Everything! Your brain needs to know about Local Anaesthetics For The FRCA Primary

Contents

• What You’ll Learn
• Episode Guide – Local Anaesthetics For The FRCA Primary
  • Listen to the Fundamentals episode here
  • Listen to the Lidocaine episode here
  • Listen to the Bupivacaine episode here
  • Listen to the Ropivacaine episode here
  • Listen to the Prilocaine episode here
  • Listen to the Cocaine episode here
  • Listen to the Local Anaesthetic Systemic Toxicity (LAST) episode here
  • Listen to the Local Anaesthetics Comparison episode here
  • Listen to the Perineural Adjuncts episode here
• Key Pharmacological Concepts** **Covered

Welcome to the comprehensive GasGasGas collection of knowledge regarding local anaesthetics for the FRCA Primary Exam.

This full series covers every major local anaesthetic you’ll encounter in uk anaesthetic practice, handles the fundamentals of sodium channel pharmacology and onset mechanics of test agents to advanced clinical decision-making and emergency management.

What You’ll Learn

Core Pharmacology: Understand how all local anaesthetics work through voltage-gated sodium channel blockade, their classification into amides and esters, and why these differences matter clinically.

Individual Drug Profiles: Complete pharmacokinetic and pharmacodynamic data for lidocaine, bupivacaine, levobupivacaine, ropivacaine, prilocaine, and cocaine.

Clinical Decision Making: Learn when to choose each local anaesthetic based on onset time, duration, toxicity profile, and patient factors.

Emergency Management: Recognise and treat local anaesthetic systemic toxicity (LAST) with intralipid rescue protocols.

Advanced Concepts: Perineural adjuncts, IV lidocaine infusions, and comparative pharmacology for exam-style viva scenarios.

Episode Guide – Local Anaesthetics For The FRCA Primary

Listen to the Fundamentals episode here

• The essential foundation
• Sodium channel blockade mechanism – must cross membrane as unionised, work as ionised
• Classification: Amides (2 i’s) vs Esters (1 i) – determines metabolism
• Nerve fibre selectivity: C fibres most sensitive → A-alpha least sensitive
• pKa determines onset speed, protein binding affects duration
• LAST recognition and intro emergency management protocols

Listen to the Lidocaine episode here

• The ubiquitous LA
• Rapid onset (20-30 seconds skin, 3-5 min nerve block)
• pKa 7.7 – “L looks like 7 backwards” – 25% unionised
• Also Class 1b antiarrhythmic agent
• Multiple formulations: sprays, gels, infiltration, IV infusions
• Never use for spinal anaesthesia – TNS risk up to 33%
• IV infusions: 120mg/hour maximum, monitored bed space and institutional awareness required

Listen to the Bupivacaine episode here

• Long-acting amide agent
• Slow onset (10-20 min) but long duration (5-16 hours)
• Racemic mixture – R and S enantiomers
• 95% protein bound creating long-lasting reservoir
• Highly cardiotoxic – respect 2mg/kg dosing limit
• Don’t mix with lidocaine – pH incompatibility impairs function

+ Levobupivacaine

• The ‘safer’ S-enantiomer (anything is a poison in a high enough dose!)
• Pure S-enantiomer of bupivacaine
• Reduced cardiotoxicity – the major selling point
• Less motor block relative to sensory at low concentrations
• Same maximum dose: 2mg/kg (but some sources suggest 2.5mg/kg)
• CNS toxicity occurs before cardiovascular – gives warning

Listen to the Ropivacaine episode here

• The somewhat differential blocker..
• Pure S-enantiomer with differential blockade properties
• Sensory block similar to bupivacaine, motor slower onset/faster recovery
• Higher safety margin: 3mg/kg toxic dose
• Patients may have numb but mobile limbs initially
• Gained prominence during levobupivacaine shortages courtesy of…????

Listen to the Prilocaine episode here

• Fast onset (33% unionised at physiological pH)
• Faster recovery than bupivacaine – motor block 158min vs 220min
• EMLA component (with lidocaine)
• Methaemoglobinaemia risk >600mg – treat with methylene blue
• Fixes quickly – position patient immediately ‘no time for conversations about trains from 1970‘

Listen to the Cocaine episode here

• The pioneer! with testicular traction and hammers vs shins
• Launched spinal anaesthesia (August Bier, 1898)
• Dual mechanism: sodium channel blockade + monoamine reuptake inhibition
• Still used in ENT for excellent vasoconstriction
• Only 6% unionised at physiological pH
• Contraindicated in IHD, uncontrolled hypertension, porphyria
• Emergency management: benzodiazepines first-line for most complications

Listen to the Local Anaesthetic Systemic Toxicity (LAST) episode here

• Recognition: Only 60% follow textbook biphasic pattern
• Any weird behaviour after LA injection should raise suspicion
• Emergency management: Stop injection, 100% O₂, call for help, QRH
• Intralipid 20%: 1.5ml/kg bolus (~100ml for 75kg), then 15ml/kg/hour
• Mechanism: Na / K / Ca Channel Blockade + Mitochondrial impairment
• Prevention: Ultrasound reduces risk 4-fold, but many ways to reduce this issue!

Listen to the Local Anaesthetics Comparison episode here

• Absorption hierarchy: Intercostal > Caudal > Epidural > Brachial > Subcutaneous
• Day surgery: Prilocaine for faster recovery
• Safety: Levobupivacaine over bupivacaine when possible
• Emergency procedures: Consider onset vs duration needs
• Special populations: Dosing adjustments for age, hepatic function etc

Listen to the Perineural Adjuncts episode here

• Off-license enhancement strategies
• All perineural adjuncts are off-license – this is a medico-legal consideration.
• Dexamethasone: IV as effective as perineural (4-8h prolongation)
• Dexmedetomidine: 4h sensory, 3h motor prolongation
• Buprenorphine: 8.5h sensory prolongation via sodium channel blockade action :O
• Drug interactions: Dexamethasone + Ropivacaine = crystallization

Key Pharmacological Concepts** **Covered

Receptor Pharmacology: All local anaesthetics work through voltage-gated sodium channels causing blockade from the internal aspect of the channel within the neuronal membrane.

Structure-Activity Relationships: Amphipathic molecules with lipophilic aromatic ring and hydrophilic amine group, linked by either ester or amide bond.

Pharmacokinetic Principles:

• pKa determines onset speed (lower pKa = faster onset)
• Protein binding affects duration (higher binding = longer duration)
• Lipophilicity affects potency and redistribution
• Metabolism: Amides hepatic, esters plasma esterases

Each episode is designed to fit into your busy (scrub ironing) schedule:

• Commute-friendly: Perfect for car journeys to work
• Exercise compatible: Learn while in the gym
• Call-room ready: Quick revision during breaks
• Structured format: Model answers you can memorize and adapt

Why This Works

• Evidence-Based: All content derived from peer-reviewed sources
• Exam-Focused: Catches the required knowledge on local anaesthetics for the FRCA primary
• Practical: Real-world applications you’ll think about immediately
• Memorable: Stories and analogies that stick
• Complete: No gaps – from basic science to emergency management

Start with any episode, but the logical progression builds understanding. Whether you’re cramming for exams or building long-term know-how, this series delivers the local anaesthetic knowledge essential for modern anaesthetic practice.

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