Managing Supraventricular Tachydysrhythmias in the Emergency Department

Supraventricular Tachydysrhythmias in the Emergency Department

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Table of Contents
About This Issue

Patients presenting to the ED with supraventricular tachydysrhythmias (SVT) require prompt diagnosis of their underlying condition in order to determine the causes and to offer treatment that is not only effective, but takes into account their comfort and safety.

What are the primary ways to determine the cause of tachycardia?

What are the ECG characteristics that differentiate unifocal, junctional, and multifocal atrial tachycardia?

What is the difference between atrioventricular re-entry tachycardia (AVRT) and atrioventricular nodal re-entry tachycardia (AVNRT)? How does treatment differ?

How does a history of Wolff-Parkinson-White syndrome affect diagnosis and treatment of SVT?

What are the toxicologic, metabolic, and behavioral conditions that can present as SVT?

Is troponin testing necessary?

Why is large-bore, proximal IV access needed for patients with SVT?

How are narrow complex and wide complex tachycardia treatments different?

How are posture-modified vagal maneuvers performed?

When is adenosine indicated and when can (and should) it be delayed?

Vagal maneuvers, calcium channel blockers, beta blockers: what is the evidence on their effectiveness?

When should synchronized electrical cardioversion be the first-line treatment?

Table of Contents
  1. Abstract
  2. Case Presentations
  3. Introduction
  4. Critical Appraisal of the Literature
  5. Etiology and Pathophysiology
  6. Differential Diagnosis
    1. Atrioventricular Nodal Re-Entry Tachycardia
    2. Atrioventricular Re-Entry Tachycardia/Ventricular Pre-Excitation
    3. Pre-Excited States and Atrial Fibrillation
  7. Prehospital Care
  8. Emergency Department Evaluation
    1. History
    2. Physical Examination
  9. Diagnostic Studies
    1. Laboratory Testing
      1. Troponin Testing
    2. 12-Lead Electrocardiogram
    3. Chest Radiograph
  10. Treatment
    1. General Approach
    2. Vagal Maneuvers
    3. Pharmacotherapy
      1. Adenosine
        • Adenosine Side Effects
        • Adenosine Versus Calcium Channel Blockers
      2. Beta Blockers
    4. Synchronized Electrical Cardioversion
  11. Special Populations
    1. Supraventricular Tachycardia in Pregnant Patients
    2. Supraventricular Tachycardia in Pediatric Patients
  12. Controversies and Cutting Edge
    1. Intranasal Etripamil
    2. Patients With Asymptomatic Ventricular Pre-Excitation
    3. Anticoagulation for Patients With Paroxysmal Supraventricular Tachydysrhythmias
  13. Disposition
    1. Outpatient Monitoring
  14. Summary
  15. Time- and Cost-Effective Strategies
  16. Risk Management Pitfalls for Supraventricular Tachycardia in the Emergency Department
  17. Case Conclusions
  18. Disclaimer
  19. Clinical Pathways
    1. Clinical Pathway for Emergency Department Management of Patients With Narrow Complex Supraventricular Tachycardia
    2. Clinical Pathway for Emergency Department Management of Patients With Wide Complex Supraventricular Tachycardia
  20. Tables, Figures, and Appendix
    1. Table 1. Supraventricular Tachycardia Differential Diagnosis
    2. Table 2. Acute Pharmacotherapy for Narrow Complex Supraventricular Tachycardia
    3. Table 3. Recommendations for the Management of Asymptomatic Patients With Pre-Excitation
    4. Figure 1. Suspected Tachydysrhythmia
    5. Figure 2. Circus Movement Entry Arrhythmias
    6. Figure 3. Single-Lead Electrocardiogram Showing Sinus Node Re-Entry Tachycardia
    7. Figure 4. Electrocardiogram of Unifocal Atrial Tachycardia
    8. Figure 5. Electrocardiogram of Junctional Tachycardia
    9. Figure 6. Electrocardiogram of Multifocal Atrial Tachycardia With Additional Features of COPD
    10. Figure 7. Electrocardiogram of Slow-Fast (Typical) Atrioventricular Nodal Re-Entry Tachycardia
    11. Figure 8. Electrocardiogram of AVNRT With Left Bundle Branch Block
    12. Figure 9. Concealed Retrograde Conduction
    13. Figure 10. Pre-Excitation, Orthodromic, and Antidromic AVRT
    14. Figure 11. Electrocardiogram of Orthodromic (Antegrade) AVRT
    15. Figure 12. Electrocardiogram of Antidromic (Retrograde) AVRT With Wolff-Parkinson-White Syndrome
    16. Figure 13. Electrocardiogram of Wolff-Parkinson-White Syndrome With Atrial Fibrillation
    17. Figure 14. Sinus Electrocardiogram Status Post Conversion From Wolff-Parkinson-White Syndrome With Atrial Fibrillation
    18. Appendix 1. Class of Recommendation and Level of Evidence for AHA/ACC/HRS Guidelines
  21. References


Diagnosing and treating supraventricular tachycardias is routine in emergency medicine, and new strategies can improve efficiency and outcomes. This review provides an overview of supraventricular tachycardias, their pathophysiology, differential diagnosis, and electrocardiographic features. Clinical evidence guiding contemporary practice is determined largely by multiple observational studies, with few randomized controlled trials. Current prehospital and emergency department management strategies beyond the use of adenosine and calcium channel blockers are addressed. Diagnostic and therapeutic recommendations are provided, based on the best available evidence.

Case Presentations

A 31-year-old woman presents to the ED with palpitations. The ECG shows a regular, narrow complex tachycardia with a rate of 170 beats/min. She has a history of AV nodal re-entry tachycardia. Her vital signs are reassuring, with a blood pressure of 127/81 mm Hg. Adenosine has successfully converted her dysrhythmia in the past, but she asks whether there is an alternative treatment, because she hates the way it makes her feel. You are considering this patient’s request when another patient’s ECG is handed to you. (See Figure 1.)

The ECG belongs to a 49-year-old man who was brought in by ambulance for “lightheadedness.” The patient reports that he feels his “heart is pounding,” but he is not in extremis. He states he has not had these symptoms before and reports only a history of hypertension. His blood pressure is 141/89 mm Hg, and he appears stable. You suspect that this is a supraventricular tachydysrhythmia, but question yourself and wonder how best to make the diagnosis and treat it.


The complaint of “heart palpitations” accounts for an estimated 50,000 visits a year to emergency departments in the United States.1 While the complaint of palpitations is often benign, emergency clinicians must rapidly and accurately recognize and treat serious dysrhythmias to maximize good outcomes. Tachycardic dysrhythmias can be challenging, with one study reporting only 18% positive recognition of Wolff-Parkinson-White (WPW) syndrome in patients with concomitant atrial fibrillation.2

Supraventricular tachycardias (SVTs) are narrow complex dysrhythmias that are dependent on the atrioventricular (AV) node or atrial tissue for their genesis and continuation. Typically, patients with SVT are awake and stable, which provides time to consider treatment options, but patients who are unstable require immediate action. The first step in approaching the patient with SVT is to correctly identify the electrocardiogram (ECG) rhythm; misdiagnosis can lead to providing the wrong treatment and concomitant clinical deterioration. Treatment options for SVT are evolving, with the recent emergence of new Valsalva techniques and a renewed interest in calcium channel blockers (CCBs), both of which pose alternatives to adenosine in select patients. This issue of Emergency Medicine Practice provides a comprehensive review of the literature on SVT and an update on the advances and controversies of management.

Critical Appraisal of the Literature

Pertinent guidelines from American College of Cardiology (ACC), American Heart Association (AHA), Heart Rhythm Society (HRS), and European Society of Cardiology (ESC) were identified and reviewed. The terms paroxysmal tachycardia, reciprocating tachycardia, atrioventricular re-entry tachycardia, atrioventricular nodal re-entry tachycardia, sinoatrial nodal re-entry tachycardia, supraventricular tachycardia, junctional tachycardia, sinus tachycardia, pre-excitation, and Wolff-Parkinson-White were searched in Ovid MEDLINE®. The Cochrane Database of Systematic Reviews, the National Guidelines Clearinghouse, and Evidence-Based Medicine Reviews, Best Evidence (ACP), Database of Abstracts of Reviews of Effectiveness (DARE), and Evidence-Based Medicine Reviews Multifile (EBMZ) were also searched. Citations were limited to full text, English-language references relating to adult patients, from 1995 to March 2020; 449 abstracts were examined for relevance to emergency medicine. The final list included several well-designed randomized controlled trials, meta-analyses, and prospective studies providing robust evidence for Valsalva maneuvers, calcium channel blockers, and adenosine. There is a paucity of studies associated with other treatment strategies. The ACC/AHA/HRS classes of recommendation (COR) and levels of evidence (LOE) linked to specific treatments are provided when available. (See Appendix 1.)

Etiology and Pathophysiology

By definition, an SVT arises at or above the AV node. The tachycardias are divided into groups based on whether the QRS is narrow or wide (> 120 ms). SVTs occur by one of two mechanisms: (1) abnormal automaticity or (2) abnormal conduction. SVTs resulting from abnormal automaticity occur when sinoatrial (SA) nodal cells or an ectopic focus of cells rapidly generate action potentials that are then propagated through the normal conduction system. These include atrial fibrillation, atrial flutter, and atrial tachycardias as well as junctional tachycardia. SVTs resulting from abnormal conduction occur when the electrical impulse is propagated though an existing pathway that is typically refractory or through an accessory pathway. These pathways may be intranodal or extranodal and include atrioventricular re-entry tachycardia (AVRT) and atrioventricular nodal re-entry tachycardia (AVNRT).

Circus movement re-entry arrhythmias, or set conduction systems, follow a course of propagation around an anatomic or functional obstacle. They allow for a secondary pathway of electrical conduction that is subject to a cellular effective refractory period. Thus, each of these rhythms is dependent on allowing sufficient time for the cells to regenerate their action potential. In normal conduction, the impulse preferentially chooses the faster of the 2 conduction pathways. In the presence of an antegrade block, however, the slower re-entry pathway is chosen. This allows for the transition from the normal conduction pathway to the aberrant one. (See Figure 2.)

Differential Diagnosis

SVTs encompass a broad range of rhythms. While the term SVT is often used synonymously in reference to AVNRT or AVRT, there are other conditions that must be taken into account. (See Table 1. The ECG characteristics are noted in Figures 3, 4, 5, and 6.)

Table 1. Supraventricular Tachycardia Differential Diagnosis

Risk Management Pitfalls for Supraventricular Tachycardia in the Emergency Department

2. “That patient had WCT, so it must be ventricular tachycardia, SVT with aberrancy, antidromic AVRT, or WPW with atrial fibrillation.”

Don’t forget about other causes of WCT. Overdoses of myocardial sodium channel blockers, illicit substances such as cocaine, over-the-counter medications such as diphenhydramine, and tricyclic antidepressants can lead to WCT. WCT may also be the result of hyperkalemia and cardiac arrest post resuscitation. Ensure you get a good patient history and consider these diagnoses, as their management is acutely distinct and nuanced. It will save your patient and your license.

6. “The patient had a history of SVT and came in for a recurrence. She was otherwise stable and healthy. Why muck around with vagal maneuvers? I gave her a dose of adenosine to expediently treat her tachycardia. Why was she so angry afterwards?”

Adenosine is a useful agent, but the experience of its administration can be quite difficult and terrifying for patients. Not all patients are alike, and some would rather try some other strategies prior to committing to 6- or 12-mg of adenosine IV push and all that entails, especially if they have suffered through adenosine in the past. Be respectful and mindful of their wishes. Remember to treat the patient, and not just the dysrhythmia. In patients with a first-time occurrence of SVT, take the time to explain the possible symptoms they may experience when adenosine is administered. With patients with recurrent episodes, remind yourself to reassure them, address fears, and consider other management strategies. Vagal maneuvers can still work, and CCBs have become a great first-line option as well.

10. “I gave the patient with WPW and tachycardia a dose of adenosine. What can possibly go wrong?”

In patients with WPW, take care to ensure that they are not presenting with atrial fibrillation. Administering adenosine, beta blockers, or a CCB to patients presenting with WPW with atrial fibrillation/atrial flutter can lead to unimpeded impulse transmission over the accessory pathway, exceptionally high ventricular rates, and decline to ventricular fibrillation. Characterization of these arrhythmias on ECG can be challenging. If ever in doubt, Synchronized electrical cardioversion or defibrillation is the wisest choice.

Tables, Figures, and Appendix

Table 1. Supraventricular Tachycardia Differential Diagnosis


Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.

To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study is included in bold type following the references, where available. In addition, the most informative references cited in this paper, as determined by the author, are highlighted.

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Publication Information

Delbert D. Clark, DO, FAAEM; Morgan McGuire, MD; Mary Jones, MD; Heather Bruner, MD, FAAEM; David Bruner, MD, FAAEM

Peer Reviewed By

James E. Morris, MD, MPH; Jennifer White, MD

Publication Date

August 1, 2020

CME Expiration Date

August 1, 2023   

Pub Med ID: 32678566

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