Supraventricular tachycardia

Last updated: August 7, 2023

Summarytoggle arrow icon

Supraventricular tachycardias (SVTs) are a group of tachyarrhythmias arising from abnormalities in pacemaker activity and/or conduction involving myocytes of the atria and/or AV node. Types of SVT include atrioventricular nodal reentrant tachycardia (AVNRT; approx. two-thirds of cases), atrioventricular reciprocating tachycardia (AVRT), focal atrial tachycardia (FAT), multifocal atrial tachycardia (MAT), and junctional tachycardia. AVNRT and AVRT are caused by abnormal conduction circuits that form an unending loop of conduction referred to as reentry. These reentry circuits can occur between parallel pathways within the AV node (as in AVNRT) or between the AV node and an accessory pathway of atrioventricular conduction (as in AVRT). Atrial tachycardias (FAT and MAT) and junctional tachycardias are usually the result of abnormal or ectopic pacemaker activity and do not involve reentry. The most common congenital accessory pathway (bundle of Kent) is seen in Wolff-Parkinson-White (WPW) syndrome and can cause ventricular preexcitation, in which supraventricular impulses bypass the AV node and are abnormally conducted to the ventricles, leading to a characteristic preexcitation pattern on ECG and a specific subset of preexcited tachyarrhythmias. SVTs have similar clinical features (typically paroxysms of tachycardia with dizziness, dyspnea, chest pain, or syncope) that may be self-limiting or progress to hemodynamic instability and sudden cardiac death. Common diagnostic steps include obtaining the patient's history and a 12-lead ECG to identify the type of SVT. The paroxysmal nature of SVTs means that continuous recording with a Holter monitor is often needed to confirm the diagnosis; in some cases, invasive electrophysiological studies (EP studies) may also be indicated. Management of SVT should be tailored to the patient. Most hemodynamically unstable patients are treated with emergency cardioversion, while patients with acute SVT episodes that are hemodynamically stable may benefit from vagal maneuvers and/or antiarrhythmic medication (typically intravenous), depending on the underlying rhythm. Long-term management may involve antiarrhythmic medication or curative catheter ablation.

The following are discussed in detail separately: “Management of tachycardia,” “Atrial fibrillation with rapid ventricular response” and “Atrial flutter.“

Definitionstoggle arrow icon


Conduction abnormalities


  • A mechanism that causes an impulse in the heart (which would normally die out) to return via conduction circuit to reexcite the tissue, leading to an extra beat (or, if it continues, an ongoing tachyarrhythmia) [4][5]
  • Examples of reentrant tachycardias include AVNRT and AVRT.

Aberrant conduction [6][7]


Overviewtoggle arrow icon

Treat unstable SVTs (except for MAT and junctional tachycardia) with electrical cardioversion.

If there is doubt about the supraventricular origin of a wide complex tachycardia, treat it as ventricular tachycardia.

Overview of SVTs [2][8]
Type of SVT Description Distinguishing ECG features Acute management of stable patients Long-term management options
  • Caused by two alternative electrical pathways within the AV node, forming a reentry circuit
Orthodromic AVRT

Antidromic AVRT

Focal AT
  • Arises from a localized atrial focus outside of the SA node
Multifocal AT
Afib with RVR
Atrial flutter
  • Caused by reentrant circuits within atrial tissue
  • Etiologies are the same as the causes of AFib.
WPW syndrome [9]
Junctional tachycardia

Epidemiologytoggle arrow icon

Epidemiological data refers to the US, unless otherwise specified.

Clinical featurestoggle arrow icon

Signs of unstable tachycardia due to SVT include acute pulmonary edema, hypotension, severe chest pain, and altered mental status.

Diagnosticstoggle arrow icon


Once the diagnosis is confirmed by ECG, do not delay acute management of SVT for additional investigations.

Initial diagnostics [11]

Additional diagnostics [11]

Consider the following tests depending on patient risk factors.

Differential diagnosestoggle arrow icon

Although differentiating between types of SVT can be challenging and may require EP studies to confirm the diagnosis, some ECG features may help to differentiate diagnoses.

Patients with SVT symptoms are frequently misdiagnosed with anxiety or panic disorders. Rule out paroxysmal tachycardia before making a psychiatric diagnosis to avoid anchoring bias.

The differential diagnoses listed here are not exhaustive.

Managementtoggle arrow icon

Acute management of SVT [2][8]

The underlying type of SVT is often unclear at presentation. A definitive diagnosis is not required to begin acute management of tachycardia following ACLS algorithms.

Pulseless patients

Patients with unstable tachycardia with pulse

Stable patients

Empiric management depends on QRS width and rhythm.

Avoid using AV nodal blockers to treat wide complex tachycardias, as they may precipitate Vfib. [16][17]

Vagal maneuvers

Valsalva maneuver

Modified Valsalva maneuver [18]

  • Patient sits in a semirecumbent position
  • Blows into a 10 mL syringe for 15 seconds (moving the plunger up achieves a strain of ∼ 40 mm Hg) [19]
  • Afterwards the patient is laid supine and the legs are passively elevated to 45° for 15 seconds.
  • Return to the semirecumbent position for 45 seconds before reassessing rhythm

Carotid sinus massage [20]

Diving reflex

  • Traditionally involves immersing the head in cold water, which is uncomfortable for most patients
  • Can be limited to applying a bag of ice water to the face (particularly the forehead and nasal area) for ∼ 10 seconds [22]

Do not simultaneously apply bilateral carotid artery pressure because this can impede cerebral blood flow.


Catheter ablation

  • Description
    • Radiofrequency or cryothermal energy is applied via a cardiac catheter to eliminate aberrant pathways or impulses from arrhythmogenic foci.
    • Usually performed in conjunction with an EP study
  • Indications [2]
    • Curative therapy in AVNRT, AVRT with concealed pathway, or drug-refractory AT
    • Symptomatic patients who want to avoid long-term drug therapy (especially younger patients)
    • Asymptomatic patients with special lifestyle considerations (e.g., pilots)

Further management and disposition [23]

  • Successful cardioversion: Consider discharge after a period of monitoring if clinically stable and no other acute medical issues.
  • Unsuccessful cardioversion
    • Urgent cardiology consult for specialist treatment, e.g., a second dose of cardioversion, antiarrhythmic infusion
    • Admit to critical care unit for further management.
  • Other indications for hospital admission

Atrioventricular nodal reentrant tachycardiatoggle arrow icon


  • A tachyarrhythmia caused by a dysfunctional AV node that contains two electrical pathways, which form a reentry circuit


  • The AV node contains two electrical pathways, one fast and one slow → the electrical impulse circles around the AV node within both pathways → a continuous circuit conducts impulses to the ventricles → tachycardia
  • Approx. 90% of cases are due to anterograde conduction across the slow-conducting pathway and retrograde conduction in the fast pathway (although the reverse is possible).

ECG findings in AVNRT [24][25]

ECG may be normal between episodes of tachycardia. Findings may be indistinguishable from those of orthodromic AVRT and include:

Treatment of AVNRT

Acute management

Long-term management

Atrioventricular reciprocating tachycardiatoggle arrow icon


Pathophysiology [11][29]

AVRT is caused by an accessory pathway, whereas in AVNRT there are two functional pathways within the AV node.

ECG findings

ECG findings in AVRT [11][33][34]
Orthodromic AVRT
Antidromic AVRT

Treatment of AVRT

Acute episodes

Long-term management [2]

Wolff-Parkinson-White syndrometoggle arrow icon




ECG findings in WPW

Treatment of WPW [8]

Acute episodes

Avoid AV nodal blocking agents and vagal maneuvers for the following preexcited tachycardias: Afib, Aflut, focal AT, and MAT.

Long-term management of WPW [2][40]

Management of WPW pattern and WPW syndrome depends on underlying risk factors and patient preference.

Risk stratification in WPW syndrome [41]

Risk stratification is determined by a cardiologist based on clinical, ECG, and electrophysiological parameters.

High-risk patients

Catheter ablation of the accessory pathway should be offered to all patients. [2]

Low-risk patients [2]

Focal atrial tachycardiatoggle arrow icon


Etiology [15]

Pathophysiology [43][44]

ECG findings in focal AT [2][46]

An isoelectric baseline between P waves can help distinguish focal AT from atrial flutter. [8]

Treatment of focal AT [2]

Acute episodes

Episodes of focal atrial tachycardia are most commonly self-limiting and asymptomatic, in which case they do not require treatment.

Avoid AV nodal blockers in patients with preexcited focal atrial tachycardia (e.g., due to WPW) because they can trigger ventricular arrhythmias.

Long-term management

Multifocal atrial tachycardiatoggle arrow icon


  • An irregular SVT featuring ≥ 3 morphologies of P waves [2]

Etiology [50][51]

Pathophysiology [53]

ECG findings in MAT [50]

Do not confuse MAT with atrial fibrillation. In Afib, there are no distinct or organized P waves, whereas in MAT there are distinct P waves with varying morphologies.

Unlike in atrial flutter, in MAT there are distinct isoelectric intervals between P waves.

Treatment of multifocal atrial tachycardia [2][11][54]

Treatment of MAT is challenging and specialists should be involved early. Patients often have severe underlying conditions and rhythm control and electrical cardioversion are not effective. For clinically-oriented management algorithms for patients with tachycardia, see “Management of tachycardia”.

Avoid AV nodal blockers in patients with preexcited MAT (e.g., due to WPW) because of the risk of ventricular arrhythmias.

Avoid electrical cardioversion and antiarrhythmic drugs (e.g., procainamide, lidocaine, phenytoin), as they are not effective in treating MAT. [2][54]

Junctional tachycardiatoggle arrow icon


Etiology [2]

Pathophysiology [2][11]

ECG findings in junctional tachycardia [2][57]

While the rate varies between paroxysmal junctional tachycardia and accelerated AV junctional rhythm, the ECG appearance is otherwise similar.

Treatment of junctional tachycardia [2]

These recommendations are for confirmed junctional tachycardia. For clinically-oriented management algorithms for patients with tachycardia, see “Management of tachycardia.”

Referencestoggle arrow icon

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