eMedicine Specialties > Cardiology > Arrhythmias

Paroxysmal Supraventricular Tachycardia

Author: Monika Gugneja, MD, Consulting Staff, Department of Emergency Medicine, William Beaumont Hospital
Coauthor(s): James V Talano, MD, MM, FACC, Director of Cardiovascular Medicine, SWICFT Institute
Contributor Information and Disclosures

Updated: Jul 13, 2006

Introduction

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. 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).

Frequency

International

PSVT incidence is approximately 1-3 cases per 1000 persons. The incidence rate of the WPW pattern on ECG tracings is 0.1-0.3% in the general population, although not all patients develop SVT (Klein, 1979; Montoya, 1991; Ganz, 1995; Xie, 1998; Al-Khatib, 1999). In a population-based study, the prevalence of PSVT was 2.25 cases per 1000 persons, with an incidence of 35 cases per 100,000 person-years (Orejarena, 1998). AVNRT is more common in patients who are of middle age or older, while adolescents are more likely to have SVT mediated by an accessory pathway. PSVT is not only observed in healthy individuals, it is also common in patients with previous myocardial infarction, mitral valve prolapse, rheumatic heart disease, pericarditis, pneumonia, chronic lung disease, and current alcohol intoxication (Klein, 1979; Montoya, 1991; Ganz, 1995; Xie, 1998). Digoxin toxicity also may be associated with PSVT (Ganz, 1995; Xie, 1998; Josephson, 2001).

Mortality/Morbidity

  • PSVT may start suddenly and last for seconds or days. Patients may or may not be symptomatic, depending on their hemodynamic reserve and their heart rate, the duration of the PSVT, and coexisting diseases. PSVT can result in heart failure, pulmonary edema, myocardial ischemia, and/or myocardial infarction secondary to an increased heart rate in patients with poor left ventricular function (Ganz, 1995; Xie, 1998; Josephson, 2001). In fact, one study found that one third of patients with SVT experienced syncope, required cardioversion, or had an episode of sudden death (Wood, 1997). Incessant SVT can cause tachycardia-induced cardiomyopathy.
  • Patients with WPW syndrome may be at risk for cardiac arrest if they develop AF or atrial flutter in the presence of a rapidly conducting (ie, short anterograde refractory period) accessory pathway. Extremely rapid ventricular rates during AF or atrial flutter can cause deterioration to ventricular fibrillation. This complication is unusual and occurs primarily in patients who have had prior symptoms due to WPW syndrome. In rare cases, sudden death may be the initial presentation of WPW syndrome.
  • In the absence of manifest preexcitation (ie, WPW syndrome), the risk of sudden death with PSVT is extremely small.

Race

  • No known racial differences exist regarding the incidence or presentation of PSVT.

Sex

  • Most series of catheter ablation reflect a higher proportion of female patients with AVNRT than male patients. This may reflect a true higher incidence in women, or it may reflect the sample of patients who are referred (or choose) to undergo extensive evaluation and/or catheter ablation.
  • In a population-based study, the risk of developing PSVT was twice as high in women compared to men (Orejarena, 1998).

Age

  • The prevalence of PSVT increases with age (Orejarena, 1998).
  • The relative frequency of tachycardia mediated by an accessory pathway decreases with age.

Clinical

History

  • Because symptom severity depends on the presence of structural heart disease and on the hemodynamic reserve of the patient, individuals with PSVT may present with mild symptoms or severe cardiopulmonary complaints. Some common presenting symptoms are listed below (Wood, 1997; Al-Khatib, 1999). Palpitations and dizziness are the most common symptoms reported by patients with SVT. Chest discomfort may be secondary to a rapid heart rate, and it frequently subsides with the termination of the tachycardia.
  • Common presenting symptoms of PSVT and their frequency rates are as follows:
    • Palpitation - Greater than 96%
    • Dizziness - 75%
    • Shortness of breath - 47%
    • Syncope - 20%
    • Chest pain - 35%
    • Fatigue - 23%
    • Diaphoresis - 17%
    • Nausea - 13%
  • History should include time of onset, any triggers, any previous episodes or arrhythmia, and previous treatment. A detailed past medical and cardiac history and a complete list of all medications should be obtained.
  • Patients who are hemodynamically unstable should be resuscitated immediately with cardioversion. An ECG should be performed as soon as possible.
  • Many patients with frequent episodes of PSVT tend to avoid activities such as exercising and driving due to past episodes of syncope or near-syncope.

Physical

  • Pertinent findings are generally limited to cardiovascular and respiratory systems. Patients often appear quite distressed. Tachycardia may be the only finding in patients who are otherwise healthy and have significant hemodynamic reserve.
  • Patients who have limited hemodynamic reserve may be tachypneic and hypotensive. Crackles may be auscultated secondary to heart failure. An S3 may be present, and large jugular venous pulsations may also be visualized (Ganz, 1995; Wood, 1997; Xie, 1998).

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References
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Further Reading

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Keywords

PSVT, supraventricular tachycardia, SVT, multifocal atrial tachycardia, MAT, tachyarrhythmia, atrial fibrillation, AF, conduction pathway disturbance, conduction pathway abnormality, conduction pathway anomaly, dysrhythmia, heart condition, heart rhythm problem, atrial tachyarrhythmia, atrioventricular tachyarrhythmia, AV tachyarrhythmia, sinus tachycardia, inappropriate sinus tachycardia, IST, sinusnodal reentrant tachycardia, SNRT, atrial tachycardia, atrial flutter, AV tachyarrhythmias, AV nodal reentrant tachycardia, atrioventricular nodal reentrant tachycardia, AVNRT, atrioventricular reentrant tachycardia, AV reentrant tachycardia, AVRT, junctional ectopic tachycardia, JET, nonparoxysmal junctional tachycardia, NPJT, heartfailure, pulmonary edema, myocardial ischemia, myocardial infarction, syncope, sudden death, tachycardia-induced cardiomyopathy, WPW syndrome

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Contributor Information and Disclosures

Author

Monika Gugneja, MD, Consulting Staff, Department of Emergency Medicine, William Beaumont Hospital
Monika Gugneja, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

James V Talano, MD, MM, FACC, Director of Cardiovascular Medicine, SWICFT Institute
James V Talano, MD, MM, FACC is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physician Executives, American College of Physicians, American Heart Association, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, and Society of Geriatric Cardiology
Disclosure: Nothing to disclose.

Medical Editor

Alan D Forker, MD, Professor of Medicine, Program Director of Cardiovascular Fellowship, Department of Medicine, Mid America Heart Institute, University of Missouri at Kansas City School of Medicine; Codirector, Lipid Diabetes Research Center, Saint Luke's Hospital
Alan D Forker, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Society of Hypertension, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Director of Cardiac Electrophysiology, Department of Internal Medicine, University of Iowa Hospitals
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, New York Academy of Sciences, and North American Society for Pacing and Electrophysiology
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Society of Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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