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  • Ultra short acting are highly lipid soluble; hence rapid effects
  • Highly protein bound

Termination of action by:

  • Redistribution: Highly lipid-soluble drugs (thiopentone) get initially distributed to organs with high blood flow, i.e. brain. Later, less vascular but more bulky tissues (muscle, fat) take up the drug. Plasma concentration falls and the drug is withdrawn from these sites. Redistribution results in termination of drug action on CNS.
  • Metabolism: Oxidation by hepatic CYP-450. Phenobarbitone is a potent inducer of later.
  • Excretion: Alkalinization of urine increases ionization and excretion. 


  • Except for phenobarbitone in epilepsy and thiopentone in anesthesia, barbiturates are seldom used now.
  • They are occasionally employed as adjuvants in psychosomatic disorders.
  • The enzyme inducing property of phenobarbitone can be utilized to hasten clearance of congenital nonhaemolytic jaundice and kernicterus

Acute barbiturate toxicity

The principles of treatment apply to any CNS depressant poisoning


Manifestations are due to excessive CNS depression patient is flabby and comatose with shallow and failing respiration, fall in BP and cardiovascular collapse, renal shut down, Pulmonary complications, bullous eruptions.


1) Gastric lavage with activated charcoal

2) Supportive measures (ABCD)

3) Forced Alkaline diuresis with Sod. Bicarbonate

4) Hemodialysis

There is no specific antidote

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