Compare and  contrast the pharmacology  of lignocaine,  magnesium  and  amiodarone when used in the treatment of ventricular tachycardia.

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College Answer


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 used in the treatment of ventricular tachycardia: 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 24 hours).

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 used in the treatment of ventricular tachycardia: 5 mmol bolus (which may be repeated), followed by infusion of 20 mmol over 4 hours.


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 used in the treatment of ventricular tachycardia: 5 mg/kg (or 300 mg in adults) which can be repeated, and followed by an infusion (15 mg/kg/hr).


Again, the college answer outlines all the important stuff.

The table below reconfigures this into a more eye-pleasing form.






Class 1a antiarrhytmic

Divalent cation

Class 3 antiarrhytmic (though it has effects of all 4 classes)

Administration / dosage

initial bolus 1-1.5mg/kg.

Then, 4 mg/kg for the first hour, then tapering infusion to 1mg/kg for 24 hrs


10-20mmol/L given over 15-60 minutes,

or 5 mmol boluses followed by 20mmol infusion


150-300mg, followed by an infusion of 900mg over 24 hrs


Rapid hepatic metabolism into inactive metabolites.
Half life 1-2hrs

Rapid distribution; some proportion becomes intracellular; the rest is renally excreted.

Rapid distribution, with a vas volume of dsitribution; becomes bound to tissue proteins.
Half-life 15-60 days


Inhibits voltage-gated sodium channels, decreasing the duration of action potentials and decreasing the  duration of repolarisation

Mechanism uncertain; appears to act as an antagonist to the entry of calcium into depolarising cells.
Depresses the activity of excitable tissues.

Voltage-gated soidum channel blockade
Potassium channel blockade
Calcium channel blockade
Prolongs the duration of both action potential and refractory period.

Adverse effects

Neurological disturbances eg. paraesthesia, seizures

Muscle weakness, decreased reflexes, hypotension

Prolongation of QT interval, risk of Torsades.
Array of chronic toxicities included pulmonary fibrosis and hypothyroidism or hyperthyroidism