Stefan Schraag, MD
Department of
Anaesthesiology
University of Ulm,
Germany
Why monitor the central
nervous system ?
Obviously, all of us have gotten along without any monitor until now, so why should we bother? The practice of anaesthesia remains one of the safest and most effective in medicine. Furthermore, like all new technologies, CNS monitoring devices will add something to the cost of delivering anaesthesia. On the other hand, there is no doubt, that significant unpredictability and uncertainty still exists in the delivery of anaesthetic drugs. This is reflected in the variety of suggested dosing regimens, especially in intravenous anaesthesia. Some patients still suffer intra-operative awareness and may consecutively develop posttraumatic stress disorder, whereas others still have prolonged recovery due to relative overdosing even with otherwise short-acting drugs. The primary reason for using any monitor, designed to reflect the anaesthetic state must be to improve patient care.
What is the rationale of anaesthetic effects on the CNS
?
The main target of drugs used in general anaesthesia is the central nervous system. Recently, several studies have suggested that movement and autonomic changes during anaesthesia do not necessarily represent the effects of anaesthetics on the central nervous system, since it has been demonstrated that forebrain structures are not essential in mediating movements to surgical stimulation. Although quite different pharmacological pathways have been suggested, by which hypnotic, analgesic and other neurotropic agents seem to act and interact on different areas of the brain and spinal cord (receptors, ion-channels, neuro-humeral transmission), there is increasing evidence that general anaesthesia may be characterised by at least two major components. Increasing concentrations of hypnotics, such as propofol or etomidate, produce unconsciousness as a suppression of cortical cognitive abilities and processing. If only unconsciousness is achieved, a noxious stimulus will cause arousal and awakening as a result of the intensity of the stimulus. To prevent arousal, the noxious stimulus needs to be inhibited to reach cortical structures. This is either achieved by the action of opioids on opiate receptors within the spinal cord or by the blockade of peripheral nerves by local anaesthetics. Both mechanisms attenuate (opioids) or abolish (local anaesthetics) the nociceptive input to ascending spino-thalamic pathways. Understanding general anaesthesia as a combination of different components achieved through the combined use of drugs with different underlying mechanisms of action has important clinical implications for measuring the overall anaesthetic effect.
What are the requirements of
an ideal monitor ?
An ideal monitor should
1. be able to reflect the level of uncounsciousness and thus detect episodes of light anaesthesia associated with the likelihood of awareness as well as episodes of excessive anaesthesia associated with side effects.
2. give an output, that reflects the overall balance between hypnotic and analgesic drug effects on one side and the intensity of stimulation by surgery on the other and alter its signal appropriately during surgical stimulation.
3. be valid both in paralysed and spontaneously breathing patients.
4. provide similar signals when different anaesthetic agents are used.
5. produce a marked signal difference during the transition from awake to asleep and vice versa.
Are
CNS effects of intravenous anaesthetics different to others ?
Interestingly, a large body of knowledge about how to measure anaesthetic effects and depth of anaesthesia has been collected by researches who are also involved in topics related to intravenous anaesthesia. This may partially be due to the fact that when continuous intravenous anaesthetic techniques became popular 10-15 years ago, the dosing regimens especially of propofol at that time were likely to produce light anaesthesia and reports of wakefulness during propofol anaesthesia were published. But since more sophisticated drug delivery systems like TCI became available, which produce more predictable drug concentrations, this discussion ended. Although the specific molecular effects of propofol, etomidate or opioids on the neural activity of the brain may be unique and therefore different to volatile agents, there is no evidence that monitoring CNS effects of intravenous anaesthetics is more difficult or cumbersome than with inhalational anaesthetics.
What are the available monitors to measure CNS effects of intravenous anaesthetics?
A comparison of selected contemporary technologies of monitoring anaesthetic effects is given in the following table.
|
Signal
(technology) |
Trade name |
Neurophysiology/Comments |
|
Auditory evoked potentials (i.e. AEP Index) |
Experimental |
Nb and Pa waves from primary auditory cortex |
|
EEG (composite) Bispectral Index (BIS) |
BIS, Aspect Medical Systems |
Weighted analysis of bispectrum, bicoherence |
|
EEG (composite) Patient state index |
PSI, Physiometrix |
Undergoing trials |
|
EEG (power sepectrum) Fast Fourier Analysis |
pEEG, Dräger |
SEF 90%, MF, relative delta power |
|
EEG (composite) Cerebrogram |
Narkotrend, MT Monitortechnik |
Stages of EEG supression (drug related profiles) |
|
EEG (composite) Topographical Electroencephalometry |
CATEEM, SFx, Medisyst |
Locoregional cortical changes, ischaemia detection |
|
Heart rate variability, RSA (mean circular resultant and moving polynomial) |
Experimental |
Brainstem (NTS medulla), linked to emotional state |
|
Heart rate variability |
Anemon-I, MCSA |
Sympathetic output, advertised as a “depth of analgesia” monitor |
|
Facial Electromyogram (EMG) |
FACE, Patient Comfort Inc. |
Development of the frontalis and other EMG signals in the brainstem (pons) |
What
are the most promising attempts of monitors to recommend ?
During the last decade, there has been a large number of studies, which tied to validate monitors designed to reflect the level of anaesthesia. However, as they were evaluated in a variety of clinical situations and with different drugs and drug combinations, their results often appear equivocal. Among the many available measures suggested, monitors based on the auditory evoked response and the bispectral index of the EEG seem to be the most promising techniques today. In comparison with other electrophysiological variables, auditory evoked potentials better discriminate the arousability of the patient and the transition from consciousness to unconsciousness, whereas BIS is better correlated with increasing drug concentrations. This lets us suggest, that both measures are valuable, but reflect different functional parts of the cortico-thalamic neuraxis. Many other approches of CNS monitoring await future validation studies.
In summary, the developments in CNS monitoring of the recent years have contributed to an increasing predictability and safety of titrating anaesthetic drug effect. Although this will definitely contribute to an improved patient care by the anaesthetist, it will remain difficult to quantify this benefit.
Selected
recommended references:
1.
Doi M, Gajraj
RJ, Mantzaridis H, Kenny GNC. Prediction of movement at laryngeal mask
insertion: comparison of auditory evoked potential index, bispectral index,
spectral edge frequency and median frequency. Br J Anaesth 1999; 82:203-7.
2.
Dutton RC,
Smith WD, Rampil IJ, Chortkoff BS, Eger EI II. Forty-hertz midlatency auditory
evoked potential activity predicts wakeful response during desflurane and
propofol anesthesia. Anesthesiology 1999; 91:1209-20.
3.
Gan TJ, Glass
PS, Windsor A, Payne F, Rosow C, Sebel P, Manberg P. Bispectral index
monitoring allows faster emergence and improved recovery from propofol,
alfentanil and nitrous oxide anesthesia. Anesthesiology 1997; 87:808-15.
4.
Ghoneim MM.
Awareness during anesthesia. Anesthesiology 2000; 92:597-602.
5.
Guignard B,
Menigaux C, Dupont X, Fletcher D, Chauvin M. The effect of remifentanil on the
bispectral index change and hemodynamic responses after orotracheal intubation.
Anesth Analg 2000; 90:161-7.
6.
Kearse LA,
Rosow C, Zaslavsky A, Conners P, Dershwitz M, Denman W. Bispectral analysis of
the electroencephalogram predicts conscious processing of information during
propofol sedation and hypnosis. Anesthesiology 1998; 88:25-34.
7.
Kenny GNC,
Mantzaridis H. Closed loop control of anaesthesia. Br J Anaesth 1999; 83:223-8.
8.
Kissin I. A
concept for assessing interactions of general anesthetics. Anesth Analg 1997;
85:204-10.
9.
Kochs E,
Kalkman CJ, Thornton C, Newton D, Bischof P, Kuppe H, Abke J, Konecny E, Nahm
W, Stockmanns G. Middle latency auditory evoked responses and
electroencephalographic derived variables do not predict movement to noxious
stimulation during 1 minimum alveolar anesthetic concentration
isoflurane/nitrous oxide anesthesia. Anesth Analg 1999; 88:1412-7.
10.
Mantzaridis
H, Kenny GNC. Auditory evoked potential index: A quantitative measure of
changes in auditory evoked potentials during general anaesthesia. Anaesthesia
1997; 52:1030-6.
11.
Pomfrett CJD.
Heart rate variability, BIS and depth of anaesthesia. Br J Anaesth 1999;
82:659-62.
12.
Rampil IJ. A
primer for EEG signal processing. Anesthesiology 1998; 89:980-1002.
13.
Schraag S,
Bothner U, Gajraj RJ, Kenny GNC, Georgieff M. The performance of
electroencephalogram bispectral index and auditory evoked potential index to
predict loss of consciousness during propofol infusion. Anesth Analg 1999;
89:1311-5.
14.
Schraag S,
Mohl U, Bothner U, Georgieff M. Clinical utility of EEG parameters to predict
loss of consciousness and response to skin incision during total intravenous
anaesthesia. Anaesthesia 1998; 53:320-5.
15.
Schwilden H,
Stoeckel H, Schüttler J. Closed loop feedback control of propofol anaesthesia
by quantitative EEG analysis in humans. Br J Anaesth 1989; 62:290-6.
16.
Zbinden AM,
Maggiorini M, Petersen-Felix S, Thomsen DA. Anesthetic depth defined using
multiple noxious stimuli during isoflurane/oxygen anesthesia: hemodynamic
responses. Anesthesiology 1994; 80:261-7.