Local Anaesthesia

1. LOCAL ANAESTHETIC AGENT
Dr. Shamvubrata Mitra
DA-11th Batch
BIRDEM General Hospital

2. DEFINITION
 Local Anaesthetics or analgesics are the
compounds that produce temporary blockade of
neural transmission when applied to the vicinity of
nerve and all excitable tissues including
myocardium.
 Analgesia- loss of pain sensation using lower
concentration of Local Anaesthetics.( Aδ & C fibre
only)
 Anaesthesia-Loss of all sensation by higher
concentration of local Anaesthetics(all fibres are
blocked)

3. HISTORY
 Cocaine- from plant “Coca”in South America in
nineteenth century.
 Karl Koller of Vienna first discovered the
advantages of cocaine,used it as a topical
opthalmic anaesthetic in 1884
 Today’s local anaestetics are synthetic chemical
descedants of cocaine.
 In 1944,lignocaine,the first amide linkage local
anaesthetic was introduced in Sweden.

4. IDEAL PROPERTIES OF LOCAL ANAESTHETICS
 It should not be irritating to the tissue to which it is
applied.
 Must be water soluble.
 Sterilisable by heat.
 Rapid onset of action.
 Duration of action appropriate to the operation to be
performed.
 Should be non-toxic.
 Leave no local after effects e.g.: Necrosis.

5. CLASSIFICATION
 According to nature of linkage between amine and arometic
parts into ester or amide group:
1)Ester:
a)Chloroprocaine
b)Cocaine
c)Procaine
d)Tetracaine

6. 2)Amide:
a)Lidocaine
b)Bupivacaine
c)Mepivacaine
d)Prilocaine
e)Ropivacaine

7.  According to duration of action:
a)Short acting:(30-60 minutes)
a)Chloroprocaine
b)Procaine
b)Intermadiate acting:(60-120 minutes)
a)Lignocaine
b)Mepivacaine
c)Prilocaine
c)Long acting:(>120 minutes)
a)Bupivacaine
b)Ropivacaine

8. STRUCTURE OF LOCAL ANAESTHETIC
o Local Anaesthetics are weak bases of
a tertiary amine.They have three
functional units-
1)Lipophilic,aromatic part
2)Hydrophillic
3)Ester or amide linkage

9. o They are classified according to
their linkage chain- Esters and Amide
group.
o LA are prepared as water soluble salt of
any acid usually hydrochloride.In the
multi dose vial it contains antifungal
agents like Na-metabisulfate.

10. MECHANISM OF LOCAL ANESTHETICS
Local anaesthetic agent (LA) __ (PH approximately 6)

In tissue, PH increase, Dissociates to release free base.

Free base is lipid soluble.

Enter into the interior of the axon.

Re-ionization takes place.

Re-ionized portion block the Na+ channel and prevent
influx of sodium ions.


11. Fails to initiation and propagation of action potential.

Impulse cannot go to the Higher centre.

No pain sensation.

12. MECHANISM OF ACTION OF LA
ionized
ionized unionized Enters into
cell
ionization
unionized

13. PHYSIOCHEMICAL AND PHARMACOKINETIC
PROPERTIES

14. FACTORS INFLUENCING ACTIVITY
Molecular weight:
Molecular weight Lipid Solubility duration of
action of local anaesthetic agents.
Lipid solubility:
lipid solubility onset and duration of action of
local anaesthetic agents.

15. pKa:
pKa degree of ionisation rapid onset of block
pH :
pH degree of ionisation amount of drug
available to cross neuronal membrane potency

16. Protein Binding:
The greater the protein binding, the longer the
duration of action of LA

17. MAXIMUM RECOMMENDED DOSES OF LA

18. ABSORPTION
 Absorption from different site is influenced by blood flow to
tissue and the uptake of drug into vascular compartment.
 Sequence:
 Intercoastal>caudal>Epidural>Plexus>Peripheral>Subcutaneous

19. METABOLISM
 Ester local anaesthetics are metabolized by plasma
cholinesterase.
 Amide local anaesthetics are metabolized by Liver.

20. TOXICITY FROM LOCAL ANAESTHETIC DRUGS
o Toxic side effects of Local anaesthetic drugs occur
when excessive blood levels is achieved.This is
usually due to-
o Accidental rapid intravenous infusion.
o Rapid absorption,such as from a very vascular site
i.e mucous membrane.
o Absolute overdose if the dose used is excessive

21. LOCAL ANAESTHETIC TOXICITY
A) Central nervous system toxicity:
1) Early symptoms:
a) Circumoral numbness.
b) Tongue Paresthesia.
c) Dizziness.
2) Sensory complain:
a) Tinnitus.
b) Blurred vision

22. 3) Excitatory:
a) Restlessness.
b) Agitation.
c) Nervousness.
4) CNS depression:
a) Slurred speech.
b) Drowsiness.
c) Unconsciousness.
d) Convulsion

23. B) Cardiovascular system:
1) Peripheral vasodilatation.
2) Hypotension.
3) Bradycardia.
4) Ventricular arrhythmias.
5) Finally cardiac arrest.
C) Allergic reaction.
D) Myotoxic.
E) Decrease coagulation (Lidocaine)

24. LIDOCAINE TOXICITY

25. FACTORS AFFECTING LA TOXICITY
1) Quantity of drug:
Increase quantity of drug  Increase toxicity.
2) Concentration of drug:
Increase concentration of drug  Increase
toxicity.
3) Absence of adrenalin:
Absence of adrenalin Increase toxicity.
4) Vascularity of the area:
Increase Vascularity of drug  Increase toxicity.

26. 5) Rate of absorption:
Increase absorption of drug  Increase toxicity
6) Rate of distribution of drug:
Increase distribution of drug  Increase toxicity.
7) Rate of metabolism:
Increase metabolism of drug  Increase toxicity.
8) Rate of protein binding:
Increase protein binding of drug  Decrease
toxicity.

27. REDUCING THE RISK OF TOXICITY
 Decide on the conc. of the local anaesthetic that is
required for the block to be performed.
 Use the least toxic drug available.
 Use lower doses in frail patients or at the extremes
of age.

28.  Always inject the and aspirate regularly looking for
blood to indicate an accidental intravenous
injection.
 Injection of test dose of 2-3 ml of LA containing
adrenaline will often cause a significant tachycardia
if accidental intravenous injection occurs .

29.  Most Nerve blocks are dependent on volume of
drug injected than total dose.Therefore if more
volume is needed it is better dilute the local
anaesthetic with 0.9% saline than to add more local
anaesthetic and increase the dose unneccesarily.

30.  Add adrenaline to reduce the speed of
absorption.The addition of adrenaline will reduce
the maximum blood conc. By about 50%.The
addition of adrenaline will make no difference to the
toxicity of LA if it is injected intravenously.

31. MANAGEMENT OF LA TOXICITY

33. ADJUVANTS
Varietes of agents are added to LA to modify the effects
in clinical practice.These are-
 Epinephrine:is added to LA to-
a)Prolong the anaesthetic effect by decreasing
absorption from site of conjugation
b)Improve the quality and reliability of central neural
blockade.
c)Decrease systemic toxicity.

34.  Opioids:all narcotics prolong the duration of action
 Hyaluronidase: allows greater spread of solution
along tissue plan thereby spread the onset of action
 Alkalinization: alkalinization of LA is used to speed
the onset of action

35.  Dextran:Dextran added to LA to increase duration
of action.
 Carbonation: addition of carbonic acid to LA
reduces the onset time and duration of action
 α-agonist: are used to prolong and potentiate the
effect of LA in all central neuraxial block.

36.  Other Agents used: mostly for epidural and SAB.
-Ketamine
-Neostigmine
-Midazolam

37. CONCLUSION
 Any unusual cardiovascular or neurological
signs,including outright cardiac arrest,after local
anaesthetic adminitration should rise suspicion of
LA systemic toxicity(LAST)
 The risk of LA systemic toxicity(LAST) is influenced
by patient factors,the site and conduct of the
block,and the LA type and dose.

38.  Education of anaesthesist and non-anaesthesists in
LAST management should improve patient safety.
 AAGBI guidelines aid emergency management of
LAST.

39. THANK YOU