A computer simulation of the haemodynamic effects of intracranial arteriovenous malformation occlusion.
To study the effect of AVM occlusion on cerebrovascular haemodynamics, a simplified model was simulated consisting of a feeding artery supplying a capillary bed in parallel with a fistula-like malformation, both emptying into a draining vein. An electrical circuit analogue of the physiologic system was developed using lumped proximal and distal pressure dependent resistances, and capacitors representing vascular compliance. Autoregulation was introduced as a pressure varying precapillary arteriolar resistance. Equations derived from the circuit model were simulated using a graphical modeling program. The model successfully simulates phenomena angiographically observed during embolization procedures. Fistula pressure is shown to rapidly fall following proximal AVM occlusion, in contrast to a marked rise seen with distal occlusion, which is associated with biphasic flow into and out of the fistula and the arterial feeder. The model predicts an increase in capillary pressure and capillary flow which, depending on the magnitude of the flow increase and the state of autoregulation, may result either in reversal of ischaemia or hyperperfusion injury. Vascular overload is predicted in the absence of autoregulation. There is, however, little potential for vascular overload when autoregulation is intact. The model represents a first step in the mathematical characterization of the phenomenon of hyperperfusion following AVM occlusion.
Ornstein
E
E
Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY 10032.
Blesser
W B
WB
Young
W L
WL
Pile-Spellman
J
J
D001157:Arterial Occlusive Diseases / Q000503:physiopathology; D001794:Blood Pressure; D002196:Capillaries / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D003198:Computer Simulation; D006439:Hemodynamics; D006706:Homeostasis; D006801:Humans; D002538:Intracranial Arteriovenous Malformations / Q000503:physiopathology*; D008955:Models, Cardiovascular; D008962:Models, Theoretical