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Ann Thorac Surg 2001;71:14-21
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

Deep hypothermic circulatory arrest: I. Effects of cooling on electroencephalogram and evoked potentials

^a Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA
^b Department of Anesthesia, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA
^c Division of Cardiothoracic Surgery, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA

Address reprint requests to Dr Stecker, Department of Neurology, Geisinger Medical Center, 100 N Academy Rd, Danville, PA 17822
e-mail: mark_stecker{at}yahoo.com

Presented at the Thirty-sixth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 31–Feb 2, 2000.

	Abstract

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Background. Deep hypothermia is an important cerebral protectant and is critical in procedures requiring circulatory arrest. The purpose of this study was to determine the factors that influence the neurophysiologic changes during cooling before circulatory arrest, in particular the occurrence of electrocerebral silence.

Methods. In 109 patients undergoing hypothermic circulatory arrest with neurophysiologic monitoring, five electrophysiologic events were selected for detailed study.

Results. The mean nasopharyngeal temperature when periodic complexes appeared in the electroencephalogram after cooling was 29.6°C ± 3°C, electroencephalogram burst-suppression appeared at 24.4°C ± 4°C, and electrocerebral silence appeared at 17.8°C ± 4°C. The N20-P22 complex of the somatosensory evoked response disappeared at 21.4°C ± 4°C, and the somatosensory evoked response N13 wave disappeared at 17.3°C ± 4°C. The temperatures of these various events were not significantly affected by any patient-specific or surgical variables, although the time to cool to electrocerebral silence was prolonged by high hemoglobin concentrations, low arterial partial pressure of carbon dioxide, and by slow cooling rates. Only 60% of patients demonstrated electrocerebral silence by either a nasopharyngeal temperature of 18°C or a cooling time of 30 minutes.

Conclusions. With the high degree of interpatient variability in these neurophysiologic measures, the only absolute predictors of electrocerebral silence were nasopharyngeal temperature below 12.5°C and cooling longer than 50 minutes.

	Introduction

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The most important cerebral protective measure used during procedures requiring circulatory arrest is deep hypothermia [1]. Therefore, the selection of an optimal temperature for circulatory arrest is critical. A circulatory arrest temperature that is too high [2] may predispose to cerebral ischemia. A circulatory arrest temperature that is too low prolongs the periods of cooling and rewarming and hence the time on cardiopulmonary bypass (CPB) and its associated risks [3]. In addition, extremely low temperatures may produce brain injury [4–7] as a result of the formation of intracellular ice crystals or denaturation of proteins [8]. At the present time, there is no agreement on the best temperature for the safe conduct of circulatory arrest [9–18] as indicated by the different protocols summarized in Table 1. Some authors use strict criteria based on nasopharyngeal and central temperature measurements. These measurements do not necessarily provide a reliable indicator of brain temperature [19], especially in the presence of cerebrovascular disease. For this reason, other investigators have used a physiologic measure such as electrocerebral silence (ECS) on electroencephalogram (EEG) to determine the best temperature for circulatory arrest.

The first purpose of this article is to describe the time course of EEG and EP changes during cooling before circulatory arrest. The second purpose is to determine whether specific patient and surgical factors influence the time course of neurophysiologic events during cooling on CPB.

	Material and methods

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Patient population
Data from 109 consecutive patients undergoing thoracic aortic surgical procedures requiring circulatory arrest at the Hospital of the University of Pennsylvania from January 1995 to December 1998 with EEG or EP monitoring were prospectively entered into a database in accordance with a protocol approved by the Institutional Review Board.

Patient age, sex, and body surface area (BSA) were recorded. When carotid ultrasonography was performed preoperatively, the degree of stenosis in the most affected carotid artery was recorded. The following surgical variables were also examined: whether the arterial cannulation site was aortic or femoral, the hemoglobin concentration at the time of circulatory arrest, the arterial carbon dioxide tension during cooling using alpha-stat management, the maximum isoflurane concentration during cooling, and the mean CPB flow rate during cooling. Although the rate of cooling was not constant, the mean rate of cooling was estimated as follows. The time required to cool from 3°C below the nasopharyngeal temperature at the onset of CPB to a temperature 3°C above the temperature at circulatory arrest is computed. The cooling rate is the ratio of the change in temperature over this range to the time required for cooling between these two temperature points.

Surgical procedure and anesthesia
All patients were anesthetized with fentanyl, midazolam, isoflurane, and pancuronium. Cardiopulmonary bypass was instituted using standard bicaval venous cannulation and arterial cannulation of either the left femoral artery, ascending aorta, or aortic arch. The left ventricle was vented through the right superior pulmonary vein. Patients were cooled on CPB (model 11160 heater/cooler unit, Sarns Inc, Ann Arbor, MI) according to a standardized protocol for a minimum of 30 minutes. Cooling on CPB was initiated with a heat exchanger setting of 1 (minimum cooling) until the blood temperature reached 27°C. After ventricular fibrillation, the heat exchanger setting was increased to 4 (maximum cooling) until circulatory arrest. The water bath temperature of the heat exchanger was permitted to decrease to less than 12°C. Antegrade cerebral perfusion was not interrupted until the EEG became isoelectric (< 2 µV for 3 minutes) and the N20-P22 component of the somatosensory evoked response had disappeared (amplitude, < 0.05 µV) bilaterally. At that time, the patient was partially exsanguinated, the superior vena cava was snared between the right atrium and the azygous vein, and retrograde cerebral perfusion was administered. Retrograde cerebral perfusion with oxygenated blood was adjusted to maintain a right internal jugular venous pressure of 25 mm Hg with the patient in an approximately 10-degree Trendelenberg position. Retrograde cerebral perfusion was interrupted for variable periods of time during deep hypothermia as required by various surgical maneuvers. The temperature of the retrograde perfusate was maintained at 12°C. After completion of aortic arch anastomoses, air was removed from the aorta and graft by allowing it to fill by retrograde cerebral perfusion. After arch deairing, a cross-clamp was placed across the ascending aortic graft, and standard CPB with antegrade cerebral perfusion (antegrade graft perfusion) was reinstituted for the final repair and rewarming.

All patients underwent a brief neurologic examination preoperatively and a standard neurologic examination postoperatively. Patients with suspected neurologic injury underwent brain imaging by computer-assisted tomography when stable. Patients with abnormal neurologic examinations postoperatively were followed up with serial clinical examinations until neurologically stable.

Electroencephalogram and evoked potential recording
Somatosensory evoked responses were monitored as described by Stecker and associates [20] with some modifications. The somatosensory stimulus consisted of 0.5-ms pulses of 25-mA intensity at the beginning of each case. From the initiation of cooling before circulatory arrest until the recovery of the evoked responses after antegrade cerebral perfusion, the stimulus current was increased to levels as high as 100 mA to ensure adequate stimulation at low temperatures [21]. The P22 cortical response, the N20 thalamic response, and the N13 response that arises from the cervicomedullary junction were identified [20]. Although the N20-P22 complex was present in all 106 patients undergoing EP monitoring, only 67 recordings in neurologically normal patients (patients without preoperative strokes, intraoperative strokes or postoperative confusion) were available for analysis. The N13 waveform was more difficult to reliably identify than the N20-P22 complex, and thus reliable serial recording of N13 throughout the process of cooling and rewarming was possible in only 34 neurologically normal patients.

Two discrete events were noted in the EP waveforms during cooling. The first event was the disappearance of the N20-P22 complex, and the second event was the disappearance of the N13 potential. The time elapsed from initiation of cooling to the disappearance of the N20-P22 complex was designated T^D_N20, and NT^D_N20 and CT^D_N20 were the nasopharyngeal and central (rectal or bladder) temperatures, respectively, at this time. In all cases, the N20-P22 complex disappeared before circulatory arrest. The N13 potential was observed to disappear in only 19 of 34 patients in whom well-formed N13 responses were recorded [22]. In the remaining 15 patients, the N13 potential was detectable at the time of circulatory arrest. The time at which N13 disappeared during cooling and the nasopharyngeal and rectal temperatures at that time were labeled T^D_N13, NT^D_N13, and CT^D_N13, respectively. Only data from patients in which the N13 did vanish before circulatory arrest were analyzed.

All EEG data reported in this article were recorded using a 16-channel electroencephalograph using gold cup electrodes placed on the scalp with collodion. In some emergent cases in this series, EEG monitoring was limited to two channels. Electroencephalogram data from these cases were not analyzed because of limitations in interpretation of such tracings. The advantage of the 16-channel recordings is that they allow the electroencephalographer to easily identify artifacts, especially those caused by the electrocardiogram and the roller pump, and hence they provide a much more accurate estimate of when the various EEG landmarks occur.

Three specific electroencephalographic events were identified during cooling. The first event was the appearance of either unilateral or bilateral periodic complexes (Fig 1) in the EEG. The elapsed time between the initiation of cooling and the appearance of periodic discharges, T_PED, occurs at a nasopharyngeal temperature designated NT_PED and a central temperature, CT_PED. With further cooling, burst suppression appeared after a time interval, T_BS, at a nasopharyngeal temperature of NT_BS and central temperature, CT_BS. The final event during cooling was the occurrence of ECS, which was defined as the absence of electrocerebral activity of more than 2 µV for at least 3 minutes on the 16-channel EEG. The time from the onset of cooling to ECS was called T_ECS. The nasopharyngeal and central temperatures at the onset of ECS were called NT_ECS and CT_ECS, respectively.

View larger version (43K): [in this window] [in a new window]   Fig 1. Distribution of nasopharyngeal temperatures at which various electroencephalogram (EEG) landmarks occur: (A) appearance of periodic complexes, (B) appearance of burst suppression, and (C) electrocerebral silence. Examples of typical EEG patterns during cooling are also shown: (D) precooling, (E) appearance of periodic complexes, (F) appearance of burst suppression, and (G) electrocerebral silence. Each of the EEG samples represents the following four channels recorded from the left hemisphere (Fp1-F7, F7-T3, T3-T5, and T5-O1).

A Spearman rank correlation analysis was used to determine which factors affected the EEG and EP events during cooling. Because of the use of multiple comparisons in the univariable analyses, statistical significance was taken as p less than 0.005, although a relationship was considered a significant trend when p was less than 0.02. Factors with a p value less than 0.2 in this analysis were selected for entry into a stepwise multiple linear regression analysis to determine whether any of the associations seen in the univariable analysis remained significant in the multivariable analysis. The F value to enter the regression was chosen as 2.0.

	Results

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Demographics
A total of 109 patients underwent circulatory arrest with deep hypothermia and were monitored with either EEG, EP, or both. Sixty-one were men and 48 were women. The mean age of the patients was 64.9 years. A total of 18 (16.5%) patients had preoperative strokes, 9 (7.3%) had intraoperative strokes, and 27 (25%) had postoperative confusion. Table 2 contains a detailed breakdown of the various patient-related and surgical factors in the neurologically normal patients, the patients with preoperative strokes, and the patients who suffered either intraoperative stroke or postoperative confusion. The only statistical trend was a tendency for longer circulatory arrest time in the patients with intraoperative strokes or postoperative confusion (p = 0.006). This relationship will be further explored in the accompanying article [25].

View larger version (31K): [in this window] [in a new window]   Fig 2. (A) The cumulative probability of electrocerebral silence on electroencephalogram (EEG) as a function of cooling time. (B) The cumulative probability that electrocerebral silence (ECS) is not achieved for temperatures above that indicated.

Univariable analysis of the correlation between the patient-specific and surgical variables and the various EEG events in the group of neurologically normal patients was performed. No significant effect of age, carotid stenosis, cannulation site, isoflurane concentration, or the arterial carbon dioxide tension on the time or temperature of any of the EEG landmarks was demonstrated. Although there was a weak relationship between the time required to cool to burst suppression (T_BS) and the BSA (r = 0.39; p = 0.008), flow rate (r = 0.38, p = 0.01), hemoglobin concentration (r = 0.33; p = 0.03), and cooling rate (r = -0.32; p = 0.04), only the effect of BSA persisted in the multivariable analysis, with longer cooling times in patients with larger BSA (p = 0.02; slope, 9.9°C/m²). Only the cooling rate correlated with T_ECS in the univariate analysis (r = -0.46; p = 0.002). In the multivariable analysis, the time to cool to ECS (T_ECS) was prolonged by increased hemoglobin concentration (p = 0.02; slope, 2.5 min · dL · mg^-1), decreased nasopharyngeal cooling rate (p = 0.008; slope, -14.4 sec²/°C), and decreased arterial carbon dioxide tension during cooling (p = 0.008; slope, -0.56 min/mm Hg). There are no significant effects of any explanatory variable on the temperature of any of the EEG events. In fact, even if all explanatory variables are included, only 30% to 50% of the variance in the time of temperature of the EEG events can be explained.

View larger version (26K): [in this window] [in a new window]   Fig 3. The distribution of nasopharyngeal temperatures at which various evoked potential landmarks occur: (A) disappearance of N20-P22, and (B) disappearance of N13. Examples of typical evoked potential patterns during cooling are also shown: (C) precooling, (D) disappearance of N20-P22 and prolongation of the latency of N13, and (E) disappearance of N13. Each evoked potential trace represents the following two channels (C4'-C3' and cervical7-Fpz).

Evoked potentials during cooling
In the group of 67 patients without preoperative or postoperative strokes (Table 3), the disappearance of the N20-P22 complex (Fig 3) occurred between 4 and 41 minutes after the initiation of cooling (mean, 17.7 minutes) at a nasopharyngeal temperature between 14.5°C and 29.2°C (mean, 21.4°C). This temperature range, although large, was similar to that reported previously by other authors [26].

Univariate analysis demonstrated significant correlations only between T^D_N20 and BSA (r = 0.36; p = 0.003), and this was confirmed by multivariable analysis demonstrating a significant prolongation in T^D_N20 in patients with larger BSA (p = 0.004; slope, 12.4°C/m²). There was a strong correlation between T^D_N20 and T_ECS (r = 0.49; p < 0.0004), although the correlation coefficient is only moderate.

Only weak effects of any surgical or patient-specific variables were seen on the times to cool to disappearance of N13 or the temperature at the disappearance of N13.

	Comment

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Although the clinical data from patients undergoing aortic arch reconstruction with hypothermic circulatory arrest and retrograde cerebral perfusion was complex and analysis involved a large number of patient-specific and surgery-specific factors, a number of important conclusions can be generated from this data.

The first conclusion is that the cortical and thalamic evoked responses disappeared at temperatures much higher than the temperature at which ECS occurred on the EEG. The major implication of this finding is that disappearance of the cortical EP should not be used as an equivalent to EEG ECS [26]. Although there was a significant correlation between the times to disappearance of the N20-P22 complex and the time to ECS, the value of the correlation was only moderate, indicating that prediction of T_ECS from T^D_N20 could not be extremely accurate.

The temperatures at which various EEG and EP events occurred were not dependent on any of the patient or surgical factors studied, although there was substantial variability from patient to patient. This might be related to individual variations in such unmeasured factors as the difference between brain temperature and systemic temperature or regional cerebral blood flow. The presence of wide variations in the nasopharyngeal temperature of ECS implies that cooling to a fixed temperature before circulatory arrest produces very different results than cooling to a physiologic end point, such as disappearance of EEG or EP, unless the fixed temperature is less than 12.5°C, which was sufficient to produce ECS in all of our cases. The total time required to cool to ECS was dependent on many factors, such as hemoglobin concentration, arterial carbon dioxide tension, and the cooling rate. These factors, however, accounted for only a small amount of the variation in times required to cool to ECS, so that the prediction of the time required to cool to ECS cannot be made accurately. In fact, only if the cooling time were greater than 50 minutes could ECS be assured, given the cooling protocol used and the range of cooling rates in our study.

Using a group of patient and surgical factors did allow predictions about the neurophysiologic consequences of hypothermia on the central nervous system on an individual basis. Thus, cooling to a fixed temperature of more than 12.5°C would have an unpredictable neurophysiologic effect on an individual patient, whereas using a neurophysiologic end point such as ECS provides a more reproducible effect of hypothermia on the nervous system.

It is quite understandable that the effects of rapid cooling on CPB are difficult to predict. There is insufficient time for thermal equilibrium to occur, such that subtle differences in flow patterns from patient to patient may produce substantially different effects of cooling in different patients. The complexity of this cooling process as well as the associated rewarming process has been studied by Markand and coworkers [23], who demonstrated that the latency changes in the somatosensory evoked responses during cooling on CPB are not solely dependent on the instantaneous temperature but also on the previous history of cooling and warming.

It was interesting to note that the hemoglobin concentration, arterial carbon dioxide tension, and BSA affected T_ECS. The increased time to cool to ECS in the setting of higher hemoglobin concentrations can be explained by increased blood viscosity causing reduced cerebral blood flow [24]. The increased time to cool with hypocarbia was also expected as this causes cerebral vasoconstriction, reduced cerebral blood flow, and thus a decreased cerebral cooling rate. The prolonged time to cool in patients with larger BSA could also be explained by a decreased rate of achieving thermal equilibrium in larger patients despite attempts to index CPB flow rates to body habitus.

Finally, this study cannot be used to determine the best temperature for circulatory arrest. We cannot predict whether an end point of ECS provides any better clinical outcome than cooling to a fixed temperature, but we have shown that these two end points are different. We have also demonstrated that the effect of ECS can be guaranteed only by cooling more than 50 minutes or cooling to a nasopharyngeal temperature of 12.5°C. None of the patient-specific or surgical factors examined allowed better predictions regarding the temperature of ECS.

	References

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