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PekkaRaatikainen

Supraventricular Tachycardia (SVT)

Essentials

  • Supraventricular tachycardia (SVT) is typically a narrow-complex regular arrhythmia with an abrupt onset and termination.
  • Vagal stimulation is the first-line treatment for an episode of acute SVT. If vagal stimulation is ineffective, the patient should be given adenosine.
  • Patients with recurrent episodes of SVT should be referred to a cardiologist with expertise in arrhythmia management (cardiac electrophysiologist); catheter ablation therapy is a curative treatment form and it has superseded drug therapy in the prophylactic treatment of SVT.
  • Wolff-Parkinson-White (WPW) syndrome must be diagnosed and the patient always referred for specialist management.

Pathogenic mechanism

  • The majority of supraventricular tachycardias are based on the re-entry phenomenon.
    • In about 60% of patients, the re-entry circuit forms within the atrioventricular node (atrioventricular nodal re-entry tachycardia = AVNRT; picture A). These patients have congenital, dual AV nodal physiology which allows re-entry to occur.
    • In about 30% of patients, the arrhythmia is atrioventricular re-entry tachycardia (AVRT; picture B) which results from the presence of an accessory conducting pathway. In the majority of cases, the accessory pathway will only allow retrograde conduction from the ventricles to the atria (so called concealed accessory pathway). In WPW syndrome, the accessory pathway will also allow antegrade conduction from the atria to the ventricles, and during normal rhythm a delta wave is seen in an ECG recording.
  • In a small proportion of patients (less than 10%), the tachycardia is maintained by an intra-atrial re-entry circuit or it occurs secondary to an increased local automaticity of atrial focus or foci (ectopic atrial tachycardia; picture C).

Diagnosis

  • An episode of SVT is characterised by an abrupt onset and termination, which distinguishes it from sinus tachycardia and most ventricular arrhythmias. Its duration varies from a few seconds to incessant tachycardia.
  • An ECG recording will confirm diagnosis. The rhythm of SVT is regular and the rate usually varies between 140 and 220/min depending on the patient's age and state of mental alertness. The QRS complexes are normally narrow. Aberrant conduction results in a wide-complex QRS, as will permanent bundle branch block or pre-excitation of the ventricles via an accessory pathway.
  • Vagal stimulation will either stop an episode of SVT, reveal atrial activity by causing a short atrioventricular block, or have no effect on heart rate (this will assist in differentiating it from sinus tachycardia).

Atrioventricular nodal re-entry tachycardia (AVNRT)

  • Typical AVNRT (slow-fast AVNRT; picture A) is likely if
    • The QRS complexes are narrow and appear at regular intervals
    • P waves are either not visible or retrograde P waves appear immediately after the QRS complexes (best seen in lead V1).
    • There are no delta waves in the resting ECG.
  • Uncommon types of AVNRT (fast-slow AVNRT, slow-slow AVNRT) will typically produce retrograde P waves that fall noticeably after the QRS complexes making these possibly difficult to differentiate from ectopic atrial tachycardia.

Atrioventricular re-entry tachycardia (AVRT)

  • AVRT (picture B) is caused by an accessory, congenital conducting pathway.
    • In a so-called concealed accessory pathway there is only retrograde conduction from the ventricle towards the atria, and no delta wave is seen in the ECG during sinus rhythm (picture ).
    • A manifest accessory pathway also conducts from the atria towards the ventricle, and a delta wave is seen in the ECG during sinus rhythm (picture ).
  • In the more common orthodromic tachycardia, impulses travel from the atria to the ventricles through the AV node and return through the accessory pathway. The QRS complexes are narrow (unless there is aberrant conduction or bundle branch block). Retrograde P waves appear later than in typical AVNRT (picture B).
  • In the rare so-called antidromic tachycardia, the direction of the re-entry is the opposite. Ventricles are activated prematurely via the accessory pathway resulting in wide QRS complexes.
  • In WPW syndrome the patient has arrhythmia sensations, and a resting ECG shows a delta wave at least in two leads (picture ), short PQ interval (< 0.10 seconds) and often also non-specific ST-T changes.
    • WPW syndrome is, besides AVRT, also associated with atrial arrhythmias, such as atrial fibrillation (picture ).
    • In WPW syndrome, atrial fibrillation may be a life-threatening arrhythmia because, due to the existence of an accessory pathway, ventricular response rate may accelerate excessively (> 300/min) leading to ventricular fibrillation. The QRS complexes are wide in pre-excited atrial fibrillation.

Atrial tachycardia

  • Atrial tachycardia (picture C) is probable if the
    • P wave morphology differs from that seen during sinus rhythm (comparison with earlier ECG recordings)
    • PQ interval is normal or prolonged
    • tachycardia usually starts and terminates gradually.

Treatment of an acute episode of SVT

  • SVT that causes haemodynamic compromise must be treated with electrical cardioversion at the first health care facility.
  • In haemodynamically stable patients, the first-line treatment of SVT is vagal stimulation Valsalva Manoeuvre for Reversion of Supraventricular Tachycardia (table T1). During the procedure, the rhythm must be observed continuously on the cardiac monitor (a paper printout must also be obtained).
  • If vagal stimulation does not produce an immediate effect in narrow-complex SVT, adenosine is given into a large vein.

Vagal stimulation may be used both in the diagnosis and treatment of arrhythmias.

ProcedureMethod
Valsalva manoeuvreAfter breathing in, the patient tries to exhale forcibly against a closed glottis. In practice, it may be easier to ask the patient to blow into a large syringe for 15-30 seconds as if trying to move the plunger outwards. Actually, the plunger cannot be moved by blowing, but this procedure brings about a really efficient Valsalva effect. If necessary, enhancement of the Valsalva effect can be tried by lifting up the patient's legs.
Carotid sinus massageThe patient's head is turned away from the side being massaged and the carotid artery is felt under the mandible on the anterior aspect of the sternocleidomastoid muscle. Only one side is massaged at a time for 5-10 seconds. Particularly in the elderly, the carotid arteries must be auscultated before the massage in order to detect possible occlusions.
Other proceduresApplying cold water to the face may also be tried, but induced vomiting (by placing fingers down the patient's throat) should be avoided.
MonitoringIn order to document any diagnostic information or the effect of the procedure, the rhythm must be monitored continuously and preferably a recording or a paper printout should be obtained.
InterpretationVagal procedures will slow down the heart rate and may terminate SVT. Further, vagal stimulation will depress atrioventricular conduction, which may reveal, for example, the characteristic flutter waves of atrial flutter.

Adenosine Adenosine Versus Intravenous Calcium Channel Antagonists for Supraventricular Tachycardia

  • Adenosine is an effective and safe first-line drug for narrow-complex, regular tachycardia.
    • It can also be used within primary care and emergency care.
    • Effectively depresses atrioventricular (AV) conduction. The rhythm will convert 20-30 seconds after the injection and its duration of action is very short (half-life about 2 seconds).
    • Will not convert atrial fibrillation or atrial flutter to sinus rhythm, but will transiently slow ventricular response rate, which may confirm diagnosis.
    • Has no effect on most ventricular tachyarrhythmias, and it may therefore be used in a hospital setting in the differential diagnosis between wide-complex SVT and VT.
    • Must not be used if the arrhythmia is irregular (variable RR interval).
  • Administration of adenosine
    • Depending on the strength of the preparation, a (3-)6 mg (3 mg/ml) or a (5-)10 mg (5 mg/ml) fast bolus is administered into an antecubital vein with cardiac monitoring (recording or paper printout). In order to improve the effect, the limb should be kept elevated and the cannula flushed with about 10 ml of sodium chloride immediately after the administration. A smaller dose should be used if a central vein is used.
    • If sinus rhythm is not restored and no AV block is detected, after 2 minutes a larger dose can be administered: 12 mg when using strength 3 mg/ml or 15 mg when using strength 5 mg/ml.
    • The benefits of adenosine as compared with verapamil are its shorter half-life and fewer haemodynamic effects. Moreover, beta-blockade is not a contraindication for its use.
  • Precautions
    • If the patient has a previously diagnosed serious functional disturbance of the sinus node or second- or third-degree AV block, adenosine must not be used.
    • There is a risk of a prolonged AV block in the elderly, and it is safer to treat these patients in a hospital.
    • The dose must be reduced in patients receiving dipyridamole as it potentiates the effect by up to 4-fold.
    • Should be given at higher doses to patients receiving theophyllamine. Transient exacerbation of asthma is possible.
    • In severe coronary heart disease, there is a risk of bradycardia and AV block.
    • Heart transplant patients are highly sensitive to adenosine and should receive very small doses.
  • Adverse effects
    • Facial flushing, dyspnoea, tightness in the chest, nausea and dizziness are common, and the patient should be warned of their appearance in advance and also told that any adverse effects are not dangerous and will be very short lived (1-2 minutes).
    • Transient sinus bradycardia followed by reflex sinus tachycardia, AV block, atrial extrasystoles and sometimes also atrial fibrillation.
    • In WPW syndrome, adenosine may accelerate conduction over the accessory pathway, and its use for the treatment and diagnosis of wide-complex tachycardia should take place only in a hospital setting.

Verapamil Adenosine Versus Intravenous Calcium Channel Antagonists for Supraventricular Tachycardia

  • If adenosine does not terminate narrow-complex SVT, verapamil may be used.
  • It depresses AV conduction effectively by blocking calcium channels.
  • Dosage
    • 5 mg by slow intravenous injection (over 5-10 minutes) in order to avoid hypotension. The dose may be repeated after about 5 minutes if necessary.
    • During the treatment, the rhythm must be observed continuously on the cardiac monitor and blood pressure measured at regular intervals.
  • Contraindicated in antidromic tachycardia

Other drugs

Electrical cardioversion

  • Electrical cardioversion should be employed when
    • the above-listed methods prove ineffective
    • the patient has severe haemodynamic disturbance or
    • avoidance of polypharmacy is preferred in patients already receiving several cardiovascular drugs.
  • The shock is delivered with the defibrillator synchronised to the QRS complexes, i.e. in the same manner as in atrial fibrillation. Carrying out electrical cardioversion: see Electrical Cardioversion.

Management of SVT in WPW syndrome

  • Adenosine is the drug of choice for the management of narrow-complex (orthodromic) SVT (see above).
  • In wide-complex (antidromic) SVT, the impulse travels through an accessory pathway from the atria to the ventricles. Verapamil, digoxin and beta-blockers may encourage preferential conduction over the accessory pathway, and they are therefore contraindicated in the treatment of antidromic SVT. Adenosine may also accelerate conduction over the accessory pathway, but due to its short duration of action it remains a fairly safe choice.
    • In antidromic SVT, the most reliable and safest way to restore sinus rhythm is electrical cardioversion.
    • Of drugs, flecainide may be considered (1-2 mg/kg as a 10-30 minute infusion, maximum dose 150 mg) or intravenous amiodarone (300 mg or 5 mg/kg over 10 minutes).
  • If atrial flutter or fibrillation occurs in the presence of WPW syndrome, the patient must not be administered verapamil, digoxin or beta-blockers due to the risk of increased ventricular response. Electrical cardioversion is the treatment option of choice.

Acute management of ectopic atrial tachycardia

  • Vagal stimulation and adenosine will not usually terminate ectopic atrial tachycardia, but they may assist in making a correct diagnosis by causing a temporary AV block during which the P waves will be easier to see.
  • Ventricular response is slowed down by blocking AV conduction with a beta-blocker, diltiazem, verapamil, or digoxin.
  • Flecainide or amiodarone may also be used in a hospital setting, but electrical cardioversion remains the quickest and most reliable way to restore normal sinus rhythm.

Prophylactic treatment

  • Irrespective of the pathogenetic mechanism, SVT has a high risk of recurrence.
  • The prophylactic drugs to be used in the primary health care include beta-blockers, verapamil or diltiazem (not in WPW syndrome). Flecainide or amiodarone may also be used if considered necessary by a specialist physician.
  • However, drug therapy is not highly effective and catheter ablation has superseded drug therapy in the prophylactic treatment of SVT. Patients with recurrent episodes of SVT should therefore always be referred to a cardiologist with expertise in arrhythmia management (cardiac electrophysiologist) for electrophysiological studies and possible ablation therapy.
  • Catheter ablation can permanently cure about 95% of atrioventricular nodal re-entry tachycardias and those caused by a congenital accessory pathway. In ectopic atrial tachycardia, the efficacy of ablation therapy is about 90%. Complications associated with the procedure are rare.
  • In WPW syndrome, atrial fibrillation is a life-threatening arrhythmia and these patients must always be referred to a cardiologist. An incidental finding of a delta wave in an asymptomatic patient is also an indication for specialist referral.

Pictures

Evidence Summaries ⬆