Assessment of dCA during CPB Introduction Coronary artery bypass graft surgery (CABG) is a common operation that is associated with significant morbidity and mortality 41. Although operative techniques, anaesthesia and cardiopulmonary bypass have improved outcomes over the past 10 years, there is inherent neurological risk associated with CABG. Stroke and postoperative cognitive decline, two major neurological outcomes, may be related to cerebral hypoperfusion during CABG 42. The frequency of any postoperative cerebral injury has been estimated at between 6 and 28% for encephalopathy alone. Moreover, 3 % of patients undergoing coronary bypass surgery have been estimated to have serious neurological sequelae (death due to cerebral injury, stroke, transient ischemic attack, or stupor) 40. Worsened control of cerebral blood flow, due to hypertension, diabetes or other conditions impose patients peri-operatively to increased risk of neurological complications 10. Despite this, evaluation of cerebral hemodynamics is not common practice. Cerebral autoregulation (CA) and carbon dioxide reactivity (CO2R) are two important mechanisms for controlling cerebral blood flow (CBF). In healthy humans CBF is controlled over a cerebral perfusion pressure range of 60-150 mmHg 35 via vasomotor effectors that control cerebrovascular resistance 3. Dysfunction of CA and impaired CO2R before and during CPB might contribute to neurological morbidity after cardiac surgery 24, 25, 45. Currently, blood pressure management during CPB is based on maintaining a minimum mean arterial blood pressure (ABP) of approximately 50 mmHg 44 and is neither monitored nor controlled for adequate function of CA and/or CO2R. In general, increasing ABP out of CA range may cause hyperperfusion with oedema formation 52, whereas reduction of CBF due to decreased ABP below the autoregulatory range may cause cerebral hypoperfusion and ischemia 35. There are two animal studies 43, 46and one in human subjects 11, indicating that CBF and mean ABP are not influenced by CPB indexed pump flow provided mean ABP is kept within the autoregulatory range. CBF will only decrease pro- portionally to a decrease in pump flow when mean ABP decreases below the sub- critical perfusion pressure, i.e. the lower limit of autoregulation. Oppositely, increasing indexed pump flow leading may lead to hyperperfusion when mean ABP rises above the upper limit of autoregulation. Thus, individualizing ABP during CPB to be within a patient’s CA working range might prevent either cerebral hypoperfusion due to low ABP and/or cerebral oedema from high ABP. However, lower and upper limits of autoregulation are not known pre- 101
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