BY MAYANK CHHABRA

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)

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

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.

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.

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

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

B)Surface Anesthetics:

1)Soluble agents- Eg Cocaine,Lidocaine, Tetracaine

2) Insoluble agents- Eg Benzocaine,Oxethazine

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….

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

 Theories of mechanism of action of local Anesthesia1) Acetylcholine Theory 

2) Calcium Displacement Theory 

3) Surface Charge Theory 

4) Membrane Expansion Theory 

5) Specific Receptor Theory

ACETYLCHOLINE THEORY, CALCIUM DISPLACEMENT THEORY andSPECIFIC CHARGE THEORY

Are discredited .

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.

Specific Receptor Theory 

Local Anesthetics act by binding to specific receptor binding site present on the sodium channels

Specific receptor site are present on either the external or internal surface of the sodium channels

Local Anesthetics are classified according to biological site & mode of action

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

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

Injectable Local Anesthetic Agents

1)Amide local anesthetics

Maximum Recommended Dosage

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.

DESCRIPTION OF INDIVIDUAL ANESTHETIC AGENTSA) ESTER-TYPE LOCAL ANESTHETICS1) 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%.

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%

B) AMIDE-TYPE LOCAL ANESTHETICS1)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

Onset of action 2-3 minutesHalf-life 1.6 hourMetabolized in liver by microsomal fixed function oxidases

2)MepivacaineAmide groupPotency-2 toxicity- 1.5 to 2pKa 7.6 pH 4.5pH with vasoconstrictor 3 to 3.5VasodilationConcentration- 3% without vasoconstrictor 2% with vasoconstrictor

Onset of action 1.5 to 2 minutesHalflife-1.9 hoursMaximum Recommended Dose- 6.6mg/kg

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%.

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%.

5)BupivacaineAmide groupPotency 4 time lidocaine toxicity 4 times less than lidocainepKa-8.1pH 4.5 to 6pH of vasoconstrictor 3 to 4.5Vasodilation more than lidocaine but less than procaineConcentration 0.5%Maximum Recommended Dose 1.3 mg\kgOnset of action 6 to 10 minutesHalflife 2.7 hoursMetaboilsm in liver by amidases

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

VasoconstrictorVasoconstrictors are important addition to local anesthetic solution due to following reasons

To decrease the perfusion To decrease absorption of local anesthetic

Minimise the risk of toxicity 

Increase the duration of action

Decrease the bleeding

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

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

Contraindications for VasoconstrictorAbsolute Contraindication :-Uncontrolled Hypertension

Severe Cardiovascular diseases such as Acute Myocardial Infarction within 6 months, Angina , Refractory Cardiac Dysrhythmias

Hyperthyroid state

Relative ContraindicationsPatients on MAO inhibitors

Patients on Tricyclic Anti-depressents

Arteriosclerosis

Diabetes Mellitus

Stanley Malamed, Handbook of Local Anesthesia, Sixth Edition

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