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Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
Local anaesthetis
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Local anaesthetis

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  • 1. LOCALLOCAL ANAESTHETICSANAESTHETICS INDIAN DENTAL ACADEMY Leader in continuing dental education www.indiandentalacademy.com www.indiandentalacademy.com
  • 2. Introduction.Introduction.  LA are drugs that produce reversibleLA are drugs that produce reversible depression of nerve impulse anddepression of nerve impulse and conduction when applied to nerve fibresconduction when applied to nerve fibres  The ester group of LA were first used inThe ester group of LA were first used in 1884 – cocaine for topical use in1884 – cocaine for topical use in opthalmologyopthalmology  Amino amide LA were manufactured inAmino amide LA were manufactured in 1943 – lidnocaine, since then many newer1943 – lidnocaine, since then many newer safer LA has been producedsafer LA has been produced www.indiandentalacademy.com
  • 3. IDEAL PROPERTIESIDEAL PROPERTIES  Physiochemical propertiesPhysiochemical properties  Easy to produce and economicalEasy to produce and economical  Stability during storageStability during storage  Easy aaccessibility; appropriate packaging andEasy aaccessibility; appropriate packaging and labellinglabelling  Formulation (where possible, additive free)Formulation (where possible, additive free)  Soluble in waterSoluble in water  Sterilisable by heat without decompositionSterilisable by heat without decomposition www.indiandentalacademy.com
  • 4. IDEAL PROPERTIES cont.IDEAL PROPERTIES cont.  PharmacokineticsPharmacokinetics  Ease of administrationEase of administration  Rapid onsetRapid onset  Duration appropriate to useDuration appropriate to use  Clearance independent of hepatic and renalClearance independent of hepatic and renal functionfunction  No active or toxic metabolitesNo active or toxic metabolites www.indiandentalacademy.com
  • 5. IDEAL PROPERTIES cont.IDEAL PROPERTIES cont.  PharmacodynamicsPharmacodynamics  High therapeutics ratioHigh therapeutics ratio  No hypersensitivity reactionNo hypersensitivity reaction  Absence of toxicity on : local tissue, liver, brain and otherAbsence of toxicity on : local tissue, liver, brain and other tissuetissue  Nervous depression, especially of sensory fibresNervous depression, especially of sensory fibres  Administration should be effective by topical application,Administration should be effective by topical application, injection near a nerve trunk or infiltrationinjection near a nerve trunk or infiltration  Specificity – only nerve tissue should be affectedSpecificity – only nerve tissue should be affected www.indiandentalacademy.com
  • 6. Chemistry and Structure ActivityChemistry and Structure Activity RelationshipRelationship  All typical LA contain h.philic and h.phobicAll typical LA contain h.philic and h.phobic domain that are separated by intermediate alkyldomain that are separated by intermediate alkyl chainchain  The h.philic grp usually tertiary amineThe h.philic grp usually tertiary amine  The h.phobic grp usually an aromatic residueThe h.phobic grp usually an aromatic residue  Intermediate bond is either of the ester or amideIntermediate bond is either of the ester or amide type – determines many of the properties of thetype – determines many of the properties of the agentagent www.indiandentalacademy.com
  • 7. Cont.Cont. Hydrophobic group Aromatic residue Hydrophilic group Tertiary amine Intermediate alkyl Intermediate alkyl www.indiandentalacademy.com
  • 8. Cont.Cont.  Intermediate chain = either ester or amideIntermediate chain = either ester or amide  Determines many of the properties of the agentDetermines many of the properties of the agent  Classification of LAClassification of LA  Changes to any part of the molecule lead toChanges to any part of the molecule lead to alteration in activity and tocxicityalteration in activity and tocxicity  Increase length of intermed. Alkyl group willIncrease length of intermed. Alkyl group will increase potency up to critical lengthincrease potency up to critical length  increaseincrease further will increase toxicityfurther will increase toxicity www.indiandentalacademy.com
  • 9. Cont.Cont.  Length of two terminal group are alsoLength of two terminal group are also equally importantequally important  Eg. Add butyl group to mepivacainEg. Add butyl group to mepivacain  bupivacainbupivacain  Inc. lipid solubilityInc. lipid solubility  Greater potencyGreater potency  Longer duration of actionLonger duration of action www.indiandentalacademy.com
  • 10. Mode of actionMode of action  All has similar MOAAll has similar MOA  Most LA bind to Na channels in the inactivated state,Most LA bind to Na channels in the inactivated state, preventing subsequent channel activation and the largepreventing subsequent channel activation and the large transient Na influx associated with mb depn.transient Na influx associated with mb depn.  Marked depression of rate of depnMarked depression of rate of depn  Failed to reach TPFailed to reach TP  no propogation of APno propogation of AP  neuralneural blockageblockage  LA act in their cationic form but most reach their site ofLA act in their cationic form but most reach their site of action by penetrating the nerve sheath and axonal mb asaction by penetrating the nerve sheath and axonal mb as unionized speciesunionized species www.indiandentalacademy.com
  • 11. Cont.Cont.  Some LA act bySome LA act by  Penetrating the mb, causing mb expansion andPenetrating the mb, causing mb expansion and channel distortion (analogous to the criticalchannel distortion (analogous to the critical volume hypothesis)volume hypothesis)  Partial penetration by LA of the axonal mb couldPartial penetration by LA of the axonal mb could increase the transmembrane potential and inhibitincrease the transmembrane potential and inhibit depn. (surface charge theory)depn. (surface charge theory) www.indiandentalacademy.com
  • 12. Differential sensitivity of nerve fibreDifferential sensitivity of nerve fibre classclass mylinationmylination diametediamete rr ConductioConductio nn velocityvelocity FunctionsFunctions AAαα heavyheavy 12-2012-20 70-12070-120 Motor and propioceptionMotor and propioception AAββ ModerateModerate 5-125-12 30-7030-70 Touch and pressureTouch and pressure AAχχ ModeratelyModerately 3-63-6 15-3015-30 Motor to muscle spindleMotor to muscle spindle AAδδ lightlylightly 2-52-5 12-3012-30 Pain, temperature, touchPain, temperature, touch BB lightlylightly 1-31-3 3-153-15 Preganglionic autonomicPreganglionic autonomic CC NoneNone nonenone 0.4-1.20.4-1.2 0.3-1.30.3-1.3 0.7-1.30.7-1.3 0.7-1.30.7-1.3 Pain & reflex responsePain & reflex response Postganglionic sympatheticsPostganglionic sympathetics www.indiandentalacademy.com
  • 13. Factors influenceFactors influence potency,speed of onset andpotency,speed of onset and duration of actionduration of action POTENCYPOTENCY  1.1. Lipophilic natureLipophilic nature = lipid solubility= lipid solubility  Inc. lipid solubility = inc potencyInc. lipid solubility = inc potency (penetrare mb more easily)(penetrare mb more easily)  less molecule required for nerve blockageless molecule required for nerve blockage  Inc alkyl substitution to aromatic ring andInc alkyl substitution to aromatic ring and amineamine  inc lipophilic natureinc lipophilic nature www.indiandentalacademy.com
  • 14. Cont.Cont.  2. Partition coefficient /2. Partition coefficient / vasodilatationvasodilatation  ? Lidocaine > potent than mepivicaine in? Lidocaine > potent than mepivicaine in vitrovitro  vasodilatationvasodilatation  Bupivacaine > Etidocaine in vivoBupivacaine > Etidocaine in vivo  inc fat uptakeinc fat uptake www.indiandentalacademy.com
  • 15.  2. SPEED OF ONSET2. SPEED OF ONSET  1. Unionized fraction / pKa & pH1. Unionized fraction / pKa & pH  Weak bases tend to be relatively ionized at highWeak bases tend to be relatively ionized at high concentration H+concentration H+  The uncharged form diffuse more readily acrossThe uncharged form diffuse more readily across nerve mbnerve mb  determine the onset of LAdetermine the onset of LA  Mechanism of ion trapping?Mechanism of ion trapping?  Onset of blockageOnset of blockage ∝∝ pKapKa www.indiandentalacademy.com
  • 16. Cont.Cont.  2. Fick’s Law of diffusion2. Fick’s Law of diffusion  DD ∝∝ A.Pc.(P1-P2)A.Pc.(P1-P2)  /MW.T/MW.T www.indiandentalacademy.com
  • 17. Cont.Cont.  3. Lipid solubility3. Lipid solubility  Its effect on onset is poorly understoodIts effect on onset is poorly understood  ?high lipid solubility?high lipid solubility  inc rate of diff andinc rate of diff and shorten onset time BUT it also incshorten onset time BUT it also inc solubility in the surrounding tissuesolubility in the surrounding tissue www.indiandentalacademy.com
  • 18. Cont.Cont.  4. Barrier eg. Nerve root4. Barrier eg. Nerve root  EpineuriumEpineurium  PerineuriumPerineurium  EndoneuriumEndoneurium  ! Subarachnoid block rapid onset because! Subarachnoid block rapid onset because nerve rootlets are almost completely barenerve rootlets are almost completely bare of fibrousof fibrous www.indiandentalacademy.com
  • 19. Cont.Cont.  SensitivitySensitivity ∝∝ 1/size1/size  Autonomic > sensory > motorAutonomic > sensory > motor  SmallSmall,, unmyelinatedunmyelinated medium, < myelinmedium, < myelin large, myelinatedlarge, myelinated  Order of blockage : B – C, Ad – Ag – Ab - AaOrder of blockage : B – C, Ad – Ag – Ab - Aa www.indiandentalacademy.com
  • 20. Cont.Cont.  Duration of blockageDuration of blockage  Protein binding regulate the duration ofProtein binding regulate the duration of anaesthetic activityanaesthetic activity  Due to protein binding of LA to protein receptorDue to protein binding of LA to protein receptor in the Na channel of nerve mbin the Na channel of nerve mb Highly protein bound will remain for a long timeHighly protein bound will remain for a long time ProcainProcain  6% protein bound6% protein bound Ropi, bupi, etidocaineRopi, bupi, etidocaine  94-96% prot. bound94-96% prot. bound www.indiandentalacademy.com
  • 21. Factors affecting anaesthetic activityFactors affecting anaesthetic activity  DosageDosage ∀ ↑↑ mass injected (vol x conc.)mass injected (vol x conc.)  Red onset timeRed onset time  Inc durationInc duration  Inc depthInc depth www.indiandentalacademy.com
  • 22. Cont.Cont.  Addition of vasoconstictorAddition of vasoconstictor  Red LA absorptionRed LA absorption  inc depthinc depth  inc durationinc duration  red toxicityred toxicity www.indiandentalacademy.com
  • 23. contcont  Site of injectionSite of injection  CarbonationCarbonation  Mixture of LAMixture of LA  Chloroprocaine & bupivacaineChloroprocaine & bupivacaine www.indiandentalacademy.com
  • 24. PHARMACOKINETICSPHARMACOKINETICS  Plasma concentration : depends onPlasma concentration : depends on   absorption kineticsabsorption kinetics   systemic disposition kineticssystemic disposition kinetics  DistributionDistribution  EliminationElimination   metabolismmetabolism   excretionexcretion www.indiandentalacademy.com
  • 25. Absorption of LAAbsorption of LA  Site of injection ( intercostal > caudal >Site of injection ( intercostal > caudal > brachial plexus etc )brachial plexus etc )  Dosage (blood level of LA related to totalDosage (blood level of LA related to total dose of drug rather than spesific volumedose of drug rather than spesific volume or concentration of solutionor concentration of solution  Addition of vasoconstrictorAddition of vasoconstrictor  Disease processDisease process www.indiandentalacademy.com
  • 26. Systemic disposition kineticsSystemic disposition kinetics  Ultimate plasma conc. Of LA is determined byUltimate plasma conc. Of LA is determined by rate of tissue distribution and rate of clearancerate of tissue distribution and rate of clearance (metabolism and excretion ) of the drug(metabolism and excretion ) of the drug  Distribution depends onDistribution depends on  Tissue perfusion ( alpha and beta phase)Tissue perfusion ( alpha and beta phase)  Tissue/blood partision coefficientTissue/blood partision coefficient  Tissue massTissue mass • Lung extract significant amount of LALung extract significant amount of LA www.indiandentalacademy.com
  • 27. Cont.Cont.  Placental transferPlacental transfer  Protein binding ( lidocaine > bupivacaine XProtein binding ( lidocaine > bupivacaine X placental )placental )  Acidosis in fetus ( ion trapping )Acidosis in fetus ( ion trapping )  Ester LA – rapid hydrolysis not available to crossEster LA – rapid hydrolysis not available to cross placental in significant amountplacental in significant amount  ClearanceClearance  Mainly hepatic metabolismMainly hepatic metabolism  Minimal renal excretionMinimal renal excretion www.indiandentalacademy.com
  • 28. Metabolism of LAMetabolism of LA  A. ESTERSA. ESTERS  Rapid hydrolysis by plasma cholinesteraseRapid hydrolysis by plasma cholinesterase  Water soluble metabolites excreted in the urineWater soluble metabolites excreted in the urine (p-aminobenzoic, diethylaminoethanol(p-aminobenzoic, diethylaminoethanol  Abnormal pseudocholinesteraseAbnormal pseudocholinesterase  inc risk ofinc risk of toxic side effecttoxic side effect  CSF lack of esterase enzymeCSF lack of esterase enzyme  Exception Cocain - partially metabolized in liverException Cocain - partially metabolized in liver and partially excreted in urine unchangedand partially excreted in urine unchanged www.indiandentalacademy.com
  • 29. Cont.Cont.  B. AMIDEB. AMIDE  Enzymatic degradation in liver by microsomalEnzymatic degradation in liver by microsomal enzymes (prilocaine > lidnocaine > mepivacaineenzymes (prilocaine > lidnocaine > mepivacaine > bupivacaine and etidocaine )> bupivacaine and etidocaine )  Much slower than ester hydrolysisMuch slower than ester hydrolysis  N-dealkylation, aromatic and amide hydrolysisN-dealkylation, aromatic and amide hydrolysis  Decrease hepatic function or hepatic blood flowDecrease hepatic function or hepatic blood flow reduce metabolic ratereduce metabolic rate  pred systemic toxicitypred systemic toxicity  Very little drug excreted unchanged by kidneyVery little drug excreted unchanged by kidney www.indiandentalacademy.com
  • 30. Cont.Cont.  Metabolite of prilocaine (o-toluidine ) whichMetabolite of prilocaine (o-toluidine ) which accumulate after large dose (>10mg/kg) convertaccumulate after large dose (>10mg/kg) convert hemoglobin to methemoglobinhemoglobin to methemoglobin  Prilocaine epidural labourPrilocaine epidural labour  Benzocaine also may causeBenzocaine also may cause methemoglobinemiamethemoglobinemia  Tx iv methylene blue @ 1-2 mg/kg of 1% over 5Tx iv methylene blue @ 1-2 mg/kg of 1% over 5 minutesminutes  reduce methemoglobin ( Fe3+ ) toreduce methemoglobin ( Fe3+ ) to hemoglobin ( Fe2+ )hemoglobin ( Fe2+ ) www.indiandentalacademy.com
  • 31. contcont  RenalRenal  Poor water solubility of LA – limit renalPoor water solubility of LA – limit renal excretion of unchange drug to < 5% ofexcretion of unchange drug to < 5% of injected dose (except cocain 10-12%injected dose (except cocain 10-12% urine)urine)  Water soluble metabolites para-Water soluble metabolites para- aminobenzoic acid readily excreted in theaminobenzoic acid readily excreted in the urineurine www.indiandentalacademy.com
  • 32. Side effectsSide effects  Toxicity often directly proportionate to itsToxicity often directly proportionate to its potencypotency  Mixture of LA roughly give additive toxicMixture of LA roughly give additive toxic effecteffect  In addition to blocking transmission in theIn addition to blocking transmission in the nerve axon, LA affect all tissue wherenerve axon, LA affect all tissue where conduction of impulse occur, therefore inconduction of impulse occur, therefore in  The CNSThe CNS  Autonomic gangliaAutonomic ganglia  The NMJThe NMJ  All form of muscle fibre, esp cardiacAll form of muscle fibre, esp cardiac www.indiandentalacademy.com
  • 33. CVSCVS  Affect both myocardium and peripheralAffect both myocardium and peripheral vascular smooth musclevascular smooth muscle  Primary site is myocardium once absorbedPrimary site is myocardium once absorbed  Effects :Effects : ↓↓conduction, contractility andconduction, contractility and excitabilityexcitability  CVS effect are seen atCVS effect are seen at ↑↑ dose, when CNSdose, when CNS effects are already evidenteffects are already evident  Inadvertent iv adm may lead to suddentInadvertent iv adm may lead to suddent death !VF, it is more likely if soln containdeath !VF, it is more likely if soln contain adrenalinadrenalin www.indiandentalacademy.com
  • 34. Cont.Cont.  At Tx conc lidocaine cause no ECG changeAt Tx conc lidocaine cause no ECG change  ↑↑ to toxic level, prolonged conductionto toxic level, prolonged conduction  ↑↑PRPR and QRS intervaland QRS interval  VeryVery ↑↑suppress SANsuppress SAN  sinus brady/arrestsinus brady/arrest and alsoand also ↓↓AVNAVN  AV blockAV block ± dissociation± dissociation  Cardiac toxicity of bupivacaine ppt VFCardiac toxicity of bupivacaine ppt VF  Bupivacaine markedly depress dV/dtBupivacaine markedly depress dV/dt  Slow rate of recoverySlow rate of recovery  arrhytmiasarrhytmias  Produce direct pulm vasoconstrictive effectProduce direct pulm vasoconstrictive effect www.indiandentalacademy.com
  • 35. ContCont  Most LA cause biphasic peripheralMost LA cause biphasic peripheral arteriolar response, with initialarteriolar response, with initial vasoconstriction then vasodilatationvasoconstriction then vasodilatation  As doseAs dose ↑↑ action change to inhibition/Vdilaction change to inhibition/Vdil  Cocaine produce vasoconstriction at mostCocaine produce vasoconstriction at most doses, inhibit noradrenalin uptake bydoses, inhibit noradrenalin uptake by tissue binding sitetissue binding site www.indiandentalacademy.com
  • 36. RESPIRATORYRESPIRATORY  Depress hypoxic driveDepress hypoxic drive  Apnoea can result from phrenic and IC nerveApnoea can result from phrenic and IC nerve paralysis or depression of medulla RCparalysis or depression of medulla RC  LA relax bronchial smooth muscleLA relax bronchial smooth muscle  Iv lidocaine 1.5 g/kg red reflex b/constrictionIv lidocaine 1.5 g/kg red reflex b/constriction upon intubationupon intubation  Occationally direct LA aerosolOccationally direct LA aerosol  b/spasmb/spasm www.indiandentalacademy.com
  • 37. NEUROLOGICALNEUROLOGICAL  Earliest signs are circumoral and tongue numbness,Earliest signs are circumoral and tongue numbness, tinnitus, nystagmus and dizzinesstinnitus, nystagmus and dizziness  Following absorption, all nitrogenous LA cause CNSFollowing absorption, all nitrogenous LA cause CNS excitationexcitation  Restlessness, tremor, eventually tonic-clonic fitsRestlessness, tremor, eventually tonic-clonic fits  CNS stimulation then followed by depressionCNS stimulation then followed by depression  Death usually d/t subsequent respiratory depressionDeath usually d/t subsequent respiratory depression  Both stimulation and depression are thought to be d/tBoth stimulation and depression are thought to be d/t neuronal depressionneuronal depression  ↓↓ in inhibitory p/w in ARAS being responsible for thein inhibitory p/w in ARAS being responsible for the excitatory effectsexcitatory effects  Ventilatory support may be req. laterVentilatory support may be req. later  Convultion can be controlled by barbiturate egConvultion can be controlled by barbiturate eg diazepamdiazepam www.indiandentalacademy.com
  • 38. Cont.Cont.  Factors affecting the occurance ofFactors affecting the occurance of CNS toxicity:CNS toxicity:  Relative toxicityRelative toxicity  approx LA potencyapprox LA potency  Rate of injectionRate of injection  r[plasma] achievedr[plasma] achieved  pCO2pCO2  inversely related to fit thresholdinversely related to fit threshold  pHpH ↓↓pHpH  ↓↓fit thresholdfit threshold www.indiandentalacademy.com
  • 39. IMMUNOLOGICALIMMUNOLOGICAL  True allergy to LA are uncommonTrue allergy to LA are uncommon  Ester are more likely – ester derivativeEster are more likely – ester derivative para aminobenzoic acid is a knownpara aminobenzoic acid is a known allergenallergen  Amide often contain methylparaben asAmide often contain methylparaben as additive – structure similar to PABAadditive – structure similar to PABA  LA may inhibit neutrophil fx andLA may inhibit neutrophil fx and theoritically may retard wound healingtheoritically may retard wound healing www.indiandentalacademy.com
  • 40. MUSCULOSKELETALMUSCULOSKELETAL  Direct inj into skeletal muscleDirect inj into skeletal muscle  LA areLA are myotoxicmyotoxic  Histopathologically cause myofibrilHistopathologically cause myofibril hypercontractionhypercontraction  lytic degenerationlytic degeneration  oedemaoedema  necrosisnecrosis www.indiandentalacademy.com
  • 41. HEMATOLOGICALHEMATOLOGICAL  Lidocaine demonstrate redn coagulationLidocaine demonstrate redn coagulation (prevent thrombosis and platelet(prevent thrombosis and platelet aggregation) and enhance fibrinolysisaggregation) and enhance fibrinolysis  Lower incident of embolic event in patientLower incident of embolic event in patient receiving epidural anaesthesiareceiving epidural anaesthesia www.indiandentalacademy.com
  • 42. ContCont  Plasma lignocaine concentration (Plasma lignocaine concentration ( µµg/ml)g/ml)    CVS collapse------------------------26 --CVS collapse------------------------26 --          Respiratory arrest------------------20 --Respiratory arrest------------------20 --          Coma--------------------------------15 ---Coma--------------------------------15 ---      Unconsciousness------------------12 ---Unconsciousness------------------12 ---  Convulsions------------------------10 ---Convulsions------------------------10 ---  Muscular twitching--------------- -8 ----Muscular twitching--------------- -8 ----  Visual disturbance-----------------6 ----Visual disturbance-----------------6 ----  4 positive inotrophy4 positive inotrophy  Light headedness,tinnitus-------- 2 -- } anticonvulsantLight headedness,tinnitus-------- 2 -- } anticonvulsant  Circumoral&tongue numbness 0 antiarrhytmicCircumoral&tongue numbness 0 antiarrhytmic www.indiandentalacademy.com
  • 43. Drug interactionDrug interaction  Non depolarising muscle relaxant blockade isNon depolarising muscle relaxant blockade is potentiated by LApotentiated by LA  Concurrent administration of succinylcholine andConcurrent administration of succinylcholine and an ester LA may potentiate the effect of bothan ester LA may potentiate the effect of both drugs (pseudocholinesterase dependant)drugs (pseudocholinesterase dependant)  Dibucaine inhibit pseudocholinesteraseDibucaine inhibit pseudocholinesterase  Cimetidine and propanolol red liver blood flowCimetidine and propanolol red liver blood flow and lidocaine clearanceand lidocaine clearance  Opiods andOpiods and aa2 agonist potentiate LA pain relief2 agonist potentiate LA pain relief www.indiandentalacademy.com
  • 44. ContraindicationContraindication  Allergy/hypersensitivity to LA / sol. AdditivesAllergy/hypersensitivity to LA / sol. Additives  Adrenalin is contraindicated forAdrenalin is contraindicated for  Tachycardia! (thyrotoxicosis,CCF,IHD)Tachycardia! (thyrotoxicosis,CCF,IHD)  Anesthesia around end arteriesAnesthesia around end arteries  Iv regional anaesthesiaIv regional anaesthesia  Epidural/spinal anaesthesia in the presence ofEpidural/spinal anaesthesia in the presence of significantsignificant  Hypotention/hypovolaemiaHypotention/hypovolaemia  CoagulopathyCoagulopathy  Presence of local tissue sepsisPresence of local tissue sepsis  Patient refusalPatient refusal www.indiandentalacademy.com
  • 45. PrecautionsPrecautions  Resuscitation equipment and drugs should be availableResuscitation equipment and drugs should be available  Reliable iv accessReliable iv access  Injection should follow aspiration TRO iv injInjection should follow aspiration TRO iv inj  Lowest effective dose possibleLowest effective dose possible  Careful in pt withCareful in pt with  Pre-existing CNS & cardiac disorderPre-existing CNS & cardiac disorder  Cardiac glycoside toxicityCardiac glycoside toxicity  Hepatic or renal impairmentHepatic or renal impairment  Pred to malignant hyperthermiaPred to malignant hyperthermia  PorphriaPorphria  Fetal bradycardia after Xcess maternal adm with subsequentFetal bradycardia after Xcess maternal adm with subsequent hypoxia and acidosishypoxia and acidosis  Retrobulbar block have been a/w respiratory areestRetrobulbar block have been a/w respiratory areest www.indiandentalacademy.com
  • 46. lidocainelidocaine pKa 7.85pKa 7.85 Plain aq solution 1, 1.5, 2% @ pH 5-7Plain aq solution 1, 1.5, 2% @ pH 5-7 Solution with adrenalin @ pH 3-4.5Solution with adrenalin @ pH 3-4.5 Ralative potency 2Ralative potency 2 T1/2T1/2ß adult 1.8 hr, neonate 2hrß adult 1.8 hr, neonate 2hr Xtremely stableXtremely stable Max dose : plain 3mg/kg, adrenalin 7mg/kgMax dose : plain 3mg/kg, adrenalin 7mg/kg E.A. of 400mg/70kg @ [blood] = 2-4ug/mlE.A. of 400mg/70kg @ [blood] = 2-4ug/ml Toxicity begin @5 ug/mlToxicity begin @5 ug/ml Relatively quickly absorbed from GITRelatively quickly absorbed from GIT Metab in liver (dealkylation)Metab in liver (dealkylation)  excreted urineexcreted urine Toxic dose lead to death by VF or cardiac arrestToxic dose lead to death by VF or cardiac arrest Suitable for surface, infiltration,nerve block, caudal, epidural and SASuitable for surface, infiltration,nerve block, caudal, epidural and SA www.indiandentalacademy.com
  • 47. BupivacaineBupivacaine  pKa 8.1pKa 8.1  Plain aq soln .25, .375, .5% @ pH 4.5-6Plain aq soln .25, .375, .5% @ pH 4.5-6  If with adrenalin pH 3.5-5.5If with adrenalin pH 3.5-5.5  Potency 8Potency 8  Protein binding 95%Protein binding 95%  > lipid solubility than lidocaine> lipid solubility than lidocaine  T1/2T1/2ß adult 3.5hr, neonate 8.1-14hrß adult 3.5hr, neonate 8.1-14hr  Amide link LAAmide link LA  Prod prolonged anaesthesia with slower onsetProd prolonged anaesthesia with slower onset  Add adrenalin -Add adrenalin - ↓↓toxicity, h/e no change in durationtoxicity, h/e no change in duration  Post op analgesia : IC 7hr, EA 3-4hrPost op analgesia : IC 7hr, EA 3-4hr  Epid/caudal peak [plasma] 30-45 minEpid/caudal peak [plasma] 30-45 min  Lower foetal/maternal ratio cf lidnocaine (! Protein binding)Lower foetal/maternal ratio cf lidnocaine (! Protein binding)  Max dose : plain/with adrenalin 2 mg/kgMax dose : plain/with adrenalin 2 mg/kg www.indiandentalacademy.com
  • 48. RopivacaineRopivacaine  Chemical analogue of bupivacaineChemical analogue of bupivacaine  The molecule is designed to modify the spesificThe molecule is designed to modify the spesific cardiotoxicity associated with bupivacainecardiotoxicity associated with bupivacaine  pKa 8.2 and pH solution 5.5-6.0pKa 8.2 and pH solution 5.5-6.0  Equally potent as bupivacaineEqually potent as bupivacaine  Its quality of clinical block appear to be veryIts quality of clinical block appear to be very similar in onset, duration and quality that ofsimilar in onset, duration and quality that of bupivacainebupivacaine  No spesific toxicity has been detectedNo spesific toxicity has been detected www.indiandentalacademy.com
  • 49. CocaineCocaine  From leaves of erytroxylon coca – is an ester of benzoicFrom leaves of erytroxylon coca – is an ester of benzoic acidacid  CNS stimulant. At low dose produce euphoria. HigherCNS stimulant. At low dose produce euphoria. Higher dose cause convulsion, coma, medullary depressant anddose cause convulsion, coma, medullary depressant and deathdeath  Stimulate vomiting centreStimulate vomiting centre  Block reuptake of catecholamineBlock reuptake of catecholamine  enhance SNSenhance SNS activityactivity  Small dose may cause bradycardia d/t central vagalSmall dose may cause bradycardia d/t central vagal stimulationstimulation  Larger dose cause tachycardia, inc TPR andLarger dose cause tachycardia, inc TPR and hypertentionhypertention  larger may produce myocardiallarger may produce myocardial depression, VF and deathdepression, VF and death www.indiandentalacademy.com
  • 50. contcont  May be used as surface anaesthesiaMay be used as surface anaesthesia  As topical LA in ENT (5%)As topical LA in ENT (5%)  Cocain itself constrict blood vessel and theCocain itself constrict blood vessel and the use of adrenalin is contraindicated as ituse of adrenalin is contraindicated as it sensitises the myocardiumsensitises the myocardium www.indiandentalacademy.com
  • 51. Uses of LAUses of LA  Surface anaesthesiaSurface anaesthesia  Infiltration anaesthesiaInfiltration anaesthesia  Nerve block anaesthesia (peripheral,plexus)Nerve block anaesthesia (peripheral,plexus)  Intravenous regional anaesthesiaIntravenous regional anaesthesia  Spinal/subarachnoid anaesthesiaSpinal/subarachnoid anaesthesia  Other uses (antiarrhytmic, reduction in ICP,Other uses (antiarrhytmic, reduction in ICP, Blunting of CVS responses to intubation andBlunting of CVS responses to intubation and extubationextubation www.indiandentalacademy.com
  • 52. Thank youThank you For more details please visitFor more details please visit www.indiandentalacademy.comwww.indiandentalacademy.com www.indiandentalacademy.com

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