74.1 Local Anaesthetics

• Amides, e.g., lidocaine, bupivacaine

• Esters, e.g., cocaine, benzocaine

• Most LAs are weak bases and exist as protonated form at body pH

• Block Na⁺ channels in axons →prevent generation of APs

• Small-diameter nerve fibres more sensitive to LAs

Therefore coarse touch and movement usually spared

• At high concentrations can depress other excitable tissues e.g., myocardium

• Main systemic effects are on CNS—sedation and light-headed; sometimes anxiety and restlessness

• High toxic doses cause twitching and visual disturbances

• Severe toxicity causes convulsions, coma, cardiorespiratory depression

• Lidocaine—rapid acting and most stable; duration of action 90 min

• Bupivacaine—slow onset (30 min) but duration 8 h

• Cocaine used for surface Anaesthesia where intrinsic vasoconstrictor action desirable

• Hypersensitivity reactions may occur with LAs, especially with atopic patients

• Opening of Na⁺ channels leads to Na⁺ entry exceeding K⁺ exit, further depolarizing membrane opening more Na⁺ channels, etc.—leads to AP

• LAs block Na⁺ channels by preventing opening of h-gates

• LAs are use dependent, i.e., degree of block proportional to rate of nerve stimulation

• More drug molecules (in protonated form) enter Na⁺ channels when they are open and cause more inactivation

• Cocaine causes vasoconstriction by blocking norepinephrine reuptake and potentiates sympathetic activity

• Most amides cause vasoconstriction at low doses and vasodilatation at higher concentrations

• Duration and potency related to lipid solubility

• Parallel use of vasoconstrictor prolongs effect

• Amides metabolized in liver

• Esters (not cocaine) hydrolyzed by plasma pseudocholinesterase

• Max. dose of lidocaine = 200 mg (500 mg with adrenaline), e.g., 5 mL of 2% lidocaine with adrenaline = 100 mg

• Bupivacaine = max. 60 mL using a 2.5 mg/mL (0.25%) solution

74.1.1 Moffat Solution

• Cocaine 10% 1 mL or 5% 2 mL @ 50 mg/mL = 100 mg (1.5 mg/kg max); adrenaline 1 mL 1:1000 (max. 100 mg/10 min); NaHCO₃ 2 mL 8.4%

• Risk of arrhythmias—especially halothane

• Risk of hypercapnia and hypertension

74.1.2 Laryngopharyngeal Local Anaesthesia

• Krause method—swab soaked in 4% lidocaine held by Krause forceps in each piriform fossa for 1 min

• Percutaneous injection of LA at greater cornu of hyoid also anaesthetizes superior laryngeal n

• Sprayed/nebulized lidocaine

• Benzocaine lozenge

74.1.3 Ear Anaesthesia

• Auriculotemporal block—2 mL of lidocaine injected anterior to meatus

• Greater auricular n block—inject anterior and posterior to mastoid tip

74.2 Neuromuscular Blocking Drugs

• Competitive, e.g., atracurium—lasts 15 to 30 min

• Depolarizing—suxamethonium—rapid onset and duration of 3 to 7 min

Drug does not dissociate rapidly from receptors at cholinergic nerve terminals

Prolonged receptor activation is produced

NM block then occurs because:

– Inactivation of voltage-sensitive Na⁺ channels in surrounding muscle fibre membrane—APs no longer generated

– Transformation of activated receptors to desensitized state—unresponsive to ACh