ◽  
Author(s):  
A. Forster ◽  
O. Juge ◽  
D. Morel
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Blood Volume ◽  
Water Soluble ◽  
Increased Intracranial Pressure ◽  
Beneficial Effects ◽  
The Mean

Although it is known that hypercarbia increases and benzodiazepines decrease cerebral blood flow (CBF), the effects of benzodiazepines on CBF responsiveness to CO2 are not well documented. The influence on CBF and CBF-C02 sensitivity of placebo or midazolam, which is a new water-soluble benzodiazepine, was measured in eight healthy volunteers using the noninvasive 133Xe inhalation method for CBF determination. Under normocarbia, midazolam decreased CBF from 40.6 ± 3.2 to 27.0 ± 5.0 ml 100 g−1 min−1 (x̄ ± SD). At a later session under hypercarbia, CBF was 58.8 ± 4.4 ml 100 g−1 min−1 after administration of placebo, and 49.1 ± 10.2 ml 100 g−1 min−1 after midazolam. The mean of the slopes correlating Paco2 and CBF was significantly steeper with midazolam (2.5 ± 1.2 ml 100 g−1 min−1 mm Hg−1) than with placebo (1.5 ± 0.4 ml 100 g−1 min−1 mm Hg−1). Our results suggest that midazolam may be a safe agent to use in patients with intracranial hypertension, since it decreases CBF and thus cerebral blood volume; however, it should be administered with caution in nonventilated patients with increased intracranial pressure, since its beneficial effects on cerebrovascular tone can be readily counteracted by the increase in arterial CO2 tension induced by this drug.

scholarly journals Peranan Hiperventilasi terhadap Penurunan Tekanan Intrakranial dalam Kasus Bedah Saraf

2020 ◽  
Vol 9 (1) ◽  
pp. 60-70
Author(s):  
Irwan Wibowo ◽  
M Sofyan Harahap
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Perivascular Space ◽  
Main Concern ◽  
Short Term ◽  
Cerebral Vasoconstriction ◽  
The Brain

AbstrakHiperventilasi telah ditemukan sebagai salah satu cara untuk menurunkan aliran darah otak (cerebral blood flow) (CBF) sejak tahun 1920-an. Pada saat itu telah dilaporkan bahwa penggunaan hiperventilasi dapat mengurangi peningkatan tekanan intrakranial (intracranial pressure/ICP) dengan vasokonstriksi serebral sehingga mampu menurunkan volume darah di daerah serebral. Secara teoritis, manfaat hiperventilasi mungkin lebih khusus diharapkan pada pasien di mana peningkatan ICP terjadi terutama karena peningkatan volume darah otak akibat mekanisme vasodilatasi. Efek vasokonstriksi tersebut akan menghilang setelah pH pada ruang perivaskular kembali normal setelah 24 jam. Yang menjadi perhatian utama dalam metode ini adalah tindakan tersebut mampu menginduksi terjadinya iskemia serebral baik secara regional maupun global. Risiko kerusakan iskemik tersebut bergantung pada sejauh mana dan seberapa lama otak mengalami aliran darah yang rendah. Masih terdapat data yang kontroversial antara yang mendukung ataupun menentang penggunaan terapi hiperventilasi, namun menurut penelitian yang telah dilakukan, tindakan ini mampu menurunkan ICP jika dilakukan dalam jangka pendek. Pemantauan multimodalitas terhadap pasien tetap diperlukan untuk memantau keberhasilan dalam tindakan ini. Hyperventilation Management for Decrease Intracranial Pressure in Neurosurgery CasesAbstractHyperventilation has been found as a way to reduce cerebral blood flow (CBF) since 1920s. At that time it was reported that the use of hyperventilation can reduce the increase in intracranial pressure (ICP) by causing cerebral vasoconstriction and decreasing cerebral blood volume. Theoretically, the benefits of hyperventilation may be more specifically expected in patients which has increasing ICP because of an increasing in blood volume and vasodilation mechanism. The vasoconstriction effect disappears after the pH in the perivascular space returns to normal after 24 hours. The main concern in treating patients with increased ICP using hyperventilation is to induce cerebral ischemia both regionally and globally. As with a stroke, the risk of ischemic damage depends on the extent and how long the brain experiences low blood flow. Controversial data still exists between those that support or oppose the use of hyperventilation therapy, but if hypocapnia monitoring is done to control the increase in ICP in the short term, hyperventilation therapy remains beneficial. Multimodality monitoring is needed so that hyperventilation therapy can be used safely in certain patients who may need this therapy. 

scholarly journals A simple mathematical model of the interaction between intracranial pressure and cerebral hemodynamics

1997 ◽  
Vol 82 (4) ◽  
pp. 1256-1269 ◽  
Author(s):  
Mauro Ursino ◽  
Carlo Alberto Lodi
Keyword(s):  
Mathematical Model ◽  
Intracranial Pressure ◽  
Blood Volume ◽  
Cerebral Autoregulation ◽  
Cerebral Blood Volume ◽  
Cerebral Hemodynamics ◽  
Arterial Hypotension ◽  
Simple Mathematical Model ◽  
Compensatory Mechanisms ◽  
Plateau Waves

Ursino, Mauro, and Carlo Alberto Lodi. A simple mathematical model of the interaction between intracranial pressure and cerebral hemodynamics. J. Appl. Physiol. 82(4): 1256–1269, 1997.—A simple mathematical model of intracranial pressure (ICP) dynamics oriented to clinical practice is presented. It includes the hemodynamics of the arterial-arteriolar cerebrovascular bed, cerebrospinal fluid (CSF) production and reabsorption processes, the nonlinear pressure-volume relationship of the craniospinal compartment, and a Starling resistor mechanism for the cerebral veins. Moreover, arterioles are controlled by cerebral autoregulation mechanisms, which are simulated by means of a time constant and a sigmoidal static characteristic. The model is used to simulate interactions between ICP, cerebral blood volume, and autoregulation. Three different related phenomena are analyzed: the generation of plateau waves, the effect of acute arterial hypotension on ICP, and the role of cerebral hemodynamics during pressure-volume index (PVI) tests. Simulation results suggest the following: 1) ICP dynamics may become unstable in patients with elevated CSF outflow resistance and decreased intracranial compliance, provided cerebral autoregulation is efficient. Instability manifests itself with the occurrence of self-sustained plateau waves. 2) Moderate acute arterial hypotension may have completely different effects on ICP, depending on the value of model parameters. If physiological compensatory mechanisms (CSF circulation and intracranial storage capacity) are efficient, acute hypotension has only negligible effects on ICP and cerebral blood flow (CBF). If these compensatory mechanisms are poor, even modest hypotension may induce a large transient increase in ICP and a significant transient reduction in CBF, with risks of secondary brain damage. 3) The ICP response to a bolus injection (PVI test) is sharply affected, via cerebral blood volume changes, by cerebral hemodynamics and autoregulation. We suggest that PVI tests may be used to extract information not only on intracranial compliance and CSF circulation, but also on the status of mechanisms controlling CBF.

Hyperacute Stroke: Simultaneous Measurement of Relative Cerebral Blood Volume, Relative Cerebral Blood Flow, and Mean Tissue Transit Time

Radiology ◽  
1999 ◽  
Vol 210 (2) ◽  
pp. 519-527 ◽  
Author(s):  
A. Gregory Sorensen ◽  
William A. Copen ◽  
Leif Østergaard ◽  
Ferdinando S. Buonanno ◽  
R. Gilberto Gonzalez ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Volume ◽  
Transit Time ◽  
Simultaneous Measurement ◽  
Cerebral Blood Volume ◽  
Hyperacute Stroke ◽  
Relative Cerebral Blood Volume

scholarly journals Effects of Acetazolamide on Cerebral Blood Flow, Blood Volume, and Oxygen Metabolism: A Positron Emission Tomography Study with Healthy Volunteers

2001 ◽  
Vol 21 (12) ◽  
pp. 1472-1479 ◽  
Author(s):  
Hidehiko Okazawa ◽  
Hiroshi Yamauchi ◽  
Kanji Sugimoto ◽  
Hiroshi Toyoda ◽  
Yoshihiko Kishibe ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Capillary Blood ◽  
Emission Tomography ◽  
Positron Emission ◽  
Capillary Blood Volume

To evaluate changes in cerebral hemodynamics and metabolism induced by acetazolamide in healthy subjects, positron emission tomography studies for measurement of cerebral perfusion and oxygen consumption were performed. Sixteen healthy volunteers underwent positron emission tomography studies with15O-gas and water before and after intravenous administration of acetazolamide. Dynamic positron emission tomography data were acquired after bolus injection of H215O and bolus inhalation of15O2. Cerebral blood flow, metabolic rate of oxygen, and arterial-to-capillary blood volume images were calculated using the three-weighted integral method. The images of cerebral blood volume were calculated using the bolus inhalation technique of C15O. The scans for cerebral blood flow and volume and metabolic rate of oxygen after acetazolamide challenge were performed at 10, 20, and 30 minutes after drug injection. The parametric images obtained under the two conditions at baseline and after acetazolamide administration were compared. The global and regional values for cerebral blood flow and volume and arterial-to-capillary blood volume increased significantly after acetazolamide administration compared with the baseline condition, whereas no difference in metabolic rate of oxygen was observed. Acetazolamide-induced increases in both blood flow and volume in the normal brain occurred as a vasodilatory reaction of functioning vessels. The increase in arterial-to-capillary blood volume made the major contribution to the cerebral blood volume increase, indicating that the raise in cerebral blood flow during the acetazolamide challenge is closely related to arterial-to-capillary vasomotor responsiveness.

Early changes measured by magnetic resonance imaging in cerebral blood flow, blood volume, and blood-brain barrier permeability following dexamethasone treatment in patients with brain tumors

1999 ◽  
Vol 90 (2) ◽  
pp. 300-305 ◽  
Author(s):  
Leif Østergaard ◽  
Fred H. Hochberg ◽  
James D. Rabinov ◽  
A. Gregory Sorensen ◽  
Michael Lev ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Magnetic Resonance ◽  
Brain Tumors ◽  
Mr Imaging ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Clinical Effects ◽  
Content Type ◽  
Fine Print

Object. In this study the authors assessed the early changes in brain tumor physiology associated with glucocorticoid administration. Glucocorticoids have a dramatic effect on symptoms in patients with brain tumors over a time scale ranging from minutes to a few hours. Previous studies have indicated that glucocorticoids may act either by decreasing cerebral blood volume (CBV) or blood-tumor barrier (BTB) permeability and thereby the degree of vasogenic edema.Methods. Using magnetic resonance (MR) imaging, the authors examined the acute changes in CBV, cerebral blood flow (CBF), and BTB permeability to gadolinium-diethylenetriamine pentaacetic acid after administration of dexamethasone in six patients with brain tumors. In patients with acute decreases in BTB permeability after dexamethasone administration, changes in the degree of edema were assessed using the apparent diffusion coefficient of water.Conclusions. Dexamethasone was found to cause a dramatic decrease in BTB permeability and regional CBV but no significant changes in CBF or the degree of edema. The authors found that MR imaging provides a powerful tool for investigating the pathophysiological changes associated with the clinical effects of glucocorticoids.

Sign in / Sign up

Export Citation Format

Share Document