FIGURE 25–5 Why induction of anesthesia is slower with more soluble anesthetic gases. In this schematic diagram, solubility in blood is represented by the relative size of the blood compartment (the more soluble, the larger the compartment). Relative partial pressures of the agents in the compartments are indicated by the degree of filling of each compartment. For a given concentration or partial pressure of the two anesthetic gases in the inspired air, it will take much longer for the blood partial pressure of the more soluble gas (halothane) to rise to the same partial pressure as in the alveoli. Since the concentration of the anesthetic agent in the brain can rise no faster than the concentration in the blood, the onset of anesthesia will be slower with halothane than with nitrous oxide.
The duration of exposure to the anesthetic can have a significant effect on the speed of emergence from anesthesia, especially in the case of the more soluble anesthetics. Accumulation of anesthetics in muscle, skin, and fat increases with prolonged exposure (especially in obese patients), and blood concentration may decline slowly after discontinuation as the anesthetic is slowly eliminated from these tissues. Although recovery after a short exposure to anesthesia may be rapid even with the more soluble agents, recovery is slow after prolonged administration of halothane or isoflurane.
1.
Ventilation—Two parameters that can be manipulated by the anesthesiologist are useful in controlling the speed of induction of and recovery from inhaled anesthesia: (1) concentration of anesthetic in the inspired gas and (2) alveolar ventilation. As stated above, since the concentration of anesthetic in the inspired gas cannot be reduced below zero, hyperventilation is the only way to speed recovery.
2.
Metabolism—Modern inhaled anesthetics are eliminated mainly by ventilation and are only metabolized to a very small extent; thus, metabolism of these drugs does not play a significant role in the termination of their effect. However, metabolism may have important implications for their toxicity (see Toxicity of Anesthetic Agents). Hepatic metabolism may also contribute to the elimination of and recovery from some older volatile anesthetics. For example, halothane is eliminated more rapidly during recovery than enflurane, which would not be predicted from their respective tissue solubility. This increased elimination occurs because over 40% of inspired halothane is metabolized during an average anesthetic procedure, whereas less than 10% of enflurane is metabolized over the same period.
In terms of the extent of hepatic metabolism, the rank order for the inhaled anesthetics is halothane > enflurane > sevoflurane > isoflurane > desflurane > nitrous oxide (Table 25–1). Nitrous oxide is not metabolized by human tissues. However, bacteria in the gastrointestinal tract may be able to break down the nitrous oxide molecule.
Organ System Effects of Inhaled Anesthetics
A. CNS Effects
Anesthetic potency is currently described by the minimal alveolar concentration (MAC) required to prevent a response to a surgical incision (see Box: What Does Anesthesia Represent & Where Does It Work?). This parameter was first described by investigators in the 1960s and remains the best clinical guide for administering inhaled anesthetics, especially since improved medical technology can now provide instantaneous, accurate determination of gas concentrations.