Hypothermia does not alter somatosensory evoked potential amplitude and global cerebral oxygen extraction during marked sodium nitroprusside-induced arterial hypotension

Background: To prevent neurologic damage, monitoring cerebral function by somatosensory evoked potentials is used in selected settings. Excision of intraocular melanoma provides a unique opportunity to assess independently during anesthesia the effects on median nerve somatosensory evoked potentials (MN-SSEPs) and cerebral oxygen extraction of sodium nitroprusside-evoked arterial hypotension with and without hypothermia. Methods: Median nerve somatosensory evoked potentials, arterial pressure, jugular venous bulb oxygen saturation (Sjo(2)) and lactate concentration, and arterial-jugular bulb oxygen content difference were assessed during propofol-remifentanil anesthesia under sodium nitroprusside-evoked arterial hypotension (mean arterial pressure, 40 mmHg) with and without surface hypothermia (32degreesC) in 11 otherwise healthy patients undergoing resection of choroidal melanoma. Results: Hypothermia alone did not affect peak-to-peak amplitude of N20/P25 but prolonged cortical latency of N20 (22.6 +/- 2.2 vs. 25.9 +/- 2.5 ms, P < 0.05), cervical latency of N13 (14.3 +/- 1.2 vs. 15.7 +/- 1.6 ms, P < 0.05), and central conduction time (8-3 +/- 1.4 vs. 10.2 +/- 1.6 ms, P < 0.05). Evoked arterial hypotension did not depress MN-SSEP N20/P25 amplitude either with or without hypothermia (-0.31 vs. -0.28 mu V, P > 0.05) or alter latency (0.08 vs. 0.1 ms, P > 0.05). Furthermore, hypotension with or without hypothermia did not change Sjo2, arterial-jugular bulb oxygen content difference, or lactate concentration. Conclusions: Thus, hypothermia to 32degreesC does not alter MN-SSEP amplitude and global cerebral oxygen extraction during marked sodium nitroprusside-induced arterial hypotension with a mean arterial pressure of 40 mmHg but prolongs MN-SSEP latencies during propofol-remifentanil anesthesia in individuals without cerebrovascular disease.