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their habits of critical inquiry and balanced judgement, and to contribute to better patient care. Disclosures: Joseph E. Marine, MD, current author of

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Supraventricular Tachycardia View online at http://pier.acponline.org/physicians/diseases/d172/d172.html

Module Updated: 2013-01-30

CME Expiration: 2016-01-30

Author

Joseph E. Marine, MD

Table of Contents

1. Diagnosis ..........................................................................................................................2

2. Consultation ......................................................................................................................7

3. Hospitalization ...................................................................................................................11

4. Therapy ............................................................................................................................12

5. Patient Counseling ..............................................................................................................15

6. Follow-up ..........................................................................................................................17

References ............................................................................................................................19

Glossary................................................................................................................................22

Tables ...................................................................................................................................23

Figures .................................................................................................................................35

http://pier.acponline.org/physicians/diseases/d172/d172.html

Supraventricular Tachycardia


Page 2 of 38

1. Diagnosis Top

Use history, physical exam, and appropriate laboratory studies to confirm and characterize SVT.

1.1 Consider the diagnosis of SVT for patients with palpitations, dyspnea, chest discomfort, or syncope.

Recommendations

• Recognize that palpitations are nonspecific and might be manifestations of several types of

arrhythmias.

• Be aware that symptoms of SVT can mimic and, therefore, be mistakenly attributed to panic

attacks, especially in women.

• Recognize that noncardiac causes of palpitations include:

Anxiety

Thyrotoxicosis

Anemia

Febrile states

Hypoglycemia

Catecholamines

Effects of drugs (e.g., caffeine, pseudoephedrine, nicotine, theophylline, cocaine)

• Remember that dyspnea and syncope or near syncope can occur in patients with SVT, but are more

likely to be manifestations of other disorders.

• Consider that chest pain and discomfort are nonspecific symptoms with multiple causes but may be

associated with cardiac arrhythmias.

• Inquire about the onset and termination of symptoms to help classify the SVT.

• Ask patients about polyuria, which can accompany SVT.

Evidence

• In a retrospective study of 107 consecutive patients with paroxysmal SVT, 55% were improperly

diagnosed for a mean of 3.3 years. In most of these patients, palpitations were attributed to panic

attacks, anxiety, or stress; such diagnoses were made more frequently in women than in men (1).

• In patients presenting with syncope, SVT is an uncommon cause, with an overall incidence of



Page 3 of 38

• Palpitations that end abruptly during vagal maneuvers suggest an AV-nodal-dependent mechanism,

such as AV nodal reentry or orthodromic reentry. Some atrial arrhythmias that are not dependent

on the AV node, such as focal atrial tachycardia, may also terminate when vagal maneuvers are

applied.

1.2 Use physical exam to look for cardiac and noncardiac causes of SVT.

Recommendations

• On physical exam, look for:

Valvular abnormalities

Evidence of congestive heart failure

Lung disease

Signs of hyperthyroidism

Evidence

• Organic heart disease is common in adults with intra-atrial reciprocating tachycardias (6.)

Rationale

• Patients with atrial dysrhythmias may have structural heart disease, lung disease, or metabolic

disorders, such as hyperthyroidism.

• The presence of structural heart disease, lung disease, or metabolic disorders may also increase in

frequency with other mechanisms of SVT.

1.3 In hemodynamically compensated patients with recurrent well-tolerated

symptoms, use an electrocardiographic recording device to confirm the presence of a cardiac dysrhythmia, and to identify its cause.

Recommendations

• Consider using an electrocardiographic recording device, such as a Holter monitor or event

recorder, in patients with symptoms suggestive of SVT.

• Consider using a cardiac event recorder rather than a Holter monitor for patients with infrequent

symptoms.

• See table Diagnostic Tests for SVT.

Evidence

• In one study of 518 consecutive ambulatory ECGs, 34% of patients who had typical symptoms

during the monitoring period had no correlating cardiac dysrhythmia (7).

• A review article discusses the electrocardiographic characteristics for different types of SVT (8).

• Three studies (of 184, 105, and 65 patients, respectively) found cardiac event recorders to be cost

effective and useful in the evaluation of patients with palpitations, syncope, and near syncope (9;

10; 11).

Rationale

• Symptoms such as palpitations or near syncope can occur during the basal rhythm and may not be

due to a cardiac dysrhythmia.

• Unless a patient's symptoms occur daily, it is unlikely that a patient would have symptoms during

the short monitoring period of ambulatory (Holter) electrocardiograms.

• An externally worn ambulatory loop recorder is a Holter-like device that continuously records the

patient's rhythm. When triggered, it saves for analysis as much as several minutes' worth of the

rhythm immediately prior to and following activation. These devices are most useful in the case of

short-duration symptoms and near or brief syncope.



Page 4 of 38

• Because patients often use nonspecific terms to describe symptoms, it is important to ascertain

that the symptoms reported during the monitoring period are the same as those for which the

patient initially sought evaluation.

1.4 Recognize that symptoms associated with cardiac arrhythmias can be

caused by other disease states.

Recommendations

• Consider other causes when the patient's symptoms cannot be correlated with a cardiac

arrhythmia.

• See table Differential Diagnosis of Symptoms Associated with SVT.

Evidence

• In a study of 190 consecutive patients presenting with palpitations, 57% had palpitations of a

noncardiac etiology (13).

Rationale

• Symptoms such as palpitations can have other causes.

1.5 Recognize that SVT may be caused or exacerbated by other concurrent illnesses such as hyperthyroidism, infection, or anemia.

Recommendations

• Consider a secondary cause, such as hyperthyroidism, myocarditis, infection, or anemia in patients

presenting with SVT.

• Perform thyroid function tests on patients presenting with atrial fibrillation, and consider

performing them on patients with an atrial tachycardia or inappropriate sinus tachycardia.

Evidence

• Expert opinion advises seeking and treating precipitating or contributing disease states when

possible (4).

Rationale

• Treatment of a concurrent illness can decrease the severity and frequency of the cardiac

arrhythmia.

Comments

• Most patients with SVT do not have a concurrent illness or disease state precipitating or

exacerbating the arrhythmia. Arrhythmias more likely to be affected by concurrent illnesses or

diseases are atrial arrhythmias (such as atrial fibrillation or flutter), atrial tachycardia, and

inappropriate sinus tachycardia.

1.6 Use electrocardiographic recording methods to classify SVT as bypass-

tract mediated, atrial, or AV-nodal reciprocating.

Recommendations

• Use the electrocardiogram to subtype SVT by determining the relationship of the P wave to the

QRS complex.

• Attempt to classify SVT into one of three types:

Bypass-tract-mediated tachycardias, also called ‘AV reciprocating tachycardias,’ are reciprocating tachycardias in which the anterograde conduction (atria-to-ventricle) is typically via the AV node, and retrograde conduction is via the bypass tract. Because bypass-tract conduction is typically faster than conduction via the AV node, atrial activation occurs rapidly after the QRS complex, resulting in a ‘short RP’ tachycardia.



Page 5 of 38

Atrial tachycardias usually appear as a ‘long RP’ tachycardia, with a PR interval equal to or slightly longer

than normal. The P-wave morphology may be upright, biphasic, or inverted in the inferior leads, depending on the site of origin.

In AV-nodal reciprocating tachycardias, atrial and ventricular activation usually occur simultaneously, and atrial activation is not easily identified, because the P wave is ‘buried’ within or at the tail of the QRS. P-wave activation at the tail of the QRS may manifest as a pseudo-R-prime deflection in V1 and as a pseudo-S wave inferiorly.

• See table Differential Diagnosis of SVT Based on Electrocardiographic Features.

• See figure Mechanisms of SVTs.

• See figure Mechanism of AV Nodal Reentrant Tachycardia.

• See figure Atrial Flutter.

• See figure Automatic Atrial Tachycardia.

• See figure Atrial Tachycardia.

• See figure AV-Nodal Reentrant Tachycardia.

• See figure AV Reciprocating Tachycardia.

Evidence

• In one study comparing bypass-tract-mediated tachycardias with AV-nodal reciprocating

tachycardia, use of atrial activation as a guide to diagnosis was 75% accurate (14).

Rationale

• Different types of SVT require different treatment.

Comments

• There are several limitations to this approach to classification:

Because atrial activity is not always obvious, some ECGs without clear atrial activity may lead to an incorrect diagnosis of AV nodal reentry.

Approximately 5% (15) of bypass tracts have decremental (slow) conduction, and SVT associated with these bypass tracts can have a ‘long RP’ morphology on the ECG, suggesting atrial tachycardia.

Among AV-nodal reciprocating tachycardias, 5% are ‘atypical’ (anterograde conduction is via the fast AV nodal pathway) and are also manifested as ‘long RP’ tachycardia.

1.7 Consider vagal maneuvers or drug therapy with adenosine to further define an SVT.

Recommendations

• Consider using vagal maneuvers or drug therapy with agents such as adenosine to terminate SVT

or to elicit transient AV block.

• Be aware that, in general:

Termination of an SVT after administration of an AV-nodal blocking agent suggests that the mechanism is AV-nodal dependent.

Persistence of an SVT after such maneuvers or drug administration suggests that the mechanism is not AV-nodal dependent.

• See table Drug Treatment for SVT.

• See table Vagal Maneuvers for Terminating SVT.

Evidence

• The usefulness of adenosine as a diagnostic tool (by causing AV block in the AV node) has been

well described (16; 17).



Page 6 of 38

Rationale

• Bypass-tract-mediated tachycardias are dependent on an AV connection and ventricular activation;

therefore, AV block should result in termination of the tachycardia.

• AV-nodal reciprocating tachycardias are dependent on AV node activation and, therefore, would

also terminate with administration of an AV block maneuver.

• Atrial tachycardias, in contrast, are not dependent on ventricular activation via the AV node, nor

are they dependent on AV node activation, and will usually persist despite AV block.

Comments

• Some focal/automatic atrial tachycardias may be adenosine sensitive, and may result in

termination of the tachycardia rather than transient AV block.



Page 7 of 38

2. Consultation Top

Consider consultation with a cardiologist when it is important to make a definitive diagnosis in symptomatic patients with suspected SVT. Consider appropriate consultation for patients with structural heart disease, Wolff-Parkinson-White syndrome, or severe symptoms associated with episodes of SVT; patients who prefer catheter ablation to medical therapy; or patients whose noncardiac illnesses contribute to the severity or frequency of their arrhythmias.

2.1 Consider cardiology consultation for definitive diagnosis in patients with

suspected SVT and hemodynamic instability during episodes of tachycardia.

Recommendations

• Consider referral for electrophysiologic testing in patients who present with syncope or near

syncope.

Evidence

• In a study of 13 patients with AV-node reentry, 8 patients with AV reentry, and 1 patient with atrial

tachycardia, syncope during SVT was shown to be related more to vasomotor factors than to heart

rate, and patients with a history of syncope during SVT were more likely to have positive results in

head-upright tilt-table tests (18).

• In a study of 74 patients with Wolff-Parkinson-White syndrome, those with syncope were more

likely to have inducible sustained atrial fibrillation with rapid ventricular rate and hypotension (19).

Rationale

• Although the prognosis of SVT is usually excellent, patients with hemodynamic instability may

cause injury to themselves or others during episodes of arrhythmia.

2.2 Consult a cardiologist to obtain electrophysiologic evaluation when there is electrocardiographic evidence of pre-excitation (Wolff-Parkinson-White

pattern).

Recommendations

• Perform an electrophysiologic evaluation in patients with Wolff-Parkinson-White syndrome and

known or suspected tachyarrhythmias.

• Be aware that electrophysiologic evaluation is warranted in patients with pre-excitation and a

history of syncope or cardiac arrest, and in asymptomatic patients with pre-excitation who have a

family history of sudden cardiac death.

• Perform electrophysiologic evaluation in asymptomatic patients with pre-excitation, especially

those in high-risk occupations, in order to document the presence and properties of the bypass

tract.

• See figure Pre-excitation (Wolff-Parkinson-White Pattern).

Evidence

• The prevalence of atrial fibrillation in patients with symptomatic Wolff-Parkinson-White syndrome

ranges from 10% to 38% (20) and the incidence of sudden cardiac death in this syndrome is

approximately 0.15% per patient year (21).



Page 8 of 38

• In 1995, the ACC/AHA issued guidelines for clinical intracardiac electrophysiological and catheter

ablation procedures; electrophysiologic evaluation and ablation of the bypass tract is a Class I

recommendation (22). A 2003 ACC/AHA guideline also recommended additional evaluation of these

patients, but did not give specific diagnostic recommendations (23).

Rationale

• The presence of a bypass tract increases the risk of rapid bypass tract conduction during atrial

fibrillation.

• In high-risk occupations in which physical injury can occur to the patient or others because of the

onset of SVT or rapidly conducting atrial fibrillation, an electrophysiology study can demonstrate

the inducibility of SVT and assess the bypass tract's conduction properties.

Comments

• Not all patients with accessory AV pathways have evidence of pre-excitation. In such patients, SVT

can nevertheless occur because of the retrograde conduction of the pathway (impulse conduction

from ventricle to atrium). Such patients are said to have a ‘concealed accessory pathway’ because

a standard ECG does not show it. Such patients without manifest pre-excitation on ECG are at very

low risk of sudden death.

2.3 Consider cardiology consultation in patients with incessant tachycardia.

Recommendations

• Patients with incessant SVT should undergo echocardiography to evaluate LV function as well as

electrophysiologic evaluation.

Evidence

• In one series of 36 patients with paroxysmal junctional reciprocating tachycardia, 20% had LV

dysfunction with a mean ejection fraction of 28±6%. After successful ablation of the bypass tract,

LV function improved in all patients (mean ejection fraction, 51±16%) (24).

Rationale

• Incessant SVT, such as paroxysmal junctional reciprocating tachycardia, autonomic atrial

tachycardia, and chronic atrial fibrillation or flutter with poorly controlled ventricular response

rates, may result in a tachycardia-induced cardiomyopathy.

• Typically, incessant SVT must persist for weeks, months, or longer, depending on the rate of the

arrhythmia.

• The LV function may normalize if these arrhythmias are treated before the LV dysfunction becomes

severe.

Comments

• Although some tachycardias may cause LV dysfunction, atrial arrhythmias, especially reciprocating

atrial dysrhythmias, are more prominent in patients with cardiomyopathies of other etiologies.

2.4 Consult a cardiologist or electrophysiologist for patients with structural heart disease, Wolff-Parkinson-White syndrome, or symptoms of

hemodynamic intolerance.

Recommendations

• Consider an electrophysiology study and radiofrequency ablation for patients who present with

syncope or near syncope or who have Wolff-Parkinson-White syndrome.

• Consider echocardiography and work-up of coronary artery disease for patients with symptoms of

congestive heart failure or angina during their arrhythmia.



Page 9 of 38

• Perform cardiac monitoring when initiating antiarrhythmic therapy for patients with structural heart

disease.

Evidence

• Patients who have syncope during SVT are more likely to have an inducible vasodepressor effect

during SVT, according to a study of 22 patients (18). In a study of 74 patients with Wolff-

Parkinson-White syndrome, patients with syncope were more likely to have inducible sustained

atrial fibrillation with rapid conduction and hypotension (19).

• A study of 39 patients found that antiarrhythmic agents, such as flecainide, may be effective in

decreasing the recurrence of atrial arrhythmias in as many as 90% of patients (43).

• Catheter ablation was curative for most patients with SVT and those with Wolff-Parkinson-White

syndrome in a study of 1050 patients (33).

Rationale

• Patients with syncope or near syncope are more likely to have poorly tolerated recurrences; thus,

definitive therapy may be warranted.

• Patients with structural heart disease are more likely to have severe symptoms associated with

arrhythmia, such as angina or congestive heart failure.

• Proarrhythmic side effects due to antiarrhythmic therapy are more likely to occur in patients with

structural heart disease.

2.5 Consider consulting a cardiologist or electrophysiologist for patients with

drug-resistant supraventricular arrhythmias or intolerance to pharmacologic

therapy.

Recommendations

• Consider consultation for patients who do not respond to initial trials of therapy or who do not wish

to be treated pharmacologically.

• Recognize that catheter ablation techniques may be required to prevent recurrent arrhythmias.

• Note that catheter ablation of the SVT also may be preferable to chronic treatment with type IA,

IC, and III antiarrhythmic agents because of their potential side effects.

Evidence

• Success rates of 96% for AV-nodal tachycardia, greater than 90% for AV nodal tachycardia, 93%

for atrial flutter, and greater than 75% for atrial tachycardias have been reported using

radiofrequency catheter ablation, along with complication rates of less than 2% (33; 44). Similar

results have been obtained using transvenous cryoablation (22; 45).

• A study involving 15 patients suggested that radiofrequency catheter ablation is cost-effective in

patients with symptomatic drug-refractory SVT (34).

Rationale

• Patients who do not respond to first-line agents, such as β-blockers and calcium antagonists, may

require more aggressive therapy with antiarrhythmic agents or an electrophysiology study with

catheter ablation.

• The safety, efficacy, and cost effectiveness of radiofrequency catheter ablation therapy makes this

procedure a reasonable first-line treatment.

Comments

• Asymptomatic patients with pre-excitation who do not have high-risk occupations may also warrant

catheter ablation if the presence of an ECG abnormality or risk of an arrhythmia affects their

insurability or mental well being or threatens other important activities (46).



Page 10 of 38

2.6 Refer to appropriate subspecialists those patients whose concurrent,

noncardiac illnesses contribute to their arrhythmias.

Recommendations

• Consider consultation for patients with atrial dysrhythmias and concurrent illnesses, such as

hyperthyroidism or lung disease.

Evidence

• Atrial dysrhythmias, including atrial fibrillation, may occur in up to 15% of patients with

hyperthyroidism (47).

Rationale

• Treat any contributing illness to improve the efficacy of SVT treatment.



Page 11 of 38

3. Hospitalization Top

Hospitalize patients with SVT who have significant cardiac diseases or severe cardiac symptoms during episodes of arrhythmia.

3.1 Hospitalize patients with specific subtypes of SVT, and those with congestive failure or hemodynamic instability.

Recommendations

• Hospitalize patients with Wolff-Parkinson-White syndrome and atrial fibrillation and patients with

pre-excited (antidromic) tachycardias requiring urgent cardiology evaluation, antiarrhythmic drug

therapy, or catheter ablation.

• Consider hospitalization for electrophysiologic study of patients with symptoms of unstable angina

or congestive heart failure during episodes of arrhythmia.

Evidence

• Retrospective studies of patients with Wolff-Parkinson-White syndrome and ventricular fibrillation

show a higher likelihood of both AV reentry and atrial fibrillation, as well as multiple bypass tracts

and rapid conduction over the bypass tract during atrial fibrillation (25).

Rationale

• Rapidly conducting atrial fibrillation due to Wolff-Parkinson-White syndrome may cause a

degeneration of the arrhythmia to ventricular fibrillation and sudden death. Furthermore, treatment

may require catheter ablation or potent antiarrhythmic agents that necessitate monitoring.

• SVT may provoke myocardial ischemia or congestive heart failure in patients with coronary artery

disease or LV dysfunction. Furthermore, the SVT may not be tolerated as well in patients with

coexisting cardiac disease.

Comments

• Patients with pre-excitation and atrial fibrillation and almost all other patients with Wolff-Parkinson-

White syndrome are best treated in the long term with radiofrequency catheter ablation (23).



Page 12 of 38

4. Therapy Top

Recognize that nonpharmacologic treatment may decrease the frequency of episodes of SVT or help terminate them, and consider using pharmacologic therapy to decrease the frequency and severity of symptoms associated with SVT.

4.1 Recommend that patients avoid catecholamines and caffeine, since they

can provoke some SVTs.

Recommendations

• Instruct patients with a history of SVT associated with certain foods or drugs to avoid those

substances.

Evidence

• Expert opinion and experience have demonstrated that exogenous catecholamines, dietary

substances, and drugs might provoke some supraventricular arrhythmias (26).

Rationale

• Advise patients not definitively treated to avoid substances known to provoke their arrhythmias.

4.2 Consider using vagal techniques, such as carotid massage and Valsalva

maneuvers, to terminate AV-nodal-dependent tachycardia.

Recommendations

• Consider teaching patients with well-tolerated AV-nodal-dependent SVT to use the Valsalva

maneuver or carotid massage to help terminate episodes of arrhythmia.

• Avoid carotid massage in patients with known carotid disease or carotid bruits.

Evidence

• In one study, as many as 53% of AV reciprocating tachycardia episodes and 33% of AV-nodal

reciprocating tachycardia episodes were terminated by means of vagal maneuvers (27).

• Another study demonstrated a 28% success rate in terminating tachycardias with either carotid

sinus massage or Valsalva maneuver (28).

Rationale

• Vagal maneuvers may terminate an episode of SVT by slowing AV nodal conduction and increasing

AV nodal refractoriness.

Comments

• The effect of vagal maneuvers can be enhanced with the administration of an AV-nodal blocking

agent. (See information on AV-nodal blocking agents in nodal-dependent arrhythmias). Carotid

sinus pressure should not be applied in patients suspected of having carotid disease or carotid

bruits because it could provoke a cerebral ischemic event.

4.3 Use AV-nodal blocking agents, preferably non-dihydropyridine calcium

channel blockers or β-blockers, to control symptoms in patients with AV-node-dependent arrhythmia.

Recommendations

• Consider a non-dihydropyridine calcium channel blocker (such as verapamil or diltiazem) as a first-

line agent to treat patients with AV-nodal reciprocating tachycardia.



Page 13 of 38

• Consider using a course of AV-nodal blocking agents to prevent recurrences, or acutely for

termination of arrhythmia when it occurs.


• See table Pharmacologic Drug Interactions for SVT.

Evidence

• As many as 71% of patients with AV-nodal reciprocating tachycardia may show at least some

improvement in their symptoms, according to one study of 17 patients with paroxysmal SVT (29).

However, most patients will not have complete suppression of symptoms with medical therapy

alone.

Rationale

• AV-nodal blocking agents slow and terminate tachycardia or prevent recurrence by slowing

conduction and increasing refractoriness in the AV node.

Comments

• There is a general lack of large, well-done studies.

4.4 Use catheter ablation in patients with hemodynamically unstable AV-node

related SVT, and consider its use in those with recurrent symptomatic AV-node dependant SVT.

Recommendations

• Perform ablation in patients with AV-nodal tachycardia who are hemodynamically unstable.

• Consider ablation in patients with recurrent symptomatic AV-nodal tachycardia.

Evidence

• The ACC/AHA/ESC guidelines for the management of supraventricular arrhythmias recommend

catheter ablation (23).

• An observational study of catheter ablations observed the highest rates of complications among

patients with modification of the AV junction (30).

• A registry of 3357 patients who underwent ablative procedures found high rates of success (94 to

97%) in procedures for SVT (31).

• An observational study of 379 consecutive patients receiving ablation for AV-node-dependant SVT

found a 97% success rate and a 0.8% rate of complete heart block (32).

• An observational study of 1050 patients who underwent ablation for AV-nodal reciprocating

tachycardias found that 996 were successful, with 32 major complications. (33)

• A study involving 15 patients suggested that radiofrequency catheter ablation is cost-effective in

patients with symptomatic drug-refractory SVT (34).

Rationale

• Catheter ablation eliminates arrhythmias in the majority of patients.

4.5 Consider using class IC antiarrhythmic agents flecainide and propafenone for patients with bypass-tract-mediated tachycardias who are not candidates

for catheter ablation.

Recommendations

• Consider use of class III drugs, such as amiodarone, sotalol, and dofetilide, in specific cases.



Page 14 of 38

• Recognize that long-term treatment using class I and class III antiarrhythmic agents may be

limited by the side effects of these agents and their potential to cause proarrhythmia.



Evidence

• The 2003 ACC/AHA and European Society of Cardiology (ESC) guidelines for the management of

supraventricular arrhythmias advise specific therapies (23). Catheter ablation is the treatment of

choice for most patients with bypass-tract-mediated tachycardias.

• Flecainide has been shown to prevent or slow the inducibility of AV reciprocating tachycardia in

70% of patients (35; 36). Most patients are not rendered free of arrhythmia symptoms.

Rationale

• Class I and class III antiarrhythmic agents terminate tachycardia by increasing the refractory

period of AV accessory pathways, as well as by slowing AV nodal conduction.

Comments

• Because of their proarrhythmic side effects, initiate class III and class IA agents (except

amiodarone) while the patient is being monitored in the hospital. Women have an increased risk of

torsades de pointes with these agents, and initial dosages for women may need to be lower than

for men. Renal insufficiency and heart failure also increase the risk of torsades de pointes with

these agents.

4.6 Consider using class I and class III antiarrhythmic agents to treat atrial arrhythmias (particularly reciprocating atrial arrhythmias).

Recommendations

• Consider amiodarone for patients with atrial dysrhythmias and structural heart disease.

• In patients without LV dysfunction, consider other antiarrhythmic agents because of the potential

long-term toxicity of amiodarone.



Evidence

• Proarrhythmia occurs more frequently in patients with structural heart disease. This effect can be

seen with both class I (35) and class III agents (37).

Rationale

• Amiodarone has the least proarrhythmic effect in patients with LV dysfunction and structural heart

disease.

Comments

• The initiation of class III and IA agents should generally occur in a hospital setting. (See

information on proarrhythmic side effects.) Specific recommendations concerning the treatment of

atrial fibrillation and flutter is discussed in the Atrial Fibrillation module.

http://pier.acponline.org/physicians/diseases/d027/d027.html



Page 15 of 38

5. Patient Counseling Top

Inform patients with paroxysmal SVT about its mechanism, treatment, and prognosis.

5.1 Inform patients of the prognosis of certain types of SVT.

Recommendations

• Assure young patients with lone paroxysmal SVT of their excellent prognosis.

• In particular, assure those with AV-nodal reciprocating tachycardia or AV reciprocating tachycardia

with normal cardiac function of their particularly good prognosis.

• Advise patients that their arrhythmias can be successfully managed with medications or cured with

catheter ablation.

• Inform patients, however, that atrial tachycardias are more commonly associated with structural

heart disease, and that incessant supraventricular arrhythmias may cause dilated cardiomyopathy.

• Advise patients with Wolff-Parkinson-White syndrome about the small but significantly increased

risk of sudden death, and refer such patients to a cardiologist for evaluation.

Evidence

• One study showed that age, organic heart disease, and recurrent syncope were associated with an

increased risk of cardiac death (38).

• In a population-based study of 113 people found to have Wolff-Parkinson-White syndrome over a

45-year period, sudden cardiac death was found to occur at the very low rate of 0.0015 per

patient-year (21).

Rationale

• Paroxysmal SVT, particularly AV-nodal reciprocating tachycardia or AV reciprocating tachycardia, is

commonly seen in patients with no other cardiac illness and does not cause other cardiac diseases,

unless the arrhythmia is incessant.

5.2 Advise patients of the potential side effects of antiarrhythmic agents.

Recommendations

• Advise patients taking class III or IA agents to avoid other QT-prolonging agents and certain other

drugs.

• Advise patients taking amiodarone to:

Use sunscreen on exposed skin

Have regular eye exams

Have periodic medical follow-up to screen for potential thyroid, hepatic, and pulmonary toxicity

Promptly report symptoms of pulmonary illness, such as persistent cough or exertional dyspnea


Evidence

• In one study, 4 of 12 patients who had syncope and polymorphic VT while taking sotalol were

concurrently taking another QT-prolonging agent (39).

• A review addresses drug-induced long QT syndrome and torsades de pointes (40).

• Although the benefit of screening for potential amiodarone toxicity is not known, screening is

generally advised (41; 42).



Page 16 of 38

Rationale

• The concurrent use of QT-prolonging agents and class III or class IA agents increases the risk of

proarrhythmia (torsades de pointes). Amiodarone is known to have a variety of potential cardiac

and noncardiac side effects, one of which is photosensitivity, which can occur even in cooler

climates.



Page 17 of 38

6. Follow-up Top

Schedule follow-up for patients with supraventricular arrhythmias in order to monitor them for recurrent arrhythmia, complications of arrhythmia, and drug toxicity.

6.1 Monitor patients taking antiarrhythmic drugs periodically for side effects,

and check digoxin levels periodically in patients receiving the drug.

Recommendations

• Be aware that digoxin levels are generally kept



Page 18 of 38

Recommendations

• Obtain a follow-up ECG in patients with recurrent symptoms who have previously undergone

bypass tract ablation for Wolff-Parkinson-White syndrome.

Evidence

• In an Italian study of 52 patients with Wolff-Parkinson-White syndrome who underwent

transcatheter ablation, evidence of pre-excitation demonstrated a recurrence of at least

anterograde conduction in patients with recurrent arrhythmias (51).

Rationale

• Bypass tracts that conduct in an anterograde direction show evidence of pre-excitation on the ECG,

and when conduction recurs following successful ablation, the ECG may again show pre-excitation.

Comments

• Some patients with pre-excitation and a recurrence of arrhythmia, after an initially successful

ablation, may have only a recurrence in retrograde conduction, which will be concealed on follow-

up ECGs. Therefore, when the patient has sinus rhythm, none of the hallmarks of ventricular pre-

excitation will be visible; nevertheless, the patient may be susceptible to the occurrence of AV-

reciprocating tachycardia.

6.4 Recognize that palpitations frequently occur following successful catheter ablation of a SVT.

Recommendations

• Note that the occurrence of brief symptoms, such as ‘skipped beats' is frequent and does not

necessitate further evaluation.

• Consider using a cardiac event recorder to evaluate frequent symptoms of longer duration.

• Consider having an electrophysiology study performed if the symptoms mimic the initial

arrhythmia.

Evidence

• In a study of 77 patients, recurrent palpitations following radiofrequency ablation occurred in as

many as 58% of patients, despite the fact that return of conduction within the ablated pathway

was demonstrated in fewer than 10% of patients (52).

Rationale

• Palpitations are a nonspecific symptom and may not necessarily be due to a recurrence of the

patient's SVT.



Page 19 of 38

References Top

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Page 22 of 38

Glossary Top

AV atrioventricular

BUN blood urea nitrogen

CBC complete blood (cell) count

ECG electrocardiogram

iv intravenous

LV

left ventricular

po oral

SVT supraventricular tachycardia

TSH

thyroid-stimulating hormone

VT ventricular tachycardia



Page 23 of 38

Tables Top

Diagnostic Tests for SVT

Test Notes

Electrocardiogram Pre-excitation on the electrocardiogram (Wolff-Parkinson-White pattern) demonstrates evidence of

accessory pathway conduction

Ambulatory electrocardiogram (Holter) Typical duration of no more than 24-48 hours; most useful for evaluating frequent symptoms

Event recorders (Ambulatory loop recorder) Long-term recording device for documenting infrequent symptoms

Implantable loop recorders A device implanted subcutaneously for as long as 4 years. Because it must be surgically implanted, this

device is best used for evaluating severe, infrequent cardiac symptoms, such as syncope

Exercise stress test Useful to evaluate patients with exertional or exercise-induced symptoms

Electrophysiology study Invasive procedure, useful as a diagnostic procedure for patients with severe symptoms or to

determine bypass-tract properties in asymptomatic patients with pre-excitation (Wolff-Parkinson-White

pattern) on ECG and high-risk occupations (12). Many forms of SVT may be ablated and eliminated by

the same procedure

Echocardiogram Noninvasive test to determine the presence of structural heart disease or valvular disease suggested by symptoms or physical findings

Thyroid function tests Some atrial arrhythmias, particularly atrial fibrillation, may be associated with hyperthyroidism

ECG = electrocardiogram; SVT = supraventricular tachycardia.



Page 24 of 38

Differential Diagnosis of Symptoms Associated with SVT

Disease Characteristics

SVT Palpitations and dizziness

Classified into 3 types based on mechanism: atrial; AV-nodal reciprocating; bypass-tract-mediated (AV

reciprocating)

Anxiety/panic disorder Palpitations and dizziness

Infrequent episodes of SVT are often mistakenly ascribed to this diagnosis

High sympathetic/catecholamine-induced states Palpitations

Examples include anemia, febrile states, hypoglycemia

Hyperthyroidism Palpitations

Consider abuse or illicit use of exogenous thyroid supplements

Ventricular tachycardia Palpitations, syncope, and near syncope, as well as any other symptoms that can occur with SVTs

The presence of structural heart disease is more common in ventricular than in supraventricular

arrhythmias (excluding atrial fibrillation and flutter)

Medications, drugs Palpitations, syncope, near syncope

Possible medications and drugs include epinephrine, ephedrine, aminophylline, atropine, thyroid

extract, monoamine oxidase inhibitors, tobacco, coffee, tea, alcohol, and illicit drugs (e.g., cocaine, amphetamines)

AV = atrioventricular; SVT = supraventricular tachycardia.

http://pier.acponline.org/physicians/diseases/d780/d780.htmlhttp://pier.acponline.org/physicians/diseases/d175/d175.html



Page 25 of 38

Drug Treatment for SVT

Drug or Drug Class Dosing Side Effects Precautions Clinical Use

AV-nodal blocking agents

Non-dihydropyridine calcium-

channel blockers

Bradycardia, hypotension, AV block,

edema, asystole, CNS side effects

Avoid with: Wolff-Parkinson-White

syndrome, advanced aortic stenosis.

Caution with: HF, hepatic disease,

reflux esophagitis. In elderly, start with

low dose

For AV-nodal reciprocating tachycardia

Diltiazem IV: 0.25 mg/kg IV over 2 min. After 15

min, may give 0.35 mg/kg IV over 2

min. Then, 5-15 mg/hr infusion for

maximum of 24 hrs

GI side effects

Verapamil (Calan) Treatment: 2.5-5 mg IV over 2 min.

May give 5-10 mg q15-30 min to a total of 20 mg. Prophylaxis: Oral

(regular-release): 240-480 mg total

daily dose, dosed tid-qid

Constipation, allergic-type reactions Caution with: CKD, neuromuscular

disease

β-blockers Bradycardia, hypotension, AV block,

bronchospasm (particularly if

nonselective), CNS side effects,

diarrhea, nausea


syndrome. Caution with: CKD, HF,

hepatic disease, hyperthyroidism,

depression

Esmolol (Brevibloc) 500 μg/kg IV loading dose over 1 min.

Then, 50 μg/kg·min infusion for 4 min.

May repeat q5min, and gradually

increase infusion up to 200 μg/kg·min

Injection site reactions β1 selective. Extremely short acting

Metoprolol (Lopressor) IV: 5 mg IV over 1-2 min, every 5 min

prn, for up to 3 doses total. Oral

(regular-release): 25-100 mg bid

Oral: Abrupt withdrawal not advised β1 selective

Nadolol (Corgard) Prophylaxis: 80-160 mg qd Abrupt withdrawal not advised Nonselective. Longest half-life in class

Propranolol (Inderal) IV: 1-3 mg IV (1 mg/min). Second

dose prn in 2 min. Then, q4hr prn. Oral (immediate-release): Initially 10-30

mg tid-qid. Up to 160-320 mg total

daily dose, dosed tid-qid

Oral: Abrupt withdrawal not advised Nonselective

Cardiac Glycoside

Digoxin (Lanoxin) IV or oral loading dose: Total of 10-15

μg/kg, split into 3 divided doses q6-

8hr, with the first dose equal to half

the total. IV or capsule maintenance

dose: 125-350 μg total daily dose,

(depending on CrCl), dosed qd-bid.

Tablet or elixir maintenance dose: 125-

500 μg qd, depending on CrCl

Arrhythmias, bradycardia, AV block, GI

side effects, CNS side effects, visual

disturbances


syndrome, ventricular fibrillation. Many

drug interactions. Narrow therapeutic

index. Dose based on CrCl and LBW.

Decrease dose in CKD. Caution with

elderly

Other



Page 26 of 38

Adenosine (Adenocard) 6 mg IV bolus followed by 20 mL saline

flush, then 12 mg IV bolus prn. May repeat 12 mg IV bolus once prn

Flushing, dyspnea, hypotension, AV

block, transient arrhythmias

Caution with: COPD, asthma Extremely short half-life. Can be useful

for making a diagnosis

Antiarrhythmics

Class Ia

Procainamide IV loading dose: 15-17 mg/kg IV infusion, infused at 20-30 mg/min. Or,

100 mg IV q5min slow IV push, up to

1000 mg maximum. IV maintenance:

1-4 mg/min (about 50 mg/kg·d)

continuous IV infusion

Arrhythmias, QT prolongation and TdP, AV block, hypotension, fever, hepatic

injury

Positive ANA titer, proarrhythmic effects, hematological disorders. Avoid

with peripheral neuropathy. Decrease

dose with: CKD, hepatic disease,

reduced cardiac output. Caution with

HF

Initiate while being monitored in the hospital

Class Ic Arrhythmias, QT prolongation and TdP,

HF, AV block, bradycardia, dizziness,

visual impairment

Avoid with structural heart disease, HF.

Decrease dose with hepatic disease

For patients with bypass-tract-

mediated tachycardias who are not

candidates for catheter ablation.

Consider for atrial arrhythmias

Flecainide (Tambocor) Prophylaxis: 50 mg q12hr. May

increase by 50 mg every 4 days.

Maximum 300 mg total daily dose

Nausea, vomiting Increased mortality, ventricular pro-

arrhythmic, hematological disorders,

pulmonary fibrosis. Caution with

CrCl60:

80 mg bid. May increase every 3 days,

up to 160 mg bid. Adults with CrCl 40-

60: 80 mg qd. May increase every 5-6 days, up to 160 mg qd

Bradycardia, hypotension, fatigue,

dyspnea, hypoglycemia

Oral: Cardiac monitoring required,

caution with CKD. Only Betapace AF

has patient PI (not Betapace). Clinical

response, CrCl, heart rate and QTc must be evaluated before initiating or

dose. Avoid with: CrCl



Page 27 of 38

Vagal Maneuvers for Terminating SVT

Maneuver Description

Valsalva Relatively deep inspiration followed by forced exhalation against a closed glottis for 5-10 seconds

Mueller Forced inspiration against a closed glottis for 5-10 seconds

Carotid sinus massage Unilateral carotid pressure

Face immersion Exposure of the face to ice water; the patient should not be alone when performing face immersion

Squatting/stooping

Gagging/vomiting

Breath holding



Page 28 of 38

Differential Diagnosis of SVT Based on Electrocardiographic Features

Disease Characteristics Notes

Atrial fibrillation, atrial flutter Atrial fibrillation is an irregular rhythm with no definitive P waves.

Atrial flutter typically has saw-tooth pattern flutter waves most

noticeable in the inferior leads

Atrial tachycardia (automatic) Long R-P tachycardia. Tends to be incessant with spontaneous

acceleration and deceleration. P-wave morphologies may vary,

depending on their site of origin. Inappropriate sinus tachycardia

has normal P-wave morphology, similar to that of normal sinus

rhythm

Atrial tachycardia (triggered) Long R-P tachycardia. Digitalis toxicity may cause a triggered

arrhythmia and should be considered as a cause in atrial tachycardia and spontaneous AV block

Commonly associated with structural heart disease

Atrial tachycardia (reciprocating) Long R-P tachycardia Commonly associated with structural heart disease

AV-nodal reentrant tachycardia In the typical variety, the atria and ventricles are simultaneously

activated, and either no P wave is visible, or a small pseudo r-prime deflection in lead V1 and a pseudo S-wave deflection inferiorly are

seen. In atypical AV-nodal reentrant tachycardia, the ECG may

show a “long RP” tachycardia with an inverted P wave inferiorly

AV reciprocating tachycardia, also known as bypass-tract-mediated In this short R-P tachycardia, the P wave is usually located within

the ST segment. Slowly conducting bypass tracts may have a “long

RP” appearance, but these are uncommon and account for ~5% of

such arrhythmias. AV reentry with anterograde conduction via the

AV node is called orthodromic; rarely, AV reciprocating arrhythmias

may be antidromic, with anterograde conduction occurring via the

accessory pathway

Accessory AV pathways can conduct either anterograde (atrium to

ventricle), retrograde (ventricle to atrium), or in both directions.

Only accessory pathways with anterograde conduction will show

pre-excitation (Wolff-Parkinson-White pattern) on the sinus rhythm

ECG

AV = atrioventricular; ECG = electrocardiogram.



Page 29 of 38

Pharmacologic Drug Interactions for SVT

Antiarrhythmic Agent Clearance Drugs That Increase the Level of

the Antiarrhythmic Agent

Drugs That Decrease the Level of

the Antiarrhythmic Agent

Effect of the Antiarrhythmic Agent

on Other Drugs

AV-nodal blocking drugs

Verapamil Liver (CYP3A3/4 and CYP1A2) CimetidineErythromycinKetoconazoleCl

arithromycin

PhenobarbitalRifampinPhenytoin Increases the level of cyclosporine ,

digoxin , quinidine , ethanol

Diltiazem Liver (CYP1A2) Moricizine Increases the level of cyclosporine ,

digoxin

Digoxin Renal

Liver (30%)

AmiodaroneQuinidinePropafenoneVerap

amilDiltiazemFlecainide

Rifampin (digitoxin)

PhenytoinCholestyramineKaolin-

pectinSulfasalazineNeomycin

Propranolol Liver (CYP2D6) FlecainidePropafenoneQuinidineCimetid

ine

CholestyramineColestipol

Class I antiarrhythmics

Procainamide Procainamide : urine, liver (acetylation

to NAPA)

NAPA: cleared renally

AmiodaroneCimetidineTrimethoprimQui

nidine

Ethanol Can prolong the QT interval in

combination with phenothiazine,

tricyclic antidepressants

Flecainide Liver (CYP2D6) AmiodaroneQuinidine Smoking Ritonavir : increase flecainide-induced

cardiotoxicity

Propranolol : increased β-blocker toxicity

Propafenone Liver (CYP2D6 – inhibitor and substrate)

QuinidineCimetidine Rifampin Warfarin : increases plasma thromboplastin

Digoxin : increases digoxin level

Propranolol : increases β-blocker

toxicity

Class III antiarrhythmics

Sotalol Renal Can prolong the QT interval in

combination with phenothiazine,

tricyclic antidepressants

Amiodarone Liver Cimetidine Cholestyramine Warfarin : increases plasma

thromboplastin

Digoxin : increases digoxin level

Phenytoin : increases phenytoin level

Theophylline : increases theophylline

level

Procainamide : increases procainamide

level

Quinidine : increases quinidine level

NAPA = n-acetyl procainamide.



Page 30 of 38



Page 31 of 38

Figures Top

Mechanisms of SVTs

A differential diagnosis of the mechanism of SVT is shown based upon the relationship of the P wave (atrial activity) to the QRS. Solid arrows demonstrate the position of the visible P waves and the open arrows show the position of atrial activity hidden within the QRS. (Lead II electrograms are shown).

AV = atrioventricular; SVT = supraventricular tachycardia.



Page 32 of 38

Atrial Flutter

A 12-lead electrocardiogram shows atrial flutter. Flutter waves (saw-tooth pattern of atrial activity) are best seen in the inferior leads–II, III, and aVF.



Page 33 of 38

Automatic Atrial Tachycardia

Automatic atrial tachycardia is shown in a patient who has hyperthyroidism. Atrial activity (P waves) can be seen between the R waves in lead II.



Page 34 of 38

AV-Nodal Reentrant Tachycardia

The common form of AV nodal reentrant tachycardia is shown. Atrial activation occurs simultaneously with ventricular activation, such that no clear atrial activity can be seen.

AV = atrioventricular.



Page 35 of 38

AV Reciprocating Tachycardia

AV reciprocating tachycardia, utilizing a left free wall bypass tract is shown. Atrial activity can be seen early in the ST segment, especially in leads I, II, and V1.

AV = atrioventricular.



Page 36 of 38

Pre-excitation (Wolff-Parkinson-White Pattern)

The sinus rhythm tracing is shown of a patient who has a right-sided bypass tract. Positive delta waves (initial up sloping of the QRS) with a short PR interval are seen in leads I, II, aVL and precordial leads V2-V6. Negative delta waves (an initial negative deflection) are seen in leads III, aVF and aVR, giving the appearance of an inferior infarct pattern.



Page 37 of 38

Atrial Tachycardia

Atrial tachycardia is caused by an ectopic focus or area of micro-reentry that fires faster than the sinus rate. Electrocardiogram shows atrial tachycardia treated with adenosine. The arrows show P waves in the absence of QRS complexes owing to adenosine-induced AV block.



Page 38 of 38

Mechanism of AV Nodal Reentrant Tachycardia

Mechanisms of typical atrioventricular nodal reentrant tachycardia. The slow pathway has a short refractory period and the fast pathway has a long refractory period. The blue line represents antegrade conduction down the slow pathway; conduction does not occur down the fast pathway because it is refractory. The yellow line represents impulse conduction into the ventricle and retrograde up the fast pathway, which is no longer refractory. The red line represents completion of the circuit with activation of the atria and ventricles.

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