Local anesthesia involves the use of drugs to achieve reversible loss of sensation in a specific area without loss of consciousness. The document covers the definition, history, pharmacodynamics, and various aspects of local anesthetics including types, composition, and clinical applications, as well as contraindications and potential complications. Key types of local anesthetics include lidocaine and bupivacaine, each with specific uses, dosage recommendations, and considerations for safety and efficacy.

1. LOCAL ANESTHESIA
PRESENTED BY-
DR.ALISHA MEHER
GUIDED BY-
DR.PROF. CHINMAYA BHAWANI PRASAD
(HOD SHALYA TANTRA)

2. EVERYTHING TO KNOW ABOUT LOCAL
ANESTHESIA:
 INTRODUCTION TO ANESTHESIA
 DEFINATION
 HISTORY
 NEURON AND NERVE
 MECHANISM OF NERVE CONDUCTION
 PHARMACODYNAMICS AND PHARMACOKINETICS OF LA
 NEED OF LA
 COMPOSITION
 IDEAL LA
 CLASSIFICATION
 LA AGENTS
 PRE-ANESTHETIC TEST
 SELECTION OF LA
 FACTORS AFFECTING LA ACTIVITY
 SYSTEMIC EFFECTS OF LA
 CONTRAINDICATIONS
 COMPICATIONS
 TOXICITY
 ANAPHYLATIC REACTION OF LA AND ITS MANAGEMENT
 PRECAUTION TAKEN FOR LA

3. ANESTHESIA :
- Greek word: “an” = without ; “aisthesia”= sensation
- Loss of sensation in all or particular part of body with or without loss of consciousness
CARDINAL FEATURES :
ANESTHESIA
ANALGESIA
(PREVENTION FROM PAIN)
AMNESIA
(LOSS OF MEMORY)
PARALYSIS
(MUSCLE RELAXATION)
UNCONCIOUSNESS

4. TYPES OF ANESTHESIA
LOCAL REGIONAL GENERAL

5. WHAT IS LOCAL
ANESTHESIA ?
• Local anaesthetics (Las) are drugs which upon topical application or local injection cause reversible loss of
sensory perception, especially of pain, in a restricted area of the body. They block generation and conduction of
nerve impulse at any part of the neuron with which they come in contact, without causing any structural
damage.
REVERSIBLE ,RECEPTOR BLOCK
• SKIN(APPLIED AREA) BRAIN
NERVE IMPULSE

6. WHAT ACHARYAS DESCRIBE ABOUT
SAGYAHARANA:

7. Cocaine(COCA PLANT;Erythroxylaceae, Erythroxylum gracilipes )is a naturally occurring
compound
It was the first anesthetic to be discovered and is the only naturally occurring local anesthetic.
Dr.Carl Koller,an austrian opthalmologist in 1884 demostrated that dropping a soluction of
cocaine into eyes of frogs and guniea pigs produced a local anesthetic effect ;also he works on
use of cocaine in catract extraction and iridectomy.
Procaine, the first synthetic derivative of cocaine, was developed in 1904 by Alfred Einhorn. Later,
Nils Lofgren,a swedish chemist later developed lidocaine(under the name XYLOCAINE).
HISTORY OF LOCAL ANESTHESIA:

8. SIGNIFICANT PERSONS IN THE FIELD OF
ANESTHESIA:

9. INTRODUCTION TO
NEURON:
A Neuron is an electically excitable cell that Processes & transmits information through
electrical & chemical signals.
NERVE:-
A whitish fibre or bundle of fibres in the body that trasmits impulses of sensation to brain or
spinal cord and impulse from these to muscles and organs

10. 3)Depending upon types of axons
2)Depending upon structure
Transmission of impulse from nerve to CNS differs depending
on whether a nerve is myelinated or unmyelinated.
1)Depending upon No. of Poles
4)Depending upon Function
CLASSIFICATION OF NEURONS

11. MECHANISM OF NERVE
CONDUCTION
Resting Member Potential (-70mV)
Threshold (-55mV) ELECTRICAL + CHEMICAL
Action Potential = DEPOLARISATION+REPOLARIZATION
1) Rising Phase +40mV
. Absolute refractory
2) Falling phage
.
Relative refractory
3) Hyperpolarisation
Impulse transmission through axons

13. HOW LOCAL ANAESTHESIA WORKS
(pharmacodynamics):
Acetylcholine theory:
• Local anesthesia prevents acetylcholine at the synapse to alter the cell permeability,Thus prevents
depolarization.This theory is less accepted as acetylcholine is not always present at the synapse.
Calcium displacement theory:
• Local anesthesia blocks calcium channels and prevents the displacement of calcium needed for
depolarization .
Surface charge theory:
• local anesthesia is positively charged and it binds to outer surface of nerve membrane,thus hindering
the depolarization process.
Membrane expansion theory:
• local anesthesia is hydrophillic and it easily diffuses into the nerve membrane,thus altering the nerve
membrane permeability.
Specific receptor theory:
• local anesthesia soluction attaches itself to specific receptors present at the external or internal
surface of nerve membrane and generally near the Na+ channel.this blocks the sodium channel and
inhibits depolarization.

14. PHARMACOKINETICS:
• ABSORPTION:
Depanding upon the vascularity of
the area .it depands whether the
drug will absorb into systemic
circulation or not.
• DISTRIBUTION:
Depands upon the degree of tissue
and plasma protein binding the
drug.
More the protein bound the
agent,the longer the duration of
action as free drug is more
slowly made available for
metabolism.
METABOLISM:
ESTERS: breakdown rapidly by plasma esterases to
inactive compounds having a short t12 .
Cocaine hydrolize in liver
AMIDES: Metabolize in liver by amidases.its a
slow process hence its t12 is longer .so if given in
repeated dose of by infusion.
EXCREATION:
BOTH ESTERS AND AMIDES ARE
EXCREATED BY KIDNEYS AS
XYLIDINES(amine).

15. NEED OF LOCAL ANESTHESIA:
• USE TO TREAT PAINFUL CONDITION E.g. mouth ulcer while
taking meal
• PREVENT PAIN DURING A PROCEDURE OR OPERATION OF A
PARTICULAR AREA OPERATED (for Dx and Rx)
• biopsy

16. • LOCAL ANESTHESIA CAN APPLIED AS IN FORM OF-
- OINTMENTS=2%
- JELLY(CATHETER,SKIN GRAFTS)=2%
- SPRAY=4%
- CREAMS 0VER SUPERFICIAL SKIN (TOPICAL)=2%
- INJECTABLES OVER SUB MUCOSA,MUCOSA,MUSCULAR AREA,INTRAVENOUS
(INFILTRATIONS= 0.5-2%)
- VISCOUS
• MINOR NERVE BLOCKER= NOT EXCEED 2%
• SPINAL= 0.5-5%
• EPIDURAL=0.25-2%

17. COMPOSITION OF LOCAL
ANASTHESIA:
• LOCAL ANESTHETIC AGENT: lignocaine hydrochloride 2%(20mgml)
• VASOCONSTRICTOR: Adrenaline – 1:80,000 to 1:2,00,000
• REDUCING AGENT(ANTIOXIDENT): Sodium metabisulphite-0.5mgml
This agent reacts with oxygen before it destroys the vasoconstrictor concentration.
• PRESERVATIVE : Methyl paraben- 0.1 mgml
This agent is added to the soluction to give a shelf life of 2yrs or more
It can cause allergic reactions.
• SALT: Sodium chloride -0.9 %- this is added to make the soluction isotonic.
• DISTILLED WATER OR RINGER LACTATE SOLUCTION: Added to give volume to the
soluction and acts as a vehicle.
• FUNGICIDE: Thymol- it is added to provide antifungal properties.

18.  LOCAL ANESTHESIA CONSIST OF HYDROPHILLIC TERTIARY AMINE GROUP LINKED WITH LIPOPHILLIC AROMATIC GROUP
 local anesthesia are alkaloid bases that are combined with acids,usually hydrochloride ,to form water soluable salts.
 SO IT MAKES LOCAL ANESTHETIC DRUG TO GET EASILY ABSORBE AND DISTRIBUTED IN THE APPLIED AREA
 the salt are used because they are stable and soulable in water ,water solubility is necessary for their diffusion through
interstitial fluids to the nerve fibers.
 some local anesthesia having 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.
Ex- bupivacaine , highly lipid soluble,is approximately 4 times more potent than lidocaine.
 local anesthesia block nerve fiber conduction by acting on nerve membrane:
inhibit Na ions activity BLOCKS DEPOLARIZATION blocks nerve conduction
 LA blocks conduction in the following order:
- Small myelinated axons
- non myelinated axons
- Large myelinated axons
Thus, a differential block can be achieved .i.e. pain sesation is blocked more readily than other sensory modalities.
 thus the loss of nerve function proceed as-
- Loss of pain
- Temperature
- Touch
- Proprioception
- Skeletal muscle tone
Thus is why people may still feel touch but not pain when using local anesthesia.

19. IDEAL LOCAL ANESTHESIA:
• RAPID ONSET OF ACTION
• LONG ACTING
• LOCAL CONSTRICTOR EFFECT
• NO LOCALSYSTEMIC TOXICITY
• NO ALLERGIC REACTION
• ECONOMICAL
• REVERSIABLE ACTION
• SAFE
• COMPATABLE ph TO LOCAL TISSUES(BASEALKALOID)
• EASY STERLIZABLE WITHOUT LOOSING ITS POTENCY AND SHELF LIFE

20. CLASSIFICATION OF LOCAL ANASTHESIA
AGENTS:
BASED ON CHEMICAL STRUCTURE:
• ESTERS:
1) ESTERS OF BENZOIC ACID:
-Butacaine
-Cocaine
- hexylcaine
- Piperacaine
- Tetracaine
- Benzocaine
2) ESTERS OF PARA AMINO BENZOIC ACID:
- CHLOROPROCAINE
- PROPOXYCAINE
• AMIDES:
BASED ON SOLUBILITY(DURATION OF
ACTION AND POTENCY):
• INJECTABLES:
- LOW POTENCY,SHORT DURATION OF ACTION:
E.g. procaine,chloroprocaine
- INTERMIDIATE POTENCY AND INTERMEDIATE
ACTION:
E.g. lidocaine,prilocaine
- HIGH POTENCY AND LONG DURATION ACTION:
E.g. bupivacaine,tetracaine,debucaine,ropivacaine
• SURFACE ANESTHESIA:
- SOLUBLE: E.g cocaine,lidocaine,tetracaine
- INSOLUABLE: .E.g. benzocaine,oxethazine
BUPIVACAINE
LIDOCAINE
PRILOCAINE
• QUINOLONES:
centbucridine

21. TYPES OF LOCAL
ANESTHESIA
SURFACE
ANESTHESIA
INFILTRATIONALA
NESTHESIA
CONDUCTION
BLOCK
ANESTHESIA
CENTRAL NERVE
BLOCK ANESTHESIA
INTRAVENOUS
REGIONAL
ANESTHESIA

22. • LOCAL ANESTHETIC AGENTS:
1) LIDOCAINE HYDROCHLORIDE:
- Introduced in 1950s.
- Excellent efficacy and safe
- 0.25-5% concentration available
- 4mgkg lasts for 90min.
- Used with or without adrenaline.with adrenaline has longer.CI : End atreries e.g. glans
penis,ear loubles, tips of nose,fingers and toes.
- Topical=2%,epidural=1.5-2%,spinal=5%,infiltration=0.5-1.5%
- 2% with1:1000000 epinephrine or 1:2000000 epinephrineor 4%.
- Due due water solubality chances of toxicity is more. So, lowest dose which provides
anasthesia should be used.
- Water soulability provides more tissue penetration than lidocaine base.
- 2% viscous-oral rinse in dental procedure
- Cotton applicators or packs- 1 to 5ml(40-200mg)or 0.6 to 3mgkg.

23. 2) BUPIVACAINE(marcaine):
- LONG ACTING
- Mostly used in post operative mangement
- Provides 4-5hrs after infiltration and 8hrs after nerve block. With epineprine
7hrs anesthesia.
- Available = 0.5%,0.5% with 1:2000000 epinephrine or 3% mepivacaine
- Dose=3mgkg, epidural=0.25%-0.5%,spinal=0.5% in 3ml

24. SELECTION OF LOCAL
ANESTHESIA:

25. FACTORS AFFECTING LA ACTIVITY:
• LIPID SOLUABILTY: higher the lipid solubility higher the ability of penetration to
lipoprotein membrane and therefore greater the potency.
• pH:Anesthesia is decreased by the acidification of tissues.e.g inflammatory
condition. (acidosis decrease the portion of nonionization of drug, reduce the
ability to cross the membrane)
• VASODILATORS:LA with a vasodilator is more effective than the same agent
without vasodilator.
• alkalization of LA increases the effectiveness and speed of action
• only LA without a vasoconstrictor are vasodilators thereby increasing the
chances of its toxicity.
• PROTEIN BINDING: the greater the degree of membrane protein binding, longer
is the duration of action.
• pKa: Acid dissociation constant

26. SAFTY LEVEL OF LA:
• WITHOUT VASOCONSTRICTORS: 3-4mgkg
• WITH VASOCONSTRICTORS: 7mgkg

27. SYSTEMIC ACTION OF LOCAL
ANESTHESIA:
• CNS-
- Readily cross BBB.
- causes depression
- On therapeautic dose,no CNS effects of clinical significance.
- anticonvulsant propertiese(lidocaine,procaine,etc) while some causes seizures.

28. • CARDIOVASCULAR SYSTEM:
Direct action on myocardium:
- LA MODIFY ELECTROPHYSIOLOGICAL CHANGES IN THE MYOCARDIUM.
- LA PRODUCES MYOCARDIAL DEPRESSION
- DECREASE CONDUCTION RATE,FORCE OF CONTRACTION
Direct action on periperal vasculature:
- cocaine, periferal cutaneous vasoconstriction
- others , vasodilation .though relaxation of smooth muscle in wall of blood vessels.
- On B.P.:
Hypotension, by direct decreasing the myocardium and smooth muscle relaxation in the vessel wall.
• RESPIRATORY SYSTEM:
- In therapeutic dose,relaxant of bronchial smooth muscle
- In overdose, produces respiratory arrest due to generalized CNS DEPRESSION.
• MALIGNANT HYPERTHERMIA:
- SYMPTOMS: TACHYCARDIA,RIGID MUSCLE SPASM,UNSTABLE B.P. ,CYANOSIS,RESPIRATORY
ACIDOSIS,MAY LEAD TO DEATH
- Amide group of LA are capable to provoke MH

29. • Alcohol and smoking
• Steriod use (.2yrs)
• ALLERGY TO LA
• BISULFIDE ALLERGY
• MI within 6months
• UNSTABLE ANGINA PECTORIS
• CARDIAC DYSRTHYRMIAS
• CEREBRAL STOKE WITHIN 6MONTHS
• SEVERE RENAL DYSFUNCTION
• D.M
• Recent hepatitis A and hepatitis B
• Jaundice
• Local infection and sepsis
• Chronic renal failure
• Hyperthyroidsm THYROTOXICOSIS
• Pregnency during 1st trimenster
• Hypertension
• MH
• Congenital methemoglobinemia. AND OTHER CONGENITAL LIVER DYSFUNCTIONS
• CONDITIONS-increased H.R. , tremor, increased basal metabolic rate, irritability, increase B.P , increase body temp.
• MEDICATIONS- anti depresents,beta blockers,etc
• BODY PARTS- END ARTERIES E.g. digits of hands and feets,ears,nose,penis.
CONTRAINDICATION:

30. • SYSTEMIC COMPLICATION:
- Toxicity
- Syncope
- Allergic reaction
- Nausea and vomiting
• LOCAL COMPLICATIONS:
- Hematoma
- pain
- Slurred speech
- Blurred vision
- Headache
- Dizziness
- Edema
- Paresthesia(trauma to the nerve)
- Trismusmuscle twitching
- Soft tissue injury
COMPLICATION:

31. • MENIFECTATION OF TOXICITY-
-visual and auditory distrubances, light headedness,numbness of tongue
- Muscular twitching
- Unconciousness
- Convulsion CNS depression
- Coma
- Cardiac depression
• Toxicity of local anesthesia depands upon various factors-
- Amount of drug injected
- site of injection-vasularity
- Addition of vasodilators
- Nature of drug given
- Presence of associated conditions such as low cardiac output , renal failure, liver diseases ,etc
• adverse effects are usually caused due to high plasma concentration, resulting from:
- intravasular injection
- Excessive dose or rate of inj.
- Delayed drug clearance
- Administration into vascular tissue
• LA TOXIC EFFECTS-
- CNS: seizures,CNS depression including respiratory arrest
- CARDIOVASCULAR: depresses heart result in bradycardia,hypotension, cardiovascular collaspe,cardiac arrest
LA TOXICITY:

32. • Maintain ‘ABC’.
• O2 mask
• Ventilation if apnea occurs
• Convulsion- i.v. dizapam,thiopentone in incremental dose
• Cardiovasular collaspe- ephedrine,CPR as needed
MANAGEMENT OF LA
TOXICITY:

33. ALLERGIC SHOCKANAPHYLATIC SHOCK DUE TO
LA:
• Esters are highly allergics, so pre anesthetic test needed.
• Pt may develop allergy only to bisulfide preservative used to stabilize the vasoconstriction.
• SIGN AND SYMPTOMS:
- Generalized body rash or skin redness
- Urticaria
- Swelling of throat
- Bronchospasm
- Asthama
- Abdominal cramping
- Irregular heartbeat
- Hypotension
- Angioneurotics edema(swelling of face and lips)

34. • Pharmacological management of anaphylatic shock:
- EPINEPHRIN-ADRENALIN:1:1000 SC INJ.
Dose= 1mg T.D.S 5min apart
Opens bronchioles allowing free breathing,increase B.P , intensify heartrate
Its effect is drastic, but short lived.
- BENEDRYL(DIPHENHYDRAMINE): 25-50mg sc inj
Pills are available to prevent serious severe allergic reaction ,given a hour
before the procedure.
- AMINOPHYLLINE: opens blocked breathing passage
- HYDROCORTISONE: iv inj
Reduces generalize allergic inflammatory reactions on long term basis
- MEPHETERMINE SULFATE: iv inj
Counteract hypotension on a prolonged basis.

35. PRE ANESTHETIC TEST:
• SKIN PRICK TESTSENSITIVITY TEST
• REQUIREMENTS-
- Cotton
- 1-3ml syringe
- 26-30 gauze needle
- Surgical spirit
- Pen
• INTRADERMAL INJECTION
• WAIT FOR 20-30 MIN FOR ANY ANAPHYLATIC REACTION

36. • Slow atraumatic insertion.
• Sharpe needle(13rd part should be seen from outside)
• PROPER STERELIZATION
• Injecjected in proper anatomical land mark.
• pre anesthetic test must be done before injection of any Las.
• inject LA slowly, not exceding max. safe dose,espicially in children.
• avoid injecting large bolus at once. Small boluses,given slowly to achieve the
desires effect are safer.
• adrenalin(vasoconstrictor) containing LA CI in pt having any type of cardiac
issues,hyrotoxicosis , uncontrolled hypertension, pt receiving betablockers,
tricyclic antidrepresants
• Propanonol(betablocker)reduces metabolism of amides group of LA reducing
hepatic blood flow.
PRECAUSIONS: