Benzodiazepine Poisoning

Basics

Potentiates the activity of γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter, by binding to its own specific site
Also facilitates GABA binding to its site
Results in chloride influx, membrane hyperpolarization, and inhibition of cellular excitation:
- Benzodiazepines (BZDs) increase the frequency of chloride channel opening
- Depresses spinal reflexes and reticular activating system
Rapidly absorbed from GI tract:
- Highly protein bound
- Large V_d
- Most have hepatic metabolism, some have active metabolites
- Duration of action is inversely proportional to lipophilicity with highly lipophilic drugs penetrating the CNS more rapidly
- Duration of diazepam > lorazepam > midazolam
- Synergistic with other sedative–hypnotic medications (e.g., ethanol, barbiturates, propofol)

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