Class I affect sodium (Na+) channels
This group slow down conduction of Na+, meaning they increase the length of the action potential, and can thus slow down fast hearts.
- Examples: quinidine, procainamide
- Conditions: ventricular arrhythmias, AF, Wolff-Parkinson-White (use procainamide)
These guys decrease conductivity, but don't affect the action potential, and are generally used for the atria.
Class II are beta blockers, such as propanolol and atenolol. In blocking the beta receptors, they slow down the heart, and make it pump less hard. They are mainly used to prevention of MIs and deal with tachyarrhythmias. See the beta blockers page for more on these.
Class III affect potassium (K+) channels
- Examples: amiodarone
- Conditions: ventricular tachycardias.
Amiodarone is most commonly used in life threatening VF and VT. It is not generally used much outside of this area as he has lots of scary side effects: it can turn your skin blue (permanently!), it causes lung toxicity, and thyroid problems, as well as others. Despite this, when nothing else has worked, it can be very effective.
This is the oddments section. There are three drugs I want to explain about here:
This is the drug you want for dealing with SVTs, since it basically turns causes temporary heart block between the AV node and the SAN. It can cure some atrial dependent SVTs and it can help to diagnose the others.
Digoxin used to have a variety of uses, but now mainly used to get AF and atrial flutter under control.
Technically not an antiarrhythmic drug, but an anticholinergic, this bad boy speeds up the heart, stimulating the AV node, and blocking the impulses from the vagal nerve that slow the heart down. You give atropine as part of advanced Life Support, when a patient goes bradycardic.