Effects of common anesthetic agents on electroencephalograms

Published on 07/02/2015 by admin

Filed under Anesthesiology

Last modified 22/04/2025

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Effects of common anesthetic agents on electroencephalograms

R. Doris Wang, MD

The electroencephalogram (EEG) is a depiction of the electrical activity occurring at the surface of the brain. This activity appears on the EEG recording as waveforms of varying frequency and amplitude measured in microvolts. Four categories of frequencies are the most clinically relevant (Table 43-1, Figure 43-1).

Table 43-1

Categories of the Most Clinically Relevant Electroencephalographic Frequencies

Wave Pattern Frequency Range (Hz) Level of Consciousness
Delta 0.5-4 Deep sleep
Theta 4-8 Drowsiness (also first stage of sleep)
Alpha 8-14 Relaxed but alert
Beta 14-30 Highly alert and focused

Intraoperative monitoring that employs raw EEG data is one of the traditional methods used to assess the adequacy of cerebral perfusion. Many electrical changes associated with increased doses of intravenously administered or inhalation anesthesia can mimic EEG changes associated with inadequate cerebral perfusion (i.e., brain ischemia).

Inhalation anesthetic agents

Inhalation anesthetic agents consistently increase slow-wave EEG activities. At doses lower than minimum alveolar concentration (MAC) levels, alpha rhythm disappears and the voltage of beta activity increases and becomes more widespread. As the end-tidal concentration of the inhalation agent increases, the EEG progressively increases in amplitude and decreases in frequency. During deep-inhalation anesthesia, burst suppression occurs. EEG changes vary somewhat depending on the specific anesthetic agent used, whether the agent is used alone or in combination with other anesthetic agents, whether hyperventilation is employed, and the patient’s age. In addition, patients with increased baseline delta (slow-wave) activity resulting from underlying intracranial pathology can show relatively little or no change in the EEG with increasing anesthesia depth, but burst suppression may eventually become evident.

Opioids

The use of opioids, such as fentanyl, sufentanil, or alfentanil, are usually not associated with beta activities but cause immediate EEG slowing with high-voltage, slow delta waves. Despite causing generalized EEG slowing, the use of an opioid anesthetic does not result in a burst-suppression pattern. In some patients, spindle-like activity with a frequency of 10 to 15 Hz appears predominately in the frontal leads. This sharp activity is not epileptiform in character and disappears after the opioid infusion is discontinued. Some patients show isolated sharp-wave activity after fentanyl induction. This phenomenon is more evident at high drug doses. For example, it is well established that opioid medications have the potential to induce epileptiform activity in both laboratory animals and humans. In patients undergoing nonlesional operations for the treatment of temporal lobe epilepsy, opioid-(particularly alfentanil and sufentanil) induced epileptiform activity facilitates intraoperative electrocorticography-guided localization of the epileptogenic zone. That is, opioids facilitate localization of the epileptogenic zone while minimizing resection of nonepileptogenic eloquent brain tissue.