GOOD MORNING

LOCAL ANESTHESIA
(DRUG PHARMACOLOGY AND BLOCKS )
DR . RITESH SINGH
History
1. 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

2. 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.

3. LIDOCAINE- Lofgren in 1948.

The discovery of its anesthetic properties was followed in 1949 by its clinical use
by T. Gordh
DEFINITION

It is reversible ,loss of sensation in a circumscribed

area of the body caused by depression of excitation in
nerve endings or inhibition of the conduction process
in peripheral nerves.
◦ STANLEY F. MALAMED
METHODS OF INDUCING LOCAL
ANESTHESIA
1. Mechanical trauma (compression of tissues)
2. Low temperature
3. Anoxia
4. Chemical irritants
5. Neurolytic agents such as alcohol and phenol
6. Chemical agents such as local anesthetics
PROPERTIES OF L.A.
It should not be irritating to the tissue to which it is applied.
It should not cause any permanent alteration of nerve structure.
Its systemic toxicity should be low.
It must be effective regardless of whether it is injected into the tissue
or is applied topically to mucous membranes.
The time of onset of anesthesia should be as short as possible.
The duration of action must be long enough to permit completion of
the procedure yet not so long as to require an extended recovery.
BENNETT ‘S ADDITION TO THESE
QUALITIES
It should have potency sufficient to give complete anesthesia without the use of
harmful concentrated solutions.

It should be relatively free from producing allergic reactions.

It should be stable in solution and should readily undergo biotransformation in

the body.

It should be sterile or capable of being sterilized by heat without deterioration.

NEUROPHYSIOLOGY OF
LOCAL ANESTHESIA
The Neuron
•The neuron or the nerve cells are the structural unit of the
nervous system.

•Two types of neurons:

(1)The sensory (afferent)
(2) Motor (efferent).
•The sensory neurons which are capable of transmitting the
sensation of pain consist of 3 major portions:

A. The peripheral process or dendritic zone

B. The axon:
C. The cell body:
NORMAL STRUCTURE OF NERVE
PHYSIOLOGY OF THE
PERIPHERAL NERVES
ELECTROPHYSIOLOGY OF NERVE
CONDUCTION
Step 1. A stimulus excites the nerve, leading to the following sequence of events:
This phase of rapid depolarization results in a reversal of the electrical potential across the
nerve membrane.
Step 2. Repolarization
Immediately after a stimulus has initiated an action
potential, a nerve is unable, for a time, to respond to another
stimulus, regardless of its strength. This is termed the
absolute refractory period

The absolute refractory period is followed by a relative

refractory period during which a new impulse can be
initiated but only by a stronger than normal stimulus.
MEMBRANE CHANNELS
IMPULSE PROPOGATION
MODE OF ACTION OF LOCAL
ANESTHETICS
Interfere with the excitation process in nerve membrane in one or more of
following ways:
1. Altering the basic resting potential of nerve membrane.
2. Altering the threshold potential (firing level).
3. Decreasing the rate of depolarization.
4. Prolonging the rate of repolarization.
Primary effect of LA occurs during depolarization.
Firing level is not achieved and action potential does not develop.
THEORIES OF L.A.
ACETYLCHOLINE THEORY
 CALCIUM DISPLACEMENT THEORY
 SURFACE CHARGE THEORY
 MEMBRANE EXPANSION THEORY
 SPECIFIC RECEPTOR THEORY
THE MEMBRANE EXPANSION
THEORY
THE SPECIFIC RECEPTOR
THEORY
 CLASSIFICATION ACCORDING TO
CHEMICAL NATURE
ESTERS
Amides
Esters of benzoic acid ESTERS OF P-
AMINOBENZOIC ACID Articaine
Butacaine
CHLOROPROCAINE Bupivacaine
Cocaine Dibucaine
PROCAINE
Ethyl aminobenzoate PROPOXYCAINE Etidocaine
(benzocaine)
Lidocaine
Hexylcaine Mepivacaine
Piperocaine Prilocaine
Tetracaine Ropivacaine
 On the Basis of Duration of
Action
Ultra-short-acting agents: Short-acting agents:
(duration of action is less than 30 minutes) (duration of action is 45–75 minutes)
•Procaine without a •2% lidocaine with 1:100,000 epinephrine
vasoconstrictor
•2% mepivacaine with 1:200,000
•2-chloroprocaine (1.2% or 3%) levonordefrin
without vasoconstrictor •4% prilocaine when used for nerve block
•2% lidocaine without a
•2% procaine, 0.4% propoxycaine with
vasoconstrictor vasoconstrictor
•4% prilocain
 MEDIUM-ACTING AGENTS :
LONG-ACTING AGENTS :
(duration of action is 90–150 minutes)
(duration of action is 180 minutes or longer)

•4% prilocaine with 1:200,000 •0.5% bupivacaine with 1:200,000

epinephrine epinephrine
•2% lidocaine and 2% •0.5% or 1.5% etidocaine with
mepivacaine with vasoconstrictor 1:200,000 epinephrine.
(pulpal anesthesia)
BIOLOGICAL SITE AND MODE OF
ACTION
CLASS A : Receptor site on external surface of nerve membrane
(Tetratoxins & Saxitoxins)

CLASS B : Receptor site on internal surface of nerve membrane

(Lidocaine & Scorpion venom)

CLASS C : Receptor independent physiochemical mechanism (Benzocaine)

CLASS D : Combination of Receptor & Receptor independent mechanisms

(Lidocaine, Mepivacaine, Prilocaine)
HOW LOCAL ANESTHETICS
WORK
1. Displacement of calcium ions from the sodium channel receptor site, which
permits…
2. Binding of the local anesthetic molecule to this receptor site, which produces…
3. Blockade of the sodium channel, and a…
4. Decrease in sodium conductance, which leads to…
5. Depression of the rate of electrical depolarization, and…
6. Failure to achieve the threshold potential level, along with…
7. Lack of development of propagated action potentials, which is called…
8. Conduction blockade.
LOCAL ANESTHETIC MOLECULES
Most injectable local anesthetics are tertiary amines.
All are amphipathic, they possess both lipophilic and hydrophilic characteristics,
generally at opposite ends of molecule with intermediate hydrocarbon chain
containing an ester or an amide linkage.
Lipophilic part is largest.
Local anesthetic without hydrophilic part are not suited for injection but are good
topical anesthetics. Eg. Benzocaine.
Histamine blockers and anticholinergic share this basic structure with local
anesthetics and commonly exhibits weak local anesthetic properties.
Nature of linkage is important in defining several properties of LA.
including the basic mode of biotransformation.
Ester-linked LA are readily hydrolyzed in aqueous solution.
Local anesthetics are basic compounds that are poorly soluble in
water and unstable on exposure to air.
However, because they are weakly basic, they combined readily with
acids to form local anesthetic salts, generally hydrochloride salt, in
which they are quite soluble in water and stable.
Increasing pH(alkalinization) of a local anesthetic
solution speeds the onset of its action, increases its
clinical effectiveness, and makes its injection more
comfortable.
Sodium bicarbonate or carbon dioxide added to the
anesthetic solution immediately before injection
provides greater comfort and a more rapid onset of
anesthesia.
 EFFECT OF pH ON LOCAL
ANESTHETIC EFFICACY
pH of LA as well as the tissue into which it is injected greatly influence its nerve blocking
action.
Acidification of tissue(as in inflammatory process) as well as acidification of LA solution
decreases LA effectiveness.
pH of normal tissue is 7.4 and of inflamed area is 5-6.
pH of solution without epinephrine is about 6.5 and with epinephrine is 3.5
When local anesthetic salts are dissolved in sterile water or saline, it exist simultaneously as
uncharged molecules, called base(RN) and as positively charged molecules, called
cation(RNH+).
RNH+ RN + H+
EFFECTIVENESS OF L.A. AT
NORMAL PH
EFFECTIVENESS OF LA AT LOW
PH OR INFLAMED TISSUE
COMPOSITION OF L.A.
Local anesthetic agent - 2%Lignocaine HCl
Vasoconstrictor - Adrenaline
Reducing agent - Sodium Meta bisulphite
Preservative - Methylparaben
Fungicide - Thymol
Vehicle - Ringers Solution
To adjust pH - Sodium Hydroxid
Nitrogen Bubble - to prevent oxygen from being trapped in cartridge
Pharmacokinetics of LA
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.
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

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.
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.

 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.
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.
 Amides v/s Esters
Major difference is method of metabolism
•Ester local anesthetics : are hydrolyzed in plasma by the enzyme pseudocholinesterase.
•The rate of hydrolysis has impact on the potential toxicity of LA.
•Procaine undergoes hydrolysis to PABA which is excreted unchanged in the urine, and to
diethylamine alcohol, which undergoes further biotransformation before excretion.
•Allergic reaction occurs due to PABA which is major metabolic product of esters.
Amide local anesthetics
The primary site of biotransformation of amide drugs is the liver.
The end product of lignocaine is monoethylglycinexylidide and glycinexylided .
 RECOVERY FROM LOCAL
ANESTHETIC BLOCK
Follows the same diffusion pattern as induction does but in reverse order.
Extraneural concentration of LA is continually depleted by diffusion, dispersion, and uptake of
drug, whereas the intraneural concentration remains relatively stable.
Thus the concentration gradient is reversed, and the anesthetic molecules begin to diffuse out of the
nerve.
Mantle bundles recovers much earlier than do the core bundles, thus proximally innervated area
recovers first.
Recovery is usually a slower process than induction because molecules are bound to the receptor
site.
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.
Causes for failure of LA
1. Anatomic variation
2. Bifid or double nerve supply
3. Secondary supply or soft tissue nerve supply
4. Inadequate dose
5. Injected into blood vessel
6. Degradation of vasoconstrictor
7. Patient having sepsis
COMPLICATIONS
ANAESTHETIC COMPLICATIONS: They can be defined as any deviation from
normally expected pattern during or after securing of regional analgesia –
Monheim

Adverse drug reaction is defined as any undesirable or unintended consequence

of drug administration.
TYPES OF SYSTEMIC
COMPLICATIONS
Overdose - A drug overdose reaction has been defined as those clinical signs and
symptoms that result from an overly high blood level of a drug in various target
organs and tissues.

is a hypersensitive state, acquired through exposure to a particular

Allergy -
allergen, re-exposure to which produces a heightened capacity to react.

◦ Idiosyncrasy - Qualitatively abnormal, unexpected response to a drug, differing from its

pharmacological actions.
 OVERDOSE - causes
- Biotransformation of the drug is unusually slow
- The unbiotransformed drug is eliminated too slowly from the body through the
kidney
- Too large dose is administered
- Absorption from the injection site is usually rapid
- Intravascular injection
INCIDENCE
 The rates of systemic toxicity due to LA have dropped significantly in the last three decades,
from 0.2 % to 0.01 %, due to the application of preventive measures such as aspiration prior to
inoculation, the use of trial doses and the establishment of maximum doses, inter alia.

 The highest toxicity rates have been reported as secondary to the peripheral nerve block
(7.5/10,000 cases). The mortality rate was 0.023 cases/100,000 (6).

 The incidence of regional anesthesia-related seizures was from 1 to 4/1,000 cases; with
regards to LA agents, bupivacaine was the LA with the highest incidence of complications .
 CENTRAL NERVOUS SYSTEM
TOXICITY
Extremely sensitive to actions of LA
Pharmacological actions of LA on CNS is depression.
LA agents cross the BBB  CNS depression
CARDIO VASCULAR SYSTEM TOXICITY
• AT NON- • AT BELOW
OVERDOSE OVERDOSE
LEVELS LEVELS

Slight increase Mild degree

or no change
in blood of
pressure hypotension

Cardiovascular Profound
collapse hypotension

• AT LETHAL • AT
LEVELS OVERDOSE
LEVELS
BASIC EMERGENCY MANAGEMENT:
P. . . POSITION
UNCONSCIOUS… SUPINE WITH FEET ELEVATED
CONSCIOUS… BASED UPON PATIENT COMFORT

A . . . AIRWAY
UNCONSCIOUS… ASSESS AND MAINTAIN AIRWAY
CONSCIOUS… ASSESS BREATHING

B . . . BREATHING
UNCONSCIOUS… ASSESS AND VENTILATE IF NECESSARY
CONSCIOUS… ASSESS BREATHING

C . . . CIRCULATION
UNCONSCIOUS… ASSESS & PROVIDE EXTERNAL CARDIAC COMPRESSION IF NECESSARY
CONSCIOUS… ASSESS CIRCULATION

D . . . DEFINITIVE CARE
DIAGNOSIS: MANAGEMENT: EMERGENCY DRUGS AND/ OR ASSISTANCE
ALLERGY - causes
Hypersensitivity to:-
Local anaesthetic itself
Methyl paraben( preservative)
Sodium metabisulfite(antioxidant / reducing agent)
 SIGNS AND SYMPTOMS

Dermatologic
al reactions urticaria angioedema

Respiratory
reactions bronchospasm Laryngeal edema

Skin Smooth Respira Cardiova

Generalized
anaphylaxis reactio muscle tory scular
ns spasms distress collapse
 MANAGEMENT
Skin reactions:
 Delayed skin reaction: (developing 1 hr after exposure) Administer oral histamine blocker- 50 mg diphenhydramine or
10 mg chlorpheniramine
Immediate skin reaction: (develop within 1 hr)
◦ Administer epinephrine 0.3 mg IM or SC
◦ Administer histamine blocker 50 mg diphenhydramine IM
◦ Observe the patient for at least 60 mins for recurrence

Respiratory reactions:
 Bronchospasm: Administer oxygen via full mask, nasal cannula at a flow of 5-6 litres/min
 Administer 0.3 ml (1:1000) epinephrine IM/SC or bronchodilator via aerosol inhaler
 Observe for 60 min
 Administer histamine blocker to minimize relapse possibility
Respiratory reactions
Bronchospasm:
 PABC
 Administer oxygen via full mask, nasal cannula at a flow of 5-6 litres/min
 Administer 0.3 ml (1:1000) epinephrine IM/SC or bronchodilator via aerosol inhaler
 Observe for 60 min
 Administer histamine blocker to minimize relapse possibility
 Summon medical assistance
Laryngeal edema:
PABC
Administer 0.3 ml epinephrine IM/SC
Summon medical assistance
Maintain airway
Additional drug management by administering histamine blocker (50mg
diphenhydramine IM/IV)
Perform cricothyrotomy if the above methods fail to secure a patent airway
Drugs for anesthetic
emergencies
DRUG DOSAGE ADMINISTRATION INDICATION

OXYGEN SUFFICIENT INHALATION RESPIRATORY OR CV

QUANTITY

EPINEPHRINE 0.3-0.5 mg IM/SC ALLERGIC REACTIONS

DIPHENHYDRAMINE 20-50 mg IV ALLERGIC REACTIONS

ATROPINE SULFATE 1mg and repeated IV BRADYCARDIA

every 3-5 minutes if
asystole persists

SUCCINYLCHOLINE 20-50 mg IV CONVULSIONS

DIAZEPAM 10 mg IV TOXIC OVERDOSE

MIDAZOLAM 5 mg IV TOXIC OVERDOSE

MALIGNANT HYPERTHERMIA
Malignant hyperthermia (MH; hyperpyrexia) is a pharmacogenic disorder in which a
genetic variant in an individual alters that person's response to certain drugs.
Incidence: reported mortality rates ranging from 28-53% occurs in 1 in 15,000
anaesthetic administrations in children and 1 in 50,000 in middle -aged adults.

Clinical signs: Tachycardia, Rigidity, Altered B.P, Tachypnea, Cyanosis, Fever [ 42◦C or
108◦ F]

Treatment : Dantrolene sodium 2.5-4.0 mg/kg initially and 1mg/kg every 4 hours upto
48 hrs after the episode.
METHEMOGLOBINEMIA
Methemoglobinemia is a reaction that can occur after administration of amide local anaesthetics, nitrates
and aniline dyes.
•Prilocaine , Benzocaine and articaine can oxidize the ferrous form of the hemoglobin to the ferric form,
creating methemoglobin.

•Prilocaine doses of >600mg are needed to produce clinically significant methemoglobinemia

Diagnosis needs clinical suspicion and confirmation by blood gas analysis.

Methemoglobinemia treated by- administration of methylene blue (1-2mg/kg of a 1% solution over 5 min)
or less successfully with ascorbic acid (2 mg/kg).
Systemic action of Local
Anesthetics
LA anesthetics readily cross the blood-brain barrier. Their pharmacological action on CNS is CNS
depression.
Effect on CVS
Direct action on the Myocardium : LA produces a myocardial depression that is
related to LA blood level.
LA decrease electrical excitability of myocardium, decrease the conduction rate, the
decrease the force of contraction.
This occurs when LA is given at range of 1.8 to 6 ug/ml.
Effect On Respiratory System
LA have a direct relaxant action on bronchial smooth muscle at non overdose levels.
Whereas at overdose level they produce respiratory arrest as a result of generalised
CNS depression.
 vasoconstrictor
Drugs that constrict blood vessels and control tissue perfusion.
Oppose inherent vasodilatory actions of local anesthetics.

I. Decrease blood flow to site of administration. ( low perfusion )

II. Slowed absorption of LA in CVS.
III. Decreases the risk of LA toxicity.
IV. Increases depth and duration of LA in nerve.
V. Decreases bleeding at site of surgery.
(= sympathomimetic/ adrenergic drugs )
 Pharmacology of
Vasoconstrictors
Any agent that causes a constriction or narrowing of an opening of a blood vessel.
Vasoconstrictors resemble adrenergic drug and are called sympathomimetic drugs.
Need Of Vasoconstrictors
Constrict blood vessels  decrease blood flow to the surgical site
Cardiovascular absorption is slowed  lower anesthetic blood levels
Local anesthetic blood levels are lowered  lower risk of toxicity
Local anesthetic remains around the nerve for longer periods 
increased duration of anesthesia
Decreases bleeding
 Selection of vasoconstrictor
• LENGTH OF THE DENTAL PROCEDURE

• REQUIREMENT FOR HEMOSTASIS

• MEDICAL STATUS OF PATIENT

Classification
Catecholamines Noncatecholamines
Epinephrine
Amphetamine
Norepinephrine
Levonordefrin Methamphetamine
Isoproterenol Ephedrine
Dopamine Hydroxyamphetamine
Modes of Action
3 Classes of Sympathomimetic Amines:
Direct Acting  directly on adrenergic receptors
Indirect Acting  act by release of norepinephrine from adrenergic nerve endings
Mixed Acting  both direct and indirect actions
Types of Adrenergic Receptors
 Alpha : Contraction of smooth muscle in blood vessels vasoconstriction
 Beta : Smooth muscle relaxation, vasodilation/ bronchodilation, cardiac stimulation, i.e.,
increased rate and strength of contraction
•Beta 1-found in heart and small intestines produces cardiac stimulation and lipolysis.
•Beta 2-found in bronchi of the lung, vascular beds and uterus produces bronchodilation and
vasodilation
EPINEPHRINE
Proprietary name: Adrenaline
It is Acid salt highly soluble in water. In Slightly acid solutions are
stable if they are protected from air. Deterioration (through
oxidation) is hastened by presence of heat and Heavy metal ions.
Sodium meta bisulfite is added to delay this deterioration.
Shelf life: LA+VC(18months)
Source: Synthetic, also obtained from adrenal medulla of animals.
MOA: Acts directly on alpha & beta receptors. Beta effects
are predominate.
Systemic actions:
-Myocardium: B1 receptor stimulation + Chronotropic action
-Pacemaker cells: Stimulates B1 receptors, Increases irritability of
pacemaker cells → increase incidence of dysrhythmias.
-Respiratory system: Potent bronchodilator.
-CNS: Stimulation when dose ↑.
Dilution of vasoconstrictor
The genesis of vasoconstrictor dilutions was given by Abel in 1897. The dilutions
are commonly referred to as Ratios.
Eg: 1:1000, 1:2500, 1:10,000, 1:100,000, 1:200,000 etc .

1:1000 – 1 g of solute in 1000 ml of solution/ 1000 mg of solute in 1000ml of

solution
1: 1000 Epinephrine – Emergency medicine ( IM/SC anaphylaxis)
1:2,500 Phenylephrine – hypotension, nasal decongestant & to produce
mydriasis ( Glaucoma )
1:10,000 Epinephrine - Emergency medicine ( IV/ET Cardiac arrest)
1:20,000 Levonordefrin – vasoconstrictor in LA, helps to provide longer
duration of anesthesia with mepivacaine.
1:30,000 Norepinephrine – vasoconstrictor in LA, for hypotension.
:50,000 Epinephrine- vasoconstrictor in LA. For hemostasis. Extended pain control.
1:80,000 Epinephrine – vasoconstrictor in LA. Longer duration of action and increase in depth of
the LA. Also reduces toxicity. Standard dilution for dental usag
1:1,00,000 Epinephrine – vasoconstrictor in LA & increases tissue oxygen consumption by
glycogenolysis. For patients with cardiovascular risk.
1:2,00,000 Epinephrine – vasoconstrictors used where they are contraindicated such as
hyperthyroidism, cardiovascular risk, hepatic failure.
1:4,00,000 Epinephrine - vasoconstrictor in LA
Concentrations of Vasoconstrictor in Local Anesthetics - 1:50,000 ,1:100,000, 1:200,000
- 0.020mg/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 Sodium metabisulfite added Known allergen

Max dose of vasoconstrictor
- Healthy patient approximately 0.2mg

- Patient with significant cardiovascular history:

Safe dose calculation of
adrenalin
2% lignocaine with1:2,00,000 of adrenaline
1000mg : 2,00,000
1000/2,00,000=0.005mg/ml of adrenaline
Safest dose of adrenaline =0.2mg in normal patients
0.2/0.005=40ml
Since one cartridge contains 1.8 ml
40/1.8 = 22 cartridges
Safest dose of adrenaline =0.04mg in cardiac compromised patients
0.04/0.005= 8ml
Since one cartridge contains 1.8 ml
8/1.8 = 4.4 cartridges
If adrenaline conc is 1:80,000
=1000/80,000=0.0125
1ml=0.0125mg
Safest dose for normal patients=0.2mg
=0.2/0.0125=16ml = 6.4 Cartridges
Safest dose for cardiac pt =0.04mg
0.04/0.0125=3ml,1.2 cartridges
Side effects & overdose:
CNS Stimulation,↑ Fear & Anxiety, Tension, Restlessness,
throbbing headache, tremor, weakness, dizziness, pallor,
respiratory difficulty & palpitation.
↑ levels- cardiac dysrythmias, ventricular fibrillation,
Cerebral haemorrhage, Anginal episodes
TACHYPHYLAXIS
Defined as an increasing tolerance to a drug that is administered repeatedly.
Much more likely to develop if nerve function is allowed to return before reinjection.
Causes:
•Edema
•Localized hemorrhage
•Clot formation
•Transudation
•Hypernatremia
•Decrease pH of tissue
Types of blocks
NERVE BLOCKS – a method of securing the regional anaesthesia by depositing the suitable LA
within close proximity of the main trunk of the nerve
FIELD BLOCKS – for securing the regional anaesthesia by deposition around larger terminals of
the nerve branches
LOCAL INFILTERATIONS – the deposition of the LA over smaller termial nerve endings in the area
of the surgery, facilitates placing the incision lines.
INTRALIGAMENTARY TECHNIQUES – the technique is intended to provide single tooth
anaesthesia, consist of forcing the LA in the PDL space.
TOPICAL ANEAESTHESIA – to the free nerve endings in the accessible regions such as the intact
mucous membrane, abraded skin or cornea of the eye
Maxillary nerve blocks
MSA/ ASA BLOCKS –
Infra-orbital blocks
◦ -bicuspid approach – in a line parallel to the supraorbital notch, pupils of eye, infra-orbital notch and
2nd bicuspid tooth
◦ - central incisor approach – by bisecting the crown of the central incisor

PSA BLOCKS –
NASOPALATINE NERVE BLOCK
ANTERIOR PALANTINE NERVE BLOCK/ GREATER PALATINE NERVE BLOCK
MAXILLARY NERVE BLOCKS
◦ - high tuberosity technique - needle progress upwards, inwards and backwards
◦ - greater palatine canal technique -
Mandibular nerve blocks
Types of mandibular techniques:
1) Direct technique
Inferior alveolar nerve [Link] nerve block.
Incisive nerve block. Mental nerve block.
2) Indirect technique
Gow gates technique.
Vazirani-Akinosi technique.
3) Extra oral technique.
Fischer 123 technique.
Kurt- Thoma technique.
Inferior alveolar nerve block:
Nerves anesthetized: Inferior alvelor nerve , Buccal nerve, Lingual
nerve
Advantages : Provides wide area of anesthesia.
Disadvantages: inadequate anesthesia( 15 to 20%) ,landmarks
not reliable, positive aspiration, lingual and lip anesthesia,
uncomfortable, partial anesthesia, in bifid mandibular canal or
bifid IAN
Technique:Needle: [Link] area: inferior alveolar nerve-
passes downwards towards mandible foramen but before it
enters the [Link] of patient: semi-supine- mouth
open, mandibular molar occlusal plain parallel to [Link] of
operator: right- 8 ‘o’ clockleft- 10 ‘o’ clock. In sittingposition.
There are three parameters that must be considered during administration of IANB.
1) height of injection*6 mm above occlusal plain.*3/4 of the anteroposterior
distance.*pterygomandibular raphe.
2) Anteroposterior site of injection:
a. point 1 falls along the horizontal line from the coronoid notch to the deepest point of
pterygomandibular rapheb. point 2 is on vertical line through point 1 about 3/4th of the distance
from the anterior border of ramus.3) Penetration depth:20-25mm or 2/3rd of the needle
shouldbe penetrated.
Amount of local anesthesia to be deposited:
1.5 ml 60 seconds, inferior alveolar nerve.0.1 ml, lingual nerve.0.6 ml 20 seconds, lingual side if
necessary.0.6 ml 20 seconds, incisive nerve if necessary.
GOW-GATES Technique
AKINOSI-VAZIRANI technique
FISHER 1-2-3 technique
anesthetic is injected using three different needle positions.

1st position - buccal anesthesia, the needle is first positioned on the midpoint of the thumbnail
when the thumb is placed on the external oblique from over the contralateral premolars and
inserted to a depth of about 6 mm
2nd position - the needle is pulled out and moved to the same side so that the needle slides onto
the internal oblique ridge. The syringe is maintained parallel to the mandible occlusal plane and
the needle is advanced about 8 mm.
3rd position - the syringe is repositioned over the opposite first premolar and the needle is
advanced 12–15 mm until the tip makes contact with bone. The needle should be withdrawn a
bit and aspirated before the anesthetic is injected.
KURT-THOMA technique
limited mouth opening like TRISMUS, ANKYLOSIS.
The needle is inserted through the skin from below the lower border of the angle of the
mandible close to the inner surface of the ramus so that the needle finally comes to lie medial to
the mandibular foramen. Aspiration is done and solution deposited.
Arched needle technique
by Ashish Chakranarayan,
the failure rate may be lowered if the needle is arched at an angle almost perpendicular to the
ramus and inserted to the medial side of the ramus. The needle is inserted slightly posterior to
that in the conventional technique and to 4–5 mm in depth parallel to the occlusal plane. Then,
the embedded tip is used as a pivot to arch the uninserted portion of the needle
posteromedially, so that the approaching angle of the needle tip is changed from acute to nearly
perpendicular
 Mandibular foramen anterior
technique
Takasugi et al. introduced this
technique which positions the needle
anterior to the mandibular foramen.
The needle tip is positioned at a
distance approximately 10 mm above
the occlusal plane of the mandible and
inserted to a depth of 10 mm towards
the lateral side of the
pterygomandibular raphe from the
contralateral first molar, creating an
approaching angle of 60
Modified IANB
1. Boonsiriseth et al.
Introduced a technique for achieving anesthesia of the inferior alveolar nerve without
periosteum contact.
The insertion point is the same as that of the conventional inferior alveolar nerve block and the
syringe is positioned parallel to the mandibular occlusal plane of the same side of the surgical
site.
The insertion depth is controlled by a rubber stop. A 30 mm needle is used and, with the rubber
stop positioned at 20 mm, the needle is advanced until the rubber stop makes contact.
As the needle does not contact the periosteum, this technique provides less pain compared to
the conventional technique and reduces the frequency of positive aspiration and the risk of
neural or vascular injury
2. Thangavelu et al.,
An anesthesia technique that uses the internal oblique ridge as the only anatomical landmark.
When the thumb is placed on the retromolar area, the internal oblique ridge is indicated by the
tip of the thumb.
The insertion point will be 6–8 mm above the midpoint of the thumb and 2 mm posterior to the
internal oblique ridge.
The syringe is placed over the contralateral premolars and the needle is advanced until it
touches the bone.
The success rate of this anesthesia technique was 95%
REFERENCES
1. HAND BOOK OF LOCAL ANESTHESIA- 5TH EDITION-STANLEY F. MALAMED
2. MONHEIM'S LOCAL ANESTHESIA AND PAIN CONTROL IN DENTAL PRACTICE-
LEONARD M. MONHEIM
3. Kim C, Hwang KG, Park CJ. Local anesthesia for mandibular third molar extraction. Journal of dental
anesthesia and pain medicine. 2018 Oct 1;18(5):287-94.
4. Khalil H. A basic review on the inferior alveolar nerve block techniques. Anesthesia, essays and
researches. 2014 Jan;8(1):3.
5. Thangavelu K, Kannan R, Kumar NS. Inferior alveolar nerve block: Alternative technique.
Anesthesia, essays and researches. 2012 Jan;6(1):53.
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