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ISHIK UNIVERSITY
FACULTY OF DENTISTRY
LOCAL ANAESTHETICS
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Local anesthetics are employed routinely in dentistry
by nerve block or by infiltration and/or regional
block techniques to carry out various operative
procedures.
Local anesthetics can also be classified into two
categories based on their chemical structure
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Local anesthetics are weak bases.
The pKa for most local anesthetics is in the range of
8.0-9.0. A balance of charged and uncharged forms
is present in the body.
The ratio between the cationic and uncharged forms
of these drugs is determined by the HendersonHasselbalch equation (Log (cationic form/uncharged
form) = pKa-pH).
The uncharged form is more lipophilic and thus
more rapidly diffuses through the membrane.
However, the charged form has higher affinity for the
receptor site of the sodium channel.
a. Ester linked local anaesthetics e.g. cocaine,
procaine, tetracaine, benzocaine, chloroprocaine.
b. Amide linked local anaesthetics e.g. lidocaine,
bupivacaine, dibucaine, prilocaine, ropivacaine.
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All the local anaesthetics possess varying degree of
water and lipid solubility.
Both the properties are essential for a local
anaesthetic, lipid solubility helps in migration of
active drug into the neuronal fibre
water solubility is essential to get the drug to site
of action from the site of administration.
Local anaesthetics block both the generation and
conduction of the nerve impulse.
CLASSIFICATION
INJECTABLE
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Low potency & short duration

Procaine

Chloroprocaine
SURFACE
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Intermediate potency & duration

Lignocaine

Prilocaine
High potency & long duration

Tetracine
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Bupivacaine
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Ropivacaine
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Soluble
 Cocaine
 Lignocaine
 Tetracaine
Insoluble : Benzocaine
Types of Local Anaesthetics

Esters
 Cocaine
 Procaine
 Tetracaine
 Chlorprocaine
 Benzocaine
Short DOA, less intense analgesia

Amides
 Lignocaine
 Mepivicaine
 Prilocaine
 Bupivacaine
More intense and longer
lasting anaesthesia
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Esters
Hydrolysed in the plasma
by a pseudo
cholinesterase
One by-product of this
reaction Para-Amino
Benzoic Acid (PABA)
Allergic reaction are
associated with PABA
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Amides
These get metabolized in
the liver to inactive
agents
Binding to amides is
provided by alpha 1
glycoprotein in plama
No allergies associated
with amides
Mechanism of action
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In simplest terms, local anesthetics bind to receptors
near the sodium channel on the nerve membrane. As
the amount of the local anesthetic accumulates, the
sodium channels become obstructed. Impulses along
the nerve are slowed, the strength and propagation
of the action potential are diminished, and
communication along the fiber is blocked.
Larger nerves require larger doses of the local
anesthetic to achieve this effect
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The uncharged form of local anesthetics is more likely
to penetrate the membrane but the charged form is
more active in blocking the Na+ channel.
At high pH, most local anesthetics are uncharged but
also have a lower affinity for the sodium channel.
At very low pH, there is a higher percentage of
charged molecules which reduces the effects of the
drugs as they are less likely to enter cells.
Differential blockade
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Peripheral nerve functions are not affected equally by
local anesthetics.
Loss of sympathetic function usually is followed by
loss of temperature sensation; sensation to pinprick,
touch, and deep pressure; and motor function. This
phenomenon is called differential blockade.
Differential blockade is the result of a number of
factors, including the size of the nerve, the presence
and amount of myelin, and the location of particular
fibers within a nerve bundle.
PHARMACOLOGICAL ACTIONS
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CNS :
 All can produce CNS stimulation followed by depression.
 Cocaine:
 Euphoria-excitement-mental Confusion-tremors-muscle
Twitching-convulsions- Unconciousness -resp. Depression.
 Procaine, Lignocaine: safe at clinical doses
CVS :
 Cardiac depressant at iv doses
 Antiarrhythmic action (procainamide)
Techniques of administration
Topical Anesthesia
 Infiltration
 Conduction block
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 Field
block
 Nerve block
Peridural
Spinal anesthesia
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Topical Anesthesia
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Done by the administering the anesthetic to mucous
membranes or skin. Relieves itching, burning and
surface pain, i.e. sunburns.
Infiltration
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Occurs by directly injecting a local anesthetic to
block the nerve endings under the skin or in the
subcutaneous tissue. Used mainly for surgeries, i.e.
cavities being filled.
Conduction block
Epidural Anesthesia

This is accomplished by
injecting a local
anesthetic into the
peridural space, a
covering of the spinal
cord
Spinal anesthesia
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Here, the local
anesthetic is injected into
the subarachnoid space
of the spinal cord
Toxicity
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CNS Toxicity:
 Systematic absorption can lead to excitement (tremors,
shivering, convulsions),
 If absorbed in even higher amounts can lead to depression
(coma, respiratory arrest and death)
Cardiovascular toxicity:
 If absorbed in excess systematically can lead to depression
of the cardiovascular system
Hypersensitivity: Rashes to anaphylaxis
Local reactions: Combination with vasoconstrictor
(combination should be avoided-feet, fingers, toes, pinna, penis)
Adverse Effects
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CNS side effects include: dizziness, mental
confusion, tremors, twitching, visual disturbances,
convulsion and respiratory depression.
CVS toxicity includes : hypotension, cardiac
arrhythmias and bradycardia. Other side effects
include allergic dermatitis, asthma, anaphylactic
shock etc.
Pharmacokinetics
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They are readily absorbed through mucous membranes
and damaged skin. These are weak bases and at tissue
pH diffuse through the connective tissue and cellular
membranes to reach the nerve fibres where ionization
can occur.
Amide type local anaesthetics (lignocaine, bupivacaine)
are metabolised in the liver and in some cases the
kidneys. These are considerably protein bound.
For certain procedures the duration of action is
prolonged by adding adrenaline 1 in 2,00,000. In
dentistry, where the total dose is small higher
concentration such as 1 in 80,000 may be used.
Therapeutic Uses
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Surface anaesthesia.
Spinal anaesthesia.
Infiltration anaesthesia.
Nerve block or conduction block
Systemic use in the treatment of cardiac arrhythmias
Dental anaesthesia: The total amount of local
anaesthetics injected is much smaller (20-80 mg of
lignocaine) than that used for other purpose.
LIGNOCAINE
Mechanism of Action
 Lignocaine stabilizes the neuronal membrane by inhibiting
ionic fluxes required for initiation and conduction of impulses
thereby affecting local anaesthetic action.
Pharmacokinetics
 Lignocaine is completely absorbed following parenteral
administration, its rate of absorption depending upon
various factors such as site of administration and the
presence or absence of vasoconstrictor agent. Lignocaine is
metabolised rapidly by the liver and metabolites and
unchanged drug are excreted by the kidneys.
Approximately 90% of lignocaine administered is excreted
in the form of various metabolites and less than 10% is
excreted unchanged.
 The elimination half-life of lignocaine following an
intravenous bolus injection is 1.5 to 2.0 hours.
Adverse Effects
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CNS manifestations are excitatory and/ or depressant
and may be characterised by light-headedness,
nervousness, apprehension, euphoria, confusion,
dizziness, drowsiness, tinnitus, blurred or double vision,
vomiting, sensation of heat, cold or numbness, twitching,
tremors, convulsions, unconsciousness, respiratory
depression.
Drowsiness following the administration of lignocaine is
usually an early sign of a high blood level of the drug
and may occur as a consequence of rapid absorption.
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Cardiovascular manifestations are usually
depressant and are characterised by bradycardia,
hypotension and cardiovascular collapse, which may
lead to cardiac arrest.
Allergic reactions are characterised by cutaneous
lesions, urticaria, edema or anaphylactoid reactions
may occur as a result of sensitivity to local
anaesthetic agent.
Indication
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Lignocaine injections are indicated for production of
local or regional anaesthesia by infiltration techniques
such as percutaneous injection, peripheral nerve block,
spinal or subarachnoid block.
Lignocaine (2%) with adrenaline (1:80,000) is mostly
used local anaesthetic in dentistry which produces good
soft tissue and pulpal anaesthesia and also reduces
post extraction bleeding. The pulpal anaesthesia is
obtained within 2-3 minutes after injection and lasts for
about on hour.
BENZOCAINE
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Inhibits conduction of nerve impulses from sensory
nerves. This action is a result of alteration of cell
membrane permeability to ions. It is poorly
absorbed from the intact epidermis.
Benzocaine has been termed by the FDA as ‘one of
the most widely used and safest external analgesic
and that the incidence of sensitivity of benzocaine is
quite low’.
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DIBUCAINE
It is another local anaesthetic with longer action but
most toxic. It is used for surface anaesthesia.
BUPIVACAINE
It is a potent and long acting local anaesthetic used for
spinal, infiltration, epidural anaesthesia and nerve
block.
Side effects include cardiac arrest, cardiac arrhythmias
and respiratory failure.
Bupivacaine (0.5%) with adrenaline (1:2,00,000) is less
frequently used in dentistry because of its poor
penetration into bone.
BENOXINATE
 It is a surface anaesthetic used in eye for producing corneal
anaesthesia for tonometry and does not cause mydriasis or any
corneal damage.
OXETHAZAINE
 A potent local anaesthetic used for anaesthetizing gastric mucosa.
Along with antacid in suspension form it is used in gastritis, gastric
irritation and gastroesophageal reflux.
 Side effects include drowsiness and dizziness.
ROPIVACAINE
 Newer compound, long acting local anaesthetic which produces less
cardiotoxicity. It is used mainly for nerve block and in postoperative
pain. It is occasionally used in dentistry.
The Use of Vasoconstrictors in Local
Anesthesia
With the exception of cocaine, local anesthetics
cause a transient vasodilation (dilatation of blood
vessels) following application or injection.
Vasodilation causes an increased perfusion of blood
to the injected area, with two possible results:
(1) the drug being carried away, and therefore
becoming less effective
(2) the anesthetic agent reaching the cardiac muscle
with the potential for undesired myocardial effects
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The effect on the heart muscle is a valid
consideration since one of the prototype drugs in
these discussions, lidocaine, has a use in medical
emergencies in the treatment for life-threatening
ventricular arrhythmia.
In order to maintain effective concentrations of local
anesthetics at the injection site, vasoconstrictive
drugs are often added to the solution.
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The primary additive is epinephrine.
The addition of epinephrine not only minimizes the
vasodilation caused by the local anesthetic agent,
but causes vasoconstriction of the blood vessels in
the area surrounding the injection. The
vasoconstriction decreases perfusion of blood to the
region, and the local anesthetic is not carried away.
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Patients with diabetes are predisposed to problems
with capillary circulation.
The addition of epinephrine can cause further
vasoconstriction to capillaries already compromised by
the disease process.
Patients with diabetes may experience an increase in
tissue damage as a result.
Another vasoconstrictor: phenylphrine, felypressin,
levonordefrin.
The most common dilution for levonordefrin 1:20,000.