Modelling the cerebral haemodynamic response in the physiological range of PaCO2

Abstract

Objective: Arterial CO₂ (PaCO₂) has a strong effect on cerebral blood flow (CBF), but its influence on CBF regulatory mechanisms and circulatory systemic variables has not been fully described over the entire physiological range of PaCO₂.

Approach: CBF velocity (CBFV, transcranial Doppler), blood pressure (BP, Finometer) and end-tidal CO₂ (EtCO₂, capnography) were measured in 45 healthy volunteers (19 male, mean age 37.5 years, range 21-71) at baseline, and in response to hypo- (-5 mm Hg and -10 mm Hg below baseline) and hypercapnia (5% and 8% CO₂), applied in random order.

Main results: CBFV, cerebral dynamic autoregulation index (ARI), heart rate (HR), arterial blood pressure (ABP), critical closing pressure (CrCP) and resistance-area product (RAP) changed significantly (all p < 0.0001) for hypo- and hyper-capnia. These parameters were shown to follow a logistic curve relationship representing a 'dose-response' curve for the effects of PaCO₂ on the cerebral and systemic circulations. The four logistic model parameters describing each 'dose-response' curve were specific to each of the modelled variables (ANOVA p < 0.0001).

Significance: The ability to model the CBFV, ARI, HR, ABP, CrCP and RAP dependency of PaCO₂ over its entire physiological range is a powerful tool for physiological and clinical studies, including the need to perform adjustments in disease populations with differing values of baseline PaCO₂.