Fifty-six subjects with carotid artery disease were assessed by measuring t
he cerebral blood flow velocity (CBFV) change in response to inhalation of
5% CO2 in air whilst continuously monitoring the blood pressure (BP). Coher
ent ave raging of the data characterised differences in CBFV, BP, resistanc
e area product and critical closing pressure during changes in end-tidal CO
2 (ETCO2). The results primarily demonstrate that the augmentation of ETCO2
increases the CBFV and BP, causing a pressure autoregulatory response, and
allows the processes of pressure autoregulation and cerebral vascular rese
rve to be differentiated.