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Barbiturates
๏ƒผused as hypnotic and sedative agents, for the induction of
anesthesia
๏ƒผ for the treatment of epilepsy and status epilepticus.
๏ƒผThey often are divided into four major groups according to
their pharmacologic activity and clinical use
They include;
ultra-short acting-Thiopental
short acting -Pentobarbital
intermediate acting- Butabarbital
long acting-Phenobarbital
Mechanism of toxicity
๏ƒผ All barbiturates cause generalized depression of neuronal
activity in the brain
๏ƒผ Interaction with a barbiturate receptor leads to enhanced
gammaaminobutyric acid (GABA)โ€“mediated chloride currents
and results in synaptic inhibition
๏ƒผ Hypotension that occurs with large doses is caused by
depression of central sympathetic tone as well as by direct
depression of cardiac contractility
Toxic dose
โ€ข toxic dose of barbiturates varies widely and depends on the
drug, the route and rate of administration, and individual
patient tolerance
โ€ข toxicity is likely when the dose exceeds 5โ€“10 times the
hypnotic dose
โ€ข abusers may have striking tolerance to depressant effects
โ€ข The potentially fatal oral dose of the shorter-acting agents such
as pentobarbital is 2โ€“3 g, compared with 6โ€“10 g for
phenobarbital
Treatment
๏ƒผ Emergency and supportive measures :Protect the airway and
assist ventilation and treat coma, hypothermia and hypotension if
they occur.
๏ƒผ Decontamination :Administer activated charcoal orally if
conditions are appropriate.
๏ƒผ Enhanced elimination
1. Alkalization : increases the urinary elimination of phenobarbital .
may potentially contribute to fluid overload and pulmonary edema.
2. Repeat-dose activated charcoal :shown to decrease the half-life
of phenobarbital and its metabolites,
3. Hemodialysis or hemo-perfusion :necessary for severely
intoxicated patients who are not responding to supportive care

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barbiturates.pptx

  • 1. Barbiturates ๏ƒผused as hypnotic and sedative agents, for the induction of anesthesia ๏ƒผ for the treatment of epilepsy and status epilepticus. ๏ƒผThey often are divided into four major groups according to their pharmacologic activity and clinical use They include; ultra-short acting-Thiopental short acting -Pentobarbital intermediate acting- Butabarbital long acting-Phenobarbital
  • 2. Mechanism of toxicity ๏ƒผ All barbiturates cause generalized depression of neuronal activity in the brain ๏ƒผ Interaction with a barbiturate receptor leads to enhanced gammaaminobutyric acid (GABA)โ€“mediated chloride currents and results in synaptic inhibition ๏ƒผ Hypotension that occurs with large doses is caused by depression of central sympathetic tone as well as by direct depression of cardiac contractility
  • 3. Toxic dose โ€ข toxic dose of barbiturates varies widely and depends on the drug, the route and rate of administration, and individual patient tolerance โ€ข toxicity is likely when the dose exceeds 5โ€“10 times the hypnotic dose โ€ข abusers may have striking tolerance to depressant effects โ€ข The potentially fatal oral dose of the shorter-acting agents such as pentobarbital is 2โ€“3 g, compared with 6โ€“10 g for phenobarbital
  • 4. Treatment ๏ƒผ Emergency and supportive measures :Protect the airway and assist ventilation and treat coma, hypothermia and hypotension if they occur. ๏ƒผ Decontamination :Administer activated charcoal orally if conditions are appropriate. ๏ƒผ Enhanced elimination 1. Alkalization : increases the urinary elimination of phenobarbital . may potentially contribute to fluid overload and pulmonary edema. 2. Repeat-dose activated charcoal :shown to decrease the half-life of phenobarbital and its metabolites, 3. Hemodialysis or hemo-perfusion :necessary for severely intoxicated patients who are not responding to supportive care