Definition

Any tachyarrhythmia arising from the atria or the atrioventricular (AV) junction is a supraventricular tachycardia (SVT). The term 'supraventricular tachycardia' is usually reserved for atrial tachycardias and arrhythmias arising from the region of the AV junction as a result of a re-entry mechanism (junctional tachycardias). Junctional tachycardias cause a narrow complex tachycardia. The two types of junctional tachycardias are:

• AV nodal re-entrant tachycardia (AVNRT) in which the entire tachycardia circuit is confined to the AV node and surrounding myocardium.
• AV re-entrant tachycardia (AVRT) in which there is an additional abnormal pathway between the atrium and ventricle completing the circuit.

Atrioventricular nodal re-entrant tachycardia

• The most common cause of paroxysmal regular narrow complex tachycardia. It usually affects young, healthy individuals with no organic heart disease.^[1]
• It is caused by having two distinct pathways in the region of the atrioventricular (AV) node.
  • The 'fast' pathway conducts more rapidly, but has a longer refractory period.
  • The 'slow' pathway has slower conduction properties but a shorter refractory period.
• During sinus rhythm, AV node conduction occurs via the fast pathway with a normal PR interval. If a premature atrial extrasystole arises, conduction in the fast pathway is blocked, but slow pathway conduction may continue. Conduction down the slow pathway may be sufficiently slow to allow the fast pathway to recover and allow retrograde activation to occur via the fast pathway, causing a re-entry circuit with anterograde conduction via the slow pathway and retrograde conduction via the fast pathway.
• Anterograde activation of the ventricles and retrograde activation of the atria occur virtually simultaneously, resulting in the P wave being obscured within the QRS complex, or producing a very small distortion of the terminal QRS.
• The tachycardia is readily initiated by atrial premature stimulation, and terminated by appropriately timed external stimuli or by overdrive pacing.
• A less common variant of AV node tachycardia may arise where anterograde conduction during tachycardia is via the fast pathway with retrograde conduction via the slow pathway. The atrium is activated well after the QRS complex, producing an inverted P wave with the RP interval greater than the PR interval during tachycardia.
• Occasionally, slow/fast and fast/slow tachycardias may coexist in the same patient.

Presentation

• Episodes of AV nodal re-entrant tachycardia (AVNRT) may begin at any age.
• AVNRT commonly presents for the first time in childhood or adolescence, although it may appear at any age.^[2]
• Episodes of tachycardia tend to start and stop abruptly. Episodes may last from a few seconds to several days. The frequency of episodes can vary between several a day or once in a lifetime.
• Attacks occur at random intervals, although there may be clustering of attacks.
• AVNRT has no specific association with other organic heart disease.
• Most patients have only mild symptoms, such as palpitations or the sensation that their heart is beating rapidly.
• Symptoms are most common in patients with a very rapid heart rate and pre-existing heart disease.
• More severe symptoms include dizziness, polyuria, dyspnoea, weakness, neck pulsation, and central chest pain.

Investigations

ECG:^[3]

• During sinus rhythm, the electrocardiogram is normal.
• During the tachycardia, the rhythm is regular, with narrow QRS complexes and a rate of 130-250 beats per minute.
• Atrial conduction is retrograde and produces inverted P waves in leads II, III, and aVF. Atrial and ventricular depolarisation often occur simultaneously and so the P waves are frequently obscured by the QRS complex.
• P waves may distort the last part of the QRS complex giving rise to a 'pseudo' S wave in the inferior leads and a 'pseudo' R wave in V1.
• In the relatively uncommon fast-slow AVNRT, atrial depolarisation lags behind depolarisation of the ventricles, and inverted P waves may follow the T wave and precede the next QRS complex.
• Fast-slow AVNRT is known as long RP1 tachycardia, and may be difficult to distinguish from an atrial tachycardia.

Management

• Termination of an episode of tachycardia is achieved by producing a transient AV nodal block.
• This may be achieved by vagal stimulation, intravenous verapamil or by intravenous adenosine.
• Drug prophylaxis of AVNRT is undertaken with betablockers, a combined betablocker/class III agent such as sotalol, or with AV nodal blocking drugs such as verapamil or digoxin.^[4]
• Curative treatment:
  • Is readily achieved by ablation and is indicated if patients are refractory to drugs, intolerant of side-effects or unwilling to take long-term medication.
  • Radiofrequency is delivered to the 'slow' pathway.
  • Ablation at this site is normally curative but carries a small risk (1-2%) of inducing complete heart block.

Atrioventricular re-entrant tachycardia

• Occurs as a result of an accessory conduction pathway, allowing the atrial impulse to bypass the atrioventricular (AV) node and activate the ventricles prematurely.
• A re-entry circuit forms and paroxysmal atrioventricular re-entrant tachycardias (AVRTs) occur.
• The most kind of AVRT occurs as part of the Wolff-Parkinson-White syndrome.

Orthodromic tachycardia

• The common form of AVRT.
• A premature atrial extrasystole may find the accessory pathway refractory, but be conducted through the AV node to the ventricles. Retrograde activation may then occur from the ventricle to atrium, causing a re-entry circuit.
• The QRS complex during re-entry tachycardia is normal, unless a rate-related, bundle branch block develops.
• Retrograde atrial activation causes a characteristic inverted P wave early in the ST segment.

Antidromic tachycardia

• A rarer form of AV tachycardia.
• Anterograde conduction occurs via the accessory pathway and retrograde conduction via the AV node.
• The QRS complexes are abnormal. The appearance depends on the site of the accessory pathway.

Management

• Orthodromic re-entry tachycardia may be terminated by blocking the AV node by vagal stimulation, verapamil or adenosine.^[4]
• Pre-excited atrial fibrillation (AF): digoxin or verapamil may paradoxically accelerate the ventricular rate and are therefore contra-indicated.
• Electrical cardioversion is indicated in the presence of severe haemodynamic disturbance.
• If the patient is stable, agents which slow anterograde conduction through the accessory pathway and restore sinus rhythm (eg intravenous flecainide, sotalol or amiodarone) are used.
• Drug prophylaxis is used to reduce the risk of recurrent orthodromic re-entry tachycardia or AF. Agents acting on both the AV node and the accessory pathway, such as flecainide and sotalol, are preferred.^[4]
• Radiofrequency ablation is indicated in patients with tachycardias due to concealed accessory pathways if they are not well controlled on drugs, intolerant of side-effects, or unwilling to take long-term medication.
• Symptomatic Wolff-Parkinson-White syndrome:
  • Radiofrequency ablation is increasingly considered as first-line therapy. It abolishes the risk of pre-excited AF as well as preventing further attacks of AVRT.
  • The success rate of ablation varies according to the location of the pathway, but is usually over 90%.