| Indication | Methohexital is indicated for use as an intravenous anaesthetic. It has also been commonly used to induce deep sedation. |
| Pharmacodynamics | Methohexital, a barbiturate, is used for the induction of anesthesia prior to the use of other general anesthetic agents and for induction of anesthesia for short surgical, diagnostic, or therapeutic procedures associated with minimal painful stimuli. Little analgesia is conferred by barbiturates; their use in the presence of pain may result in excitation. |
| Mechanism of action | Methohexital binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged. |
| Absorption | The absolute bioavailability following rectal administration of methohexital is 17%. |
| Volume of distribution | Not Available |
| Protein binding | 73% |
| Metabolism | Metabolism occurs in the liver through demethylation and oxidation. Side-chain oxidation is the most important biotransformation involved in termination of biologic activity. |
| Route of elimination | Excretion occurs via the kidneys through glomerular filtration. |
| Half life | 5.6 ± 2.7 minutes |
| Clearance | Not Available |
| Toxicity | The onset of toxicity following an overdose of intravenously administered methohexital will be within seconds of the infusion. If methohexital is administered rectally or is ingested, the onset of toxicity may be delayed. The manifestations of an ultrashort-acting barbiturate in overdose include central nervous system depression, respiratory depression, hypotension, loss of peripheral vascular resistance, and muscular hyperactivity ranging from twitching to convulsive-like movements. Other findings may include convulsions and allergic reactions. Following massive exposure to any barbiturate, pulmonary edema, circulatory collapse with loss of peripheral vascular tone, and cardiac arrest may occur. |