Cerebral blood flow (CBF) can be altered by a change in partial pressure of arterial CO2 (pCO2), being reduced during hyperventilation (HPV). Critical closing pressure (CrCP) and resistance area product… Click to show full abstract
Cerebral blood flow (CBF) can be altered by a change in partial pressure of arterial CO2 (pCO2), being reduced during hyperventilation (HPV). Critical closing pressure (CrCP) and resistance area product (RAP) are parameters which can be studied to understand this change, but their dynamic response has not been investigated during paced HPV (PHPV). Seventy five participants had recordings at rest and during PHPV. Blood pressure (BP) (Finometer), bilateral CBF velocity (CBFV) (transcranial Doppler), end-tidal CO2 (capnography) and heart rate (HR) were recorded continuously. Subcomponent analysis (SCA) and time-varying CrCP, RAP and dynamic cerebral autoregulation (Autoregulation Index, ARI) were estimated comparing PHPV to poikilocapnia. PHPV caused a change in CBFV (p<0.01), EtCO2, (p<0.01), HR (p<0.001) and RAP (p<0.01). SCA demonstrated RAP was the main parameter explaining the changes in CBFV due to PHPV. The time-varying step responses for CBFV and RAP during PHPV demonstrated considerable non-stationarity compared to poikilocapnia (p<0.00001). Although time-varying ARI was temporarily depressed, after 60 s of PHPV it was significantly higher (6.81 ± 1.88) (p<0.0001) than in poikilocapnia (5.08 ± 1.86). The mean plateau of the RAP step response was -98.3 ± 58.8 % 60 s after the onset of PHPV but -71.7 ± 45.0 % for poikilocapnia (p=0.0026), with no corresponding changes in CrCP (p=0.6). Further work is needed to assess the role of sex and aging in our findings, and the potential for using RAP and CrCP to improve the sensitivity and specificity of CO2 reactivity studies in cerebrovascular conditions.
               
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