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tivity ceases. There is some variation in the EEG changes seen with the various general anesthetic agents. Thiopental initially causes increased amplitude of the 18 to 30-Hz activity, and as consciousness is lost, the appearance of 5 to 12-Hz activity is superimposed on faster activity. This frequently occurs in spindle-shaped bursts. Halothane initially produces 10 to 20-Hz activity that persists until consciousness is lost. As the concentration of the gas is increased, slower theta and delta activity becomes more prominent. Various combinations of inhalation anesthetic gases can also have unique effects on the EEG. Patients receiving 0.5% isoflurane with 70% nitrous oxide/oxygen showed 15 to 20 Hz activity of low to moderate voltage. At 2% isoflurane with oxygen, or 1% isoflurane with 70% nitrous oxide/oxygen most EEGs showed 2- to 6-Hz moderate to high voltage activity with superimposed 15- to 20-Hz activity. When the concentration of isoflurane is raised above 2% in oxygen, or 1.5% in nitrous oxide, a burst-suppression pattern or total electrical silence most typically occurs. Changes in the blood levels of carbon dioxide in patients under general anesthesia can also cause fluctuations in the EEG. The narcotic fentanyl is notable for having a rapid onset and short duration at low doses. There is general agreement that the EEG is a sensitive indicator of cerebral ischemia in the conscious patient. Ischemia is initially recognized by changes from background activity to beta activity, frequently with the disappearance of alpha waves. As cerebral ischemia becomes more profound, low to moderate voltage theta and then high voltage delta appear. With severe and prolonged ischemia, a complete loss of electrical activity may be observed. In the awake patient, the sensitivity of the EEG to ischemia is such that the EEG changes often precede clinical signs. EEG is also an accurate indicator of cerebral ischemia under general anesthesia. In fact, its prime clinical utility in cerebrovascular surgery is that it permits an assessment of regional cerebral perfusion in the unconscious patient. Under deep general anesthesia, however, the EEG becomes dominated by waves of 2 to 6 Hz with loss of the faster components. These generalized EEG changes make the detection of focal abnormalities much more difficult. Therefore, in order for the EEG to be adequately sensitive to the detection of cerebral ischemia in a patient under general anesthesia, the level of anesthesia must be maintained in a range that permits a stable baseline EEG. In such cases, minor alterations in the EEG secondary to ischemia will not be masked.
Sharbrough found a stereotypic EEG response to ischemia in patients monitored under general anesthesia. These EEG changes generally consisted of replacement of the faster background frequencies by higher amplitude theta components. This was followed by lower amplitude irregular delta waves. In patients with extreme changes, the residual EEG tracing was ultimately reduced to low voltage irregular delta activity. The EEG is less sensitive to the detection of cerebral ischemia in patients who have major (Continued on page 107)
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