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The sedative-hypnotics belong to a chemically heterogeneous class of drugs, almost all of which produce dose-dependent CNS depressant effects. A major subgroup is the benzodiazepines, but representatives of other subgroups, including barbiturates, and miscellaneous agents (carbamates, alcohols, and cyclic ethers) are still in use. Newer drugs with distinctive characteristics include the anxiolytic buspirone, several widely used hypnotics (zolpidem, zaleplon, eszopiclone), and ramelteon, a novel drug used in sleep disorders.

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SedationReduction of anxiety
AddictionThe state of response to a drug whereby the drug taker feels compelled to use the drug and suffers anxiety when separated from it
AnesthesiaLoss of consciousness associated with absence of response to pain
AnxiolyticA drug that reduces anxiety, a sedative
DependenceThe state of response to a drug whereby removal of the drug evokes unpleasant, possibly life-threatening symptoms, often the opposite of the drug's effects
HypnosisInduction of sleep
REM sleepPhase of sleep associated with rapid eye movements; most dreaming takes place during REM sleep
SedationReduction of anxiety
ToleranceReduction in drug effect requiring an increase in dosage to maintain the same response

Absorption and Distribution

Most sedative-hypnotic drugs are lipid-soluble and are absorbed well from the gastrointestinal tract, with good distribution to the brain. Drugs with the highest lipid solubility (eg, thiopental) enter the CNS rapidly and can be used as induction agents in anesthesia. The CNS effects of thiopental are terminated by rapid redistribution of the drug from brain to other highly perfused tissues, including skeletal muscle. Other drugs with a rapid onset of CNS action include eszopiclone, zaleplon, and zolpidem.

Metabolism and Excretion

Sedative-hypnotics are metabolized before elimination from the body, mainly by hepatic enzymes. Metabolic rates and pathways vary among different drugs. Many benzodiazepines are converted initially to active metabolites with long half-lives. After several days of therapy with some drugs (eg, diazepam, flurazepam), accumulation of active metabolites can lead to excessive sedation. Lorazepam and oxazepam undergo extrahepatic conjugation and do not form active metabolites. With the exception of phenobarbital, which is excreted partly unchanged in the urine, the barbiturates are extensively metabolized. Chloral hydrate is oxidized to trichloroethanol, an active metabolite. Rapid metabolism by liver enzymes is responsible for the short duration of action of zolpidem. A biphasic release form of zolpidem extends its plasma half-life. Zaleplon undergoes even more rapid hepatic metabolism by aldehyde oxidase and cytochrome P450. Eszopiclone is also metabolized by cytochrome P450 with a half-life of 6 h. The duration of CNS actions of sedative-hypnotic drugs ranges from just a few hours (eg, zaleplon < zolpidem = triazolam = eszopiclone < chloral hydrate) to more than 30 h (eg, chlordiazepoxide, clorazepate, diazepam, phenobarbital).

No single mechanism of action for sedative-hypnotics has been identified, and the different chemical subgroups may have different actions. Certain drugs ...

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