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Barbiturates (Thiopentone)

Derived from urea + malonic acid
  1. Mechanism: Depression of RAS, GABA facilitatory.
    Thiopentone has greater potency, rapid onset, shorter duration of action because of sulphur atom.
  2. Route - I.V., I.M. or P.R. (thio and methohexitone) highly protein bound 80%, lipid soluble, uptake to brain with in 20sec., termination of action – redistribution, elimination – hepatic metabolism T ½ - 10-11 hrs. execration via kidney. Dose 4-7 mg/kg

Systemic effects

  1. CVS: Decrease B.P., increase H.R., Cardiac output is maintained
  2. R/s: Decrease R.R., decrease T.V., apnea, does not suppresses upper airway reflexes
  3. CNS: Decrease Cerebral Blood Flow(CBF), decrease ICP, decrease Cerebral Metabolic Requirement of O2(CMRO2), increases seizure threshold, Anti analgesic effect by decrease pain threshold, no muscle relaxation.
  4. Renal: Decrease R.B.F. and G.F.R.; decrease hepatic blood flow
  1. Highly alkaline solution – causes irritation, pain, phlebitis
  2. Shivering- thiopental shakes
  3. Excitatory phenomenon, decrease B.P., decrease respiration, increase airway reflexes, hiccough
  4. Intra arterial – Agonizing pain, shooting down the forearm, anesthesia, motor weakness, gangrene, loss of finger or forearm.
  5. T/t: Leave the needle in situ, lignocaine/heparin/procaine/ papaverine / brachial or stellate ganglion block/surgical removal of clot.
    C/I: Porphyria, hypersensitivity, hypovolemia, cardiac insufficiency or failure, hypersensitive airway disease, myxedema


Phencyclidine derivative
  1. Dissociates the thalamus from Limbic system
  2. Dissociative anesthesia- Eye opening, swallowing, muscle contraction unable to feel or respond to sensory stimulus.
  3. Inhibits excitatory neurotransmitter- N.M.D.A.
  4. Awakening due to redistribution (10-15 min), metabolized in liver.
  5. Elimination t½-2 hrs , excretion-renal.
  6. Increase H.R, B.P, ICP,CBF, CMRO2 (Cerebral metabolic requirement of oxygen), decrease seizure threshold.
  7. Depresses ventilation, potent bronchodilator, increased salivation.
  8. Hallucinations, illusion, delirium during emergence.
  9. Good analgesic, amnesia & unconsciousness


  1. CAD,
    1. uncontrolled hypertension,
    2. CHF
    3. arterial aneurysm;
    4. space occupying intracranial lesions,
    5. open eye surgery.


-2,6 diisopropyl phenol contains – Propofol 1%, soya bean oil 10%, glycerol 2.25%, egg lecithin 1.2% pale straw (white), milky, shouldn’t be mixed with any other except 5% D and lignocaine
  1. MOA: GABA facilitatory and mimetic, 98% protein bound , highly lipid soluble metabolized in liver, distribution T ½ - 2-8min. Excretion renal
  2. Decrease CBF, ICP, decrease CMRO2 (Cerebral metabolic requirement of oxygen), decrease HR and B.P., anticonvulsant
  3. Apnea, inhibits hypoxic drive, depresses upper airway reflexes
  4. Antipruritic, antiemetic, excitatory phenomenon, hiccough
  5. Cause pain on injection, support growth of bacteria


  1. Imidazole derivative
  2. Depresses RAS, GABA mimetic, dose 0.2 – 0.4mg/kg
  3. Decrease B.P., Cardiac output unchanged
  4. Maintains ventilation
  5. Decrease ICP, CBF and CMRO2 no analgesic property.
  6. S/E Myoclonus, vomiting, adrenocortical suppressions


GABA facilitatory increase Cl- conductance. Highly protein bound, lipid soluble except midazolam (WATER SOLUBLE). Redistribution t1/2 3-10 min. Metabolized in liver into active metabolites
  1. Depresses R/S and CVS (inc HR), Midazolam lesser than Diazepam
  2. Decrease ICP, CBF, CMRO2, control seizure, sedative, antianxiety, amnesic and muscle relaxant no analgesia.
  3. Antagonist is flumazenil.







Elimination t1/2






a. premedication
b. induction

0.04 - 0.2mg/kg

0.3 - 0.6 mg/kg

0.01- 0.1mg/kg

0.1 - 0.4mg/kg

0.03 - 0.05mg/kg

usually not used

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