Local anaesthetics

Question 1

Examples of amide local anaesthetics

Answer 1

Lidocaine
Bupivacaine
Ropivacaine
Prilocaine
Mepivacaine
Dibucaine

Question 2

Examples of ester local anaesthetics

Answer 2

Tetracaine (amethocaine) - present in ametop
Cocaine
Benzocaine
Procaine

Question 3

Ametop vs EMLA

Answer 3

Ametop (amethocaine / tetracaine)
* Ester
* Faster onset ~30 mins
* Longer duration ~4-6 hours
* Local vasodilatation and erythema

EMLA = Eutectic mixture of local anaesthetic
* 2.5% lidocaine and 2.5% prilocaine
* Slower onset ~60 mins
* Less duration ~1-2 hours
* Vasoconstriction and blanching
* Avoid in patients at risk of methaemoglobinaemia

Question 4

Mechanism of action

Answer 4

• Local anaesthetic drugs bind to fast sodium channels in the axon to prevent depolarization and action potential propagation
• Smaller nerves are blocked first
• Only the unionized form of LA can cross the axon membrane to take its effect

Question 5

General principles

Answer 5

• Local anaesthetics are weak bases with a pKa >7.4, therefore at physiological pH they are mostly in their ionized form
• Formulated as hydrochloride salts to render them water soluble
• Potency is related to lipid solubility
• Duration of action is related to extent of protein bindings - more extensive protein binding = longer duration of action. Amide LAs exhibit more protein binding
• Onset of action is related to pKa - lower = less ionized = quicker onset
• Esters are hydrolysed rapidly by plasma cholinesterases to inactive compounds
• Amides undergo hepatic metabolism by amidases