U.S. flag

An official website of the United States government

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Paroxysmal Supraventricular Tachycardia

; ; ; .

Author Information and Affiliations

Last Update: February 5, 2023.

Continuing Education Activity

Paroxysmal supraventricular tachycardia (PSVT) describes a narrow complex tachycardia involving episodic supraventricular tachycardia with sudden onset and termination. In contrast to multifocal atrial tachycardia, atrial fibrillation, and atrial flutter, PSVT involves a regular ventricular response. This activity illustrates the evaluation and treatment of paroxysmal supraventricular tachycardia and reviews the role of the interprofessional team in managing those with this condition.


  • Describe the exam of a patient with paroxysmal supraventricular tachycardia.
  • Review the evaluation of paroxysmal supraventricular tachycardia.
  • Describe management options for paroxysmal supraventricular tachycardia.
  • Outline interprofessional team strategies to improve care coordination and communication to enhance outcomes for patients affected by paroxysmal supraventricular tachycardia.
Access free multiple choice questions on this topic.


Paroxysmal supraventricular tachycardia (PSVT) accounts for intermittent episodes of supraventricular tachycardia with sudden onset and termination. PSVT is part of the narrow QRS complex tachycardias with a regular ventricular response in contrast to multifocal atrial tachycardia, atrial fibrillation, and atrial flutter. SVTs are classified based on the origin of the rhythm and whether the rhythm is regular or irregular.[1][2][3][4][5][6]

Atrial in Origin and Regular Rhythm

  • Sinus tachycardia
  • Inappropriate sinus tachycardia
  • Sinoatrial nodal reentrant tachycardia
  • Atrial flutter
  • Atrial fibrillation

Atrial in Origin and Irregular Rhythm

  • Multifocal atrial tachycardia
  • Atrial flutter with variable block
  • Atrial fibrillation

AV Node in Origin and Regular Rhythm

  • Junctional tachycardia 
  • Atrioventricular nodal reentrant tachycardia
  • Atrioventricular reentrant tachycardia

AV Node in Origin and Irregular Rhythm

  • None

SVT is known to occur in individuals of all ages, but treatment is often difficult. The clinical presentation of SVT is variable- ranging from asymptomatic to severe palpitation. Electrophysiologic studies are usually necessary to determine the pathophysiology of impulse formation and pathways of conduction.[7]


Numerous conditions and medications can lead to PSVT in patients. [1][8][9][10]

Some of these conditions and medications are listed below:

  • Hyperthyroidism
  • Caffeinated beverages
  • Nicotine
  • Hydralazine
  • Atropine
  • Adenosine
  • Verapamil
  • Salbutamol
  • Ecstasy
  • Cocaine
  • Amphetamines
  • Alcohol 
  • Digoxin toxicity
  • Myocardial infarction
  • Structural heart disease
  • Ebstein anomaly
  • Pericarditis
  • Myocarditis
  • Cardiomyopathy
  • Pulmonary embolism
  • Rheumatic heart disease
  • Mitral valve prolapse
  • Pneumonia
  • Chronic lung disease
  • Chest wall trauma
  • Anxiety
  • Hypovolemia
  • Hypoxia


In the United States, the prevalence of PSVT is approximately 0.2%, and it has an incidence of one to three cases every thousand patients. The most common type of PSVT is atrial fibrillation, with a prevalence rate of approximately 0.4% to 1% occurring in men and women equally; it is projected to affect as many as 7.5 million patients by 2050. The risk of developing PSVT was found to be twice in women compared to men in a population-based study, with the prevalence of the PSVT higher with age. Atrioventricular nodal reentrant tachycardia is found more commonly in patients who are middle-aged or older. Whereas PSVT with an accessory pathway is most common in adolescents, and their occurrence decreases with age.[11][12][13]

Besides occurring in healthy people, PSVT can also occur after a myocardial infarction (MI), rheumatic heart disease, mitral valve prolapse, pneumonia, chronic lung disease, and pericarditis. Digoxin toxicity is often associated with PSVT.


PSVT is often due to different reentry circuits in the heart, where less frequent causes include enhanced or abnormal automaticity and triggered activity. Reentry circuits include a pathway within and around the sinus node, within the atrial myocardium, within the atrioventricular node, or an accessory pathway involving the atrioventricular node.[14][15][16] Different types of PSVT result depending on the existing circuits, and examples are:

  • Sinus node: Sinoatrial node reentrant tachycardia
  • Atrial myocardium: Atrial flutter, atrial fibrillation, and multifocal atrial tachycardia
  • Atrioventricular node: Atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia


Under most circumstances, careful examination in patients with PSVT will show reentry circuits discussed above. No specific histopathologic findings are found in patients with PSVTs secondary to triggered activity and enhanced or abnormal automaticity.[16]

History and Physical

The severity of symptoms in patients with PSVT depends on any underlying structural heart disease, the frequency of PSVT episodes, and the patient's hemodynamic reserve. Usually, patients with PSVT present with symptoms of dizziness, syncope, nausea, shortness of breath, intermittent palpitations, pain or discomfort in the neck, pain or discomfort in the chest, anxiety, fatigue, diaphoresis, and polyuria secondary atrial natriuretic factor secreted mainly by the heart's atria in response to atrial stretch. The most common symptoms are dizziness and palpitations. Patients with PSVT and a known history of coronary artery disease may present with a myocardial infarction secondary to the stress on the heart. Patients with PSVT and a known history of heart failure may come in with acute exacerbation. Frequent PSVTs in a patient can result in new-onset heart failure secondary to tachycardia-induced cardiomyopathy.[17]

A detailed history of the patient with PSVT should include past medical and cardiac history, time of symptom onset, prior episodes, and treatments. The patients' current medication list must be obtained. Investigations of involvement in physical activities such as exercise or outdoor sports should be made, as patients who have symptomatic PSVT's avoid such hobbies. Patients presenting with PSVTs should get a thorough physical exam, including vital signs (respiratory rate, blood pressure, temperature, and heart rate), to assess their hemodynamic stability.[18]


A significant component of evaluation for a patient who presents with signs and symptoms of PSVT is history and physical exam. These should include vital signs (respiratory rate, blood pressure, temperature, and heart rate), a review of the patient's medication list, and a 12-lead electrocardiogram. During an evaluation, a health care provider should establish if the patient is hemodynamically stable and whether they have any underlying ischemic heart disease or heart failure. Digoxin toxicity should be ruled out.

Healthcare providers should consider thyroid function testing, pulmonary function testing, including routine blood work, and echocardiography as part of their initial evaluation of patients presenting with symptomatic PSVTs.[19][20]

ECG features:

  1. Sinus tachycardia with a heart rate more than 100 bpm with normal P waves
  2. Atrial tachycardia with a heart rate between 120 to 150 bpm. The P wave morphology may be different from normal sinus rhythm.
  3. Multifocal atrial tachycardia with heart rates from 120 to 200 bpm with 3 or more different P wave morphologies
  4. Atrial flutter with a heart rate of 200 to 300 bpm
  5. Atrial fibrillation with irregularly irregular rhythm and no visible P waves
  6. AVNRT with a heart rate of 150 to 250 bpm, P waves before or within the QRS complex, short PR interval
  7. AVRT with a heart rate between 150 to 250 bpm, narrow QRS complex in orthodromic conduction, and wide QRS complex in antidromic conduction

Treatment / Management

Treatment of PSVT in a patient is dependent on the type of rhythm present on the electrocardiogram and the patient's hemodynamic stability. Patients presenting with hypotension, shortness of breath, chest pain, shock, or altered mental status are considered hemodynamically unstable, and their electrocardiogram evaluation must be done to determine if they are in sinus rhythm or not. If they are not in sinus rhythm, these patients should undergo urgent cardioversion. If they are determined to be in appropriate sinus tachycardia, then their underlying etiology must be treated. For any manifestations of cardiac ischemia, intravenous beta-blockers should be considered. If they have inappropriate sinus tachycardia on the electrocardiogram and are determined to be hemodynamically unstable, treatment with intravenous beta-blockers may be appropriate.[21][22][23]

If, on the initial evaluation, a patient is found to be hemodynamically stable, then the treatment of the patient depends on the specific PSVT present on the electrocardiogram. If the 12-lead electrocardiogram shows that the rhythm is irregular and P waves are absent, the patient should be appropriately treated for atrial fibrillation. If the rhythm on the electrocardiogram is irregular and flutter waves are present, then the patient should be treated for atrial flutter. If the rhythm on the electrocardiogram is irregular and multiple P wave morphologies are present, the patient should be treated for multifocal atrial tachycardia.[24]

In patients who are hemodynamically stable and showing a regular rhythm with visible P waves on the electrocardiogram, then an assessment of the atrial rate, the relationship between the atrial and ventricular pacing, P-wave morphology, and the P-wave position in the rhythm cycle is required. Type of PSVT present (atrial tachycardia, multifocal atrial tachycardia, atrial flutter, atrial flutter with a variable block, intra-atrial reentrant tachycardia, sinus tachycardia, sinoatrial node reentrant tachycardia, atrioventricular nodal reentrant tachycardia, atrioventricular reciprocating tachycardia, junctional ectopic tachycardia, and nonparoxysmal junctional tachycardia) determines the treatment.[25][26]

Patients who are hemodynamically stable and have an electrocardiogram that shows a regular rhythm with undetectable P waves, Valsalva maneuvers, carotid sinus massage, or intravenous adenosine might be used to slow the ventricular rate or convert the rhythm into sinus rhythm and thus aid in the diagnosis. In some instances, increasing the electrocardiogram paper speed from 25 mm per second to 50 mm per second might help as well. If intravenous adenosine does not work, then intravenous or oral calcium channel blockers or beta-blockers should be used. Patients with PSVTs must also undergo evaluation for any underlying pre-excitation syndrome, and patients who fail medical treatment or those who might need radiofrequency catheter ablation need cardiology consultation.[27][28][29]

Differential Diagnosis

The differential includes: [30][31]

  • Atrial tachycardia
  • Multifocal atrial tachycardia (MAT)
  • Atrial flutter
  • Atrial flutter with variable block
  • Atrial fibrillation
  • Intra-atrial reentrant tachycardia
  • Sinus tachycardia
  • Inappropriate sinus tachycardia
  • Sinoatrial node reentrant tachycardia
  • Atrioventricular nodal reentrant tachycardia
  • Atrioventricular reciprocating (reentrant) tachycardia
  • Junctional ectopic tachycardia
  • Nonparoxysmal junctional tachycardia


In cases with no structural heart disease, the prognosis of PSVT is reasonably good. For patients with structural heart disease, the prognosis is often guarded. The arrhythmia may come on suddenly and last anywhere from a few seconds to several days. Most patients develop anxiety, a sense of doom, and others may develop hemodynamic compromise. The arrhythmia can result in congestive heart failure, myocardial infarction, and pulmonary edema.


If not identified promptly, symptomatic complications such as syncope, fatigue, or dizziness can occur. 

Deterrence and Patient Education

Educating patients at risk for this rhythm and making a closed-loop communication between them and their providers can help further improve the management of these rhythms. If available, patient education should be provided using resources familiar to the patient, including online resources and pamphlets. 

Pearls and Other Issues

Frequent PSVT can result in tachycardia-induced cardiomyopathy; a study on pregnant females found that PSVT in the first to second gestational month increased the chances of the child developing ostium secundum atrial septal defect.

Enhancing Healthcare Team Outcomes

Treatment of PSVT can involve an interprofessional team, including emergency department physicians and nurses, cardiologists and cardiology nurses, primary care providers, and pharmacists. Emergency medical technicians are often the first to encounter patients and provide treatment. The team should evaluate, as outlined above. Nurses, pharmacists, and physicians can provide education. Pharmacists should educate patients about medication side effects and compliance, as well as check for drug interactions. [Level 5] 

Review Questions



Lead II (2) Supraventricular tachycardia SVT Contributed by Wikimedia Commons, James Heilman, MD (Public Domain-Self)



A graphical representation of the Electrical conduction system of the heart showing the Sinoatrial node, Atrioventricular node, Bundle of His, Purkinje fibers, and Bachmann's bundle Contributed by Wikimedia Commons (Public Domain)

This is a recording of the termination of a supraventricular tachycardia at about 130/min


This is a recording of the termination of a supraventricular tachycardia at about 130/min. which terminates and leaves a pause and then sinus bradycardia. This is a from of "tachy/brady" syndrome where a tachycardia is followed by a bradycardia. Contributed (more...)



atrial fibrillation Contributed by S Bhimji MD



Atrial fibrillation Image courtesy S Bhimji MD


Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med. 1995 Jan 19;332(3):162-73. [PubMed: 7800009]
Chauhan VS, Krahn AD, Klein GJ, Skanes AC, Yee R. Supraventricular tachycardia. Med Clin North Am. 2001 Mar;85(2):193-223, ix. [PubMed: 11233946]
Akhtar M, Jazayeri MR, Sra J, Blanck Z, Deshpande S, Dhala A. Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations. Circulation. 1993 Jul;88(1):282-95. [PubMed: 8319342]
Rosen KM, Mehta A, Miller RA. Demonstration of dual atrioventricular nodal pathways in man. Am J Cardiol. 1974 Feb;33(2):291-4. [PubMed: 4810028]
Orejarena LA, Vidaillet H, DeStefano F, Nordstrom DL, Vierkant RA, Smith PN, Hayes JJ. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. 1998 Jan;31(1):150-7. [PubMed: 9426034]
Waldo AL, Wit AL. Mechanisms of cardiac arrhythmias. Lancet. 1993 May 08;341(8854):1189-93. [PubMed: 8098085]
Klein GJ, Sharma AD, Yee R, Guiraudon GM. Classification of supraventricular tachycardias. Am J Cardiol. 1987 Aug 31;60(6):27D-31D. [PubMed: 3630922]
Luca AC, Curpan AS, Miron I, Horhota EO, Iordache AC. Paroxysmal Supraventricular Tachycardia in Wolff-Parkinson-White Syndrome in a Newborn-Case Report and Mini-Review. Medicina (Kaunas). 2020 Nov 05;56(11) [PMC free article: PMC7694453] [PubMed: 33167583]
Accardi AJ, Miller R, Holmes JF. Enhanced diagnosis of narrow complex tachycardias with increased electrocardiograph speed. J Emerg Med. 2002 Feb;22(2):123-6. [PubMed: 11858914]
Trohman RG. Supraventricular tachycardia: implications for the intensivist. Crit Care Med. 2000 Oct;28(10 Suppl):N129-35. [PubMed: 11055681]
Murdock CJ, Leitch JW, Teo WS, Sharma AD, Yee R, Klein GJ. Characteristics of accessory pathways exhibiting decremental conduction. Am J Cardiol. 1991 Mar 01;67(6):506-10. [PubMed: 1998282]
Porter MJ, Morton JB, Denman R, Lin AC, Tierney S, Santucci PA, Cai JJ, Madsen N, Wilber DJ. Influence of age and gender on the mechanism of supraventricular tachycardia. Heart Rhythm. 2004 Oct;1(4):393-6. [PubMed: 15851189]
Tada H, Oral H, Greenstein R, Pelosi F, Knight BP, Strickberger SA, Morady F. Analysis of age of onset of accessory pathway-mediated tachycardia in men and women. Am J Cardiol. 2002 Feb 15;89(4):470-1. [PubMed: 11835934]
Xie B, Thakur RK, Shah CP, Hoon VK. Clinical differentiation of narrow QRS complex tachycardias. Emerg Med Clin North Am. 1998 May;16(2):295-330. [PubMed: 9621846]
Krahn AD, Yee R, Klein GJ, Morillo C. Inappropriate sinus tachycardia: evaluation and therapy. J Cardiovasc Electrophysiol. 1995 Dec;6(12):1124-8. [PubMed: 8720214]
Brugada P, Wellens HJ. The role of triggered activity in clinical ventricular arrhythmias. Pacing Clin Electrophysiol. 1984 Mar;7(2):260-71. [PubMed: 6200854]
Link MS. Clinical practice. Evaluation and initial treatment of supraventricular tachycardia. N Engl J Med. 2012 Oct 11;367(15):1438-48. [PubMed: 23050527]
Fox DJ, Tischenko A, Krahn AD, Skanes AC, Gula LJ, Yee RK, Klein GJ. Supraventricular tachycardia: diagnosis and management. Mayo Clin Proc. 2008 Dec;83(12):1400-11. [PubMed: 19046562]
Josephson ME, Wellens HJ. Electrophysiologic evaluation of supraventricular tachycardia. Cardiol Clin. 1997 Nov;15(4):567-86. [PubMed: 9403161]
Obel OA, Camm AJ. Supraventricular tachycardia. ECG diagnosis and anatomy. Eur Heart J. 1997 May;18 Suppl C:C2-11. [PubMed: 9152669]
Ferguson JD, DiMarco JP. Contemporary management of paroxysmal supraventricular tachycardia. Circulation. 2003 Mar 04;107(8):1096-9. [PubMed: 12615783]
Josephson ME, Kastor JA. Supraventricular tachycardia: mechanisms and management. Ann Intern Med. 1977 Sep;87(3):346-58. [PubMed: 332025]
Basta M, Klein GJ, Yee R, Krahn A, Lee J. Current role of pharmacologic therapy for patients with paroxysmal supraventricular tachycardia. Cardiol Clin. 1997 Nov;15(4):587-97. [PubMed: 9403162]
Pieper SJ, Stanton MS. Narrow QRS complex tachycardias. Mayo Clin Proc. 1995 Apr;70(4):371-5. [PubMed: 7898144]
Lévy S, Ricard P. Using the right drug: a treatment algorithm for regular supraventricular tachycardias. Eur Heart J. 1997 May;18 Suppl C:C27-32. [PubMed: 9152672]
Blomström-Lundqvist C, Scheinman MM, Aliot EM, Alpert JS, Calkins H, Camm AJ, Campbell WB, Haines DE, Kuck KH, Lerman BB, Miller DD, Shaeffer CW, Stevenson WG, Tomaselli GF, Antman EM, Smith SC, Alpert JS, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Hiratzka LF, Hunt SA, Jacobs AK, Russell RO, Priori SG, Blanc JJ, Budaj A, Burgos EF, Cowie M, Deckers JW, Garcia MA, Klein WW, Lekakis J, Lindahl B, Mazzotta G, Morais JC, Oto A, Smiseth O, Trappe HJ., American College of Cardiology. American Heart Association Task Force on Practice Guidelines. European Society of Cardiology Committee for Practice Guidelines. Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation. 2003 Oct 14;108(15):1871-909. [PubMed: 14557344]
Smith GD, Dyson K, Taylor D, Morgans A, Cantwell K. Effectiveness of the Valsalva Manoeuvre for reversion of supraventricular tachycardia. Cochrane Database Syst Rev. 2013 Mar 28;(3):CD009502. [PubMed: 23543578]
Shaker H, Jahanian F, Fathi M, Zare M. Oral verapamil in paroxysmal supraventricular tachycardia recurrence control: a randomized clinical trial. Ther Adv Cardiovasc Dis. 2015 Feb;9(1):4-9. [PubMed: 25297337]
Lesh MD, Van Hare GF, Epstein LM, Fitzpatrick AP, Scheinman MM, Lee RJ, Kwasman MA, Grogin HR, Griffin JC. Radiofrequency catheter ablation of atrial arrhythmias. Results and mechanisms. Circulation. 1994 Mar;89(3):1074-89. [PubMed: 8124793]
Katritsis DG, Josephson ME. Differential diagnosis of regular, narrow-QRS tachycardias. Heart Rhythm. 2015 Jul;12(7):1667-76. [PubMed: 25828600]
Kalbfleisch SJ, el-Atassi R, Calkins H, Langberg JJ, Morady F. Differentiation of paroxysmal narrow QRS complex tachycardias using the 12-lead electrocardiogram. J Am Coll Cardiol. 1993 Jan;21(1):85-9. [PubMed: 8417081]

Disclosure: Yamama Hafeez declares no relevant financial relationships with ineligible companies.

Disclosure: Bryan Quintanilla Rodriguez declares no relevant financial relationships with ineligible companies.

Disclosure: Intisar Ahmed declares no relevant financial relationships with ineligible companies.

Disclosure: Shamai Grossman declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK507699PMID: 29939521


  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Similar articles in PubMed

See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...