Cocaine

Chemical

Ester local anaesthetic – an ester of benzoic acid

1860 – purified and named (Niemann)

1884 – first used topically for LA (Koller)

Use

Topical anaesthesia

Vasoconstriction on nasopharynx

Presentation

Solution & Liquid

Dose

1.5-2.0mg/kg up to 100mg

Route

Topical

Onset

3-8mins

DoA

Intermediate

MoA

Na channel blockade – inhibits nerve conduction

Inhibits NA & DA reuptake by adrenergic nerve terminal (Uptake 1), increasing plasma NA & DA concentrations

PD

CNS – euphoria, excitement, restlessness at low doses.  Convulsions, coma, medullar depression and death at high doses

Peripheral nerves – blocks nerve conduction when applied directly to nervous tissue

CVS

Vessels – vasoconstriction at most doses (other LAs display biphasic vascular smooth muscle effects) – an indirect effect due to elevated NA due to inhibition of NA update in adrenergic n terminals

Myocardium – bradycardia at low doses (central vagal stimulation).  Moderate dauses cause tachycardia.  High doses cause direct myocardial depression, VF & death

PK

A

Peak absorption:

Intranasal 30mins

IV/smoked 5mins

D

N/A

M

The only ester to undergo significant liver metabolism

Metabolised by liver & plasma cholinesterase

E

Metabolites excreted in urine

10% unchanged

Adverse Effects

Life threatening arrythmias

Addictive

Coronary vasospasm and increased myocardial O2 consumption

Hyperpyrexia

CVA

HTN

Contraindicated with IHD, MAOI, Adrenaline