As is well known, the heart contains specialized conduction system consisting of excitatory myocytes that regulate the rate and rhythm of cardiac contraction and are essential for normal cardiac function. This system is influenced by direct neural inputs (e.g., vagal stimulation), adrenergic agents (e.g., epinephrine [adrenaline]), hypoxia, and potassium concentrations (i.e., hyperkalemia can block signal transmission altogether).
The components of the conduction system include (1) the sinoatrial (SA) node pacemaker (located at the junction of the right atrial appendage and superior vena cava), (2) the atrioventricular ( AV) node (located in the right atrium along the atrial septum), (3) the bundle of His , connecting the right atrium to the ventricular septum, and the subsequent divisions into (4) the right and left bundle branches that stimulate their respective ventricles.
Abnormalities in myocardial conduction can be sustained or sporadic ( paroxysmal ). Aberrant rhythms can be initiated anywhere in the conduction system, from the SA node down to the level of an individual myocyte ; they are typically designated as originating from the atrium ( supraventricular ) or within the ventricular myocardium.
Arrhythmias can manifest as tachycardia (fast heart rate), bradycardia (slow heart rate), an irregular rhythm with normal ventricular contraction, chaotic depolarization without functional ventricular contraction ( ventricular fibrillation ), or no electrical activity at all ( asystole ). Patients may be unaware of a rhythm disorder or may note a “racing heart” or palpitations ; loss of adequate cardiac output due to sustained arrhythmia can produce lightheadedness (near syncope), loss of consciousness ( syncope ), or sudden cardiac death .
Ischemic injury is the most common cause of rhythm disorders, because of direct damage or due to the dilation of heart chambers with consequent alteration in conduction system firing.