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.
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.
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.)
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.)
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.)
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.
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.
Delbert D. Clark, DO, FAAEM; Morgan McGuire, MD; Mary Jones, MD; Heather Bruner, MD, FAAEM; David Bruner, MD, FAAEM
James E. Morris, MD, MPH; Jennifer White, MD
August 1, 2020
September 1, 2023
4 AMA PRA Category 1 Credits™, 4 ACEP Category I Credits, 4 AAFP Prescribed Credits, 4 AOA Category 2-A or 2-B Credits
Date of Original Release: August 1, 2020. Date of most recent review: July 10, 2020. Termination date: August 1, 2023.
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