Combined transfer function analysis and modelling of cerebral autoregulation.
The clinical importance of cerebral autoregulation has resulted in a significant body of literature that attempts both to model the underlying physiological processes and to estimate the mathematical relationships between clinically measurable variables, the most common of which are Arterial Blood Pressure and Cerebral Blood Flow Velocity. These approaches have, however, rarely been used together to interpret clinical data. A simple model of cerebral autoregulation is thus proposed here, based on a flow dependent feedback mechanism with gain and time constant that adjusts arterial compliance. Analysis of this model shows that it closely approximates a second order system for typical values of physiological parameters. The model parameters can be optimally estimated from available experimental data for the Impulse Response (IR), yielding physiologically reasonable values, although there is one free parameter that must be fixed. The effects of changes in feedback gain and time constant are found to be significant on the predicted IR and can thus be estimated robustly from experimental data. The effects of elevated baseline Intracranial Pressure (ICP) are found to be exactly equivalent to a reduced feedback gain, although the solution is much less sensitive to the former effect. A transfer function approach can be used to estimate autoregulation status clinically using a physiologically-based model, thus providing greater insight into the processes that govern cerebral autoregulation.
Payne
S J
SJ
Department of Engineering Science, University of Oxford, Parks Road, OX1 3PJ, Oxford, UK.
Tarassenko
L
L
D000465:Algorithms; D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001921:Brain / Q000098:blood supply* / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D003198:Computer Simulation; D005246:Feedback / Q000502:physiology; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D008955:Models, Cardiovascular