Inhalation Anesthetics

F_a: Ventilation–perfusion mismatches are the primary cause for changes in F_a because they restrict normal flow and increase the alveolar–arterial difference (i.e., venous admixture, alveolar dead space).

Elimination: The most important route for elimination for inhalational anesthetics is the alveolus. Many of the factors that speed induction also speed recovery.

Minimum alveolar concentration (MAC): Defined as the alveolar concentration of an inhalational anesthetic at which 50% of patients do not move in response to surgical stimulation. Important because it allows anesthesiologists to compare potencies among various agents and mirrors brain partial pressure. MAC values are additive between anesthetics and can be altered by various factors.

• MAC decreased (anesthetic potency increases): Hypoxia with a PaO₂ below 40, anemia, benzodiazepines, barbiturates, hypercarbia with a PaCO₂ above 95, cholinesterase inhibitors, chronic amphetamines, cloni-dine, narcotics, ketamine, pregnancy (normal by 72 hours postpartum), lithium, local anesthetics, opioids, elderly age (6% decrease in MAC per decade of age).

• MAC unchanged: Duration of anesthesia, gender, hyper- or hypothyroidism.

• MAC increased (anesthetic potency decreases): Chronic alcoholism, hyperthermia, hypernatremia, drugs that increase catecholamines (e.g., ephedrine, acute cocaine or amphetamines, monoamine oxidase inhibitors).

Inhalational Pharmacology

Shared properties: Almost all inhalational anesthetics (IAs) result in an increase in cerebral blood flow (CBF) and intracranial pressure, depression of myocardial activity, rapid shallow breathing pattern, pulmonary bronchodilation, decrease in renal blood flow and glomerular filtration rate and, to a certain degree, cause a relaxation of skeletal muscle.

Nitrous oxide (NO): Colorless, odorless gas that antagonizes the N-methyl-D-aspartic acid (NMDA) receptor. Unlike volatile agents, nitrous oxide is a gas at room temperature and ambient pressure. It can be kept as a liquid under pressure because its critical temperature lies above room temperature. It also does not provide significant muscle relaxation and has been shown to cause postoperative nausea and vomiting. Even though nitrous oxide directly depresses myocardial contractility, arterial blood pressure, cardiac output, and heart rate are essentially unchanged or slightly elevated because of its stimulation of catecholamines. Importantly, NO is contraindicated in patients with pneumothorax, pulmonary embolus, pneumocephalus, and bowel obstruction because NO is 35 times more soluble then nitrogen in blood.

Halothane is no longer used in the United States. Its use results in a dose-dependent reduction of arterial blood pressure from a direct myocardial depression (most pronounced of the IA). Although halothane is a coronary artery vasodilator, coronary blood flow decreases because of the drop in systemic arterial pressure. By dilating cerebral vessels, halothane lowers cerebral vascular resistance and increases CBF. Autoregulation, the maintenance of constant CBF during changes in arterial blood pressure, is blunted. Halothane is oxidized in the liver by a particular isozyme of cytochrome P-450 (2EI) to its principal metabolite, trifluoroacetic acid.

Only gold members can continue reading. Log In or Register to continue