FRCA Notes

Lidocaine

  • Lidocaine is an amide local anaesthetic and Vaughan-Williams class 1b anti-arrhythmic drug
  • As a local anaesthetic:
    • Via the epidural route e.g. epidural top-up
    • Topically to the airway to facilitate awake tracheal intubation
    • Subcutaneously for wound anaesthesia/analgesia and/or superficial surgery
    • Topically to the skin to facilitate cannulation e.g. EMLA cream

  • Class 1b anti-arrhythmic
  • Analgesic e.g. lidocaine patches, post-operative lidocaine infusion
  • To blunt airway reflexes at intubation/extubation in lieu of neuromuscular blocking drugs
  • To reduce pain on injection from propofol

Presentation

  • Formulated as the hydrochloride salt in a variety of forms depending on use:
    • A colourless solution of 1% or 2% lidocaine in 2ml, 5ml or 10ml glass vials stored at room temperature
    • A 2% gel e.g. for urinary catheterisation
    • A 4% cream for topical use on mucous membranes
    • A 5% ointment or as plasters
    • A 10mg/dose spray for airway topicalisation (xylocaine)

Potential additives

  • Adrenaline (1:80,000 - 1:200,000)
  • Prilocaine (EMLA cream, see below)
  • Tetracaine (as LAT gel for paediatric wound management)
  • Phenylephrine (as co-phenylcaine for airway topicalisation)

Dosing

  • The toxic plasma concentration is described as 5μg/ml, although it may actually be higher than this (9-10μg/ml in a fantastic 1961 paper by Bromage)

  • Seeing as one is unlikely to know the patient's plasma concentration, the toxic dose is deemed to be 3mg/kg IBW
  • This is increased by the presence of adrenaline to 7mg/kg
  • For airway topicalisation the safe dose is deemed to be 4.5mg/kg (paediatrics) - 9mg/kg (adults)

  • pKa 7.9 (i.e. 25% unionised at physiological pH)
  • Relative potency vs. cocaine: 2x
  • Relative lipid solubility vs. cocaine: 150x

Absorption

  • The low pKa (compared to some of the other local anaesthetics) mean it has a relatively fast onset

Distribution

  • 70% protein bound to ɑ1-acid-glycoprotein
  • This gives lidocaine a moderate duration of action compared to its more heavily protein-bound relatives

Metabolism

  • In short, hepatic metabolism to xylidines

  • In long, hepatic metabolism via de-alkylation to eitherL
    • Acetaldehyde - which undergoes hydroxylation to the main metabolite 4-hydroxy-2,6-xylidine
    • Monoethylglycine-xylidide - this mouthful undergoes further hydrolysis

  • Some metabolites have anti-arrhythmic properties, others potentiate lidocaine-induced seizures
  • Metabolism is reduced when hepatic blood flow is reduced (owing to a high hepatic extraction ratio)

Excretion

  • The main metabolite, 4-hydroxy-2,6-xylidine, is excreted in the urine and may accumulate in renal failure
  • Elimination half-life 100mins

  • Reduces the rate of rise of phase 0 of the cardiac action potential by blocking inactivated Na+ channels and raising the threshold potential
  • This shortens the duration of the action potential (and refractory period) as the repolarisation (phase 3) is shortened
  • Can be used to treat sustained ventricular tachyarrhythmias when associated with ischaemia - 1mg/kg bolus (i.e. 100mg) ± 1-3mg/min infusion
  • Features in the Resus Council's adult cardiac arrest guideline as an alternative to amiodarone in the shockable algorithm (100mg after 3rd shock ± a further 50mg after the 5th shock

  • A eutectic mix is when two compounds mix to produce a substance that behaves with a single set of physical characteristics
  • 5% EMLA contains a mixture of the crystalline bases of 2.5% lidocaine and 2.5% prilocaine in a white, oil-in-water emulsion
  • Despite the individual components being crystalline, EMLA is an oil
  • It has a lower melting point and lower boiling point than either of its two individual components
  • Tends to cause a slight vasoconstriction

Presentation & use

  • As an emulsion in tubes containing 5g or 20g
  • Can be used pre-cannulation or before harvesting skin for grafts
  • Should be applied to intact skin at least 60mins before procedure

Cautions

  • Methaemoglobinaemia can be caused by o-toluidine, a prilocaine metabolite, and it shouldn't be used in:
    • Those with congenital or idiopathic methaemoglobinaemia
    • Infants <12months receiving treatment with drugs that can also induce methaemoglobinaemia e.g. sulphonamides and phenytoin
  • Should not be used on mucous membranes due to rapid systemic absorption
  • Should be used with caution in those receiving Class I anti-arrhythmic drugs as the toxic effects are additive/synergistic

  • Intubating, and to a slightly lesser extent extubating, patients is associated with a number of adverse physiological sequelae, such as:
    • Coughing (unless NMBA are used)
    • Elevated MAP
    • Elevated HR ± dyshrhythmia
    • Raised ICP and/or IOP
  • Blunting said responses is beneficial in patients where they can have deleterious consequences e.g. the patient with a head injury, ruptured globe or significant cardiovascular disease
  • Lidocaine can do just that, with putative mechanisms including:
    • Direct myocardial depressant effect
    • Selective depression of pain transmission in the spinal cord
    • A peripheral vasodilatory effect, which accommodates the raised MAP
    • Suppression of excitatory C-fibres within the airway, preventing transmission of noxious stimuli
  • A deep dive into the literature supporting lidocaine's use in this realm is beyond the purview of the FRCA exams
  • In short:
    • Doses of 0.5mg - 2mg/kg can be used, with a dose-response relationship
    • The effect seems to be maximal 1-3mins post-administration, after which it starts to diminish
    • It may be only as, or perhaps less, effective in this regard than esmolol, high-dose opioids, dexmedetomidine or propofol