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Ann Thorac Surg 2001;71:22-28
© 2001 The Society of Thoracic Surgeons


Original article: cardiovascular

Deep hypothermic circulatory arrest: II. Changes in electroencephalogram and evoked potentials during rewarming

Mark M. Stecker, MD, PhDa, Albert T. Cheung, MDb, Alberto Pochettino, MDc, Glenn P. Kent, BSa, Terry Patterson, PhDa, Stuart J. Weiss, MD, PhDb, Joseph E. Bavaria, MDc

a Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA
b Department of Anesthesia, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA
c Division of Cardiothoracic Surgery, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA

Address reprint requests to Dr Stecker, Department of Neurology, Geisinger Medical Center, 100 N Academy Rd, Danville, PA 17822
e-mail: mark_stecker{at}yahoo.com

Presented at the Poster Session of the Thirty-sixth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 31–Feb 2, 2000.

Background. Electrophysiologic studies during rewarming after deep hypothermic circulatory arrest probe the state of the brain during this critical period and may provide insight into the neurological effects of circulatory arrest and the neurologic outcome.

Methods. Electroencephalogram (EEG) and evoked potentials were monitored during rewarming in 109 patients undergoing aortic surgery with hypothermic circulatory arrest.

Results. The sequence of neurophysiologic events during rewarming did not mirror the events during cooling. The evoked potentials recovered first followed by EEG burst-suppression and then continuous EEG. The time to recovery of the evoked potentials N20-P22 complex was significantly correlated with the time of circulatory arrest even in patients without postoperative neurologic deficits (r = 0.37, (p = 0.002). The nasopharyngeal temperatures at which continuous EEG activity and the N20-P22 complex returned were strongly correlated (r = 0.44, p = 0.0002; r = 0.41, p = 0.00003) with postoperative neurologic impairment. Specifically, the relative risk for postoperative neurologic impairment increased by a factor of 1.56 (95% CI 1.1 to 2.2) for every degree increase in temperature at which the EEG first became continuous.

Conclusions. No trend toward shortened recovery times or improved neurologic outcome was noted with lower temperatures at circulatory arrest, indicating that the process of cooling to electrocerebral silence produced a relatively uniform degree of cerebral protection, independent of the actual nasopharyngeal temperature.


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