The normal cardiac rhythm arises from and is conducted by the tissues of the cardiac conduction system. These specialized structures include the sinus node, the AV node, and the His-Purkinje system. The sinus node or the sinoatrial node is located at the junction of the superior vena cava and the high right atrium. The sinus node is surrounded by a rim of tissue that connects the specialized sinus nodal cells to the rest of the atrial myocardium. The AV nodal complex includes the compact AV node located in the atrial septum adjacent to the tricuspid annulus and transitional fibers in the anterior and posterior aspect of the AV node, which funnel the atrial signals into the node itself. These transitional fibers likely represent the “fast” (anterior) and “slow” (posterior) AV nodal pathways discussed later in the section on PSVT. The AV node is connected to the bundle of His, which dives into the central fibrous body of the heart and divides into the right bundle branch (which runs under the moderator band of the right ventricle) and the left bundle branch, which functionally splits into anterior and posterior hemifascicles. These bundles of Purkinje fibers provide for a rapid conduction of the electrical signal and allow for an organized, synchronized contraction of the ventricular myocardium.
The sinus nodal complex and the AV node are “calcium-dependent,” meaning that depolarization of those cells occurs due to slow movement of calcium ions into the cells during phase 0 of the action potential. All other electrically active cardiac tissues, including the atrial and ventricular myocardium, the His-Purkinje system, and accessory AV pathways found in the Wolff-Parkinson-White (WPW) Syndrome are “sodium-dependent” since they depolarize because of rapid movement of sodium ions into the cells. This difference helps to explain why calcium channel blockers such as verapamil and diltiazem have their predominant effect on the sinus node and the AV node, while Class I antiarrhythmic drugs, which block the sodium channels, exert their predominant effects on the sodium-dependent tissues of the heart.