Modeling cerebral autoregulation and CO2 reactivity in patients with severe head injury.
The mathematical model presented in a previous work is used to simulate the time pattern of intracranial pressure (ICP) and of blood velocity in the middle cerebral artery (VMCA) in response to maneuvers simultaneously affecting mean systemic arterial pressure (SAP) and end-tidal CO2 pressure. In the first stage of this study, a sensitivity analysis was performed to clarify the role of some important model parameters [cerebrospinal fluid (CSF) outflow resistance, intracranial elastance coefficient, autoregulation gain, and the position of the regulation curve] during CO2 alteration maneuvers performed at different SAP levels. The results suggest that the dynamic "ICP-VMCA" relationship obtained during changes in CO2 pressure may contain important information on the main factors affecting intracranial dynamics. In the second stage, the model was applied to the reproduction of real ICP and velocity tracings in neurosurgical patients. Ten distinct tracings, taken from six patients during CO2 changes at different mean SAP levels, were reproduced. Best fitting between model and clinical curves was achieved by minimizing a least-squares criterion function and adjusting certain parameters that characterize CSF circulation, intracranial compliance, and the strength of the regulation mechanisms. A satisfactory reproduction was achieved in all cases, with parameter numerical values in the ranges reported in clinical literature. It is concluded that the model may be used to give reliable estimations of the main factors affecting intracranial dynamics in individual patients, starting from routine measurements performed in neurosurgical intensive care units.
Lodi
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CA
Department of Electronics, Computer Science and Systems, University of Bologna, Italy.
Ter Minassian
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Beydon
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Ursino
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M
D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000502:physiology; D002536:Cerebral Arteries / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D006259:Craniocerebral Trauma / Q000503:physiopathology*; D006801:Humans; D007427:Intracranial Pressure / Q000502:physiology; D008954:Models, Biological; D008962:Models, Theoretical