Abstract

The aim of this work was to study the impact of acute cerebral perfusion pressure (CPP) changes and autoregulation on cerebral hemodynamics, intracranial pressure (ICP), and estimation of the pressure-volume index (PVI) and the possible involvement of these factors in the development of secondary brain damage. The study was performed by using a mathematical model of intracranial hemodynamics and cerebrospinal fluid (CSF) dynamics. The model includes the biomechanics of proximal and distal arterial intracranial vessels, cerebral veins, and CSF circulation, the intracranial pressure-volume relationship, and the action of autoregulation mechanisms on proximal and distal vessels. In the case of normal intracranial dynamics, lowering mean systemic arterial pressure (SAP) in the range of 100 to 60 mm Hg causes only a mild ICP increase (+1-2 mm Hg). In contrast, in the case of severe impairment of intracranial dynamics (reductions in CSF outflow and storage capacity), even a modest mean SAP decrease (from 100 to 90 mm Hg) may induce a transient abrupt ICP rise (+30-40 mm Hg), because of the presence of a vicious cycle among CPP, cerebral blood volume, and ICP. In the case of intact autoregulation, PVI shows a mild positive correlation with SAP in the central autoregulation range and a strongly negative correlation below the autoregulation lower limit. In the case of impaired autoregulation, PVI exhibits higher values than in the regulated case, with a mild negative correlation with SAP. The present study emphasizes the relevant role of CPP changes, elicited by acute arterial hypotension, in intracranial dynamics. To achieve intracranial stability, CPP should be maintained above 80 to 90 mm Hg. PVI is significantly affected by the active response of cerebral vessels. Hence, it may provide misleading information on craniospinal capacity if it is considered as an autonomous index: rather, it should always be considered together with information on CPP and the status of autoregulation.

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