Objective: To investigate the influence of hemodilution and arterial pCO2 on cerebral autoregulation and cerebral vascular CO2 reactivity.
Design: Prospective interventional study.
Setting: University hospital-based single-center study.
Participants: Forty adult patients undergoing elective cardiac surgery using normothermic cardiopulmonary bypass.
Interventions: Blood pressure variations induced by 6/minute metronome-triggered breathing (baseline) and cyclic 6/min changes of indexed pump flow at 3 levels of arterial pCO2.
Measurements and main results: Based on median hematocrit on bypass, patients were assigned to either a group of a hematocrit ≥28% or<28%. The autoregulation index was calculated from cerebral blood flow velocity and mean arterial blood pressure using transfer function analysis. Cerebral vascular CO2 reactivity was calculated using cerebral tissue oximetry data. Cerebral autoregulation as reflected by autoregulation index (baseline 7.5) was significantly affected by arterial pCO2 (median autoregulation index amounted to 5.7, 4.8, and 2.8 for arterial pCO2 of 4.0, 5.3, and 6.6 kPa, p≤0.002) respectively. Hemodilution resulted in a decreased autoregulation index; however, during hypocapnia and normocapnia, there were no significant differences between the two hematocrit groups. Moreover, the autoregulation index was lowest during hypercapnia when hematocrit was<28% (autoregulation index 3.3 versus 2.6 for hematocrit ≥28% and<28%, respectively, p = 0.014). Cerebral vascular CO2 reactivity during hypocapnia was significantly lower when perioperative hematocrit was<28% (p = 0.018).
Conclusions: Hemodilution down to a hematocrit of<28% combined with hypercapnia negatively affects dynamic cerebral autoregulation, which underlines the importance of tight control of both hematocrit and paCO2 during CPB.
Keywords: cardiopulmonary bypass; cerebral autoregulation; cerebral carbon dioxide reactivity; hemodilution.
Copyright © 2015 Elsevier Inc. All rights reserved.