local anesthesia in oral and maxillofacial surgery

1. LOCALANESTHESIA –
DEFINITION,
NEUROPHYSIOLOGY & MODE
OFACTION
Moderated by: Dr. Rachana Ma’am
Presented by: Dr. Rishitha Kodali

2. CONTENTS
 MODE AND SITE OF LA
 COMPOSITION OF LA
 TOPICALANAESTHESIA
 LOCAL AND SYSTEMIC
COMPLICATIONS
 LA IN GENERAL ANAESTHESIA
 PRECAUTIONS
 SUBSTITUTES
 RECENT ADVANCES
 CONCLUSION
 REFERENCES
 INTRODUCTION
 HISTORY OF L.A.
 DEFINITION
 PHARMACOLOGY OF LA:
 CLASSIFICATION
 PHARMACOKINETICS
 PHARMACODYNAMICS
 NEUROPHYSIOLOGY
 ANATOMIC CONSIDERATION
 PHYSIOLOGIC CONSIDERATION

3. INTRODUCTION
Giovannitti JA Jr, Rosenberg MB, Phero JC. Pharmacology of local anesthetics used in oral surgery. Oral Maxillofac Surg Clin North Am. 2013
Aug;25(3):453-65
 The efforts of human kind to find the means to control pain presents as one of the greatest challenges in medicine.
 Pain is the phenomenon wisely instituted by nature as a warning sign of a condition that may be detrimental to our
bodies.
 Pain free operating is of obvious benefit to the patient, it also helps the operator as treatment can be performed in a
calm, unhurried manner.
 The ability to provide safe, effective local anesthesia is the cornerstone of clinical oral surgical practice. Its use and
effectiveness depends on patient considerations, the extent and duration of the procedure, the choice of drug and
technique, and the skill and experience of the practitioner.

4. • Alcohol is the oldest known sedative. It was used in the ancient Mesopotamia
thousands of years ago.
• 3400 B.C The ‘Euphoric’ effect of opium was discovered by summerians.
• Joseph Priestly(1733-1804) – discovered various gases like – nitrous oxide,
ammonia, oxygen.
• 1801- Humphry Davy
-anaesthetic properties of nitrous oxide.
- coined the term ‘laughing gas’
HISTORY

5. 5
HORACEWELLS
11 Dec 1844, Nitrous oxide was
administered to Dr. Horace well,
rendering him unconscious and able
to have wisdom tooth extracted
without awareness of pain.
T.Y. Euliano, J.S. Gravestein, Essential Anaesthesia- From Science To Practice: United States Of Amesrica By Cambridge
University Press, New York; 2004: Introduction A Very Short History Of Anesthesia: P 1-4

6. Robert Hinkley’s painting from 1882 depicts the first
ether anaesthetic, provided on oct 16th 1846, in Boston,
Massachusetts. William T.G Morton(left) is holding the
globe inhaler, while the surgeon, John C Warren
operates on the patient Edward Gilbert Abbott.
• 16th oct 1846, ether was administered by Sir William
Morton for the removal of mandibular tomur.
• Experiment was published in Boston daily journal.
• And led to the discovery of Surgical anaesthesia.
T.Y. Euliano, J.S. Gravestein, Essential Anaesthesia- From Science To Practice: United States Of Amesrica By Cambridge
University Press, New York; 2004: Introduction A Very Short History Of Anesthesia: P 1-4

7. • 1850’s cocaine isolated, hypodermic needle developed.
• 1853 chloroform used as anesthetic by Dr. John Snow
This chloroform inhaler was the type John Snow
used on Queen Victoria to ease the pain of
childbirth. Chloroform vapours were delivered
down a tube via the brass and velvet face mask.

8. CARL KOLLER
WILLIAM
HALSTED
1884 Carl Koller introduces cocaine intlo medical
practice
1884 Halsted injected cocaine directly into mandibular nerve and
brachial plexus
T.Y. Euliano, J.S. Gravestein, Essential Anaesthesia- From Science To Practice: United States Of Amesrica By Cambridge
University Press, New York; 2004: Introduction A Very Short History Of Anesthesia: P 1-4

9.  1905 Procaine synthesized by Einhorn
 1948 First amide L.A (Lidocaine) synthesized
by Lofgren
 1960 Mepivacaine
 1983 Bupivacaine
 2000 Articaine
Joseph A Et Al,pharmacology Of Local Anaesthetics Used In Oral Surgery, Anaesthesia: Oral And Maxillofacial Clinics Of North
America Volume 25 Issue 3 Pages 453-66 (August 2013)

10. DEFINITION
 LA is defined as loss of sensation in a circumscribed area of body caused by depression of
excitation in nerve endings or an inhibition of conduction process in peripheral nerves –
SANTLEY F MALAMED.
It produce loss of sensation without inducing loss of consciousness.
 The direct administration of an anaesthetic agent to tissues to induce the absence of
sensation in a small area of the body.” MOSBY’S DICTIONARY

11. IDEAL PROPERTIES OF LOCALANESTHETIC
1. Should have sufficient potency to give complete anesthesia
2. Action must be reversible
3. Non irritating to the tissues and produce no secondary local reaction
4. Should have low degree of systemic toxicity
5. Relatively free from allergic reactions
6. Should have rapid onset and sufficient duration
7. Sufficient penetrating properties
8. Low cost
9. Should be stable in solution (long shelf life) and undergoes biotransformation
readily
10. Either sterile or capable of being sterilized

12. BASED ON CHEMICAL STRUCTURE
ESTER
PABA
BENZOIC ACID
QUINOLONE AMIDES KETONES
Butacaine
Cocaine
Benzocaine
Hexylcaine
Piperocaine
2-Chlorprocaine
Procaine
Propoxycaine
Tetracaine
Centbucridine
Articaine
Bupivacaine
Dibucaine
Etidocaine
Lidocaine
Mepivacaine
prilocaine
Dyclonine

13. BASED ON BIOLOGICAL SITE & MODE OF ACTION
CLASS A CLASS B CLASS C CLASS D
• Tetrodotoxin
• Saxitoxin
•Quaternary
ammonium
analogues of
lidocaine
• Scorpion
venom
• Lidocaine
• Mepivacane
• Prilocaine
Benzocaine

14. Based on mode of application
Topical
Insoluble
Soluble
Injectable
Cocaine
Lidocaine
Tetracaine
Benoxinate
Benzocaine
Butylamino-
Benzoate
Lidocaine
Mepivacaine
Tetracaine
Bupivacaine
Dibucaine

15. BASED ON DURATION OF ACTION
ULTRA SHORT SHORT MEDIUM LONG
Pulpal
< 10 min
Soft tissue
30 – 45 min
• 2-Chlorprocaine
• Procaine without
vasoconstrictor
• Lidocaine
without
vasoconstrictor
Pulpal 45 – 90 min
Soft tissue 120 – 240
min
• 4%Prilocaine with
1:2,00,000
epinephrine
• 2%Lidocaine and
2%Mepivacaine
with vasoconstrictor
• Articaine
Pulpal 5-10 min
Soft tissue 60 – 120
min
• 2%Lidocaine with
1:1,00,000
epinephrine
• 4%Prilocaine
• 2%Mepivacaine
with 1:20,000
levonordefrin
• 2% procine .4%
propoxycaine
Pulpal
90 – 180 min
Soft tissue
240 – 540 min
• 0.5%Bupivacaine
• 0.5-
1.5%Etidocaine
with 1:2,00,000
epinehrine

16. BASED ON POTENCY
LOW MEDIUM HIGH
BASED ON POTENCY
LOW MEDIUM HIGH
Procaine
chlorprocaine
Lidocaine
mepivacaine
Tetracaine
Bupivacaine
Dibucaine

17. COMPARATIVE FEATURES OFGENERALAND LOCAL
ANAESTHESIA
GENERAL ANAESTHESIA LOCAL ANAESTHESIA
SITE OF ACTION CNS Peripheral nerves
AREA OF BODY INVOVLED Whole body Restricted area
CONSCIOUSNESS Lost Unaltered
CARE OF VITAL FUNCTIONS Essential Usually not needed
PHYSIOLOGICAL TRESSPASS High Low
POOR HEALTH PATIENT Risky Safer
USE IN NON-COOPERATIVE PATIENT Possible Not possible
MAJOR SURGERY Preferred Cannot be used
MINOR SURGERY Not preferred Preferred

19. CHEMISTRY

20. PHARMACOKINETICS
• Uptake:
• Injection-degree of Vaso activity
• Oral route-poorly absorbed
• Topical route-absorption at differing rates
• Distribution:
Throughout body, more in highly perfused organs
Influenced by:
• Rate at which it is absorbed into CVS
• Rate of distribution from vascular compartment to
tissues
• Rate of elimination
Metabolism (Biotransformation, Detoxification):
Esters- Hydrolyzed in plasma by
PSEUDOCHOLINESTERASE
Amides- LIVER
Excretion:
Kidneys

21. Mechanism of Action
Normal depolarization causes conformational changes in the nerve membrane that allow for the passage of
sodium ions through specified channels resulting in the propagation of the action potential along the nerve.
Local anesthetics bind to specific sites within the sodium channels, preventing these conformational changes,
and thus impair conduction.

22. 1. Local anesthetics disrupt nerve conduction by affecting a critical length of the nerve. Larger
myelinated fibers, with greater internodal distance, are more sensitive.
2. The effectiveness of local anesthetics on nerves is also influenced by impulse frequency. Higher-
frequency impulses increase the availability of sodium channels for local anesthetics, causing faster
blockage. This use-dependent block is clinically significant as pain impulses, with higher frequencies
than motor impulses, are preferentially and rapidly blocked, enhancing pain management.
3. The clinical onset and recovery characteristics of nerve blocks are influenced by the organization of
nerve trunks. Local anesthetic diffusion affects outer (mantle) axons first, followed by the inner (core)
axons. The inferior alveolar nerve, proximal structures are innervated by the mantle fibers and distal
structures are innervated by the core.

23. IONIZATION
• The rate of onset for a local anesthetic is determined by its degree of ionization after injection.
• The acidic solution is buffered in the body, leading to the formation of an uncharged base and a
cationic form.
• The uncharged base diffuses through the nerve membrane, and the onset speed depends on the pKa of
the anesthetic and tissue ph.
• A lower pKa, closer to tissue pH, results in faster onset.
• In the presence of inflammation, the tissue becomes more acidic, making achieving local anesthesia
more challenging.

24. LIPID SOLUBILITY AND PROTEIN BINDING
• The lipid solubility of a local anesthetic is determined by its aromatic ring, influencing
its potency as nerve membranes are predominantly lipid. Greater lipid affinity results in
higher potency.
• Duration of action is determined by protein-binding properties. Local anesthetics
binding tightly to protein, especially in sodium channels and receptor sites, exhibit
prolonged action. Protein binding creates a reservoir, contributing to a longer duration
of action as unbound drug is gradually removed by vascular uptake

25. PHARMACODYNAMICS
CNS
Euphoria, excitement, mental confusion, restlessness,
tremor and twitching of muscles, convulsions,
unconsciousness, respiratory depression, death in a
dose dependent manner.
CVS
Inhibit cardiac conduction, reduced cardiac output,
systemic hypotension, and ultimately leading to
cardiovascular collapse.
Peripheral vasculature
• Vasodilatory impact
• Cocaine, uniquely causing vasoconstriction, can lead to
severe complications, such as malignant hypertension,
stroke, myocardial infarction, and death

26. PAIN PATHWAY
 Sensory receptors receive
stimulus from external or internal
sources-present all over body
 Neural pathways-conduct
information from receptors to
brain
 Parts of brain that deals with
processing information and
perceives pain

27. ANATOMIC CONSIDERATION
Sensory
neuron
Dendritic
zone
Axon Cell body

28.  Function of nerve is to carry messages from 1 part of the body to another
 Messages in form of electrical action potentials called impulses
 Action potentials are transient depolarizations of membrane, result from brief increase in
permeability of membrane to sodium, from a delayed increase in its permeability to potassium
 Impulses are initiated by chemical, thermal, mechanical, or electrical stimuli.
 Impulse is initiated, amplitude and shape of that impulse remain constant, regardless of changes in
the quality of the stimulus or in its strength
PHYSIOLOGIC CONSIDERATION-PHYSIOLOGY OF
PERIPHERAL NERVES

29. PHYSIOLOGICCONSIDERATION-
ELECTROPHYSIOLOGYOFNERVECONDUCTION
• Nerve possess resting potential of -70mv
• Interior of nerve is negative relative to exterior
• Stimulus excites nerves:
• Initial slow depolarisation
• Rapid phase depolarisation
• Reversal of electric potential
• After depolarisation, repolarisation occurs

30. MODEAND SITE OFLA
• Altering the basic resting potential of nerve membrane
• Altering the threshold potential
• Decreasing the rate of depolaraization
• Prolonging rate of repolarisation

31. THEORIES
ACETYLCHOLINE THEORY(DETT BARN,1967)
CALCIUM DISPLACEMENT THEORY(GOLDMAN, 1966)
SURFACE CHARGE(REPULSION)THEORY(WEI, 1969)
MEMBRANE EXPANSION THEORY(LEE, 1976)
SPECIFIC RECEPTOR THEORY(STRICHARTZ, 1987)

32. ACETYLCHOLINE THEORY
 Stated that acetylcholine was involved in
nerve conduction in addition to its role as
a neurotransmitter at nerve synapses.
 DRAWBACK: There is no evidence that
acetylcholine is involved in neural
transmission.

33. • Stated that local anesthetic nerve block was
produced by displacement of calcium from
some membrane site that controlled
permeability of sodium.
• DRAWBACK :- Evidence that varying the
concentration of calcium ions bathing a nerve
does not affect local anesthetic potency has
diminished the credibility of this theory.
CALCIUM DISPLACEMENT
THEORY

34. SURFACE CHARGE(REPULSION)THEORY
• Acted by binding to nerve membrane and changing the
electrical potential at membrane surface.
• Drawback:- current evidence indicate that resting potential
of nerve membrane is unaltered by local anaesthetic and that
conventional local anaesthetics act within membrane
channels rather than at membrane surface. They cannot
explain the activity of the uncharged anesthetic molecules in
blocking nerve impulses(eg.Benzocaine)

35. MEMBRANE EXPANSIONTHEORY
• Local anaesthetic molecule diffuse to hydrophobic regions of
excitable membranes, producing a general disturbance of bulk
membrane structure, expanding membrane, and thus preventing
an increase in permeability to sodium ions.
• Lipid soluble LA can easily penetrate the lipid portion of cell
membrane changing the configuration of lipoprotein matrix of
nerve membrane. This results in decreased diameter of sodium
channel, which leads to inhibition of sodium conduction and
neural excitation.

36. SPECIFIC RECEPTOR THEORY
• Act by binding to specific receptors on the
sodium channels The specific site exists in the
sodium channels either on its external surface
or on the intenal axoplasmic surface As LA
gains access to receptors, permeability to
sodium ions is decreased or eliminated Nerve
conduction is interrupted

37. RNH+ = RN + H+
Nerve membrane
RN
RN
H+ RNH+
Outside nerve membrane
Inside nerve membrane
DISSOCIATION OFLA

38. • The relative proportion of ionic forms also depend upon pKa, or dissociation constant of specific
local anesthesia.
• It is a measure of the affinity of a molecule for hydrogen ions (H+).
Percentage of drug existing in either form can be determined from the Henderson-Hasselbach
equation.
Log Base / Acid = pH – pKa
• A local anesthetic with a high pKa value has very few molecules available in the RN form at a
tissue pH of 7.4. The onset of anesthetic action of this drug is slow because too few base molecules
are available to diffuse through the nerve membrane (e.g., procaine, with a pKa of 9.1).
• The rate of onset of anesthetic action is related to the pKa of the local anesthetic.
• A local anesthetic with a lower pKa (<7.5) has a greater number of lipophilic free base molecules
available to diffuse through the nerve sheath; however, the anesthetic action of this drug is
inadequate because at an intracellular pH of 7.4, only a very small number of base molecules
dissociate back to the cationic form necessary for binding at the receptor site.

39. RNH+ > RN + H+
RNH+ < RN + H+
If pH is low
If pH is high
EFFECT OF pH ON DIFFUSION OF LOCAL
ANESTHETIC

40. INDUCTIONAND
RECOVERYFROM
LOCAL
ANAESTHESIA

41.  Dissociation constant (Pka )
 Type and size of nerve
 Lipid solubility
 Protein binding
 Perineurium thickness
 Concentration of LA agent
 Non-nervous tissue diffusibility
 Vasodilator activity
 Too high too low Ph
 Excessive dilution with blood or
tissue fluids
 Too rapid absorption
 Vascularity of site
 Infection
 Volume of drug
 Vasoconstrictors
FACTORS AFFECTING LA ACTION

42. PATIENT RELATED FACTORS
Age
Body size
Renal dysfunction
Hepatic dysfunction
Pregnancy

43. REVERSAL OF ANAESTHESIA
 Phentolamine - reversible
nonselective α-adrenergic
antagonist
 Action-vasodilation due to α1
blockade
 Reverse the local
vasoconstrictor properties

44.  Lignocaine Hcl-(Anesthetic)24.64 mg (2 %)
 Adrenaline- (Vasoconstrictor) 0.0125 mg (1:80,000)
 Sodium metabisulphite -(Reducing Agent)0.5 mg
• Methyl paraben -(Preservative)
• Thymol - (Fungicide)
• Salts (NaCl) - (Isotonicity) 5-6 mg
• Distilled Water- (Vehicle)100 ml or Ringer’s Lactate
COMPOSITION OF LA

45. % Vasoconstrictor Duration (hours)
2 Without 1 – 2
2 1:50,000
epinephrine
3 – 5
2 1:100,000
epinephrine
3 – 5
Maximum recommended dose
 w/o epinephrine: 4.4 mg/kg (2 mg/lb)
 with epinephrine: 7 mg/kg (3.2 mg/lb)
Maximum safe dose –
2% with 1:1,00,000 epinephrine
LIDOCAINE
• Concentration - 2%
• Metabolized - Liver
• Excreted - Kidney
• Time of onset : 2-3 mins
• Half life : 90 mins

46. MEPIVACAINE
CONCENTRATION –
• 3%WITHOUT
VASOCONSTRICTOR
• 2% WITH LEVONORDEFRIN
• METABOLIZED - LIVER
• EXCRETED – KIDNEY
• TIME TO ONSET 3-5 MINS
• HALF LIFE 1.9 HRS
% Vasoconstrictor
Duration (minutes)
Pulp Tissue
3 Without
20 with
infiltration
120 – 180
2 levonordefrin
40 with
never block
180 – 300

47. ARTICAINE
• Only amide having an ester group
• Biotransformation occurs in both plasma and liver
• Excretion via kidneys
• Pka-7.8
• Onset of action- 1 to 2 mins
• Effective dental concentration- 4% with 1:1,00,000 epinephrine
• Half life – 0.5 hours
• Maximum recommended dose- 7mg/kg adult body weight

48. ROPIVACAINE
o Long- acting amide anesthetic
o Prepared as a isomer
o Greater margin of safety
o (t ½= 1.9 hour)
o Decreased cardio-toxicity
o Uses: regional nerve block mainly epidural

49. BUPIVACAINE
• Potency. Four times that of lidocaine, mepivacaine, and prilocaine.
• Toxicity. Less than four times that of lidocaine and mepivacaine.
• Metabolism. Metabolized in the liver by amidases.
• Excretion. Via the kidney; 16% unchanged bupivacaine has been recovered from human urine.
Vasodilating properties. Relatively significant: greater than those of lidocaine, prilocaine, and
mepivacaine, yet considerably less than those of procaine.
• pKa. 8.1.
• pH of plain solution. 4.5 to 6.0.
• pH of vasoconstrictor-containing solution. 3.0 to 4.5.
• Pregnancy classification. C
• Maximum recommended dose. The MRD is 2.0 mg/kg to a maximum of 200 mg.

50. PRILOCAINE
• Classification- Amide
• Metabolism- The metabolism of prilocaine differs significantly from that of lidocaine and mepivacaine as it is a
secondary amine, prilocaine is hydrolyzed straight forwardly by hepatic amidases to o-toluidine and N-propylalanine.
Carbon dioxide is a major end product of prilocaine biotransformation.
• prilocaine causes cyanosis and methemoglobinemia.
• Prilocaine undergoes biotransformation more rapidly and completely than lidocaine.
• prilocaine considered to be less toxic systemically than comparably potent local anesthetic amides.
• Excretion- primarily via kidney
• pKa. 7.9. pH of plain solution. Approximately 6.0 to 6.5
• pH of vasoconstrictor-containing solution is 4
• Maximum recommended dose. The FDA MRD for is 8.0 mg/kg (3.6 mg/lb) body weight for the adul

51. CENTBUCRIDINE
• Quinolone derivative five to eight times more potent than lidocaine
• Does not effect CNS & CVS
• Uses: subarachnoid, extradural , I.V reg. Anesthesia , intraocular
surgery
• 1:1 mixture of 0.5% ropivacaine and 3% chloroprocaine
• Used for surgical procedures in cardiac compromised patients
WEAVERCAINE

52. VASOCONSTRICTORS
o To counteract vasodilation
o Decrease blood flow
o Lower anesthetic blood levels
o Decrease the risk of toxicity
o Increases duration of action
o Decrease bleeding
All vasoconstrictors are
Sympathomimetic amines, unstable in
solutions so preservative should be
used to prevent oxidation

53. CLASSIFICATION OFVASOCONSTRICTORS
Natural: Epinephrine, norepinephrine and Dopamine.
Synthetic: Isoproterenol and Levonordefrin.
 Catecholamines (when it contains 2
hydroxyl group on carbon 3 and 4 )
 Epinephrine
 Nor-epinephrine
 Dopamine
 Levonordefrin
 Isoproterenol
 Non catecholamines
 Amphetamine
 Methamphetamine
 Hydroxy-amphetamine
 Ephedrine
 Mephetermine

54. CONCENTRATIONS OFCLINICALUSEDVASCONSTRICTORS
Dilution Mg/ml Therapeutic Use
1:1,000 1.0
Emergency medicine
(Im/Sc anaphylaxis)
1:2,500 0.4 Phenylephrine
1:10,000 0.1
Emergency medicine (IV
cardiac arrest)
1:20,000 0.05 Levonordefrin
1:30,000 0.033 Norepinephrine
Dilution Mg/ml Therapeutic use
1:50,000 0.02
Local anesthesia
1:80,000 0.0125
Local anesthesia
1:1,00,000 0.01
Local anesthesia
1:2,00,000 0.005
Local anesthesia
1:4,00,000 0.0025
Local anesthesia

55. ADRENERGIC RECEPTORS
Receptors Α1 Α2 Β1 Β2 Β3
Location Blood Vessels Brain Heart Lungs Adipose
Tissue
Vas Deferens Pancreas Small
Intestines
Uterus
Urethra And
Uterus
G.I. Tract Blood Vessels
Pupil
CNS Intestine and
Liver

56. EPINEPHRINE
o Most potent and widely
used vasoconstrictor
o Source: 80% of medullary
secretion, also synthetic
o Acts on both  and , with
 being predominate
Recommended maximum Doses
• Normal healthy patient 0.2
mg per appointment
• Significant cardiovascular
impairment 0.04 mg per
appointment

57. EFFECTS OFADRENALINE ONBODY
CNS
 Produces “ ALERTING EFFECTS”
 Jitteryness
 Apprehension
 Mild excitation
Others
 Increase in blood sugar levels
 Increase in glycogenolysis in liver and muscle
 Pupillary dilatation
CVS
 1 Stimulation :
 Increase in HR
 Increase in stroke volume
 Increase in cardiac output
 Increase in oxygen consumption
 Irritability of myocardium
 Premature ventricular contractions
 2 causes vasodilatation causes vasoconstriction at
higher doses

58. USES OFADRENALINE
Therapeutic dose
0.3 to 0.5 mg
Clinical Applications for Epinephrine
• Acute allergic reaction
• Bronchospasm
• Cardiac arrest
• Hemostasis
• Produce mydriasis
• Vasoconstrictor

59. NOREPINEPHRINE
• Constitutes 20% catecholamine production of medulla
• White crystalline monohydrate salt
• Soluble in water
• Ph 3.4
• Predominantly on  receptors
• Available as 1:30000 per ml
• Max dose 0.34mg or 10 ml of 1:30,000 concentration
• Cardiac patients- 0.14 mg or 4 ml of 1:30,000 concentration

60. CVS
Increase in HR
Increase in stroke volume
Increase in force of contraction
Increase in systolic and diastolic BP
Respiratory system
No effect
CNS
Produces mild“ ALERTING EFFECTS

61. LEVONORDEPHRINE
CVS
•Reflex decrease in HR
•Increase in cardiac output
RESPIRATORY SYSTEM
•No effect
CNS
•No effect
• White crystalline monohydrate salt
• Soluble in water and alcohol
• pH 3.4
• Predominantly on  receptors
• Available as 1:10000 per ml
• Max dose 1mg or 10 ml of 1:10000
concentration
• Cardiac patients .4 mg

62. PHENYLEPHRINE
CVS
• Cardiac arrythmias less likely to occur
as it does not affect beta receptors
• Reflex decrease in HR
RESPIRATORY SYSTEM
• No effect
CNS
• “NO EFFECT”
o White crystalline salt
o Soluble in water
o Ph 3.4
o Almost pure  agonist
o Available as 1:2500 per ml
o Vasoconstrictor effect less than epinephrine,
norepinephrine, levonordephrine
o Long lasting
o Max dose 4mg or 10 ml of 1:2500 concentration
o Cardiac patients 1.6 mg

63. FELYPRESSIN
 Analogue of vasopressin (0.03 IU/ml with 3% prilocaine)
 Little direct effect on heart & CNS
 Uses
 Hyperthyroidism
 Hypertension
 Advanced cardiac diseases
 Patients on TCA, MAO inhibitors
 Disadvantage : poor hemostasis
 contraindicated in pregnancy

64. SELECTION OFVASOCONSTRICTOR
DURATION OF
DESIRED
EFFECT
PHYSICAL
CONDITION
OF PATIENT
DESIRE TO
ACHIEVE
HEMOSTASIS
CONCURRENT
MEDICATION

65. For “stable” cardiac disease, prudent to administer minimal amount of epinephrine while always
avoiding intravascular injections.
Pain control is of paramount importance, potentially deleterious effect of epinephrine can be
minimized by limiting amount to 40 μg.
Although half life of epinephrine is short, exceeding 40 μg epinephrine per appointment cannot be
recommended unless the patient’s cardiac status is monitored continuously during procedure.

66. CONSIDERATIONS
• Congenital heart disease: vasoconstrictors to kept minimal or eliminated
• Rheumatic heart disease: vasoconstrictors to kept minimal with profound analgesia
• Coronary artery disease: concentration of 1:100000 or .04mg + aspiration + advised to
eat lightly
• Mailgnant hypertension: moderately sedated + vasoconstrictors kept minimal
• Pending congestive heart failure: sedation + good pain control + vasoconstrictors to
kept minimal

67. Chronic valvular heart disease : vasoconstrictors to kept
minimal
Diabetes mellitus: vasoconstrictors to kept minimal
Hypothroidism: amount of vasoconstrictor should be
chosen wisely
Hyperthroidism: reduced amount of vasoconstrictor

68. EMLA

69. Local anesthetics are absorbed at different rates after
application to mucous membranes, in the tracheal mucosa
uptake is as rapid as with intravenous administration.
In pharyngeal mucosa uptake is slow . In bladder mucosa
uptake is even slower.
Eutectic mixture of local anesthesia (EMLA) has been
developed to provide surface anesthesia for intact skin.
TOPICALANAESTHESIA

70. WATER INSOLUBLETOPICALANESTHETICS
ETHLYAMINOBENZOATE (BENZOCAINE)
• Lacks basic nitrogen group
• Used topically
• Poorly soluble in water
• Rapid onset
• On injecting: irritating, toxic
• Used in cough drops, sunburn lotions
LIDOCAINE
 Lidocaine base
 Onset 15 secs
 Duration 30 mins
 Poorly absorbed so toxicity minimal

71. WATERSOLUBLETOPICALANESTHETICS
3. Lidocaine hydrochloride: 2% or 4%
o Onset 15 secs
o Duration 30 mins
o absorbed so more toxicity
o Available as syrup for rinses
o max recommended dose 200 mg
1. Benzyl alcohol
Irritating on injection available as 4% and 10%
o 2. Tetracaine:2%
o Duration 45 mins
o Combination with benzocaine
o Onset: 30secs
o Long lasting
o Available in liquid, ointment, spray, gel form

72. RATESATWHICHLOCALANESTHETICSAREABSORBEDANDREACHTHEIRPEAK
BLOODLEVEL
ROUTE TIME PEAK LEVEL(MIN)
IV 1
TOPICAL 5
IM 5-10
SC 30-90

73. A simple formula for quick and accurate calculation of maximum allowable volume of local
anaesthetic agents
British Journal of Dermatology (2015) 172, pp805–840
maximum allowable
dose (mg/kg)
(weight in kg/10)
(1/concentration
of local
anesthetic)
mL
Thus, if maximal dose is 7 mg/kg for lidocaine with epinephrine, using 1% lidocaine with epinephrine
for a 60-kg patient:
7 x 60/10 x 1/1
i.e. 7 x 6 x 1 = 42 mL lidocaine
Same, for using 2% lidocaine with epinephrine for a 60-kg patient
7 x 6 x 0.5 = 21 ml lidocaine

74. LAIN GENERALANAESTHESIA
• Used for gaining multimodal analgesia.
• Ga will not provide intra-op as well as post operative analgesia . therefore to have pain free post operative
period la is given
• Intra-op it prolongs the GA effect as the LA will reduce the painfull stimulus to the patient.
Hence patient will not be stimulated. Therefore prolonged action of muscle relaxants and reduces usage of GA
drugs
• Vasconstrictor effect is an added advantage of lignocaine+adrenaline.To reduce small vessels bleed

75. LAIN PREGNANCY
o Highest concentrations in the fetal circulation follow injection of prilocaine, and the
lowest follow bupivacaine, with lidocaine in between.
o Felypressin, which is a derivative of vasopressin and is related to oxytocin, has the
potential to cause uterine contractions.
o Although this is a highly unlikely effect at the low dose of felypressin used in local
anesthetics, it is best avoided during pregnancy.
o Lidocaine with epinephrine is commonly used for pregnant dental patients.

76. GERIATRICS
Changes in the
• systemic absorption,
• distribution and clearance
• Decreases in neural population, neural conduction velocity and
inter Schwann cell distance can lead to an increased sensitivity to
local anaesthetics in the elderly.

77. COMPLICATIONS
Local complications
• Pain on injection
• Burning on injection
• Needle breakage
• Paresthesia
• Facial nerve paralysis
• Trismus
• Soft tissue injury
• Hematoma
• Infection
• Edema
• Sloughing of tissues
• Postanesthetic intraoral lesions

78. Systemic complications
CNS
• La crosses the blood brain barrier producing CNS depression .
• Therapeutic advantage can be taken of lidocaine at blood levels between
0.5-4ug/ml because it has anticonvulsant properties.
• Mechanism of action is depression of hyper excitable neurons found in
amygdala of seizing patient. signs of toxicity appear at blood levels
greater than 4.5ug/ml where general cortical sensitivity, agitation,
talkativeness and irritability is seen.
• Tonic clonic seizures occur at levels greater than 7.5 ug/ml
CVS –
• Higher blood level 5.0 to 10.0 mild ECG alteration ,myocardial
depression decreased cardiac output
• Above 10ug/ml there is intensification of these effects primarily
massive vasodilation, marked reduction in myocardial contractility,
severe bradycardia and possible cardiac arrest.
RESPIRATORY SYSTEM
• Local anesthetic drugs exert a
dual effect on respiration.
• non overdose levels - direct
relaxant actions on bronchial
smooth muscles.
• At overdose level -
respiratory arrest as a result of
generalized CNS depression

79. Severe Overdose Reaction
 Rapid onset (within one minute)
 Remove syringe (if in the process of an injection)
 Protect patient for trauma if convulsions are
present
 Call 911
 Basic life support
 Administer anticonvulsant
 Allow patient to recover
 Do not let patient leave alone
Management of epinephrine overdose
Terminate dental procedure
Sit patient upright in the dental chair
Reassure patient
Monitor blood pressure
Administer oxygen
Mild Overdose Reaction
1. Slow onset
2. Reassure patient
3. Administer oxygen
4. Monitor vital signs
5. Allow patient to recover as long as
necessary

80. Allergic Reactions to Local Anesthetic Agents
• Hypersensitive state as a result of exposure to an allergen
• Re-exposure can heighten the initial reaction
Clinical Manifestations of an Allergy
 Fever
 Angioedema
 Urticaria
 Dermatitis
 Depression of blood-forming organs
 Photosensitivity
 Anaphylaxis

81. Allergic responses to local anesthetic
Dermatitis (hives)
Bronchospasm
Systemic anaphylaxis
Hypersensitivity to esters
(Atypical pseudo cholinesterase, PABA)
ANAPHYLACTIC REACTION

82.  The cartridge opening into which the needle is
inserted is aluminum with a very thin
diaphragm of latex in the middle
 Though patients with a latex allergy are at an
increased risk, there are no known cases or
reports of an allergic response from the latex
on a local anesthetic cartridge
LatexAllergy

83. Sodium BisulfiteAllergy
• Allergy to sodium bisulfite or sodium metabisulfite is being reported today with increasing frequency.
• People who are allergic to bisulfites (most often steroid-dependent asthmatics) may develop a severe response
(bronchospasm)
• A history of allergy to bisulfites should alert the dentist to the possibility of this same type of response if
sodium bisulfite or sodium metabisulfite is included in the local anesthetic solution.
• Sodium bisulfite or sodium metabisulfite is found in all dental local anesthetic cartridges that contain a
vasoconstrictor, and is not found in plain local anesthetic solutions.
• In the presence of a documented sulfite allergy, local anesthetic solution without a vasoconstrictor
(“plain local anesthetic”) should be used (e.g., 3% mepivacaine hydrochloride, 4% prilocaine hydrochloride

84. TopicalAnestheticAllergy
• Topical anesthetics possess the potential to induce allergy.
• The most commonly used topical anesthetics in dentistry are esters, such as
benzocaine and tetracaine.
• However, because benzocaine (an ester topical anesthetic) is poorly absorbed
systemically, allergic responses that develop in response to its use are normally limited
to the site of application.
• When other topical formulations, ester or amide, that are absorbed systemically are
applied to mucous membranes, allergic responses may be localized or systemic.
• Many contain preservatives such as methylparaben, ethylparaben, or propylparaben.

85.  Mepivacaine, lidocaine, halothane, succinylcholine
 Autosomal dominant disorder include defect in distribution of myoplasmic calcium.
 Acute episode of rising ca++ concentration
 Ca++  increase phosphorylation  increase atp production - heat formation.
 C/f- muscular rigidity, metabolic acidosis , high fever more than 110 ‘f monitored.
 Tachycardia, tachypnoea, dysrythmias, cyanosis and death
 Management : dantrolene sodium i.V 2.5mg/kg , bicarbonate 1-2 meq/kg
MALIGNANT HYPERTHERMIA

86. METHEMOGLOBINEMIA
• Prilocaine,
• Benzocaine
• Articaine
• Methemoglobin- 1.5-3g/dl(10-20%)
• Management :
1% methylene blue 1.5mg/kg (electron acceptor) ;
Ascorbic acid 100-200mg/day

87. ADVANCEMENTS IN LOCAL
ANESTHETICS

88. Vibra Ject
• A small battery-operated attachment that snaps
on to the standard dental syringe.
• Takes advantage of the gate control theory of
pain management, which suggests that pain can
be reduced by simultaneous activation of nerve
fibers through the use of vibration

89. DENTALVIBE
o A cordless, rechargeable, hand held device that
delivers soothing, pulsed, percussive micro-
oscillations to the site where an injection is
being administered.
o U-shaped vibrating tip attached to a
microprocessor-controlled Vibra-Pulse motor
gently stimulates the sensory receptors at the
injection site, effectively closing the neural pain
gate, blocking the painful sensation of
injections.

90. Accupal
• A cordless device that uses both vibration and
pressure to precondition the oral mucosa

91. WAND
Advantages
• Precise control of flow rates and pressure
• Comfortable even in tissues of low elasticity
• Increased tactile sensation
• Light weight
• Automatic aspiration
• Minimal needle deflection
Disadvantages
• Requires additional armamentarium
• High cost

92. JET INJECTORS
Principle:
Anaesthesia of surface to a depth
over 1cm without use of needle
Advantages:
Fast
Easy to use
Less pain

93. Safety dental syringes
Hypo Safety
Syringe
Safety Wand
Ultra safety plus
XL syringe

94. STA(SINGLE TOOTHANAESTHESIA
SYSTEM)
Dynamic Pressure Sensing – provides continuous feedback to the
user about the pressure at the needle tip to identify the ideal needle
placement for PDL injections.

95. EMLA
5% emulsion preparation, containing 2.5%
each of lidocaine/prilocaine

96. INTRAOSSEOUS
The devices used for this technique,
inject the solution into the cancellous
bone adjacent to the root apex

97. IONTOPHORESIS
Lidocaine and epinephrine molecules are
drawn into the tissue by an electrical
current

98. • The local anesthetics currently available are satisfactory for the vast majority of
indications.
• Although safety, particularly in the context of accidental intravascular injection,
remains a concern
• Use of adjuvants and also the newer chiral compounds provide an increased safety
margin.
• However, there is still room for the improvement of painless techniques in
administrating local anesthetics.
CONCLUSION

99. REFERENCES
1. Handbook of local anesthesia- stanley F. Malamed.
2. Neural blockade in clinical anesthesia & management of pain – michael j. Cousins , philip
O. Bridenbaugh
3. Textbook of pharmacology & pharmacotherpautics- goodman & gilman- 10th edition
4. Regional anesthesia of the oral cavity- J . theodore jastak, john A. Yagiela
5. Monehims local anesthesia and pain control, benett
6. Principles of anesthesiology- vincent J. Collins