3. Definition of LA
Local Anaesthesia has been defined as a
“ Reversible loss of sensation in a
circumscribed area of the body caused by a
depression of excitation in nerve endings or
an inhibition of conduction process in
peripheral nerves”
5. Based on chemical structure
Esters
• Cocaine
• Procaine
• Benzocaine
• Tetracaine
Amides
• Articaine
• Bupivacaine
• Lidocaine
• Mepivacaine
• Prilocaine
• Ropivacaine
6. Based on duration of action
• 2% Lignocaine without vasoconstrictorUltra short duration
• Procaine
• 2% Lignocaine with 1:1,00,000
Epinephrine
Short duration
• Articaine
• Mepivacaine
• Prilocaine
• 2% Lignocaine with 1:2,00,000
Epinephrine
Intermediate
Duration
• Bupivacaine
• Etidocaine
• 5% Lignocaine with 1:2,00,000
Epinephrine
Long Duration
8. Composition
• Local anaesthetic solution contains:
1. Local anaesthetic agent-
Ester linkage- procaine,cocaine,tetracaine
Amide linkage-Lignocaine, prilocaine,
bupivacaine , mepivacaine
2. Vasoconstrictor-
Adrenaline- a synthetic substance similar to that
secreted in human body. Concentration from
1:50,000-1:250,000 (optimal 1:200,000)
9. Advantage
• Reduces toxic effect by retarding the absorption of
the constituents.
• It increases the depth & duration of the anaesthesia
and produces bloodless field for the surgical
procedure.
3. Reducing agent – Sodium bimetasulphite.
• Small quantity in the solution prevents oxidation of
the vasoconstrictor as they are unstable in solution
especially on exposure to sunlight.
10. 4. Preservative- caprylhydrocupeinotoxin
• It helps to maintain sterility of the solution & also
increases its shelf life.
5. Fungicide- Thymol
• To prevent proliferation of the minute fungi which
cause cloudiness of the solution.
6. Vehicle – Ringer’s solution.
• In which all constituents are dissolved to minimize
discomfort during injection of the L.A.
7. Sodium chloride - Isotonicity of the solution
11. Indications
• The patient remains awake and cooperative.
• Poor risk patients.
• Low incidence of morbidity
• Patients leaves office unescorted.
• No additional trained personnel is necessary.
• Techniques are not difficult to master.
• % of failure is small
• No additional expense to patient
• Patient need not omit the previous meal
12. Contraindications
• Patient refuses regional anaesthesia because
of fear or apprehension
• Infection
• Allergy
• Patient is below the age of reason
• Major surgery- regional anaesthesia
unfeasible
• Anomalies
14. Electrophysiology of nerve
conduction
• Electrical events occur within a nerve during
the conduction of an impulse.
• A nerve possesses a resting potential which is
-70mV that exists across the nerve membrane,
produced by differing concentration of ions on
either side is the membrane.
• A stimulus excites the nerve, in the following
sequence of events:-
15. • Step 1a- An initial phase of slow
depolarization.
• Step 1b- Falling electrical
potential reaches a critical level,
it gives result of rapid phase of
depolarization. This is termed as
Threshold or firing potential.
• Step 1c- This phase of rapid
depolarization results in a
reversal of electrical potential
across the nerve membrane.
Electric potential of +40mV
exists on the interior of the
nerve cell.
16. Depolarization
• Excitation of the nerve
segment leads to an
increase in permeability of
the cell membrane to
sodium ions. The rapid influx
of the sodium ions to the
interior of the nerve cell
causes depolarization of the
nerve membrane from its
resting level to its firing
threshold of approx. -50 to -
60mV. Exposure of the nerve
to Local anaesthetic raises
its firing threshold.
17. • The action potential is terminated when the
membrane repolarises. This is caused by the
inactivation of the increased permeability to
sodium. In many cells potassium also
increases, resulting in the reflux of K+ , and
leading to more rapid membrane
repolarisation and return to its resting
potential.
• The entire process requires 1 millisecond;
depolarisation(step1)takes 0.3msec;
repolarisation (step2) takes 0.7 msec.
18. Theories for Mechanism of LA
The Acetylcholine theory.
The Calcium displacement theory.
The surface charge theory.
Membrane Expansion theory
Specific Receptor theory
19. The Acetylcholine theory
• Stated that acetylcholine was involved in
nerve conduction in addition to its role as
a neurotransmitter at nerve synapse.
20. The Calcium Displacement theory
• Local Anaesthetic nerve block was produced
by displacement of the calcium from some
membrane site that controlled permeability of
sodium. That varying the concentration of
calcium ion bathing a nerve does not affect
local anaesthetic potency has diminished the
credibility of this theory.
21. The Surface charge theory
• Proposed that La acts by binding to the nerve
membrane and changing the electrical
potential at the membrane surface.
22. Membrane expansion theory
• Stated that Local anaesthetic molecules diffuse to
hydrophobic regions of excitable membranes,
producing a general disturbance in the bulk
membrane structure, expanding some critical
regions in the membrane & preventing an increase
in the permeability to sodium ions.
23. Specific receptor theory by strichartz
1987
• Drug molecules bind to specific receptors present
on the external or internal axoplasmic surface of
the sodium channel & by acting directly on them,
decrease or eliminate permeability to Na2⁺ leading
to interruption of nerve conduction.
24. Local anaesthesia acts as follows:
Displacement of calcium ions from
the sodium channel receptor site,
which permits
Binding of L.A molecules to the
receptor site, which thus produces
Blockade of the sodium channel
25. Decrease in sodium conductance, which
leads to
Depression of the electrical
depolarization
Failure to achieve the threshold
potential level along with
Lack of development of the propagated
action potential, which is called
Conduction blockade
26. Doses and Duration of Block
Drug Conc. Total dose (mg) Dose(mg/kg) Duration of
block
Procaine 1-2% 400 6 30-60 min.
Lidocaine 0.5-2% 300 4.5 60-120 min.
Bupivacaine 0.25-0.5% 90 1.4 180-360 min.
Tetracaine 0.25-0.5% 80 1.3 180-480 min.
28. Complications
• CNS stimulation (more sensitive than cardiac)
• Dose related spectrum of effects and all effects are due
to depression of neurons.
• First an apparent CNS stimulation ( convulsion most
serious)
• Premonitory signs include: ringing in ears, metallic
taste, numbness around lips
• Followed by CNS depression (death due to respiratory
depression)
• Cocaine- Euphoria
• Lidocaine – Sedation even at non toxic dose
29. ARRHYTHMIAS
• Decrease cardiac
excitability and
contractibility
• Decreased conduction rate
• Increased refractory rate
(bupivacaine)
• ALL can cause arrhythmias
if conc. Is high enough
• ****Cocaine is exception
(it stimulates heart)
HYPOTENSION: Arteriolar
dilation as a result of:
• Direct effect(procaine and
lidocaine have most effect)
• Block of postganglionic
sympathetic fibre function
• CNS depression
• Avoid by adding
vasoconstrictor to the
preparation
• Cocaine is exception
(produces
vasoconstriction)
30. • Hypersensitivity:
• Common with ester linked LA
• Rashes, angio oedema, dermatitis an rare
anaphylaxis
• Sometimes typical asthmatic attack
• Neurotoxicity:
• La can cause concentration dependent nerve
damage to central and peripheral NS
• Mechanism not clear
• Permanent neurologic injury is rare
• May account for transient neurological
symptoms.
31. • Others:
• Ischemia and necrosis of soft tissues when
highly conc. Vasoconstriction solution used for
homeostasis over a prolonged period
• Hematoma is possible but rarely occurs
• Inflammation or infection at the injection site
• Palatal ulcers
• Facial paralysis
• Trismus
• Needle breakage
• Pain/burning on injection site
• Sloughing of tissue