Local anesthesia has been defined as 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.

1. MECHANISM OF LOCAL
ANESTHESIA
-Ishita Singhal

2. DEFINITION
 Local anesthesia has been defined as 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.

3. METHODS OF INDUCING LOCAL
ANESTHESIA
 Mechanical trauma (compression of tissues)
 Low temperature
 Anoxia
 Chemical irritants
 Neurolytic agents such as alcohol and phenol
 Chemical agents such as local anesthetics

4. IDEAL PROPERTIES OF LOCAL ANESTHESIA
 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 locally to mucous membranes.
 The time of onset of anesthesia should be as short as possible.

5.  The duration of action must be long enough to permit completion
of the procedure yet not so long as to require an extended recovery.
 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.

6. COMPOSITION OF LOCAL ANESTHESIA
 Local anesthetic agent: Lignocaine HCL-2%.
 Vasoconstrictor: Epinephrine-1:80000
– Absorption of the local anesthetic into the cardiovascular system is
slowed.
– Decrease the risk of local anesthetic toxicity.
– Higher volume of the local anesthetic agent remains in and around
the nerve for longer period, thereby increasing the duration of
action.
– Vasoconstrictors decrease bleeding at the site of their administration.

7.  Reducing agents: Vasoconstrictors are unstable in solution and may
oxidize, especially on a prolonged exposure to sunlight. Sodium
Metabisulfite which competes for the available oxygen is added in
the concentration between 0.05% and 0.1%.
 Preservative: Stability of modern local anesthetic solution is
maintained by adding Caprylhydrocuprienotoxin and Methyl
Paraben-0.1%
 Fungicide: Thymol
 Isotonic solution: Sodium Chloride-6mg.
 To adjust pH: Sodium Hydroxide
 Diluting agent: Distilled Water

8.  Vehicle: All the above solutions and local anesthetic agent are
dissolved in a modified Ringer’s solution. This isotonic vehicle
minimizes discomfort during injection.

9. STRUCTURE OF LOCAL ANESTHESIA
The basic components of local anesthetic (LA) structure are:
 A lipophilic aromatic portion
 A hydrophilic amine portion
 An intermediate hydrocarbon chain containing either an ester or an
amide linkage.

14. THEORIES
 Acetylcholine theory (dett barn 1967)
Acetylcholine was involved in nerve conduction in addition to its role as
neurotransmitter at nerve synapses. No evidence indicates that
acetylcholine is involved in neural transmission along the body of the
neuron.
 Calcium displacement theory(goldman 1966)
Stated that local anesthetic nerve block is produced by the displacement of
calcium from some membrane site that controlled permeability to sodium.
There is evidence that varying the concentration of ca++ ions bathing a
nerve does not affect local anesthetic potency.

15.  Surface charge (repulsion) theory(wei 1969)
Local anesthetics act by binding to the nerve membrane and changing the
electrical potential at the membrane surface. Cationic (RNH+)drug molecules were
aligned at the membrane–water interface, and because some of the local anesthetic
molecules carried a net positive charge, they made the electrical potential at the
membrane surface more positive, thus decreasing the excitability of the nerve by
increasing the threshold potential.
Current evidence indicates that the resting potential of the nerve membrane is
unaltered by local anesthetics (they do not become hyperpolarized), and that
conventional local anesthetics act within membrane channels rather than at the
membrane surface.
This theory cannot explain the activity of uncharged anesthetic molecules, e.g.
Benzocaine.

16.  Membrane expansion theory (lee 1976)
Local anesthetic molecules diffuse to hydrophobic regions of excitable membranes,
producing a general disturbance of the bulk membrane structure, expanding some
critical region(s) in the membrane and preventing an increase in permeability to
NA+ ions. LA that are highly lipid soluble can easily penetrate the lipid portion of
the cell membrane, producing a change in configuration of the lipoprotein matrix
of the nerve membrane.
This theory explains the action of benzocaine which does not exist in cationic
form, yet still exhibits potent topical anesthetic activity.
It has been demonstrated that nerve membranes in fact, do expand and become
more “fluid” when exposed to local anesthesia. However, there is no direct evidence
that nerve conduction is entirely blocked by membrane expansion per se.

17.  Specific receptor theory(strichartz 1987)
Local anesthesia act by binding to specific receptors on the sodium
channel either on its external surface or on the internal axoplasmic
surface. Once access is gained to these receptors, permeability to NA+
ions is decreased or eliminated and nerve conduction is interrupted.
There are at least four sites within the sodium channel at which
drugs can alter nerve conduction.

19. MECHANISM OF ACTION OF LOCAL
ANESTHESIA
• Altering the basic resting potential of the nerve membrane
• Altering the threshold potential (firing level)
• Decreasing the rate of depolarization
• Prolonging the rate of repolarization

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