EEG Monitoring is Required During Hypothermic Circulatory Arrest

PRO:

Stuart J. Weiss MD, PhD
Associate Professor
Department of Anesthesia
Hospital of the University of Pennsylvania
Philadelphia, PA

Neurologic complications are common after complex aortic reconstruction. Therapeutic opportunities for interventions to prevent neurologic injury during these types of operations are possible, but require the ability to continuously assess neurologic function during general anesthesia. Electroencephalography (EEG) permits the continuous online detection of neuronal ischemia. Intraoperative EEG monitoring during aortic reconstruction can detect cerebral malperfusion upon initiation of extracorporeal circulation, diagnose cerebral hypoperfusion caused by an inadequate arterial pressure, and provide physiologic criteria for optimal cerebral metabolic suppression during deliberate hypothermia for circulatory arrest. Acute detection of neurologic events enables the surgeon, anesthesiologist, or perfusionist to intervene to prevent complications.

The relationship between EEG activity and the adequacy of cerebral blood flow has been well demonstrated for carotid endarterectomy.1 Decreased cerebral blood flow producing cerebral ischemia causes changes in the EEG within seconds.2 Although EEG has been used for many years, early attempts to demonstrate a benefit for routine cardiac surgical cases have been inconclusive.3,4 In order to demonstrate efficacy, a diagnostic monitor must provide information in a timely fashion and assess the outcome of therapeutic interventions. For example, EEG monitoring

would have little impact in routine cardiac operations where neurologic dysfunction is primarily caused by cerebral emboli and outcome is unlikely to be affected by clinical intervention after the event. In contrast, the onset of abnormal EEG activity during aortic reconstruction indicates acute cerebral malperfusion that can be corrected surgically or by changes in circulation management. Because there is greater risk of neurologic complications with aortic surgery EEG monitoring should have a greater potential for improving clinical outcome.

The event associated with the greatest risk for cerebral malperfusion in patients undergoing complex aortic reconstruction is the termination of native cardiac ejection with the onset of cardiopulmonary bypass (CPB). The consequent alteration in the pattern of blood flow in the aorta can reposition the intimal flap in patients with aortic dissection causing ostial obstruction of arch vessels leading to cerebral ischemia. The author's personal experiences and anecdotal reports in the literature support such occurrences. On more than one occasion, unilateral EEG slowing has detected and averted malperfusion of the right carotid artery caused a dissection flap obstructing the innominate artery with the onset of CPB. In several situations, the detection of acute global EEG slowing detected insufficient aortic blood flow in the true lumen that was created by inadvertent CPB perfusion via the false lumen that had a relatively intact intimal layer. Immediate detection averted a disastrous outcome by prompting the surgeon to open the aorta and fenestrate the intimal flap permitting perfusion of the cerebral vessels.

In less acute conditions, generalized EEG slowing may represent hypoperfusion caused by unrecognized cerebrovascular disease and often improves in response to pharmacologic interventions to increase the arterial pressure. The ability to detect and treat intraoperative cerebral hypoperfusion using EEG may not only decrease the risk of stroke, but may decrease the risk of postoperative neurocognitive dysfunction. Although we would like to believe that we are effectively treating cerebral ischemia in this scenario, the efficacy of this approach remains to be proven.

Circulatory arrest is often required in operations performed on the aortic arch. The only proven neuroprotective strategy for circulatory arrest is deep hypothermia to decrease cerebral metabolic requirements. There is no consensus as to the best temperature or cooling duration for the conduct of circulatory arrest. Further, no peripheral site exists to accurately measure brain temperature. EEG monitoring provides a physiologic indicator of the effects of hypothermia on the brain. The cessation of EEG activity or electrocortical silence during deliberate hypothermia has been the advocated as a means to detect the adequacy of cerebral metabolic suppression for circulatory arrest.5,6 Cosselli and others have shown that body temperatures during active cooling were not reliable indicators of hypothermic-induced changes in brain function. No single site or combination of sites consistently predicted electrocerebral silence. Several studies have found that there was substantial variability from patient to patient in the absolute temperature and time to achieve electrocortical silence.6-8 In a prospective observational study by Stecker, the total cooling time required to achieve electrocortical silence was dependent on several factors including hemoglobin concentration, arterial carbon dioxide tension, and cooling rate.7 The temperature required to achieve electrocortical silence in their study of 109 adult aortic surgical patients ranged from 12.5°C to 27.2°C and had a median value of 18° C. Therefore, cooling to a set temperature would be expected to produce non-uniform levels of cerebral protection compared to cooling to a specific a physiologic endpoint, such as electrocortical silence. Cooling patients to 18°C would have failed to establish electrocerebral silence in 50% of the patients, potentially increasing their risk of postoperative neurologic morbidity. Conversely, cooling all patients to 12°C would have needlessly subjected some patients to the inherent risks of excess hypothermia or prolonged CPB. 9,10

Opponents to the routine use of EEG monitoring for complex aortic operations argue that electrical artifacts and "nonspecific changes" limit one's ability to interpret the EEG in the operating room. Improvements in instrumentation and the elimination of electrical artifacts caused by the roller pumps of the bypass machine by the use of centripetal flow pumps have improved the diagnostic capabilities of intraoperative EEG. By recognizing the suppressive effects of general anesthetics on the EEG, one can increase its' diagnostic potential by maintaining a stable anesthetic state.

In conclusion, intraoperative EEG monitoring for aortic reconstruction is noninvasive and provides a method for detecting cerebral malperfusion to enable therapeutic intervention. EEG monitoring also provides physiologic criteria for optimizing deliberate hypothermia prior to circulatory arrest. Prospective randomized studies to verify the efficacy of EEG have not been performed, but to conduct such a study would deny control subjects the potential benefits of this monitor. Based on our understanding, the only risk of EEG monitoring is not using it.

References:

1. Sundt TH Jr, Sharbrough FW, Piepgras DG, et al. Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy with results of surgery and hemodynamics of cerebral ischemia. Mayo Clin Proc 1981; 56: 533-543

2. de Vries JW, Visser GH, Bakker PF. Neuromonitoring in defibrillation threshold testing. A comparison between EEG, near-infrared spectroscopy and jugular bulb oximetry. J Clin Monit 1997; 13: 303-307

3. Edmonds HL Jr, Griffiths LK, van der Laken J, et al. Quantitative EEG monitoring during myocardial revascularization predicts postoperative disorientation and improves outcome. J Thorac Cardiovasc Surg 1962; 103: 555-563

4. Grote CL, Shannon PT, Salmon P, et al. Cognitive outcome after cardiac operations. J Thorac Cardiovasc Surg 1992; 104: 1405-1409

5. Mizrahi EM, Patel VM, Crawford ES, et al. Hypothermic-induced electrocerebral silence, prolonged circulatory arrest, and cerebral protection during cardiovascular surgery. Electroencephalogr Clin Neurophysiol 1989; 72: 81-85

6. Coselli JS, Crawford ES, Beall AC, Jr. et al. Determination of brain temperatures for safe circulatory arrest during cardiovascular operation. Ann Thorac Surg 1988; 45: 638-642

7. Stecker MM, Cheung AT, Pochettino A, et al. Deep hypothermic circulatory arrest: I. Effects of cooling on electroencephalogram and evoked potentials. Ann Thorac Surg 2001; 71: 14-21

8. Ganzel BL, Edmonds HL, Jr., Pank JR, Goldsmith LJ: Neurophysiologic monitoring to assure delivery of retrograde cerebral perfusion. J Thorac Cardiovasc Surg. 1997; 113: 748-755

9. Egerton N, Egerton WS, Kay JH. Neurologic changes following profound hypothermia. Ann Surg 1963; 157: 366-374

10. DeLeon SY, Thomas C, Roughneen PT, et al. Experimental evidence of cerebral injury from profound hypothermia during cardiopulmonary bypass. Pediatr Cardiol 1998; 19:398-403

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