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VINAY JAIN
PG 1ST YEAR
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DEFINITION
Local Anaesthesia is defined as a transient reversible loss of
malamed)
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CLASSIFICATION OF
LOCAL ANAESTHESIA
1. Esters (of benzoic acid)
-Butacaine
-Cocaine
-Benzocaine
-Hexylcaine
-Piperocaine
-Tetracaine
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Esters (of paraaminobenzoic acid)
-Chloroprocaine
-Procaine
-Propoxycaine
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2. Amides
-Articaine
-Bupivacaine
-Dibucaine
-Etidocaine
-Lidocaine
-Mepivacaine
-Prilocaine
3. Quinoline 4. Combinations
Lidocaine/Prilocaine(EMLA)
Centbucridine
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CLASSIFICATION ACCORDING TO DURATION OF ACTION
SHORT DURATION (pulpal anesthesia approximately 30 minutes)
Lidocaine HCl 2%
Mepivacaine HCl 3%
Prilocaine HCl 4% (by infiltration)
INTERMEDIATE DURATION (pulpal anesthesia approximately 60 minutes)
Articaine HCl 4% + epinephrine 1:100,000
Lidocaine HCl 2% + epinephrine 1:50,000 and 1:100,000
Mepivacaine HCl 2% + levonordefrin 1:20,000
Mepivacaine HCl 2% + epinephrine 1:100,000
Prilocaine HCl 4% (via nerve block only)
LONG DURATION (pulpal anesthesia approximately 90+ minutes)
Bupivacaine HCl 0.5% + epinephrine 1:200,000
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General Structure
A lipophilic group…usually a benzene ring
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Ester Amide
Ester linkage is more easy Not broken easy
broken
More stable in solution
Less stable in solution
Stored for long time
Cannot be stored for long time
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Fundamentals Of Impulse
Generation And Transmission
Concept behind action of local anaesthesia- prevent
conduction and generation of nerve impulse, set up
chemical roadblock between the source of impulse
and the brain.
NEURON is the fundamental unit of nerve cell.
It transmits messages between CNS and all parts of the
body.
It is of 2 types:-
Sensory (afferent)
Motor (efferent)
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Sensory Neuron
It transmits pain sensation with 3 major portions:-
Peripheral process (dendritic zone) composed of free
nerve endings .The most distal segment of sensory
neuron.
Axon- Thin cable like structure, has free nerve endings
that respond to stimulation produced in the tissues in
which they lie provoking an impulse transmitted via
axon.
Cell Body- located at a distance from axon, provide vital
metabolic support for the entire neuron.
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Motor Neuron
They transmit nerve impulses from the CNS to the
periphery
Their cell body is interposed between axon and
dendrites.
Axon branches with each branch ending as a bulbous
axon terminal (or button)
Axon terminals synapse with muscle cells.
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Physiology Of Peripheral Nerves
The function of nerve is to carry messages from one part
of the body to another in the form of electrical action
potential called IMPULSES initiated by chemical,
mechanical, thermal or electrical stimuli.
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ELECTRICAL IMPULSE
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Electrophysiology Of Nerve Conduction
Nerve possesses a resting potential (step 1) which is
negative electrical potential of -70mV because of
differing in concentration of ions on either side of
membrane.
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RESTING POTENTIAL Internal to the nerve
membrane is negative in respect to the outer part.
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STEP 1
Stimulation excites the nerve cells.
A. Initial phase of slow depolarization, the electrical
potential in the nerve becomes slightly less negative.
B. When the falling electrical potential reaches a
critical level,extremely rapid phase of depolarisation
results. This term threshold potential or firing
threshold.
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C. This phase of rapid depolarization result in a reversal of the
electrical potential across the nerve membrane . Internal to
the membrane becomes positive in respect to the outside
(+40mV).
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STEP 2
This is a phase of Repolarisation.
Electrical potential gradually becomes more negative
in respect to the outside until -70mv is achieved.
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Electrochemistry of Nerve Conduction
Resting State. In its resting state the nerve
membrane is
• Slightly permeable to sodium ions (Na+)
• Freely permeable to potassium ions (K+)
• Freely permeable to chloride ions (Cl−)
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Membrane Excitation
Depolarization--Excitation of a nerve segment leads to
an increase in permeability of the cell membrane to
sodium ions.
The rapid influx of sodium ions to the interior of the
nerve cell causes depolarization of the nerve membrane
from its resting level to its firing threshold of approximately−50 to
−60 mV.
A decrease in negative transmembrane potential of
15 mV (e.g., from −70 to −55 mV) is necessary to reach the
firing threshold.
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Exposure of the nerve to a local anesthetic raises its
firing threshold. Elevating the firing threshold means
that more sodium must pass through the membrane to
decrease the negative transmembrane potential to a level
where depolarization occurs.
Repolarization--The action potential is terminated
when the membrane repolarizes. This is caused by the
extinction (“inactivation”) of increased permeability to
sodium.
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Mechanism of action of local
anesthetics
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Non-specific membrane
expansion theory:
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The lipophilic part of the local anaesthetic attaches to the cell
membrane to cause swelling. This then reduces the size of the
sodium channel to obstruct the flow of sodium ions.
This results in a decreased diameter of sodium channels, which
leads to an inhibition of both sodium conductance and neural
excitation.
There is no direct evidence that nerve conduction is entirely
blocked by membrane expansion.
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Specific receptor theory:
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The hydrophilic charged amino terminal binds to specific
receptors of the sodium gates to block the passage of sodium
ions.
Both biochemical and electrophysiological studies have
indicated that a specific receptor site for local anesthetic
agents exists in the sodium channel either on its external
surface or on the internal axoplasmic surface.
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Local anesthetics are classified by ability to react
with specific receptor sites in the sodium channel
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•Drugs in Class C exist only in the uncharged form (RN)
• Class D drugs exist in both charged and uncharged forms.
•Approximately 90% of the blocking effects of Class D drugs are caused by the
cationic form of the drug; only 10% of blocking action is produced by the base.
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PHARMACOLOGY
OF
LOCAL ANESTHESIA
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KINETICS OF LOCAL ANESTHETIC ONSET
AND DURATION OF ACTION
Diffusion. The rate of diffusion is governed by several
factors, the most significant of which is the
concentration gradient. The greater the initial
concentration of the local anesthetic, the faster is the
diffusion of its molecules and the more rapid its onset
of action.
Blocking Process. After deposition of the local
anesthetics close to the nerve as possible, the solution
diffuses in all directions according to prevailing
concentration gradients.
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Induction Time->> Induction time is defined as the
period from deposition of the anesthetic solution to
complete conduction blockade. Several factors control
the induction time
Under the operator’s control are-> the concentration
of the drug and the pH of the local anesthetic solution.
Factors not under the operator’s control are-> the
diffusion constant of the anesthetic drug and the
anatomical diffusion barriers of the nerve.
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Effect of PH On LA
Local anesthetics are available as salts (usually the hydrochloride)
for clinical use. The local anesthetic salt, both water soluble and
stable, is dissolved in either sterile water or saline. In this solution
it exists simultaneously as uncharged molecules (RN),also called
the base, and positively charged molecules (RNH+),called the
cation.
RNH+ ↔ RN + H+
Ionic form in the solution varies with the pH of the solution or
surrounding tissues.
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In the presence of a high concentration of hydrogen ions
(low pH), the equilibrium shifts to the left and most of the
anesthetic solution exists in cationic form:
RNH+ > RN + H+
RNH+ < RN + H+
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The relative proportion of ionic forms also depends on the pKa, or
dissociation constant, of the specific local anesthetic. The pKa is a
measure of a molecule’s affinity for hydrogen ions (H+). When the pH
of the solution has the same value as the pKa of the local anesthetic,
exactly 50% of the drug exists in the RNH+ form and 50% in the RN
form Henderson-Hasselbalch equation.
BASE
Log ==pH–pKa
ACID
Benzocaine 3.5
Lidocaine 7.7
Prilocaine 7.7
Articaine 7.8
Etidocaine 7.9
Procaine 9.1
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A local anesthetic with a high pKa value has very few
molecules available in the RN form at a tissue pH of 7.4.
The onset of anesthetic action of this drug is slow
because too few base molecules are available to diffuse
through the nerve membrane
The rate of onset of anesthetic action is related to the
pKa of the local anesthetic .
A local anesthetic with a lower pKa (<7.5) has a very
large number of lipophilic free base molecules that are
able to diffuse through the nerve sheath;
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Physical Properties and Clinical
Actions
1)The effect of the dissociation constant (pKa):
The anesthetic are important in neural blockade, drugs
with a lower pKa possess a more rapid onset of action than
those with a higher pKa.
2)Lipid solubility->Increased lipid solubility permits the
anesthetic to penetrate the nerve membrane (which itself
is 90% lipid) more easily. This is reflected biologically in
the increased potency of the anesthetic. Local anesthetics
with greater lipid solubility produce more effective
conduction blockade at lower concentrations than the less
lipid soluble local anesthetics.
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3) The degree of protein binding of the local anesthetic
molecule is responsible for the duration of anesthetic
activity.
In the sodium channel itself, the RNH+ ions bind at the
receptor site. Proteins constitute approximately 10% of
the nerve membrane, and local anesthetics (e.g.,
etidocaine, ropivacaine, and bupivacaine) possessing a
greater degree of protein binding than others (e.g.,
procaine) appear to attach more securely to the protein
receptor sites and to possess a longer duration of
clinical activity.
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4)Vasoactivity affects both the anesthetic potency and
the duration of anesthesia provided by a drug.
Injection of local anesthetics, such as procaine, with
greater vasodilating properties increases perfusion of
the local site with blood.
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Duration of Action
The duration of action of the drug is also related to the
length of the intermediate chain joining the aromatic and
amine groups.
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MAXIMUM DOSES OF LOCAL ANESTHETICS
The doses of local anesthetic drugs are presented in terms of milligrams of drug per unit of
body weight.
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Each ml of local anesthesia 1:2,00,000 contains:-
Lignocaine hydrochloride 21.3mg
Adrenaline 0.0125mg
Methylparaben 1.00mg
Sodium meta bisulfite 0.5mg
In 30ml of local anesthesia, the quantity of lignocaine is approx. 640 mg.
According to manufacturer, MRD of lidocaine with vasoconstrictor is 6.6 mg/kg.
In a person of weight 60kg MRD is 396 mg .
396/21.3=18.5 ml of LA can be given as a MRD in a person of 60 kg .
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Absorption and Distribution
Absorption of local anesthetics is affected by following
factors:1)dosage 2)site of injection 3) drug –tissue –
binding 4) presence of vasoconstricting drug
The distribution of the drug is influenced by the degree of
tissue and plasma binding protein of the drug. The more
protein bound the agent, the longer the duration of
action, as free drug is more slowly made available for
metabolism.
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Metabolism
Ester Local Anesthetics. Ester local anesthetics are hydrolyzed in
the plasma by the enzyme pseudocholinesterase.
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Amide Local Anesthetics- The biotransformation of amide
local anesthetics is more complex than that of the esters. The
primary site of biotransformation of amide drugs is the liver.
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Excretion
The kidneys are the primary excretory organ for both the local
anesthetic and its metabolites.
Esters appear in only very small concentrations as the parent
compound in the urine. This is because they are hydrolyzed almost
completely in the plasma.
Amides usually are present in the urine as the parent compound in
a greater percentage than the esters, primarily because of their
more complex process of biotransformation.
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Adverse Effects
CNS: excitation followed by depression (drowsiness to
unconsciousness and death due to respiratory depression.
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Properties of ideal LA
Reversible action.
It should be Non-irritant to the tissue
It should not cause any permanent alteration of nerve
structure.
No allergic reaction.
Its systemic toxicity should be low.
It should be rapid onset of action.
Sufficient duration of action.
Stable in solutions.
Not expensive
It should have potency sufficient to give complete anesthesia
without the use of harmful concentrated solution.
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Sequence of clinical anesthesia
•Sympathetic block (vasodilatation)(Type B fiber)
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SIGNS AND SYMPTOMS OF LOCAL
ANAESTHETIC TOXICITY:
1-CNS toxicity :
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ALLERGIC REACTIONS TO LOCAL
ANESTHETICS
Hypersensitivity reactions to local anesthetics are
quite rare and generally account for less than 1% of all
reported adverse drug reactions.
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Testing for anesthetic allergy using
skin test
T.R.U.E. Test (thin –layer rapid use epicutanous patch
test)
This is a patch test applied 23 allergens to the skin
contained 12 polyester patches.
The mixture of anesthetics is called the caine mix, in
this
Benzocaine,
Tetracaine hydrochloride,
Dibucaine hydrochloride,
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1.Peel open the package and remove the test panel (Figure 1).
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Sign and symptoms of allergic
reaction
Generalized body rash or skin redness
Itching ,urticaria
Bronco spasm
Swelling of the throat
Asthma
Abdominal cramping
Irregular heart beat
Hypotension
Swelling of the face and lips
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ADVANTAGES OF LOCAL ANAESTHESIA
Non inflammable.
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Less pulmonary complications
Postoperative analgesia.
Earlier
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Suitable for patients who recently ingested food or fluids.
Less bleeding.
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Contraindications for local anesthesia
- Heart block, second or third degree (without pacemaker)
- Severe sinoatrial block (without pacemaker).
- Serious adverse drug reaction to lidocaine or amide local
anaesthetics.
- Concurrent treatment with quinidine, disopyramide, procainamide
(class 1 antiarrhythmic agents).
- Hypotension not due to arrhythmia.
- Bradycardia.
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VASOCONSTRICTORS
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What happens if you don’t use a vasoconstrictor?
5) Decreases bleeding
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Vasoconstrictors should not be used in the
following locations
Fingers
Toes
Nose
Ear lobes
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Contraindications to Using Vasoconstrictors
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Other agents with LA properties
Meperidine
TCAs (amitriptyline)
Volatile anesthetics
Ketamine
Tetrodotoxin (blocks Na channels from the outside of
the cell membrane) Animal studies suggest that when
used in low doses with vasoconstrictors it will
significantly prolong duration of action of LA.
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Thanks
for
your attentions
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Steps in Administration of Local Anesthesia
1. Patient should be in supine position. This is preferred because it favors good blood supply and pressure to
brain.
2. Syringe aspiration: Before injecting the solution into the body, first a little aspiration in the syringe is done
to avoid chances of injecting solution in the blood vessels and consequently preventing toxic effect of local
anesthesia.
3. The local anesthetic solution should not be injected into the inflamed and infected tissues to prevent
possible spread of infection. In inflamed areas, the local anesthetic solution does not work properly due to
acidic medium of inflamed tissues.
4. In every patient, disposable needle and syringe should be used.
5. Before loading syringe the temperature of the solution should be brought to body temperature to make
injecting a painless procedure.
6. Before loading the solution in the syringe, it should be confirmed that anesthetic solution is fresh and not
expired.
7. Before injecting the local anesthesia, the site of injection should be cleaned free of debris and saliva by a
sterile cotton pellet.
8. Topical surface anesthetic solution or jelly may be applied before injecting the needle for painless
penetration of needle.
9. Needle should be inserted at the junction of alveolar mucosa and vestibular mucosa and the angle of needle
should not be parallel to the long axis of the tooth . Injection parallel to long axis causes more pain (Fig. 15.1).
10. Anesthetic solution is injected slowly not more than 1 ml per minute and in small increments to provide
enough
time for tissue diffusion of the solution. Needle should be continuously inserted inside till the periosteum or
bone is felt by way of slight increase in resistance of the needle movement The needle is slightly withdrawn
and here the remaining
solution is injected. 11: Two minutes after injection the effect of anesthesia is checked before starting operative
procedure. 12. Patient should be carefully watched during and after local anesthesia for about half an hour for
delayed
1/11/2016 13. After use. the needle and syringe should be discarded in a container.
reactions 75
The primary afferent nerve fibres have been divided into seven different groups depending on their
function.
Aa - Somatic motor and proprioception
Ab - Touch and pressure - circumvent the dorsal horn by giving off collaterals that ascend in the
posterior columns
Ag - Proprioception, motor to muscle spindles
Ad - Pain, cold T o and touch - synapse in Rexed's lamina I of the dorsal horn.
B - Autonomic preganglionic
C dorsal root - Pain, T o , mechanoreception and reflex responses - synapse in Rexed's lamina II (the
substantia gelatinosa) of the dorsal horn.
C sympathetic - Postganglionic sympathetics
Preferential blockade of a nerve requires a minimal length of fibre exposed to an adequate
concentration (Cm) of local anaesthetic. The blocking of three sequential nodes of Ranvier is always
sufficient. As thick fibers have an increased distance between nodes of Ranvier this explains the onset
of fiber blockade
B - Autonomic preganglionic - vasodilatation with associated decrease in BP.
C - Pain and T o - loss of thermal appreciation
Ad - Pain and T o
Ag - Proprioception - loss of awareness of limbs
Ab - Touch and pressure
Aa - Motor
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