Inhaled Anesthetics
Nitroux Oxide
Used alone, nitrous oxide causes a decrease in amplitude and frequency
of the dominant occipital α rhythm (see Chapter
5
, Chapter 6
, Chapter
7
, and Chapter 8
).
With the onset of analgesia and depressed consciousness, frontally dominant fast
oscillatory activity (>30 Hz) is frequently seen.[33]
This activity may persist to some extent for up to 50 minutes after discontinuation
of nitrous oxide. When nitrous oxide is
TABLE 38-3 -- Anesthetic drugs and the electroencephalogram
|
Drug |
Effect on EEG Frequency |
Effect on EEG Amplitude of Dominant Frequency |
Burst Suppression |
|
Isoflurane |
|
|
Yes, >1.5 MAC |
|
Subanesthetic |
Loss of α, ↑ frontal β |
↑ |
|
|
Anesthetic |
Frontal 4–13 Hz activity |
↑ |
|
|
Increasing dose >1.5 MAC |
Diffuse theta and δ → burst suppression →
silence |
↑ → 0 |
|
|
Desflurane |
Similar to equi-MAC dose of isoflurane |
Similar to equi-MAC dose of isoflurane |
Yes, >1.5 MAC |
|
Sevoflurane |
Similar to equi-MAC dose of isoflurane |
Similar to equi-MAC dose of isoflurane |
Yes, >1.5 MAC |
|
Nitrous oxide (alone) |
Frontal fast oscillatory activity (>30 Hz) |
↑, especially with inspired concentration >50% |
No |
|
Enflurane |
|
|
Yes, >1.5 MAC |
|
Subanesthetic |
Loss of α, ↑ frontal β |
↑ |
|
|
Anesthetic |
↑ Frontal 7–12 Hz activity |
↑ |
|
|
Increasing dose >1.5 MAC |
Spikes/spike and slow waves → burst suppression; hypocapnia
→ seizures |
↑↑ → 0 |
|
|
Halothane |
|
|
Not seen in clinically useful dosage range |
|
Subanesthetic |
↑ Frontal 10–20 Hz activity |
↑ |
|
|
Anesthetic |
↑ Frontal 10–15 Hz activity |
↑ |
|
|
Increasing dose >1.5 MAC |
Diffuse theta, slowing with increasing dose |
↑ |
|
|
Barbiturates |
|
|
Yes, with high doses |
|
Low dose |
Fast frontal β activity |
Slight ↑ |
|
|
Moderate dose |
Frontal α-frequency spindles |
↑ |
|
|
Increasing high dose |
Diffuse δ → burst suppression → silence |
↑↑↑ → 0 |
|
|
Etomidate |
|
|
Yes, with high doses |
|
Low dose |
Fast frontal β activity |
↑ |
|
|
Moderate dose |
Frontal α-frequency spindles |
↑ |
|
|
Increasing high dose |
Diffuse δ → burst suppression → silence |
↑↑ → 0 |
|
|
Propofol |
|
|
Yes, with high doses |
|
Low dose |
Loss of α, ↑ frontal β |
↑ |
|
|
Moderate dose |
Frontal δ, waxing or waning α |
↑ |
|
|
Increasing high dose |
Diffuse δ → burst suppression → silence |
↑↑ → 0 |
|
|
Ketamine |
|
|
No |
|
Low dose |
Loss of α, ↑ variability |
↑↓ |
|
|
Moderate dose |
Frontal rhythmic δ |
↑ |
|
|
High dose |
Polymorphic δ, some β |
↑↑ (β is low amplitude) |
|
|
Benzodiazepines |
|
|
No |
|
Low dose |
Loss of α, increased frontal β activity |
↑ |
|
|
High dose |
Frontally dominant δ and theta |
↑ |
|
|
Opiates |
|
|
No |
|
Low dose |
Loss of β, α slows |
↔↑ |
|
|
Moderate dose |
Diffuse theta, some δ |
↑ |
|
|
High dose |
δ, often synchronized |
↑↑ |
|
|
EEG, electroencephalographic; MAC, minimum alveolar concentration;
α, 8–13 Hz frequency; β, >13 Hz frequency; δ, <4 Hz
frequency; theta, 4–7 Hz frequency. |
Figure 38-6
electroencephalographic effects of intravenous administration
of thiopental in humans. A, Rapid activity. B,
Barbiturate spindles. C, Slow waves. D,
Burst suppression. (From Clark DL, Rosner BS: Neurophysiologic effects
of general anesthetics. Anesthesiology 38:564, 1973.)
used in combination with other agents, it increases the clinical and electroencephalographic
effects that are associated with the agent alone.
Isoflurane, Sevoflurane, Enflurane, Halothane, and
Desflurane
Potent inhaled anesthetics follow the basic anesthesiarelated
electroencephalographic pattern. For example, isoflurane initially causes an activation
of the EEG, followed by a slowing of the electroencephalographic activity that escalates
with increasing dose. Isoflurane begins to produce periods of electroencephalographic
suppression at 1.5 minimum alveolar concentration (MAC), which become longer with
increasing dose until electrical silence is produced at 2 to 2.5 MAC. Sometimes,
isolated epileptiform patterns can be seen during intersuppression activity at 1.5
to 2.0 MAC of isoflurane.[34]
Sevoflurane causes
similar dose-dependent electroencephalographic effects. Equi-MAC concentrations
of sevoflurane and isoflurane cause similar electroencephalographic changes.[35]
Epileptiform activity has been induced by administration of sevoflurane in patients
without epilepsy, and seizure activity on EEG, but not clinical seizure activity,
has been reported in pediatric patients with a history of epilepsy during induction
of anesthesia with sevoflurane.[36]
[37]
Despite these observations, sevoflurane, like other inhalation agents, is not suitable
for use during electrocorticography for localization of seizure foci.[38]
The electroencephalographic patterns seen with enflurane are similar to those seen
with isoflurane, except that epileptiform activity is considerably more prominent.
At 2 to 3 MAC, burst suppression is seen, but virtually all intersuppression activity
consists of large spike and wave pattern discharges. Hyperventilation with high
concentrations of enflurane increases the length of suppression, decreases the duration
of bursts, but increases the amplitude and main frequency component of the intersuppression
epileptiform activity. Frank seizures seen on the EEG may also occur with enflurane,
which produces the same cerebral metabolic effects as pentylenetetrazol, a known
convulsant. Halothane also produces electroencephalographic patterns
similar to those of isoflurane, but dosages of halothane that would produce burst
suppression on the EEG (3 to 4 MAC) are associated with profound cardiovascular toxicity.
Desflurane produces electroencephalographic changes similar in nature to equi-MAC
concentrations of isoflurane. In limited clinical studies, there has been no evidence
of epileptiform activity with desflurane, despite hyperventilation and 1.6 MAC dosage,
[39]
and desflurane has been used as a treatment
of refractory status epilepticus.[40]
Clinical studies have demonstrated that the EEG of inhalational
anesthetic agents is influenced by age and baseline electroencephalographic characteristics.
Older patients and those with electroencephalographic slowing at baseline were more
sensitive to the electroencephalographic effects of isoflurane and desflurane. As
anesthesia was deepened, similar electroencephalographic pattern changes were observed,
but these changes occurred at lower end-tidal anesthetic concentrations.[41]
