Compare and contrast the pharmacology of lignocaine, magnesium and amiodarone when used in the treatment of ventricular tachycardia.
• Lignocaine: Class I (membrane stabilising) antiarrhythmic agent. Sodium channel blockades results in decreased action potential duration and shortened refractory period. Rapidly distributed to all body tissues. Approximately 65% protein bound; elimination half-life 1.6 hours (80% metabolised in liver). Adverse effects: lightheaded, hypotension, cardiovascular collapse, heart block, confusion and convulsions. Dosage 1 to 1.5mg/kg with subsequent boluses (up to 3 mg/kg total), followed by infusion (1-4 mg/min, at decreasing dose, up to
• Magnesium (as sulphate or chloride): second most abundant intracellular cation. Depresses neuronal activation. Widely distributed, duration of action about 30 minutes. Filtered by kidneys, but most is reabsorbed. Adverse effects include: nausea, flushing, CNS depression, coma, and heart block. Dose 5 mmol bolus (which may be repeated), followed by infusion
of 20 mmol over 4 hours.
• Amiodarone: Class III antiarrhythmic. Prolongs action potential duration, and prolongs refractory period of atrial, nodal and ventricular tissues. Highly protein bound with very high apparent volume of distribution (6 L/kg); accumulates in adipose tissue and highly perfused organs. Half-life (with chronic dosing) is 14 to 59 days, mainly excreted via the liver and bile. Adverse effects: hypotension/circulatory collapse, bradycardia, sinus arrest, nausea and flushing. Torsades de pointes can be induced. Hyper- or hypo-thyroidism can be
induced. Multiple other potential organ dysfunctions with more chronic use (including some potentially fatal). Dosage 5 mg/kg which can be repeated, and followed by an infusion (15 mg/kg/hr).
This question is identical to Question 12 from the first paper of 2006.