The document provides information on the history and properties of local anesthesia. It discusses how cocaine was the first local anesthetic isolated in 1860 and procaine was the first widely used synthetic agent in 1905. Key events include the discovery of lidocaine in 1948 and its clinical introduction in 1949. Local anesthesia works by reversibly blocking nerve conduction, producing loss of sensation while maintaining consciousness. The mechanisms of action and properties of various local anesthetic agents are explained.
2. Cocaine- first local anesthetic agent isolated by NIEMAN-
1860 from the leaves of the coca tree.
Its anesthetic action was demonstrated by KARL KOLLER In
1884.
First effective and widely used synthetic local anesthetic-
PROCAINE-produced by EINHORN in 1905 from benzoic acid
and diethyl amino ethanol.
Its anesthetic properties were identified by BIBERFIELD and
the agent was introduced into clinical practice by BRAUN.
HISTORY
3. LIDOCAINE-LOFGREN in 1948.
The discovery of its anesthetic properties was followed in
1949 by its clinical use by T.GORDH.
4. Local anesthesia is defined as a loss of sensation in a
circumscribed area of the body caused by depression of
excitation in nerve endings or an inhibition of the conduction
process in peripheral nerves. STANLEY F. MALAMED
LOSS OF SENSATION WITHOUT LOSS OF CONSCIOUSNESS…
DEFINITION
An important feature of local anesthesia is that it
produces:
5. PROPERTIES OF LOCAL ANESTHESIA
I==It should not be irritating to tissue to which it is applied
N==It should not cause any permanent alteration of nerve
structure
S==Its systemic toxicity should be low
T==Time of onset of anesthesia should be short
E== It should be effective regardless of whether it is injected
into the tissue or applied locally to mucous membranes
D==The duration of action should be long enough to permit
the completion of procedure
6. It should have the potency sufficient to give complete
anesthesia with out the use of harmful concentration
solutions
It should be free from producing allergic reactions
It should be free in solution and relatively undergo
biotransformation in the body
It should be either sterile or be capable of being sterilized by
heat with out deterioration.
8. STEP 1:
A stimulus excites the nerve, leading to following sequence of
events:
A. An initial phase of slow depolarization.The electrical
potential within nerve become lightly less negative
B. When the falling electrical potential reaches a critical level,
an extremely rapid phase of depolarization results. This is
termed threshold potential or firing threshold.
C. This phase of rapid depolarization results in a reversal of the
electrical potential across the nerve membrane.The interior of
the nerve is now electrically positive in relation to the exterior.
An electrical potential of +40 mV exists on the interior of the
nerve cell.
9. STEP 2: -
After these steps of depolarization,
repolarization occurs. The electrical
potential gradually becomes more
negative inside the nerve cell relative to
outside until the original resting potential
of -70 mV again achieved.
10.
11.
12. MODE AND SITE OF ACTION OF LOCAL
ANESTHETICS
Local anesthetic agent interferes with excitation process in a
nerve membrane in one of the following ways:
Altering the basic resting potential of nerve membrane
Altering the threshold potential
Decreasing the rate of depolarization
Prolonging the rate of repolarization
13. Many theories have been promulgated over the years to explain
the mechanism of action of local anesthetics.
ACETYLECHOLINE THEORY: Stated that acetylcholine was
involved in nerve conduction in addition to its role as a
neurotransmitter at nerve synapses. There is no evidence that
acetylcholine is involved in neural transmission.
WHERE DO LOCAL ANESTHETIC WORKS?
14. CALCIUM DISPLACEMENT THEORY:
States that local anesthetic nerve block was produced by
displacement of calcium from some membrane site that
controlled permeability of sodium. Evidence that varying the
concentration of calcium ions bathing a nerve does not affect
local anesthetic has diminished the credibility of those theory
15. SURFACE CHARGE (REPULSION) THEORY:
Proposed that local anesthetic acted by binding to nerve
membrane and changing the electrical potential at the
membrane surface. Cationic drug molecule were aligned at the
membrane water interface, and since some of the local
anesthetic molecule carried a net positive charge, they made
the electrical potential at the membrane surface more positive,
thus decreasing the excitability of nerve by increasing the
threshold potential. Current evidence indicate that resting
potential of nerve membrane is unaltered by local anesthetic.
16. MEMBRANE EXPANSION THEORY
It states that local anesthetic 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.
17.
18. SPECIFIC RECEPTOR THEORY:
The most favored today, proposed that local anesthetics
act by binding to specific receptors on sodium
channel the action of the drug is direct, not mediated
by some change in general properties of cell
membrane. Biochemical and electrophysiological
studies have indicated that specific receptor sites for
local anesthetic agents exists in sodium channel
either on its external surface or on internal
axoplasmic surface. Once the LA has gained access
to receptors, permeability to sodium ion is decreased
or eliminated and nerve conduction is interrupted.
19. DISSOCIATION OF LOCAL ANESTHETICS
• Local anesthetics are available as salts (usually
hydrochlorides) for clinical use.
• The salts, both water soluble and stable, is dissolved in either
sterile water or saline.
• In this solution it exists simultaneously as
unchanged molecule (RN), also called base and
positively charged molecules (RNH+) called cations.
RNH+ ==== RN+ H+
20. The relative concentration of each ionic form in the solution
varies in the pH of the solution or surrounding tissue.
In the presence of high concentration of hydrogen ion (low
pH) the equilibrium shifts to left and most of the anesthetic
solution exists in cationic form.
RNH+ > RN + H+
As hydrogen ion concentration decreases (higher pH) the
equilibrium shifts towards the free base form.
RNH+ < RN + H+
21. • The relative proportion of ionic form also depends on pKa or
DISSOCIATION CONSTANT, of the specific local anesthetic.
• The pKa is a measure of molecules affinity for H+ ions.
• When the pH of the solution has the same value as pKa of the
local anesthetic, exactly half the drug will exists in the RNH+
form and exactly half in RN form.
• The percentage of drug existing in either form can be
determined by Henderson Hasselbalch equation
22. • Henderson hasselbach equation
Determines how much of a local anesthetic will be in a non-
ionized vs ionized form . Based on tissue pH and anesthetic Pka
.
• Injectable local anesthetics are weak bases (pka=7.5-9.5)
When a local anesthetic is injected into tissue it is neutralized
and part of the ionized form is converted to non-ionized
The non-ionized base is what diffuses into the nerve.
23. • Hence if the tissue is infected, the pH is lower (more acidic) and
according to the HH equation; there
will be less of the non-ionized form of the drug to cross into the
nerve (rendering the LA less effective)
• Once some of the drug does cross; the pH in the nerve will be
normal and therefore the LA re-equilibrates to both the ionized and
non-ionized forms; but there are fewer cations which may cause
incomplete anesthesia.
24. MECHANISM OF ACTION OF LOCAL ANESTHETICS
The following sequence is proposed mechanism of action of LA:
Displacement of calcium ions from the sodium channel
receptor site
Binding of local anesthetic molecule to this receptor site
Blockade of sodium channel
25. Decrease in sodium conductance
Depression of rate of electrical depolarization
Failure to achieve the threshold potential level
Lack of development of propagated action potential
Conduction blockade…
27. COMERCIALLY PREPARED LOCAL ANESTHESIA CONSISTS OF:
Local anesthetic agent : lignocaineHCL 2%(20mg/ml)
Vasoconstrictor -adrenaline 1:80,000)
Reducing agent -sodium metabisulphite
Preservative -methylparaben,capryl hydrocuprienotoxin
Fungicide -thymol
Diluting agent: Distillded water
Isotonic solution: NaCl or Ringers solution-6mg
Nitogen bubble: 1-2 mm in diameter and is present to
prevent oxygen from being trapped in the cartridge and
potentially destroying the vasopressor.
28. LOCAL ANESTHETIC AGENT
The local anesthetics used in dentistry are divided into two
groups:
ESTER GROUP
AMIDE GROUP
29. ESTER GROUP:
It is composed of the following
An aromatic lipophilic group
An intermediate chain containing an ester linkage
A hydrophilic secondary or tertiary amino group
AMIDE GROUP:
It is composed of the following
An aromatic, lipophilic group
An intermediate chain containing amide linkage
A hydrophilic secondary or tertiary amino group
30.
31. CLASSIFICATION OF LOCAL ANESTHETICS ESTERS
Esters of benzoic acid
Butacaine
Cocaine
Benzocaine
Hexylcaine
Piperocaine
Tetracaine
Esters of Para-amino
benzoic acid
Chloroprocain
Procaine
Propoxycaine
33. CLASSIFICATION OF LOCAL
ANESTHETIC SUBSTANCES
ACCORDING TO BIOLOGICAL SITE
AND MODE OF ACTION
CLASS A: Agents acting at receptor site on external
surface of nerve membrane
Biotoxins (e.g., tetrodotoxin and saxitoxin)
CLASS B: Agents acting on receptor sites on internal
surface of nerve membrane.
Quaternary ammonium analogues of lidocaine, scorpion venom
34. CLASS C: Agents acting by receptor independent of physiochemical
mechanism
Chemical substance: Benzocaine.
CLASS D: Agents acting by combination of receptors and receptor
independent mechanisms
Chemical substance: most clinically useful
anesthetic agents.(e.g. lidocaine, mepivacaine, prilocaine)
35. PHARMACOKINETICS OF LOCAL ANESTHETICS
UPTAKE:
When injected into soft tissue most local anesthetics produce
dilation of vascular bed.
Cocaine is the only local anesthetic that produces
vasoconstriction, initially it produces vasodilation which is
followed by prolonged vasoconstriction.
Vasodilation is due to increase in the rate of absorption of the
local anesthetic into the blood, thus decreasing the duration of
pain control while increasing the anesthetic blood level and
potential for over dose.
36. ORAL ROUTE:
Except cocaine, local anesthetics are poorly absorbed from
GIT
Most local anesthetics undergo hepatic first-pass effect
following oral administration.
72% of dose is biotransformed into inactive metabolites
TOCAINIDE HYDROCHLORIDE an analogue of lidocaine is
effective orally
37. TOPICAL ROUTE:
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.
38. INJECTION:
The rate of uptake of local anesthetics after injection is
related to both the vascularity of the injection site and the
vasoactivity of the drug.
IV administration of local anesthetics provide the most rapid
elevation of blood levels and is used for primary treatment of
ventricular dysrhythmias.
39. DISTRIBUTION
Once absorbed in the blood stream local anesthetics are
distributed through out the body to all tissues.
Highly perfused organs such as brain, head, liver, kidney,
lungs have higher blood levels of anesthetic than do less
higher perfused organs.
40. The blood level is influenced by the following factors:
Rate of absorption into the blood stream.
Rate of distribution of the agent from the vascular
compartment to the tissues.
Elimination of drug through metabolic and/or excretory
pathways.
All local anesthetic agents readily cross the blood-brain
barrier, they also readily cross the placenta.
41. METABOLISM (BIOTRANSFORMATION)
ESTER LOCAL ANESTHETICS:
Ester local anesthetics are hydrolyzed in the plasma by the
enzyme pseudocholinesterase.
Chloroprocaine the most rapidly hydrolyzed, is the least toxic.
Tertracaine hydrolyzed 16 times more slowly than
Chloroprocaine ,hence it has the greatest potential toxicity.
42. AMIDE LOCAL ANESTHETICS
The metabolism of amide local anesthetics is more
complicated then esters. The primary site of
biotransformation of amide drugs is liver.
Entire metabolic process occurs in the liver for lidocaine,
articaine, etidocaine, and bupivacaine.
Prilocaine undergoes more rapid biotransformation then the
other amides.
43. EXCREATION
Kidneys are the primary excretory organs for both the local
anesthetic and its metabolites
A percentage of given dose of local anesthetic drug is
excreted unchanged in the urine.
Esters appear in only very small concentration as the parent
compound in urine.
Procaine appears in the urine as PABA (90%) and 2%
unchanged.
10% of cocaine dose is found in the urine unchanged.
Amides are present in the urine as a parent compound in a
greater percentage then are esters.
44. VASOCONSTRICTORS
Constrict vessels and decrease blood flow to the site of
injection.
Absorption of LA into bloodstream is slowed, producing
lower levels in the blood.
Lower blood levels lead to decreased risk of overdose (toxic)
reaction.
Higher LA concentration remains around the nerve
increasing the LA's duration of action.
45. Minimize bleeding at the site of administration.
Naturally Occurring Vasoconstrictors:
- Epinephrine
- Norepinephrine
Vasoconstrictors should be included unless contraindicated.
Mode of Action - Attach to and directly stimulate adrenergic
receptors . Act indirectly by provoking the release of
endogenous catecholamine from intraneuronal storage sites.
46. Concentrations of Vasoconstrictor in Local Anesthetics -
1:50,000, 1:80,000, 1:100,000,
1:200,000 - 0.020mg/ml, 0.012mg/ml, 0.010mg/ml, 0.005
mg/ml
Calculation 1:50,000= 1gram/50,000ml=1000mg/50,000ml=
1mg/50ml= 0.02mg/ml
Levonordefrin - One fifth as active as epinephrine
Vasoconstrictors - Unstable in Solution
49. OTHER COMMON NAMES- Tuberosity block, zygomatic block.
NERVE ANESTHETIZED- Posterior superior alveolar nerve and
branches.
AREA ANESTHETIZED-
1.Pulps of the maxillary third, second, and first molars (entire
tooth=72%; mesiobuccal root of the maxillary first molar not
anesthetized=28%)
2.Buccal periodontium and bone overlying these teeth.
INDICATION
1.When treatment involves two or more maxillary molars.
50. 1. A 27- gauge short needle recommended
2. Area of insertion: height of the mucobuccal fold above the
maxillary second molar
3. Target area: PSA nerve- posterior, superior, and medial to
the posterior border of the maxilla
4. LANDMARKS :
a. Mucobuccal fold
b. Maxillary tuberocity
c. Zygomatic process of maxilla
TECHNIQUE
51.
52. 5.Procedure:
a. Assume the correct position
1)For a left PSA nerve block, a right handed administrater should
sit at the 10 o’ clock position facing the patient.
2)For a right PSA block, a right handed administrater should sit at
the 8 ‘ clock position .
b. Prepare the tissues at the height of the mucobuccal fold for
penetration.
c. Orient the bevel of the needle toward bone.
d. Partially open the patients mouth, pulling the mandible to the side
of injection.
e.Insert the needle into height of mucobuccal fold over second molar
f.Advance the needle slowly in an upward, inward, and backward
direction in one movement.
g.Advanc the needle to the desired depth ( in an adult of normal
size, needle penetration depth is 16 mm)
h. Aspirate in two plane, if both aspirations are negative , deposi
0.9 to 1.8 ml of anesthetic solution slowly over 30 to 60 seconds.
54. Provides pulpal anaesthesia to the maxillary premolars and
the mesiobuccal root of the maxillary first molar,and
supporting buccal soft and hard tissues.
Recommended needle-27 gauge short.
MIDDLE SUPERIOR ALVEOLAR NERVE BLOCK
55. INICATIONS:
1.Where the ASA nerve block fails to provide pupal anesthesia
distal to the maxillary canine
2.Dental procedures involving both maxillary premolars only.
TECHNIQUE:
-Area of insertion: height of mucobuccal fold above the
maxillary second premolar
-Assume the correct position
-Insert the needle into height the height of mucobuccal fold
above second premolar with the bevel directed toward bone
-Penetrate the mucous membrane slowly advance the needle
until its tip is located well above the apex of second premolar.
-Aspirate
56. Slowly deposit 0.9 to 1.2 ml of solution( approx. in 30 to 40
seconds)
60. AREA ANESTHETIZED:
1.Pulps of the maxillary central incisor to the canine on
injected side
2.In about 72% of patients, pulps of the maxillary premolars
and mesiobuccal root of the first molar
3. Buccal periodontium and bone of these same teeth
4. Lower eyelid ,lateral aspect of nose, upper lip
61. AREA OF INSERTION: height of mucobuccal fold directly over first premolar
TARGET AREA: infraorbital foramen
LANDMARKS:
Mucobuccal fold
infraorbital notch
infraorbital foramen
PROCEDURE
-Assume the correct position
-prepare the tissue at the injection site
-Locate the infraorbital foramen
-Maintain finger on the foramen or mark the skin at the site
-Insert the needle into the height o mucobuccal fold over the first premolar with
the bevel facing bone
-Orient syringe toward the infraorbital foramen
-The needle should be hel parellel with the long axis of the tooth as it is
advanced, to avoid premature contact with bone
-Advance the needle slowly until bone is gently contacted.
-Aspirate in two planes
-Slowly deposit 0.9 to 1.2 ml solution.
TECHNIQUE
63. AREA ANESTHETIZED:
Provides anesthesia to the posterior portion of the hard
palate and its overlying soft tissues extending anteriorly as
far as the first premolar and medially to the midline
64. TARGET AREA: greater palatine nerve as it passes anteriorly between
soft tissues and bone of the hard palate
LANDMARK:greater palatine foramen and junction of maxillary
alveolar process and palatine bone
AREA OF INSERTION: soft tissue slightly anterior to greater palatine
foramen
PATH OF INSRTION: advance the syringe from opposite side of the
mouth at a right angle to the target area
PROCEURE
-Assume the correct position
-Locate greater palatine foramen
-Direct the syringe into the mouth from opposite side with the needle
approching the injection site at right angle
Place the bevel of needle gently against the previously blanched soft
tissue at the injection site
-Slowly advance the needle until palatine bone is gently contacted.
Aspirate , slowly deposite 0.45 to 6ml of LA solution
TECHNIQUE
66. Provides anaesthesia to the anterior portion of the hard
palate,affecting both soft and hard tissues,from the mesial of
the right first premolar to the mesial of the left first premolar.
AREA ANESTHETIZED
67. AREA OF INSERTION: palatal mucosa just lateral to the incisive papilla(
located in the midline behind the central incisor)
TARGET AREA: incisive foramen beneath the incisive papilla
LANDMARK: Central incisor and incisive papilla
PATH OF INSERTION: approach the injection site at a 45 degree angle
toward incisive papilla.
PROCEDURE:
-Assume the correct position
-prepare the tissue just lateral to the incisive papilla
-Place the bevel against the ischemic soft tissues at the injection site
-Straighten the needle and permit the bevel to penetrate the mucosa.
-Slowly advance the needle toward incisive foramen until bone is gently
contacted
-Withdraw the needle 1 mm to prevent subperiosteal injection
-Aspirate
-Slowly deposit 0.45 ml of local anesthetic solution
70. Mandibular teeth to the midline
Body of the mandible, inferior portion of the ramus
Buccal mucoperiosteum, mucous membrane anterior to the
mental foramen
Anterior two third of the tongue and floor of the oral cavity
Lingual soft tissues and periosteum
AREA ANESTHETIZED
71. A long dental needle is recommended for the adult patient.
A 25-gauge long needle is preferred
LANDMARKS:
-Coronoid notch( greatest concavity on the anterior border of
ramus)
-Pterygomandibular raphe
-Occlusal plane of mandibular posterior teeth
TARGET AREA: Inferior alveolar nerve as it passes downward
toward the mandibular foramen
AREA OF INSERTION: Mucous membrane on the medial side of
mandibular ramus
TECHNIQUE
72. PROCEDURE
-locate the needle penetration site
three parameters must be considered during administration of
IANB:
1)The height of injection
2)The antero-posterior placement of needle
3)The depth of penetration
-Place the syringe barrel in the corner of the mouth on the
contralateral side
-Insert the needle: when bone is contacted, withdraw
approximately 1 mm to prevent subperiosteal injection
-Aspirate in two plan. If negative, slowly deposit 1.5 ml of
anesthetic solution over a minimum of 60 seconds.
-Slowly withdraw the syringe, and when approximately half of its
length remains within tissues, reaspirate. If negative, deposit a
portion of the remaining solution(0.2 ml) to anesthetize the
lingual nerve.
74. AREA ANESTHETIZED: Soft tissue and periostium buccal to
the mandibular molar teeth.
LONG BUCCAL NERVE BLOCK
75.
76. TECHNIQUE:
LANDMARK: Mandibular molars, mucobuccal fold
TARGET AREA: Buccal nerve as it passes over the anterior border of the
ramus
AREA OF INSERTION: Mucous membrane distal and buccal to the most
distal molar tooth in the arch
-Prepare the tissues for penetration distal and buccal to the most
posterior molar.
-Penetrate mucous membrane at the injection site, distal and buccal to
the last molar
-Advance the needle slowly untill mucoperiosteum is gently contacted
-The depth of penetration is seldom more than 2 to 4 mm, and usually
only 1 or 2 mm.
-Aspirate
-If negative, slowly deposit 0.3 ml over 10 seconds.
80. AREA ANESTHETIZED:
Mandibular teeth to the midline
Buccal mucoperiosteum and mucous membranes on the side
of injection
Anterior two third of the tongue and floor of the oral cavity
Lingual soft tissues and periosteum
Body of the mandible, inferior portion of the ramus
Skin over the zygoma, posterior portion of the cheek, and
temporal regions
81.
82. AREA OF INSERTION: Mucous membrane on the mesial of the
mandibular ramus, on a line from the intertragic notch to the
corner of the mouth, just distal to the maxillary second molar
