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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
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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
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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
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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
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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
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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
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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
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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
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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)
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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22. Cont.Cont.
Addition of vasoconstictorAddition of vasoconstictor
Red LA absorptionRed LA absorption
inc depthinc depth
inc durationinc duration
red toxicityred toxicity
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23. contcont
Site of injectionSite of injection
CarbonationCarbonation
Mixture of LAMixture of LA
Chloroprocaine & bupivacaineChloroprocaine & bupivacaine
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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
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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
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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
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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
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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
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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+ )
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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52. Thank youThank you
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