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Hypothermia Does Not Alter Somatosensory Evoked Potential Amplitude and Global Cerebral Oxygen Extraction during Marked Sodium Nitroprusside–induced Arterial Hypotension
Author Affiliations & Notes
  • Eva Kottenberg-Assenmacher, M.D.
    *
  • Wolf Armbruster, M.D.
    *
  • Norbert Bornfeld, M.D.
  • Jürgen Peters, M.D.
  • *Staff Anesthesiologist, ‡Professor of Anesthesiology and Intensive Care Therapy and Chairman, Klinik für Anästhesiologie und Intensivmedizin. †Professor of Ophthalmology and Chairman, Abteilung für Erkrankungen des hinteren Augenabschnittes.
  • Received from the Klinik für Anästhesiologie und Intensivmedizin and the Abteilung für Erkrankungen des hinteren Augenabschnittes, Essen, Germany.
Article Information
Education
Education   |   May 2003
Hypothermia Does Not Alter Somatosensory Evoked Potential Amplitude and Global Cerebral Oxygen Extraction during Marked Sodium Nitroprusside–induced Arterial Hypotension
Anesthesiology 5 2003, Vol.98, 1112-1118. doi:
Anesthesiology 5 2003, Vol.98, 1112-1118. doi:
CEREBRAL ischemia is one of the most devastating complications of perioperative arterial hypotension. Somatosensory evoked potentials (SEPs), used to assess neural function during anesthesia for cerebrovascular surgery 1,2 or hypothermia, 3–7 may be particularly important to prevent neuronal damage by directing the anesthesiologist‘s attention to possible ischemia. Unfortunately, knowledge of the relationship of median nerve somatosensory evoked potentials (MN-SSEPs) amplitude or latency to hypotension and hypothermia is scarce, with most data derived from experiments in animals in which graded hypotension was induced by blood withdrawal, 8,9 by ganglion-blocking agents, 10,11 or during cardiac bypass. 12 In fact, the relation between hypotension, hypothermia, or their combination and MN-SSEP amplitude in humans has not been systematically studied. However, if MN-SSEPs are to be used as an intraoperative monitoring tool or to define limits of arterial hypotension, temperature-dependent and arterial pressure–dependent effects on MN-SSEPs and cerebral oxygen extraction must be separated. This is particularly true when hypotension is deliberately induced by sodium nitroprusside (SNP) since both hypothermia and SNP may or may not 13–20 interfere with cerebrovascular autoregulation.
Accordingly, we report our experience with evoked arterial hypotension and hypothermia during propofol–remifentanil anesthesia for excision of intraocular malignant melanoma. Technically, this surgery involves lamellar dissection of sclera, regional en bloc  removal of sclera and choroid, and resuturing the remaining sclera to cover the resected area. 21 This transscleral resection is performed in a few centers worldwide for large uveal tumors that cannot be eradicated by radiotherapy alone, to preserve visual function and avoid enucleation. Since surgery can easily result in intraocular hemorrhage leading to loss of vision or of the eye, controlled arterial hypotension with a mean arterial pressure around 40 mmHg during the critical parts of surgery is required. 22 Furthermore, since hypotension in this range is near if not below the lower inflection point of the cerebral autoregulatory pressure–flow relation, surface hypothermia has been suggested to lessen the risk of cerebral ischemia and improve surgical conditions. 23 
Accordingly, this setting provides a unique opportunity to assess independently in the same individuals the effects on MN-SSEPs and cerebral oxygen extraction of SNP-evoked arterial hypotension with and without hypothermia.
Materials and Methods
Patients
Nineteen otherwise healthy patients (American Society of Anesthesiologists physical status class I) were scheduled for possible resection of intraocular melanoma under hypotension and hypothermia following informed written consent. To minimize risks evoked by unrecognized cerebrovascular or coronary artery disease, all patients had undergone extensive preoperative assessment, including history, physical examination, 24-h arterial pressure measurements, echocardiography, stress electrocardiography, cerebrovascular duplex sonography, pulmonary function tests, and standard laboratory tests. In 8 patients, the tumor eventually proved to be nonresectable intraoperatively, leaving for final analysis 11 patients undergoing evoked hypotension both before and during induced hypothermia (5 men, 6 women; age, 54 ± 13.7 yr [mean ± SD]; weight, 74 ± 13.5 kg; height, 173 ± 8.6 cm).
General Procedures
After premedication with 1 mg oral flunitrazepam, both on the evening before surgery and in the morning 1 h before induction of anesthesia, preoperative MN-SSEPs were recorded. A five-lead electrocardiography was applied to monitor heart rate, rhythm, and ST segments (leads II and V5), a pulse oximeter was attached, and a peripheral venous cannula was placed. For continuous measurement of arterial pressure and arterial blood sampling, a radial artery catheter was inserted under local anesthesia. General anesthesia was induced by 200 μg · kg−1· min−1propofol (Klimofol®; IVAmed, Mannheim, Germany) and 0.5 μg · kg−1· min−1remifentanil (Ultiva®; Glaxo Welcome, Hamburg, Germany) followed by 0.1 mg/kg vecuronium (Norcuron®; Organon Teknika, Oberschleißheim, Germany). Following tracheal intubation, patients were mechanically ventilated with 30% oxygen in air. Anesthesia was maintained with propofol (120 μg · kg−1· min−1), remifentanil (0.3 μg · kg−1· min−1), and vecuronium (2 mg/h), and no bolus injections were administered at any time. A gastric tube, esophageal and rectal temperature probes, and a Foley catheter were also placed. Normocapnia was established using mainstream capnography (Siemens, Erlangen, Germany) and repeatedly confirmed by arterial blood gas analysis (α-stat). For central venous pressure measurements, drug infusion and blood sampling, a triple-lumen catheter was inserted via  the right internal jugular vein, and its position close to the right atrium was confirmed by intravascular electrocardiography. For cerebrovenous blood sampling, a catheter (20 gauge; Braun, Melsungen, Germany) was advanced into the jugular bulb via  a 6-French introducer following retrograde cannulation of the left internal jugular vein, as described. 24 Jugular bulb blood was sampled at a rate of 0.5 ml/min to avoid extracranial contamination. 25 In three patients, jugular bulb blood could not be analyzed because samples turned out to be coagulated.
Following anesthetic induction, 500 ml hydroxyethyl starch, 10%, and 500 ml normal saline were infused to compensate for fluid losses, to optimize cardiac preload, and to minimize possible reflex tachycardia during induced arterial hypotension.
Measurements
Cardiovascular Variables.
Heart rate was determined from the electrocardiogram (Sirecust 1281; Siemens), lead II. Arterial and central venous pressures were continuously measured by electromanometry relative to barometric pressure with transducers referenced to the mid axillary line (Sirecust 1281) and recorded on a multichannel strip chart recorder (Siredoc 220; Siemens) at slow speed.
Body Temperature.
Esophageal and rectal temperatures were continuously measured (Sirecust 1281) with thermistor probes.
Blood Gas Tensions, Lactate concentration, and Oxygen Saturation.
Blood oxygen and carbon dioxide partial pressures, pH, oxygen saturations, hemoglobin concentration, and lactate concentrations were measured using electrodes at 37°C (α-stat) or spectrophotometry (ABL-725; Radiometer, Copenhagen, Denmark) in arterial, central venous, and jugular bulb blood samples withdrawn simultaneously into chilled tubes and placed in crushed ice until analysis.
Neurophysiological Measurements.
For median nerve stimulation and MN-SSEP acquisition, a commercially available system was used (Viking IV; Nicolet Biomedical Instruments, Madison, WI). Right and left median nerves were identified at the wrists with a stimulator probe and marked. Pairs of platinum needle stimulating electrodes were inserted subcutaneously over the median nerve at both wrists with the cathode placed 3 cm proximal to the anode. The median nerve was stimulated with 25 mA using a constant square wave impulse with a duration of 0.1 ms.
Median nerve somatosensory evoked potentials were recorded using platinum needle electrodes inserted subcutaneously and with an electrode impedance of less than 1 kΩ. The recording electrode positions over the left and right primary somatosensory cortex were chosen according to the international 10–20 classification system. The cortical MN-SSEP N20/P25 component was recorded from the C3′ and C4′ electrode positions over the left and right primary somatosensory cortex. The cervical MN-SSEP N13 component was recorded from an electrode over the spinous process C2. A midfrontal electrode (Fz) served as the reference for all channels. The central electrode (Cz) was used as ground.
Cortical responses to 200 stimuli delivered at a frequency of 4.7 Hz were averaged by computer and recorded simultaneously with cervical MN-SSEPs. The low-frequency response of the recording apparatus was 30 Hz, and the high-frequency response was 1,000 Hz. During measurements, averaged wave forms were displayed on an oscilloscope, and the data were stored on floppy discs until analysis. Peak-to-peak amplitudes of N20/P25 and latencies of N13 and N20 waves were determined by cursor measurements, and central conduction time was calculated as the difference between cortical N20 latency and cervical N13 latency. Continuous recordings of MN-SSEPs then commenced and lasted throughout surgery.
Clinical Interventions and Data Sampling
Two episodes of evoked arterial hypotension were evaluated, i.e.  , a hypotensive period of approximately 15 min before induced hypothermia (with body temperature allowed to decrease without attempts of active warming), and a second, more prolonged hypotensive period following induction of hypothermia, as required for completion of surgery. The initial hypotensive period allowed the surgeon to safely dissect the tissues in the vicinity of the tumor, making a final determination of its resectability, and also served as a final clinical check that the patient would likely tolerate more prolonged arterial hypotension as indicated by absent ST-segment changes and no major decrease in MN-SSEP amplitude. In eight patients, following the first hypotensive episode, the surgeon decided that the tumor could not safely be resected, and anesthesia was terminated without data acquisition.
In case the surgeon determined that the tumor appeared resectable (n = 11), further surgery was halted at normotension until hypothermia to an esophageal temperature of approximately 32°C had been induced using ice packs and a cool (8°C) circulating-water mattress. Once target hypothermia was reached, arterial hypotension was induced again, and surgery proceeded.
For evoked hypotension, SNP was infused together with sodium thiosulfate, with doses being increased as needed to evoke a decrease of mean arterial pressure to a final plateau of 40 mmHg, with mean arterial pressure decreased gradually at a rate of approximately 5 mmHg every 2 min.
Mean arterial blood pressure, heart rate, and esophageal temperature were recorded with each evoked potential recording. Arterial and jugular venous bulb blood gas tensions, pH, hemoglobin concentration, lactate concentrations, and oxygen saturations were determined before and after 15 min of arterial hypotension both before or during marked hypothermia, i.e.  , at the nadir decrease of arterial pressure.
Statistical Analysis
Data are reported as mean ± SD. Differences in mean values of MN-SSEP variables between interventions (before/during hypothermia: yes/no) over mean arterial pressure were assessed by two-way repeated-measures analysis of variance followed by the Newman-Keuls post hoc  test, if indicated. Other variables were compared during normotension and plateau hypotension (approximately 40 mmHg) both before and during hypothermia. To assess temperature-dependent effects on MN-SSEP latencies, regression analysis was used. The following a priori  null hypotheses were tested: There is no difference in means of variables (latencies and amplitudes) when compared between (1) normotension and hypotension and (2) before and during hypothermia. An α-error P  of less than 0.05 was considered statistically significant.
Results
High-quality MN-SSEPs were recorded in all patients, and a representative course of anesthesia and surgery is depicted in figure 1.
Fig. 1. Time course of mean arterial pressure, MN-SSEP amplitude, esophageal temperature, and heart rate during anesthesia and surgery in a patient undergoing resection of a choroidal melanoma delineating the two episodes of evoked arterial hypotension in their relation to body temperature. A similar time course was observed in other patients except for variation in the duration of the final stage of tumor resection. Values of variables during hypotension before and during hypothermia were compared 15 min after hypotension had been achieved. Hypotension with a mean arterial pressure of 40 mmHg lasted approximately 20 min before hypothermia and averaged approximately 60 min during hypothermia of 32°C. Heart rate continuously decreased as esophageal temperature decreased from 36.1°C to 31.9°C.
Fig. 1. Time course of mean arterial pressure, MN-SSEP amplitude, esophageal temperature, and heart rate during anesthesia and surgery in a patient undergoing resection of a choroidal melanoma delineating the two episodes of evoked arterial hypotension in their relation to body temperature. A similar time course was observed in other patients except for variation in the duration of the final stage of tumor resection. Values of variables during hypotension before and during hypothermia were compared 15 min after hypotension had been achieved. Hypotension with a mean arterial pressure of 40 mmHg lasted approximately 20 min before hypothermia and averaged approximately 60 min during hypothermia of 32°C. Heart rate continuously decreased as esophageal temperature decreased from 36.1°C to 31.9°C.
Fig. 1. Time course of mean arterial pressure, MN-SSEP amplitude, esophageal temperature, and heart rate during anesthesia and surgery in a patient undergoing resection of a choroidal melanoma delineating the two episodes of evoked arterial hypotension in their relation to body temperature. A similar time course was observed in other patients except for variation in the duration of the final stage of tumor resection. Values of variables during hypotension before and during hypothermia were compared 15 min after hypotension had been achieved. Hypotension with a mean arterial pressure of 40 mmHg lasted approximately 20 min before hypothermia and averaged approximately 60 min during hypothermia of 32°C. Heart rate continuously decreased as esophageal temperature decreased from 36.1°C to 31.9°C.
×
Sodium nitroprusside–evoked arterial hypotension with a mean nadir pressure of 40 mmHg did not significantly alter either MN-SSEP N20/P25 amplitude or latency (figs. 2A and Band table 1) at an esophageal temperature of approximately 36°C. Furthermore, there was no evidence of increased global cerebral oxygen extraction or lactate production, as shown by unchanged jugular venous bulb oxygen saturation (Sjo2), arterial–jugular bulb oxygen content difference, and lactate concentrations (table 1). Arterial oxygen partial pressure and pHadid not change (data not shown), nor did arterial carbon dioxide partial pressure or hemoglobin concentration (table 1).
Fig. 2. MN-SSEP peak to peak amplitude of N20/P25 (A  ) and MN-SSEP latency of N20 (B  ) in relation to mean arterial pressure before (open circles) and during hypothermia (full circles). Means ± SDs from 11 patients undergoing resection of intraocular melanoma during progressive arterial hypotension with or without hypothermia of approximately 32°C.
Fig. 2. MN-SSEP peak to peak amplitude of N20/P25 (A 
	) and MN-SSEP latency of N20 (B 
	) in relation to mean arterial pressure before (open circles) and during hypothermia (full circles). Means ± SDs from 11 patients undergoing resection of intraocular melanoma during progressive arterial hypotension with or without hypothermia of approximately 32°C.
Fig. 2. MN-SSEP peak to peak amplitude of N20/P25 (A  ) and MN-SSEP latency of N20 (B  ) in relation to mean arterial pressure before (open circles) and during hypothermia (full circles). Means ± SDs from 11 patients undergoing resection of intraocular melanoma during progressive arterial hypotension with or without hypothermia of approximately 32°C.
×
Table 1. Data from Patients Undergoing Resection of Intraocular Melanoma during Sodium Nitroprusside–evoked Arterial Hypotension before and during Induced Hypothermia
Image not available
Table 1. Data from Patients Undergoing Resection of Intraocular Melanoma during Sodium Nitroprusside–evoked Arterial Hypotension before and during Induced Hypothermia
×
Hypothermia per se  did not alter MN-SSEP N20/P25 amplitude but increased latencies. During arterial normotension, the decrease in esophageal temperature to 31.6 ± 0.25°C was associated with a slight but highly significant increase in latency of all MN-SSEP components (fig. 3). Cortical N20 latency increased by 14.6% (22.6 ± 2.2 vs.  25.9 ± 2.5 ms, P  < 0.05), and cervical N13 latency increased by 9.8% (14.3 ± 1.2 vs.  15.7 ± 1.6 ms, P  < 0.05). Central conduction time, i.e.  , the interval between N13 and N20 also increased (8.3 ± 1.4 vs.  10.2 ± 1.6 ms, P  < 0.05) by 22.9% during hypothermia. Latencies as a function of body temperature are presented in figure 3, demonstrating a linear relation (P  < 0.05) between latency of MN-SSEP components and esophageal temperature. Thus, for a 1°C decline in temperature (at unchanged pressure), N20 latency increased by 1 ms, N13 latency increased by 0.4 ms, and central conduction time increased by 0.1 ms. Hypothermia alone was associated with a slight but nonsignificant increase in Sjo2and decrease in arterial–jugular bulb oxygen content difference (table 1).
Fig. 3. MN-SSEP latencies of cortical N20 and cervical N13 at arterial normotension in relation to esophageal temperature. Central conduction time (CCT), i.e.  , the difference between N13 and N20, is also presented. Means ± SDs from 11 patients undergoing resection of intraocular melanoma during hypothermia of approximately 32°C.
Fig. 3. MN-SSEP latencies of cortical N20 and cervical N13 at arterial normotension in relation to esophageal temperature. Central conduction time (CCT), i.e. 
	, the difference between N13 and N20, is also presented. Means ± SDs from 11 patients undergoing resection of intraocular melanoma during hypothermia of approximately 32°C.
Fig. 3. MN-SSEP latencies of cortical N20 and cervical N13 at arterial normotension in relation to esophageal temperature. Central conduction time (CCT), i.e.  , the difference between N13 and N20, is also presented. Means ± SDs from 11 patients undergoing resection of intraocular melanoma during hypothermia of approximately 32°C.
×
In contrast, arterial hypotension to a mean arterial pressure as low as 40 mmHg during hypothermia per se  did not change latencies (fig. 2Band table 1).
Effects on MN-SSEP amplitude of SNP-evoked arterial hypotension during hypothermia are shown in figure 2A. Like before induced hypothermia, N20/P25 amplitude did not change during combined hypothermia and hypotension (table 1). Thus, arterial hypotension did not evoke different effects on MN-SSEP amplitude before and after hypothermia at plateau hypotension. Furthermore, the course of pressure-related MN-SSEP amplitudes was not significantly different before and during hypothermia (fig. 2A).
Arterial hypotension during hypothermia did not significantly change Sjo2, arterial–jugular bulb oxygen content difference, or lactate concentration difference (table 1).
The SNP dose required to decrease mean arterial pressure to a plateau of 40 mmHg averaged 0.7 ± 0.5 μg · kg−1· min−1before and 1.0 ± 0.7 μg · kg−1· min−1during (P  > 0.05) induced hypothermia.
Duration of arterial hypotension during hypothermia averaged 60 ± 17 min, as required for resection of choroidal melanoma, and all patients underwent successful surgery. None of the patients showed neurologic deficits or other anesthesia-related complications.
Discussion
In this confirmatory study, we assessed and compared in humans the effects on MN-SSEP amplitude and latency of marked arterial hypotension evoked by SNP with or without marked hypothermia along with variables of global cerebral oxygen extraction. SNP-evoked hypotension to a mean arterial pressure of as low as 40 mmHg did not significantly alter MN-SSEP amplitude or latency or cerebral oxygen extraction before or during hypothermia of 32°C. Furthermore, hypothermia per se  did not change MN-SSEP amplitude but significantly prolonged MN-SSEP latency. Thus, in individuals without evidence of cerebrovascular disease, hypothermia does not alter effects on MN-SSEP amplitude and global cerebral oxygen extraction of prolonged SNP-evoked arterial hypotension with a mean arterial pressure of 40 mmHg.
These results were observed during propofol–remifentanil anesthesia and with arterial partial pressure of carbon dioxide (Pco2) maintained unchanged (α-stat). Remifentanil does not accumulate even during long procedures and, in dosages of 0.125–0.4 μg · kg−1· min−1, does not change MN-SSEP amplitude or latency. 26,27 Propofol has also been recommended during MN-SSEP monitoring since MN-SSEPs are affected to a lesser degree compared to inhaled anesthetics. 28 It might be speculated that the anesthetic effect of propofol and remifentanil may have increased during hypothermia by decreased clearance because of decreased hepatic blood flow and/or metabolism. However, this effect, if any, on MN-SSEP variables is likely small and would only introduce a conservative error with regard to MN-SSEP depression. In fact, MN-SSEP amplitude remained unchanged as body temperature decreased to 32°C, excluding major effects of increased anesthetic depth.
The SNP dose required to decrease mean arterial pressure to 40 mmHg was not different before and during hypothermia, excluding differential effects of SNP dose. Progressive decreases in mean arterial pressure were evoked by increasing SNP dosage, resulting in a pressure decrease of approximately 2.5 mmHg/min. This rate is considered consistent with unimpaired autoregulation within the known autoregulatory pressure range in rats subjected to graded hypotension by bleeding. 29 Thus, neither the anesthetics used nor the rate of arterial pressure changes are likely to have introduced a bias on results observed.
Monitoring cortical function by MN-SSEPs during evoked hypotension or hypothermia is considered important for prevention of neural damage. 1,2,10 Unfortunately, for obvious reasons, safe limits of SNP-evoked arterial hypotension in humans and effects of marked hypotension on MN-SSEPs have not been defined. Controlled arterial hypotension during intraocular tumor resection, providing a bloodless surgical field, facilitating dissection, and possibly decreasing surgical time, 22 is believed to be essential in preventing choroidal hemorrhage and loss of the eye but obviously carries a risk of cerebral ischemia. Accordingly, this setting can provide insights since interpretation is not corroborated by the simultaneous presence of hypothermia, hypotension, or hemodilution, such as during cardiopulmonary bypass, allowing effects of hypotension to be clearly separated from those of hypothermia. Furthermore, it allows assessment of whether hypothermia interacts with SNP-evoked arterial hypotension.
In the intact brain, autoregulation maintains cerebral blood flow constant over a wide pressure range, with a lower limit in humans believed to be 60 or 50 mmHg. 30–32 During normothermia and SNP-induced hypotension with a mean arterial blood pressure of 50–55 mmHg or even less, cerebral blood flow appears to be little affected in the awake or anesthetized state. 33–39 This has been attributed to an intact cerebral autoregulation 36,40 but may or may not 17 also be explained by a direct vasodilating effect of SNP. However, others have reported a disturbed autoregulation with SNP 13–15,41–43 and longer hypotension. 13 In our study, SNP-evoked hypotension with a mean pressure to 40 mmHg, i.e.  , 10–20 mmHg below the presumed limit of autoregulation, failed to decrease MN-SSEP amplitude and was not associated with a change in global cerebral oxygen extraction. Absence of critical cortical ischemia despite marked SNP-evoked hypotension is supported by unchanged Sjo2and unchanged global cerebral oxygen content difference.
Hypothermia alone during propofol–remifentanil anesthesia did not significantly affect MN-SSEP amplitude but linearly prolonged cortical latency, cervical latency, and central conduction time, with prolongation of the N20 component by 1 ms/°C. This is consistent with decreased axonal conduction and delayed synaptic transmission 44 and close to values of 1–1.6 ms/°C reported by others. 45–47 In our study, however, unlike studies using cardiopulmonary bypass, arterial pressure and body temperature were assessed independently, and arterial oxygen content did not change.
The effect of body temperature on MN-SSEP amplitude is not well defined. Larger temperature decreases to 25.8°C 7 or 27.8°C 46 using cardiopulmonary bypass in humans decreased MN-SSEP amplitude by 11–19%. In our study, N20/P25 peak-to-peak amplitude remained unchanged, indicating in humans during remifentanil–propofol anesthesia that surface hypothermia with a mean core temperature of 31.8°C alone does not alter MN-SSEP amplitude but only delays MN-SSEP latency.
Few studies, all performed in cats or rats, have addressed the impact of hypothermia on cerebrovascular autoregulation without using cardiopulmonary bypass, 18–20 and whether hypothermia interacts with effects of SNP evoked hypotension is unknown. Surface hypothermia (30.5–32°C) blunts the vasodilatory response of pial arterioles to hemorrhagic hypotension, suggesting impaired cerebral autoregulation in anesthetized cats and rats. 18–20 Finally, hypothermia may decrease vascular nitric oxide release, resulting in less vasodilatation during hypotension. 48 Although these data suggest that cerebral blood flow autoregulation or SNP response may be impaired by hypothermia, our data indicate in humans that even hypothermia of 32°C alters neither the MN-SSEP response nor global cerebral oxygen extraction during marked SNP-evoked arterial hypotension.
In conclusion, during remifentanil–propofol anesthesia in individuals without evidence of cerebrovascular disease, marked SNP-evoked arterial hypotension with a mean arterial pressure of 40 mmHg does not depress either MN-SSEP amplitude nor prolong MN-SSEP latency and is associated with unchanged global cerebral oxygen extraction and lactate production. Furthermore, surface hypothermia with a core temperature of 32°C alone does not depress MN-SSEP amplitude but prolongs MN-SSEP latencies. Finally, there is no evidence that hypothermia alters the effects of SNP-evoked marked arterial hypotension.
References
Markand ON, Dilley RS, Moorthy SS, Warren C: Monitoring of somatosensory evoked potentials responses during carotid endarterectomy. Arch Neurol 1984; 41: 375–8Markand, ON Dilley, RS Moorthy, SS Warren, C
Buchthal A, Belopavlovic M, Mooij JJA: Evoked potential monitoring and temporary clipping in cerebral aneurysm surgery. Acta Neurochir 1988; 93: 28–36Buchthal, A Belopavlovic, M Mooij, JJA
Coles JG, Wilson GJ, Sima AF, Klement P, Tait GA: Intraoperative detection of spinal cord ischemia using somatosensory cortical evoked potentials during thoracic aortic occlusion. Ann Thorac Surg 1982; 34: 299–306Coles, JG Wilson, GJ Sima, AF Klement, P Tait, GA
Kopf GS, Hume AL, Durkin MA, Hammond GL, Hashim SW, Geha AS: Measurement of central somatosensory conduction time in patients undergoing cardiopulmonary bypass: An index of neurologic function. Am J Surg 1985; 149: 445–8Kopf, GS Hume, AL Durkin, MA Hammond, GL Hashim, SW Geha, AS
Markand ON, Warren CH, Moorthy SS, Stoelting RK, King RD: Monitoring of multimodality evoked potentials during open heart surgery under hypothermia. Electroenceph Clin Neurophysiol 1984; 59: 432–40Markand, ON Warren, CH Moorthy, SS Stoelting, RK King, RD
Coles JG, Taylor MJ, Pearce JM, Lowry NJ, Stewart DJ, Trusler GA: Cerebral monitoring of somatosensory potentials during profoundly hypothermic circulatory arrest. Circulation 1984; 70 (suppl I): 96–102Coles, JG Taylor, MJ Pearce, JM Lowry, NJ Stewart, DJ Trusler, GA
Russ W, Sticher J, Scheld H, Hempelmann G: Effects of hypothermia on somatosensory evoked responses in man. Br J Anesth 1987; 59: 1484–91Russ, W Sticher, J Scheld, H Hempelmann, G
Sato M, Pawlik G, Umbach C, Heiss WD: Comparative studies of regional CNS blood flow and evoked potentials in the cat: Effects of hypotensive ischemia on somatosensory evoked potentials in cerebral cortex and spinal cord. Stroke 1984; 15: 97–101Sato, M Pawlik, G Umbach, C Heiss, WD
Skarphedinsson JO, Stage L, Thoren P: Cerebral function during hypotensive haemorrhage in spontaneously hypertensive rats and Wistar Kyoto rats. Acta Physiol Scand 1986; 128: 445–52Skarphedinsson, JO Stage, L Thoren, P
Dong WK, Bledsoe SW, Chadwick HS, Shaw CM, Hornbein TF: Electrical correlates of brain injury resulting from severe hypotension and hemodilution in monkeys. A nesthesiology 1986; 65: 617–25Dong, WK Bledsoe, SW Chadwick, HS Shaw, CM Hornbein, TF
Dong WK, Bledsoe SW, Eng DY, Heavner JE, Shaw CM, Hornbein TF, Anderson JL: Profound arterial hypotension in dogs: Brain electrical activity and organ integrity. A nesthesiology 1983; 58: 61–71Dong, WK Bledsoe, SW Eng, DY Heavner, JE Shaw, CM Hornbein, TF Anderson, JL
Dolman J, Silvay G, Zapulla R, Toth C, Erickson N, Mindich BP: The effect of temperature, mean arterial pressure, and cardiopulmonary bypass flows on somatosensory evoked potential latency in man. J Thorac Cardiovasc Surg 1986; 34: 217–22Dolman, J Silvay, G Zapulla, R Toth, C Erickson, N Mindich, BP
Ivankovich AD, Miletich DJ, Albrecht RF, Zahed MD: Sodium nitroprusside and cerebral blood flow in the anesthetized and unanesthetized goat. A nesthesiology 1976; 44: 21–6Ivankovich, AD Miletich, DJ Albrecht, RF Zahed, MD
Weiss MH, Spence J, Apuzzo M, Heiden JS, McComb JG, Kurze T: Influence of nitroprusside on cerebral pressure autoregulation. Neurosurgery 1979; 4: 56–9Weiss, MH Spence, J Apuzzo, M Heiden, JS McComb, JG Kurze, T
Stange K, Lagerkranser M, Sollevi A: Nitroprusside-induced hypotension and cerebrovascular autoregulation in the anesthetized pig. Anesth Analg 1991; 73: 745–52Stange, K Lagerkranser, M Sollevi, A
Stulken EH, Sokoll MD: Intracranial pressure during hypotension and subsequent vasopressor therapy in anesthetized cats. A nesthesiology 1975; 42: 425–31Stulken, EH Sokoll, MD
Joshi S, Young WL, Duong H, Aagaard BA, Ostapkovich ND, Sander Connolly E, Pile-Spellman J: Intracarotid nitroprusside does not augment cerebral blood flow in human subjects. A nesthesiology 2002; 96: 60–6Joshi, S Young, WL Duong, H Aagaard, BA Ostapkovich, ND Sander Connolly, E Pile-Spellman, J
Verhaegen MJJ, Todd MM, Hindman BJ: Cerebral autoregulation during moderate hypothermia in rats. Stroke 1993; 24: 407–14Verhaegen, MJJ Todd, MM Hindman, BJ
Irikura K, Miyasaka Y, Nagai S: Moderate hypothermia reduces hypotensive, but not hypercapnic vasodilation of pial arterioles in rats. J Cereb Blood Flow Metab 1998; 18: 1294–7Irikura, K Miyasaka, Y Nagai, S
Kishi K, Kawaguchi M, Kurehara K, Inoue S, Sakamato T, Einaga T, Kitaguchi K, Furuya H: Hypothermia attenuates the vasodilatory response of pial arterioles to hemorrhagic hypotension in the cat. Anesth Analg 2000; 91: 140–4Kishi, K Kawaguchi, M Kurehara, K Inoue, S Sakamato, T Einaga, T Kitaguchi, K Furuya, H
Damato BE: Local resection of uveal melanoma. Bull Soc Belge Ophtalmol 1993; 248: 11–7Damato, BE
Foulds WS, Damato BE, Burton RL: Local resection versus enucleation in the management of choroidal melanoma. Eye 1987; 1: 676–9Foulds, WS Damato, BE Burton, RL
Papadopoulos G, Lang M, Link J, Schäfer M: Loss of brainstem auditory evoked potentials waves I and II during controlled hypotension. Anaesthesist 1995; 44: 785–8Papadopoulos, G Lang, M Link, J Schäfer, M
Jakobsen M, Enevoldsen E: Retrograde catheterization of the right internal jugular vein for serial measurements of cerebral venous oxygen content. J Cereb Blood Flow Metab 1989; 9: 717–20Jakobsen, M Enevoldsen, E
Matta BF, Lam AM: The rate of blood withdrawal affects the accuracy of jugular venous bulb oxygen saturation measurements. A nesthesiology 1997; 4: 806–8Matta, BF Lam, AM
Samra SK, Dy EA, Welch KB, Lovely LK, Graziano GP: Remifentanil- and fentanyl-based anesthesia for intraoperative monitoring of somatosensory evoked potentials. Anesth Analg 2001; 92: 1510–5Samra, SK Dy, EA Welch, KB Lovely, LK Graziano, GP
Bürkle H, Stuart D, Van Aken H: Remifentanil: A novel, short-acting, mu-opioid. Anesth Analg 1996; 83: 646–51Bürkle, H Stuart, D Van Aken, H
Scheepstra GL, De Lange JJ, Booij LHDJ, Ros HH: Median nerve evoked potentials during propofol anesthesia. Br J Anesth 1989; 62: 92–4Scheepstra, GL De Lange, JJ Booij, LHDJ Ros, HH
Barzo P, Bari F, Doczi T, Jansco G, Bodosi M: Significance of the rate of systemic change in blood pressure on the short-term autoregulatory response in normotensive and spontaneously hypertensive rats. Neurosurgery 1993; 32: 611–8Barzo, P Bari, F Doczi, T Jansco, G Bodosi, M
Lassen NA, Christensen MS: Physiology of cerebral blood flow. Br J Anaesth 1976; 48: 719–34Lassen, NA Christensen, MS
Paulson OB, Strandgaard S, Edvinsson L: Cerebral autoregulation. Cerebrovasc Brain Metab Rev 1990; 2: 161–92Paulson, OB Strandgaard, S Edvinsson, L
Rosner MJ, Rosner SD, Johnson AH: Cerebral perfusion pressure: Management protocol and clinical results. J Neurosurg 1995; 83: 949–62Rosner, MJ Rosner, SD Johnson, AH
Henriksen L, Paulson OB: The effects of sodium nitroprusside on cerebral blood flow and cerebral venous blood gases: II. Observations in awake man during successive blood pressure reduction. Eur J Clin Invest 1982; 12: 389–93Henriksen, L Paulson, OB
Henriksen L, Paulson OB, Lauritzen M: The effects of sodium nitroprusside on cerebral blood flow and cerebral venous gases: I. Observations in awake man of rebound effects following moderate blood pressure reduction. Eur J Clin Invest 1982; 12: 383–7Henriksen, L Paulson, OB Lauritzen, M
Larsen R, Teichmann J, Hilfiker O, Busse C, Sonntag H: Nitroprusside-hypotension: cerebral blood flow and cerebral oxygen consumption in neurosurgical patients. Acta Anaesthesiol Scand 1982; 26: 327–30Larsen, R Teichmann, J Hilfiker, O Busse, C Sonntag, H
Henriksen L, Thorshauge C, Harmsen A: Controlled hypotension with sodium nitroprusside: Effects on cerebral blood flow and cerebral venous blood gases in patients operated for cerebral aneurysms. Acta Anaesthesiol Scand 1983; 27: 62–7Henriksen, L Thorshauge, C Harmsen, A
Bünemann L, Jensen K, Thornsen L, Riisager S: Cerebral blood flow and metabolism during controlled hypotension with sodium nitroprusside and general anesthesia for total hip replacement. Acta Anaesthesiol Scand 1987; 31: 487–90Bünemann, L Jensen, K Thornsen, L Riisager, S
Pinaud M, Souron R, Lelausque J-N, Gazeau M-F, Lajat Y, Dixneuf B: Cerebral blood flow and cerebral oxygen consumption during nitroprusside-induced hypotension to less than 50 mmHg. A nesthesiology 1989; 70: 255–60Pinaud, M Souron, R Lelausque, J-N Gazeau, M-F Lajat, Y Dixneuf, B
Griffiths DPG, Cummins BH, Greenbaum R, Griffith HB, Staddon GE, Wilkins DG, Zorab JSM: Cerebral blood flow and metabolism during hypotension induced with sodium nitroprusside. Br J Anesth 1974; 46: 671–9Griffiths, DPG Cummins, BH Greenbaum, R Griffith, HB Staddon, GE Wilkins, DG Zorab, JSM
Candia GJ, Heros RC, Lavyne MH, Zervas NT, Nelson CN: Effect of intravenous sodium nitroprusside on cerebral blood flow and intracranial pressure. Neurosurgery 1978; 3: 50–3Candia, GJ Heros, RC Lavyne, MH Zervas, NT Nelson, CN
Miller CL, Lampard DG, Griffith RI, Brown WA: Local cerebral blood flow and the electrocorticogram during sodium nitroprusside hypotension. Anaesth Intensive Care 1978; 6: 290–6Miller, CL Lampard, DG Griffith, RI Brown, WA
Larsen R, Drobnik L, Teichmann J, Radke J, Kettler D: The effects of halothane-, nitroprusside- and trimethaphan-induced hypotension on cerebral blood flow and intracranial pressure. Anaesthesist 1979; 28: 494–6Larsen, R Drobnik, L Teichmann, J Radke, J Kettler, D
Fitch W, Pickard JD, Tamura A, Graham DI: Effects of hypotension induced with sodium nitroprusside on the cerebral circulation before, and one week after, the subarachnoid injection of blood. J Neurol Neurosurg Psychiatr 1988; 51: 88–93Fitch, W Pickard, JD Tamura, A Graham, DI
Benita M, Conde H: Effects of local cooling upon conduction and synaptic transmission. Brain Res 1972; 36: 133–51Benita, M Conde, H
Markand ON, Warren C, Mallik GS, King RD, Brown JW, Mahomed Y: Effects of hypothermia on short latency somatosensory evoked potentials in humans. Electroenceph Clin Neurophysiol 1990; 77: 416–24Markand, ON Warren, C Mallik, GS King, RD Brown, JW Mahomed, Y
Porkkala T, Kaukinen S, Häkkinen V, Jäntti V: Effects of hypothermia and sternal retractors on median nerve somatosensory evoked potentials. Acta Anesthesiol Scand 1997; 41: 843–8Porkkala, T Kaukinen, S Häkkinen, V Jäntti, V
Sebel PS, De Bruijn NP, Neville WK: Effect of hypothermia on median nerve somatosensory evoked potentials. J Cardiothorac Vasc Anesth 1988; 2: 326–9Sebel, PS De Bruijn, NP Neville, WK
Booth BP, Brien JF, Marks GS: Effect of temperature on glyceryl trinitrate induced relaxation of rabbit aorta. Can J Physiol Pharmacol 1993; 71: 629–32 Arterial hypotension with a mean arterial pressure of 40 mmHg evoked by sodium nitroprusside does not depress median nerve somatosensory evoked potential amplitude or alter cerebral oxygen extraction with or without hypothermia of 32°C during intraocular tumor resection.Booth, BP Brien, JF Marks, GS
Fig. 1. Time course of mean arterial pressure, MN-SSEP amplitude, esophageal temperature, and heart rate during anesthesia and surgery in a patient undergoing resection of a choroidal melanoma delineating the two episodes of evoked arterial hypotension in their relation to body temperature. A similar time course was observed in other patients except for variation in the duration of the final stage of tumor resection. Values of variables during hypotension before and during hypothermia were compared 15 min after hypotension had been achieved. Hypotension with a mean arterial pressure of 40 mmHg lasted approximately 20 min before hypothermia and averaged approximately 60 min during hypothermia of 32°C. Heart rate continuously decreased as esophageal temperature decreased from 36.1°C to 31.9°C.
Fig. 1. Time course of mean arterial pressure, MN-SSEP amplitude, esophageal temperature, and heart rate during anesthesia and surgery in a patient undergoing resection of a choroidal melanoma delineating the two episodes of evoked arterial hypotension in their relation to body temperature. A similar time course was observed in other patients except for variation in the duration of the final stage of tumor resection. Values of variables during hypotension before and during hypothermia were compared 15 min after hypotension had been achieved. Hypotension with a mean arterial pressure of 40 mmHg lasted approximately 20 min before hypothermia and averaged approximately 60 min during hypothermia of 32°C. Heart rate continuously decreased as esophageal temperature decreased from 36.1°C to 31.9°C.
Fig. 1. Time course of mean arterial pressure, MN-SSEP amplitude, esophageal temperature, and heart rate during anesthesia and surgery in a patient undergoing resection of a choroidal melanoma delineating the two episodes of evoked arterial hypotension in their relation to body temperature. A similar time course was observed in other patients except for variation in the duration of the final stage of tumor resection. Values of variables during hypotension before and during hypothermia were compared 15 min after hypotension had been achieved. Hypotension with a mean arterial pressure of 40 mmHg lasted approximately 20 min before hypothermia and averaged approximately 60 min during hypothermia of 32°C. Heart rate continuously decreased as esophageal temperature decreased from 36.1°C to 31.9°C.
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Fig. 2. MN-SSEP peak to peak amplitude of N20/P25 (A  ) and MN-SSEP latency of N20 (B  ) in relation to mean arterial pressure before (open circles) and during hypothermia (full circles). Means ± SDs from 11 patients undergoing resection of intraocular melanoma during progressive arterial hypotension with or without hypothermia of approximately 32°C.
Fig. 2. MN-SSEP peak to peak amplitude of N20/P25 (A 
	) and MN-SSEP latency of N20 (B 
	) in relation to mean arterial pressure before (open circles) and during hypothermia (full circles). Means ± SDs from 11 patients undergoing resection of intraocular melanoma during progressive arterial hypotension with or without hypothermia of approximately 32°C.
Fig. 2. MN-SSEP peak to peak amplitude of N20/P25 (A  ) and MN-SSEP latency of N20 (B  ) in relation to mean arterial pressure before (open circles) and during hypothermia (full circles). Means ± SDs from 11 patients undergoing resection of intraocular melanoma during progressive arterial hypotension with or without hypothermia of approximately 32°C.
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Fig. 3. MN-SSEP latencies of cortical N20 and cervical N13 at arterial normotension in relation to esophageal temperature. Central conduction time (CCT), i.e.  , the difference between N13 and N20, is also presented. Means ± SDs from 11 patients undergoing resection of intraocular melanoma during hypothermia of approximately 32°C.
Fig. 3. MN-SSEP latencies of cortical N20 and cervical N13 at arterial normotension in relation to esophageal temperature. Central conduction time (CCT), i.e. 
	, the difference between N13 and N20, is also presented. Means ± SDs from 11 patients undergoing resection of intraocular melanoma during hypothermia of approximately 32°C.
Fig. 3. MN-SSEP latencies of cortical N20 and cervical N13 at arterial normotension in relation to esophageal temperature. Central conduction time (CCT), i.e.  , the difference between N13 and N20, is also presented. Means ± SDs from 11 patients undergoing resection of intraocular melanoma during hypothermia of approximately 32°C.
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Table 1. Data from Patients Undergoing Resection of Intraocular Melanoma during Sodium Nitroprusside–evoked Arterial Hypotension before and during Induced Hypothermia
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Table 1. Data from Patients Undergoing Resection of Intraocular Melanoma during Sodium Nitroprusside–evoked Arterial Hypotension before and during Induced Hypothermia
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