in this seminar contain all enquiry about local anasthsisa

1. DR.VINAY JAIN
PG 1ST YEAR
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2. DEFINITION
Local Anaesthesia is defined as a transient reversible loss of
sensation in a circumscribed area of the body caused by a
depression of excitation in nerve endings or an inhibition of
the conduction process in peripheral nerves.(stanley f.
malamed)
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3. CLASSIFICATION OF
LOCAL ANAESTHESIA
1. Esters (of benzoic acid)
-Butacaine
-Cocaine
-Benzocaine
-Hexylcaine
-Piperocaine
-Tetracaine
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4. Esters (of paraaminobenzoic acid)
-Chloroprocaine
-Procaine
-Propoxycaine
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5. 2. Amides
-Articaine
-Bupivacaine
-Dibucaine
-Etidocaine
-Lidocaine
-Mepivacaine
-Prilocaine
3. Quinoline 4. Combinations
Lidocaine/Prilocaine(EMLA)
Centbucridine
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6. CLASSIFICATION ACCORDING TO DURATION OF ACTION
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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

7. General Structure
 A lipophilic group…usually a benzene ring
 A Hydrophilic group…usually a tertiary amine
 These are connected by an intermediate chain that
includes an ester or amide linkage
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8. 2/5/2015 8

9. Ester Amide
 Ester linkage is more easy
broken
 Less stable in solution
 Cannot be stored for long time
 Metabolism of most esters
results in the production of para
aminobenzoate (PABA) which is
associated with allergic reaction.
 Not broken easy
 More stable in solution
 Stored for long time
 Amides, very rarely cause
allergic phenomena
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10. 2/5/2015 10

11. 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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12. 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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13. 2/5/2015 13

14. 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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15. 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.
 Action Potential- Transient depolarization of membrane
that result from a brief increase in permeability of the
membrane to sodium, and usually also from a delayed
increase in permeability of potassium.
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16. ELECTRICAL IMPULSE
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17. 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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18.  RESTING POTENTIAL Internal to the nerve
membrane is negative in respect to the outer part.
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19. 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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20. 2/5/2015 20
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).

21. 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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22. 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−)
 Potassium remains within the axoplasm
 Chloride remains outside the nerve membrane
 Sodium ions remains outside.
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23.  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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24. 2/5/2015 24

25.  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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26. Mechanism of action of local
anesthetics
1. Non-specific membrane expansion theory
2. Specific receptor theory
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27. 2/5/2015 27
Non-specific membrane
expansion theory:

28. 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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29. 2/5/2015 29
Specific receptor theory:

30.  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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31. Local anesthetics are classified by ability to react
with specific receptor sites in the sodium channel
1. Within the sodium channel (tertiary amine local
anesthetics)
2. At the outer surface of the sodium channel (tetrodotoxin,
saxitoxin)
3–4. At either the activation or the inactivation gates
(scorpion venom)
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32. 2/5/2015 32
•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.

33. 2/5/2015 33
PHARMACOLOGY
OF
LOCAL ANESTHESIA

34. 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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35.  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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36. 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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37.  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+
 Hydrogen ion concentration decreases (higher pH),the
equilibrium shifts toward the free base form:
RNH+ < RN + H+
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38.  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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39.  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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40. 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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41. 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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42. 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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43. 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.
 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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44. 2/5/2015 44
MAXIMUM DOSES OF LOCAL ANESTHETICS
The doses of local anesthetic drugs are presented in terms of milligrams of drug per unit of
body weight.

45. 2/5/2015 45

46. 2/5/2015 46
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 .

47. 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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48. Metabolism
Ester Local Anesthetics. Ester local anesthetics are hydrolyzed in
the plasma by the enzyme pseudocholinesterase.
 The rate of hydrolysis has an impact on the potential toxicity of a
local anesthetic.
 Chloroprocaine, the most rapidly hydrolyzed, is the least toxic,
whereas tetracaine, hydrolyzed 16 times more slowly than
chloroprocaine, has the greatest potential toxicity.
 Procaine undergoes hydrolysis to paraaminobenzoic acid (PABA),
which is excreted unchanged in the urine
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49. 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.
 The entire metabolic process occurs in the liver for lidocaine,
mepivacaine, articaine,etidocaine, and bupivacaine.
 Prilocaine undergoes primary metabolism in the liver, with
some also possibly occurring in the lung.
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50. 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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51. Adverse Effects
 CNS: excitation followed by depression (drowsiness to
unconsciousness and death due to respiratory depression.
 Cardiovascular System: bradycardia, heart block,
vasodilation (hypotension)
 Allergic reactions: allergic dermatitis to anaphylaxis (rare,
but occur most often by ester-type drugs). Very uncommon
 Esters more likely because of p-aminobenzoic acid
(allergen)
 Methylparaben preservative present in amides is also a
known allergen
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52. Clinical Consideration
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53. 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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54. •Sympathetic block (vasodilatation)(Type B fiber)
•Loss of pain and temperature sensation(Type C and type A
delta)
•Loss of Proprioception(Type A gamma)
•Loss of touch and pressure sensation(Type A beta)
•Loss of motor function(Type A alpha)
Sequence of clinical anesthesia
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55. SIGNS AND SYMPTOMS OF LOCAL
ANAESTHETIC TOXICITY:
1-CNS toxicity :
 Early or mild toxicity: light-headedness, tinnitus,
circumoral numbness, abnormal taste, confusion and
drowsiness.
 Severe toxicity: tonic-clonic convulsion leading to
progressive loss of consciousness, coma,.respiratory
depression, and respiratory arrest.
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56. 2-CVS toxicity:
 Early or mild toxicity: tachycardia and rise in blood
pressure. This will usually only occur if there is adrenaline
in the local anaesthetic. If no adrenaline is added then
bradycardia with hypotension will occur.
 Severe toxicity: Usually about 4 - 7 times the convulsant
dose needs to be injected before cardiovascular collapse
occurs. Collapse is due to the depressant effect of the local
anaesthetic acting directly on the myocardium.
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57. 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.
2/5/2015 57

58. 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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59. 2/5/2015 59
1.Peel open the package and remove the test panel (Figure 1).

60. 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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61. ADVANTAGES OF LOCAL ANAESTHESIA
 During local anesthesia the patient remains conscious
 Maintains his own airway.
 Excellent muscle relaxant effect.
 It requires less skilled nursing care as compared to other
anesthesia like general anesthesia.
 Non inflammable.
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62.  Less pulmonary complications
 Aspiration of gastric contents unlikely.
 Less nausea and vomiting.
 Contracted bowel so helpful in abdominal and pelvic
surgery.
 Postoperative analgesia.
 There is reduction surgical stress.
 Earlier discharge for outpatients.2/5/2015 62

63.  Suitable for patients who recently ingested food or fluids.
 Local anesthesia is useful for ambulatory patients having
minor procedures.
 Ideal for procedures in which it is desirable to have the
patient awake and cooperative.
 Less bleeding.
 Expenses are less.
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64. DISADVANTAGES OF LOCAL
ANAESTHESIA
 There are individual variations in response to local
anesthetic drugs.
 Rapid absorption of the drug into the bloodstream can cause
severe, potentially fatal reactions.
 Apprehension may be increased by the patient's ability to see
and hear. Some patients prefer to be unconscious and
unaware.
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65.  Direct damage of nerve.
 Post-dural headache from CSF leak.
 Hypotension and bradycardia through blockade of the
sympathetic nervous system.
 Not suitable for extremes of ages.
 Multiple needle pricks may be needed.
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66. 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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67. VASOCONSTRICTORS
- Vasoconstrictors are the drugs that constricts the blood vessels
and thereby control tissue perfusion.
- They are added to local anaesthesia to oppose the vasodilatory
action of local anesthetic agent.
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68. What happens if you don’t use a vasoconstrictor?
Plain local anesthetics are vasodilators by nature
1) Blood vessels in the area dilate
2) Increase absorption of the local anesthetic into the
cardiovascular system (redistribution)
3) Higher plasma levels  increased risk of toxicity
4) Decreased depth and duration of anesthesia  diffusion
from site
5) Increased bleeding due to increased blood perfusion to the
area
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69. Why You Need Vasoconstrictors
1) Constrict blood vessels  decrease blood flow to the surgical site
2) Cardiovascular absorption is slowed  lower anesthetic blood levels
3) Local anesthetic blood levels are lowered  lower risk of toxicity
4) Local anesthetic remains around the nerve for longer periods 
increased duration of anesthesia
5) Decreases bleeding
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70. Vasoconstrictors should not be used in the
following locations
 Fingers
 Toes
 Nose
 Ear lobes
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71. Contraindications to Using Vasoconstrictors
1) Blood pressure > 200/115 mm Hg
2) Severe cardiovascular disease
3) Acute myocardial infarction in the last 6 months
4) Anginal episodes at rest.
5) Cardiac dysrhythmias that are refractory to drug treatment
6) Patient is in a hyperthyroid state
7) Levonordefrin and Norepinephrine are absolutely
contraindicated in patients taking tricyclic antidepressants
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72. Drug Interactions
 Chloroprocaine epidurally may interfere with the analgesic
effects of intrathecal morphine.
 Opioids and a2 agonists potentiate LA’s.
 Propranolol and cimetidine decrease hepatic blood flow
and decrease lidocaine clearance.
 Pseudocholinesterase inhibitors decrease Ester LA
metabolism.
 Dibucaine (amide LA) inhibits pseudocholinesterase.
 LA potentiate nondepolarizing muscle relaxant blockade.
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73. 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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74. Thanks
for
your attentions
2/5/2015 74

75.  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
 reactions 13. After use. the needle and syringe should be discarded in a container.2/5/2015 75

76.  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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