To understand how anti-arrythmic drugs work, we must review automaticity and refractories. If any of this sounds foreign to you, read this quick refresher on cardiac physiology.
Automaticity
All cardiac cells can initiate electrical activity but they won’t fire if the SA node fires first. If the impulse doesn’t come from the SA node, that is arrythmia. This is a great safety mechanism in case the SA node doesn’t work.  The ability for cardiac cells to fire on their own is meant to be a backup if they sense nothing is happening but these “latent pacemakers” will fire slower than the SA node and won’t fire normally.
On the heart, there may be ectopic foci which are specific points that are firing abnormally. Ectopic means abnormal and foci means point. They may exist due to ischemia, acidosis, and suppressant drugs.
Refractories
The action potential cannot occur during the refractory period due to the “all or nothing” phenomenon. The anti-arrhythmical drugs will lengthen this refractory period.
All antiarrhythmics have two therapeutic actions:
- Decrease automaticity
- Increase the refractory period
They also have other pharmacological effects that may not be therapeutic.
There’s different classes of drugs. Class 1A drugs tend to treat atrial arrhythmia. Class 1B and 1C tend to treat ventricular arrhythmia.
We’ll look more info these when we review anti-arrhythmial agents next.
