Mechanisms of reduced cerebral blood flow in cerebral edema and elevated intracranial pressure

Abstract

A mechanism of elevated intracranial pressure (ICP) in cerebral edema and its effects on cerebral blood flow (CBF) are presented in this paper. To study and demonstrate these effects, a mathematical model of intracranial hydrodynamics was developed. The model simulates the intracranial hydrodynamics and the changes that occur when cerebral edema predominates. To account for an edema pathology, the model includes resistances to cerebrospinal fluid (CSF) and interstitial fluid (ISF) flows within the parenchyma. The resistances change as the intercellular space becomes smaller due to swelling of brain cells. The model demonstrates the effect of changes in these resistances on ICP and venous resistance to blood flow by accounting for the key interactions between pressure, volume, and flow in the intracranial compartments in pathophysiological conditions. The model represents normal intracranial physiology as well as pathological conditions. Simulating cerebral edema with increased resistance to cerebral ISF flow resulted in elevated ICP, increased brain volume, markedly reduced ventricular volume, and decreased CBF as observed in the neurointensive care patients. The model indicates that in high ICP values, alternation of the arterial-arteriolar resistance to flow minimally affects CBF, while at low ICP they have a much greater effect on CBF. The model demonstrates and elucidates intracranial mechanisms related to elevated ICP.

Limitation of cerebral blood flow by increased venous outflow resistance in elevated ICP

“…A lumped parameter model representing interactions between brain tissue, CSF, and blood compartments was developed and described in-depth in previous articles [14,15].…”

“…However, it is observed that the point of equalization between venous pressure and intracranial pressure (ICP) shifts with the elevation of ICP. Figure 2 demonstrates the incorporation of the FCZ into our previously published model of intracranial physiology [14,15] with the FCZ component as the essential component influencing venous outflow.…”