Junctional tachycardia - Junctional arrhythmias

Junctional arrhythmias

Junctional tachycardia

Definition

Tachycardia with the source being at or involving the AV node (also called AV nodal tachycardias) usually with rates 140–220 bpm.

Aetiology/pathophysiology

The majority of junctional tachycardias are due to re-entry circuits.

·        These may be confined to the AV node (AV nodal re-entry tachycardia – AVNRT). The abnormal AV node consists of both slow and fast conducting pathways. Usually there is a slow anterograde pathway from atria to ventricles and a fast retrograde pathway back to the atria, which forms the re-entry circuit. The ECG during normal sinus rhythm is unremarkable. The re-entrant circuit is concealed as it slow, close to the node and does not interfere with normal AV node activity.

·        Alternatively there may be an aberrant conduction pathway at a distance from the AV node (AV re-entry tachycardia AVRT). The most well-recognised condi tion of tachycardia due to aberrant pathway is Wolff– Parkinson–White syndrome. The AV node acts as a fast or slow anterograde pathway and the accessory pathway conducts back to the atria to form the re-entry circuit.

Junctional tachycardias may occur spontaneously or may be triggered by exertion, tobacco, coffee or alcohol. They last for minutes to hours or rarely days. The frequency of occurrence is very variable even in a single individual.

Clinical features

The characteristic clinical picture is of sudden onset of palpitations sometimes accompanied by chest pain, dyspnoea and polyuria due to high circulating levels of atrial naturetic peptide. During an attack the pulse is between 140 and 220 bpm, and in severe cases, the rapid rate impairs cardiac filling and may result in hypotension.

Investigations/management

·        During a paroxysm patients require a 12-lead ECG and continuous ECG monitoring. Normal rapid regular QRS complexes are seen. In AV nodal tachycardia P waves are usually hidden within the QRS complex. If the retrograde pathway is slow with delayed atrial contraction, inverted P waves appear between complexes. Carotid sinus massage or bolus injection of adenosine may produce an immediate cessation of the arrhythmia. In contrast, atrial tachycardia and atrial flutter will produce only transient slowing of the ventricular rate due to the increase in AV node block.

·        Between paroxysms diagnosis is often difficult. Exercise testing, 24-hour Holter monitors or patient activated recorders may be useful.

·        Prophylaxis involves identification and avoidance of trigger factors where possible. Pharmacological prophylaxis may be achieved using anti-arrhythmic drugs (e.g. flecainide). Radiofrequency ablation of the AV node or accessory pathway is being increasingly used as an effective method to prevent recurrence.