The complexity of cerebral blood flow regulation: the interaction of posture and vasomotor reactivity.

Abstract

Arterial carbon dioxide (PaCO₂) and posture influence the middle (MCAv) and posterior (PCAv) cerebral artery blood velocitiesbut there is paucity of data about their interaction and need for an integrated model of their effects, including dynamic cerebral autoregulation (dCA). In 22 participants (11 male, age 30.2 ± 14.3 years), blood pressure (BP, Finometer), dominant MCAv and non-dominant PCAv (transcranial Doppler ultrasound), end-tidal CO₂ (EtCO₂, capnography) and heart rate (HR, ECG) were recorded continuously. Two recordings (R) were taken when the participant was supine (R1, R2), two taken when the participant was sitting (R3, R4), and two taken when the participant was standing (R5, R6). R1, R3 and R5 consisted of 3 minutes of 5% CO₂ through a mask and R2, R4 and R6 consisted of 3 minutes of paced hyperventilation. The effects of PaCO2 were expressed with a logistic curve model (LCM) for each parameter. dCA was expressed by the autoregulation index (ARI), dervived by transfer function analysis. Standing shifted LCM to the left for MCAv (p<0.001), PCAv (p<0.001), BP (p=0.03) and ARI (p=0.001); downwards for MCAv and PCAv (both p<0.001), and upwards for HR (p<0.001). For BP, LCM was shifted downwards by sitting and standing (p=0.024). For ARI, the hypercapnic range of LCM was shifted upwards during standing (p<0.001). A more complete mapping of the combined effects of posture and arterial CO₂ on the cerebral circulation and peripheral variables can be obtained with the LCM over a broad physiological range of EtCO₂ values.