Ashman phenomenon

Ashman’s Phenomenon is an aberrant intra-ventricular conduction abnormality that occurs because of variable cycle length in atrial fibrillation. It presents as isolated wide complex beats manifesting as a right bundle branch block morphology with short RR cycle length immediately following a longer RR cycle. It represents an aberrantly conducted complex that originates above the AV node, rather than a complex that originates in either the right or left ventricle.

In an emergency setting, this phenomenon can be easily confused with non-sustained ventricular tachycardia which also presents with a wide ORS complex. Misinterpretation of this finding can potentially result in unnecessary testing and health care costs.

Ashman’s phenomenon was first described in a patient with atrial fibrillation in 1947 by Gouaux JL and Ashman R^[1].

Ashman’s phenomenon classically occurs in atrial fibrillation, in which not all impulses originating the atrium are regularly conducted through the AV node. This variability in RR cycle lengths predisposes to the aberrant conduction.

The key to understanding the pathophysiology of Ashman’s phenomenon is the fact that refractory period of an impulse that travels in the ventricular muscle varies from beat to beat in patients with an underlying atrial fibrillation. Longer RR cycles(slower hear rate) have longer refractory period whereas shorter RR cycles(faster hear rate) have a shorter refractory period.

When a long RR cycle is followed by a shorter RR cycle, the cardiac muscle cells are still in the refractory period from the preceding longer beat. This gives rise to a bundle branch block like pattern, more commonly a right bundle, leading to aberrant conduction. Also, in atrial fibrillation, there is no P wave to indicate that the tachycardia is supraventricular and not due to aberrant conduction.

Besides atrial fibrillation, Ashman’s phenomenon is also seen in multifocal atrial tachycardia and premature atrial tachycardia.

Lead V1 being a right ventricular lead demonstrates the right bundle branch block pattern of the aberrant conduction better than the other leads^[2].

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  Ashman phenomenon

The above EKG strip shows:

1. Irregular heart rate and rhythm (atrial fibrillation)
2. V1 shows aberrant conduction with short RR interval
3. Preceding long RR interval
4. No compensatory pause

• Ventricular tachycardia
• Supraventricular tachycardia with aberrancy

The following criteria favors Ashman’s phenomenon and is routinely used to differentiate it from a ventricular origin of the wide complex beats^[3][4]:

• Right bundle branch block morphology
• The wide ORS complex occurs immediately following a long RR interval cycle
• No compensatory pause
• No fixed coupling interval

Also, Sandler and Marriot^[5] further extended the criteria to include demonstration of wide complex beats in lead V1 and appearance of triphasic QRS complex strongly suggesting aberrant conduction, whereas mono and biphasic QRS complexes suggests ventricular tachycardia. Furthermore the initial depolarization vector in same direction as the preceding beat favors aberrancy.

However, these criteria have a poor sensitivity and specificity and are termed unreliable, as there seems to be an exception for every rule. Later, Ashman’s index was developed to clearly differentiate between the two. Ashman’s index was defined as the ratio of long cycle length to short cycle length. The study of this index showed that no ratio examined on intracardiac study could differentiate between VT and aberrancy. Thus, the best way to differentiate between the two is in the electrophysiologic laboratory.

When in dilemma, it should be assumed that the wide complex beat is ventricular in origin and managed accordingly.

The management of Ashman’s phenomenon revolves around correct interpretation of the origin of wide complex tachycardia as a non-sustained ventricular tachycardia can signify structural heart defects, electrolyte abnormalities and progression to sustained VT if not corrected. It also puts the patient at risk for sudden cardiac death.

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