eMedicine Specialties > Cardiology > Arrhythmias

Paroxysmal Supraventricular Tachycardia

Monika Gugneja, MD, Consulting Staff, Department of Emergency Medicine, William Beaumont Hospital
Phillip L Kraft, MD, Director, Interventional Cardiology and Cardiac Catheterization Laboratory, William Beaumont Hospital

Updated: Aug 12, 2009

Introduction

Background

Supraventricular tachycardia (SVT), a common clinical condition, is any tachyarrhythmia that requires 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.^15,41,3,50 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.^27,7

Atrial tachyarrhythmias include (1) sinus tachycardia, (2) inappropriate sinus tachycardia (IST), (3) sinus nodal reentrant tachycardia (SNRT), (4) atrial tachycardia, (5) multifocal atrial tachycardia, (6) atrial flutter, and (7) atrial fibrillation.

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 Media file 1). Underlying physiological stresses such as hypoxia, hypovolemia, fever, anxiety, pain, hyperthyroidism, and exercise usually induce sinus tachycardia.^47,19 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.

Sinus tachycardia. Note that the QRS complexes are narrow and regular. The patient's heart rate is approximately 135 bpm. P waves are normal in morphology.

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.^8,29,55 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.^8,29,55

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.^8,29,55

Atrial tachycardia

Atrial tachycardia is an arrhythmia originating in the atrial myocardium. Enhanced automaticity, triggered activity, or reentry may result in this rare tachycardia.^{51,17,10,30,55} 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 Media file 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.^{51,17,10,30,55}

Atrial tachycardia. The patient's heart rate is 151 bpm. P waves are upright in lead V₁.

Multifocal atrial tachycardia 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 atrial fibrillation (see Media file 3). Treatment involves correcting the underlying disease process.^38,22,43 Magnesium and verapamil may sometimes be effective.

Multifocal atrial tachycardia. Note the different P-wave morphologies and irregularly irregular ventricular response.

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 atrial fibrillation. 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 Media file 4).^2,47,24

Atrial flutter. The patient's heart rate is approximately 135 bpm with 2:1 conduction. Note the sawtooth pattern formed by the flutter waves.

Atrial fibrillation 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 Media file 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.^2,47,24 When atrial fibrillation occurs in young or middle-aged patients in the absence of structural heart disease or any apparent cause, it is called lone or idiopathic atrial fibrillation.

Atrial fibrillation. The patient's ventricular rate varies from 130-168 bpm. Rhythm is irregularly irregular. P waves are not discernible.

AV Tachyarrhythmias

AV nodal reentrant tachycardia

The most common cause of paroxysmal supraventricular tachycardia is AVNRT. AVNRT is diagnosed in 50-60% of patients who present with regular narrow QRS tachyarrhythmia.^25,2,23,3 The heart rate is 120-250 bpm and is typically quite regular (see Media files 6-7). AVNRT may occur in healthy, young individuals, and it occurs most commonly in women.²³ 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.^25,3,23,3

Atrioventricular nodal reentrant tachycardia. The patient's heart rate is approximately 146 bpm with a normal axis. Note the pseudo S waves in leads II, III, and aVF. Also note the pseudo R' waves in V₁ and aVR. These deflections represent retrograde atrial activation.

Same patient as in Media file 6. Patient is in sinus rhythm following atrioventricular nodal reentrant tachycardia.

Image A displays the slow pathway and the fast pathway, with a regular impulse being conducted through the atrioventricular node. Image B displays a premature impulse that is conducted in an anterograde manner through the slow pathway and in a retrograde manner through the fast pathway, as is seen in typical atrioventricular nodal tachycardia. Image C displays the premature impulse conducting in a retrograde manner through the pathway and the impulse reentering the pathway with anterograde conduction, which is seen commonly in patients with atypical atrioventricular nodal tachycardia.

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.^25,3,2,20,24 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.^{25,54,2,23,3,20,26,24}

AV reentrant tachycardia

AVRT is the second most common form of paroxysmal supraventricular tachycardia. 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.^25,33,20,55

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.^{52,14,25,18,33,37,20,55} 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 Media file 9).⁵²

Wolff-Parkinson-White pattern. Note the short PR interval and slurred upstroke (delta wave) to the QRS complexes.

The left image displays the atrioventricular node with the accessory pathway. The impulse is conducted in an anterograde manner in the atrioventricular node and in a retrograde manner in the accessory pathway. This circuit is known as orthodromic atrioventricular reentrant tachycardia and can occur in patients with concealed accessory tracts or Wolff-Parkinson-White syndrome. The right image displays the impulse being conducted in an anterograde manner through the accessory pathway and in a retrograde manner via the atrioventricular node. This type of circuit is known as antidromic atrioventricular reentrant tachycardia and only occurs in patients with Wolff-Parkinson-White syndrome. Both patterns may display retrograde P waves after the QRS complexes.

Orthodromic atrioventricular reentrant tachycardia. This patient has Wolff-Parkinson-White syndrome.

The left panel depicts antidromic atrioventricular reentrant tachycardia. The right panel depicts sinus rhythm in a patient with antidromic atrioventricular reentrant tachycardia. Note that the QRS complex is an exaggeration of the delta wave during sinus rhythm.

Atrial fibrillation in a patient with Wolff-Parkinson-White syndrome. Note the extremely rapid ventricular rate and variability in QRS morphology. Several minutes later, the patient developed ventricular fibrillation.

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.^20,39,48

Frequency

International

Paroxysmal supraventricular tachycardia 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.^{28,32,20,55,4} In a population-based study, the prevalence of paroxysmal supraventricular tachycardia was 2.25 cases per 1000 persons, with an incidence of 35 cases per 100,000 person-years.³⁶ 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. Paroxysmal supraventricular tachycardia 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.^28,32,20,55 Digoxin toxicity also may be associated with paroxysmal supraventricular tachycardia.^20,55,24

Mortality/Morbidity

• Paroxysmal supraventricular tachycardia 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 paroxysmal supraventricular tachycardia, and coexisting diseases. Paroxysmal supraventricular tachycardia 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.^20,55,24 In fact, one study found that one third of patients with SVT experienced syncope, required cardioversion, or had an episode of sudden death.⁵³ Incessant SVT can cause tachycardia-induced cardiomyopathy.
• Patients with WPW syndrome may be at risk for cardiac arrest if they develop atrial fibrillation or atrial flutter in the presence of a rapidly conducting (ie, short anterograde refractory period) accessory pathway. Extremely rapid ventricular rates during atrial fibrillation 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 paroxysmal supraventricular tachycardia is extremely small.

Race

No known racial differences exist regarding the incidence or presentation of paroxysmal supraventricular tachycardia.

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 paroxysmal supraventricular tachycardia was twice as high in women compared to men.³⁶

Age

• The prevalence of paroxysmal supraventricular tachycardia increases with age.³⁶
• 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 paroxysmal supraventricular tachycardia may present with mild symptoms or severe cardiopulmonary complaints. Some common presenting symptoms are listed below.^53,4 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. Persistent SVT may lead to tachycardia-induced cardiomyopathy.
• Common presenting symptoms of paroxysmal supraventricular tachycardia 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 paroxysmal supraventricular tachycardia 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.^20,53,55

Causes

Supraventricular tachycardia or paroxysmal supraventricular tachycardia are triggered by reentry mechanism. This may be induced by premature atrial or ventricular ectopic beats. Other triggers include hyperthyroidism and stimulants, including caffeine, drugs, and alcohol.

Differential Diagnoses

Workup

Laboratory Studies

• A cardiac enzyme evaluation should be ordered for patients with chest pain; patients with risk factors for myocardial infarction; and patients who are otherwise unstable and present with heart failure, hypotension, or pulmonary edema. Young patients with no structural heart defects have a very low risk of myocardial infarction.
• Electrolyte levels should be checked because electrolyte abnormalities can contribute to paroxysmal supraventricular tachycardia.
• A complete blood cell count helps assess whether anemia is contributing to the tachycardia or ischemia.
• The results from thyroid studies are rarely diagnostic of hyperthyroidism.
• Obtain a digoxin level for patients on digoxin because paroxysmal supraventricular tachycardia is one of the many dysrhythmias that can be caused by supratherapeutic levels of this drug.

Imaging Studies

• Obtain a chest radiograph to assess for the presence of pulmonary edema and cardiomegaly. Infections such as pneumonia, which are associated with paroxysmal supraventricular tachycardia in certain cases, can also be confirmed with findings from this imaging method.^{20,39,55,48,24} Congenital heart defects such as Ebstein anomaly of the tricuspid valve can be suspected.
• A transthoracic echocardiogram may be helpful if structural or congenital heart disease is suggested. Cardiac MRI can be useful, especially if a congenital heart disease is being considered.

Other Tests

ECG findings allow classification of the tachyarrhythmia, and they may allow a precise diagnosis. P waves may not be visible; when present, they may be normal or abnormal depending on the mechanism of atrial depolarization.^20,34,55

• ECG characteristics of the various SVTs are as follows:
  • Sinus tachycardia - Heart rate greater than 100 bpm; P waves similar to sinus rhythm
  • Inappropriate sinus tachycardia - Findings similar to sinus tachycardia; P waves similar to sinus rhythm
  • Sinus node reentrant tachycardia - P waves similar to sinus rhythm; abrupt onset and offset
  • Atrial tachycardia - Heart rate 120-250 bpm; P-wave morphology different from sinus rhythm; long RP interval (in general); AV block does not terminate tachycardia
  • Multifocal atrial tachycardia - Heart rate 100-200 bpm; 3 or more different P-wave morphologies
  • Atrial flutter- Atrial rate of 200-300 bpm; flutter waves; AV conduction of 2:1 or 4:1
  • Atrial fibrillation - Irregularly irregular rhythm; lack of discernible P waves
  • AV nodal reentrant tachycardia - Heart rate of 150-200 bpm; P wave located either within the QRS complex or shortly after the QRS complex; short RP interval in typical AVNRT and long RP interval in atypical AVNRT
  • AV reentrant tachycardia - Heart rate of 150-250 bpm; narrow QRS complex in orthodromic conduction and wide QRS in antidromic conduction; diagnosis excluded by AV block during SVT; P wave after QRS complex
• Following the termination of the tachycardia, an ECG should be performed during the sinus rhythm to screen for WPW syndrome. Echocardiography and/or Holter monitoring also may be useful. These tests can help assess the frequency and duration of SVT episodes, although they have a low yield. Echocardiography may be helpful in screening for structural or congenital heart disease.
• Characterizing the SVT by comparing the RP interval to the PR interval is helpful. Long RP tachycardias result when atrial activity precedes the QRS complex. In short RP tachycardias, atrial activity occurs with or shortly after ventricle excitation. In short RP tachycardias, the P wave is found within the QRS complex or shortly after the QRS complex.^20,39,55,48 The classifications of SVTs based on the RP interval are as follows:
  • Short RP tachycardias – Typical AVNRT, AVRT, JET, and NPJT
  • Long RP tachycardias – Sinus tachycardia, SNRT, atrial tachycardia, atrial flutter, atypical AVNRT, and a permanent form of junctional reciprocating tachycardia

Procedures

• Electrophysiology studies have dramatically changed the diagnosis of SVT. Intracardiac recordings have helped map accessory pathways and reentry circuits in patients, and they have also assisted cardiologists and electrophysiologists in understanding the mechanisms behind these tachyarrhythmias.
• At present, electrophysiologic studies are generally performed in combination with radiofrequency catheter ablation. Catheter ablation is indicated in patients with severe symptoms, symptomatic preexcitation syndrome, incessant tachycardia, and those who do not tolerate or do not desire medical therapy. Catheter ablation procedures are generally performed in an outpatient setting or with an overnight stay for observation.

Treatment

Medical Care

Most of the patients who present with paroxysmal supraventricular tachycardia have AVNRT or AVRT. These arrhythmias depend on AV nodal conduction and therefore can be terminated by transiently blocking AV nodal conduction.

Vagal maneuvers are the first-line treatment in hemodynamically stable patients. Vagal maneuvers, such as breath-holding and the Valsalva maneuver (ie, having the patient bear down as though having a bowel movement), all slow conduction in the AV node and can potentially interrupt the reentrant circuit.

Carotid massage is another vagal maneuver that can slow AV nodal conduction. Massage the carotid sinus for several seconds on the nondominant cerebral hemisphere side. This maneuver is usually reserved for young patients. Due to the risk of stroke from emboli, auscultate for bruits before attempting this maneuver. Do not perform carotid massage on both sides. A Valsalva maneuver, if performed properly by the patient, can frequently avert an attack.

Synchronized cardioversion starting at 50 J can be used immediately in patients who are hypotensive, have pulmonary edema, have chest pain with ischemia, or are otherwise unstable.

• Short-term medical management
  • When SVT is not terminated by vagal maneuvers, short-term management involves intravenous adenosine or calcium channel blockers. Adenosine is a short-acting drug that blocks AV node conduction; it terminates 90% of tachycardias due to AVNRT or AVRT.^{39,11,13,16,48} Adenosine does not usually terminate atrial tachycardia, although it is effective for terminating SNRT.^{39,11,13,21,48} Typical adverse effects of adenosine include flushing, chest pain, and dizziness. These effects are temporary because adenosine has a very short half-life of 10-20 seconds.⁴⁴
  • Other alternatives for the acute treatment of SVT include calcium channel blockers like verapamil, diltiazem or beta-blockers like metoprolol or esmolol. Verapamil is a calcium channel blocker that also has AV blocking properties. Verapamil has a longer half-life than adenosine and may help maintain sinus rhythm following the termination of SVT. It is also advantageous for controlling the ventricular rate in patients with atrial tachyarrhythmia.^{20,12,13,31,55,21,44,24}
  • Acute management of a wide complex tachycardia in a hemodynamically unstable patient requires immediate cardioversion whereas in a stable patient, IV procainamide, propafenone, or flecainide is acceptable. Amiodarone is preferred in patients with impaired left ventricular function or in patients with heart failure or structural heart disease.⁹
  • Treatment of AF and atrial flutter involves controlling the ventricular rate, restoring the sinus rhythm, and preventing embolic complications. The ventricular rate is controlled with calcium channel blockers, digoxin, amiodarone, and beta-blockers. The sinus rhythm may be restored with either pharmacological agents or electrical cardioversion. Pharmacological agents such as ibutilide convert AF and atrial flutter of short duration to sinus rhythm in approximately 30% and 60% of patients, respectively.
  • Electrical cardioversion is the most effective method for restoring sinus rhythm. If AF has been present for longer than 24-48 hours, defer cardioversion until the patient has been adequately anticoagulated to prevent thromboembolic complications.^{39,11,13,31,40,21,44,48}
• Long-term medical management
  • The choice of long-term therapy for patients with SVT depends on the type of tachyarrhythmia and the frequency and duration of episodes, symptoms, and risks associated with the arrhythmia (eg, heart failure, sudden death). Evaluate patients on an individual basis, and tailor the best therapy for the specific tachyarrhythmia.
  • Patients with paroxysmal supraventricular tachycardia may initially be treated with calcium channel blockers, digoxin, and/or beta-blockers. Class IA, IC, or III antiarrhythmic agents are used less frequently because of the success of radiofrequency catheter ablation.^{39,11,13,31,40,21,44,48,56} Consider radiofrequency ablation for any patient with symptomatic paroxysmal supraventricular tachycardia in whom long-term medical treatment is not effectively tolerated or desired. In addition, because of the risk of sudden cardiac death, perform catheter ablation on patients with symptomatic WPW syndrome. Radiofrequency catheter ablation is more than 90% effective in curing paroxysmal supraventricular tachycardia.^{20,39,55,48,19}
  • Radiofrequency ablation involves focally ablating the crucial component of the arrhythmia mechanism. For example, in AVNRT, the slow pathway is ablated, which prevents the reentry cycle. The accessory pathway is targeted in patients with AVRT. Focal atrial tachycardia, atrial flutter, and, in some cases, AF can also be cured with ablation. Radiofrequency ablation has a high success rate and is performed using conscious sedation in an outpatient setting or with overnight hospitalization. Complications, which occur at a rate of 1-3%, include deep vein thrombosis, systemic embolism, infection, cardiac tamponade, and hemorrhage. The risk of death is approximately 0.1%. The lifetime risk of fatal malignancy as a result of radiation exposure is low.
  • Radiofrequency ablation is cost-effective for patients who have frequent episodes of SVT that require antiarrhythmic agents and frequent emergency visits. It is also indicated for patients with incessant tachycardia and for patients with symptomatic WPW syndrome. The optimal management strategy for patients with asymptomatic preexcitation syndromes remains uncertain.^{42,45,30,20,19}

Surgical Care

Prior to the advent of percutaneous radiofrequency catheter ablation, open cardiac surgical procedures were the only means of curing paroxysmal supraventricular tachycardia. Currently, open surgical procedures are rarely performed.

Consultations

• A cardiologist should be consulted for patients with frequent episodes of paroxysmal supraventricular tachycardia, syncope, and/or preexcitation syndromes.
• Consultation with a cardiologist should also be obtained for patients in whom medical management has failed.
• An electrophysiologist should be consulted for patients considered for radiofrequency catheter ablation.

Diet

Dietary changes depend on underlying medical problems.

Activity

Changes in physical activity depend on underlying cardiac problems and other comorbidities.

Medication

The goals of pharmacotherapy are to correct arrhythmia, to prevent complications, and to reduce morbidity.

Antiarrhythmic agents

Used to treat or prevent arrhythmia.

Flecainide (Tambocor)

Blocks sodium channels, producing dose-related decrease in intracardiac conduction in all parts of heart. Increases electrical stimulation of threshold of ventricle, HIS-Purkinje system. Shortens Phase 2 and 3 repolarization, resulting in a decreased action potential duration and effective refractory period.
Indicated for the treatment of paroxysmal atrial fibrillation/flutter (PAF) associated with disabling symptoms and PSVT, including atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, and other supraventricular tachycardias of unspecified mechanism associated with disabling symptoms in patients without structural heart disease. Indicated also for prevention of documented life-threatening ventricular arrhythmias, such as, sustained ventricular tachycardia. Not recommended in less severe ventricular arrhythmias even if patients are symptomatic.

Dosing

Adult

100 mg PO bid q12h; increase q4d to a maximum of 400 mg/d

Pediatric

3-6 mg/kg/d or 100-150 mg/m²/d PO divided tid to 11 mg/kg/d or 200 mg/m²/d

Interactions

May increase toxicity of digoxin; beta-adrenergic blockers, verapamil, and disopyramide may have additive inotropic effects when administered with flecainide; CYP4502D6 inhibitors (ritonavir, cimetidine, amiodarone) may increase serum levels and cardiotoxicity of flecainide

Contraindications

Documented hypersensitivity, preexisting second- or third-degree AV block, right bundle branch block associated with left hemi-block (bifascicular block) or trifascicular block), unless a pacemaker is present to sustain the cardiac rhythm if complete heart block occurs; concurrent use of ritonavir or amprenavir; recent MI

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in pre-existing sinus node dysfunction, history of congestive heart failure, sick-sinus syndrome, post-MI, or myocardial dysfunction; reserve use for life-threatening arrhythmias only due to deaths associated with proarrhythmic effects of Class IC antiarrhythmics; adjust dose in renal or hepatic impairment

Propafenone (Rythmol)

Shortens upstroke velocity (Phase 0) of monophasic action potential. Reduces fast inward current carried by sodium ions in Purkinje fibers, and to a lesser extent myocardial fibers. May increase diastolic excitability threshold and prolong effective refractory period prolonged. Reduces spontaneous automaticity and depresses triggered activity.
Indicated for the treatment of documented life-threatening ventricular arrhythmias, such as sustained ventricular tachycardia. Appears to be effective in the treatment of supraventricular tachycardias including atrial fibrillation and flutter. Not recommended in patients with less severe ventricular arrhythmias, even if patients are symptomatic.

Dosing

Adult

150 mg PO q8h and increase at 3-4 d intervals up to 300 mg q8h

Pediatric

Not established

Interactions

Rifampin may decrease plasma levels; quinidine may increase pharmacologic effects; propafenone may increase plasma levels of beta-blockers, cyclosporine, warfarin, and digoxin; CYP4502D6 inhibitors (ritonavir, cimetidine, amiodarone) may increase serum levels and cardiotoxicity of propafenone

Contraindications

Documented hypersensitivity, second or third-degree AV block, right bundle-branch block associated with left hemi-block (bifascicular block) or trifascicular block; concurrent use of ritonavir or amprenavir

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in pre-existing sinus node dysfunction, history of congestive heart failure, sick-sinus syndrome, post MI, or myocardial dysfunction; reserve use for life-threatening arrhythmias only due to deaths associated with proarrhythmic effects of Class IC antiarrhythmics; adjust dose in renal or hepatic impairment

Adenosine (Adenocard)

First-line medical treatment for termination of PSVT. Short-acting agent that alters potassium conductance into cells and results in hyperpolarization of nodal cells. This increases the threshold to trigger an action potential and results in sinus slowing and blockage of AV conduction (Pieper, 1995; Orejarena; 1998; Siberry, 2000; Trohman, 2000).
Effective in terminating both AVNRT and AVRT. More than 90% of patients convert to sinus rhythm with adenosine at 12 mg. As a result of its short half-life, adenosine is best administered in an antecubital vein as an IV bolus followed by rapid saline infusion (Pieper, 1995; Orejarena; 1998; Siberry, 2000; Trohman, 2000).

Dosing

Adult

Initial: 6 mg rapid IV bolus (antecubital vein), followed by saline flush; second bolus of 12 mg may be given if initial bolus is unsuccessful

Pediatric

0.1-0.2 mg/kg rapid IV push, increasing increments of 0.05 mg/kg IV bolus q2min until PSVT resolves; not to exceed 12 mg

Interactions

Coadministration with carbamazepine may produce higher degrees of heart block; dipyridamole may potentiate effects; methylxanthines or caffeine may antagonize effects

Contraindications

Third-degree heart block, asthma, or sick sinus syndrome; documented hypersensitivity; atrial flutter or AF in setting of ventricular preexcitation (WPW syndrome)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Associated with flushing, chest tightness, dyspnea, lightheadedness, nausea, and palpitation; patients may have sinus bradycardia or sinus arrest; due to ultrashort half-life, adverse effects rarely require specific interventions; adenosine-induced bronchoconstriction may occur in patients with asthma

Class IV calcium channel blockers (nondihydropyridine)

Decrease conduction velocity and prolong refractory period.

Verapamil (Isoptin, Calan)

Calcium channel blockers prevent calcium influx in slow channels of AV node, decrease conduction velocity, and prolong refractory period, which effectively terminates reentrant conduction.

Dosing

Adult

2.5-5 mg IV over 2-3 min; repeat in 5-10 min if arrhythmia is not slowed or converted to sinus rhythm; monitor BP and pulse
240-480 mg SR PO qd to prevent recurrent PSVT

Pediatric

<1 year: Not established
>1 year: 0.1 mg/kg IV bolus; not to exceed 0.3 mg/kg; continuous ECG monitoring

Interactions

Risk of serious bradycardia and AV block with beta-blockers; increases digoxin blood levels, leading to arrhythmia and complete AV block; may increase levels of carbamazepine, digoxin, cyclosporine, and theophylline; coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; cimetidine may increase levels

Contraindications

Children <1 year; documented hypersensitivity; cardiogenic shock, sick sinus syndrome, or severe CHF; second- or third-degree AV block

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients on beta-blockers, digoxin, antidysrhythmics, and antihypertensives because effects may be additive, resulting in serious conduction abnormalities and hypotension; adjust dose with renal insufficiency; hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued treatment); periodically monitor liver function

Diltiazem (Cardizem, Tiazac, Dilacor)

Similar to verapamil, this agent decreases conduction velocity in AV node. Also increases refractory period via blockade of calcium influx. This, in turn, stops reentrant phenomenon.

Dosing

Adult

0.25 mg/kg IV bolus converts 75-100% of PSVTs; usual dose is 20 mg IV over 2 min

Pediatric

1.5-2 mg/kg/d IV

Interactions

Levels increased with cimetidine; increases levels/effects of cyclosporins, carbamazepine, theophylline, fentanyl, digoxin, and beta-blockers; with amiodarone, may cause bradycardia and decreased cardiac output

Contraindications

Sick sinus syndrome, second- or third-degree heart block, heart failure, acute MI; documented hypersensitivity; hypotension (<90 mm Hg systolic)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Warn patients that headache, nausea, vomiting, and dizziness may occur; caution in patients on beta-blockers or digoxin because effects may be additive and result in serious conduction abnormalities and hypotension; caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur

Class II beta-blockers

Increase refractory period of AV node.

Propranolol (Inderal)

Beta-blockers abolish reentry-induced PSVT by increasing refractory period of AV node. Other beta-blockers effective in treating PSVT are esmolol, metoprolol, atenolol, and nadolol.

Dosing

Adult

IV: 0.5-1 mg bolus; not to exceed 5 mg
PO: 10-30 mg tid/qid; 80-160 mg qd long-acting formulation

Pediatric

0.01-0.1 mg/kg IV over 10 min, repeat q6-8h prn; not to exceed 1 mg/dose for infants or 3 mg/dose for children

Interactions

Calcium channel blockers result in additive effects and increase risk of AV block; barbiturates, rifampin, and indomethacin may decrease effects; cimetidine, quinidine, chlorpromazine, and verapamil may increase effects; aluminum salts, NSAIDs, penicillins, calcium salts, and cholestyramine may decrease effects; loop diuretics and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase

Contraindications

Asthma, second- or third-degree heart block, heart failure; documented hypersensitivity; bradycardia, cardiogenic shock

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely

Esmolol (Brevibloc)

Short-acting beta-blocker that abolishes reentry-induced PSVT by increasing refractory period of AV node.

Dosing

Adult

Loading dose of 0.5 mg/kg IV over 1 min, followed by a maintenance infusion of 50 mcg/kg/min for 4 min; if unsuccessful, a second bolus of 0.5 mg/kg is infused over 1 min, with a maintenance rate of 100 mcg/kg

Pediatric

Not established; suggested dose is 100-500 mcg/kg administered IV over 1 min

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity of esmolol may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of esmolol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents

Contraindications

Documented hypersensitivity; uncompensated CHF, bradycardia, cardiogenic shock, and AV conduction abnormalities

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Category D in second or third trimester; beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn; withdraw drug slowly and monitor patient closely

Cardiac glycosides

Increase vagal activity, which decreases conduction velocity through AV node.

Digoxin (Lanoxin)

Indirectly increases vagal activity, thereby decreasing conduction velocity through AV node, which can result in termination of PSVT.

Dosing

Adult

0.125 mg PO qod to 0.375 mg PO qd

Pediatric

<5 years: Not established
5-10 years: 20-35 mcg/kg PO
>10 years: 10-15 mcg/kg PO
Maintenance dose is 25-35% of PO loading dose

Interactions

Medications that may increase levels include quinidine, verapamil, diltiazem, amiodarone, alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, aminoglycosides, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, and tolbutamide
Drugs that increase hepatic microsomal enzyme activity (eg, rifampin, phenobarbital, phenytoin) may increase metabolism; diuretics may result in hypokalemia, which may increase risk of digoxin toxicity
Medications that may decrease serum levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, and procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, kaolin/pectin, and aminosalicylic acid

Contraindications

Ventricular dysrhythmia; documented hypersensitivity; beriberi heart disease, hypertrophic cardiomyopathy, constrictive pericarditis, and carotid sinus syndrome

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Dose adjustment in patients with renal insufficiency; monitor levels to avoid toxicity or symptoms (eg, confusion, headache, ataxia, vomiting, weakness, visual disturbances, delirium, diarrhea); most serious effects of toxicity are dysrhythmia and PVC (most common), but ventricular tachycardia and AV block also occur; monitor for electrolyte abnormalities because hypokalemia may increase risk of toxicity; toxicity can be treated with Digibind IV calcium but may produce arrhythmia in digitalized patients; hypercalcemia predisposes patients to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis

Follow-up

Further Inpatient Care

Patients who require cardioversion, are unstable, and have comorbid illnesses should be admitted to the hospital. Patients who are young, healthy, and asymptomatic may be discharged and advised to have a follow-up examination with their primary physician or cardiologist. If the patient is having more frequent episodes of paroxysmal supraventricular tachycardia and medical therapy is not successful or desired, then radiofrequency ablation should be proposed.

Further Outpatient Care

Patients treated medically should be monitored regularly. Patients cured with radiofrequency catheter ablation are typically seen once in a follow-up examination following the procedure, then as needed for recurrent symptoms.

Transfer

Transfer to a center with radiofrequency catheter ablation is reasonable if this therapy is planned. Alternatively, patients can be discharged home and scheduled for outpatient procedures. Exceptions include patients with syncope, profound symptoms, or preexcited atrial fibrillation or atrial flutter.

Complications

• Rare complications of paroxysmal supraventricular tachycardia include myocardial infarction, congestive heart failure, syncope, and sudden death.
• Potential complications of radiofrequency catheter ablation include hematoma, bleeding, infection, pseudoaneurysm, myocardial infarction, cardiac preformation, heart block that requires a pacemaker, thromboembolic complications, stroke, need for emergency surgery, radiation burn, increased risk of malignancy, and death.

Prognosis

Patients with symptomatic Wolff-Parkinson-White syndrome have a small risk of sudden death. Otherwise, prognosis is dependent on any underlying structural heart disease. Patients with paroxysmal supraventricular tachycardia in the setting of a structurally normal heart have an excellent prognosis.

Patient Education

For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education articles Supraventricular Tachycardia, Atrial Fibrillation, Atrial Flutter, and Heart Rhythm Disorders.

Miscellaneous

Medicolegal Pitfalls

• Patients with symptomatic Wolff-Parkinson-White syndrome should be told of the potential for cardiac arrest. In general, these patients should not be treated longitudinally with calcium channel blockers or digoxin unless the pathway is known to be of low risk (long anterograde refractory period). This is because of the potential for more rapid ventricular rates should atrial fibrillation or atrial flutter occur.
• Patients with preexcited atrial fibrillation should not be treated with intravenous AV nodal blocking agents such as adenosine, beta-blockers, calcium channel blockers, and digoxin. Rather, if the patient is hemodynamically stable, intravenous procainamide should be administered. If the patient is unstable, direct current cardioversion should be performed.

Special Concerns

Pediatric patients should be referred to a pediatric electrophysiologist.

Multimedia

Media file 1: Sinus tachycardia. Note that the QRS complexes are narrow and regular. The patient's heart rate is approximately 135 bpm. P waves are normal in morphology.

Media file 2: Atrial tachycardia. The patient's heart rate is 151 bpm. P waves are upright in lead V₁.

Media file 3: Multifocal atrial tachycardia. Note the different P-wave morphologies and irregularly irregular ventricular response.

Media file 4: Atrial flutter. The patient's heart rate is approximately 135 bpm with 2:1 conduction. Note the sawtooth pattern formed by the flutter waves.

Media file 5: Atrial fibrillation. The patient's ventricular rate varies from 130-168 bpm. Rhythm is irregularly irregular. P waves are not discernible.

Media file 6: Atrioventricular nodal reentrant tachycardia. The patient's heart rate is approximately 146 bpm with a normal axis. Note the pseudo S waves in leads II, III, and aVF. Also note the pseudo R' waves in V₁ and aVR. These deflections represent retrograde atrial activation.

Media file 7: Same patient as in Media file 6. Patient is in sinus rhythm following atrioventricular nodal reentrant tachycardia.

Media file 8: Image A displays the slow pathway and the fast pathway, with a regular impulse being conducted through the atrioventricular node. Image B displays a premature impulse that is conducted in an anterograde manner through the slow pathway and in a retrograde manner through the fast pathway, as is seen in typical atrioventricular nodal tachycardia. Image C displays the premature impulse conducting in a retrograde manner through the pathway and the impulse reentering the pathway with anterograde conduction, which is seen commonly in patients with atypical atrioventricular nodal tachycardia.

Media file 9: Wolff-Parkinson-White pattern. Note the short PR interval and slurred upstroke (delta wave) to the QRS complexes.

Media file 10: The left image displays the atrioventricular node with the accessory pathway. The impulse is conducted in an anterograde manner in the atrioventricular node and in a retrograde manner in the accessory pathway. This circuit is known as orthodromic atrioventricular reentrant tachycardia and can occur in patients with concealed accessory tracts or Wolff-Parkinson-White syndrome. The right image displays the impulse being conducted in an anterograde manner through the accessory pathway and in a retrograde manner via the atrioventricular node. This type of circuit is known as antidromic atrioventricular reentrant tachycardia and only occurs in patients with Wolff-Parkinson-White syndrome. Both patterns may display retrograde P waves after the QRS complexes.

Media file 11: Orthodromic atrioventricular reentrant tachycardia. This patient has Wolff-Parkinson-White syndrome.

Media file 12: The left panel depicts antidromic atrioventricular reentrant tachycardia. The right panel depicts sinus rhythm in a patient with antidromic atrioventricular reentrant tachycardia. Note that the QRS complex is an exaggeration of the delta wave during sinus rhythm.

Media file 13: Atrial fibrillation in a patient with Wolff-Parkinson-White syndrome. Note the extremely rapid ventricular rate and variability in QRS morphology. Several minutes later, the patient developed ventricular fibrillation.

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Keywords

paroxysmal supraventricular tachycardia, 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 reentranttachycardia, 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

Contributor Information and Disclosures

Author

Monika Gugneja, MD, Consulting Staff, Department of Emergency Medicine, William Beaumont Hospital
Disclosure: Nothing to disclose.

Coauthor(s)

Phillip L Kraft, MD, Director, Interventional Cardiology and Cardiac Catheterization Laboratory, William Beaumont Hospital
Phillip L Kraft, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Alan D Forker, MD, Professor of Medicine, Program Director of Cardiovascular Fellowship, University of Missouri at Kansas City School of Medicine; Director, Outpatient Lipid Diabetes Research Center, MidAmerica Heart Institute of St 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: Research Grant Grant/research funds Hospital contracts to do research; I am a hospital employee with no personal profit; Speakers Bureau Honoraria Speaking and teaching

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Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
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, and New York Academy of Sciences
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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 Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
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The authors and editors of eMedicine gratefully acknowledge the contributions of previous author James V Talano, MD to the development and writing of this article.

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