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Sedatives and hypnotics: Clinical use and abuse

INTRODUCTION

The term "sedative-hypnotics" refers to a heterogeneous class of drugs that include benzodiazepines, barbiturates, and various hypnotics. A sedative lowers excitement and calms the awake patient, whereas a hypnotic produces drowsiness and promotes sleep. By tradition, they are categorized into a single class because of their common ability to induce sedation and sleep.

This topic will discuss the medical and non-medical use of these drugs, including treatment to prevent withdrawal. The pharmacology and pharmacoepidemiology of sedative and hypnotic medications, the management of sedative hypnotic intoxication and withdrawal syndromes, and the treatment of specific medical conditions for which these drugs are indicated are discussed separately. (See "Sedatives and hypnotics: Pharmacology and epidemiology" and "Benzodiazepine poisoning and withdrawal" and "Overview of generalized anxiety disorder" and "Overview of panic disorder" and "Treatment of insomnia" and "Overview of the recognition and management of the drug abuser".)

INDICATIONS FOR MEDICAL USE

Barbiturates — Short-acting barbiturates are only used for anesthesia induction. Longer-acting barbiturates are used for management of epilepsy and have a role in management of sedative withdrawal; their use for treatment of anxiety and insomnia has largely been replaced by benzodiazepines.

Benzodiazepines — Benzodiazepines are most commonly used for management of anxiety and for insomnia [1]. They can also be used for muscle relaxation, sedation/amnesia before medical or surgical procedures, treatment of epilepsy and seizure states, treatment of alcohol or sedative withdrawal, or acute agitation. They are used intravenously as a component of balanced anesthesia. Additionally, they have a role in the initial management of acute mania or agitated psychosis, as well as for control of drug-induced hyperexcitable states (eg, stimulant or PCP intoxication).

ADVERSE EFFECTS

Adverse effects of sedative drugs result from dose-dependent depression of the central nervous system, and include [2]:
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