RT Book, Section A1 Butterworth IV, John F. A1 Mackey, David C. A1 Wasnick, John D. SR Print(0) ID 1190603935 T1 Inhalation Anesthetics T2 Morgan & Mikhail’s Clinical Anesthesiology, 7e YR 2022 FD 2022 PB McGraw-Hill Education PP New York, NY SN 9781260473797 LK accessanesthesiology.mhmedical.com/content.aspx?aid=1190603935 RD 2024/03/28 AB KEY CONCEPTS The greater the uptake of anesthetic agent, the greater the difference between inspired and alveolar concentrations and the slower the rate of induction. Three factors affect anesthetic uptake: solubility in the blood, alveolar blood flow, and the difference in partial pressure between alveolar gas and venous blood. Low-output states predispose patients to overdosage with soluble agents as the rate of rise in alveolar concentrations will be markedly increased. Many of the factors that speed induction also speed recovery: elimination of rebreathing, high fresh gas flows, low anesthetic-circuit volume, low absorption by the anesthetic circuit, decreased solubility, high cerebral blood flow, and increased ventilation. The unitary hypothesis proposes that all inhalation agents share a common mechanism of action at the molecular level. This was previously supported by the observation that the anesthetic potency of inhalation agents correlates directly with their lipid solubility (Meyer–Overton rule). The implication is that anesthesia results from molecules dissolving at specific lipophilic sites; however, the correlation is only approximate. The minimum alveolar concentration (MAC) of an inhaled anesthetic is the alveolar concentration that prevents movement in 50% of patients in response to a standardized stimulus (eg, surgical incision). Prolonged exposure to anesthetic concentrations of nitrous oxide can result in bone marrow depression (megaloblastic anemia) and even neurologic deficiencies (peripheral neuropathies). “Halothane hepatitis” is extremely rare. Patients exposed to multiple halothane anesthetics at short intervals, middle-aged obese women, and persons with a familial predisposition to halothane toxicity or a personal history of toxicity are considered to be at increased risk. Isoflurane dilates coronary arteries but not nearly as potently as nitroglycerin or adenosine. Dilation of normal coronary arteries could theoretically divert blood away from fixed stenotic lesions. The low solubility of desflurane in blood and body tissues causes very rapid induction of and emergence from anesthesia. Rapid increases in desflurane concentration lead to transient but sometimes worrisome elevations in heart rate, blood pressure, and catecholamine levels that are more pronounced than occur with isoflurane, particularly in patients with cardiovascular disease. Nonpungency and rapid increases in alveolar anesthetic concentration make sevoflurane an excellent choice for smooth and rapid inhalation inductions in pediatric and adult patients.