EEG Signal Analysis in Anesthesia - Quantitative EEG Analysis Methods and Clinical Applications - page 227

anesthesia, nondepolarizing muscle relaxants, and female gender. These risk fac-
tors, however, account for only about half of the cases of recall. Many other cases
occur in the setting of inadvertent failure of intended anesthetic agent delivery,
extreme pharmacological tolerance, and even, occasionally, simple errors in
anesthetic management.
In unmedicated subjects pain or fear can elicit a substantial increase in blood
pressure and heart rate due to activation of the sympathetic nervous system. Several
lines of evidence suggest that routine monitoring of vital signs (e.g., blood pressure
and heart rate) is insensitive to the patient's level of consciousness in current anes-
thetic practice [10-12]. In the face of widespread use of opiates, beta-blockers, and
central alpha agonists, and the general anesthetic agents themselves, the likelihood
of a detectable sympathetic response to painful stimulus or even consciousness is
diminished. Domino et al.'s [13] review of the ASA Closed Claims database failed to
find a correlation between recorded vital signs and documented recall events. Other
attempts to score vital sign plus diaphoresis and tearing have also failed to establish
a link between routine vital signs and recall [10-12].
Because existing hemodynamic monitors have definitively failed to detect ongo-
ing recall in the current environment of mixed pharmacology (if they ever did), a
new, sensitive monitor could be useful, especially for episodes of recall not predicted
by preexisting risk factors. Real-time detection of inadequate anesthetic effect and a
prompt therapeutic response with additional anesthetics appear likely to reduce the
incidence of overt recall.
With the goal of monitoring anesthetic effect justified, it is now appropriate to
review the effect of anesthetic drugs on the human EEG. It is important to first note
that anesthesiologists in the OR and intensivists in the critical care unit use a wide
range of drugs, some of which alter mentation, but only some of which are true gen-
eral anesthetics. Invoking the spirit of William Thompson, Lord Kelvin, who said
one could not understand a phenomenon unless one could quantify it, the state of
general anesthesia is poorly understood, in part because there have been no quanti-
tative measures of its important effects until very recently.
This author has defined general anesthesia as a therapeutic state induced to
allow safe, meticulous surgery to be tolerated by patients [14]. The “safe and metic-
ulous” part of the definition refers to the lack of responsiveness to noxious stimula-
tion defined most commonly as surgical somatic immobility, a fancy way of saying
that the patient does not move perceptibly or purposefully in response to incision. In
practice, this unresponsiveness also mandates stability of the autonomic nervous
system and the hormonal stress response. These are the features central to surgeons'
and anesthesiologists' view of a quality anesthetic. Patients, on the other hand,
request and generally require amnesia for intraoperative events including disrobing,
marking, positioning, skin prep, and, of course, the pain and trauma of the surgery
itself. Also best to avoid is recall of potentially disturbing intraoperative

conversation.
General anesthetics are those agents which by themselves can provide both
unresponsiveness and amnesia. Anesthetic drugs include inhaled agents such as
diethyl ether, halothane, isoflurane, sevoflurane, and desflurane. Barbiturates such
as thiopental and pentobarbital as well as certain GABA A agonists, including
propofol and etomidate, are also general anesthetics. Other GABA A agonists such as