Barbiturates are central nervous system (CNS) depressants (downers). These drugs produce sedative, hypnotic, and anesthetic effects. Depending on the dose used, any single drug in this class may produce sedation (decreased responsiveness), hypnosis (sleep), and anesthesia (loss of sensation). A small dose will produce sedation and relieve anxiety and tension; a somewhat larger dose taken in a quiet setting will usually produce sleep; an even larger dose will produce unconsciousness. The sleep produced by barbiturates, however, is not identical with normal sleep. Normal sleep consists of several phases, including slow-wave sleep, or deep sleep, and rapid-eye-movement (REM) sleep. In the REM sleep phase, skeletal muscles relax, eyes move rapidly and frequently, and dreaming occurs. Dreaming is believed to play an important role in learning and memory. Barbiturates decrease REM (or dreaming) sleep, which may explain why the sleep associated with barbiturates is less restorative than natural sleep.
As is true for most drugs that act on the CNS, the effects of these drugs are also influenced markedly by the user's previous drug experience, the circumstances in which the drug is taken, and the route of administration of the drug. For example, a dose taken at bedtime may produce sleep, whereas the same dose taken during the daytime may produce a feeling of euphoria, incoordination, and emotional response. This, in many ways, is what happens with alcohol intoxication. In fact, the behavioral effects of this class of drugs is very similar to those observed after drinking alcohol, and the user may experience impairment of skills and judgment not unlike that experienced with alcohol. It is therefore not surprising that the effects of barbiturates are enhanced when taken in combination with alcohol, anti-anxiety drugs (benzodiazepines), and other CNS depressants such as opioids, antihistamines, and over-the-counter cough and cold medications containing these drugs. Barbiturates, however, differ from some other sedative-hypnotic drugs in that they do not elevate the pain threshold. In fact, patients experiencing severe pain may become agitated and delirious if they are given barbiturates without also receiving analgesics (pain killers).
Barbiturates are generally classified as being long, intermediate, short, and ultra-short acting on the basis of their duration of effect. The long-acting barbiturates, such as phenobarbital, which were at one time mainly employed as daytime sedatives for the treatment of anxiety, produce sedation that lasts from twelve to twenty-four hours. Although no longer prescribed widely for that purpose, phenobarbital is one of the drugs used for the treatment of grand mal epilepsy. The short- and intermediate-acting drugs such as pentobarbital and secobarbital, which were once mainly employed as hypnotics, produce CNS depression that lasts for three to twelve hours, depending on the compound used. The ultra-short-acting barbiturates (e.g., thiopental) are used for the induction of anesthesia because of the ease and rapidity with which they induce sleep when given intravenously. The effects of barbiturates on judgment and other mental as well as motor skills, however, may persist much longer than the duration of the hypnotic effect. For this and other reasons, for the treatment of anxiety or insomnia, barbiturates have largely been replaced by the generally safer group of drugs called benzodiazepines.
The respiratory system is significantly depressed by the administration of barbiturate doses that are larger than those usually prescribed. Furthermore, there is a synergistic effect (i.e., one that is greater than simply adding the drugs' effects) when barbiturates are combined with alcohol and other central nervous system depressants—often with a fatal outcome. Barbiturates are frequently used for suicides. For this reason, too, barbiturates have been displaced by less toxic benzodiazepines. The symptoms of acute barbiturate toxicity resemble the effects observed after excessive alcohol ingestion. Although repeated administration of barbiturates results in CNS tolerance, thus producing less intoxication, tolerance does not appear to develop to the same extent for the respiratory depressant and lethal effects of the barbiturates; the person addicted to barbiturates may therefore be at a greater risk of respiratory toxicity Page 208 | Top of Articlebecause of less pronounced CNS euphoric effects with higher doses, which may lead the individual to increase the dosage, resulting in respiratory depression. Tolerance to barbiturates also affects metabolism; the administration of these drugs speeds up not only their own metabolism (i.e., shortens their effectiveness) but also the metabolism of a large number of other drugs. This property has been of use in some special cases (as in jaundice of the newborn), but it can be hazardous in others when it decreases the effectiveness of another drug (e.g., an anticoagulant used to treat blood clots).
Long-term users experience withdrawal symptoms when the barbiturate is stopped abruptly. Abrupt cessation also leads to an increase in the amount and intensity of REM sleep (REM rebound). The intensity of the withdrawal symptoms varies with the degree of abuse and may range from sleeplessness and tremor in mild cases to delirium and convulsions in severe cases. Fatalities have occurred as a result of barbiturate withdrawal; this is more likely to occur with short-acting barbiturates. In some individuals, barbiturates may produce CNS excitement rather than CNS depression. This type of idiosyncratic reaction occurs most frequently in elderly people. Among the side effects sometimes seen, there may be rashes and muscle and body aches.
See alsoExpectancies; Sleep, Dreaming, and Drugs.
Charney, D. S., Mihic, S. J., & Harris, R. A. (2005). Hypnotics and sedatives. In L. Brunton, J. Lazo, & K. Parker (Eds), The pharmacological basis of therapeutics (11th ed.). New York: McGraw-Hill.
Kalant, H., & Roschlau, W. H. E. (1989). Principles of medical pharmacology, 5th ed. Toronto: B. C. Decker.
JAT M. KHANNA
REVISED BY BY LEAH R. ZINDEL (2009)