Paroxysmal Supraventricular Tachycardia

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. Certain drugs, such as stimulants (eg, nicotine, caffeine), medications (eg, atropine, salbutamol), recreational drugs (eg, cocaine, amphetamines, ecstasy), and hydralazine, can also induce sinus tachycardia.
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 and heart rates. 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 sometimes 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 other disorders of the mitral valve, and digitalis toxicity (Akhtar, 1984; Tintinalli, 2000; Josephson, 2001). When AF occurs in young or middle-aged patients in the absence of structural heart disease or any apparent cause, it is called lone or idiopathic AF.
AV tachyarrhythmias
AV nodal reentrant tachycardia
The most common cause of PSVT is AVNRT. AVNRT is diagnosed in 50-60% of patients who present with regular narrow QRS tachyarrhythmia (Josephson, 1977; Akhtar, 1984; Jazayeri, 1992; Akhtar, 1993). The heart rate is 120-250 bpm and is typically quite regular (see Images 6-7). AVNRT may occur in healthy, young individuals, and it occurs most commonly in women (Jazayeri, 1992). Most patients do not have structural heart disease. However, occasionally these individuals may have an underlying heart condition such as rheumatic heart disease, pericarditis, myocardial infarction, mitral valve prolapse, or preexcitation syndrome (Josephson, 1977; Akhtar, 1984; Jazayeri, 1992; Akhtar, 1993).
An understanding of the electrophysiology of AV nodal tissue is very important in order to comprehend the mechanism of AVNRT. In most people, the AV node has a single conducting pathway that conducts impulses in an anterograde manner to depolarize the bundle of His. In certain cases, AV nodal tissue may have 2 conducting pathways with different electrophysiological properties (see Image 8). One pathway (alpha) is a relatively slow conducting pathway with a short refractory period, while the second pathway (beta) is a rapid conducting pathway with a long refractory period. The coexistence of these functionally different pathways serves as the substrate for reentrant tachycardia (Josephson, 1977; Akhtar, 1984; Akhtar, 1993; Ganz, 1995). Electrophysiologic studies have demonstrated dual AV nodal pathways in 40% of patients.
Onset of AVNRT is triggered by a premature atrial impulse. A premature atrial impulse may reach the AV node when the fast pathway (beta) is still refractory from the previous impulse but the slow pathway (alpha) may be able to conduct. The premature impulse then conducts through the slow pathway (alpha) in an anterograde manner; the (beta) pathway continues to recover because of its longer refractory period. After the impulse conducts in an anterograde manner through the slow (alpha) pathway, it may find the fast (beta) pathway recovered; the impulse then conducts in a retrograde manner via the fast (beta) pathway. If the slow pathway (alpha) has repolarized by the time the impulse completes the retrograde conduction, the impulse can then reenter the slow (alpha) pathway and initiate AVNRT (see Image 8).
Importantly, note that AVNRT does not involve the ventricles as part of the reentry circuit; the necessity of perinodal atrial tissue to the circuit is controversial. Because the impulse typically conducts in an anterograde manner through the slow pathway and in a retrograde manner through the fast pathway, the PR interval is longer than the RP interval. Thus, in patients with typical AVNRT, the P wave is usually located at the terminal portion of the QRS complex (Josephson, 1977; Akhtar, 1984; Akhtar, 1993; Ganz, 1995; Josephson, 2001). In patients with atypical AVNRT, anterograde conduction is via the fast pathway, while retrograde conduction is via the slow pathway. For these atypical patients, the RP interval is longer than the PR interval (Josephson, 1977; Wu, 1977; Akhtar, 1984; Jazayeri, 1992; Akhtar, 1993; Ganz, 1995; Josephson, 1997; Josephson, 2001).
AV reentrant tachycardia
AVRT is the second most common form of PSVT. The incidence rate of AVRT in the general population is 0.1-0.3%. AVRT is more common in males than in females (male-to-female ratio of 2:1), and patients with AVRT commonly present at a younger age than patients with AVNRT. AVRT is associated with the Ebstein anomaly, although most patients with AVRT do not have evidence of structural heart disease. AVRT occurs in the presence of accessory pathways, or bypass tracts. Accessory pathways are errant strands of myocardium that bridge the mitral or tricuspid valves (Josephson, 1977; Murdock, 1991; Ganz, 1995; Xie, 1998).
AVRT is the result of 2 or more conducting pathways: the AV node and 1 or more bypass tracts. In a normal heart, only a single route of conduction is present. Conduction begins at the sinus node, progresses to the AV node, and then to the bundle of His and the bundle branches. However, in AVRT, 1 or more accessory pathways connect the atria and the ventricles. The accessory pathways may conduct impulses in an anterograde manner, a retrograde manner, or both (Wolff, 1930; Coumel, 1967; Josephson, 1977; Gallagher, 1978; Murdock, 1991; Oren, 1993; Ganz, 1995; Xie, 1998). When impulses travel down the accessory pathway in an anterograde manner, ventricular preexcitation results. This produces a short PR interval and a delta wave as is observed in persons with Wolff-Parkinson-White (WPW) syndrome (see Image 9) (Wolff, 1930).
Importantly, note that not all accessory pathways conduct in an anterograde manner. Concealed accessory pathways are not evident during sinus rhythm, and they are only capable of retrograde conduction. A reentry circuit is most commonly established by impulses traveling in an anterograde manner through the AV node and in a retrograde manner through the accessory pathway; this is called orthodromic AVRT. A reentry circuit may also be established by a premature impulse traveling in an anterograde manner through a manifest accessory pathway and in a retrograde manner through the AV node; this is called antidromic AVRT (see Image 10) (Bardy, 1984; Obel, 1997). While the orthodromic AVRT is typically a narrow-complex tachycardia (see Image 11), antidromic AVRT inscribes a bizarre, wide-complex tachycardia (see Image 12) (Bardy, 1984; Atie, 1990; Obel, 1997).
Patients with WPW syndrome can develop AF and atrial flutter (see Image 13). The rapid nondecremental conduction via the accessory pathways can result in extremely rapid rates, which can degenerate to ventricular fibrillation and cause sudden death. Patients with preexcitation syndromes with AF must not be administered an AV nodal blocking agent; these agents can further increase conduction via the accessory pathway, which increases the risk of ventricular fibrillation and death (Campbell, 1977; Sung, 1977; Klein, 1979; Bardy, 1984; Vidaillet, 1987; Montoya, 1991; Obel, 1998).
Junctional ectopic tachycardia and nonparoxysmal junctional tachycardia
JET and NPJT are rare and presumably arise because of increased automaticity, triggered activity, or both. They are usually observed following valvular surgery, after myocardial infarction, during active rheumatic carditis, or with digoxin toxicity. These tachycardias are also observed in children following congenital heart surgery. ECG findings include a regular narrow QRS complex, although P waves may not be visible. Patients with AV dissociation have also been described (Ganz, 1995; Pieper, 1995; Trohman, 2000).