The mechanism of nonparoxysmal atrioventricular junctional tachycardia (NPJT) is related to increased automaticity or triggered activity in the atrioventricular junctional tissue. The most common cause is digitalis toxicity, followed by inferior myocardial infarction, myocarditis, acute rheumatic fever, or cardiac valve surgery. It may also occasionally occur in healthy individuals.
The onset and termination of this tachycardia are gradual, distinguishing it from the sudden start and stop of paroxysmal reentrant tachycardia. The heart rate ranges from 70 to 150 beats per minute or faster, and the rhythm is usually regular with normal QRS complexes. Changes in autonomic nervous system tone can affect the heart rate. Atrioventricular dissociation may occur if atrial activity is controlled by the sinus node or an ectopic atrial pacemaker. In case of digitalis overdose, Wenckebach block may occur, causing irregular ventricular rhythms.
Treatment primarily targets the underlying cause. This type of arrhythmia often resolves spontaneously. If patients are well tolerated, close monitoring and treatment of the primary disease are sufficient. If digitalis is being used or digitalis toxicity is suspected, it should be discontinued immediately, and potassium supplements should be given; electrical cardioversion is not recommended. If unrelated to digitalis, β-blockers, non-dihydropyridine calcium channel blockers, or digitalis may be used. Other options include class Ia, Ic, and III (amiodarone) antiarrhythmic drugs.