Adequacy of Anesthesia

Introduction to the concept of general anesthesia

Michel Struys, MD, PhD
Ghent University Hospital
Department of Anesthesia
B-9000 Ghent, Belgium

Email: michel.struys@rug.ac.be

The article also available in PDF: 36 KB

Introduction

The quality control of anesthesia has become increasingly important, owing the recent evolution in perioperative management. Due to new surgical techniques and changing needs in patient care, it is more and more essential to find ways to manage anesthesia in a fast, simple, and safe way. In this respect, to control the state of general anesthetic, a wide spectrum of pharmacological actions need to be utilized. This includes not only analgesia and hypnosis, but also the suppression of somatic and autonomic responses to noxious stimuli [1].

When a specific dose of anesthetic or analgesic drugs is administered, the ultimate goal is to obtain a desired clinical effect. For this, a specific therapeutic concentration of the drug at the site of action at the receptor is required. Typically, each individual anesthetic produces its unique spectrum of pharmacological actions. Hence, the traditional concept of common drug titration may need to be adjusted to reflect separate clinical components of an ideal anesthetic state [2]. In order to reach today’s high standards of care, the anesthetist has to simultaneously optimize the administration of multiple drugs by titrating doses for a specific therapeutic effect. Therefore, he or she needs a theoretical understanding of the "conceptual components of anesthesia"

Evolution of the anesthetic concept

Classic theories

In 1847, Plombey [3] was the first to classify depth of anesthesia in three characteristic stages: intoxication, excitement (both conscious and unconscious), and the deeper level of narcosis. In 1937, Guedel [4] used clinical definitions to describe the four stages of ether anesthesia based on respiratory, hemodynamic, and ocular signs plus muscle tone.

Since 1942, when neuromuscular blocking agents were first introduced into clinical use, the incidence of reports of awareness started increasing. Paralyzed patients’ traditional clinical signs were no longer detectable. In 1954, Artusio [5] divided the first stage in Guedel's classification into three planes (Table 1).

The traditional clinical signs were quite relevant at the time they were developed, as they could be utilized effectively during the administration of ether, cyclopropane, and chloroform. In today’s anesthesia practice, however, the effectiveness of clinical signs would be questionable, as there are new volatile anesthetics often used in combination with opioids and other drugs. In addition, the modern monitoring techniques offer information that was not available then.

The unitary non-specific mechanisms of anesthetic actions

The above mentioned classic anesthesia theories were based on unitary, non-specific mechanisms of anesthetic actions. It was assumed that one anesthetic could be replaced freely by another, and in the case of anesthetic combinations, the anesthetic effect of such mixtures was expected to be additive [6].

In the classic concept of anesthesia, the state of general anesthesia was taken as a multi-featured phenomenon, which was caused by a single underlying mechanism. In order to bind all general anesthetics with diverse chemical structures with a common hypothesis, that mechanism was supposed to be non-specific.

Taking distance from the classic concept

The problem with the classic concept of the state of anesthesia became obvious when neuromuscular blocking agents, opioids, and barbiturates were increasingly used in combination with inhaled anesthetics.

In 1957, Woodbridge [7] examined the use of anesthetic drugs at that time and defined anesthesia as having four components:

1. Sensory blockade of afferent nerve impulses
2. Motor blockade of efferent impulses.
3. Reflex blockade of the respiratory, cardiovascular, or gastrointestinal tract, and
4. Mental block, sleep, or unconsciousness.

In Woodbridge’s classification, different drugs could be used to achieve each effect. However, he made no effort to define methods of assessing each of these components. In 1986, Pinsker [8] sent a letter to the editor of a recognized anesthesia journal, and postulated anesthesia as a concept with three components: paralysis, unconsciousness, and attenuation of the stress response. In that theory, any drug or combination of drugs that reversibly provided these three conditions could be used in anesthesia.

Perception of pain vs. state of anesthesia

In 1987, Prys-Roberts [9] raised a noteworthy topic: perception of pain. If pain was to be considered as a "conscious perception of noxious stimulus", then "a state of anesthesia" could be defined as drug-induced unconsciousness, in which the patient neither perceived nor recalled pain. According to his theory, surgery causes noxious stimuli which resulted in a series of somatic (i.e. pain or movement), autonomic, and hemodynamic responses that could then be modified by different drugs.

Subsequently, Kissin [1,6] expanded, refined, and further contributed to the definition of anesthesia. He stated that a wide spectrum of pharmacological actions via different drugs could be used to create a general anaesthetic state. These pharmacological actions could include analgesia, anxiolysis, amnesia, unconsciousness, and suppression of somatic, motor, cardiovascular, and hormonal responses to the stimulus of surgery. He also emphasized that one should not understand the spectrum of effects that constituted the state of general anesthesia, as multiple components of anesthesia resulting from one anesthetic action. Instead, the spectrum merely represented separate pharmacological actions, even if the anesthesia was produced by one drug only.

Recent understanding of depth of anesthesia

To confirm the theories and to further advance our understanding of depth of anesthesia, it was clear that we need more scientific information on the interaction of combinations of clinically relevant anaesthetic drugs.

Modern hypothesis of general anesthesia

In 1998, an editorial appeared where Glass [10] discussed the interaction of hypnotics and opioids in achievement of two major endpoints in general anesthesia, namely loss of consciousness and the inhibition of movement at skin incision.

He suggested that the interaction between hypnotics and opioids might explain loss of consciousness and response to skin incision. These did not appear to be a single continuum of increasing "anesthetic depth", but rather were two separate phenomena.

Combining his observations, Glass then proposed the following hypothesis of general anesthesia. He explained general anesthesia as a process requiring a state of unconsciousness of the brain, primarily produced by the volatile or intravenous anesthetics. If only unconsciousness has been achieved, the noxious stimulus needs to be inhibited from reaching higher centers, where it could cause an arousal reflex. Such an inhibition can be achieved by the action of opiates at opiate receptors within the spinal cord. Alternatively, local anesthetics can be injected on the peripheral nerves. In fact, volatile anesthetics can be administered in concentrations exceeding the minimum alveolar concentration (MAC), to have similar effect on the spinal cord [10]. Special effects should be obtained by specific therapeutics. For example, in the case of neuromuscular block, neuromuscular relaxants should be used.

In conclusion, today’s anesthetist needs knowledge of specific effects of drugs and their pharmacological interactions. Monitoring of drug effects during anesthesia, utilizing the specific effect-monitoring technology available today, will help to maintain high therapeutic quality.

References:

1. Kissin I: General anesthetic action: an obsolete notion? [editorial]. Anesth Analg 1993, 76, 215-218
2. Glass PS, Bloom M, Kearse L, Rosow C, Sebel P, Manberg P: Bispectral analysis measures sedation and memory effects of propofol, midazolam, isoflurane, and alfentanil in healthy volunteers. Anesthesiology 1997, 86, 836-847
3. Plombey F. Operations upon the eye. Lancet 1847, 1, 1847
4. Guedel AE. Inhalational anesthesia: a fundamental guide. New York: Macmillan, 1937
5. Artusio JF. Di-ethyl ether analgesia: a detailed description of the first stage of ether analgesia in man. J Pharmacol Exp Ther 1954, 111, 343-334
6. Kissin I. A concept for assessing interactions of general anesthetics. Anesth Analg 1997, 85, 204-210
7. Woodbridge PD. Changing concepts concerning depth of anesthesia. Anesthesiology 1957, 18, 536
8. Pinsker MC. Anesthesia : a pragmatic construct, letter. Anesth Analg 1986, 65, 819-820
9. Prys-Roberts C. Anaesthesia: a practical or impractical construct? Br J Anaesth 1987, 11, 1341-1345
10. Glass PS. Anesthetic drug interactions: an insight into general anesthesia – its mechanism and dosing strategies. Anesthesiology 1998, 88, 5-6
    

Last updated: 1 November 2001Created
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