EEG Monitoring is Required During Hypothermic Circulatory Arrest


Ronald A. Kahn, MD
Divisional Director, Vascular Anesthesiology
The Mount Sinai Medical Center
New York, NY

Deep hypothermic circulatory arrest (DHCA) is currently the most common method of providing cerebral protection for patients undergoing repair of the distal ascending aorta, transverse aortic arch, proximal descending aorta and other surgical procedures necessitating complete interruption of cerebral blood flow. The major disadvantages of this technique include prolonged cardiopulmonary bypass time and adverse neurologic outcomes. It is therefore important to provide optimum perioperative cerebral protection.1,2

Since the major mechanism of cerebral protection during circulatory arrest is hypothermia, an adequate and homogenous degree of cerebral hypothermia must be provided. Although hemodilution, proper blood gas management, as well as the assurance of adequate times for complete cooling help ensure homogenicity, the adequacy of cerebral protection needs to be assured. Jugular bulb oxygen saturation monitoring is a better monitor of overall homogeneity of cerebral hypothermia than electroencephalography (EEG).

Ideally, any presumptive perioperative monitor should have the ability to detect changes early in the parameter being monitored, have support based upon outcome studies, and have theoretical support for its use. During cooling prior to deep hypothermic circulatory arrest, EEG measurements may be used to monitor the degree of hypothermic metabolic suppression. Cooling is continued until cortical electrical silence is assured. EEG monitoring is however limited to the recording of postsynaptic potentials of cortical neurons in the vicinity of the electrical lead and is not able to fully monitor the metabolic status of the most vulnerable areas of the brain (hippocampus and basal nuclei). Finally EEG monitoring is only able to monitor the energy expended on neuronal transmission and not the energy consumption necessary for the maintenance of cellular integrity.

EEG has also been used to titrate agents (such as barbiturates) to provide burst suppression, which had been felt to provide optimal metabolic suppression. Although frequently utilized, metabolic suppression with anesthetic agents as a clinical neuroprotective strategy has not been well established. Nussemeier et. al. randomized patients undergoing open chamber cardiac surgery to perioperative barbiturate or no barbiturate administration.3 They reported a decrease in postoperative neuropsychological complications and delayed awakening in the group receiving barbiturates. In a similar study Zaidan et. al. examined neurologic outcome after coronary artery bypass grafting surgery in patients receiving thiopental or placebo.4 This group of investigators did not find a significant difference between the two groups. Other investigators have also failed to observe differences in outcome with barbiturate administration.5,6,7

Although it would be easy to attribute the beneficial effects of hypothermia strictly by its ability to lower cerebral oxygen consumption (CMRO2) and brain energy demands, the actual mechanism is not entirely clear. Although intellectually appealing, the use of these cerebral metabolic suppressive drugs do not necessarily effect cerebral outcome after cerebral ischemia.8 Anesthetic agents and mild hypothermia that are equally suppressant of cerebral metabolism do not confer equal degrees of protection to ischemic insult. Anesthetic agents decrease overall CMRO2 and hence forestall the development of a neurotoxic cascade. Realistically, this metabolic suppression would only provide a short window of protection. It is likely, therefore, that hypothermia may provide significant neuronal protection by mechanisms, such as reducing excitatory neurotransmitter release, decreasing free radical production, decreasing post-ischemic edema, and stabilizing central nervous system blood flow.9,10 Because of the ineffectiveness of metabolic suppression to protect the brain after ischemic insults, we do not use EEG to monitor burst suppression.

We are presently using jugular bulb saturations rather than EEG monitor to assure the adequacy of cooling prior to circulatory arrest. Since esophageal, tympanic membrane, and nasopharyngeal temperatures may not accurately reflect brain temperature, jugular bulb oxyhemoglobin saturation may be used as an indirect index of cerebral hypothermia.11 Cerebral cooling decreases the cerebral metabolic rate for oxygen, decreases cerebral oxygen extraction, and results in increased jugular bulb oxyhemoglobin saturation (satJBO2). A low satJBO2 (high cerebral oxygen extraction) is evidence that additional cerebral cooling is warranted. A high satJBO2, therefore, is a reassuring clinical sign of global cerebral hypothermia, but does not guarantee that all regions are sufficiently hypothermic. EEG monitoring may produce false positive results, indicating electrical silence in the presence of a low satJBO2, indicating residual metabolism.12 Moreover, satJBO2 may not be a sensitive indicator of focal ischemic events. Prior to initiating DHCA at the authors' institution, cooling on CPB is continued until the satJBO2 is at least 95%.13,14

In conclusion, EEG monitor is not necessary prior to deep hypothermic circulatory arrest. Although it is an effective monitor of cortical electric activity, its inability to monitor deeper vulnerable structures limit its clinical usefulness. Its use for the titration of burst-suppression is limited by the paucity of scientific evidence supporting metabolic suppression as an effective cerebral protectant strategy. Finally, the monitoring of jugular bulb saturations may be a more effective modality than EEG of the homogenicity and adequacy of cerebral cooling.


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