Local anesthesia is a transient loss of sensation in a localized area caused by blocking nerve conduction without loss of consciousness. It works by binding to receptor sites on nerve membranes and blocking sodium channels, preventing the transmission of nerve impulses. Common local anesthetics are lidocaine, prilocaine, mepivacaine and bupivacaine. Vasoconstrictors like epinephrine are often added to prolong the effects and reduce systemic absorption. Proper dosage calculation and contraindications must be considered for safe administration of local anesthesia.
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.
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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.
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“Local Anaesthetics”
These are agents which upon topical application or local injection cause reversible loss of pain sensation in a restricted area of the body. They act by blocking both sensory and motor nerve conduction to produce temporary loss of sensation without loss of consciousness.
Mechanism of action
These drugs reversibly prevent the generation and propagation of impulses in all excitable membranes including nerve fiber by stabilizing the membrane.
Local anesthetics block the nerve conduction by decreasing the entry of Na+ during action potential. They interact with a receptor situated within the voltage sensitive Na+ channel and raise the threshold of Na+ channel opening.
Therefore, Na+ can’t enter into the cell in response to an impulse which prevents depolarisation. Thus, action potential is not generated.
This action affecting the depolarization which leads to failure of conduction of impulse without affecting the resting membrane potential (RMP) is known as membrane stabilizing effect.
History- Cocaine is a naturally occurring compound indigenous to the Andes Mountains, West Indies, and Java.
It was the first anesthetic to be discovered and is the only naturally occurring local anesthetic; all others are synthetically derived.
Cocaine was introduced into Europe in the 1800s following its isolation from coca beans. Sigmund Freud, the noted Austrian psychoanalyst, used cocaine on his patients and became addicted through self-experimentation.
In the latter half of the 1800s, interest in the drug became widespread, and many of cocaine's pharmacologic actions and adverse effects were elucidated during this time. In the 1880s, Koller introduced cocaine to the field of ophthalmology, and Hall introduced it to dentistry
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2. Definition of local anesthesia
1) It is a transient loss of all modalities of sensation such as pain,
touch , temperature and pressure in a localized circumscribed
anatomical area by blocking the nerve conduction without loss of
consciousness.
2) Local anesthesia is defined as a 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 nerve.
(Handbook of Local Anesthesia , Stanley.F.Malamed
6th
ed)
3. Composition of Local AnestheticSolution
Local Anesthetic agent- 2% Lidocaine
Vasoconstrictor- Epinephrine1:80,000 to1:200,000
Reducing Agent- Sodium Metabisulphite
Preservative- Methyl Paraben
Solvent- Distilled Water
4. 1) It should not be irritating to the tissue to which it is applied.
2) It should not cause any permanent alteration of nerve
structure.
3) It’s systemic toxicity should be low.
4) It must be effective regardless of whether it is injected into
the tissue or is applied locally to mucous membranes.
5) The time of onset of anesthesia should be as short as
possible.
6) The duration of action must be long enough to permit
completion of the procedure yet not so long as to require an
extended recovery.
5. Other desirable qualities listed by Bennett :-
7) It should have have potency sufficient to give complete
anesthesia without the use of harmful concentrated
solutions.
8) It should be relatively free from producing allergic
reactions.
9) It should be stable in solution and should readily undergo
biotransformation in the body.
10) It should be sterile or capable of being sterilised by heat
without deterioration.
6. A) Based on duration of action:
1) Ultra Short acting anesthetics (less than 30 mins)-
2-Chloroprocaine without a vasoconstrictor
2% Lidocaine without vasoconstrictor
2) Short acting anesthetics(45 to 75 mins)-
2% Lidocaine with 1:1,00,000 epinephrine
4% Prilocaine when used for nerve block
7. 3) Medium acting anesthetics (90-150 mins)-
a) 4% Prilocaine with 1:2,00,000 epinephrine
b) 2% Lidocaine and 2% Mepivacaine with
vasoconstrictor
4) Long acting anesthetics (180 mins or longer)-
a) 0.5% Bupivacaine with 1:2,00,000
epinephrine
b) 0.5% or 1.5% etidocaine with 1:2,00,000
epinephrine
10. MECHANISM OF ACTION OF LOCAL ANESTHESIA
1. Displacement of calcium ions from the sodium
channel receptor site, which permits……
2. Binding of the local anesthetic molecule to this
receptor site , which thus produces….
3. Blockade of the sodium channel, and a …
4. Decrease in sodium conductance, which leads to….
11. 5. Depression of rate of electrical
depolarization…
6. And a failure to achieve threshold potential
level….along with
7. A lack of development of propagated action
potentials… which brings about..
8. CONDUCTION BLOCKADE
12. Theories of mechanism of action of local
Anesthesia
1) Acetylcholine Theory
2) Calcium Displacement Theory
3) Surface Charge Theory
4) Membrane Expansion Theory
5) Specific Receptor Theory
14. Membrane Expansion Theory
Local Anesthetics are highly lipid soluble & easily penetrate
lipid portion of cell membrane
Thus causing expansion of nerve membrane &
resulting in the decrease of the diameter of the sodium
channels
Thereby inhibiting the influx of sodium & nerve impulse
generation.
17. 1)Agents acting at receptor site on external surface of nerve
membrane- biotoxins (eg. tetrodotoxin)
2)Agents acting at receptor site on internal surface
of nerve membrane - quaternary ammonium analogues of
lidocaine
3)Agents acting by a receptor-independent physico-
chemical mechanism -benzocaine,
4)Agents acting by combination of receptor &
receptor - independent mechanism -articaine
lidocaine, mepivacaine, prilocaine
18.
19. Biologically active substances are frequently
administered as very dilute solutions which can be
expressed as parts of active drug per 100 parts of
solution (grams percent)
Ex.: 2% solution =
_2 grams = _2000 mg = __20 mg
100 cc’s 100 cc’s 1 cc
22. A)To calculate the maximum amount of Lidocaine 2% with 1:100,000
epinephrine and the number of carpules that can be safely administered to a
30 pound patient
B)To calculate the maximum amount of Mepivacaine 3% plain and the number
of carpules that can be administered to a 30 pound patient the clinician would
perform the following calculations.
23. DESCRIPTION OF INDIVIDUAL ANESTHETIC AGENTS
A) ESTER-TYPE LOCAL ANESTHETICS
1) PROCAINE- Present as Procaine HCl.
-Is an ester type local anesthetic , is ester of
PABA.
-Prepared by Alfred Einhorn in 1904.
- Potency= 1.
-Toxicity= 1.
- Metabolized rapidly by hydrolysis, in plasma by
pseudocholinesterase.
- Onset of action= 6 to 10 minutes.
- Half life= 6 minutes.
- Effective concentration in dental use= 2% , 4%.
24. 2)PROPOXYCAINE-Present as Propoxycaine HCl.
- Is an ester type local anesthetic,is ester of PABA.
- Prepared by Clinton and Laskowski in 1952.
- Potency= 7 compared to Procaine= 1.
- Toxicity= 7 compared to Procaine= 1.
- Metabolized by hydrolysis in both plasma and
liver.
- Onset of action= 2 to 3 minutes.
- Effective concentration in dental use= 0.4%
25. B) AMIDE-TYPE LOCAL ANESTHETICS
1)Lidocaine
Potency is 2 & toxicity is 2
pKa is 7.9 ph 6.5
pH with vasoconstrictor 5 to 5.5
Vasodilating
Concentration available-
2% Dental Concentration
5% Topical Agent
10% Spray
Maximum Recommended Dose with
vasoconstrictor 7 mg/kg and without vasoconstrictor 4.4
mg/kg
26. Onset of action 2-3 minutes
Half-life 1.6 hour
Metabolized in liver by microsomal fixed function oxidases
2)Mepivacaine
Amide group
Potency-2 toxicity- 1.5 to 2
pKa 7.6 pH 4.5
pH with vasoconstrictor 3 to 3.5
Vasodilation
Concentration- 3% without vasoconstrictor 2%
with vasoconstrictor
27. Onset of action 1.5 to 2 minutes
Halflife-1.9 hours
Maximum Recommended Dose- 6.6mg/kg
28. 3) PRILOCAINE-Present as Prilocaine HCl.
- Is an amide type local anesthetic.
- Prepared by Lofgren and Tegner in 1953.
- Potency= 2 compared to Procaine= 1.
- Toxicity= 2 compared to Procaine= 1.
- Metabolized in liver by amidases.
- Onset of action= 2 to 4 minutes.
- Half life= 90 minutes.
- Effective concentration in dental use= 4%.
29. 4) ARTICAINE-Present as Articaine HCl.
-Is an amide type local anesthetic.
-Prepared by H.Rusching et al in 1969.
-Potency= 3 compared to Procaine= 1.
-Toxicity= 2 compared to Procaine= 1.
-Metabolized both in plasma and liver by plasma
esterase and microsomal enzymes.
-Onset of action= 2 to 3 minutes.
-Half life= 30 minutes.
-Effective concentration in dental use= 4%.
30. 5)Bupivacaine
Amide group
Potency 4 time lidocaine toxicity 4 times less than lidocaine
pKa-8.1
pH 4.5 to 6
pH of vasoconstrictor 3 to 4.5
Vasodilation more than lidocaine but less than procaine
Concentration 0.5%
Maximum Recommended Dose 1.3 mgkg
Onset of action 6 to 10 minutes
Halflife 2.7 hours
Metaboilsm in liver by amidases
31. Eutectic Mixture of Local Anesthetics
EMLA cream is emulsion with oil phase composed of
lidocaine 2.5% & prilocaine 2.5%(1:1)
It was designed as a topical anesthetic able to provide
surface anesthesia of intact skin
Used primarily before painful procedure
EMLA has become popular during circumcision , leg
ulcer debridement & gynecological procedure
It is applied 1hour before procedure
EMLA is contraindicated for use in patient with
congenital or idiopathic methemoglobinemia, infants
under 1 2 months receiving methemoglobin-inducing
agents or patients with sensitivity with amide group
33. Epinephrine
It is most potent & widely used vasoconstrictor in
dentistry
It is available in following dilution
1:50,000,1:80,000,1:100,000,1:200,000,
1:300,000
Systemic Actions
On myocardium increases force of contraction & rate of
contraction
Increased heart rate & cardiac output
On coronary arteries causes dilation thus increases
coronary blood flow
Systolic blood pressure increases & diastolic pressure
decreases in small doses
34. In large doses diastolic pressure is increased
On blood vessels supplying skin , mucous membranes
& kidneys produces vasoconstriction
On blood vessels supplying smooth muscles cause
vasodilation on small doses & vasoconstriction on large
doses
It is potent bronchodilator
35. Contraindications for Vasoconstrictor
Absolute Contraindication :-
Uncontrolled Hypertension
Severe Cardiovascular diseases such as Acute
Myocardial Infarction within 6 months, Angina , Refractory
Cardiac Dysrhythmias
Hyperthyroid state