Patient was educated on sodium channel blockers and their mechanism of action as follows:
- Sodium channel blockers are medications that block the movement of sodium ions into the cells in the cardiac and nervous tissues.
- Blocking the entry of sodium ions into the cells of cardiac and nervous tissues results in reduced excitation of these tissues.
- Slowing down the excitation of the cardiac and nervous tissues results in reduced conduction of the impulse in both these tissues. Slowing down the conduction of an impulse along the cardiac muscle will also reduce the number of impulses per minute, thus reducing the heart rate.
- Slowing of excitation in the cardiac muscle tissues by sodium channel blockers will help in controlling abnormal heart rate and rhythm in conditions, such as, atrial flutter, atrial fibrillation, ventricular tachycardia, ventricular flutter, and ventricular fibrillation.
- Slowing of excitation in the nervous tissues by sodium channel blockers will help controlling abnormal firing of nervous tissues and thus, finds utility with preventing convulsions and controlling pain. So, medications belonging to this group can also be used as anticonvulsants and anesthetics.
- These agents also increase the refractory period of the cardiac muscle cell. Tissues in refractory period cannot initiate a new impulse. For tissues to initiate a new impulse, the refractory period should end. Class I antiarrhythmic medications increase the refractory period of cardiac muscle and thereby, help to prevent arrhythmia.
- Examples of sodium channel blockers include Quinidine, Procainamide, Disopyramide, Lidocaine, Flecainide, and Mexiletine.
