SVT (Supraventricular Tachycardia) - Adult

Quick Reference Card

Critical Alerts

⚠️ Red Flag: - Unstable = Cardiovert NOW: Hypotension (SBP less than 90), altered mental status, severe chest pain, acute heart failure

• Adenosine is diagnostic AND therapeutic: Terminates most re-entrant SVTs
• Give adenosine RAPIDLY: Push fast with immediate 20mL NS flush, via antecubital vein closest to heart
• Wide complex SVT may be VT: If uncertain, treat as VT (safer approach)
• Vagal maneuvers first: Safe, effective in up to 43% with modified Valsalva technique [1]
• WPW with AF is LIFE-THREATENING: AVOID all AV nodal blockers - can precipitate VF

Key Diagnostic Features

Emergency Treatment Algorithm

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Overview

Supraventricular tachycardia (SVT) represents a heterogeneous group of arrhythmias arising from or involving atrial tissue or the atrioventricular (AV) junction, characterised by a heart rate exceeding 100 bpm with QRS complexes typically narrower than 120 milliseconds. [2] In clinical practice, the term "SVT" commonly refers specifically to paroxysmal supraventricular tachycardia (PSVT), encompassing atrioventricular nodal re-entrant tachycardia (AVNRT), atrioventricular re-entrant tachycardia (AVRT), and focal atrial tachycardia. [3]

SVT represents one of the most common arrhythmias encountered in emergency departments and primary care, affecting approximately 2.29 per 1,000 persons in the general population. [4] While generally considered benign with a low mortality risk in structurally normal hearts, SVT causes significant morbidity through debilitating symptoms, impaired quality of life, and rarely, tachycardia-induced cardiomyopathy with prolonged uncontrolled episodes. [5] The condition is particularly amenable to curative therapy with catheter ablation, which has transformed the management paradigm from lifelong medication to definitive single-procedure treatment for appropriate candidates. [6]

Understanding the electrophysiological mechanisms underlying different SVT subtypes is crucial for acute management, as therapeutic interventions target specific components of the re-entrant circuit or automaticity focus. The ability to rapidly recognise, stabilise, and appropriately manage SVT is a core competency for emergency physicians, cardiologists, and general internists. [3]

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Epidemiology

Prevalence and Incidence

Demographics and Distribution

Age Distribution:

• AVNRT: Peak incidence in adults aged 30-50 years; more common in middle-aged women
• AVRT: More common in younger patients (adolescents and young adults)
• Atrial tachycardia: Can occur at any age; focal AT more common in elderly

Sex Differences:

• AVNRT demonstrates 2:1 female predominance [4]
• AVRT shows slight male predominance due to WPW association
• Overall SVT risk 2-fold higher in women compared to men [4]

SVT Subtype Distribution:

Risk Factors

Predisposing Factors:

Exam Detail: High-Yield Epidemiological Points:

• The 2:1 female predominance in AVNRT is attributed to hormonal influences on AV nodal electrophysiology
• Ebstein's anomaly is associated with accessory pathways in 20-30% of cases, typically right-sided
• Athletes may have increased vagal tone, which can paradoxically facilitate SVT initiation by enhancing conduction heterogeneity
• First SVT episode commonly occurs between ages 12-30 years for AVRT and 30-50 years for AVNRT

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Classification

Mechanistic Classification

SVT Mechanisms:

Primary SVT Classification (Narrow Complex)

AVNRT (Atrioventricular Nodal Re-entrant Tachycardia):

AVRT (Atrioventricular Re-entrant Tachycardia):

Atrial Tachycardia:

Other Supraventricular Tachycardias (Broader Definition)

Clinical Pearl: Distinguishing SVT Subtypes:

• Rate of exactly 150 bpm should prompt consideration of atrial flutter with 2:1 AV block
• "Pseudo R' " in V1 or "pseudo S" in inferior leads suggests retrograde P waves of AVNRT
• Long RP interval (RP > PR) suggests atrial tachycardia or atypical AVNRT
• Alternating QRS amplitude during tachycardia ("electrical alternans") is common in AVRT at fast rates

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Pathophysiology

The Re-entry Mechanism

Prerequisites for Re-entry (All Must Be Present):

1. Two distinct pathways with different electrophysiological properties
2. Unidirectional block in one pathway (usually due to longer refractory period)
3. Slow conduction in the alternative pathway (allows recovery of blocked pathway)
4. Completed circuit enabling continuous circus movement

Initiation of Re-entry: A premature atrial contraction (PAC) arrives when the fast pathway is still refractory but the slow pathway has recovered. The impulse conducts anterograde down the slow pathway, allowing time for the fast pathway to recover, then conducts retrograde up the fast pathway to complete the circuit. [8]

AVNRT Electrophysiology

Dual AV Nodal Physiology: The AV node contains functionally distinct pathways:

• Fast pathway: Rapid conduction, longer refractory period (located superior/anterior)
• Slow pathway: Slow conduction, shorter refractory period (located inferior/posterior)

Typical AVNRT (Slow-Fast):

Exam Detail: Atypical AVNRT (Fast-Slow):

• Less common (5-10% of AVNRT cases)
• Antegrade conduction via fast pathway, retrograde via slow pathway
• Produces long RP tachycardia (RP > PR interval)
• Can be difficult to distinguish from atrial tachycardia or PJRT
• May not respond to typical slow pathway ablation; requires different ablation approach

AVRT and Accessory Pathway Physiology

Accessory Pathway Characteristics:

Orthodromic AVRT:

Antidromic AVRT:

WPW Syndrome: Delta Wave and Pre-excitation

Pre-excitation Physiology: During sinus rhythm, the ventricles are activated simultaneously via the AV node-His-Purkinje system AND the accessory pathway. The accessory pathway conducts faster, causing early ventricular activation (pre-excitation) manifested as:

WPW Classification by Pathway Location:

Critical Danger: WPW with Atrial Fibrillation

⚠️ Red Flag: Life-Threatening Scenario: When AF develops in a patient with WPW, the accessory pathway can conduct rapid atrial impulses directly to the ventricles without the protective rate-limiting function of the AV node.

Pathophysiological Cascade:

Why AV Nodal Blockers Are Dangerous:

• Block AV nodal conduction → paradoxically enhances accessory pathway conduction
• Adenosine, beta-blockers, calcium channel blockers, digoxin all contraindicated
• Can precipitate VF and sudden cardiac death [7]

Haemodynamic Consequences

Immediate Effects of Tachycardia:

Tachycardia-Induced Cardiomyopathy: Prolonged or frequent SVT episodes can lead to reversible ventricular dysfunction:

• Develops over weeks to months of uncontrolled tachycardia
• LVEF can decline to 20-30%
• Mechanism: Myocardial remodelling, calcium handling abnormalities
• Reversible with rate/rhythm control; may take 3-6 months to recover [9]

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Clinical Presentation

Symptoms

Cardinal Symptoms:

• instantly starts | | Lightheadedness/dizziness | 60-70% | Pre-syncopal sensation | | Dyspnoea | 50-60% | Air hunger, chest tightness | | Chest discomfort | 40-50% | Pressure, rarely true angina | | Anxiety/panic | 40-50% | Sense of impending doom | | Neck pulsations | 20-30% | "Frog sign"
• cannon A waves | | Polyuria | 20-50% | During or after episode (ANP release) |

Pathognomonic Features:

• Abrupt onset and termination: Unlike sinus tachycardia, SVT starts and stops instantaneously
• Polyuria: Release of atrial natriuretic peptide during atrial stretch
• "Flip" sensation: Moment of PAC initiation or sudden termination

Syncope:

• Relatively uncommon (less than 15%) in structurally normal hearts
• Higher risk with very fast rates (> 220 bpm)
• More common in elderly and those with structural heart disease
• Should prompt consideration of WPW with pre-excited AF [3]

History Taking

Essential Questions:

Physical Examination

Vital Signs:

Cardiovascular Examination:

Signs of Haemodynamic Instability:

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Red Flags and High-Risk Features

Immediate Life Threats

⚠️ Red Flag: Cardiovert Immediately If:

1. Haemodynamic instability: SBP less than 90 mmHg, signs of shock
2. Altered consciousness: Confusion, decreased GCS
3. Acute coronary syndrome: ST changes, troponin rise, ongoing ischaemic chest pain
4. Acute heart failure: New pulmonary oedema, cardiogenic shock
5. Pre-excited AF: Wide complex, irregular, variable QRS morphology

High-Risk Presentations

WPW Sudden Death Risk Stratification

High-Risk Accessory Pathway Features:

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Differential Diagnosis

Narrow Complex Tachycardia (QRS less than 120 ms)

Wide Complex Tachycardia (QRS ≥120 ms)

Clinical Pearl: Brugada Algorithm for Wide Complex Tachycardia:

1. Absence of RS complex in all precordial leads → VT
2. RS interval > 100 ms in any precordial lead → VT
3. AV dissociation → VT
4. Morphology criteria for VT in V1/V2 and V6 → VT

When in Doubt: Treat wide complex tachycardia as VT - it is safer to treat SVT as VT than to give AV nodal blockers to true VT [10]

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Investigations

Electrocardiogram (12-Lead ECG)

During Tachycardia - Systematic Analysis:

ECG Features by SVT Type:

Baseline ECG (Sinus Rhythm):

Laboratory Investigations

Additional Investigations

Echocardiography:

Ambulatory Monitoring:

Electrophysiology Study:

Exam Detail: EP Study Findings by SVT Type:

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Management

Principles of Acute Management

Stepwise Approach:

Unstable SVT: Immediate Synchronized Cardioversion

Indications (Any One):

• Hypotension (SBP less than 90 mmHg)
• Altered mental status
• Severe chest pain with ischaemic features
• Acute pulmonary oedema
• Signs of shock

Cardioversion Protocol:

Stable SVT: Vagal Maneuvers

Modified Valsalva Maneuver (REVERT Trial): [1]

The modified Valsalva technique significantly improves conversion rates compared to standard Valsalva (43% vs 17%, pless than 0.001).

Technique:

Other Vagal Maneuvers:

Stable SVT: Adenosine

Mechanism: Adenosine activates A1 receptors on AV nodal cells, increasing potassium conductance and hyperpolarising the cell membrane, resulting in transient AV nodal block. [11]

Dosing Protocol:

Dose Modifications:

Pre-Administration Counselling: Warn patient: "You will feel strange for a few seconds - chest tightness, flushing, and a sense that something is wrong. This is normal and lasts only seconds."

Responses to Adenosine:

Contraindications:

Clinical Pearl: Adenosine Administration Tips:

• Use the most proximal IV site possible (antecubital preferred over hand)
• Use a 3-way stopcock for simultaneous drug and flush delivery
• Have the patient's arm elevated during administration
• Keep defibrillator nearby (very rare VF reported)
• Record continuous rhythm strip during administration

Stable SVT: Second-Line Pharmacotherapy

If Adenosine Fails:

Calcium Channel Blockers (Non-dihydropyridine):

Diltiazem Infusion (for rate control): 5-15 mg/hour after bolus

Beta-Blockers:

Contraindications to Calcium Channel Blockers and Beta-Blockers:

WPW with Atrial Fibrillation: Specific Management

⚠️ Red Flag: NEVER GIVE to Pre-excited AF:

• Adenosine
• Beta-blockers
• Calcium channel blockers
• Digoxin
• Amiodarone (controversial, but many guidelines advise avoidance)

These agents block AV nodal conduction, paradoxically enhancing accessory pathway conduction and risking VF.

Safe Options:

Refractory or Recurrent SVT

Options:

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Long-Term Management

Lifestyle Modifications

Pharmacological Prophylaxis

Indications for Medical Therapy:

• Recurrent symptomatic episodes
• Patient preference over ablation
• Ablation not feasible or declined
• Bridge to ablation

Options:

Pill-in-Pocket Strategy: For infrequent episodes, patients can take a single dose of flecainide (200-300 mg) or propafenone (450-600 mg) at episode onset after initial supervised trial. [3]

Contraindications:

• Flecainide/propafenone contraindicated in coronary artery disease and structural heart disease
• Verapamil contraindicated in WPW syndrome

Catheter Ablation

Overview: Catheter ablation delivers radiofrequency or cryothermal energy to eliminate the arrhythmogenic substrate and is the definitive curative treatment for most SVTs. [6]

Success Rates:

Indications for Ablation (ESC 2019 Guidelines): [2]

Complications:

Exam Detail: Ablation Targets by SVT Type:

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Special Populations

Pregnancy

Considerations:

• SVT is the most common arrhythmia requiring treatment in pregnancy
• Haemodynamic changes increase arrhythmia susceptibility
• Fetal considerations affect drug and intervention choices

Management:

WPW Syndrome

Risk Stratification:

Management Approach:

Elderly

Considerations:

• More likely to have structural heart disease
• More sensitive to haemodynamic effects
• Higher drug sensitivity
• Greater risk of drug interactions

Modifications:

• Lower initial drug doses
• Avoid carotid massage if carotid disease suspected
• Consider ablation for recurrent episodes (effective and safe in elderly)
• Careful assessment for coronary artery disease

Paediatric SVT

Key Differences:

• AVRT more common than AVNRT (opposite of adults)
• WPW syndrome more prevalent
• Ice to face (diving reflex) effective vagal maneuver
• Adenosine dose: 0.1 mg/kg (max 6 mg), then 0.2 mg/kg (max 12 mg)
• Higher ablation success rates; procedure can be delayed until adolescence if symptoms controlled

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Prognosis

Natural History

Outcomes

Quality of Life:

• Significant impairment during episodes
• Inter-episode anxiety common
• Marked improvement after successful ablation [12]

Tachycardia-Induced Cardiomyopathy:

• Develops with prolonged uncontrolled SVT
• Reversible with rate/rhythm control
• Recovery of LV function typically over 3-6 months [9]

Sudden Cardiac Death:

• Rare in typical SVT (AVNRT, orthodromic AVRT)
• Risk present in WPW with AF (estimated 0.1-0.3% per year in symptomatic patients)
• Eliminated by successful accessory pathway ablation [7]

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Complications

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Follow-Up

Post-Episode Care

Monitoring

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Patient Education

Condition Explanation

Simple Explanation: "Your heart has an electrical 'short circuit' that sometimes makes it beat very fast. This is called SVT. While it feels scary, it's usually not dangerous in a healthy heart. We can often stop it with simple techniques or medications, and there's a procedure called ablation that can cure it permanently."

Self-Management Techniques

Teaching Modified Valsalva:

1. Sit up at a 45-degree angle
2. Take a deep breath and blow hard against resistance (like blowing up a balloon) for 15 seconds
3. Immediately lie flat and have someone lift your legs up
4. Hold for 15 seconds
5. Sit back up

When to Seek Emergency Care:

• Episode lasting > 15-20 minutes despite vagal maneuvers
• Feeling faint or actually fainting
• Severe chest pain
• Severe shortness of breath
• First episode ever (get evaluated)

Lifestyle Advice

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Viva Questions and Model Answers

Opening Statement

Viva Point: "Supraventricular tachycardia encompasses arrhythmias arising from above the ventricles, most commonly AVNRT and AVRT. These are typically benign re-entrant tachycardias that present with paroxysmal palpitations and are amenable to acute termination with vagal maneuvers or adenosine, and definitive cure with catheter ablation."

Common Viva Questions

Q1: How do you differentiate AVNRT from AVRT on the ECG?

Model Answer: "Both AVNRT and AVRT are regular narrow complex tachycardias that can be difficult to distinguish. Key differentiating features include:

• P wave location: In typical AVNRT, atrial and ventricular activation are nearly simultaneous, so P waves are buried within the QRS or appear immediately after as a pseudo R' in V1 or pseudo S in inferior leads. In orthodromic AVRT, the P wave typically appears in the ST segment after the QRS (short RP tachycardia) because the atria are activated later via the accessory pathway.

• RP interval: AVNRT typically has RP less than 70 ms or P wave buried in QRS. Orthodromic AVRT typically has RP 70-120 ms.

• Baseline ECG: Pre-excitation (delta wave) on the baseline ECG during sinus rhythm confirms an accessory pathway and makes AVRT more likely.

Definitive diagnosis requires an electrophysiology study."

Q2: A patient presents with an irregularly irregular wide complex tachycardia at 220 bpm. What is your approach?

Model Answer: "This presentation is concerning for pre-excited atrial fibrillation in a patient with WPW syndrome. The irregular rhythm with wide, variable QRS complexes at a very fast rate is highly suggestive of AF conducting via an accessory pathway.

My immediate approach:

1. Assess stability: If unstable, immediate synchronized DC cardioversion (120-200 J biphasic)
2. AVOID AV nodal blockers: Adenosine, beta-blockers, calcium channel blockers, and digoxin are absolutely contraindicated as they can accelerate accessory pathway conduction and precipitate VF
3. If stable: Procainamide (20-50 mg/min IV) or ibutilide (1 mg IV over 10 min) can be used
4. Prepare for defibrillation: Have defibrillator ready as VF can occur
5. Urgent EP referral: For definitive ablation of the accessory pathway

This is a life-threatening arrhythmia with risk of degeneration to VF and sudden cardiac death."

Q3: What is the mechanism of the modified Valsalva maneuver?

Model Answer: "The modified Valsalva maneuver works by manipulating autonomic tone to terminate re-entrant SVT:

1. Straining phase: Bearing down against resistance increases intrathoracic pressure, initially increasing venous return briefly, then decreasing it, leading to reduced cardiac output and reflex sympathetic activation.

2. Leg elevation and supine position: Immediately after straining, lying flat with passive leg raise causes a surge in venous return to the heart.

3. Vagal surge: This increased venous return stretches the right atrium and stimulates baroreceptors, triggering a reflex vagal response that slows conduction through the AV node.

4. Circuit interruption: This transient AV nodal block interrupts the re-entrant circuit, terminating the tachycardia.

The REVERT trial demonstrated that the modified technique (with leg elevation) achieves 43% conversion rate compared to 17% with standard Valsalva, making it the recommended first-line intervention." [1]

Q4: When would you recommend catheter ablation for SVT?

Model Answer: "According to ESC guidelines, catheter ablation is recommended in the following situations:

Class I indications:

• Symptomatic recurrent SVT when the patient prefers definitive therapy over long-term medication
• WPW with documented arrhythmias (SVT or AF)
• SVT with haemodynamic compromise

Class IIa indications:

• First documented SVT episode if patient prefers ablation
• Asymptomatic pre-excitation with high-risk features (short pathway refractory period, high-risk occupation)
• Pre-excitation in competitive athletes

Advantages of ablation:

• Curative in > 95% for AVNRT and 90-95% for AVRT
• Eliminates need for long-term medication
• Low complication rates (less than 1% AV block for slow pathway ablation)
• Improves quality of life

Relative contraindications:

• Very elderly with minimal symptoms
• Significant comorbidities precluding procedure
• Patient preference for medical management"

Common Mistakes That Fail Candidates

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Key Guidelines

ESC 2019 Guidelines for SVT Management [2]

ACC/AHA/HRS 2015 Guidelines [3]

Key differences and additions:

• Emphasis on adenosine as diagnostic tool (reveals underlying rhythm)
• Detailed recommendations for chronic management options
• Specific guidance on WPW risk stratification

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Quality Metrics and Documentation

Performance Indicators

Documentation Checklist

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Clinical Pearls Summary

Diagnostic Pearls

• Rate of exactly 150 bpm: Think atrial flutter with 2:1 block before assuming SVT
• Pseudo R' in V1: Classic for AVNRT (compare to baseline ECG)
• Wide complex + irregular: Pre-excited AF until proven otherwise - DO NOT give AV nodal blockers
• Adenosine is diagnostic: Watch carefully what happens (terminates vs reveals underlying rhythm)
• Compare to prior ECG: Identify pre-existing BBB or pre-excitation

Treatment Pearls

• Modified Valsalva superiority: Leg elevation is the key - nearly 3x more effective than standard
• Push adenosine FAST: Slow administration = metabolism before AV node = failure
• Warn the patient: "You'll feel strange for a few seconds"
• prevents panic
• When adenosine fails twice, move on: Rate control agents or cardioversion
• WPW + AF = Procainamide or shock: Never AV nodal blockers

Disposition Pearls

• Most stable SVT patients can go home: If converted, stable, simple episode
• Always teach vagal maneuvers: Empowers patients, reduces ED visits
• All SVT needs cardiology follow-up: Consider ablation for recurrence
• WPW needs EP referral: Even asymptomatic patients need risk stratification discussion

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References

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2. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. Eur Heart J. 2020;41(5):655-720. doi:10.1093/eurheartj/ehz467

3. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia. Circulation. 2016;133(14):e506-e574. doi:10.1161/CIR.0000000000000311

4. Orejarena LA, Vidaillet H Jr, DeStefano F, et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. 1998;31(1):150-157. doi:10.1016/S0735-1097(97)00422-1

5. Wood KA, Drew BJ, Scheinman MM. Frequency of disabling symptoms in supraventricular tachycardia. Am J Cardiol. 1997;79(2):145-149. doi:10.1016/S0002-9149(96)00699-7

6. Katritsis DG, Boriani G, Cosio FG, et al. European Heart Rhythm Association (EHRA) consensus document on the management of supraventricular arrhythmias, endorsed by Heart Rhythm Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS), and Sociedad Latinoamericana de Estimulación Cardiaca y Electrofisiología (SOLAECE). Europace. 2017;19(3):465-511. doi:10.1093/europace/euw301

7. Al-Khatib SM, Arshad A, Balk EM, et al. Risk Stratification for Arrhythmic Events in Patients With Asymptomatic Pre-Excitation: A Systematic Review for the 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia. Circulation. 2016;133(14):e575-e586. doi:10.1161/CIR.0000000000000309

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9. Gopinathannair R, Etheridge SP, Marchlinski FE, et al. Arrhythmia-Induced Cardiomyopathies: Mechanisms, Recognition, and Management. J Am Coll Cardiol. 2015;66(15):1714-1728. doi:10.1016/j.jacc.2015.08.038

10. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991;83(5):1649-1659. doi:10.1161/01.CIR.83.5.1649

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12. Bathina MN, Mickelsen S, Brooks C, Jaramillo J, Heywood T, Kusumoto FM. Radiofrequency catheter ablation versus medical therapy for initial treatment of supraventricular tachycardia and its impact on quality of life and healthcare costs. Am J Cardiol. 1998;82(5):589-593. doi:10.1016/S0002-9149(98)00416-0

13. Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary. Circulation. 2003;108(15):1871-1909. doi:10.1161/01.CIR.0000091380.04100.84

14. Chen SA, Chiang CE, Yang CJ, et al. Sustained atrial tachycardia in adult patients. Electrophysiological characteristics, pharmacological response, possible mechanisms, and effects of radiofrequency ablation. Circulation. 1994;90(3):1262-1278. doi:10.1161/01.CIR.90.3.1262

15. Calkins H, Yong P, Miller JM, et al. Catheter ablation of accessory pathways, atrioventricular nodal reentrant tachycardia, and the atrioventricular junction: final results of a prospective, multicenter clinical trial. Circulation. 1999;99(2):262-270. doi:10.1161/01.CIR.99.2.262

16. Jackman WM, Wang XZ, Friday KJ, et al. Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med. 1991;324(23):1605-1611. doi:10.1056/NEJM199106063242301

17. Link MS. Evaluation and Initial Treatment of Supraventricular Tachycardia. N Engl J Med. 2012;367(15):1438-1448. doi:10.1056/NEJMcp1111259

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19. Morady F. Catheter ablation of supraventricular arrhythmias: state of the art. J Cardiovasc Electrophysiol. 2004;15(1):124-139. doi:10.1046/j.1540-8167.2004.03394.x

20. Klein GJ, Bashore TM, Sellers TD, Pritchett EL, Smith WM, Gallagher JJ. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl J Med. 1979;301(20):1080-1085. doi:10.1056/NEJM197911153012003