Describe the pharmacology of lidoocaine
The answers for this question were generally of a good standard. Lidocaine is a core drug in intensive care practice and thus a high level of detail was expected. This question was best structured using a standard pharmacology template (pharmaceutics, pharmacokinetics and pharmacodynamics). A small number of answers omitted any pharmaceutic elements. Another common error was the use of vague and imprecise statements. For example, many answers stated that the maximum dose (without adrenaline) is 3 mg/kg, without specifying that this is subcutaneous. The concept of the ratio of the dose required to produce cardiovascular collapse to that required to induce seizures (CC/CNS ratio) was often mentioned. However, in many cases this was conveyed simply as an abbreviated statement without any additional explanation leaving the examiner unsure as to whether the candidate understood the concept (and thus unable to award any additional marks). In addition, many candidates confused the order of this ratio (incorrectly referring to it as a CNS/CC ratio of 7). Lastly, few answers made specific mention of the narrow therapeutic index and the associated implications for use in the ICU
|Class||Class Ib antiarrhythmic and local anaesthetic|
|Routes of administration||IV, inhaled, subcutaneous|
Anaesthetic (regional infiltration) maximum dose 4mg/kg, with adrenaline 8mg/kg
Infused dose for antiarrhythmic effect = 1-2mg/kg loading dose,
|Absorption||Oral bioavailability = 35%|
|Solubility||pKa = 7.9; about 25% is not ionised at pH 7.4|
|Distribution||VOD= 0.9L/kg; 70% protein-bound|
|Target receptor||Nav1.5 subunit of the fast voltage-gated sodium channels|
|Metabolism||Hepatic metabolism (90-95%)|
|Elimination||Minimally renally excreted; half-life 10-20 minutes following IV bolus, closer to 45-90 minutes with subcutaneous infiltration|
|Time course of action||Duration of action is similar to half-life|
|Mechanism of action||Regional anaesthesia, by differential block (pain and temperature fibres are blocked earliest). With higher doses, also motor block. In toxicity, CNS effects (visual disturbances, perioral numbness, delirium, seizures, coma) and cardiovascular side effects (initially tachycardia and hypertension followed by bradycardia, negative inotropy, vasodilation and arrhythmias) Does not prolong the QRS, and actually shortens the QT.|
|Clinical effects||Antiarrhythmic effect, analgesic and local anaesthetic effects. Lowers seizure threshold, causes CNS excitation. Does not prolong the QRS, and actually shortens the QT.|
|Single best reference for further information||Weinberg et al (2015)|
HOLMDAHL, M. H: SON. "Xylocain (lidocaine, lignocaine), its discovery and Gordh's contribution to its clinical use." Acta Anaesthesiologica Scandinavica 42 (1998): 8-12.
Eipe, N., S. Gupta, and J. J. B. E. Penning. "Intravenous lidocaine for acute pain: an evidence-based clinical update." Bja Education 16.9 (2016): 292-298.
Weinberg, Laurence, et al. "Pharmacokinetics and pharmacodynamics of lignocaine: A review." World Journal of Anesthesiology 4.2 (2015): 17-29.