Final answer:
Class IA sodium channel blockers slow the upstroke of the action potential in cardiac cells, affecting the rapid depolarization phase by decreasing the inflow of Na+. Potassium channel blockers like amiodarone and procainamide prolong the action potential by interfering with the repolarization phase, which can be therapeutic in cardiac dysrhythmias.
Step-by-step explanation:
Class IA sodium channel blockers affect the action potential of cardiac cells by altering the flow of sodium ions during the cardiac cycle. These medications slow the upstroke velocity of the action potential, which leads to a decrease in the conduction velocity within the heart tissue. This effect is particularly visible during Phase 0, the rapid depolarization phase, where the entry of Na+ is crucial. By inhibiting the sodium channels, these blockers can delay the return of the channels to their active state, prolong the refractory period, and potentially prevent abnormal rapid heart rhythms, known as cardiac dysrhythmias.
Potassium channel blockers, such as amiodarone and procainamide, interrupt the movement of K+ through voltage-gated K+ channels, specifically affecting the repolarization phase. This is where the outflow of K+ ions restores the membrane potential back to its resting state. As a result, these blockers prolong the duration of the action potential and the refractory period, which can assist in the treatment of cardiac dysrhythmias.