Anesthesia 5th year, 4th & 5th lectures (Dr. Aamir)

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The lecture has been given on Oct. 19th & 26th, 2010 by Dr. Aamir.
  • 1. MUSCLE RELAXANTS Muscle relaxants are drugs that interrupt transmission of neural impulses at the neuromuscular junction
  • 2. History <ul><li>Involved research using Banded Krait (bungarotoxins) and cobra as well as curare from South American plants </li></ul>
  • 3. Banded Krait from Taiwan
  • 5. Most potent source of curare
  • 6. Clinical uses
  • 7. <ul><li>Provide skeletal muscle relaxation to facilitate intubation of the trachea </li></ul><ul><li>Provide optimal surgical working conditions </li></ul><ul><li>In the intensive care setting to facilitate mechanical ventilation of the lungs </li></ul>
  • 8. Note <ul><li>MR lack anesthetic or analgesic effects and must not be used to render an inadequately anesthetized patient immobile </li></ul>
  • 9. The choice of MR is influenced by: <ul><li>Its speed of onset </li></ul><ul><li>Duration of action </li></ul><ul><li>Rout of elimination </li></ul><ul><li>Associated side effects </li></ul>
  • 10. Neuromuscular junction <ul><li>Consist of a prejuctional motor nerve ending separated from the highly folded postjunctional membrane by synaptic cleft </li></ul><ul><li>Neuromuscular transmission is initiated by arrival of an impulse at the motor nerve terminal with an associated influx of calcium and a resultant release of neurotransmitter acetylcholine </li></ul>
  • 11. <ul><li>Ach binds to nicotinic cholinergic receptors on postjunctional membrane, causing a change in membrane permeability to ions, principally K & Na ions </li></ul><ul><li>Ach is rapidly hydrolyzed by enz. Acetylcholine esterase (true cholinesterase) </li></ul><ul><li>Nicotinic cholinergic receptors </li></ul><ul><li>1.Prejunctional </li></ul><ul><li>2.Postjunctional </li></ul><ul><li>3.extrajunctional </li></ul>
  • 12. Neuromuscular Junction
  • 13. Acetate and choline 50% recaptured by nerve terminal Voltage-dependent Ca 2+ channels High affinity choline carrier Empty vesicle choline Na + Ca 2+ Ca 2+ Ca 2+ ACh ACh ACh Na + K + nAChR Na + Muscle fibre ACh (8-10,000 molecules) ~100mM CAT AcCoA CoA choline ACh active transport AChE
  • 14. Muscle relaxants Depolarizing noncompetitive Nondepolarizing competitive
  • 15. Depolarizing (succinylcholine or Suxamethonium) <ul><li>Clinical use: - - - - - - </li></ul>
  • 16. Averse effects <ul><li>Cardiac dysrthymia: Bradycardia, arrest </li></ul><ul><li>Myalgia </li></ul><ul><li>Myoglobinuria </li></ul><ul><li>Increased Intraocular pressure </li></ul><ul><li>Increased Intragastric pressure </li></ul><ul><li>Increased Intracranial pressure </li></ul><ul><li>Trismus </li></ul><ul><li>Allergic reactions </li></ul><ul><li>Trigger for malignant hyperthermia </li></ul>
  • 17. <ul><li>10. Hyperkalemia </li></ul><ul><li>Denervation injury (spinal cord transection) </li></ul><ul><li>Unhealed skeletal muscle injury as produced by 3 rd degree burn </li></ul><ul><li>Upper motor neuron injury </li></ul><ul><li>Multiple trauma </li></ul>
  • 18. Causes of delayed recovery from succinylcholine <ul><li>Sever liver disease </li></ul><ul><li>Potent anticholine esterase (insecticides) </li></ul><ul><li>Chemotherapy (cyclophosphamide) </li></ul><ul><li>A typical pseudo cholinesterase </li></ul>
  • 19. Nondepolarizing competitive Nondepolarizing competitive Long acting (>30 min) Pancuronium D-tubocurarine Gallamine Intermediate acting (15-25 min) Vecuronium Cis (atracurium) rocuronuim Short acting (<15 min) Mivacurium
  • 20. Factors enhance effects of NDMR <ul><li>Volatile anesthetics </li></ul><ul><li>Aminoglycosides Antibiotics </li></ul><ul><li>Mg </li></ul><ul><li>Local analgesics </li></ul><ul><li>Calcium channel blockers (verapamil) </li></ul><ul><li>Cardiac antiarrythmias (quinidine) </li></ul><ul><li>Hypothermia </li></ul><ul><li>Acidosis </li></ul><ul><li>Hypokalemia </li></ul>
  • 21. Drug-assisted antagonism of Nondepolarizing muscle relaxants Anti-choline esterase Neostigmine edrophonium pyridostigmine
  • 22. Anticholinesterase <ul><li>Drug accelerates the already established pattern of spontaneous recovery at the neuromuscular junction by inhibiting the activity of acetylcholinesterase leading to accumulation of ach. At nicotinic (neuromuscular junction) and muscarinic sites </li></ul>
  • 23. <ul><li>The competition between ach and a Nondepolarizing MR in favor of the neurotransmitter (Ach) and restores neuromuscular transmission </li></ul><ul><li>Anticholinesterase does not cross blood brain barrier </li></ul><ul><li>Peripheral muscarinic effects block by anticholinergic drugs like Atropine </li></ul>
  • 24. <ul><li>Thank you </li></ul>
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