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Class local anaesthetics 2
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  • 2.  Drugs that cause reversible loss of sensory perception specially of pain in a restricted area of the body, when applied topically or local injection.  LA if applied to a mixed nerve—sensory and motor impulses are interrupted—resulting in muscular paralysis and loss of autonomic control.
  • 3.  Reversibly block the impulse conduction  Transient loss of sensation  Local anaesthesia blockade  C,B > Aδ > Aα,ß,γ
  • 6. E S T E R S  Short duration of action  Less intense anesthesia  Higher risk of hypersensitivity -PABA.  Hydrolyzed by Plasma Cholinesterase in blood.  Rarely used for Infiltration anesthesia But useful for topical anesthesia on mucous membranes. A M I D E S Produce more intense and longer lasting anesthesia Bind to alpha1 acid glyco- protein in plasma Rarely cause hypersensitivity reactions- no cross reactivity with ESTER L A s Not hydrolyzed by Plasma Cholinesterase, but in liver
  • 7.  Vasoconstrictor is a substance used to keep the anesthetic solution in place at a longer period and prolongs the action of the drug  Vasoconstrictor delays the absorption which slows down the absorption into the bloodstream  Vasoconstrictor used ---the natural hormone called epinephrine (adrenaline).
  • 8.  Blockage of membrane depolarisation in all excitable tissues, usually intended on peripheral nerve  Membrane stabilizer  They prevent the  Initiation and propa-  Gation of the nerve  Impulse by reducing  the passage of Na
  • 9.  Effects of LA: injection as acid (hydrochloric salt)= ionized form  at physiological pH dissociation to free base (lipid soluble) passage through cell membrane to interior of axon re-ionisation enter and blockage of Na+-channel and thereby preventing influx of Na+ no generation of AP conduction blockade  They block nerve conduction by reducing the permeability of Na ions during depolarisation
  • 10.  Should not be coadministered for nerve block in areas such as fingers and toes that are supplied with end-arteries because it may cause ischemia or necrosis  It should be used cautiously in patients in labour and in patients with thyrotoxicosis or cardiovascular disease.
  • 11.  Usually at range 7.6 – 8.9  Decrease in pH shifts equilibrium toward the ionized form, delaying the onset action.  Lower pH, solution more acidic, gives slower onset of action  Presence of Pus and inflammation will retard the action of LA. ( probably low acidic pH)
  • 12.  Most widely used Amide linked LA and most versatile ana.  Has variety of applications like Local, nerve block, spinal, epidural, IVRA.  When used locally action starts within 3 mts and causes vasodilatation.  Overdose causes muscle twitchings, convulsions, cardiac arrhythmias, fall in BP, coma, respiratory arrest.  Most popular ant arrhythmic drug
  • 13. • Standard agent for infiltrations, regional blocks or topical • Short onset time, intermediate duration of action • Class Ib antiarrhythmic properties • Medium toxicity • Maximal recommended dose: 3 mg/kg, 6 mg/kg with vasconstrictor
  • 14.  A potent long acting ---Amide linked LA available in India, most widely used allover.  Not used for IVRA but all others like local, spinal epidural blocks.  Action lasts for 2 to 3 hours. Strength for epidural is 0.25 to 0.5 % solution.  Has high lipid solubility, distributes more in tissues than in blood
  • 15.  It is similar to Bupivacaine  One of the metabolites are toxic and can cause Methamoglobinemia  Used for Nerve Blocks and IVRA.
  • 16.  Causes more sensory block, than motor block the advantage taken in during Caesarean Section. (Walking Epidural)  Bupivacaine is more prone to prolong QTc interval and induce ventricular tachycardia or Cardiac depression----( Membrane Stabilization action ) ( toxic doses and accidental entry into vessel)-should not be used for IVRA.  Longest acting LA available in India now.
  • 17. 1. Surface anesthesia 2. Infiltration anesthesia 3. Conduction block a. Field block b. Nerve Block 4. Spinal anesthesia 5. Epidural anesthesia 6. I V R A (Bier’s Block)
  • 18.  Amethocaine ---eye, throat, urethra, rectum and skin.  Benzocaine and Lidocaine hydrochloride—same --- except for eye.  Procaine is unsuitable as a surface ana. Because of its poor penetrating power  Lignocaine --4 % topical solution, 2 % Jelly 2 % vials for injections
  • 19.  Eutectic : Lowering of melting point of two solids when they are mixed.  combination of Lidocaine and Prilocaine.  For Pediatric purpose. It can penetrate intact skin.  I v .cannula inserting.  Split skin graft harvesting  Other superficial procedures.
  • 20.  Mech. of action : Nerve endings as exposed to the drug there by action.  Procaine, Lignocaine 2 % are used either with or without Adrenaline 1 : 2,00,000  C/I : blocking where end arteries are involved either for Penis, or for Digits, C A D patients.
  • 21.  Drug is injected close to the nerve or big nerve trunks eg. Brachial Block, Sciatic, Femoral Nerve, Radial, Ulnar Nerves.
  • 22.  LA is injected into the subarachnoid space. Injection is made heavy by adding dextrose or light by adding saline.  When the anesthetic in injected outside the dura, the technique is known as Epidural anesthesia.  Lignocaine, Bupivacaine the two agents most commonly used regularly in anesthesia practice.
  • 24.  Intravenous regional anesthesia  Agent of choice------ Lignocaine (Xylocaine )  20 to 40 ml of 0.5 % Lidocaine is used  Used for only for Upper Limb orthopedic surgeries and others on Up. Limb.
  • 25.  We have seen all Local actions of LA s  Systemic action when given IV : Bupivacaine is relatively more cardiotoxic , produces ventricular tachycardia or fibrillation.  Lidocaine has little effect on contractility and conductivity, used as antiarrhythmic.  The prominent cardiac action of Xylocaine is suppression of automaticity in ectopic foci.
  • 26.  Depression of function of CNS and CVS when high plasma concentrations are reached  CNS toxicity : usually before cardiovacular effects First signs of excitation due to initial blockade of inhibitory pathways mild: circumoral tingling, metallic taste, tinnitus, visual disturbance, slurred speech moderate: altered consicous state, convulsions Later sings of generalized CNS depression with potentially fatal toxicity: coma,respiratory arrest
  • 27.  1.Bradycardia, 2.Hypotension 3.Headache  4.Cauda Equina syndrome 5.Septic meningitis  EPIDURAL ANESTHESIA :  Here the drug is injected outside the dura. Drug spread is restricted to a specific region causes fewer complications.
  • 28.  Allergic reactions: common with ESTERS like Procaine, caused by para-aminobenzoic acid (also found to cause arachnoiditis), less common with AMIDES, then mostly through preservatives  Drug interactions: i.e. Anticholinesterases, other competing drugs hydrolyzed by Plasma CE  Attention with heavy sedation with anticonvulsants: may mask early signs of toxicity  Methaemoglobinaemia: after large doses Prilocaine