A theoretical model of cerebral hemodynamics: application to the study of arteriovenous malformations

Abstract

A comprehensive computer model of the cerebral circulation, based on both hydrodynamics and electrical network analysis, was used to investigate the influences of arteriovenous malformations (AVM) on regional cerebral hemodynamics. The basic model contained 114 normal compartments: 55 arteries, 37 veins, 20 microvessel groups (MVG), one compartment representing systemic and extracranial vascular resistance, and one representing the heart. Each microvessel group, which represented the arteriolar bed, consisted of 5000 microvessels. Cerebral blood flow autoregulation was simulated by a formula that determined the resistance and therefore the flow rate of the microvessel groups (arterioles) as a function of perfusion pressure. Elasticity was introduced to describe the compliance of each vessel. Flow rate was made a controlling factor for the positive regulation of the diameters of conductance vessels by calculation of shear stress on the vessel wall (vessel dilation). Models containing an AVM were constructed by adding an AVM compartment and its feeding arteries and draining veins. In addition to the basic model, AVM models were simulated with and without autoregulation and flow-induced conductance vessel dilation to evaluate the contributions of these factors on cerebral hemodynamics. Results for the model with vessel dilation were more similar to clinical observations than those without vessel dilation. Even in the presence of total vasoparalysis of the arteriolar bed equivalent, obliteration of a large (1000 mL/min) shunt flow AVM resulted in a near-field CBF increase from a baseline of 21 to a post-occlusion value of no more than 74 mL/100 g/min, casting doubt on a purely hemodynamic basis for severe hyperemia after treatment. The results of the simulations suggest that our model may be a useful tool to study hemodynamic problems of the cerebral circulation.