Modeling modulation of intracranial pressure by variation of cerebral venous resistance induced by ventilation.

To test, theoretically, the hypothesis that: (1) cyclic extravascular compressional modulation of the terminal venous bed occurs with positive pressure inhalation; and (2) the degree of modulation is diminished with increasing vascular dilation induced by increasing the level of the partial pressure of arterial blood carbon dioxide (PCO2), two modifications of Ursino's model of cerebrospinal fluid dynamics were made: (1) terminal venous bed resistance was synchronously modulated with the ventilation cycle; and (2) both the depth of modulation and cerebrovascular resistance were progressively reduced with increasing levels of PCO2. Recordings of intracranial pressure (ICP) and arterial blood pressure of piglets were obtained and correlated at different levels of hypercapnia. Simulated and experimental correlation values progressively increased monotonically as the level of PCO2 increased. Group (n = 4) mean values of correlation (+/- standard deviation) were 0.54 (+/- 0.17), 0.61 (+/- 0.08), 0.79 (+/- 0.06), 0.86 (+/- 0.04), 0.87 (+/- 0.05) for respective mean PCO2 levels (+/- standard deviation) of 32.9 (+/- 1.75), 41.4 (+/- 2.5), 55.9 (+/- 4.0), 72.5 (+/- 6.45), and 87.4 (+/- 7.25) mmHg. These results support the stated premise that dilation of the cerebrovasculature reduces the influence of positive pressure ventilation on the ICP recording by increasing the venous pressure and thus diminishing the likelihood of vascular compression.