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Ann Thorac Surg 2001;71:14-21
© 2001 The Society of Thoracic Surgeons

Original article: cardiovascular

Deep hypothermic circulatory arrest: I. Effects of cooling on electroencephalogram and evoked potentials

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

Background. Deep hypothermia is an important cerebral protectant and is critical in procedures requiring circulatory arrest. The purpose of this study was to determine the factors that influence the neurophysiologic changes during cooling before circulatory arrest, in particular the occurrence of electrocerebral silence.

Methods. In 109 patients undergoing hypothermic circulatory arrest with neurophysiologic monitoring, five electrophysiologic events were selected for detailed study.

Results. The mean nasopharyngeal temperature when periodic complexes appeared in the electroencephalogram after cooling was 29.6°C ± 3°C, electroencephalogram burst-suppression appeared at 24.4°C ± 4°C, and electrocerebral silence appeared at 17.8°C ± 4°C. The N20-P22 complex of the somatosensory evoked response disappeared at 21.4°C ± 4°C, and the somatosensory evoked response N13 wave disappeared at 17.3°C ± 4°C. The temperatures of these various events were not significantly affected by any patient-specific or surgical variables, although the time to cool to electrocerebral silence was prolonged by high hemoglobin concentrations, low arterial partial pressure of carbon dioxide, and by slow cooling rates. Only 60% of patients demonstrated electrocerebral silence by either a nasopharyngeal temperature of 18°C or a cooling time of 30 minutes.

Conclusions. With the high degree of interpatient variability in these neurophysiologic measures, the only absolute predictors of electrocerebral silence were nasopharyngeal temperature below 12.5°C and cooling longer than 50 minutes.




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