Local anesthetics work by reversibly blocking nerve impulses through inhibition of sodium ion channels. The first local anesthetic was cocaine in 1884, and the first synthetic was procaine in 1905. Local anesthetics are classified as esters or amides and are commonly used for regional anesthesia techniques. Potential side effects include central nervous system toxicity, cardiovascular effects, allergic reactions, and methemoglobinemia. Careful dosing and monitoring can prevent local anesthetic toxicity.

1. LOCAL ANESTHETICS
DR GEETANJALI S VERMA
DEPT OF ANESTHESIA
© DR GEETANJALI S VERMA

2. WHAT?
• Produce reversible conduction blockade of
impulses along central & peripheral nerve
pathways after RA
• Increasing conc – autonomic, somatic sensory,
somatic motor impulse transmission
interrupted – ANS system blockade, sensory
anesth, skeletal muscle paralysis in area
innervated by the nerve
© DR GEETANJALI S VERMA

3. HISTORY
• 1st LA – COCAINE 1884 (used by KOLLAR in
ophtho surg) – fm erythroxylon cola plant
• 1st synthetic LA – PROCAINE (EINHORN 1905)
• LIDOCAINE – logfren 1943
© DR GEETANJALI S VERMA

4. CHARACTERISTICS
• Poorly soluble in water
• Marketed as water soluble HCl salts – acidic
(pH 6) – stability
• Acidity also useful with epinephrine (unstable
at alkaline pH)
• Sodium bisulfite added to LA epinephrine soln
(pH 4) – prevents oxidative decomposition of
epinephrine
© DR GEETANJALI S VERMA

5. CLASSIFICATION
• ESTERS
– Procaine
– Chloroprocaine
– tetracaine
• AMIDES
– Lidocaine
– Etidocaine
– Prilocaine
– Mepivacaine
– Bupivacaine
– Levobupivacaine
– ropivacaine
© DR GEETANJALI S VERMA

6. © DR GEETANJALI S VERMA

7. MOA
• Inhibit passage of Na+ ions thru ion selective
Na+ ch in nerve memb
• Failure of Na ion ch permeability to increase
• Slows rate of depol (threshold pot. Not
reached)
• Action pot not propagated
• Also block voltage dependent K+ ion ch
• ? Ca2+ ch blockade
© DR GEETANJALI S VERMA

8. © DR GEETANJALI S VERMA

9. METABOLISM
• ESTERS: rapid hydrolysis in plasma and liver
• AMIDES: hepatic metabolism
© DR GEETANJALI S VERMA

10. © DR GEETANJALI S VERMA

11. • Regional anesth
– Topical anesth
– Local infiltration
– Periph N block
– IVRA
– Epidural
– Spinal
• Tumescent liposuction© DR GEETANJALI S VERMA

12. • SYSTEMIC
– CNS
– CVS
– Allergy
– Met Hb
• LOCAL
© DR GEETANJALI S VERMA

13. CNS
• Light headedness, dizziness
• Visual/ aud disturbances, tinnitus, disorientn
• Excitability – shivering, tremors, musc twitching,
convulsions
• CNS depression, rest depr, resp arrest
• Cause: blockade of inhibitory pathways in
cerebral cortex, incr release of glutamate
• t/t: BZD, thiopentone (conv)
ventilatory/ circulatory support
© DR GEETANJALI S VERMA

14. CVS
• Decrease rate of depol in fast conducting
tissues of Purkinje fibres & ventricular musc
• ECG: incr PR interval, incr QRS complex
duration
• High doses – depress spont pacemaker activity
in sinus node – sinus brady & arrest
• t/t: ABC, ECG monitoring
intralipid 20% 1.5ml/kg bolus IV foll by
0.25ml/kg/min over next 10mins
© DR GEETANJALI S VERMA

15. ALLERGY
• Esters (PABA)
– t/t: oxygen, epinephrine, hydrocort
• Vasoconstriction – pallor, anxiety, palpitations,
tachy, HTN, tachypnea
– t/t: B blockers
© DR GEETANJALI S VERMA

16. MET HEMOGLOBINEMIA
• Prilocaine (600mg)
• Hepatic metabolism of prilocaine
↓
O – toluidine
↓
Oxidises Hb to Met Hb
t/t: methylene blue 1-2mg/kg IV over 5mins
© DR GEETANJALI S VERMA

17. LOCAL
• Radicular symptoms
• Cauda equina syndrome
• Neurological symp – back pain, paresthesia,
radicular pain, hypoaesthesia
© DR GEETANJALI S VERMA

18. PREVENTION OF TOXICITY
• Liposomal encapsulation of drug
• Incorporation into biodegradable polymer
microspheres for sustained release
• Use of site 1 Na+ ch toxins with LA
© DR GEETANJALI S VERMA

19. © DR GEETANJALI S VERMA