Book Text

DEFINITIONS OF ANESTHETIC DEPTH

Historical Definitions

The word "anesthesia" was first used by the Greek philosopher Dioscorides in the first century of the current era to describe the narcotic effect of the plant mandragora.

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The word reappeared in the 1771 Encyclopaedia Britannica, where it was defined as a "privation of the senses."^[1] After the introduction of ether anesthesia by Morton in 1846, Oliver Wendell Holmes coined the word to describe the new phenomenon that made surgical procedures possible.

Plomley,^[2] in 1847, was the first to attempt to define depth of anesthesia. He described three stages: intoxication, excitement (both conscious and unconscious), and the deeper levels of narcosis. In that same year, John Snow^[3] described "five degrees of narcotism" for ether anesthesia. The first three stages encompassed induction of anesthesia, and the last two represented surgical anesthesia. Eleven years later, Snow^[4] turned his attention to chloroform. Snow's excellent characterizations of ether and chloroform anesthesia described the following signs: conjunctival reflex; regular, deep, automatic breathing; movement of the eyeballs; and inhibition of the intercostal muscles. Many of these clinical signs were later "rediscovered."^[5] Because oxygen was not readily available until the early 1900s, Snow and his successors tried to minimize the use of deep anesthesia to decrease morbidity and mortality.

The early 1900s saw the introduction of premedication with sedatives or opioids. In addition, anesthetics with more rapid onset, such as nitrous oxide and ethylene, became available. Therefore, the anesthetic excitement phase could be traversed more rapidly with the use of preanesthetic medication and rapid-onset inhaled anesthetics. In 1937, Guedel published his classic description of the clinical signs of ether anesthesia.^[6] He used clear physical signs involving somatic muscle tone, respiratory patterns, and ocular signs ( Fig. 31-1 ) to define four stages. The first stage, analgesia, is characterized by slow, regular breathing with the diaphragm and intercostal muscles and the presence of the lid reflex. The subject experiences complete amnesia, analgesia, and sedation. In the second

Figure 31-1 Guedel's classic text described the stages and planes of ether anesthesia (A) and then related them to clinical signs or relevant reflexes (B). (From Guedel AE: Inhalational Anesthesia: A Fundamental Guide. New York, Macmillan, 1937.)

stage (delirium), the subject experiences excitement, unconsciousness, and a dream state with uninhibited activity. Ventilation is irregular and unpredictable. Reflex dilatation of the pupils occurs, the lid reflex is intact, and the risk of clinically important reflex activity (e.g., vomiting, laryngospasm, or arrhythmias) increases. The third stage (surgical anesthesia) consists of four progressive planes. Plane 1 is characterized by slight somatic relaxation, regular periodic breathing, and active ocular muscles. During plane 2, breathing changes, inhalation becomes briefer than exhalation, and a slight pause separates inhalation and exhalation. The eyes become immobile. In plane 3, the abdominal muscles are completely relaxed, and diaphragmatic breathing is very prominent. The eyelid reflex is absent. In plane 4, the intercostal muscles are completely paralyzed, and paradoxical rib cage movement occurs. Breathing is irregular, and the pupils are dilated. In Guedel's fourth stage (respiratory paralysis), muscles become flaccid, and the eyes widely dilate. Cardiovascular and respiratory arrest occurs, as does cardiovascular collapse.

In 1954, Artusio^[7] expanded Guedel's description of ether analgesia (stage 1) into three planes. In plane 1, the patient has no amnesia or analgesia. In plane 2, the patient has total amnesia and partial analgesia. In plane 3, the patient has complete analgesia and amnesia, but is comfortable and responsive to verbal stimulation; there is little depression of reflexes. The clinical signs of depth of anesthesia defined by Guedel and others had significant practical utility for the administration of ether, cyclopropane, and chloroform anesthesia. The success of using clinical signs to assess ether anesthetic depth arises partly from the established hypnotic and analgesic effects that ether provides, which differ from those of the current inhaled anesthetics used in modern anesthetic practice.

Beginning in 1942, small doses of the muscle relaxant d-tubocurarine were used with the deep levels of ether

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anesthesia that produced plane 2 or 3 of Guedel's stage III. Respiration was assisted when necessary. Over time, the dose of d-tubocurarine began to increase as fully controlled ventilation became commonplace. Anesthesiologists soon realized that they could combine controlled ventilation and large doses of muscle relaxants with low concentrations of inhaled anesthetics to reduce the risk of toxicity (cardiovascular and respiratory depression) and increase the speed of emergence from anesthesia. However, the use of muscle relaxants eliminated two valuable types of clinical signs of depth of anesthesia: the rate and volume of respiration and the degree of muscle relaxation induced by the anesthetic.^[7] Seven of the nine components of Guedel's classification system involved skeletal muscle activity. When muscle relaxants are used with ether anesthesia, only pupil size and lacrimation are left as clinical signs. These signs are inadequate to judge anesthetic depth clinically.^[8] A 1945 editorial in the Lancet discussed the clinical problems that muscle relaxants would create,^[9] and descriptions of patient awareness during surgery later began to appear in the literature.^[10]

In 1957, Woodbridge^[11] examined the diverse use of anesthetic drugs at that time. He 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. Different drugs could be used to achieve each effect. However, Woodbridge made no effort to define methods of assessing each of these components.

In a 1987 editorial, Prys-Roberts^[12] contributed to the concept of depth of anesthesia by redefining which elements are truly relevant to anesthesia. He began by observing that depth of anesthesia is difficult to define because anesthetists have approached the issue in terms of the drugs available to them rather than the patient's needs during surgery. Prys-Roberts believed that the noxious stimulation of surgery induces a variety of reflex responses that may be independently modified to the benefit of the patient. One important premise is that pain is the conscious perception of noxious stimuli. Thus, he defined anesthesia as a state in which the patient neither perceives nor recalls noxious stimuli as a result of drug-induced unconsciousness. The loss of consciousness is considered a threshold or all-or-none (quantal) phenomenon. By this definition, there can be no degrees of anesthesia or any variable depth of anesthesia. Prys-Roberts defined

Figure 31-2 Depth of anesthesia can be defined by suppression of the relevant clinical responses to noxious stimuli, as proposed by Prys-Roberts. (Modified from Prys-Roberts C: Anaesthesia: A practical or impossible construct [editorial]? Br J Anaesth 59:1341, 1987.)

anesthesia in terms of the drugs producing unconsciousness and modification of noxious stimuli, and he classified them by pharmacologic properties of the drugs and not by their ability to produce components of the state of anesthesia.

Prys-Roberts focused his concepts on the body's response to noxious stimuli, which he defined as factors causing potential or actual cell damage: mechanical, chemical, thermal, or radiation induced. Figure 31-2 shows the somatic and autonomic responses to noxious stimuli. In this scheme, one reads from left to right and from top to bottom to see the order in which reflex responses are suppressed by anesthetic drugs. For example, somatic responses include both sensory and motor activity. Sensory input obtained through the central nervous system (CNS) can originate from somatic or visceral tissue. The subject must be conscious to perceive pain. Low concentrations of inhaled or intravenously administered anesthetics can eliminate recall of pain, but they allow a motor response. The motor response to noxious stimuli is typically an all-or-none reflex withdrawal of the stimulated part. Eger and colleagues^[13] used this movement response as a clinical end point in developing the concept of minimum alveolar concentration (MAC).

The response of the respiratory system is part of the autonomic response described by Prys-Roberts. The motor response to noxious stimuli can involve an increase in tidal volume or the frequency of breathing. This ventilatory response may occur even if there is no somatic motor response to surgical stimulation. A higher concentration is required to suppress the breathing response than to suppress the somatic response to noxious stimuli.

Prys-Roberts divided autonomic responses into three categories. The hemodynamic response consists of autonomic responses to noxious stimuli, namely, increased sympathoadrenal activity that elevates arterial blood pressure and the heart rate. The sudomotor response consists of sweating. Release of hormones is an extremely difficult response to eliminate completely.

Prys-Roberts considered pain relief, muscle relaxation, and suppression of autonomic activity to be discrete pharmacologic events. These events may be engendered by specific drugs. Some drugs can produce all these end points; others can achieve only one or two. The only feature common to most anesthetics is suppression of sensory perception and production of unconsciousness. He considered inclusion of muscle relaxation in the definition of

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the anesthetic state illogical and confusing. Although muscle relaxation is necessary for laryngoscopy and surgical access, it is neither a component of anesthesia nor an alternative to adequate anesthesia.

Kissin,^[14] in a 1993 editorial, expanded, refined, and further contributed to the definition of anesthesia. He began by indicating that a wide spectrum of pharmacologic actions by different drugs can be used to create the general anesthetic state. These pharmacologic actions include analgesia, anxiolysis, amnesia, unconsciousness, and suppression of somatic motor, cardiovascular, and hormonal responses to the stimulation of surgery. Kissin stated that the spectrum of effects that constitute the state of general anesthesia should not be regarded as several components of anesthesia resulting from one anesthetic action but, instead, should be considered as separate pharmacologic actions, even if the anesthesia is produced by one drug. Kissin then reviewed a series of investigative studies and concepts that supported his hypothesis:

Several groups of drugs (benzodiazepines, opioids, α₂ -agonists) that induce anesthesia by acting on specific receptors can have their anesthetic effects reversed by the administration of a specific receptor antagonist.
There is growing understanding that the molecular mechanisms of general anesthesia are more specific than was suggested by the previous unitary hypothesis of anesthesia.
The rank order of effects for two important goals of anesthesia (hypnotic effect and blockade of somatic motor response to noxious stimuli) can be different for different classes of anesthetics. Opioids induce blockade of the movement response to noxious stimulation before hypnosis occurs. For intravenous anesthetics, the opposite occurs.
When studies of anesthetic interactions are undertaken, the type of interaction (synergism, antagonism, summation) for one component of anesthesia may differ from that of another component.
Classic theories of anesthesia, based on the unitary nonspecific mechanisms of anesthetic action, suggest that one anesthetic may be freely replaceable by another and that the anesthetic effects of combinations of anesthetics should be additive. Many combinations of anesthetic drugs prove to be supra-additive for the hypnotic effects, a finding suggesting that the mechanisms of hypnotic action of different components of a combination are different.

If one understands general anesthesia as a spectrum of separate pharmacologic actions that vary according to the goals of anesthesia, certain conclusions can be made regarding the measurement of anesthetic potency and depth of anesthesia. Kissin stated that "Diversity of pharmacological actions that in combination provide anesthesia make[s] it almost impossible to determine the potency of different actions with one measure."^[14]