antiarrhythmic
An antiarrhythmic restores order to a heartbeat that has lost its rhythm. The heart relies on precisely timed electrical signals to fire its chambers in sequence; when those signals race, stall or short-circuit, the pump loses efficiency. An antiarrhythmic re-tunes the electrical system so the beat returns to a steady, coordinated pace.
These drugs are organized by the Vaughan Williams classification according to which electrical process they affect. Class I blocks sodium channels (for example lidocaine, flecainide); Class II are beta-blockers that slow the pacemaker and node; Class III blocks potassium channels to lengthen recovery (amiodarone, sotalol); Class IV are the rate-slowing calcium channel blockers verapamil and diltiazem. Digoxin and adenosine act outside this scheme. The choice depends on the type of arrhythmia and the patient's heart structure.
Antiarrhythmics carry a paradoxical danger: by altering cardiac electrical timing they can themselves cause new, sometimes lethal, arrhythmias, a property called proarrhythmia. Several, notably those that prolong the QT interval, can trigger dangerous rhythms, and amiodarone in particular causes long-term toxicity to the thyroid, lungs, liver and eyes. They are therefore prescribed and monitored carefully, often by specialists.
A patient with atrial fibrillation and a fast ventricular rate is given amiodarone, a Class III antiarrhythmic, to help restore and maintain a normal rhythm.
Amiodarone is broadly effective but its long-term organ toxicity demands periodic monitoring.
Because antiarrhythmics can provoke arrhythmias, a landmark trial found that suppressing minor irregular beats after a heart attack actually increased deaths, a sobering lesson in not treating the monitor instead of the patient.