Chapter 6 operatively. Moreover, it is unethical to change blood pressure over such large ranges other measures are necessary to determine the level of cerebral blood flow regulation. Consequently, dynamic cerebral autoregulation (dCA) should be assessed during CPB. Instead of determining static lower and upper limits of cerebral autoregulation, dCA quantifies the response of CBF to transient and/or periodic changes in ABP. Bradyet al 7 have evaluated cerebral blood flow autoregulation continuously during CPB using Transcranial Doppler sonography (TCD) calculating cross- correlation (Mx) between slow waves (f < 0.05 Hz) of middle cerebral artery blood flow velocity (CBFV) and mean arterial blood pressure (ABP). Similarly, cerebral oximetry index (COx), recorded through Near-Infrared Spectroscopy (NIRS), was calculated for slow waves of cerebral oximetry and ABP. They show high values of Mx and COx during CPB suggesting impaired cerebral autoregula- tion. However, they do not mention whether sufficient blood pressure variability occured during CPB to reliably calculate signal cross-correlation. An important point since a patient on CPB usually shows very little spontaneous ABP variabil- ity. Furthermore, Mx is essentially an intermediate indicator of static CA and dynamic cerebral autoregulation, since it does not take into account the phase relationship in the autoregulatory response 1. Apart from Mx we are not aware of any other method evaluating dCA during CPB. A common approach to quantify dynamic cerebral autoregulation (dCA) is to analyse ABP oscillations as input and CBFV, measured in the middle cerebral artery (MCA) using TCD, as output signal in the frequency domain using trans- fer function analysis (TFA) 31, 53. Under the assumption of a constant MCA diameter CBFV is linearly related to CBF 6, 48. A positive phase shift is present when CBFV oscillations precede ABP oscillations in the low frequency range around 0.1 Hz and is interpreted as intact dCA 13. In a previous study in healthy volunteers under normal supine conditions we found average values of phase shift of 0.9 ± 0.3 rad 15. CO2R is an index of cerebrovascular dilatory capacity to an increase in arterial carbon dioxide (paCO2) level, and is defined as the change in CBF per unit change in paCO2. CO2R is not a dynamic measure but represents the capacity of arterioles to respond to changes in p aCO2. CO2R can readily be assessed using TCD 51 or NIRS 47. Normal CO2R is estimated to be 2-3% decrease in CBF per mmHg decrease in paCO2between 3-4% increase per mmHg increase in paCO2 9. Additionally, the CO2R measured with NIRS in supine position is found to be 0.36 ± 0.1 per mmHg change in paCO239. 102
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