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Ann Thorac Surg 1988;45:206-209
© 1988 The Society of Thoracic Surgeons
From the Divisions of Cardiovascular Surgery, Neurology, and the Department of Pathology, Hospital for Sick Children, and the Department of Surgery, University of Toronto, Toronto, Ont, Canada
Accepted for publication October 15, 1987.
* Address reprint requests to Dr. Wilson, Department of Pathology, Hospital for Sick Children, 555 University Ave, Toronto, Ont, Canada M5G 1x8
We assessed somatosensory evoked response (SSER) as a monitor of cerebral protection during nonpulsatile, hypothermic cardiopulmonary bypass (CPB). In 13 dogs under CPB, extracorporeal flow rate (EFR) thresholds for loss of SSER were determined by stepwise reduction of the EFR from 2.0 to 0.25 L/min/m2 at perfusion temperatures of 35°C, 30°C, 25°C, and 20°C. Testing began at 35°C in Group 1 (N = 6) and at 20°C in Group 2 (N = 7). Immediately on loss of SSER (denoted as a decrease of 80% or more in the amplitude of the somatosensory evoked potentials), EFR was restored to 2.0 L/min/m.
Thresholds for loss of SSER ranged between 0.75 and 0.25 L/min/m2. SSER was always restored on return of EFR to 2.0 L/min/m2; thus loss of SSER was a reversible ischemic change. Both groups had similar threshold values at 35°C, but at lower temperatures, Group 1 thresholds were significantly higher than those in Group 2. Since 35°C was the first test temperature for Group 1 but the last for Group 2, EFR reduction at 35°C apparently caused neurophysiological changes (depletion of cortical energy reserves), which diminished subsequent tolerance to ischemia, but EFR reduction at 20°C did not. Our findings show that loss of SSER warns of reversible cerebral ischemia, and support SSER monitoring as a useful measure of cerebral function during low-flow, hypothermic CPB.
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