Supraventricular Tachycardia in Adults

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Supraventricular Tachycardia written for patients

Supraventricular tachycardia (SVT) is generally used to refer to atrioventricular nodal re-entry tachycardia (AVNRT), atrioventricular re-entry tachycardia (AVRT), and atrial tachycardia.[1] 

SVT is usually paroxysmal and episodes may occur regularly or very infrequently (sometimes years apart). Episodes may only last for a few minutes or may last for up to several months.

SVT is caused by:

  • Abnormalities of impulse conduction (re-entrant tachycardias).
  • Disorders of impulse initiation (automatic tachycardias) causing a narrow complex tachycardia.

These are the most common type:

  • Atrioventricular nodal re-entrant tachycardia (AVNRT):
    • Due to the presence of two functionally and anatomically distinct conducting pathways in the atrioventricular node. One of these is fast-conducting, the other slow-conducting.
    • During an episode of SVT one of these acts as the antegrade limb of a re-entrant circuit, while the other acts as the retrograde limb. AVNRT is the most common form of SVT.
  • Atrioventricular re-entrant tachycardia (AVRT):
    • Due to the presence of accessory pathways that connect the atria and ventricles, but that lie outside the atrioventricular node.
    • Accessory pathways may be capable of antegrade or retrograde conduction, or both.
    • Wolff-Parkinson-White syndrome is the most well-known type of AVRT.

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  • Focal junctional tachycardia:
    • Due to abnormally rapid discharges from the junctional region.
    • This type of SVT originates from the atrioventricular node, or bundle of His.
    • This type is also known as automatic or paroxysmal junctional tachycardia.
  • Focal atrial tachycardia:
    • Due to regular atrial activation from atrial areas with centrifugal spread.
    • Neither the sinus nor the atrioventricular node plays a role in the initiation or continuation of this type of SVT.
  • Incidence of paroxysmal supraventricular tachycardia (PSVT) is approximately 2 per 1,000.[1]

Risk factors

SVT may occur at any age but often occurs in younger people in the absence of heart disease.

Risk factors include:

  • PSVT may be associated with minimal symptoms or present with syncope.
  • Symptoms vary with the ventricular rate and duration of the SVT. Symptoms are more likely in those with underlying heart disease, and include:
    • Palpitations and dizziness, which are the most common symptoms reported.
    • Other symptoms, including fatigue, light-headedness, chest discomfort, dyspnoea, polyuria and syncope (uncommon).
  • Examination may be normal if seen after the attack, with normal cardiac function and no underlying heart abnormality.
  • During an attack, tachycardia may be the only finding if the patient is otherwise healthy and there is no cardiac dysfunction. During an episode of SVT the pulse rate is 140-250 beats per minute (bpm).
  • Resulting heart failure may cause tachypnoea, hypotension, raised JVP, third heart sound and basal lung crepitations.
  • Drug adverse effects - eg, amiodarone, digoxin, theophylline
  • Narrow QRS-complex tachycardia:
    • Irregular: atrial fibrillation (AF).
    • Regular:
      • Sinus tachycardia - eg, due to anxiety, infection, medication, panic attack, thyrotoxicosis. The heart rate rarely exceeds 150 bpm except during exercise.
      • No visible P waves: atrioventricular nodal re-entrant tachycardia (AVNRT).
      • Visible P waves:
        • Atrial rate greater than ventricular rate: atrial flutter or AF.
        • Atrial rate not greater than ventricular rate: long RP interval: atrial tachycardia, permanent form of junctional re-entrant tachycardia, atypical AVNRT
        • Short RP interval:
          • Less than 70 ms: AVNRT.
          • Longer than 70 ms: atrioventricular re-entrant tachycardia (AVRT), AVNRT, atrial tachycardia.
  • Wide QRS tachycardia (broad complex tachycardia):
  • ECG:[2]
    • Allows classification of the tachyarrhythmia, and may allow a precise diagnosis.
    • P waves may not be visible; when present, they may be normal or abnormal depending on the mechanism of atrial depolarisation.
    • Presence of pre-excitation on the resting ECG and a history of paroxysmal regular palpitations is very likely to signify an atrioventricular re-entrant tachycardia (AVRT).
    • A history of paroxysmal irregular palpitations - very likely to be AF, associated with baseline pre-excitation on the ECG needs urgent specialist assessment, as there is a risk of sudden death.
    • All patients with Wolff-Parkinson-White syndrome should be referred.[3] 
  • Ambulatory 24-hour Holter recording can be used for patients with frequent but transient tachycardias.
  • Exercise ECG testing may be useful if arrhythmia is triggered by exercise.
  • Cardiac enzymes: if there is chest pain; patients with risk factors for myocardial infarction, and patients who are otherwise unstable and present with heart failure, hypotension, or pulmonary oedema.
  • Electrolyte levels: electrolyte disturbances may be an underlying cause.
  • FBC: helps assess whether anaemia is contributing to the tachycardia.
  • TFTs.
  • Digoxin level for patients on digoxin: paroxysmal supraventricular tachycardia (PSVT) can be caused by high levels of digoxin.
  • CXR: pulmonary oedema; infections such as pneumonia, which are associated with PSVT in certain cases.
  • Echocardiogram may be helpful if structural heart disease is suggested.
  • Possible precipitating factors - eg digoxin, caffeine, alcohol, nicotine intake, recreational drugs or hyperthyroidism - should be addressed.
  • An ECG should be performed as soon as possible.
  • The choice of long-term therapy depends on the exact nature of the tachyarrhythmia and the frequency and duration of episodes and risks associated with the arrhythmia (eg, heart failure, sudden death).
  • The most effective and rapid means of terminating any haemodynamically unstable tachycardia is direct current (DC) cardioversion.
  • In haemodynamically stable regular narrow QRS-complex tachycardia, vagal manoeuvres - eg, Valsalva, carotid massage, facial immersion in cold water. Carotid massage is usually reserved for young patients. Due to the risk of stroke from emboli, auscultate for bruits before attempting this manoeuvre. Do not perform carotid massage on both sides simultaneously.
  • If vagal manoeuvres fail, intravenous adenosine or verapamil can be used:
    • Intravenous adenosine is the treatment of choice except for people with severe asthma. Adenosine has a rapid onset and short half-life. It blocks conduction through the atrioventricular node. Adenosine has a high incidence of minor but unpleasant side-effects (eg, nausea, chest tightness, shortness of breath and headache).[4]
    • Intravenous verapamil, although effective, is rarely used now. It has a more prolonged action than adenosine on blocking atrioventricular node conduction, and there is a risk of prolonged depression of ventricular function and hypotension, especially if the person is taking a beta-blocker. It still has a place if adenosine is contra-indicated (eg, in somebody with severe asthma).[5] 
  • Sinus tachycardia:
    • Beta-blocker or non-dihydropyridine calcium-channel blocker - eg, diltiazem, verapamil.
    • Exclude any secondary cause - eg, hyperthyroidism, phaeochromocytoma.
  • Sinus node re-entry tachycardia:
    • Beta-blockers are first-line and diltiazem or verapamil are also effective.
    • Radiofrequency catheter ablation is generally successful.[6]
  • Focal atrial tachycardia:
    • Calcium-channel blockers or beta-blockers are considered first-line.
    • Flecainide, sotalol or amiodarone may also be effective.
  • Multifocal atrial tachycardia:
    • Therapy is mainly directed at chronic pulmonary disease (usually associated) and electrolyte disturbances, which may be the underlying cause. Digoxin toxicity is also an uncommon cause.
    • Long-term therapy is otherwise with calcium-channel blockers.
    • Beta-blockers are usually contra-indicated because of pulmonary disease and there is no role for DC cardioversion or ablation.
  • Long-term preventative treatment:
    • Not required in all people.
    • The frequency and severity of the episodes of SVT need to be balanced against the risks of long-term therapy.
    • The choice of maintenance therapy depends on the underlying type of SVT.
  • Radiofrequency catheter ablation:
    • Is associated with a high success rate and low complication rate for people with SVT.
    • Radiofrequency catheter ablation is indicated in the following situations:
      • As first-line therapy as a curative option.
      • If the SVT is refractory to antiarrhythmic drug therapy.
      • If the person is intolerant of antiarrhythmic drug therapy.
      • If antiarrhythmic drug therapy is contra-indicated.
  • Driver and Vehicle Licensing Agency (DVLA) advice:[7]
    • Group 1 (car or motorcycle):
      • Must stop driving if the arrhythmia has caused or is likely to cause incapacity.
      • Driving may be permitted when the underlying cause has been controlled for at least four weeks.
    • Group 2 (lorry or bus):
      • Disqualifies from driving if the arrhythmia has caused or is likely to cause incapacity.
      • Driving may be permitted when:
        • The arrhythmia is controlled for at least three months.
        • The LV ejection fraction is ≥0.4.
        • There is no other disqualifying condition.

Urgent referral:

  • Syncope with palpitations on exertion
  • Broad complex tachycardia
  • Pre-excitation (delta wave) on a 12-lead ECG
  • Structural heart disease
  • Severe symptoms

Routine referral:

  • Drug resistance or intolerance
  • Preference not to take medication
  • Diagnostic uncertainty
  • Prognosis is dependent on any underlying structural heart disease.
  • Patients with a structurally normal heart have an excellent prognosis.
  • In the absence of manifest pre-excitation (Wolff-Parkinson-White syndrome), the risk of sudden death is very small.

Further reading & references

  1. Whinnett ZI, Sohaib SM, Davies DW; Diagnosis and management of supraventricular tachycardia. BMJ. 2012 Dec 11;345:e7769. doi: 10.1136/bmj.e7769.
  2. ECG Library
  3. Colucci RA, Silver MJ, Shubrook J; Common types of supraventricular tachycardia: diagnosis and management. Am Fam Physician. 2010 Oct 15;82(8):942-52.
  4. Holdgate A, Foo A; Adenosine versus intravenous calcium channel antagonists for the treatment of supraventricular tachycardia in adults. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD005154.
  5. Delaney B, Loy J, Kelly AM; The relative efficacy of adenosine versus verapamil for the treatment of stable paroxysmal supraventricular tachycardia in adults: a meta-analysis. Eur J Emerg Med. 2011 Jun;18(3):148-52. doi: 10.1097/MEJ.0b013e3283400ba2.
  6. Supraventricular Arrhythmias; European Society of Cardiology Guideline (2003)
  7. Assessing fitness to drive: guide for medical professionals; Driver and Vehicle Licensing Agency

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Colin Tidy
Current Version:
Peer Reviewer:
Dr John Cox
Document ID:
2576 (v23)
Last Checked:
Next Review:

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