Inhaled anesthetics produce reversible loss of consciousness through diffuse + low-affinity binding at multiple targets: GABA-A potentiation (sedation/hypnosis), glycine-receptor potentiation (spinal immobility), background K⁺ leak channels (TASK/TREK — neuronal hyperpolarization), and NMDA inhibition for some agents (xenon, nitrous oxide). MAC (minimum alveolar concentration) is the standardized potency measure. Sevoflurane + isoflurane + desflurane are halogenated ethers with different blood-gas solubilities (lower = faster on/off); sevoflurane is preferred for inhalational induction in children due to non-pungent odor. Volatile anesthetics + succinylcholine + RYR1 polymorphism are the MH-trigger triad; dantrolene is the antidote (releases the RYR1 calcium leak — cross-link: ros_oxidative_stress / dantrolene appears across multiple pathways).
Organ Systems
nervous
Pathway Steps
alveolar-gas-phase → systemic-equilibration — via low blood/gas partition coefficient → faster on/off; high lipid/blood partition → potent (MAC↓). Volatile anesthetics are delivered as gases whose alveolar partial pressure equilibrates with blood and brain; the blood-gas partition coefficient governs induction speed and MAC quantifies potency. At the molecular level they act largely by potentiating inhibitory GABA-A and glycine receptors (and inhibiting some excitatory channels), though a unified mechanism of anesthesia is still debated.