Efficacy of multimodal neuromonitoring by transcranial doppler and EEG to assess cerebral hemodynamic changes during cardiopulmonary bypass.

The overall incidence of neurological complications in cardiac surgery is 3-5%. The most important mechanisms involved in neurological damage during cardiopulmonary bypass (CPB) are global or focal hypoperfusion and embolic phenomena. While most neuromonitoring studies highlighted the role of embolism during CPB, only a few studies focused on the relationship between cerebral hemodynamic changes and neurological outcome. We developed a study protocol based on intraoperative bilateral continuous monitoring of middle cerebral arteries by transcranial doppler (TCD) and digital 32-channel EEG recording (10-20 system). Patients underwent clinical, neuropsychological, TCD and EEG evaluation at baseline and postoperatively at the 2 "d, 7 th and 30 th day. Including criteria were: age < 75 years, number of vascular risk factors < 3, absent history of cerebral ischemic attacks, no significant intracranial and/or extracranial carotid plaques on carotid color duplex and TCD, no significant cognitive dysfunction. Eight patients were recruited and 4 ofthem, submitted to coronary-aortic bypass, could undergo the complete protocol study. Four patients were excluded from the intraoperative monitoring: 2 cases due to abad temporal windows for TCD study, 1 case for a significant carotid plaque, and 1 case for a sudden worsening of cardiac conditions. In all patients, we found a significant increase of mean cerebral blood flow velocity (CBFV) soon after the aortic clamping and during the whole phase of extracorporeal circulation. CBFV remained significantly higher than basal values also after aortic decannulation, despite a transient decrease at the clamping removal. EEG showed diffuse slowing and voltage reduction in all patients, suggesting cerebral hypoperfusion. The apparent contradictory changes of TCD andEEG could be explained by a pseudo-inflammatory reaction leading to a concomitant arteriolar vasodilatation and impaired blood-tissue exchange with neuronal dysfunction. Mean arterial blood pressure decreased during CPB and returned to basal values soon after aortic decannulation. This suggested that CBFV and arterial blood pressure changed independently and that a merely loss of cerebral autoregulation did not occur. Our on-progress study indicated that multimodal neuromonitoring provided interesting data on pathophysiological mechanisms during CPB