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 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.
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 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.
|
Features |
Lignocaine |
Magnesium |
Amiodarone |
|
Class |
Class 1b antiarrhytmic |
Divalent cation |
Class 3 antiarrhytmic (though it has effects of all 4 classes) |
|
Administration / dosage |
IV Then, 4 mg/kg for the first hour, then tapering infusion to 1mg/kg for 24 hrs |
IV 10-20mmol/L given over 15-60 minutes, or 5 mmol boluses followed by 20mmol infusion |
IV 150-300mg, followed by an infusion of 900mg over 24 hrs |
|
Pharmacokinetics |
Rapid hepatic metabolism into inactive metabolites. |
Rapid distribution; some proportion becomes intracellular; the rest is renally excreted. |
Rapid distribution, with a vas volume of dsitribution; becomes bound to tissue proteins. |
|
Mechanism |
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. |
Beta-blockade |
|
Adverse effects |
Neurological disturbances eg. paraesthesia, seizures |
Muscle weakness, decreased reflexes, hypotension |
Prolongation of QT interval, risk of Torsades. |