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Local Anesthetics
Dr.K.R.Prabhakar
Asst.Professor
Introduction
 LA reversibly block the impulse conduction.
 Transient loss of sensation in area of contact.
 Used for performing minor surgeries.
 Neither cause unconsciousness nor need proper
maintenance of vital functions during surgery.
 Mixed nerve- not only sensory but also motor
impulses are interrupted.
 Results in muscular paralysis and loss of
autonomic control as well.
Susceptibility of nerve fibers to LA
blockade
 Differs on the basis of size & myelination.
 Small unmyelinated C&B fibers blocked first.
 Pain, temp & touch sensation are blocked
first.
 Proprioception disappears in succession.
 Small typeA-delta fibers(myelin) are blocked
next.
 Heavily myelinated A-α, β & ɣ fibers blocked
last.
 Skeletal muscle tone is lost in the end.
 Recovery takes place in reverse order.
Classification
Amide type
Long acting
 Bupivacaine
 Levo-Bupivacaine
 Ropivacaine
 Dibucaine
Intermediate acting
 Lidocaine
(lignocaine)
 Mepivacaine
 Prilocaine
 Articaine
Ester type
Long acting
 Tetracaine
(amethocaine)
Intermediate acting
 Cocaine
Short acting
 Procaine
 Chloroprocaine
 Benzocaine
 Proparacaine
Miscellaneous
 Pramoxine (pramocaine)
 Dyclonine
 Oxethazaine (mucaine)
Mechanism of action
 LA molecules consist of an aromatic part
liked by an ester or amide bond to a basic
amine side chain.
 LA are weak bases
 Remain partly ionized at physiological pH.
 Unionized form penetrates the N membrane.
 In axon- ionized form of LA is active at
receptor site.
 LA block the voltage gated Na+ channels..
 Blocking action is favored by repetitive
stimulation- voltage dependence.
 Activation gate (AG) on extracellular site.
 Inactivation gate (IG) on intracellular site.
 These gates are called voltage sensors.
 Voltage sensors movement is regulated by
conformational change due to voltage
gradient.
Effect of pH on LA action
 LA action is strongly pH dependent.
 Partly ionized & partly unionized at physiolog
pH.
 Unionized form diffuses through axon.
 Inside axon it is ionized to cationic form BH+
 LA are less effective in infected tissue due to-
1. Acidic pH
2. ↑Blood supply at inflamed site.
3. Effectiveness of Adr ↓ at inflamed site.
4. Inflammatory products may oppose LA
action.
Prolongation of action by
vasoconstrictors
 Drugs that delays absorption of LA in to
circulation will prolong its action & reduce
systemic toxicity.
 Adrenaline (1:100,000 to 1: 200,000) in
dentistry (1:50,000 to 1: 100,000) MC used
with LA- doubles the duration of LA action.
 Vasoconstrictor shouldn’t be used for N block
of an extremity or end organs e.g. on fingers,
toes, nose & penis.
 One ampoule of 1:1000 adrenaline in 1 ml volume.
 This equals 1mg in 1 ml
 This equals 1000 μg/ml

 If one ampoule is diluted to 10ml
 This equals 0.1 mg/ml
 This equals 100 μg/ml
 This is 1:10,000 adrenalin

 If one ampoule is diluted to 100ml
 This equals 0.01 mg/ml
 This equals 10 μg/ml
 This is 1:100,000 adrenalin
 Adr can cause cardiac complications.
 Felypressin can be used as an
alternative.
 Preferable in pts with cardiovascular
diseases.
 Alternatively prilocaine can be used.
Systemic actions
C.N.S
 Stimulation followed by depression.
Symptoms of overdose with clinically used LAs
are-
 Circumoral numbness,
 Abnormal sensation in the tongue,
 Dizziness, blurred vision, tinnitus followed by
 Drowsiness, dysphoria and lethargy.
 Still higher doses produce excitation,
restlessness, agitation, muscle twitching,
seizures and finally unconsciousness.
cvs
Heart
 No significant effects at conventional doses.
 High doses- LAs are cardiac depressants.
 Decrease automaticity, excitability,
contractility, conductivity and prolong ERP.
 Quinidine like antiarrhythmic action.
 Procainamide is a class IA antiarrhythmic.
 QTc interval is prolonged and LAs can induce
cardiac arrhythmias
 Bupivacaine is relatively more cardiotoxic
 Lidocaine used as an antiarrhythmic.
Blood vessels
 ↓ BP due to sympathetic blockade
 High conc locally- direct relaxation of arterial
SM.
 Bupivacaine> Lidocaine> prilocaine
 Toxic doses of LAs- cardiovascular collapse.
 Cocaine has sympathomimetic property;
 ↑sympathetic tone, causes local
vasoconstriction, marked rise in BP and
Pharmacokinetics
 Ester/amide bond in LA governs its
metabolism & ability to cause hypersensitivity
reactions.
 Ester LA are hydrolysed by plasma esterases
& liver esterases.
 Spinal fluids contain negligible esterases.
 Amide LA are degraded by hepatic
microsomes by N-dealkylation & hydrolysis.
 Hypersensitivity more common with ester Las.
 First pass metabolism is significant for both
procaine & lidocaine, not used orally in
arrhythmias
Adverse effects
CNS
Low doses
 Tongue numbness
 Sleepiness
 Mild headache
 Visual & auditory disturbances
High doses
 Nystagmus & muscle twitching.
 Convulsions
 Cocaine- long lasting CNS stimulation &
euphoria.
CVS
 Bradycardia,
 Hypotension,
 Cardiac arrhythmias and
 Vascular collapse
Blood
 Orthotoludine – metabolite of prilocaine.
 Oxidises Hb to metHb, ↑levels cause
cyanosis.
 Rx- reducing agents like methylene blue or
ascorbic acid I.V to convert metHb to Hb.
Allergic reactions
 Ester LA are metabolized to PABA derivatives
.
 Responsible for allergic reactions.
1. Rashes,
2. Angioedema,
3. Dermatitis,
4. Contact sensitization,
5. Asthma and
6. Rarely anaphylaxis occur.
 Methylparaben added as preservative in
certain LA solutions is responsible for allergic
Precautions and interactions
 Pts on propranolol are very sensitive to
pressor responses of Adr- unopposed 1
action.
 Drugs with 1blocking property may lead to
hypotension if co-administered with L+A.
 Pts on acute alcohol intoxication need higher
doses of X+A.
 In pts on digoxin- accidental I.V inj of Adr
cause arrhythmias.
 Propranolol can lead to xylocaine toxicity due
to-
1. Inhibition of metabolic oxidation of xylocaine.
Amide group
Long duration
Bupivacaine & Levo-Bupivacaine (4>lignocaine)
0.25-0.5%
Uses: nerve block, epidural & spinal anesthesia
 More sensory than motor block.
 Least placental transmission- painless delivery.
 Intermediate onset of action.
 Shouldn’t be used for IV regional analgesia or
obstetrical paracervical block anesthesia.
Toxicity
 Cardiotoxic- prolongs QTc interval- VT & VA.
 Blocks Na channels both in systole &
diastole.
 Aggrevated by acidosis & hypoxemia.
 Levo-bupivacaine equally potent but less
toxic.
Ropivacaine (equipotent to bupivacaine)
Uses: infiltration, epidural & regional
anesthesia.
 Continous epidural used for relief of post op
& labor pain.
 Less cardiotoxic & more motor sparing than
bupi.
 Intermediate onset of action.
Toxicity
 Available as S-sterioisomer-
 Less affinity for cardiac Na+ channels.
 R-isomer is toxic.
Dibucaine (Cinchocaine)
 Very potent, longest acting LA.
 Slow onset of action.
Use: surface anesthetic in anal canal & rectum.
 Ocasionally for SA of longer duration. Rarely
used
Toxicity
 More toxic than bupivacaine
Other uses
 Pseudocholinesterase inhibitor.
 Used for dibucaine number test.
 Normal dibucaine number is 80.
Medium duration
Lidocaine (Lignocaine) or Xylocaine
 Most widely used multipurpose LA
Uses:
 Topically on mucous membrane- Aq.sol, jelly
etc.
 Infiltration, nerve block & epidural anesthesia.
 Spinal analgesia- high conc 5% made
hyperbaric with 7.5% dextrose is used.
 Rapid onset of action, lasts for 1-2 hrs.
 Opiods are synergistic for intrathecal &
epidural.
 Transdermal patch- for post herpetic
Toxicity
 CNS: dizziness, paresthesia & euphoria.
 High doses- confusion, vertigo, tinnitus &
nausea.
 Severe toxicity ppt seizures.
 Overdose- arrhythmias, ↓BP, coma, resp
arrest.
 Propranolol enhances toxicity by ↓
clearance.
Other uses
 Ventricular arrhythmias during MI.
Mepivacaine (50% potent as lignocaine)
 Similar to lidocaine
 Not effective as topical anesthetic.
 Can be used without epinephrine.
Articaine (almost equipotent to lidocaine)
 Rapid onset of action (5min)
 Recently approved for dental & periodontal
procedures. Contains epinephrine.
 Also used for spinal & epidural anesthesia
 Mainly metabolized by liver, partly by plasma
cholinesterase.
Prilocaine (equipotent to lidocaine)
Uses: mostly for dental procedures.
 Administered by infiltration or nerve block.
 Can be used without epinephrine.
Toxicity
 Similar to lidocaine
 Metabolite orthotoludine
causes metHb.
 CI in obstetric practice.
Eutectic lidocaine/prilocaine
 Anaesthetise intact skin after surface
application.
 Eutectic mixture refers to lowering of melting
point of two solids when they are mixed.
 Lidocaine and prilocaine are mixed in equal
proportion at 25°C.
 The resulting oil is emulsified into water to
form a cream
Use:
 Applied under occlusive dressing for 1 hr
before
1. I.V. cannulation,
2. Split skin graft harvesting and
3. Other superficial procedures.
 Anaesthesia up to a depth of 5 mm lasts for
1–2 hr after removal.
 It has been used as an alternative to
lidocaine infiltration.
 PRILOX 5% cream.
Ester group
Long duration
Tetracaine or Amethocaine (4> lignocaine)
Uses: topically on eye, nose, troat &
tracheobronchial tree.
 Eye: no effect on pupil, accomdation & IOP.
 Very suitable for SA of long duration.
 Onset of action is slow.
Toxicity:
 Slowly metabolized
 Being PABA ester may antaonise-
sulfonamides.
 I.V doses may produce arrhythmias.
Medium duration
Cocaine (50% potent as lidocaine)
 Earlier it was used as ocular anesthetic.
 Vasoconstrictor, Adr not necessary.
 Protoplasmic poison, causes necrosis on
injection.
Toxicity
 CNS stimulant- euphoria, delays fatigue,
strong psychological dependence
 Bradycardia, ↑BP, ↑temp
 Nausea & vomiting
Short duration
Procaine (25% potent as lidocaine)
 No longer used
 Slow onset of action, Ineffective topically
Toxicity
 Bradycardia, vasodilation, ↓CO.
 Anxiety, restlessness & shivering.
 Hydrolysed to PABA
Other uses
 Procaine + Benzylpenicillin= procaine
penicillin
 Procainamide- class IA antiarrhythmic.
Chloroprocaine (slightly > procaine)
 Better & safer than procaine.
 Use: infiltration, nerve block, caudal &
epidural block.
 Rapid onset of action.
 Not effective topically.
 Less toxic than procaine.
Benzocaine & Proparacaine
 Used as topical (surface) anesthetics.
 Included in preparations of ointment, lozenges
& suppositories- ulcer, sore throat &
inflammation.
 Proparacaine preferred in minor ocular
procedures. Non irritant & less antigenic.
Toxicity
 PABA derivatives- antagonize sulfonamides.
 Too toxic for injection
Miscellaneous group
Uses and techniques of LA
Surface anaesthesia
 Applied topically on mucous membranes and
abraded skin.
 Superficial layer is anaesthetised and motor
function not affected.
 Onset and duration -site, the drug, conc and
form.
 Lidocaine (10%) sprayed in the throat acts in
2–5 min and produces anaesthesia for 30–45
min.
 Adr no affect on duration of topical
anaesthesia.
 Phenylephrine can cause mucosal
vasoconstrion.
 Absorption of soluble LAs from mucous
membranes is rapid, may attain IV conc.
 Eutectic lidocaine/prilocaine is capable of
anaesthetizing intact skin.
Sites & uses of SA
Infiltration anaesthesia
 Dilute sol of LA is injected under the skin to
reach sensory nerve terminals.
 Uses; minor surgical procedures like incisions
& excisions.
 Onset of action is almost immediate.
 Duration:lidoc 30-60 min, bupiva 90-180 min.
 Motor function is not affected.
Conduction block anesthesia
 LA injected around the nerve trunk.
 Area distal to injection site is anesthetized &
paralysed.
 Lidocaine (1–2%) with intermediate duration
of action is most commonly used,
 Longer lasting anaesthesia bupivacaine may
be selected.
Two types
 Field block
 Nerve block
Field block
 LA is injected SC in a manner that all nerves
coming to a particular field are blocked.
 Uses: herniorrhaphy, appendicectomy, dental
procedures, scalp stitching, operations on
forearms and legs, etc.
 Larger area beginning 2–3 cm distal to the
line of injection can be anaesthetised with
lesser drug compared to infiltration.
 The same concentration of LA as for
infiltration is used for field block.
Nerve block
 LA injected around the appropriate nerve
trunks or plexuses.
 Latency of anaesthesia depends on the
drug and the area to be covered.
 Frequently performed nerve blocks are—
lingual, intercostal, ulnar, sciatic, femoral,
brachial plexus, trigeminal, facial, phrenic,
etc.
 Used for tooth extraction, operations on
eye, limbs, abdominal wall, fracture setting,
trauma to ribs, neuralgias, persistent
hiccup, etc
Spinal anaesthesia
 LA is injected in the subarachnoid space
between L2–3 or L3–4.
 Nerve roots in the cauda equina are targeted.
 Adr may be enhancing spinal anaesthesia by
reducing spinal cord blood flow or
 By its own analgesic effect exerted through
spinal α2 adrenoceptors.
 Intrathecal clonidine, an α2 agonist, produces
spinal analgesia by itself.
 Spinal anaesthesia is used for operations on
the-lower limbs, pelvis, lower abdomen, e.g.
prostatectomy,
 Fracture setting, obstetric procedures,
caesarean section, etc
 Advantages of spinal anaesthesia over GA
are:
(i) It is safer.
(ii) Produces good analgesia and muscle
relaxation
without loss of consciousness.
(iii) Cardiac, pulmonary, renal disease and
diabetes pose less problem
Complications of spinal anaesthesia
Respiratory paralysis
 Due to Hypotension and ischaemia of
respiratory centre.
Hypotension
 due to blockade of sympathetic outflow to
blood vessels & venous pooling.
 Raising the foot end overcomes the
hypotension.
 Prevented by ephedrine, mephentermine.
Headache
Septic meningitis
Cauda equina syndrome
 Prolonged loss of control over bladder and
bowel sphincters.
 It may be due to traumatic damage to nerve
roots or chronic arachnoiditis caused by
 inadvertent introduction of the antiseptic or
particulate matter in the subarachnoid space.
Nausea and vomiting
 Due to reflexes triggered by traction on
abdominal viscera.
 Premedication with opioid analgesics prevents
it.
Epidural anaesthesia
 LA injected in dural space, acts on nerve
roots.
Thoracic
 Injection is made in the midthoracic region.
 Epidural space in this region is relatively
narrow.
 Analgesia obtained in middle and lower
thoracic dermatomes.
Lumbar
 epidural space is wide.
 Produces anaesthesia of lower abdomen,
pelvis and hind limbs.
 Use is similar to that of spinal anaesthesia.
Caudal
 Injection is given in the sacral canal through
the sacral hiatus.
 Produces anaesthesia of pelvic and perineal
region.
 Used mostly for vaginal delivery, anorectal and
genitourinary operations.
Complications
 Cardiovascular complications are similar to
spinal.
 Headache & neurological complications are
less.
Intravenous regional anaesthesia

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Local anesthetics

  • 2. Introduction  LA reversibly block the impulse conduction.  Transient loss of sensation in area of contact.  Used for performing minor surgeries.  Neither cause unconsciousness nor need proper maintenance of vital functions during surgery.  Mixed nerve- not only sensory but also motor impulses are interrupted.  Results in muscular paralysis and loss of autonomic control as well.
  • 3. Susceptibility of nerve fibers to LA blockade  Differs on the basis of size & myelination.  Small unmyelinated C&B fibers blocked first.  Pain, temp & touch sensation are blocked first.  Proprioception disappears in succession.  Small typeA-delta fibers(myelin) are blocked next.  Heavily myelinated A-α, β & ɣ fibers blocked last.  Skeletal muscle tone is lost in the end.  Recovery takes place in reverse order.
  • 4.
  • 5. Classification Amide type Long acting  Bupivacaine  Levo-Bupivacaine  Ropivacaine  Dibucaine Intermediate acting  Lidocaine (lignocaine)  Mepivacaine  Prilocaine  Articaine Ester type Long acting  Tetracaine (amethocaine) Intermediate acting  Cocaine Short acting  Procaine  Chloroprocaine  Benzocaine  Proparacaine
  • 6. Miscellaneous  Pramoxine (pramocaine)  Dyclonine  Oxethazaine (mucaine)
  • 7. Mechanism of action  LA molecules consist of an aromatic part liked by an ester or amide bond to a basic amine side chain.  LA are weak bases  Remain partly ionized at physiological pH.  Unionized form penetrates the N membrane.  In axon- ionized form of LA is active at receptor site.
  • 8.
  • 9.  LA block the voltage gated Na+ channels..  Blocking action is favored by repetitive stimulation- voltage dependence.  Activation gate (AG) on extracellular site.  Inactivation gate (IG) on intracellular site.  These gates are called voltage sensors.  Voltage sensors movement is regulated by conformational change due to voltage gradient.
  • 10.
  • 11. Effect of pH on LA action  LA action is strongly pH dependent.  Partly ionized & partly unionized at physiolog pH.  Unionized form diffuses through axon.  Inside axon it is ionized to cationic form BH+  LA are less effective in infected tissue due to- 1. Acidic pH 2. ↑Blood supply at inflamed site. 3. Effectiveness of Adr ↓ at inflamed site. 4. Inflammatory products may oppose LA action.
  • 12. Prolongation of action by vasoconstrictors  Drugs that delays absorption of LA in to circulation will prolong its action & reduce systemic toxicity.  Adrenaline (1:100,000 to 1: 200,000) in dentistry (1:50,000 to 1: 100,000) MC used with LA- doubles the duration of LA action.  Vasoconstrictor shouldn’t be used for N block of an extremity or end organs e.g. on fingers, toes, nose & penis.
  • 13.  One ampoule of 1:1000 adrenaline in 1 ml volume.  This equals 1mg in 1 ml  This equals 1000 μg/ml   If one ampoule is diluted to 10ml  This equals 0.1 mg/ml  This equals 100 μg/ml  This is 1:10,000 adrenalin   If one ampoule is diluted to 100ml  This equals 0.01 mg/ml  This equals 10 μg/ml  This is 1:100,000 adrenalin
  • 14.  Adr can cause cardiac complications.  Felypressin can be used as an alternative.  Preferable in pts with cardiovascular diseases.  Alternatively prilocaine can be used.
  • 15. Systemic actions C.N.S  Stimulation followed by depression. Symptoms of overdose with clinically used LAs are-  Circumoral numbness,  Abnormal sensation in the tongue,  Dizziness, blurred vision, tinnitus followed by  Drowsiness, dysphoria and lethargy.  Still higher doses produce excitation, restlessness, agitation, muscle twitching, seizures and finally unconsciousness.
  • 16. cvs Heart  No significant effects at conventional doses.  High doses- LAs are cardiac depressants.  Decrease automaticity, excitability, contractility, conductivity and prolong ERP.  Quinidine like antiarrhythmic action.  Procainamide is a class IA antiarrhythmic.  QTc interval is prolonged and LAs can induce cardiac arrhythmias  Bupivacaine is relatively more cardiotoxic  Lidocaine used as an antiarrhythmic.
  • 17. Blood vessels  ↓ BP due to sympathetic blockade  High conc locally- direct relaxation of arterial SM.  Bupivacaine> Lidocaine> prilocaine  Toxic doses of LAs- cardiovascular collapse.  Cocaine has sympathomimetic property;  ↑sympathetic tone, causes local vasoconstriction, marked rise in BP and
  • 18. Pharmacokinetics  Ester/amide bond in LA governs its metabolism & ability to cause hypersensitivity reactions.  Ester LA are hydrolysed by plasma esterases & liver esterases.  Spinal fluids contain negligible esterases.  Amide LA are degraded by hepatic microsomes by N-dealkylation & hydrolysis.  Hypersensitivity more common with ester Las.  First pass metabolism is significant for both procaine & lidocaine, not used orally in arrhythmias
  • 19. Adverse effects CNS Low doses  Tongue numbness  Sleepiness  Mild headache  Visual & auditory disturbances High doses  Nystagmus & muscle twitching.  Convulsions  Cocaine- long lasting CNS stimulation & euphoria.
  • 20. CVS  Bradycardia,  Hypotension,  Cardiac arrhythmias and  Vascular collapse Blood  Orthotoludine – metabolite of prilocaine.  Oxidises Hb to metHb, ↑levels cause cyanosis.  Rx- reducing agents like methylene blue or ascorbic acid I.V to convert metHb to Hb.
  • 21. Allergic reactions  Ester LA are metabolized to PABA derivatives .  Responsible for allergic reactions. 1. Rashes, 2. Angioedema, 3. Dermatitis, 4. Contact sensitization, 5. Asthma and 6. Rarely anaphylaxis occur.  Methylparaben added as preservative in certain LA solutions is responsible for allergic
  • 22. Precautions and interactions  Pts on propranolol are very sensitive to pressor responses of Adr- unopposed 1 action.  Drugs with 1blocking property may lead to hypotension if co-administered with L+A.  Pts on acute alcohol intoxication need higher doses of X+A.  In pts on digoxin- accidental I.V inj of Adr cause arrhythmias.  Propranolol can lead to xylocaine toxicity due to- 1. Inhibition of metabolic oxidation of xylocaine.
  • 23. Amide group Long duration Bupivacaine & Levo-Bupivacaine (4>lignocaine) 0.25-0.5% Uses: nerve block, epidural & spinal anesthesia  More sensory than motor block.  Least placental transmission- painless delivery.  Intermediate onset of action.  Shouldn’t be used for IV regional analgesia or obstetrical paracervical block anesthesia.
  • 24. Toxicity  Cardiotoxic- prolongs QTc interval- VT & VA.  Blocks Na channels both in systole & diastole.  Aggrevated by acidosis & hypoxemia.  Levo-bupivacaine equally potent but less toxic.
  • 25. Ropivacaine (equipotent to bupivacaine) Uses: infiltration, epidural & regional anesthesia.  Continous epidural used for relief of post op & labor pain.  Less cardiotoxic & more motor sparing than bupi.  Intermediate onset of action. Toxicity  Available as S-sterioisomer-  Less affinity for cardiac Na+ channels.  R-isomer is toxic.
  • 26. Dibucaine (Cinchocaine)  Very potent, longest acting LA.  Slow onset of action. Use: surface anesthetic in anal canal & rectum.  Ocasionally for SA of longer duration. Rarely used Toxicity  More toxic than bupivacaine Other uses  Pseudocholinesterase inhibitor.  Used for dibucaine number test.  Normal dibucaine number is 80.
  • 27. Medium duration Lidocaine (Lignocaine) or Xylocaine  Most widely used multipurpose LA Uses:  Topically on mucous membrane- Aq.sol, jelly etc.  Infiltration, nerve block & epidural anesthesia.  Spinal analgesia- high conc 5% made hyperbaric with 7.5% dextrose is used.  Rapid onset of action, lasts for 1-2 hrs.  Opiods are synergistic for intrathecal & epidural.  Transdermal patch- for post herpetic
  • 28. Toxicity  CNS: dizziness, paresthesia & euphoria.  High doses- confusion, vertigo, tinnitus & nausea.  Severe toxicity ppt seizures.  Overdose- arrhythmias, ↓BP, coma, resp arrest.  Propranolol enhances toxicity by ↓ clearance. Other uses  Ventricular arrhythmias during MI.
  • 29. Mepivacaine (50% potent as lignocaine)  Similar to lidocaine  Not effective as topical anesthetic.  Can be used without epinephrine. Articaine (almost equipotent to lidocaine)  Rapid onset of action (5min)  Recently approved for dental & periodontal procedures. Contains epinephrine.  Also used for spinal & epidural anesthesia  Mainly metabolized by liver, partly by plasma cholinesterase.
  • 30. Prilocaine (equipotent to lidocaine) Uses: mostly for dental procedures.  Administered by infiltration or nerve block.  Can be used without epinephrine. Toxicity  Similar to lidocaine  Metabolite orthotoludine causes metHb.  CI in obstetric practice.
  • 31. Eutectic lidocaine/prilocaine  Anaesthetise intact skin after surface application.  Eutectic mixture refers to lowering of melting point of two solids when they are mixed.  Lidocaine and prilocaine are mixed in equal proportion at 25°C.  The resulting oil is emulsified into water to form a cream
  • 32. Use:  Applied under occlusive dressing for 1 hr before 1. I.V. cannulation, 2. Split skin graft harvesting and 3. Other superficial procedures.  Anaesthesia up to a depth of 5 mm lasts for 1–2 hr after removal.  It has been used as an alternative to lidocaine infiltration.  PRILOX 5% cream.
  • 33. Ester group Long duration Tetracaine or Amethocaine (4> lignocaine) Uses: topically on eye, nose, troat & tracheobronchial tree.  Eye: no effect on pupil, accomdation & IOP.  Very suitable for SA of long duration.  Onset of action is slow. Toxicity:  Slowly metabolized  Being PABA ester may antaonise- sulfonamides.  I.V doses may produce arrhythmias.
  • 34. Medium duration Cocaine (50% potent as lidocaine)  Earlier it was used as ocular anesthetic.  Vasoconstrictor, Adr not necessary.  Protoplasmic poison, causes necrosis on injection. Toxicity  CNS stimulant- euphoria, delays fatigue, strong psychological dependence  Bradycardia, ↑BP, ↑temp  Nausea & vomiting
  • 35. Short duration Procaine (25% potent as lidocaine)  No longer used  Slow onset of action, Ineffective topically Toxicity  Bradycardia, vasodilation, ↓CO.  Anxiety, restlessness & shivering.  Hydrolysed to PABA Other uses  Procaine + Benzylpenicillin= procaine penicillin  Procainamide- class IA antiarrhythmic.
  • 36. Chloroprocaine (slightly > procaine)  Better & safer than procaine.  Use: infiltration, nerve block, caudal & epidural block.  Rapid onset of action.  Not effective topically.  Less toxic than procaine.
  • 37. Benzocaine & Proparacaine  Used as topical (surface) anesthetics.  Included in preparations of ointment, lozenges & suppositories- ulcer, sore throat & inflammation.  Proparacaine preferred in minor ocular procedures. Non irritant & less antigenic. Toxicity  PABA derivatives- antagonize sulfonamides.  Too toxic for injection
  • 39. Uses and techniques of LA Surface anaesthesia  Applied topically on mucous membranes and abraded skin.  Superficial layer is anaesthetised and motor function not affected.  Onset and duration -site, the drug, conc and form.  Lidocaine (10%) sprayed in the throat acts in 2–5 min and produces anaesthesia for 30–45 min.
  • 40.  Adr no affect on duration of topical anaesthesia.  Phenylephrine can cause mucosal vasoconstrion.  Absorption of soluble LAs from mucous membranes is rapid, may attain IV conc.  Eutectic lidocaine/prilocaine is capable of anaesthetizing intact skin.
  • 41. Sites & uses of SA
  • 42. Infiltration anaesthesia  Dilute sol of LA is injected under the skin to reach sensory nerve terminals.  Uses; minor surgical procedures like incisions & excisions.  Onset of action is almost immediate.  Duration:lidoc 30-60 min, bupiva 90-180 min.  Motor function is not affected.
  • 43. Conduction block anesthesia  LA injected around the nerve trunk.  Area distal to injection site is anesthetized & paralysed.  Lidocaine (1–2%) with intermediate duration of action is most commonly used,  Longer lasting anaesthesia bupivacaine may be selected. Two types  Field block  Nerve block
  • 44. Field block  LA is injected SC in a manner that all nerves coming to a particular field are blocked.  Uses: herniorrhaphy, appendicectomy, dental procedures, scalp stitching, operations on forearms and legs, etc.  Larger area beginning 2–3 cm distal to the line of injection can be anaesthetised with lesser drug compared to infiltration.  The same concentration of LA as for infiltration is used for field block.
  • 45.
  • 46. Nerve block  LA injected around the appropriate nerve trunks or plexuses.  Latency of anaesthesia depends on the drug and the area to be covered.  Frequently performed nerve blocks are— lingual, intercostal, ulnar, sciatic, femoral, brachial plexus, trigeminal, facial, phrenic, etc.  Used for tooth extraction, operations on eye, limbs, abdominal wall, fracture setting, trauma to ribs, neuralgias, persistent hiccup, etc
  • 47.
  • 48. Spinal anaesthesia  LA is injected in the subarachnoid space between L2–3 or L3–4.  Nerve roots in the cauda equina are targeted.  Adr may be enhancing spinal anaesthesia by reducing spinal cord blood flow or  By its own analgesic effect exerted through spinal α2 adrenoceptors.  Intrathecal clonidine, an α2 agonist, produces spinal analgesia by itself.
  • 49.  Spinal anaesthesia is used for operations on the-lower limbs, pelvis, lower abdomen, e.g. prostatectomy,  Fracture setting, obstetric procedures, caesarean section, etc  Advantages of spinal anaesthesia over GA are: (i) It is safer. (ii) Produces good analgesia and muscle relaxation without loss of consciousness. (iii) Cardiac, pulmonary, renal disease and diabetes pose less problem
  • 50.
  • 51. Complications of spinal anaesthesia Respiratory paralysis  Due to Hypotension and ischaemia of respiratory centre. Hypotension  due to blockade of sympathetic outflow to blood vessels & venous pooling.  Raising the foot end overcomes the hypotension.  Prevented by ephedrine, mephentermine. Headache Septic meningitis
  • 52. Cauda equina syndrome  Prolonged loss of control over bladder and bowel sphincters.  It may be due to traumatic damage to nerve roots or chronic arachnoiditis caused by  inadvertent introduction of the antiseptic or particulate matter in the subarachnoid space. Nausea and vomiting  Due to reflexes triggered by traction on abdominal viscera.  Premedication with opioid analgesics prevents it.
  • 53. Epidural anaesthesia  LA injected in dural space, acts on nerve roots. Thoracic  Injection is made in the midthoracic region.  Epidural space in this region is relatively narrow.  Analgesia obtained in middle and lower thoracic dermatomes. Lumbar  epidural space is wide.  Produces anaesthesia of lower abdomen, pelvis and hind limbs.  Use is similar to that of spinal anaesthesia.
  • 54. Caudal  Injection is given in the sacral canal through the sacral hiatus.  Produces anaesthesia of pelvic and perineal region.  Used mostly for vaginal delivery, anorectal and genitourinary operations. Complications  Cardiovascular complications are similar to spinal.  Headache & neurological complications are less.