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Halothane

  1. Excreted unchanged in lungs
  2. Auto Regulation Blunted
  3. No analgesia
  4. Tissue: Blood ratio is maximum in fat
  5. Dissolves rubber
  6. Trichloracetic acid is found in urine
  7. Drager Narco test is done for halothane
  8. Causes dilation of:
  1. Physical Properties
    1. Colourless liquid volatile agent
    2. Pleasant to smell
    3. Stored in amber colour bottles (to prevent decomposition by light 0.01% thymol also added)
    4. Non inflammable
    5. Non explosive
    6. Non irritant
    7. stabilize by thymol (Preservative) and amber coloured bottle,
  2. For Induction - 2-4% Maintenance - 0.5 to 2%
  3. MAC - 0.74%
     
    Blood gas coefficient - 2.4
  4. Metabolism - 20% is metabolized , main metabolites - Trifluroacetic acid (TFA)
  5. Effects
     
    CVS
    1. C.O (Cardiac output)
    2. Bradycardia
    3. Direct depression of myocardium
    4. B.P
    5. Sensitizes heart to ADRENALINE (both exogenous & endogenous) arrhythmias like
    6. Ventricular Extrasystoles, Ventricular - tachycardia & Ventricular fibrillation may occur
       
      Important: Halothane usually causes sinus or nodal bradycardia which is reversed by atropine.
  6. Malignant Hyperthermia
  7. CNS
    1. Potent anaesthetic
    2. Not a good analgesic  
    3. Muscle relaxation - moderate.

NOTE: Most commonly implicated drugs in malignant hyperthermia are:

  1. Halothane (MCQ)
  2. Suxamethonium (MCQ)
     
    Treatment of choice for malignant hyperthermia is intravenous dantrolene. (MCQ)
  1. Respiratory system
    1. Resp. depressant
    2. ↓ tidal volume frequency
    3. C. BRONCHODILATION - This is due to inhibition of reflexes pathways for bronchoconstriction

Important: Halothane tends to accentuate perfusion-ventilation mismatch in lungs by causing vasodilatation in hypoxic alveoli. (MCQ)

  1. Uterus
    1. Can cause uterine atony & PPH
    2. Agent of choice for version & manual removal of placenta
  2. Liver
    1. Halothane hepatitis , causes centrilobular hepatitis necrosis. 
    2. Incidence of massive hepatic necrosis 1:35,000
    3. Patients predisposed to halothane hepatitis- 
      1. Middle age
      2. Female
      3. Obese
      4. Preexisting liver disease
      5. Previous exposure to halothane within 3 months
    4. MOA --
      1. Directly hepatocellular (its metabolite causes direct injury), or
      2. Immunologic (more acceptable theory now)
      3. Blood supply to liver
         
        So, guidelines are
        • Avoid repeated administration at frequent interval (say 3 months)
        • Pre- existing liver disease is not an absolute C/I, but use cautiously in acute liver diseases.
Other causes of post op. Jaundice
  1. Drugs
  2. Blood transfusion
  3. Shock
  4. Benign post - operative cholestasis
  5. Septic cholangitis
  6. Coincidental viral hepatitis
  7. Familial hyperbilirubinemia




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