Local Anaesthesia Basics
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Introduction to Local Anaesthesia
Dr. Rudraprasad Chakraborty1st year PG Student
Department of Oral & Maxillofacial SurgeryRama Dental college Hospital & Research Centre
Kanpur, UP
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Inclusions…..
IntroductionPain PathwayNerve and Nerve conductionMode of Action of LAProperties of LAComposition of LAThe Vasoconstrictors mainly used with LA
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“A Doctor who can control pain and give the patient relief from it, is the Best Doctor for the Patient”
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INTRODUCTION
The first LA, cocaine, was isolated in 1860. Cocaine introduced into practice in 1884 as a
topical ophthalmic anesthetic. Despite its addictive property, cocaine was
used for 30 years. In 1905 procaine was synthesized, which
became the dominant LA for the next 50 years. Lidocaine, which is still a widely used LA, was
synthesized in 1943
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PAIN
One of the most commonly experienced symptoms .
An unpleasant emotional experience usually initiated by a noxious stimulus and transmitted over a specialized neural network to the CNS where it is Interpreted as such.
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PAIN PATHWAY
…THE TRRIGEMINOTHALAMIC PATHWAY
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3rd Ventricle
Left Thalamus
Right Thalamus
Pituitary
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Anterior Nucleus
Medial
Nucleus
VLDL
Lateral nucleus
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SUB DIVISIONS OF LATERAL NUCLEUS OF THALAMUS
VAL
VIL
VPL
VPM
DL
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THE TRIGEMINOTHALAMIC TRACT
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DISCRIMINATIVE TOUCH PATHWAY FROM HEAD
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CONTROL OF PAIN
1.Removal of the cause
2.Blocking the pathways of pain impulses
3.Raising the pain threshold
4.Preventing pain reaction by cortical depression
5.Using psychosomatic methods
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ANALGESIA, ANASTHESIA
ANALGESIA : Condition in which pain can not be appreciated but the patient is aware of what is happening.
ANAESTHESIA : Complete loss of all sensation including that of Pain.
LOCAL ANAESTHESIA : Temporary loss of all modalities of sensation in a limited region of the body.
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LOCAL ANAESTHESIA
Defined as reversible and transient 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
Loss of sensation without inducing loss of consciousness
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THE NERVE/ THE NEURON
The Sensory neuron : Transmitting the sensation of Pain
Consist three major part1. The Peripheral Process2. The Axon3. The Cell Body
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THE AXON
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THE NERVE CONDUCTION
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SODIUM CHANNEL TRANSITION STAGES
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DIFFERENTIAL CONDUCTION BLOCKADE
A and B fibers are Myelinated…….. Tend to be blocked First
C fibers are Nonmyelinated…………Tend to be blocked Last
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In Unmyelinated Nerve : 35 per μmIn Myelinated Nerve/ at nodes : 20000 per μm
Sodium Channel on Nerve Membrane
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IMPULSE SPREAD
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In Myelinated Nerve, two to three Nodes of Ranvier needed for ensuring proper nerve block
At 0.5 to 3mm distance, there are constrictions
That means, 8 to 10mm of Length area of nerve is to be in contact with LA
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ORDER OF BLOCKADE
Smaller Myelinated B fibers…………………Sympathetic A delta fibers………….Temperature sharp pain
Large Myelinated A alfa and beta fibers…..Motor and Proprioception
Small Unmyelinated C fibers……. ……………..Dull Pain
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Nerve fiber…………………..…….. Single nerve cell
Endoneurium ………………Covers each nerve fiber
Fasciculi ……...Bundles of 500 to 1000 nerve fibers
Perineurium …………..…………… Covers fasciculi
Perilemma ………….Innermost layer of perineuriumEpineurium ….............Connective tissue supporting fasciculi and carrying nutrient vesselsEpineural sheath….…Outer layer of epineurium
Structure Description
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SITE OF ACTION OF LA
Obviously… The Nerve Membrane
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THE PERINEURIUM AND PERILEMMA CONSTITUTE THE GREATEST ANATOMIC
BARRIERS TO DIFFUSION IN A PERIPHERAL NERVE.
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M = MANTLE, M= MOLAR/ C=CORE, C = CANINE
LA diffuses from periphery to centre of the nerve
Mantle fibers are anaesthetised first
Core fibers are anaesthetised last
Recovery occurs at Reverse Direction
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MODE OF ACTION OF LA
1.Altering the basic resting membrane potential of nerve membrane
2.Altering the threshold potential ( Firing Level )
3.Decreasing the rate of Depolarization
4.Prolonging the rate of repolarization
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MECHANISM THEORIES
The acetylcholine Theory
The Calcium Displacement Theory
The Surface Charge ( repulsion ) Theory
The Membrane Expansion Theory
The Specific Receptor Theory
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Acetylcholine was inolved in nerve membrane conduction & also it work as a neurotransmitter at nerve synapes.
ACETYL CHOLINE THEORY-
Nerve block was produced by the displacement of ca from membrane site that control permeability to sodium
CALCIUM DISPLACEMENT THEORY-
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Local anesthesia acted by binding to the nerve membrane & changing the electrical potential at the membrane surface.
Decrease excitability of the nerve by increase the threshold potential
SURFACE CHARGE THEORY
Can not explain the activity of uncharged anesthetic
molecule in blocking nerve impulses ex-benzocaine
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MEMBRANE EXPANSION THEORYPreventing an increase permeability of sodium LA are highly soluble to lipid & can easily penetrate the lipid portion of cell membrane
Resulting decrease of sodium channel which lead to an inhibition of both sodium conduction & neural exicitation
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Most favored today.
Proposed that local anesthetics act by binding to specific receptors on the sodium channel.
SPECIFIC RECEPTOR THEORY
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THE SODIUM CHANNELcomposed of three subunits known as alpha, beta1 and beta2
The pore through which sodium enters is contained in the alpha subunit
The alpha subunit is made up of four similar domains (I–IV) each of which contains six protein segments (S1–S6).
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THE ALPHA SUBUNIT OF THE SODIUM CHANNEL:
Sliding helix
in the resting state with S4 segments in the body of the channel;
In the firing configuration with S4 segments in wall of the channel;
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In the refractory orientation with a protein loop extended into the channel
Exposure of binding site for local anesthetics in segment S6
Binding of LA maintaining refractory orientation.
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ACCORDING TO BIOLOGICAL SITE & MODE OF ACTION
CLASS(A) •Agent acting at receptor site on external surface of nerve membrane•Ex-Biotoxin
CLASS(B) •Agent acting at receptor site on internal surface of nerve membrane•Ex-quaternary ammonium analogues of lidocaine
CLASS(C) •Agent acting by a receptor-independent physicochemical mechanism•Ex-benzocaine
Class(D) •Combination of recepter&receptor independent mechanism•Ex-articaine,lidocaine, mepivacaine
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OTHER METHODS OF CONTROLLING PAIN
Acupuncure Analgesia
Hypnotism
Audio Analgesia
Electric Anaesthesia/ Anelectrotonus
Anaesthesia by Cold Air
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Displacement of Ca++ from the sodium channel receptor site. Which permits.
Binding of the local anesthetics molecules to
this receptor site. Which thus produces.
Blockade Of the sodium channel.
HOW LA WORKS ?
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Decrease in sodium conductance which leads to
Depression of the rate of electrical depolarizatioN.
Failure to achieve the threshold potential level along with a….
Lack of development of propagated action potentials which is called as …..
Conduction blockadeCONDUCTION
BOLCKADE
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PROPERTIES OF LA
Non Irritating to the tissues
No Permanent Alteration in Nerve Structures
Low Systemic Toxicity
Effective on tissue or mucous membrane
Short Time of Onset
Long Duration of Action
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ADDITION OF BENETT
Potency without Harmful Concentrated Solution
Free From Producing Allergy
Stable in Solution and Readily Undergo Biotransformation
Should Be Sterile or capable of being Sterilised without Deterioration
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THE STRUCTURE OF LA
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Ester:
Amide:
Procaine
Lidocaine
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PHYSICOCHEMICAL CHARACTERISTICS OF A LOCAL ANAESTHETIC AFFECT ITS FUNCTION
The aromatic ring structure and hydrocarbon chain length determine the lipid solubility of the drug.
The more lipid soluble drug penetrates the cell membrane more easily to exert its effect.
Thus bupivacaine – which is highly lipid soluble – is approximately four times more potent than lidocaine.
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THE DURATION OF ACTION
Related to the length of the intermediate chain joining the aromatic and amine groups.
Protein binding , Procaine is only 6% protein bound and has a very short duration of action, wherease bupivacaine is 95% protein bound. bupivacaine have a longer duration of action .
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04/19/2023
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Esters BA Ester
Butacaine Cocaine Piperocaine Tetracaine
PABA Ester Procaine Propoxycain
CLASSIFICATION OF LOCAL ANESTHESIA
Amides Bupivacaine Etidocaine Lidocaine Mepivacane
Quinoline Centbucridine
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THE CHEMISTRY
LA Agents are weak base, unstable, insoluble and UNIONIZED as FREE BASE
Mixing with Acid, Salt is produced ….Stable & soluble in water.
RN + H(+) RNH(+)+ RN
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THE DISSOCIATION CONSTANT
The pKa : is the pH at which the Free Base (RN) and Ionized cation ( RNH+) are at equilibrium .
LA comes with pKa Value of 7.7 to 8.1Normal Tissue pH : 7.4
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LA UPON ALTERED TISSUE ENVIRONMENT pKa : 7.6 Tissue pH : 6.5 More Acidic More H+ ions More RNH(+)…. Less RN to enter
Axoplasm
LA will not work Properly
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ESTERS
First group of LA to be developed Short to Moderate duration of Action ( except Tetracain) Produces more vasodialation (Except Cocain ) Pseudocholinesterase in blood metabolise it End product PABA is highly allergic Not used now a days
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ATYPICAL PSEUDOCHOLINESTERASE
1:2800 ppl have this condition Ester bond is not broken easily Delayed metabolism More Toxicity
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AMIDES
Longer Duration of action Causes less Vasodialation Greater potency Metabolised by Liver primarily (prilocaine : Liver + Lung) (Articaine: Liver + Blood ) Rarely Allergic
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QUINOLINE
Centbucridine
4-N-butylamino-1,2,3,4-tetrahydro acridine hydrochloride
Non Ester, Non Amide type L.A.
Study showes long action of Local anaesthesia on human trial
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ELEMINATION HALF LIFE
Rate of which LA is removed from blood
Time needed for 50% reduction = 1st half life
for 75% reduction = 2nd half life
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COMPOSITION OF LA
LA itself The Acid to Make it Stable The Vasoconstrictor The Antioxidant to make VC stable The Preservatives The Vehicle in the form of Normal
Saline Nitrogen Bubbles to prevent O2
entrapement
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Preservative: Stability of modern L.A is maintained by adding Capryl hydro-cuprienotoxin which includes Xylotox and Methyl Paraben.
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Reducing agent: Act as preservatives for the vasoconstictor agents. Vasoconstrictors are unstable in solution and may
oxidize,especially on exposure to prolonged sunlight. Sodium metabisulphite which competes for the
available oxygen is added in the concentration between 0.05% and 0.1%
Vehicle:The isotonic vehicle reduces discomfort during injection.
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VASOCONSTRICTOR
Sympathomimetic drugs Acts on receptors which take
sympathetic mediators and receptors 1 and 1 are stimulatory 2 and 2 are inhibitory
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EPINEPHRIN AND NOR EPINEPHRIN
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Stimulatory Receptors Maximum 1
Except : Heart 1 J.G. Apparatus 1 Lipocyte/
Adipocyte 3
Inhibitory Receptors Maximum 2 Except : Presynaptic Nerve Endings, Platelets and some parts of
GIT 2
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Coronary and Cerebral vasculature have equal number of Alfa 1 and Beta 2, so not so much significant on circulation of these two area
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ACTION OF VC UPON DIFFERENT AREA Heart : Beta 1 ( Stimulatory) Present in
S.A. Node : +ve Chronotropic action A.V. Node : +ve Dromotropic action Purkinze Fibers : +ve Bathmotropic action Ventricular Muscles : +ve Ionotropic action
………….Resulting in Rise in Systolic BP
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Skin : alpha 1 ( stimulatory) present in Peripheral blood vessels smooth
muscles Vasoconstriction
Increase in peripheral resistance
Rise in Diastolic BP
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Exposedshaftof hair
Sebaceousgland
Arrectorpilimuscle
Connectivetissue sheath
Root hairplexus
The Arrector Pili Muscle has Alpha 1 Stimulatory receptors
If Constricts
Goose Bump
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Pupil : Dialator pupilae ( radial Muscle ) have Alpha 1 Stimulatory
Constriction makes Pupil to dialate
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Respiratory System :
Needs more Air More Resp Rate
Dialation of Broncheoles needed
Broncheal Smooth Muscle Inhibition needed
(Beta 2 receptors)
BUT…. No Vasodialation Needed . Alpha 1 receptors stimulated in Blood
Vessels
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Mast Cell
Histamine
Broncho constriction
Mast Cell has to be inhibited to keep potent airway
Beta 2 Receptors work over there
Respiratory System Cont..
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Renal System : Alpha1 Stimulatory in Blood vessels
Decrease Blood Flow Decrease
Filtration
Less Urinary Output
• Beta 1 in Juxta Glomerular apparatus
Stimulation of which increases fluid retention in body
Rise in Blood Pressure
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GIT : Absorption and Secretory activity should
be decreased Depends upon Mesenteric Blood Flow,
should have vasoconstriction ( Alpha 1)
Peristalsis should be Inhibited ( Beta 2 )
Pyloric and cecal sphincture constricts ( Alpha 1)
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Effect on Na-K movement Na-K ATPase takes back exhailed K+ ion
in.
Sensitive to Epinephrin by Alpha 1 Receptors
Hyperkaelimia does not occur
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Effect on skeletal muscle
Due to improper signaling to CNS, propermuscle tone is not maintained.
When Epinephrin goes up…
we feel TREMOR
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Effect on Endocrine system
More glucose is needed
Insuline should be less secreted
Pancreatic Beta Cells are Inhibited
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Effect on Endocrine system
More glucose is needed
Insuline should be less secreted
Pancreatic Beta Cells are Inhibited
Alpha 2
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Norepinephrine 1 1 2
Epinephrine 1 = 1 = 2
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TERMINATION OF CATECHOLAMINES
C.O.M.T enzyme and M.A.O enzyme act on both epinephrine and norepinephrine.
COMT removes 3 and 4 hydroxyl group
MAO removes carbon Hydroxyl group
End products are reuptaken by the system
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DOSE CALCULATION Example ……… 1: 100000 Adrenaline 1gram adrenaline in 100000ml of
solution i.e 1000mg in 100000ml i.e 0.01mg per ml solution
Preparation comes with 1 : 50000 1 : 80000
1 : 100000 1 : 200000
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Norepinephrine : Normal patient : 0.34mg per
appointment i.e 34 ml of 1:100000 i.e 18 inj of 1.8ml
CVS patient : 0.14mg per appointment
i.e 14 ml of 1: 100000 i.e 7.7 injections of
1.8ml
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Epinephrine : Maximum 0.2 mg , i.e 20ml of 1:
100000 Around 11 inj of 1.8 lakhs can be given
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TO BE CONTINUED WITH…
EMLA Doses of LA Techniques of LA Complications of LA
Thanks