Two-breath CO2 test detects altered dynamic cerebrovascular autoregulation and CO2 responsiveness with changes in arterial PCO2

The new two-breath CO2 method was employed to test the hypotheses that small alterations in arterial PCO2 had an impact on the magnitude and dynamic response time of the CO2 effect on cerebrovascular resistance (CVRi) and the dynamic autoregulatory response to fluctuations in arterial pressure. During a 10-min protocol, eight subjects inspired two breaths from a bag with elevated PCO2, four different times, while end-tidal PCO2 was maintained at three levels: hypocapnia (LoCO(2), 8 mmHg below resting values), normocapnia, and hypercapnia (HiCO(2), 8 mmHg above resting values). Continuous measurements were made of mean blood pressure corrected to the level of the middle cerebral artery (BPMCA), PCO2 ( estimated from expired CO2), and mean flow velocity (MFV, of the middle cerebral artery by Doppler ultrasound), with CVRi = BPMCA/MFV. Data were processed by a system identification technique (autoregressive moving average analysis) with gain and dynamic response time of adaptation estimated from the theoretical step responses. Consistent with our hypotheses, the magnitude of the PCO2-CVRi response was reduced from LoCO(2) to HiCO(2) [from - 0.04 (SD 0.02) to - 0.01 (SD 0.01) ( mmHg . cm(-1) . s) . mmHg PCO2-1] and the time to reach 95% of the step plateau increased from 12.0 +/- 4.9 to 20.5 +/- 10.6 s. Dynamic autoregulation was impaired with elevated PCO2, as indicated by a reduction in gain from LoCO(2) to HiCO(2) [ from 0.021 +/- 0.012 to 0.007 +/- 0.004 (mmHg . cm(-1) . s) . mmHg BPMCA-1], and time to reach 95% increased from 3.7 +/- 2.8 to 20.0 +/- 9.6 s. The two-breath technique detected dependence of the cerebrovascular CO2 response on PCO2 and changes in dynamic autoregulation with only small deviations in estimated arterial PCO2.