Supraventricular tachycardia


Any arrhythmia originating in the upper cardiac chambers with atrial rate greater than 100 beats/min.

Gradual onset = tachycardia gradually accelerates and decelerates (gradual shortening/prolongation of P-P interval.

Sudden onset = abruptly starts and ends, typically with symptoms.

We can divide these by duration on:

  • Paroxysmal supraventricular tachycardia (PSVT) – rapid tachycardia with ventricular rate usually > 120 beats/min, sudden onset and termination. (prevalence 2,25 per 1000 persons)
  • Non-paroxysmal/ incessant SVT – episodes of tachycardia alternate with the normal sinus rhythm at least 50% of the time or totally replace it. Usually 120-190 beats/min

Symptoms during SVT

  • palpitations
  • syncope or dizziness
  • chest pain, dyspnoea
  • polyuria (atrial stretch-induced atrial natriuretic peptide activity)
  • altered consciousness

Complications of SVT

  • worsened quality of life – anxiety, prolonged tiredness after an episode, fear of dying
  • paroxysmal SVT can degenerate into ventricular fibrillation – often fatal
  • incessant SVT – may develop into post-tachycardial cardiomyopathy
  • tachycardias over 150 bpm dramatically reduce cardiac output and coronary blood flow (diastole is very short),  potentially causing myocardial ischaemia. The faster the heart rate, the less well it will be tolerated

ECG features

A four-step approach to diagnose the underlying rhythm: 

  1. QRS complex
  • The width of the QRS complex during SVT is usually 80–100 ms
  • QRS can be wide >120ms e.g. in these situations:
    - if the patient has a permanent LBBB or RBBB
    - if during tachycardia a functional bundle branch block develops
    - if AV conduction during tachycardia is over an AV accessory pathway (AVNRT, AVRT)
  1. Is the rhythm regular or irregular?
  • regular – AVNRT, AVRT, atrial tachycardia or atrial flutter with stable conduction
  • irregular – atrial fibrillation, multifocal atrial tachycardia or atrial flutter with variable conduction (basically excludes AVNRT and AVRT)
  1. Presence and morphology of the P waves
  1. Duration of RP intervals
  • by this criteria, we can divide tachycardia to long RP and short RP

Picture 1 Differential diagnosis of narrow complex tachycardia


Acute management

Initial treatment of SVT depends on hemodynamic stability of the patient.

  1. Hemodynamically unstable patient with narrow or wide complex tachycardia – urgent synchronized cardioversion
  2. Hemodynamically stable patient

Acute therapy of narrow complex tachycardia

Vagal manoeuvres

  • Carotid sinus massage - Pressure is applied to one carotid sinus for 5 to 10 seconds. Steady pressure is recommended because it may be more reproducible. If the expected response is not obtained, the procedure is repeated on the other side after a one- to two-minute delay.
  • Valsalva manoeuvres – patient is instructed to exhale forcefully against a closed glottis (against closed mouth and compressed nose) for 10 – 15s and then release.
  • Modified Valsalva manoeuvre – patient does classical Valsalva manoeuvre followed by 15 seconds of passive leg raise at 45 degree angle – this may be more successful in restoring sinus rhythm.

If this fails -

Adenosine – through cardiac adenosine A1 receptor > transient AV block

  • 6 mg i.v. as a rapid bolus with saline flush
  • second dose – 12 mg i.v., safe within 1 min of the last dose
  • maximum dose = 18 mg


  • AVNRT, AVRT > termination
  • atrial flutter, focal atrial tachycardia > demasking atrial rhythm during AV blockade
  • no response – probably underdosed or ventricular tachycardia
  • CAVE: contraindication in patients with asthma and patients with preexcitation on resting ECG!
  • Adenosine may induce a wide range of transient bradycardias as well as atrial fibrillation, SVT and ventricular tachycardia
  • Adenosine should always be administered with an external pacemaker or defibrillator nearby

If Vagal manoeuvres and adenosine application fails: 

  • Verapamil [0.075 - 0.15 mg/kg i.v. (average 5 - 10 mg) over 2 min] or i.v. diltiazem [0.25 mg/kg (average 20 mg) over 2 min] has been shown to terminate SVT in 64-98% of patients, but is associated with a risk of hypotension
  • application intravenously over 20 minutes has been shown to reduce the rate of hypotension
  • i.v. esmolol - 0.5 mg/kg i.v. bolus or 0.05 - 0.3 mg/kg/min infusion
  • i. v. metoprolol - 2.515 mg given i.v. in 2.5 mg boluses

If all pharmacological therapies fail - synchronized cardioversion is recommended, even in hemodynamically stable patients.

Chronic management

  • catheter ablation
  • paroxysmal tachycardia – vagal maneuvers, “pill in the pocket” – BB, verapamil, flecainide
  • symptomatic, incessant tachycardia
    - pharmacological therapy – BB, verapamil
    - radiofrequency catheter ablation

Acute therapy of wide complex tachycardia

  • Vagal manoeuvres
  • Adenosine – if there is no evidence of preexcitation on resting ECG
  • if ineffective:
    - Procainamide (i.v.) should be considered if vagal manoeuvres and adenosine fail.
    - Amiodarone (i.v.) may be considered if vagal manoeuvres and adenosine fail.
  • If drug therapy fails -synchronized cardioversion – to convert or control the tachycardia.

Picture 2 and 3  Treatment of narrow and wide complex tachycardias as per ESC guidelines


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Picture no. 1  HARAN BURRI. Oxford Medicine Online [online]. [cit. 30.1.2021]. Accessible at WWW:

Picture no. 2  Acute therapy of narrow QRS tachycardia in the absence of an established diagnosis (2019). [Graph]. Accessible at:

Picture no. 3 Acute therapy of wide complex tachycardia in the absence of an established diagnosis.[Graph]. Accessible at: