The effect of increased intracranial pressure on cerebrovascular hemodynamics

Abstract

✓ Both brain edema (increased water content) and enlargement of the vascular compartment have been implicated as being responsible for intracranial hypertension following trauma. In this study pertinent cerebrovascular hemodynamic parameters have been investigated in states of increased intracranial pressure (ICP) and graded trauma to determine whether cerebral edema or vascular factors are of major importance. Utilizing the monkey-epidural balloon experimental model, continuous measurements of the mean arterial pressure (MABP) , jugular outflow pressure (MJVP), and sagittal sinus wedge pressure (SSWP) were obtained. Shulman's observations that the sagittal sinus wedge pressure accurately reflects the intracranial pressure have been confirmed. The total cerebral blood flow (CBF) and mean transit time (t̄) were determined and the total cerebral blood volume (CBV) computed. From these data the venous (Rv), arterial (Ra), and total resistances (Rt) were calculated. Analysis of these parameters during both the acute elevation of ICP and that following graded trauma has demonstrated: 1) a progressive decrease in the total cerebral blood flow and volume and a concomitant increase in the mean transit time; 2) a progressive increase in the total resistance with a shift from the arterial to the venous side; 3) a progressive decrease in the perfusion pressure (PP = MABP-SSWP); 4) impairment of CO2 reactivity pari passu with vasomotor activity and autoregulation of flow to pressure. The findings did not support the concept that increased intracranial pressure following trauma is the result of an increase in the size of the cerebrovascular compartment.