Supraventricular Arrhythmias: An Electrophysiology Primer

Carol Chen-Scarabelli, MSN, APRN, BC, CCRN


Prog Cardiovasc Nurs. 2005;20(1):24-31. 

In This Article


In the normal heart, impulse formation occurs in the sinoatrial node and conducts sequentially to the atrioventricular (AV) node, the Bundle of His, the bundle branches, and finally to the Purkinje fibers located in the ventricles. The mechanism of cardiac arrhythmias involves either disturbances in impulse formation (often referred to as automatic), or abnormalities in impulse conduction (often referred to as reentrant).[13,14] Enhanced or abnormal automaticity, reentry, and reflection (reflected reentry) are the mechanisms for SVT and ventricular tachycardia.[13] Automaticity is the inherent property of the myocardial cells to spontaneously depolarize (i.e., impulse formation), whereas reentry refers to abnormalities in impulse conduction.

SVTs, most commonly due to the reentry mechanism, occur above the ventricle and are defined as any tachyarrhythmia that requires only the atrial tissue and/or AV node for the initiation and maintenance of the arrhythmia.[14,15] In SVT, abnormalities in automaticity may originate from tissue in the atria, the AV junction, or vessels communicating directly with the atria, such as the vena cava or pulmonary veins,[14] and may result from either enhanced pacemaker activity or from a protected ectopic focus.[13] On the other hand, abnormal impulse conduction (i.e., reentrant arrhythmias) may result from circus movement reentry or from reflection of the impulse back into excitable tissue.[13]

Arrhythmias due to enhanced or abnormal automaticity include sinus tachycardia, atrial tachycardia (AT), and junctional or nodal tachycardia, while arrhythmias due to triggered activity include PSVT.[13] Reentry arrhythmias include AT, AFL, PSVT, atrioventricular reentrant tachycardia (AVRT), and atrioventricular nodal reentrant tachycardia (AVNRT) ( Table I ).[13,14]

According to the site of origin of the impulse, the two classifications of SVT are atrial tachyarrhythmia and AV tachyarrhythmia. Atrial arrhythmias include sinus tachycardia, inappropriate sinus tachycardia, AT, sinus node reentrant tachycardia, AFL, AF, and multifocal AT. AV tachyarrhythmias consist of AVNRT, AVRT, nonparoxysmal junctional tachycardia, and junctional ectopic tachycardia.[15]

Supraventricular arrhythmias may occur in the pre- and post-MI setting. Causes of SVT include: irritation of atrial myocardium as a result of pericarditis; elevated atrial pressures resulting in stretch and distention of the atria; vagal activation and increased parasympathetic tone, such as in the setting of inferior wall MI; increased sympathetic tone and elevated levels of circulating catecholamines; and atrial ischemia.[9]