Local Anaesthetics
Local anaesthetics (LAs) block nerve conduction by inhibiting voltage-gated sodium channels (VGSC) in neuronal membranes, preventing action potential generation and propagation. Classification: Esters (procaine,...
What matters first
Local anaesthetics (LAs) block nerve conduction by inhibiting voltage-gated sodium channels (VGSC) in neuronal membranes, preventing action potential generation and propagation. Classification: Esters (procaine,...
Local anaesthetic systemic toxicity (LAST) with seizures and cardiac arrest
2 Feb 2026
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Clinical board
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Urgent signals
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- Local anaesthetic systemic toxicity (LAST) with seizures and cardiac arrest
- Methemoglobinaemia with prilocaine
- Allergic reaction to para-aminobenzoic acid (PABA) metabolites
- Neurotoxicity with high intrathecal concentrations
Exam focus
Current exam surfaces linked to this topic.
- ANZCA Primary Written
- ANZCA Primary Viva
Content status and exam context
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Topic family
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1. Define - What are local anaesthetics, classification... CICM First Part Written, CICM First Part Viva exam preparation.
Local anaesthetics (LAs) block nerve conduction by inhibiting voltage-gated sodium channels (VGSC) in neuronal membranes, preventing action potential generation and propagation. Classification: Esters (procaine,...
Clinical explanation and evidence
Quick Answer
Local anaesthetics (LAs) block nerve conduction by inhibiting voltage-gated sodium channels (VGSC) in neuronal membranes, preventing action potential generation and propagation. Classification: Esters (procaine, chloroprocaine, tetracaine, benzocaine) metabolized by plasma cholinesterases; amides (lidocaine, prilocaine, mepivacaine, bupivacaine, ropivacaine) metabolized by hepatic CYP1A2 (lidocaine, mepivacaine) and CYP3A4 (bupivacaine, ropivacaine). Potency: Related to lipid solubility (partition coefficient) — bupivacaine > ropivacaine > lidocaine; Onset: Related to pKa and unionized fraction at physiological pH — lidocaine (pKa 7.7, 35% unionized) faster than bupivacaine (pKa 8.1, 15% unionized); Duration: Related to protein binding (α1-acid glycoprotein) — bupivacaine (95% bound) > lidocaine (65% bound). Toxicity (LAST): CNS effects first (circumoral numbness, tinnitus, metallic taste, visual disturbances, agitation, seizures, coma), then cardiovascular (hypotension, arrhythmias, cardiac arrest — bupivacaine most cardiotoxic due to strong protein channel binding). Treatment: Stop injection, call for help, lipid emulsion 20% 1.5 mL/kg bolus then 0.25 mL/kg/min infusion (lipid sink mechanism), benzodiazepines for seizures, ACLS with prolonged resuscitation. Additives: Adrenaline 1:200,000 (5 μg/mL) reduces systemic absorption by 30-50%, prolongs block, allows detection of intravascular injection (tachycardia). Indigenous considerations: Higher rates of obesity alter distribution volume; cautious dosing required to prevent LAST. [1-10]