Effect of Mild Hypothermic Cardiopulmonary Bypass on the Amplitude of Somatosensory-evoked Potentials

Abstract

Several neurophysiological techniques are used to intraoperatively assess cerebral functioning during surgery and intensive care, but the introduction of hypothermia as a means of intraoperative neuroprotection has brought their reliability into question. The present study aimed to evaluate the effect of mild hypothermia on somatosensory-evoked potentials' (SSEPs) amplitude and latency in a cohort of cardiopulmonary bypass (CPB) patients as the temperature reached the steady-state. The amplitude and latency of 4 different SSEP signals--N9, N13, P14/N18 interpeak, and N20/P25--were evaluated retrospectively in 84 patients undergoing CPB during normothermic (36°C±0.43°C) and mild hypothermic (32°C±1.38°C) conditions. SSEPs were recorded in normothermia immediately after the induction of anesthesia and in hypothermia as the temperature reached its steady-state, specifically, when the nasopharyngeal temperature was equivalent to the rectal temperature (±0.5°C). A paired-samples t test was performed for each SSEP to test the differences in latencies and amplitudes between normothermic and hypothermic conditions. Compared with normothermia, hypothermia not only significantly increased the latency of all SSEPs, N9 (P<0.001), N13 (P<0.001), P14/N18 (P<0.001), and N20/P25 (P<0.001), but also the amplitude of N9 (P<0.001) and N20/P25 (P<0.001). The increased amplitude in particularly of cortical SSEPs (N20/P25), detected specifically during steady-state hypothermia, seems to support the clinical utility of this methodology in monitoring the brain function not only during cardiac surgery with CPB, but also in other settings like therapeutic hypothermia procedures in an intensive care unit.