20 Inhalation anesthesia
CO2 Absorption Canisters: Located in a circle system on an anesthesia machine that clears rebreathed gas that contains carbon dioxide by passing through a canister containing a chemical carbon dioxide absorbent.
Diffusion Hypoxia: Sometimes referred to as the Fink phenomenon; refers to the rapid exit of nitrous oxide and thus partial reduction of the percentage of oxygen that can be inhaled during the immediate (first 4 to 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 certain effect in a certain percentage of patients. For example, the ED50 is the term for when a drug produces a particular effect in 50% of patients.
Minimal Alveolar Concentration (MAC): A measure of 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 surgical skin incision in 50% of human subjects.
Scavenger System: Used to reduce exposure to escaping gases from the anesthesia machine; a waste gas suction tube (scavenger) is connected to the adjustable positive-pressure relief valve and anesthesia ventilator relief valve, and the gases are then vented to the outside atmosphere via an operating room suction system.
Vaporizer: A device on the anesthesia machine that converts liquid anesthetics into metered amounts of vapor that are added to the fresh gas mixture to produce a known concentration of the vaporized form of the inhalational anesthetic agent.
The inhalation anesthetic agents have undergone a significant transition over the last three decades. Inhalation agents used in the past possessed many positive attributes to include postoperative analgesia and sedation. The emergence from the inhalation anesthetic was slow and not without its difficulties. Research on the inhalational anesthetic agents has beenpositive and productive, leading to the use of 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 important to understand the many physiologic and pharmacologic effects of all the anesthetic agents, both used presently and in the past.
The inhalation anesthetic agents in use today have survived the many examinations of research, and clinically they have been shown to add significant safety factors and improved outcomes for perianesthesia patients. Research continues in this area; for example, xenon is under evaluation as an inhalation anesthetic agent.1 Other volatile agents are undergoing evaluation, all in an effort to find the inhalational agent that best represents all the facets of anesthesia, such as muscle relaxation, sedation, analgesia, amnesia, with minimal effects on the major organ systems of the body.
To anticipate a patient’s reaction on emergence from an inhalation anesthetic in the postanesthesia care unit (PACU), the perianesthesia nurse should have a thorough understanding of the pharmacologic concepts of inhalation anesthesia. 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. An understanding of some general principles prepares the perianesthesia nurse for the most commonly expected outcomes.
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; the patient could be monitored by assessing the pupils, respiratory activity, muscle tone, and various reflexes. The ether signs and stages were devised to provide a means of assessing the depth of anesthesia. The first three stages were described by Plomley in 1847; 1 year later, John Snow added a fourth stage: overdose.2 During World War I, Guedel more accurately defined and described the signs and stages of anesthesia. A graphic representation of these signs and stages is provided in Fig. 20-1.
(Adapted from Gillespie NA: Signs of anesthesia, Anesth Analg 22:275, 1943.)
With the advent of modern anesthesia, which includes the addition of fluorinated inhalation anesthetic agents, muscle relaxants, and various pharmacologic adjuncts, the usual predictable signs and stages as described by Guedel were abolished. Currently in the PACU, many of these pharmacologic adjuncts have an affect on predicting 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 the incorporation of some of the pharmacology of the 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. This stage has been described as the lightest level of anesthesia and represents sensory and mental depression. Stage I is the level of anesthesia used with nitrous oxide. Patients are able to 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 pattern of breathing and the disappearance of the lid reflex; this is also called the stage of delirium. This stage is characterized by excitement, and so many untoward responses such as vomiting, laryngospasm, and even cardiac arrest can take place during this stage. With the use of anesthetic agents that act much more rapidly than ether, this stage is passed rather quickly. In addition, the induction of anesthesia is usually facilitated with short-acting barbiturates 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 pattern of breathing to the cessation of respiration. At this stage of anesthesia, response to surgical incision is absent. The modern concept of minimal alveolar concentration (MAC) is predicated in part with 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 level of anesthesia. Patients who receive 1.3 MAC anesthesia3 have a depression in all elements of nervous system function—that is, sensory depression, loss of recall, reflex depression, and some skeletal muscle relaxation. From this point, with the modern anesthetics, increased MAC results in further 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 of the level of anesthesia depends on the particular properties of each agent.
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.
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.
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.
The determinants of the PA are the inspired partial pressure of the inhalation anesthetic, the characteristics of the anesthesia machine’s delivery system, and the patient’s alveolar ventilation. The inhaled partial pressure (PI) is the concentration of the inhalation anesthetic that is delivered from the anesthesia machine. The effect of the PI on the rate of increase in the PA is called the concentration effect. The higher the inhaled concentration, the more rapid the induction of anesthesia. The anesthesia machine’s delivery system has an effect on the depth of anesthesia and the speed of induction and emergence. For example, the rate of uptake of an anesthetic agent administered via inhalation can be reduced with the diffusion of the anesthetic agent into the rubber tubing of the anesthesia machine, the small losses of anesthetic agent from the body via diffusion across skin and mucous membranes, and, to a lesser extent, the metabolism of the agents by the body.
Alveolar ventilation plays the primary role in delivery of the anesthetic gas. It is determined in large part by the minute ventilation (V.E). If the V.E is high, the anesthetic concentration increases quickly in the alveoli, as does the concentration in the arterial blood. This concept is important to understand because the reverse also is true. In the emergence phase of anesthesia, a good V.E is important to ensure elimination of the anesthetic agent.
The movement of the inhalation anesthetic agent from the alveoli to the arterial blood depends on the blood-gas partition coefficient and the cardiac output. The rate at which the anesthetic is taken up by the blood and tissues is governed in part by the solubility of the agent in blood. This is expressed as the blood-gas partition coefficient, or the Oswald solubility coefficient, and is defined as the ratio of the concentration of an anesthetic in blood to that in a gas phase when the two are in equilibrium (Table 20-1). This concept is difficult to understand because the more soluble the anesthetic agent is, the slower the agent is in producing anesthesia. This effect is because the blood serves as a reservoir and a large volume of the agent must be introduced to attain an equilibrium between the blood partial pressure and the partial pressure in the lungs.
The blood conveys the anesthetic agent to the tissues. Consequently, a normal cardiac output is needed for facilitation of the movement of the inhalation anesthetic 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 great variation in blood perfusion of certain tissues in the body. The body tissue compartments can be divided into the following major groups:
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 takes place, 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 the affinity of anesthesia agents to adipose tissue and ultimately the emergence from anesthesia. The oil-gas partition coefficient is defined as the ratio of the concentration of the anesthetic agent in oil (adipose tissue) to that in a gaseous phase when the two are in equilibrium (see Table 20-1). The oil-gas partition coefficients seem to parallel anesthetic requirements. In fact, it is possible to calculate the MAC by knowing the oil-gas partition coefficient. With the 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 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 termination of the anesthesia. Redistribution then takes place; some of the agent is eliminated by the lungs, which are vessel rich, and some is distributed to the brain. The recovery period becomes significantly extended when the administration time of the anesthetic agent is prolonged to allow for complete saturation of the adipose tissue.
Halothane (Fluothane) was the classic inhalation anesthetic from the 1960s to the 1990s. Inclusion of halothane in the discussion is helpful because all the inhalation anesthetic agents currently in use have almost the same partition coefficients. Halothane has an oil-gas partition coefficient that is approximately twice that of isoflurane, desflurane, or sevoflurane; therefore, with use of halothane as the marker, the newer inhalation agents are twice as fast during induction and emergence as before. All three of the inhalational anesthetics currently in use are used in a variety of settings, and all possess a blood-gas partition coefficient less than 1 (see Table 20-1).