Background: Supraventricular tachycardia (SVT), a common clinical condition, is any tachyarrhythmia that requires only atrial and/or atrioventricular (AV) nodal tissue for its initiation and maintenance. It is usually a narrow-complex tachycardia that has a regular, rapid rhythm; exceptions include atrial fibrillation (AF) and multifocal atrial tachycardia (MAT). Aberrant conduction during SVT results in a wide-complex tachycardia. SVT occurs in persons of all age groups, and treatment can be challenging.
Paroxysmal supraventricular tachycardia (PSVT) is episodic, with an abrupt onset and termination. Manifestations of SVT are quite variable; patients may be asymptomatic or they may present with minor palpitations or more severe symptoms. Results from electrophysiology studies have helped determine that the pathophysiology of SVT involves abnormalities in impulse formation and conduction pathways. The most common mechanism identified is reentry (Denes, 1973; Rosen, 1974; Akhtar, 1984; Waldo, 1993). This article focuses on SVT, including the pathophysiology, clinical presentation, diagnosis, management, and treatment options of this condition.
Pathophysiology: The development of intracardiac electrophysiology studies has dramatically changed the classification of SVT. Intracardiac recordings have identified the various mechanisms of SVT. Depending on the site of origin of the dysrhythmia, SVTs may be classified as an atrial or AV tachyarrhythmia (Klein, 1987; Basta, 1997).
Atrial tachyarrhythmias include (1) sinus tachycardia, (2) inappropriate sinus tachycardia (IST), (3) sinus nodal reentrant tachycardia (SNRT), (4) atrial tachycardia, (5) MAT, (6) atrial flutter, and (7) AF.
AV tachyarrhythmias include (1) AV nodal reentrant tachycardia (AVNRT), (2) AV reentrant tachycardia (AVRT), (3), junctional ectopic tachycardia (JET), and (4) nonparoxysmal junctional tachycardia (NPJT).
Atrial tachyarrhythmias
Sinus tachycardia
Sinus tachycardia is an accelerated sinus rate that is a physiologic response to a stressor. It is characterized by a heart rate faster than 100 beats per minute (bpm) and generally involves a regular rhythm (see Image 1). Underlying physiological stresses such as hypoxia, hypovolemia, fever, anxiety, pain, hyperthyroidism, and exercise usually induce sinus tachycardia (Tintinalli, 2000; Ganz, 2002). Treatment involves addressing the basic underlying stressor.
Inappropriate sinus tachycardia
IST is an accelerated baseline sinus rate in the absence of a physiological stressor. In this situation, healthy adults may have an elevated resting heart rate and an exaggerated heart rate response to even minimal exercise. This tachyarrhythmia is observed most commonly in young women without structural heart disease (Bellet, 1963; Krahn, 1995; Xie, 1998). The underlying mechanism of IST may be hypersensitivity of the sinus node to autonomic input or an abnormality within the sinus node, its autonomic input, or both (Bellet, 1963; Krahn, 1995; Xie, 1998).
Sinus nodal reentrant tachycardia
SNRT is frequently confused with IST. SNRT is due to a reentry circuit, either in or near the sinus node. Therefore, it has an abrupt onset and offset. The heart rate is usually 100-150 bpm, and ECG tracings usually demonstrate normal sinus P-wave morphology (Bellet, 1963; Krahn, 1995; Xie, 1998).
Atrial tachycardia
Atrial tachycardia is an arrhythmia originating in the atrial myocardium. Enhanced automaticity, triggered activity, or reentry may result in this rare tachycardia (Wellens, 1978; Farre, 1981; Brugada, 1984; Lesh, 1994; Xie, 1998). The heart rate is regular and is usually 120-250 bpm. The P-wave morphology is different from the sinus P waves and is dependent on the site of origin of the tachycardia (see Image 2). Because the arrhythmia does not involve the AV node, nodal blocking agents such as adenosine and verapamil are usually unsuccessful in terminating this arrhythmia. Atrial tachycardia has also been associated with digoxin toxicity via the triggered mechanism (Wellens, 1978; Farre, 1981; Brugada, 1984; Lesh, 1994; Xie, 1998).
Multifocal atrial tachycardia
MAT is a tachyarrhythmia that arises within the atrial tissue; it is composed of 3 or more P-wave morphologies. This arrhythmia is fairly uncommon and is typically observed in elderly patients with pulmonary disease. The heart rate is greater than 100 bpm, and ECG findings typically include an irregular rhythm, which may be misinterpreted as AF (see Image 3). Treatment involves correcting the underlying disease process (Phillips, 1969; Habibzadeh, 1980; Scher, 1989). Magnesium and verapamil may be effective.
Atrial flutter
Atrial flutter is a tachyarrhythmia arising above the AV node with an atrial rate of 250-350 bpm. The mechanism behind atrial flutter is generally reentrant in nature. Typically, counterclockwise atrial flutter is due to a macroreentrant right atrial circuit. It is commonly observed in patients with ischemic heart disease, myocardial infarction, cardiomyopathy, myocarditis, pulmonary embolus, toxic ingestion (eg, alcohol), or chest trauma. It may be a transitional rhythm and can progress to AF. ECG findings of typical atrial flutter include negative sawtooth flutter waves in leads II, III, and aVF. AV conduction is most commonly 2:1, which yields a ventricular rate of approximately 150 bpm (see Image 4) (Akhtar, 1984; Tintinalli, 2000; Josephson, 2001).
Atrial fibrillation
AF is an extremely common arrhythmia arising from chaotic atrial depolarization. The atrial rate is usually 300-600 bpm, while the ventricular rate may be 170 bpm or more. ECG findings characteristically include an irregular rhythm with fibrillatory atrial activity (see Image 5). This arrhythmia is associated with rheumatic heart disease, hypertension, ischemic heart disease, pericarditis, thyrotoxicosis, alcohol intoxication, mitral valve prolapse, and digitalis toxicity (Akhtar, 1984; Tintinalli, 2000; Josephson, 2001). When AF occurs in young patients in the absence of structural heart disease or any apparent cause, it is called lone or idiopathic AF.
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