Noninvasive estimation of cerebral perfusion pressure and zero flow pressure in healthy volunteers: the effects of changes in end-tidal carbon dioxide

Zero flow pressure (ZFP) in the cerebral circulation is defined as the arterial pressure at which flow ceases. Noninvasive methods of estimating cerebral perfusion pressure (CPP) and ZFP using transcranial Doppler ultrasonography have been described. There is a paucity of normal physiological data related to changes in estimated CPP (eCPP) and ZFP induced by changes in carbon dioxide (CO(2)). We studied the effects of CO(2) on eCPP and ZFP in 17 healthy volunteers. After baseline measurements of middle cerebral artery blood-flow velocity and blood pressure, subjects voluntarily hyperventilated to decrease their end-tidal CO(2) (PE'CO(2)) by approximately 7.5 mm Hg, and then they increased their PE'CO(2) by approximately 7.5 mm Hg by breathing through a Mapleson D circuit. Blood-flow velocity and blood pressure were recorded at each stage. The eCPP and ZFP were calculated by using established formulas, and the results were analyzed with analysis of variance. With increasing PE'CO(2), eCPP increased from 50.67 mm Hg (8.33 mm Hg) (mean [SD]) to 60.87 mm Hg (9.28 mm Hg) (20% increase; P < 0.001), with a corresponding decrease in ZFP (P = 0.017); hypocapnia resulted in the opposite effects on eCPP and ZFP. These results indicate physiological changes in eCPP and ZFP that can be expected from changes in CO(2) in subjects without any neurological disorder. IMPLICATIONS: Increasing end-tidal CO(2) increases the estimated cerebral perfusion pressure and vice versa. These results are opposite to those expected from the known effects of CO(2) on intracranial pressure. Thus, we support the suggestion that, in the absence of intracranial hypertension, vascular tone remains a major determinant of effective downstream pressure and cerebral perfusion.