Abstract
Barbiturates have sedative-hypnotic properties and are classified by duration of action into short- and long-acting agents. Their primary mechanism of action is binding of the central γ-aminobutyric acid (GABA) receptor, causing prolonged chloride channel opening which hyperpolarizes the postsynaptic neuron resulting in central nervous system (CNS) depression. Many clinical manifestations of toxicity are related to their GABA-ergic effects. The duration of these effects are dependent on the half-life of each specific agent and may be augmented by co-ingestants. Treatment in a minor overdose setting is usually supportive but severe overdoses may require advanced airway management, gastrointestinal decontamination or dialysis.
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