Supraventricular Tachycardia (SVT): Strategies for Diagnosis, Risk Stratification, and Management in the Emergency Department Setting
Authors: Monika Ahluwalia, MD, Emergency Physician, Emory University, Atlanta, GA; Tammie Quest, MD, Assistant Professor, Department of Emergency Medicine, Emory University School of Medicine, Atlanta, GA.
Peer Reviewers: Sandra M. Schneider, MD, FACEP, Professor and Chair, Department of Emergency Medicine, University of Rochester, NY; Raymond L. Fowler, MD, FACEP, Assistant Professor, Emergency Medicine, The University of Texas Southwestern Medical Center, Dallas.
Supraventricular tachycardia (SVT) is a common clinical condition encountered in the emergency department (ED) that often is a challenge to treat. SVT is defined as any rapid heart rhythm arising above the ventricles, utilizing either the atria or atrioventricular nodal tissue. SVT may be a physiologic response, such as sinus tachycardia, or any of a number of pathological tachyarrhythmias. It includes sinus tachycardia, multifocal atrial tachycardia, ectopic atrial tachycardias, atrial flutter, atrial fibrillation, atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and Wolff-Parkinson-White syndrome (WPW).
Distinguishing physiologic sinus tachycardia from other types of pathologic SVTs can be difficult. This distinction is important in the clinical management of SVT because the therapeutic approaches differ widely. The distinction between physiologic and pathologic tachycardias is best made by careful examination of the patient’s vital signs, the history and physical exam, and careful analysis of the electrocardiogram (ECG). Although physiologic tachycardia is a type of SVT, it may be a result of states such as sepsis, dehydration, or hemorrhagic shock. This article will use the term SVT to refer solely to those pathological tachyarrhythmias that are not considered physiologic. (See Table 1.)
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SVT can occur in any age group and in patients with or without structural heart disease. In fact, SVT is the most common cardiac arrhythmia of childhood. Initial clinical presentation may range from no symptoms to palpitations, dizziness, chest pain, or syncope. Electrophysiology dramatically has changed the field of tachyarrhythmias by identifying the basic mechanism underlying SVT. Defects in impulse propagation and conduction in the heart are the hallmark pathophysiologic findings of SVT. Pharmacological therapies available for termination and prevention of SVT are based on the underlying rhythm, the frequency and severity of the episodes, and the mechanism of the arrhythmia.
With these issues in mind, the purpose of this review is provide a systematic approach to the diagnosis and management of this common clinical emergency.—The Editor
Incidence and Prevalence
SVT has been recognized as a cardiac arrhythmia since 1909. However, the prevalence of this condition only recently was determined to be approximately 2.25 per 1000 persons, with an incidence of 35 per 100,000 person-years. This equals approximately 89,000 new cases each year. More than 1 million people in United States suffer from SVT.1
Clinical Presentation
Patients with SVT present with a range of clinical symptoms. The overwhelming majority (96%) present with palpitations.2,3 Other common symptoms include: dizziness (75%); shortness of breath (47%); fatigue (23%); chest pain (35%); diaphoresis (17%); and nausea (13%).2,3 Note that "neck pounding" is a pathognomonic sign for AVNRT.2,3 SVT largely is considered to be a fairly benign condition. However, recent studies indicate that more than 20% of patients with SVT have syncope or life-threatening arrhythmias such as ventricular fibrillation.2 Many patients with frequent episodes of SVT and syncope or near-syncopal episodes restrict daily life activities.2
The onset and duration of SVT is associated with a variety of factors, such as circadian rhythms, physical or mental stressors, pregnancy, and drugs. SVT has been found to follow circadian rhythms, with episodes occurring much more commonly during the day than at night.4 This pattern is thought to be due to the increased sympathetic tone, higher levels of circulating epinephrine, and physical and mental stressors found during the day.4 Further studies are needed to determine if a change in the circadian rhythm, such as in patients who work at night, alters the frequency and incidence of SVT. Pregnancy, with its accompanying dramatic hormonal changes, also increases the frequency of SVT.2 Drugs such as digitalis, albuterol, and sympathomimetics can increase the risk of developing SVT as well.4,5
Classification
SVT encompasses many tachyarrhythmias, including atrial fibrillation, atrial flutter, AVNRT, AVRT, sinus node reentrant tachycardia (SNRT), and multifocal atrial tachycardia (MAT). These tachyarrhythmias are classified based on two principles: the tissue involved (atrial, atrioventricular nodal and/or its surrounding tissue) and the underlying mechanism generating the tachyarrhythmia determined by intracardiac monitoring. This classification is important, as it assists in understanding the underlying circuitry utilized by the various types of SVT.6-11 (See Table 1 for the current classification.)
Pathophysiology
Sinus Tachycardia. Sinus tachycardia is a narrow, complex, regular tachycardia that usually is a response to an underlying stressor. Sinus tachycardia is not considered to be an arrhythmia. Stressors can be physiologic, pharmacologic, or pathophysiologic, including fever, pain, anxiety, exercise, sympathomimetic agents (caffeine, methylxanthines, amphetamines, etc.), anemia, hypoxia, hypotension, hyperthyroidism, or hypovolemia.6-10 Sinus tachycardia has a gradual onset and can be undulating. It does not have a sudden onset or termination; rather, it gradually accelerates and decelerates depending on the reversal, or lack thereof, of its cause. Treatment involves correcting the underlying stressor.
Electrocardiographic Features. Electrocardiographic features include a narrow complex regular tachycardia with an upright P wave in leads I, II, III, and aVF that precedes each QRS complex. (See Figure 1.) The heart rate usually ranges between 100 and 180 beats per minute (bpm), although in young patients it may be more than 180 bpm.6-10,16 The expected maximum heart rate can be calculated by using a formula (220 minus patient’s age). Thus, for a 40-year-old, the maximum heart rate would be 180 bpm.
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Inappropriate Sinus Tachycardia. In contrast to sinus tachycardia, inappropriate sinus tachycardia (IST) is defined as a baseline accelerated heart rate without a physiologic or pharmacologic stressor. This may be an arrhythmia. Found more commonly in young women, IST is a rare tachyarrhythmia that involves a diagnosis of exclusion. Pheochromocytoma and hyperthyroidism may mimic this arrhythmia and, therefore, must be excluded whenever IST is considered as a diagnosis. Currently, the mechanism of this tachycardia is considered to be an ectopic atrial focus located in close proximity to the sinoatrial node or a hypersensitivity to catecholamines. Therefore, even minimal exertion, such as standing from a supine position or walking, can result in an elevated heart rate.6-10,12
Electrocardiographic Features. Electrocardiographic features of IST usually are indistinguishable from sinus tachycardia. However, P waves may show slight differences if the mechanism is an ectopic atrial focus in close proximity to the sinoatrial node.9-12,16
Sinus Node Reentrant Tachycardia. SNRT is a rare clinical condition that arises due to a reentry circuit involving the sino-atrial node. Because SNRT and sinus tachycardia both utilize the sino-atrial node, they have many electrocardiographic features in common. The difference lies chiefly in its onset and termination. In contrast to sinus tachycardia, SNRT has an abrupt onset and termination.6-10
Electrocardiographic Features. As with sinus tachycardia, the heart rate usually ranges between 100 and 150 bpm. In addition, P wave morphology on the electrocardiogram is identical or nearly identical to sinus P waves seen in sinus tachycardia.7-10,16
Multifocal Atrial Tachycardia. MAT is an arrhythmia that has at least three or more P wave morphologies and a heart rate typically between 100 and 200 bpm. It is an irregular tachycardia, and is misinterpreted most commonly as atrial fibrillation. The distinction between MAT and atrial fibrillation has important clinical implications. Atrial fibrillation may require anticoagulation, whereas MAT clearly does not. Distinct physical exam findings can help differentiate MAT from atrial fibrillation. The presence of "a" waves in jugular venous pulsations, coupled with the presence of discreet P waves on ECG, lead the clinician to the diagnosis of MAT. (See Figure 2.) The mechanism leading to MAT is considered to be either enhanced automaticity or triggered activity. It commonly is seen in ill, elderly patients with chronic obstructive pulmonary disease, sepsis, acidosis, and hypoxia. Certain drugs such as theophylline and beta-agonists, and electrolyte disturbances such as hypokalemia and hypomagnesiumia also have been associated with MAT. The treatment focuses on correcting the underlying physiological abnormalities: hypoxia, acidosis, and electrolyte abnormalities. MAT is not considered to be a clinically significant tachycardia, but it serves as an indicator of an underlying physiological stressor.6,9-11,13-15
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Electrocardiographic Features. MAT has three or more types of P waves and an irregular rhythm. The heart rate is 100-200 bpm.13-15
Ectopic Atrial Tachycardia. Ectopic atrial tachycardia is a rare arrhythmia that arises due to reentry, abnormal automaticity, or both. It may occur in patients without any structural heart disease, but it often occurs in the presence of cardiac or pulmonary disease. The most important characteristic of this arrhythmia is that it utilizes the atrial tissue rather than the atrioventricular node for its circuit. Therefore, drugs or maneuvers such as carotid massage or Valsalva, which delay AV nodal conductions, often are not effective in terminating this abnormal rhythm. Because prolonged, untreated atrial tachycardias can result in tachycardia-induced cardiomyopathy, treatment of atrial tachycardia focuses of controlling the ventricular rate.6-11
Electrocardiographic Features. Electrocardiographic features include P wave morphology different from sinus rhythm, because the P wave morphology depends on the site of the ectopic focus. For example, a low, right atrial ectopic focus will produce negative P waves in inferior leads. (See Figure 3.)6-11,16 Atrial tachycardia usually has a ventricular rate between 120 and 250 bpm, and the QRS complexes are regular and narrow.
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Atrial Flutter. Atrial flutter is an arrhythmia that forms a reentrant circuit using the inferior vena cava, tricuspid valve, Eustachian ridge, and coronary sinus ostium.7,11,16-18 It commonly is seen in patients with surgical repair of congenital heart disease, chronic obstructive pulmonary disease, mitral and tricuspid valve disease, thyrotoxicosis, and an enlarged right atrium.7,11,16-18 Clinically, atrial flutter is significant because it can convert to atrial fibrillation, which increases the risk of thromboembolic complications. In addition, the fast atrial rates with 1:1 or 2:1 conduction to ventricles can have untoward clinical consequences, including congestive heart failure, ventricular fibrillation, and/or cardiac arrest.7,11,16-18
Electrocardiographic Features. The reentrant circuit established in atrial flutter depolarizes the atrial tissue, resulting in atrial rates ranging between 250 and 350 bpm. Characteristic "sawtooth" flutter waves are seen on electrocardiogram.16-18 Often, the conduction of the flutter waves is 2:1 or 4:1 with ventricular rates at approximately 150 bpm. (See Figures 4a-b.)
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Atrial Fibrillation. Atrial fibrillation is the most common persistent supraventricular arrhythmia, with a prevalence of 0.4% in the general population, and more than 9% in patients older than age 80.17,19,20 More than 2 million people in the United States suffer from atrial fibrillation. The frequency of this arrhythmia increases dramatically after age 60. Atrial fibrillation arises due to chaotic depolarization of the atrial tissue from multiple reentrant circuits. It often is associated with structural and valvular heart disease; hypertension; pericarditis; metabolic disorders like thyrotoxicosis; and alcohol intoxication.9,11,17,19,20 Atrial fibrillation with an uncontrolled ventricular response results in poor cardiac performance, which may result in myocardial ischemia or infarction. In addition, the abnormal atrial contractions during atrial fibrillation result in blood accumulation in the atria, increasing the risk of thromboembolic events such as stroke.9,11,17,19,20
Electrocardiographic Features. The ECG of patients with atrial fibrillation displays an irregularly irregular rhythm evident in the variable RR interval with an absence of discrete P waves. However, the QRS complexes are narrow unless there is a bundle-branch block. The conduction properties of the atrioventricular node determine the ventricular rates, which can vary from 75 bpm to 200 bpm.9,11,16,17,19,20 Atrial fibrillation with very rapid, uncontrolled ventricular response can be difficult to distinguish from sinus tachycardia with a very rapid rate. (See Figure 5.)
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Atrioventricular Nodal Reentrant Tachycardia. AVNRT is one of the three most common causes (> 60%) of SVT, along with sinus tachycardia and atrial fibrillation. The overall prevalence of AVNRT is unknown. AVNRT is twice as common in females as in males, and it can be encountered in all age groups.9,11,21,22 AVNRT may present in patients with or without structural heart disease. The symptoms, which include palpitations, dizziness, weakness, and near-syncope, usually are mild and are similar to those of other SVTs.
The mechanism of AVNRT is reentrant phenomena of the AV node, as indicated by its name.9,11,21-26 AVNRT has characteristic "longitudinal dissociation," implying that there is more than one type of conducting fiber in the AV node. One side of the circuit has slow conduction with fast repolarization, and the other side has fast conduction with slow repolarization. The typical conduction of impulses is from the SA node through the AV node, the bundle of His, and finally, to the right and left branches of the ventricles. In AVNRT, an atrial premature impulse enters the node and depolarizes the slow pathway, traveling anterogradely down the slow pathway of the circuit. It does not depolarize the fast pathway because it still is in the refractory period. When the impulse reaches the end of the slow pathway, however, the fast pathway has repolarized, and thus, the impulse depolarizes the fast pathway.
The impulse travels retrogradely up the fast pathway and then reenters the circuit as the slow pathway has repolarized. This reentry circuit induces clinical tachycardia.9,11,21-26 (See Figure 6.) Because the impulse travels fast retrogradely and redepolarizes the atria after the ventricles, the RP is noted to be less than the PR interval. AVNRT typically follows anterogradely down the slow pathway and retrogradely up the fast pathway. However, some patients have atypical conduction whereby the impulse travels anterogradely down the fast pathway and retrogradely up the slow pathway. This produces a long RP interval and a short PR interval.9,11,21-26
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Electrocardiographic Features. The rate usually is greater than 150 bpm, and the QRS complexes are regular and narrow if no aberrant conduction is present in the bundle branches. Retrograde P waves may be seen shortly after the QRS complexes on ECG, though sometimes no P waves may be visible. (See Figure 7.) Typical AVNRT has a short RP interval and a long PR interval, whereas atypical AVNRT has a long RP interval and a short PR interval.9,11,21-26
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Atrioventricular Reentrant Tachycardia. AVRT is the next most common cause of SVT, accounting for more than 30% of SVT. It commonly is seen in children and adolescents. AVRT results when there are accessory conducting pathways between the atria and ventricles in addition to the normal atrioventricular conducting system. These accessory pathways have electrophysiologic properties that are different from the normal atrioventricular conduction system.9,27-31 Accessory pathways are capable of rapid nondecremental conduction in either anterograde or retrograde direction or both. When an impulse travels down the accessory pathway rapidly, preexcitation of the ventricles occurs, resulting in a short PR interval, a wide QRS, and a delta wave. This constellation of electrophysiologic findings also is known as WPW.9,11,27-31
WPW prevalence is 0.13.1 per 1000 persons. Men are twice as likely to have preexcitation as women. The rate usually is 150250 bpm, and patients usually do not have any structural heart disease.9,11,27-31 In general, patients with WPW are at high risk of developing potentially dangerous, fast arrhythmias, such as atrial fibrillation and ventricular fibrillation, due to nondecremental conduction in the fast accessory pathways. Atrial fibrillation has been noted to occur in 11.539% of the patients with WPW. Patients with atrial fibrillation and multiple access pathways are at increased risk of developing ventricular fibrillation that can result in sudden cardiac death. Sudden cardiac death in patients with WPW has been reported at a rate of 0.6% per year.9,11,27-31
AVRT utilizes both the atria and ventricles along with the AV node to form a reentry circuit, which is the main mechanism for the tachycardia. There are two types of AVRT: orthodromic tachycardia and antidromic tachycardia. Orthodromic tachycardia, the most common form in WPW patients, occurs when an impulse travels anterogradely from the atria to the atrioventricular node to the bundle branches and then travels retrogradely up the accessory pathway to the atrium. (See Figure 8.) Because the ventricles are depolarized by the slow pathway, which is part of the normal atrioventricular conducting system, no delta waves are seen. Because the retrograde impulse traveling via the fast accessory pathway depolarizes the atrium after the ventricles, a short RP interval is seen on the ECG with P waves that occur shortly after the QRS complexes.9,11,16,27-31
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In antidromic tachycardia, impulses travel anterogradely from the atrium to the ventricles via the fast accessory pathways and retrogradely up the normal conducting system (the bundle of His to the AV node and then to the atrium)—not via an accessory pathway. Antidromic tachycardia conduction is opposite to the orthodromic AVRT and typically produces wide QRS complexes, short PR intervals, and delta waves. Antidromic tachycardia is associated with a higher risk of developing atrial fibrillation and ventricular fibrillation than orthodromic tachycardia.9,11,27-31
Electrocardiographic Features. In WPW syndrome, the ECG commonly displays a delta wave, a short PR interval, and a wide QRS. Orthodromic AVRT presents with a narrow QRS with P waves occurring shortly after the QRS complexes, while antidromic tachycardia presents with wide QRS complexes and a short PR interval, if P waves are visible.9,11,16,27-31 (See Figure 9.)
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Management
Acute management of SVT depends on a number of issues: hemodynamic status of the patient, type of SVT, and duration of symptoms.
Hemodynamically Unstable Patients. If the patient is hemodynamically unstable (i.e., hypotension, mental status changes, ischemia), and the rhythm is not attributable to physiologic sinus tachycardia, then immediate direct current synchronized cardioversion should be performed.
Hemodynamically Stable Patients. If the patient is hemodynamically stable and the underlying rhythm is atrial fibrillation or atrial flutter, then the following issues must be considered to initiate optimal therapy: 1) controlling the rate; 2) converting the patient to sinus rhythm; and 3) preventing recurrences.
If the patient has been in atrial fibrillation for fewer than 48 hours, then the patient’s rate can be controlled with calcium channel blockers, beta-blockers, amiodarone, or digoxin and, in some cases when indicated and appropriate, the patient can be converted to sinus rhythm with either DC cardioversion or with chemical agents such as ibutilide, procainamide, or amiodarone.33-36,39 (See Figure 10.)
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If the patient has been in atrial fibrillation for more than 48 hours, or if duration is unknown, then the patient should be treated with anticoagulants for three weeks and then cardioverted. Another approach is to start heparin or enoxaparin and perform transesophageal echo to exclude atrial clot and then to cardiovert within 24 hours, continuing anticoagulation for four more weeks. Chronic atrial fibrillation treatment involves controlling ventricular rate with calcium channel blockers, beta-blockers, and/or digoxin.33-36,39 Catheter ablation recently has been utilized for patients who cannot be managed medically and in patients who have severe symptoms and co-morbid diseases. (See Table 2: Click here.)
Supraventricular Tachycardia. If the patient is hemodynamically stable, and the underlying rhythm is SVT excluding atrial flutter or fibrillation, then a number of maneuvers and medications can convert the arrhythmia to sinus rhythm. The first technique that can slow or terminate the SVT is vagal maneuvers. Vagal maneuvers include Valsalva, immersion of the face in cold water, bearing down, and ocular massage. These maneuvers stimulate the parasympathetic system, increasing AV block and thus slowing or terminating the arrhythmia.37,38 If the vagal stimulations terminate the tachy- arrhythmia, the likely etiology is either AVNRT or AVRT, both of which involve the AV node. Carotid massage, which involves rubbing the carotid sinus for 10-15 seconds, also increases AV block and can slow, if not terminate, the SVT. Carotid massage should not be used in elderly patients, because a carotid plaque can be dislodged. Both carotid massage and vagal maneuvers convert SVT to sinus in approximately 10% to 19% of patients.37,38 (See Table 2 and Insert. For Insert, click here.)
If vagal maneuvers and carotid massage are not effective, then the next step is to use adenosine. Adenosine is an endogenous nucleoside that has significant effects on the heart, including depression of the AV node and prolongation of the AV refractory period. Its ultra-fast action reaches peak effect in 15-30 seconds, and it has an equally short-lived half-life of 8 seconds. Adenosine is given at a dose of 6 mg as a rapid bolus in a peripheral vein, followed by a 10-30 mL normal saline flush. If the 6 mg dose is not effective in terminating the SVT, then a second dose of 12 mg should be used. A last dose of 12 mg or 18 mg also can be used if the second dose is unsuccessful. A 12-mg dose of adenosine is effective in terminating 90% of the SVT (AVNRT/AVRT), and it is as effective as verapamil.39-42
Ectopic atrial tachycardias, atrial flutter, and atrial fibrillation usually are not converted to sinus with adenosine. Adenosine, however, may slow the heart enough to visualize the underlying rhythm so that appropriate treatment can be started for the respective arrhythmias. Patients should be warned about the short-lived side effects of adenosine, including facial flushing, chest pain, dsypnea, and dizziness. Importantly, clinicians and patients should be aware that transient asystole is common with adenosine. Use caution with heart transplant patients because they are supersensitive to adenosine due to denervation. Precaution also should be used with patients who have asthma, because adenosine may cause bronchospasm.
If adenosine is unsuccessful in terminating the SVT, then the calcium channel blockers verapamil or diltiazem should be used. The choice of calcium channel blocker depends on the patient’s medical history and electrocardiographic findings. Verapamil selectively blocks calcium from entering cells during depolarization, hence slowing AV node conduction. The dose administered is 5-10 mg intravenously over 2-3 minutes. If the initial dose is ineffective, then a repeat dose may be given 15-30 minutes after the first dose. Verapamil starts working within 1-2 minutes and peaks within 10-15 minutes.41-44 Side effects include hypotension, bradycardia, and high-degree AV block; therefore, it should not be given to patients with second- or third-degree AV block or sick sinus syndrome. Verapamil-induced hypotension can be prevented somewhat by pretreating with intravenous calcium gluconate.
Diltiazem, another calcium channel blocker with properties similar to verapamil, also can be used to terminate SVT. The recommended dose is 0.25 mg/kg, with an average dose of 20 mg given intravenously over 2-3 minutes. If the first dose is inadequate, a second dose of 25 mg may be given 15 minutes after the initial dose. Diltiazem is preferred in patients with low ejection fraction or heart failure. A diltiazem drip may be required to control ventricular rates in patients with atrial fibrillation or atrial flutter. The drip should be started at 10 mg/hour and titrated up to achieve the desired effect.41-44
Esmolol, a short-acting beta-blocker, also can be used to control the rapid ventricular rates of SVT. The dose of esmolol ranges from 50 mcg/kg/min to 200 mcg/kg/min. Beta-blockers should be avoided in patients with asthma and in patients with second- and third-degree heart blocks.7,9,11
Digoxin, a common cardiac glycoside, commonly is used to control ventricular rates of SVT in patients with congestive heart failure and left ventricular dysfunction. An initial loading dose of 0.5 mg is given intravenously, and additional doses between 0.125 mg and 0.5 mg may be given 30-60 minutes after the first dose to achieve an adequate response. The total dose should not exceed 0.02 mg/kg.7,9,11,41-44
Other agents that may be considered for acute treatment of SVT include amiodarone, procainamide, and sotalol. (See Insert.)
WPW. Verapamil is contraindicated for rate control in patients with WPW syndrome. Verapamil can block the normal conducting tracts and provoke conduction down accessory pathways in WPW, thereby increasing ventricular rates and resulting in hemodynamic instability and even cardiac arrest.9,11,27-31 Concomitant use of beta-blockers and verapamil can cause significant hypotension, bradycardia, and heart block and, therefore, both agents should not be used together. Patients with WPW in atrial fibrillation should be treated with procainamide and, if needed, electrical cardioversion.41-44
Chronic Management
Patients with SVT do not always need to be placed on antiarrhythmic agents. Patients with frequent episodes, co-morbid diseases, and severe symptoms during episodes (heart failure), however, should be treated with antiarrhythmics. Class Ia (quinidine, procainamide), Ic (propafenone, flecainide), and III (amiodarone) all have been used to control ventricular rates, convert and maintain sinus rhythms, and prevent recurrences. If the patient is unable to tolerate antiarrhythmic therapy, or if frequent episodes of SVT are occurring despite antiarrhythmic therapy, then catheter ablation may be considered.9,45,46 Due to the risk of sudden death, patients who have pre-excitation syndromes like WPW with symptomatic SVT should have ablation over medical management. All patients with breakthrough or frequent episodes of SVT should be followed by a cardiologist.9,11,41-46
Conclusion
Supraventricular tachycardia is a very common clinical condition presenting to the ED. For emergency physicians, it is critical to differentiate the many types of tachyarrhythmias that are classified under SVT and to treat the specific arrhythmia appropriately. Treatment strategies are dictated by history and electrocardiographic findings. Management includes accurately diagnosing and treating the acute rhythm, discerning and treating underlying etiologies, initiating pharmacologic or electrical therapy, and referring to a cardiologist if chronic treatment is necessary.
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