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
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
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
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
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