What is the primary mechanism of action of calcium channel blockers in the treatment of arrhythmias?

Calcium channel blockers primarily function by slowing down AV nodal conduction, which plays a crucial role in managing certain types of arrhythmias. These medications inhibit the influx of calcium ions through voltage-gated calcium channels in the cardiac tissue, particularly within the atrioventricular (AV) node. This action results in a decreased conduction velocity and an increased refractory period, which can help control heart rate and prevent or mitigate abnormal electrical impulses in the heart.

By reducing the conduction through the AV node, calcium channel blockers can effectively decrease the rate of ventricular response in conditions such as atrial fibrillation or atrial flutter. This makes them valuable for rate control in patients with rapid atrial arrhythmias. The ability to modulate the conduction system is pivotal in avoiding the risks associated with tachyarrhythmias.

Other mechanisms listed are not the primary actions of calcium channel blockers in this context. For instance, increasing heart rate is not a desired effect of these medications, nor do they block sodium channels; such actions would be characteristic of different classes of antiarrhythmic medications. Additionally, while calcium channel blockers can have a minor effect on contractility, enhancing contractility is not their primary mechanism and can vary based on the specific drug and individual patient