Barbiturates are sedatives/hypnotics used mainly for anesthesia and epilepsy treatment. They affect the gamma-aminobutyric acid (GABA) system and cause a CNS suppressive effect, which ranges from anxiolysis, sedation, and coma to fatal cardiovascular and respiratory arrest upon overdose.  They are classified as short-acting, intermediate-acting, and long-acting. See Table 1 for classification and properties.
Table 1. Classification and Properties of Barbiturates (Open Table in a new window)
|Drug||Half-life (h)||Duration of Effect (h)||Hypnotic Dose, mg||Minimum Toxic level, mg/L|
Minimally toxic levels of barbiturates (see Table 1) are considered toxic since even a slightly elevated level is sufficient to produce toxicity. When the barbiturate level is measured, the patient’s body weight, renal function, liver function, age, and the specific barbiturate used should all be considered, since all of these variables alter the clinical correlation.
For example, a phenobarbital level of 31 mg/L in an older patient with renal and/or liver dysfunction is more critical than a thialbarbital level of 10 mg/L in a younger healthy patient.
Collection and Panels
Container: Red-top tube
Collection method: Routine venipuncture
Specimen: Blood serum
Specimen volume: 1 mL (minimum, 0.4 mL)
Analysis method: Immunoassay and gas chromatography-mass spectrometry
Barbiturates work primarily on GABA-A receptors, which are the main neurosuppressant receptors in the brain cortex. Stimulation of GABA-A receptors results in increasing seizure threshold by decreasing postsynaptic excitation. However, this mechanism also produces the well-known side effects of barbiturates, such as drowsiness, sedation, and coma. Activation of the GABA system in the cerebellum causes ataxia.
The metabolic/excretory characteristics of barbiturates are as follows:
Absorption: Fast absorption in the stomach when given orally
Half-life: Varies by category
Metabolism: CYP450 system and mainly by 2C9 substrate
Excretion: 25%-50% of the long-acting barbiturates are excreted unchanged in urine (the remainder is excreted via hepatic oxidation); the vast majority of short-acting barbiturates are metabolized and excreted through the liver
Currently, barbiturates are used to induce anesthesia and to treat seizures (especially generalized seizures) and intracranial pressure in pediatric patients. 
Barbiturates were first used in 1903 as anticonvulsants, anxiolytics, sedatives, and anesthetics; currently, their clinical utility is limited to epilepsy and anesthesia because of various side effects and difficulty in monitoring. Barbiturate use may lead to tolerance, dependence, and addiction; in 1970, several barbiturates were designated as controlled substances in the United States.
Potential adverse effects of barbiturates include the following:
Neurologic: Confusion, hallucinations, coma
Cardiopulmonary: Hypoventilation, apnea, syncope
Hematologic (rare): Agranulocytosis, megaloblastic anemia
Hepatic (rare): Liver injury
Dermatologic (rare): Stevens-Johnson syndrome, erythroderma
Since barbiturates have a very narrow therapeutic index, patients can easily develop side effects and toxicity. Patients should be extremely careful when another medication is given along with barbiturates, such as opioids, benzodiazepines, or antidepressants, since these combinations could be fatal. In addition, over-the-counter medications that include antihistamines are also CNS depressants; when taken with barbiturates, the combination can lead to fatal respiratory failure.
Table 2. Chemical, Trade, and Street Names for Some Barbiturates (Open Table in a new window)
|Chemical Name||Street Name||Trade Name|