Chapter 6 hypovolemic bleeding patients and cerebral autoregulation can be compromised 18 which is improbable in patients undergoing CPB. Ogawaet al 27 showed impaired dCA due to hypervolemic hemodilution with increased gain after infusion of 15-30 ml/kg of saline with a mean Hct of 43 %. Also phase decreased, but this did not reach statistical significance. Hemodilution during CPB therefore seems to be a plausible explanation for the reduced dCA capability, since Hct with 27 % is much lower in our study group. Because the induced sinusoidal variations at 0.1 Hz are the main content of ABP and CBFV signals and their shapes are very similar, coherence is high, even close to 1, expressing the strong linear relation between ABP and CBFV. Because the shape is not a purely sinusoidal, also at higher harmonics (0.3 Hz and 0.5 Hz) coherence is high. These high coherence values are unprecedented in beating heart measurement and indicate a strong linear relationship between ABP and CBFV under the conditions of this study. It also shows that in univariate analysis all variance of CBFV can be explained by ABP variance and coherence can reach values of nearly 1 when signal to noise ratio is high. However, in beating heart measurements, these signal to noise ratios are not easily achieved possibly due to others sources of CBFV variations that are not related to ABP variations, such as the influence of changing paCO2 and/or sympathetic tone as was shown by others studying multiple coherence 33, 37. Gain decreases with increasing paCO2, not only at 0.1 Hz, but also at higher 0.3 and 0.5 Hz frequencies at which dCA is thought not to function. In an earlier study in awake lacunar infarct patients we found decreased gain after acetazola- mide infusion 17. Since acetazolamide is an anhydrase inhibitor it has the same effect as hypercapnia. Others did not report dCA gain 5 or report no reduction 4 or even an increase 53 at hypercapnia. However, they all investigated much smaller number (10-14) of subjects. An explanation for our finding is that de- creased gain with increased paCO2 might be due to increased vessel dilation causing less responsiveness to changes in pressure. Given the different results for dCA gain it seems not to be a very robust parameter of dCA as Panerai demon- strated using simulations with the Tiecks model 29. The reduction of the initial rise of the step response function, which is clearly shown in figure 4, may be explained by a decrease in critical closing pressure. With increasing paCO2 a decrease of critical closing pressure occurs as was shown by others 4, 32. Since we investigated patients during CPB we cannot evaluate critical closing pressure using the available per beat techniques 2, 30, 114
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