A mathematical model of the relationship between cerebral blood volume and intracranial pressure changes: The generation of plateau waves

1991 ◽  
Vol 19 (1) ◽  
pp. 15-42 ◽  
Author(s):  
Mauro Ursino ◽  
Patrizia Di Giammarco
Keyword(s):  
Mathematical Model ◽  
Intracranial Pressure ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Plateau Waves ◽  
Pressure Changes ◽  
The Relationship

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.

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.

Rheographic assessment of cerebral blood volume and correlations with changes in intracranial pressure

1976 ◽  
Vol 34 (1-4) ◽  
pp. 287-294 ◽  
Author(s):  
A. L. Benabid ◽  
J. C. Persat ◽  
J. F. Piquard ◽  
M. Barge ◽  
J. P. Chirossel
Keyword(s):  
Intracranial Pressure ◽  
Blood Volume ◽  
Cerebral Blood Volume

Effects of increased intracranial pressure on cerebral blood volume, blood flow, and oxygen utilization in monkeys

1975 ◽  
Vol 43 (4) ◽  
pp. 385-398 ◽  
Author(s):  
Robert L. Grubb ◽  
Marcus E. Raichle ◽  
Michael E. Phelps ◽  
Robert A. Ratcheson
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Metabolic Rate ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Blood Volume ◽  
Cerebral Perfusion ◽  
Cerebral Blood Volume ◽  
Perfusion Pressure ◽  
Cerebral Metabolic Rate

✓ The relationship of cerebral blood volume (CBV) to cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and the cerebral metabolic rate for oxygen (CMRO2) was examined in rhesus monkeys. In vivo tracer methods employing radioactive oxygen-15 were used to measure CBV, CBF, and CMRO2. Cerebral perfusion pressure was decreased by raising the intracranial pressure (ICP) by infusion of artificial cerebrospinal fluid (CSF) into the cisterna magna. The production of progressive intracranial hypertension to an ICP of 70 torr (CPP of 40 torr) caused a rise in CBV accompanied by a steady CBF. With a further increase in ICP to 94 torr, CBV remained elevated without change while CBF declined significantly. Cerebral metabolic rate for oxygen did not change significantly during intracranial hypertension. For comparison, CPP was lowered by reducing mean arterial blood pressure in a second group of monkeys. Only CBF was measured in this group. In this second group of animals, the lower limit of CBF autoregulation was reached at a higher CPP (CPP ∼ 80 torr) than when an increase in ICP was employed (CPP ∼ 30 torr).

scholarly journals Intracranial pressure dynamics in patients with acute brain damage

1997 ◽  
Vol 82 (4) ◽  
pp. 1270-1282 ◽  
Author(s):  
M. Ursino ◽  
C. A. Lodi ◽  
S. Rossi ◽  
N. Stocchetti
Keyword(s):  
Intracranial Pressure ◽  
Brain Damage ◽  
Blood Volume ◽  
Time Constant ◽  
Cerebral Blood Volume ◽  
Volume Index ◽  
Parameter Estimates ◽  
Time Pattern ◽  
Pressure Dynamics ◽  
Parameter Values

Ursino, M., C. A. Lodi, S. Rossi, and N. Stocchetti.Intracranial pressure dynamics in patients with acute brain damage. J. Appl. Physiol. 82(4): 1270–1282, 1997.—The time pattern of intracranial pressure (ICP) during pressure-volume index (PVI) tests was analyzed in 20 patients with severe acute brain damage by means of a simple mathematical model. In most cases, a satisfactory fitting between model response and patient data was achieved by adjusting only four parameters: the cerebrospinal fluid (CSF) outflow resistance, the intracranial elastance coefficient, and the gain and time constant of cerebral autoregulation. The correlation between the parameter estimates was also analyzed to elucidate the main mechanisms responsible for ICP changes in each patient. Starting from information on the estimated parameter values and their correlation, the patients were classified into two main classes: those with weak autoregulation (8 of 20 patients) and those with strong autoregulation (12 of 20 patients). In the first group of patients, ICP mainly reflects CSF circulation and passive cerebral blood volume changes. In the second group, ICP exhibits paradoxical responses attributable to active changes in cerebral blood volume. Moreover, in two patients of the second group, the time constant of autoregulation is significantly increased (>40 s). The correlation between the parameter estimates was significantly different in the two groups of patients, suggesting the existence of different mechanisms responsible for ICP changes. Moreover, analysis of the correlation between the parameter estimates might give information on the directions of parameter changes that have a greater impact on ICP.

Management of Elevated Intracranial Pressure

2002 ◽  
Vol 15 (2) ◽  
pp. 167-185 ◽  
Author(s):  
Beth A. Vanderheyden ◽  
Brian D. Buck
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Blood Volume ◽  
Vital Signs ◽  
Elevated Intracranial Pressure ◽  
Neurologic Injury ◽  
Barbiturate Coma ◽  
Therapeutic Modalities ◽  
Neurologic Disorders ◽  
Pharmacologic Management ◽  
The Relationship

Elevated intracranial pressure (ICP) is a primary cause of morbidity and mortality for many neurologic disorders. The relationship between ICP and brain volume is influenced by autoregulatory processes that can become dysfunctional. As a result, neurologic damage can occur by systemic and intracranial insults such as ischemia and excitatory amino acids. Therefore, survival is dependent on optimizing ICP and cerebral perfusion pressure. Treatment of intracranial hypertension requires intensive monitoring and aggressive therapy. Intracranial pressure monitoring techniques such as intraventricular catheters are useful for determining ICP elevations before changes in vital signs and neurologic status. Therapeutic modalities, generally aimed at reducing cerebral blood volume, brain tissue, and cerebrospinal fluid (CSF) volume, include nonpharmacologic (CSF removal, controlled hyperventilation, and elevating the patient’s head) and pharmacologic management. Mannitol and sedation are first-line agents used to lower ICP. Barbiturate coma may be beneficial in patients with elevated ICP refractory to conventional treatment. The use of prophylactic antiseizure therapy and optimal nutrition prevents significant complication. Currently, investigations are directed at discovering useful neuroprotective agents that prevent secondary neurologic injury.

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