Inhalation Anesthesia

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Inhalation anesthesia had its beginnings almost two centuries ago. Many excellent papers and books highlight exciting accounts of the inhalational agents—including Dr. Crawford Long’s account of administering ether in Georgia.1 Another report is William T.G. Morton’s account of a young man who inhaled ether administered by Morton. The young man felt little or no pain during the removal of a mass on his neck. Surgeon John Collins Warren performed the surgery in front of an audience in Boston at Massachusetts General Hospital (MGH) on October 16, 1846. Modern anesthesia providers celebrate “Ether Day” annually on October 16. Table 20.1 provides an overview of the historical timeline of inhalational anesthetics.1

Table 20.1

History of the Introduction of the Inhalational Anesthetic Agents
Anesthetic Agent
(Generic Name; Trade Name)
Year Anesthetic Property Demonstrated or Introduced
Diethyl ether 1842
Nitrous oxide 1845
Chloroform 1847
Cyclopropane 1934
Fluroxene (Fluomar) 1951
Halothane (Fluothane) 1956
Methoxyflurane (Penthrane) 1960
Enflurane (Ethrane) 1973
Isoflurane (Forane) 1981
Desflurane (Suprane) 1993
Sevoflurane (Ultane) 1995

Modified from Elisha E, Heiner JS, Nagelhout JJ. Nurse Anesthesia. 7th ed. Philadelphia, PA: Elsevier; 2023.

Anesthesia providers appreciate that the inhalation anesthetic agents used in the early years of anesthesia had an extremely long induction time and emergence time. The long emergence phase did provide the patient with significant postoperative analgesia and sedation. Research on inhalational anesthetic agents has been positive and productive and has led to rapid-acting agents. Patients emerge from anesthesia in minutes instead of hours. As a result, patients can be discharged rapidly from perianesthesia care and, ultimately, the health care facility. It is essential to understand the physiologic and pharmacologic effects of anesthetic agents used both presently and in the past.

The inhalation anesthetic agents in use today have survived the many examinations of research. Clinically, modern inhalation agents add significant safety factors and improved outcomes for perianesthesia patients. Research continues in this area to find the inhalational agent that best represents all anesthesia facets, such as muscle relaxation, sedation, analgesia, and amnesia, with minimal effects on the body’s major organ systems.

The perianesthesia nurse should have a thorough understanding of the pharmacologic concepts of inhalation anesthesia to anticipate a patient’s reaction upon emergence from an inhalation anesthetic in the postanesthesia care unit (PACU). It is difficult to predict the exact nature of each patient’s emergence from inhalation anesthesia because of the complexity of these agents coupled with drug interactions and the various levels of physical health of the patient. An understanding of some general principles prepares the perianesthesia nurse for the most commonly expected outcomes.


Adjustable Pressure-Limiting (APL) Valve An outlet valve located in the breathing circuit used during manual or assisted ventilation for waste anesthesia gases and titration of positive pressure ventilation.

Amnesia A component of anesthesia in which the patient cannot recall the events during the inhalational anesthetic administration.

Analgesia A component of anesthesia in which the patient is unable to experience pain.

CO2Absorption Canisters These canisters are located in a circle system on an anesthesia machine that clears rebreathed gas containing carbon dioxide by passing it through a canister containing a chemical carbon dioxide absorbent.

Delirium A portion of a stage of anesthesia in which the patient has a transient disturbance during a loss of consciousness accompanied by a change in cognition with a fluctuating course.

Diffusion Hypoxia Sometimes referred to as the Fink phenomenon, the rapid exit of nitrous oxide and partial reduction of the percentage of oxygen that can be inhaled during the immediate (first 4–5 minutes) emergence phase of recovery from anesthesia. Supplemental oxygen and the use of the modified stir-up regime negate this effect of nitrous oxide on emergence.

Effective Dose (ED) The dose of a drug necessary to produce a specific effect in a certain percentage of patients. For example, the ED50 is when a drug produces a particular effect in 50% of patients.

Hypnosis A component of anesthesia in which the patient becomes unconscious.

Inhalation Anesthesia Anesthetic substances, in either volatile or gaseous form, are inhaled via an anesthesia machine.

Lacrimation Tears from the lacrimal glands on the medial side of the tissue surrounding the eyes.

Minimal Alveolar Concentration (MAC) A measure of the potency of inhalation anesthetic agents; occurs when the equilibrium end-tidal anesthetic concentrations, expressed as a fraction of 1 atm, prevent movement in response to a surgical skin incision in 50% of human subjects.

Muscle Relaxation A component of anesthesia in which the patient has reduced tension of the skeletal muscle.

Nociception The unconscious perception of a stimulus, for example, surgery, which is expressed through a response of the autonomous nervous system. Local anesthetics, opioids, and other agents such as ketamine are usually used to blunt nociception as a component during general anesthesia and surgery.

Scavenger System Used to reduce exposure to escaping gases from the anesthesia machine; a waste gas suction tube (scavenger) is connected to the APR valve and anesthesia ventilator relief valve, and the gases are then vented to the outside atmosphere via an operating room suction system.

Solubility Coefficient The ratio of the concentration of an anesthetic in blood or other tissue to that in a gas phase when the two are in equilibrium.

Sympatholysis Describes the component of anesthesia’s effect that blocks the patient from having an autonomic response to nociceptive (painful) stimuli.

Vaporizer A device on the anesthesia machine that converts liquid anesthetics into metered amounts of vapor added to the fresh gas mixture to produce a known concentration of the vaporized form of the inhalational anesthetic agent.

Basic concepts

Evolution of the Signs and Stages of Anesthesia

The observation of anesthesia by John Snow and Arthur Guedel influenced the early assessment of anesthesia effects. Both Snow and Guedel described the anesthesia effect assessment based on the autonomic sympathetic nervous system response and subsequent neurologic signs to evaluate the depth of anesthesia.2 The five components of anesthesia are hypnosis, analgesia, muscle relaxation, sympatholysis, and amnesia. In the past, when diethyl ether was the primary general anesthetic, assessment of anesthetic depth with the signs and stages of anesthesia was simple; monitor the patient by assessing the pupils, respiratory activity, muscle tone, and various reflexes. During World War I, Guedel more accurately defined and described the signs and stages of anesthesia.3 A graphic representation of these signs and stages is provided in Fig. 20.1.

Chart shows signs and reflex reactions of stages of anesthesia. The data are as follows: • Intercostal and diaphragm respiration is increased in stage 3 plane 1. Intercostal respiration is absent in plane 4. • Ocular movements are maximum in stage 2 and reduced to minimum in stage 3 plane 1, depicted as triangular shape. Stage 1 has voluntary control. • Pupils no pre-med: Pupil size is increased from stage 1 through stage 4. • Eye reflexes: Stage 2: lid tone, plane 2: corneal and pupillary light reflex. • Pharynx larynx reflexes: Stage 2: Swallow, retch, stage 3 plane 1: vomit, plane 2: glottis, plane 4; carinal. • Lacrimation: Stage 1: Normal, maximum in between plane 1 and plane 2. Reduced to minimum in plane 4. • Muscle tone: Stage 1: normal, stage 2: increased tense struggle. Tense struggle is decreased from stage 2 through plane 4. • Response incision: Maximum in plane 1. Very less in plane

Chart shows signs and reflex reactions of stages of anesthesia. The data are as follows: • Intercostal and diaphragm respiration is increased in stage 3 plane 1. Intercostal respiration is absent in plane 4. • Ocular movements are maximum in stage 2 and reduced to minimum in stage 3 plane 1, depicted as triangular shape. Stage 1 has voluntary control. • Pupils no pre-med: Pupil size is increased from stage 1 through stage 4. • Eye reflexes: Stage 2: lid tone, plane 2: corneal and pupillary light reflex. • Pharynx larynx reflexes: Stage 2: Swallow, retch, stage 3 plane 1: vomit, plane 2: glottis, plane 4; carinal. • Lacrimation: Stage 1: Normal, maximum in between plane 1 and plane 2. Reduced to minimum in plane 4. • Muscle tone: Stage 1: normal, stage 2: increased tense struggle. Tense struggle is decreased from stage 2 through plane 4. • Response incision: Maximum in plane 1. Very less in plane

Fig. 20.1 Signs and reflex reactions of stages of anesthesia. (Adapted from Gillespie NA. Signs of anesthesia. Anesth Analg. 1943;22:275.)

With the advent of modern anesthesia, which includes fluorinated inhalation anesthetic agents, muscle relaxants, and various pharmacologic adjuncts, the usual predictable signs and stages described by Guedel were abolished. Currently, in the PACU, many of these pharmacologic adjuncts affect prediction of the depth of anesthesia. The classic signs and stages provide some help in the assessment and care of the patient after surgery. Many times in modern anesthesia practice, these signs and stages provide a basic language for describing the level of anesthesia during and after surgery. Consequently, a brief description, including incorporating some of the pharmacology of modern anesthetics, is given.

Stage I begins with the initiation of anesthesia and ends with the loss of consciousness. It is commonly called the stage of analgesia. Stage 1 has been described as the lightest level of anesthesia and represents sensory and mental depression, and it is the level of anesthesia used with nitrous oxide. Patients can open their eyes on command, breathe normally, maintain protective reflexes, and tolerate mild painful stimuli.

Stage II starts with the loss of consciousness and ends with the onset of a regular breathing pattern and the disappearance of the lid reflex; this is also called the stage of delirium. This stage is characterized by excitement, but many untoward responses such as vomiting, laryngospasm, and even cardiac arrest can occur. With anesthetic agents that act much more rapidly than ether, this stage is passed rather quickly. Also, anesthesia induction is usually facilitated with short-acting sedative-hypnotic agents that expedite a short duration of stage II.

Stage III is the stage of surgical anesthesia. With ether anesthesia, this stage is defined as lasting from the onset of a regular breathing pattern to respiration cessation. At this stage of anesthesia, response to surgical incision is absent. The modern concept of MAC is predicated in part on the signs and stages of surgical anesthesia. MAC is exceeded by a factor of 1.3 in stage III because most patients do not respond to surgical incision at this anesthesia level. Patients who receive 1.3 MAC anesthesia3 have a depression in all nervous system function elements—sensory depression, loss of recall, reflex depression, and skeletal muscle relaxation. With modern anesthetics, increased MAC results in escalating respiratory, cardiovascular, and central nervous system (CNS) depression. The difficulty is that each of the newer agents affects the clinical signs, such as blood pressure, differently. Consequently, monitoring the level of anesthesia depends on the particular properties of each agent.

Most surgical procedures in which ether anesthesia was used were performed at anesthesia stage III, divided into four planes.4 Plane 1 occurs with elimination of the lid reflex and when respiration becomes regular. During this plane, the vomiting reflex disappears gradually. 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 when the eyeballs cease to move and become concentrically fixed to the beginning of decreased activity of the intercostal muscles or thoracic respiration. The reflex of laryngospasm disappears during this plane. Plane 3 occurs 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 the diaphragm’s unopposed action, displaces the lung’s hilum, and increases trachea traction.

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.

During early ether administration as the sole inhalation agent, these signs and stages occurred in reverse order on emergence from the anesthetic. No single 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 anesthesia’s depth for the more modern inhalation anesthetics include changes in breathing pattern, eye movement, lacrimation, and muscle tone. Because ventilation is under autonomic control, it is the most sensitive indicator of the depth of anesthesia. A patient who uses diaphragmatic ventilation without their intercostal muscles in the PACU should be considered still in a state of 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. More profound 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, light anesthesia is present if a patient received one of those drugs and has eye tearing. As the depth of anesthesia increases, 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 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 muscle tone criterion. Finally, because anesthesia depth determinants have such a high degree of variability, all possible assessment tools should be incorporated into the patient’s care in the PACU. The bottom line is the constant vigilance of the patient’s physiologic parameters during the emergence of 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. The pharmacokinetic process 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 the 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 anesthesia’s depth. For classification, the more potent the anesthetic, the lower the agent’s partial pressure needed to produce a certain depth of anesthesia.

Movement of Inhalation Anesthetic From Anesthesia Machine to Alveoli

An anesthesia machine’s delivery system affects the depth of anesthesia and the speed of induction and emergence. In practice, the higher the inhaled concentration, the more rapid the induction of anesthesia. The inhaled partial pressure (PI) concentrates on the inhalation anesthetic delivered from the anesthesia machine. The effect of the PI on the rate of increase in the PA is called the concentration effect. The PA’s determinants are the inspired partial pressure of the inhalation anesthetic, the anesthesia machine’s delivery system’s characteristics, and the patient’s alveolar ventilation. Several factors can reduce the rate of uptake of an anesthetic agent administered via inhalation. For example, the diffusion of the anesthetic agent into the rubber tubing of the anesthesia machine, the small losses of the anesthetic agent from the body via diffusion across the skin and mucous membranes, and, to a lesser extent, the metabolism of the agents by the body can reduce the uptake of anesthetic agents.

Alveolar ventilation plays the primary role in the delivery of the anesthetic gas. It is determined in large part by the minute ventilation (V¯Esi1_e). If the V¯Esi1_e is high, the anesthetic concentration increases quickly in the alveoli, as does the arterial blood concentration. This concept is vital to understand because the reverse also is true. In the emergence phase of anesthesia, a good V¯Esi1_e is essential to ensure the anesthetic agent’s elimination.

Movement of Inhalation Anesthetic From Alveoli to Arterial Blood

The inhalation anesthetic agent’s movement from the alveoli to the arterial blood depends on the cardiac output and blood-gas partition coefficient. The rate at which the blood and tissues take up the anesthetic is governed in part by the agent’s solubility in blood. The blood-gas partition coefficient or the Oswald solubility coefficient describes this relationship. It is defined as the ratio of the concentration of an anesthetic in the blood to that in a gas phase when the two are in equilibrium (Table 20.2). This concept is difficult to understand because the more soluble the anesthetic agent is, the slower the agent is producing anesthesia. The blood serves as a reservoir, and a large volume of the agent must be introduced to attain equilibrium between the partial pressure in the blood and the partial pressure in the lungs.

Table 20.2

Properties of Inhalant Anesthetic Agents
Partition Coefficient
Alveolar Agent Blood-Gas Oil-Gas Blood-Brain Minimal Alveolar Concentration (MAC)
(As a % in 1 Atmosphere)
Isoflurane (Forane) 1.4–1.46 98 1.6 1.15–1.2
Desflurane (Suprane) 0.45 19 1.3 6
Sevoflurane (Ultane) 0.65 47 1.7 1.85–2.0
Nitrous oxide 0.46 1.4 1.1 104.0

Adapted from Pardo M, Miller RD. Basics of Anesthesia. 7th ed. Elsevier; 2018; Hemmings HC, Egan TD. Pharmacology and Physiology for Anesthesia: Foundations and Clinical Application. 2nd ed. Elsevier; 2019.

The blood conveys the anesthetic agent to the tissues. Consequently, normal cardiac output is needed to facilitate the inhalation anesthetic movement through the tissues to the brain. The partial pressure increases most rapidly in the tissues with the highest rates of blood flow. Of interest is the significant variation in blood perfusion of specific tissues in the body. The body tissue compartments can be divided into the following major groups:

  •  The vessel-rich group, which consists of the heart, brain, kidneys, hepatoportal system, and endocrine glands
  •  The intermediate group of perfused tissues, which consists of muscle and skin
  •  The fat group, which includes marrow and adipose tissue
  •  The vessel-poor group, which has the lowest circulation per unit volume and comprises tendons, ligaments, connective tissue, teeth, bone, and other avascular tissue

The vessel-rich group of tissues receives 75% of the cardiac output; thus, the brain becomes saturated rapidly with an anesthetic agent administered via inhalation. On termination of the anesthetic, the reverse occurs, and the agent is rapidly removed from the brain.

The tissue tensions of the inhaled anesthetic increase and approach the arterial blood tension and ultimately the PA. One of the tissue groups that affects both the induction and the emergence from anesthesia is the fat group. The oil-gas partition coefficient best exemplifies the process involved with anesthesia agents’ affinity to adipose tissue and ultimately the emergence from anesthesia. The oil-gas partition coefficient is defined as the ratio of the anesthetic agent’s concentration in oil (adipose tissue) to that in a gaseous phase when the two are in equilibrium (see Table 20.2). The oil-gas partition coefficients seem to parallel anesthetic requirements. It is possible to calculate the MAC by knowing the oil-gas partition coefficient. With a constant of 150, the calculated MAC for an anesthetic with an oil-gas partition coefficient of 100 is 1.5%.

Because some anesthetic agents are highly fat-soluble, they tend to be readily absorbed by the adipose tissue. This characteristic affects the uptake of the anesthetic agent, but of more importance is the prolonged recovery phase that usually ensues with a high oil-gas partition coefficient, such as in the case of halothane. Because adipose tissue is poorly perfused by blood, the adipose tissue releases the agent slowly to the blood at the anesthesia’s termination. Redistribution occurs as the vessel-rich lungs eliminate the agents, and some distribute to the brain. The recovery period becomes significantly extended when the anesthetic agent’s administration time is prolonged to allow for the adipose tissue’s complete saturation.

Halothane (Fluothane) was the classic inhalation anesthetic from the 1960s to the 1990s. The inclusion of halothane in the discussion is helpful because all the inhalation anesthetic agents currently have almost the same partition coefficients. Halothane has an oil-gas partition coefficient approximately twice that of isoflurane, desflurane, or sevoflurane; therefore, with halothane as the marker, the newer inhalation agents are twice as fast during induction and emergence as before. All three of the current inhalational anesthetics are used in various settings, and all possess a blood-gas partition coefficient of less than 1 (see Table 20.2).

Movement of Inhalation Anesthetic From Arterial Blood to the Brain

The transfer of the inhalation anesthetic from the arterial blood to the brain depends on the agent’s blood-brain partition coefficient and cerebral blood flow. The blood-brain partition coefficient for most of the inhalation anesthetics is between 1.3 and 2 (see Table 20.2). The concentration gradient during induction of anesthesia is as follows:



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May 20, 2023 | Posted by in NURSING | Comments Off on Inhalation Anesthesia

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