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 (Sjo2) 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 (32°C) 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 &mgr;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 32°C 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.

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