Post on 06-Jun-2020
Quality Ratings: The preponderance of data supporting guidance statements are derived from:
level 1 studies, which meet all of the evidence criteria for that study type;
level 2 studies, which meet at least one of the evidence criteria for that study type; or
level 3 studies, which meet none of the evidence criteria for that study type or are derived from expert opinion, commentary, or consensus.
Study types and criteria are defined at http://smartmedicine.acponline.org/criteria.html
Disclaimer: The information included herein should never be used as a substitute for clinical judgement and does not represent an official position of the American College of Physicians. Because all PIER modules are updated regularly, printed web pages or PDFs may rapidly become obsolete.
Therefore, PIER users should compare the module updated date on the offical web site with any printout to ensure that the information is the most
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CME Statement: The American College of Physicians is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide
continuing education for physicians. The American College of Physicians designates this enduring material for a maximum of 1 AMA PRA Category 1
CreditTM. Physicians should claim only credit commensurate with the extent of their participation in the activity. Purpose: This activity has been
developed for internists to facilitate the highest quality professional work in clinical applications, teaching, consultation, or research. Upon completion
of the CME activity, participants should be able to demonstrate an increase in the skills and knowledge required to maintain competence, strengthen
their habits of critical inquiry and balanced judgement, and to contribute to better patient care. Disclosures: Joseph E. Marine, MD, current author of
this module, has no financial relationships with pharmaceutical companies, biomedical device manufacturers, or health-care related organizations. Deborah Korenstein, MD, FACP, Co-Editor, PIER, has no financial relationships with pharmaceutical companies, biomedical device manufacturers, or
health-care related organizations. Richard B. Lynn, MD, FACP, Co-Editor, PIER, has no financial relationships with pharmaceutical companies,
biomedical device manufacturers, or health-care related organizations.
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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
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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
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• 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.
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• 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.
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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).
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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.
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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).
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• 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.
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• 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).
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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.
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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).
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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.
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• Consider using a course of AV-nodal blocking agents to prevent recurrences, or acutely for
termination of arrhythmia when it occurs.
• See table Drug Treatment for SVT.
• 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.
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• 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.
• See table Drug Treatment for SVT.
• See table Pharmacologic Drug Interactions for SVT.
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.
• See table Drug Treatment for SVT.
• See table Pharmacologic Drug Interactions for SVT.
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
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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
• See table Pharmacologic Drug Interactions for SVT.
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).
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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.
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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
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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.
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References Top
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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
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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.
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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.
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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
Avoid with: Wolff-Parkinson-White
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
Avoid with: Wolff-Parkinson-White
syndrome, ventricular fibrillation. Many
drug interactions. Narrow therapeutic
index. Dose based on CrCl and LBW.
Decrease dose in CKD. Caution with
elderly
Other
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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
Supraventricular Tachycardia
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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
Supraventricular Tachycardia
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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.
Supraventricular Tachycardia
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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.
Supraventricular Tachycardia
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Supraventricular Tachycardia
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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.
Supraventricular Tachycardia
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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.
Supraventricular Tachycardia
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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.
Supraventricular Tachycardia
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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.
Supraventricular Tachycardia
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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.
Supraventricular Tachycardia
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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.
Supraventricular Tachycardia
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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.
Supraventricular Tachycardia
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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.