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