Most surgical procedures in which ether anesthesia was used were performed at this stage of anesthesia, which is divided into four planes.⁴ Plane 1 is entered when the lid reflex is abolished and respiration becomes regular. During this plane, the vomiting reflex is gradually abolished. The nurse working in the PACU must know that swallowing, retching, and vomiting reflexes tend to disappear in that order during induction and reappear in the same order during emergence from anesthesia.

Plane 2 lasts from the time the eyeballs cease to move and become concentrically fixed to the beginning of a decrease of activity of the intercostal muscles, or thoracic respiration. The reflex of laryngospasm disappears during this plane. Plane 3 is entered when intercostal activity begins to decrease. Complete intercostal paralysis occurs in lower plane 3, and respiration is produced solely by the diaphragm. Plane 4 lasts from the time of paralysis of the intercostal muscles to the cessation of spontaneous respiration.

Tracheal tug often appears in association with deep anesthesia and intercostal paralysis. This effect represents an unopposed action of the diaphragm, which displaces the hilum of the lung and thereby increases traction on the trachea.

Stage IV lasts from the time of cessation of respiration to failure of the circulatory system. This level of anesthesia is called the stage of overdose.

When ether was used as the sole inhalation agent, these signs and stages were seen in reverse order on emergence from the anesthetic. No one clinical sign can be considered a reliable indicator of anesthetic depth by itself. All clinical signs must be viewed in the context of the patient’s status along with the particular characteristics of the individual anesthetic agent used.

Some of the more reliable indicators of depth of anesthesia for the more modern inhalation anesthetics include changes in breathing pattern, eye movement, lacrimation, and muscle tone. Because the ventilation is under autonomic control, it is the most sensitive indicator of depth of anesthesia. In the PACU, a patient who uses diaphragmatic ventilation without the intercostal muscles should be considered to be in surgical anesthesia. As the ventilatory pattern returns to a more normal rate, rhythm, and pattern, the patient can be considered to be in light anesthesia and about to have total emergence. Eye movement as opposed to pupillary size is a good indicator of anesthetic depth. Light anesthesia is present with eye movement. Deeper anesthesia is present when the eyes are close together in a cross-eyed position. Lacrimation does not occur during surgical anesthesia when a patient receives desflurane (Suprane), isoflurane (Forane), or sevoflurane (Ultane). Conversely, if a patient received one of those drugs and has tearing, light anesthesia can be considered to be present. As the depth of anesthesia is increased, the amount of muscle tone decreases. Therefore, if a patient in the PACU lacks muscle tone, especially in the jaw and abdomen, the patient should be considered to be in a surgical depth of anesthesia. With the assessment of the degree of muscle tone, the perianesthesia nurse must critically assess the degree of reversal of skeletal muscle relaxants (see Chapter 23) before determining the depth of anesthesia with the criterion of muscle tone. Finally, because the determinants of anesthesia depth have such a high degree of variability, all possible assessment tools should be incorporated into the care of the patient in the PACU. The bottom line is constant vigilance of the patient’s physiologic parameters during emergence from anesthesia and the institution of appropriate nursing interventions based on an ongoing assessment.

Pharmacokinetics of inhalation anesthetics

The pharmacokinetics of inhalation anesthetics involve uptake, distribution, metabolism, and elimination. Basically, this involves a series of partial pressure gradients starting in the anesthesia machine to the patient’s brain for induction, and vice versa for emergence. The object of anesthesia is a constant and optimal partial pressure in the brain. The key to attainment of anesthesia is the alveolar partial pressure (PA) in equilibrium with the arterial partial pressure (Pa) and brain partial pressure (Pbr) of the inhaled anesthetic.⁴ The partial pressure of an inhalation anesthetic in the brain is used to determine the depth of anesthesia. The more potent the anesthetic, the lower the partial pressure of the agent needed to produce a certain depth of anesthesia.

Emergence of inhalation anesthesia

When the administration of the anesthetic is terminated, a reverse gradient takes place. In this instance, the PA is almost zero because only oxygen is administered during the emergence phase. The gradient that develops is as follows:

This gradient favors the removal of the anesthetic agent from the brain tissue. The partial pressure in the tissues declines first and is followed by that in the arterial blood. The agent returns to the lungs and is then eliminated into the atmosphere. The factors that affect the rate of elimination of the agent are the same ones that determine how rapidly an anesthetic agent takes a patient to surgical anesthesia. If a short procedure is performed (less than 1 hour), complete equilibrium among PA, Pa, and Pbr might not have occurred, and the recovery from anesthesia is more rapid. The reverse is true; during long procedures in which equilibrium occurs, a prolonged emergence may be anticipated.

Potency of inhalation anesthetic agents

Potency is determined by factors such as absorption, distribution, metabolism, excretion, and affinity for a receptor. The potency of the anesthetic agent refers to its ability to take the patient through all the stages of anesthesia to respiratory and circulatory arrest without the occurrence of hypoxia or the use of preanesthetic medication. Certainly, circulatory and respiratory arrests are not desired outcomes of the use of anesthetic agents; these features are used merely to describe the potency of anesthetic agents that are used clinically. For example, isoflurane is 100% potent compared with nitrous oxide, which is 15% potent. Isoflurane, when administered with oxygen to meet the patient’s metabolic needs and when given without premedication, takes the patient to circulatory and respiratory arrest, whereas nitrous oxide administered with oxygen takes the patient only to the first portion of surgical anesthesia and no further. Therefore, clinically speaking, potency of a drug makes little difference as long as the drug that is to be administered has an effective dose for a particular patient, which is why the concept of ED was developed. The ED is the dose of a drug necessary to produce certain effects in a certain percentage of patients. For example, an ED₅₀ means that a drug produces a particular effect in 50% of the patients.⁴

Another method of determination of potency is with the use of the MAC. The MAC is found with determining the alveolar concentration (at 1 atm) needed for prevention of gross muscular movement in response to painful stimuli in 50% of anesthetized patients. The lower the MAC value, the more anesthetic potency of the inhalation anesthetic. Consequently, the MAC defines the therapeutic effect of inhalational anesthetics as the prevention of movement in response to surgical stimulation.⁴

The potency of an inhalation anesthetic agent with the MAC as the tool of assessment varies with the patient’s age, state of health, clinical conditions, and concurrent use of other drugs (with depressant effects). The factors that modify the MAC are presented in Box 20-1. MAC awake is the anesthetic dose at which a patient responds to commands; it is also the dose of anesthetic at which most patients lose consciousness and recall. MAC awake usually corresponds with stage I of anesthesia. Another term used with MAC is MAC-Block Adrenergic Response, which is the MAC needed to block the adrenergic and cardiovascular responses to incision; it corresponds to stage III, plane III anesthesia.

BOX 20-1 Factors That Modify Minimum Alveolar Concentration

Factors that increase MAC

Factors that decrease MAC

MAC, Minimum alveolar concentration; CNS, central nervous system.

Modified from Longnecker D, et al: Anesthesiology, New York, 2007, McGraw Hill Medical.

Techniques of administration

The inhalation anesthetics are usually administered by means of an anesthesia machine (Fig. 20-2). The anesthesia machine is essentially a breathing circuit that conveys the agent and oxygen to the patient. It consists of a mask, corrugated tubing, an absorber for removal of expired carbon dioxide, a reservoir bag, unidirectional valves, adjustable positive-pressure relief (APR) valve, and vaporizers (Fig. 20-3).⁵

FIG. 20-2 Anesthesia machine apparatus.

(Used with permission from Datex-Ohmeda, Madison, Wis.)

FIG. 20-3 Anesthesia machine circuit. Oxygen and nitrous oxide enter the machine from cylinders or from hospital service supply. Pressure regulators reduce cylinder pressure to approximately 3 kg/cm². Check valves to prevent transfilling of cylinders or gas flow from cylinders to service line. Fail-safe valve prevents flow of nitrous oxide if oxygen supply fails. Needle valves in flowmeters control flows to rotameters. Calibrated vaporizers provide preselected concentration of volatile anesthetics. Gases are delivered to the circle absorber, where unidirectional valves ensure flow from patient through the carbon dioxide absorber. Excess gas is vented through exhaust valve into waste gas scavenger system. Reservoir bag compensates for variations in respiratory demand.

(Adapted from Dripps RD, et al: Introduction to anesthesia: the principles of safe practice, ed 7, Philadelphia, 1988, Saunders.)

Circle systems

A variety of techniques can be used to deliver gaseous agents with the anesthesia machine by adding or removing certain features. The most common technique used is the semiclosed circle method, in which some rebreathing of expired gases occurs by opening the APR valve to vent some of the gas to the atmosphere. The closed circle method is used when low gas flows are desired. In this technique, the APR valve is completely closed and complete rebreathing of expired gases occurs. A carbon dioxide absorber is used in both the semiclosed and the closed techniques.

Inhalation agents

Inhalation anesthetic substances can be divided into the following two groups: volatile and gaseous. Volatile anesthetic agents are chemicals in the liquid state at room temperature that have a boiling point above 20° C. Ethyl chloride, which has a boiling point of 12° C, is also included in this class of anesthetic agents. The volatile inhalation anesthetic agents are divided into two major categories: the halogenated hydrocarbons and the ethers. Examples of the halogenated hydrocarbons are isoflurane, desflurane, and sevoflurane; diethyl ether is an example of the ethers. The gaseous anesthetic agents, such as nitrous oxide, are in the gaseous state at room temperature. The anesthetic agents currently in use have evolved from the traditional inhalation anesthetics that are not in use today: cyclopropane, chloroform, and diethyl ether.

Modern inhalation anesthetics

Isoflurane (forane)

Isoflurane, an analogue of enflurane, is also a halogenated methyl ethyl ether; it produces a dose-related depression of the CNS.⁶ In contrast with enflurane, this anesthetic agent does not produce convulsive electroencephalographic abnormalities. Isoflurane reduces the systemic arterial blood pressure and total peripheral resistance; however, during isoflurane anesthesia, the heart rate is usually increased and the cardiac output usually remains within normal limits. This agent produces respiratory depression and skeletal muscular relaxation in a dose-related fashion, because isoflurane markedly potentiates the actions of the nondepolarizing muscle relaxants. Of interest to the perianesthesia nurse is the fact that isoflurane does not sensitize the myocardium to catecholamines to the same extent as halothane does. Thus, the chance of dysrhythmias is reduced when the patient has received isoflurane anesthesia.

The recovery phase is rapid because of isoflurane’s low blood-gas partition coefficient of 0.97.³^,⁶ The patient awakens promptly and is lucid within 15 to 30 minutes after termination of the anesthetic. However, clinical observation indicates that if the anesthesia time with isoflurane is longer than 45 to 60 minutes, the patient will probably have a slower emergence phase than expected, given that the drug has such a low blood-gas partition coefficient.

The lung volumes and capacities, as measured with the Wright respirometer, return to normal in less than 30 minutes along with the ability to raise the head, protrude the tongue, cough on command, and converse clearly. The blood pressure and pulse remain stable. Shivering is seen in 2% of patients, and nausea and vomiting occur only occasionally.

Isoflurane possesses some excellent qualities: a lack of sensitization of the heart to catecholamines, cardiovascular stability, limited biodegradation, good neuromuscular relaxation, and no CNS excitatory effects. Isoflurane isa major component in the practice of most anesthesia practitioners.

Sevoflurane (ultane)

Sevoflurane is a 100% potent inhalation anesthetic agent that has a blood-gas solubility coefficient of 0.69,⁶ which is near nitrous oxide and thus makes it an extremely rapid-acting agent. Consequently, patients emerge from sevoflurane anesthesia in a matter of minutes when they have received this drug as the sole agent. One must remember that a rapid recovery from an inhalation anesthetic usually mandates the need for analgesic drugs in the immediate postoperative period.⁷

The drug is not irritating to the respiratory tract, and the degree of patient acceptance is high. Sevoflurane can be used in place of halothane for the induction of anesthesia in children ⁸; it tends to decrease the blood pressure by decreasing the systemic vascular resistance. Like all other inhalation agents, this drug is a respiratory depressant and blunts the ventilatory response to an increased PaCO₂. This drug undergoes some metabolism at approximately the same degree as does enflurane. The metabolites of sevoflurane include fluoride and hexafluoroisopropanol. On the basis of a number of studies, no evidence of toxicity has been shown in regard to the biodegradation of this agent, probably because of sevoflurane’s rapid ventilatory excretion, in which the metabolic byproducts do not seem to be significantly detrimental to the patient.

Like the other ethers, sevoflurane does not sensitize the heart to catecholamines and hence does not predispose to arrhythmias. This inhalation agent reduces cerebrovascular resistance and can increase intracranial pressure in a dose-related manner. In regard to its effect on skeletal muscle function, it enhances the action of the skeletal muscle relaxants. However, because of the drug’s rapid elimination, this characteristic does not have a significant effect on the care of a patient in the PACU who has received sevoflurane during surgery.

Sevoflurane possesses many outstanding qualities. It has great precision and control over anesthetic depth, it does not depress kidney or liver function, it has little effect on heart rate, and, most of all, it is extremely rapid, which speeds up the emergence of the patient in the PACU.

Desflurane (suprane)

Desflurane is a fluorinated ether that is similar to isoflurane. This drug has a blood-gas partition coefficient that is the same as cyclopropane (0.42) and even less than nitrous oxide, which makes it extremely rapid acting.⁶ As with sevoflurane, patient emergence is extremely rapid and analgesia is needed in the immediate postoperative period. This drug produces a dose-related decrease in blood pressure and cardiac output that is slightly greater than the depression seen with equivalent doses of isoflurane. Because this drug is an ether-type inhalation agent, the incidence rate of cardiac dysrhythmias when epinephrine is administered is extremely low.

The pungency of desflurane irritates the respiratory tract and causes coughing, breathholding, and laryngospasm. Consequently, the drug is not recommended as an inhalation induction agent, especially in the pediatric age group. This drug depresses respiration in the same fashion as does sevoflurane and thus blunts the response to an increased PaCO₂. Desflurane produces a dose-related reduction in cerebrovascular resistance. Desflurane also enhances the neuromuscular blockade produced by skeletal muscle relaxants. However, like sevoflurane, this action is not of consequence for the patient in the PACU because of its extremely rapid ventilatory excretion during emergence.⁸ Finally, as opposed to sevoflurane, this drug resists biodegradation and is almost totally eliminated by the respiratory system and therefore does not have a negative effect on the kidney or liver.

Desflurane represents a new era in inhalation anesthesia in regard to its effects on the care of the patient in the PACU. More specifically, because of the low solubility of desflurane, rapid emergence will become common, and a more rapid release from the PACU and a shorter length of stay in the hospital may be possible.

Nitrous oxide

Nitrous oxide is the only inorganic gas used as an anesthetic agent. It is marketed in blue steel cylinders as a colorless liquid at a pressure of 30 atm. As the pressure is released, nitrous oxide returns to the gaseous state. It is readily soluble in water and heavier than air. Nitrous oxide was probably the first anesthetic agent to be used extensively. The fact that it is still used indicates that, when used properly, it is a valuable and safe anesthetic agent.

Nitrous oxide supports combustion—that is, if a burning match is put into a jar that contains nitrous oxide, it will continue to burn. However, this agent is not explosive. Although the nitrous oxide molecule contains oxygen, that oxygen is unavailable for respiration because nitrous oxide does not decompose in the body.

Nitrous oxide is a 15% potent agent; therefore the maximum depth of anesthesia that can be produced while the patient’s metabolic need for oxygen is supplied is the middle of plane 1 of stage III anesthesia. This agent has no side effects unless hypoxia is present. It is nontoxic and nonirritating; however, nitrous oxide can cause postoperative nausea and vomiting, particularly in the ambulatory surgical setting when the procedure lasts for 1 hour, and probably for 2 hours or more.⁹ Nitrous oxide is a rapid-acting agent in part because of its blood-gas partition coefficient of 0.47.⁶ This agent does not combine with hemoglobin but is carried in physical solution in the blood. It is excreted mostly unchanged by the lungs, although a small fraction is excreted through the skin. It does not sensitize the heart to epinephrine, and it provides a fair amount of analgesia. Even in subanesthetic concentrations, nitrous oxide has an analgesic effect in humans, and 20% concentrations of the gas have been claimed to be as effective as 15 mg of morphine sulfate. If this agent were more potent, it would probably be considered an almost perfect anesthetic.

In current anesthesia practice, nitrous oxide serves an important role because it is administered alone and in combination with various agents. Recently, the balanced technique of anesthesia has been favored because of the number of negative factors associated with some of the more potent volatile inhalation anesthetics. The balanced technique consists of the administration of opioids that may or may not be in combination with a tranquilizer, a muscle relaxant, nitrous oxide, oxygen, and barbiturates.³ All the elements of anesthesia or nervous system depression are met: sensory block (analgesia), motor block (muscle relaxation), reflex block, and mental block (narcosis). When nitrous oxide is administered with a potent volatile inhalation anesthetic such as desflurane, it acts as a carrier and provides an additional analgesic effect. The second gas effect occurs because of nitrous oxide’s rapid uptake, after which the potent volatile agent takes the patient to the desired surgical plane. The reverse takes place at termination of the anesthetic.

The solubilities of nitrogen and nitrous oxide differ greatly. Nitrous oxide is 30-fold more soluble than nitrogen. An enclosed gas-filled space in the body expands if gas within it is more soluble than the gas respired. For this reason, any enclosed gas-filled cavity in the body expands because of the slow exchange of nitrogen from the cavity for the rapid exchange of large volumes of nitrous oxide from the blood, which is why the use of nitrous oxide is not recommended in surgical procedures for intestinal obstruction or pneumothorax. Nitrous oxide has been shown to dislodge a tympanoplasty graft because of the expansion of the air pocket in the middle ear. Consequently, in surgical procedures that involve the middle ear, the administration of nitrous oxide is usually avoided. Of interest to the perianesthesia nurse is the possible role of nitrous oxide in altering the pressures in the middle ear; nitrous oxide has been suggested to cause nausea and vomiting from the resulting increased pressure in that area.

Diffusion hypoxia after nitrous oxide anesthesia is another area of concern for the perianesthesia nurse. This effect is sometimes called the Fink phenomenon. It occurs when not enough nitrous oxide is removed from the lungs at the end of the surgical procedure. Normally, 100% oxygen is administered at the end of the procedure for removal of the nitrous oxide, which is called nitrous oxide washout. Diffusion hypoxia is directly related to the dilution of alveolar gas by the rapid diffusion of the nitrous oxide out of the blood. This outpouring of nitrous oxide into the alveoli occurs during the first 1 to 5 minutes after the nitrous oxide has been discontinued. In addition, the rapid movement into the alveoli can cause a dilutional effect of the PACO₂ and ultimately a reduction in the stimulus to breathe. Therefore administration of oxygen via mask to all patients who are admitted to the PACU is highly advisable. This maneuver forestalls the development of severe hypoxia if some unpredicted airway problem occurs. Another measure for avoiding this complication is the provision of adequate verbal and physical stimulation to the patient to promote good ventilatory effort. This approach should include encouraging the patient to sigh every 5 minutes to ensure adequate removal of the anesthetic gases.

Assessment of the effects of inhalation agents in the perianesthesia care unit

In assessment of the patient’s degree of emergence from inhalation anesthesia, the nurse must understand the pharmacologic effects of each anesthetic agent and of the preoperative medications used. In addition, the rate of recovery from inhalation anesthesia is predictable based on the solubility of the anesthetic agent, alveolar ventilation, and duration of the anesthetic. Each anesthetic agent is essentially a depressant drug. Certain volatile agents, such as sevoflurane, desflurane, and isoflurane, possess a high degree of myocardial and respiratory depressant properties. One parameter for monitoring of the emergence phase with administration of these agents is the vital signs. Preanesthetic baseline vital sign readings are reliable postoperative indicators of the patient’s cardiorespiratory status and can be used in the assessment of the patient’s stage of recovery. When this assessment is made, however, all other factors of the patient’s condition must also be considered.¹⁰ Total assessment of the patient recovering from anesthesia is discussed in Chapter 27. Most inhalation anesthetics cause some degree of depression of the respiratory system. Consequently, the PaCO₂ increases in a dose-related manner, frequency increases, and tidal volume is reduced. Because of the respiratory depression that all patients have after anesthesia and surgery, the perianesthesia nurse must use the stir-up regimen that encourages the patient to perform the sustained maximal inspiration maneuver (see Chapter 27).

To understand the emergence phase of inhalation anesthesia, the nurse also needs a basic understanding of blood-gas and oil-gas partition coefficients. Anesthetic agents are usually administered in combinations, often with nitrous oxide as the carrier gas. The combination of agents usually consists of a 100% potent agent, a carrier agent, and oxygen to meet the metabolic needs of the patient. The agent with the highest blood-gas partition coefficient takes the longest time to be removed from the body. Therefore, if a isoflurane–nitrous oxide–oxygen combination is administered to a patient, the isoflurane, which has the highest blood-gas partition coefficient, is eliminated the most slowly.

Along with the factors attributed to the blood-gas partition coefficient, those attributed to the oil-gas partition coefficient should be considered in an evaluation of length of time of emergence from the anesthetic. When the intraoperative phase is of long duration, an agent with a high oil-gas partition coefficient redistributes into the adipose tissue. As mentioned previously, because the vascular supply to adipose tissue is sparse, the release of the agent to the blood is slow and the emergence is prolonged. Both coefficients must be kept in mind in prediction of the length of the emergence phase from an inhalation anesthetic agent. Isoflurane, for example, has the low blood-gas partition coefficient of 0.97, and a rapid recovery from its administration would be expected. However, isoflurane has a high oil-gas partition coefficient of 93.7; therefore, when it is administered for longer than 2 hours, the adipose tissue is saturated and emergence from the anesthetic agent is prolonged. Nitrous oxide, desflurane, and isoflurane have low blood-gas and oil-gas partition coefficients.⁷

Inhalation agents, because of their depressant effect on the hypothalamus, disrupt the regulation of body temperature that may be manifested by either a reduction or an elevation, depending on the environmental temperature.¹⁰ In the recovery phase, the emerging patient should be monitored for hypothermia or hyperthermia. Serious heat loss can occur in newborns and create difficulties in the reestablishment of adequate ventilatory effort after surgery. Body temperature should be monitored in patients who were febrile before surgery and who received atropine before or during the operative procedure. Agents such as isoflurane that have a direct vasodilatory effect on vascular smooth muscle can cause a temperature drop of 1° C in esophageal temperature. Shivering and tremors have been reported during the postoperative period after isoflurane anesthesia, although these phenomena have mostly been associated with a generalized loss of muscle tone during surgery and anesthesia.

Water and electrolyte balance is affected by inhalation anesthesia.¹ Pituitary and adrenocortical systems appear to be affected in such a way that water and sodium retention and potassium loss occur after anesthesia. This balance is also affected in part by the stress of surgical trauma. Decreased glomerular filtration, increased tubular reabsorption, and varying degrees of oliguria exist in the recovery phase because of renal vasoconstriction. If renal blood flow is not impaired, glomerular function quickly returns to normal after the operation. The increased tubular reabsorption of water usually persists for 36 to 48 hours, but may continue for several days in elderly patients.