Many agents can depress the function of the central nervous system and produce calming or drowsiness (sedation). The CNS depressants discussed in this chapter include benzodiazepines, other benzodiazepine receptor agonists (the "Z compounds"), barbiturates, and sedative-hypnotic agents of diverse chemical structure. Older sedative-hypnotic drugs depress the CNS in a dose-dependent fashion, progressively producing a spectrum of responses from mild sedation to coma and death.
A sedative drug decreases activity, moderates excitement, and calms the recipient, whereas a hypnotic drug produces drowsiness and facilitates the onset and maintenance of a state of sleep that resembles natural sleep in its electroencephalographic characteristics and from which the recipient can be aroused easily.
Sedation is a side effect of many drugs that are not general CNS depressants (e.g., antihistamines and antipsychotic agents). Although such agents can intensify the effects of CNS depressants, they usually produce more specific therapeutic effects at concentrations far lower than those causing substantial CNS depression. For example, they cannot induce surgical anesthesia in the absence of other agents. The benzodiazepine sedative-hypnotics resemble such agents; although coma may occur at very high doses, neither surgical anesthesia nor fatal intoxication is produced by benzodiazepines in the absence of other drugs with CNS-depressant actions; an important exception is midazolam, which has been associated with decreased tidal volume and respiratory rate. Moreover, specific antagonists of benzodiazepines exist. This constellation of properties sets the benzodiazepine receptor agonists apart from other sedative-hypnotic drugs and imparts a measure of safety such that benzodiazepines and the newer Z compounds have largely displaced older agents for the treatment of insomnia and anxiety.
The sedative-hypnotic drugs that do not specifically target the benzodiazepine receptor belong to a group of agents that depress the CNS in a dose-dependent fashion, progressively producing calming or drowsiness (sedation), sleep (pharmacological hypnosis), unconsciousness, coma, surgical anesthesia, and fatal depression of respiration and cardiovascular regulation. They share these properties with a large number of chemicals, including general anesthetics (Chapter 19) and aliphatic alcohols, most notably ethanol (Chapter 23). Only two landmarks on the continuum of CNS depression produced by increasing concentrations of these agents can be defined with a reasonable degree of precision: surgical anesthesia, a state in which painful stimuli elicit no behavioral or autonomic response (Chapter 19), and death, resulting from sufficient depression of medullary neurons to disrupt coordination of cardiovascular function and respiration. The "end points" at lower concentrations of CNS depressants are defined with less precision—in terms of deficits in cognitive function (including attention to environmental stimuli) or motor skills (e.g., ataxia) or of the intensity of sensory stimuli needed to elicit some reflex or behavioral response. Other important indices of decreased CNS activity, such as analgesia and seizure suppression, do not necessarily fall along this continuum; they may not be present at sub-anesthetic concentrations of a CNS depressant drug (e.g., a barbiturate), or they may be achieved with minimal ...
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