Paroxysmal Supraventricular Tachycardias

Supraventricular tachycardia (SVT) is caused by abnormalities of impulse conduction (re-entrant tachycardias) or disorders of impulse initiation (automatic tachycardias), causing a narrow complex tachycardia.

• SVT is most often due to the junctional tachycardias, atrioventricular nodal re-entrant tachycardia (AVNRT) or atrioventricular re-entrant tachycardia (AVRT).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 for several months.

• Atrioventricular nodal reciprocating tachycardia (AVNRT)
  • Due to the presence of two functionally and anatomically distinct conducting pathways in the atrioventricular (AV) 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 reciprocating tachycardia (AVRT)
  • Due to the presence of accessory pathways that connect the atria and ventricles, but that lie outside the AV 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.

• Focal junctional tachycardia:
  • Due to abnormally rapid discharges from the junctional region
  • This type of SVT originates from the AV 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 AV node plays a role in the initiation or continuation of this type of SVT

• Incidence of paroxysmal supraventricular tachycardia is approximately 1-3 per 1000.
• Prevalence is twice as high in women compared to men and the prevalence increases with age.²

Risk factors

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

• Previous myocardial infarction
• Mitral valve prolapse
• Rheumatic heart disease
• Pericarditis
• Pneumonia
• Chronic lung disease
• Current alcohol intoxication
• Digoxin toxicity

• Paroxysmal SVT 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 are the most common symptoms reported.
  • Other symptoms include 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 otherwise healthy and no cardiac dysfunction. During an episode of SVT the pulse rate is 140-250 per minute.
• Resulting heart failure may cause tachypnoea, hypotension, raised JVP, third heart sound and basal lung crepitations.

• Drug adverse effects, e.g. amiodarone, digoxin, theophylline
• Narrow QRS-complex tachycardia
  • Irregular: atrial fibrillation
  • Regular:
    • Sinus tachycardia, e.g. due to anxiety, infection, medication, panic attack, thyrotoxicosis. The heart rate rarely exceeds 150 except during exercise
    • No visible P waves: atrioventricular nodal reciprocating tachycardia (AVNRT)
    • Visible P waves:
      • Atrial rate greater than ventricular rate: atrial flutter or atrial fibrillation
      • Atrial rate not greater then ventricular rate: Long RP interval: atrial tachycardia, permanent form of junctional reciprocating tachycardia (PJRT), atypical AVNRT
      • Short RP interval:
        • Less than 70 ms: AVNRT
        • Longer than 70 ms: atrioventricular reciprocating tachycardia (AVRT), AVNRT, atrial tachycardia.
• Wide QRS tachycardia (broad complex tachycardia):
  • SVT with bundle branch block or aberration
  • SVT with AV conduction over an accessory pathway
  • Ventricular tachycardia

• ECG:³
  • 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 AVRT.
  • A history of paroxysmal irregular palpitations (very likely to be atrial fibrillation) 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.
• 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 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.
• Full blood count: helps assess whether anaemia is contributing to the tachycardia.
• Thyroid function tests
• Digoxin level for patients on digoxin: PSVT can be caused by high levels of digoxin.
• Chest x-ray: 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, e.g. 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 (e.g. heart failure, sudden death). .
• The most effective and rapid means of terminating any haemodynamically unstable tachycardia is DC cardioversion.
• In haemodynamically stable regular narrow QRS-complex tachycardia, vagal manoeuvres, e.g. 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 maneuver. 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 AV node. Adenosine has a high incidence of minor but unpleasant side effects (e.g. 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 AV 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 contraindicated (e.g. in somebody with severe asthma).
• Sinus tachycardia:
  • Beta-blocker or non-dihydropyridine calcium-channel blocker, e.g. diltiazem, verapamil.
  • Exclude secondary cause, e.g. 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.⁵
• 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 contraindicated because of pulmonary disease and there is no role for DC cardioversion or ablation.
• Treatment of atrial fibrillation and atrial flutter (see separate articles):
  • Includes controlling the ventricular rate, restoring the sinus rhythm, and preventing embolic complications.
  • The ventricular rate can be controlled with amiodarone or sotalol.
  • Sinus rhythm may be restored with either drugs or electrical cardioversion.
• 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 anti-arrhythmic drug therapy
    • If the person is intolerant of anti-arrhythmic drug therapy
    • If anti-arrhythmic drug therapy is contraindicated
• Driver and Vehicle Licensing Agency advice:
  • 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 4 weeks.

• Haemodynamic collapse can occur. This is more likely in people with underlying heart disease who are unable to tolerate increases in heart rate.
• Deep vein thrombosis
• Systemic embolism
• Cardiac tamponade
• Rare complications include myocardial infarction, congestive heart failure, syncope, and sudden death.
• SVT that persists for weeks or months may lead to a tachycardia-mediated cardiomyopathy.

• 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.