In
1947 Gouaux and Ashman first reported an aberrant ventricular
conduction during atrial fibrillation secondary to change
in QRS cycle length. This conduction pattern, known as
Ashman Phenomenon, is typically seen when a relatively
long cycle is followed by a relatively short cycle. The
beat with a short cycle often has right bundle-branch
block (RBBB) morphology.
Ashman
Phenomenon is caused by a change in the heart rate affecting
electrophysiological properties of the heart. The pathophysiology
of Ashman Phenomenon depends on the relative refractory
period of the conduction tissues and the heart rate. Refractory
period changes with the R-R interval of the preceding
cycle; shorter duration of action potential is associated
with a short R-R interval and prolonged duration of action
potential is associated with a long R-R interval. A longer
cycle lengthens the ensuing refractory period, and, if
a shorter cycle follows, the beat terminating the cycle
is likely to be conducted with aberrancy. Because one
of the bundle branch, usually right is still in refractory
period and resulting complex has bundle branch block pattern
as shown in Fig. 1.
Bundle
branch block pattern in aberrant conduction occurs when
a supraventricular impulse reaches the His-Purkinje system
while one of its branches is still in the relative or
absolute refractory period. This results in slow or blocked
conduction through this bundle branch and delayed depolarization
through the ventricular muscles, causing a bundle-branch
block configuration on electrocardiogram. Because refractory
period of right bundle branch is longer than left bundle
branch so right bundle branch block pattern is more frequent
than left bundle branch block.
Figure
I. Rhythm strip demonstrating atrial fibrillation
with aberrant conduction “a” (Ashman Phenomenon).
Aberrant conduction has right bundle block configuration
and occurs when a short R-R interval follows a
long R-R interval.
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Ashman
phenomenon is related to the underlying pathologic conditions
and is a common electrocardiographic finding in atria
fibrillation, atrial tachycardia, and atrial ectopy. These
conditions cause a change in the refractory period of
bundle branches or ventricular tissue.
Clinically,
Ashman Phenomenon by itself is asymptomatic. Symptoms,
if present, are related to the premature complexes but
not due to aberrantly conducted complexes. No specific physical examination findings are described for Ashman
Phenomenon, however in associated atrial fibrillation
an irregular pulse, pulses deficit or fast
heart rate may be seen.
Understanding
Ashman Phenomenon helps to differentiate it from ventricular
premature contractions and ventricular tachycardia. A
supraventricular impulse with aberrant conduction is confused
with ventricular premature contractions and a series of
consecutive aberrantly conducted supraventricular impulses
may look like ventricular tachycardia. Thus differentiating
wide complex arrhythmias of ventricular origin from supraventricular
arrhythmias with aberrancy is important because the prognosis
and treatment of these conditions are different.
Ashman
phenomenon is typically diagnosed by 12 lead surface electrocardiogram.
However in difficult cases more invasive electrophysiological
studies are required to establish the origin of supraventricular
or ventricular arrhythmia.
Criteria
described by Fisch are useful to establish diagnosis of
Ashman phenomenon and are 1) relatively long cycle immediately preceding the cycle terminated
by the aberrant QRS complex: A short-long-short interval
is even more likely to initiate aberration. Aberration
can be LBBB and RBBB, even in the same patient.
2) RBBB-form aberrancy with normal orientation
of the initial QRS vector: Concealed perpetuation of aberration
is possible, such that a series of wide QRS supraventricular
beats is possible. 3) Irregular coupling of aberrant QRS complexes
4) Lack of a fully compensatory pause.
Treatment
includes diagnosis and appropriate management of disease
entities associated with Ashman Phenomenon, such as atrial
fibrillation and atrial tachycardia. No treatment is needed
for isolated complexes.
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