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Latest revision as of 00:35, 15 March 2016

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]

Overview

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.

Historical Perspective

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

Pathophysiology

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.

EKG Examples

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

Ashman phenomenon

The above EKG strip shows:

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

Differential Diagnosis

Ventricular tachycardia
Supraventricular tachycardia with aberrancy

Differentiating Ashman's Phenomenon from Ventricular Beats

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.

Management

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.

Reference

↑ J. L. GOUAUX & R. ASHMAN (1947). "Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia". American heart journal. 34 (3): 366–373. PMID 20262631. Unknown parameter |month= ignored (help)
↑ I. A. SANDLER & H. J. MARRIOTT (1965). "THE DIFFERENTIAL MORPHOLOGY OF ANOMALOUS VENTRICULAR COMPLEXES OF RBBB-TYPE IN LEAD V; VENTRICULAR ECTOPY VERSUS ABERRATION". Circulation. 31: 551–556. PMID 14275993. Unknown parameter |month= ignored (help)
↑ I. A. SANDLER & H. J. MARRIOTT (1965). "THE DIFFERENTIAL MORPHOLOGY OF ANOMALOUS VENTRICULAR COMPLEXES OF RBBB-TYPE IN LEAD V; VENTRICULAR ECTOPY VERSUS ABERRATION". Circulation. 31: 551–556. PMID 14275993. Unknown parameter |month= ignored (help)
↑ I. I. Chaudry, E. K. Ramsaran & D. H. Spodick (1994). "Observations on the reliability of the Ashman phenomenon". American heart journal. 128 (1): 205–209. PMID 7517096. Unknown parameter |month= ignored (help)
↑ I. A. SANDLER & H. J. MARRIOTT (1965). "THE DIFFERENTIAL MORPHOLOGY OF ANOMALOUS VENTRICULAR COMPLEXES OF RBBB-TYPE IN LEAD V; VENTRICULAR ECTOPY VERSUS ABERRATION". Circulation. 31: 551–556. PMID 14275993. Unknown parameter |month= ignored (help)

Template:WikiDoc Sources CME Category::Cardiology

[1] J. L. GOUAUX & R. ASHMAN (1947). "Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia". American heart journal. 34 (3): 366–373. PMID 20262631. Unknown parameter |month= ignored (help)

[2] I. A. SANDLER & H. J. MARRIOTT (1965). "THE DIFFERENTIAL MORPHOLOGY OF ANOMALOUS VENTRICULAR COMPLEXES OF RBBB-TYPE IN LEAD V; VENTRICULAR ECTOPY VERSUS ABERRATION". Circulation. 31: 551–556. PMID 14275993. Unknown parameter |month= ignored (help)

[3] I. A. SANDLER & H. J. MARRIOTT (1965). "THE DIFFERENTIAL MORPHOLOGY OF ANOMALOUS VENTRICULAR COMPLEXES OF RBBB-TYPE IN LEAD V; VENTRICULAR ECTOPY VERSUS ABERRATION". Circulation. 31: 551–556. PMID 14275993. Unknown parameter |month= ignored (help)

[4] I. I. Chaudry, E. K. Ramsaran & D. H. Spodick (1994). "Observations on the reliability of the Ashman phenomenon". American heart journal. 128 (1): 205–209. PMID 7517096. Unknown parameter |month= ignored (help)

[5] I. A. SANDLER & H. J. MARRIOTT (1965). "THE DIFFERENTIAL MORPHOLOGY OF ANOMALOUS VENTRICULAR COMPLEXES OF RBBB-TYPE IN LEAD V; VENTRICULAR ECTOPY VERSUS ABERRATION". Circulation. 31: 551–556. PMID 14275993. Unknown parameter |month= ignored (help)

[1]

[2]

[3]

[4]

[5]

@@ Line 7: / Line 7: @@
 {{SI}}
-{{CMG}}
+{{CMG}} {{AE}} {{AN}}
 ==Overview==
@@ Line 24: / Line 24: @@
 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]].
+Besides atrial fibrillation, Ashman's phenomenon is also seen in [[multifocal atrial tachycardia]] and premature atrial tachycardia.
 ==EKG Examples==
-Lead V1 being a right ventricular lead demonstrates the right bundle branch block pattern of the aberrant conduction better than the other leads.
+Lead V1 being a right ventricular lead demonstrates the right bundle branch block pattern of the aberrant conduction better than the other leads<ref>{{Cite journal | author = [[I. A. SANDLER]] & [[H. J. MARRIOTT]] | title = THE DIFFERENTIAL MORPHOLOGY OF ANOMALOUS VENTRICULAR COMPLEXES OF RBBB-TYPE IN LEAD V; VENTRICULAR ECTOPY VERSUS ABERRATION | journal = [[Circulation]] | volume = 31 | pages = 551–556 | year = 1965 | month = April | pmid = 14275993 }}</ref>.
 <gallery>
 image:Ashman phenomenon.jpg|Ashman phenomenon
@@ Line 33: / Line 33: @@
 The above EKG strip shows:
-# Irregular heart rate and rhythm (atrial fibrillation)
+# Irregular heart rate and rhythm ([[atrial fibrillation]])
 # V1 shows aberrant conduction with short RR interval
 # Preceding long RR interval
 # No compensatory pause
-==Reference==
+==Differential Diagnosis==
-{{reflist|2}}
+* [[Ventricular tachycardia]]
+* [[Supraventricular tachycardia]] with aberrancy
+==Differentiating Ashman's Phenomenon from Ventricular Beats==
+The following criteria favors Ashman's phenomenon and is routinely used to differentiate it from a ventricular origin of the wide complex beats<ref>{{Cite journal | author = [[I. A. SANDLER]] & [[H. J. MARRIOTT]] | title = THE DIFFERENTIAL MORPHOLOGY OF ANOMALOUS VENTRICULAR COMPLEXES OF RBBB-TYPE IN LEAD V; VENTRICULAR ECTOPY VERSUS ABERRATION | journal = [[Circulation]] | volume = 31 | pages = 551–556 | year = 1965 | month = April | pmid = 14275993 }}</ref><ref>{{Cite journal | author = [[I. I. Chaudry]], [[E. K. Ramsaran]] & [[D. H. Spodick]] | title = Observations on the reliability of the Ashman phenomenon | journal = [[American heart journal]] | volume = 128 | issue = 1 | pages = 205–209 | year = 1994 | month = July | pmid = 7517096 }}</ref>:
+* 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<ref>{{Cite journal
+| author = [[I. A. SANDLER]] & [[H. J. MARRIOTT]]
+ | title = THE DIFFERENTIAL MORPHOLOGY OF ANOMALOUS VENTRICULAR COMPLEXES OF RBBB-TYPE IN LEAD V; VENTRICULAR ECTOPY VERSUS ABERRATION
+ | journal = [[Circulation]]
+ | volume = 31
+ | pages = 551–556
+ | year = 1965
+ | month = April
+ | pmid = 14275993
+}}</ref> 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.
-. Ashman R, Byer E. Aberration in the conduction of premature ventricular impulses. J La State Med Soc 8:62, 1946
+When in dilemma, it should be assumed that the wide complex beat is ventricular in origin and managed accordingly.
-==See also==
+==Management==
-* [[Atrial fibrillation]]
+The management of Ashman's phenomenon revolves around correct interpretation of the origin of wide complex tachycardia as a [[ventricular tachycardia|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]].
-* [[Electrocardiogram]]
+==Reference==
+{{reflist|2}}
 {{Electrocardiography}}
@@ Line 52: / Line 75: @@
 {{WikiDoc Help Menu}}
 {{WikiDoc Sources}}
+[[CME Category::Cardiology]]
 [[Category:Electrophysiology]]
 [[Category:Cardiology]]
-[[Category:Medical signs]]
-[[Category:Signs and symptoms]]

v t e Electrocardiography
Overview	History of the EKG • EKG interpretation basics • Normal sinus rhythm
EKG Complexes	P wave • QRS complex • ST Segment • T wave • T wave alternans • Tombstone T wave • U wave Osborn wave • H wave • K wave • Delta wave NSSTW changes
EKG Intervals	PR Interval • QRS Interval • ST Interval • QT Interval
Conduction System & Bradycardia	Cardiac pacemaker • SA node • AV node• Bundle of His • Purkinje fibers • Sinus bradycardia • First Degree AV Block • Second Degree AV Block • Complete or Third-Degree AV Block • Concealed conduction • AV Junctional Rhythms • LBBB • LAHB • LPHB • RBBB • Trifascicular block
Atrial Arrhythmias	Sinus tachycardia • Premature Atrial Contractions (PACs) • Ectopic Atrial Rhythm • Paroxysmal Atrial Tachycardia (PAT) • Paroxysmal Atrial Tachycardia (PAT) with Block • Multifocal Atrial Tachycardia (MAT) • Atrial Flutter • Atrial Fibrillation • Wandering atrial pacemaker
Ventricular Arrhythmias	Differential Diagnosis of Tachycardia with a Wide QRS Complex • Accelerated Idioventricular Rhythm • Ventricular Parasystole • Premature Ventricular Contractions (PVCs) • Ventricular tachycardia • Ventricular Fibrillation • Sudden cardiac death
EKG Abnormalities in Disease States	Hypertrophy & Dilatation • Right atrial enlargement • Left atrial enlargement • Biatrial enlargement • Left Ventricular Hypertrophy • Right Ventricular Hypertrophy • Biventricular Hypertrophy • Acute myocardial infarction • NSTEMI • STEMI • Tombstone ST elevation • Right ventricular myocardial infarction • Atrial infarction Pre-excitation Syndromes • Wolff-Parkinson-White Syndrome • Lown Ganong Levine Syndrome • Mahaim Type Preexcitation Cardiomyopathies • Arrhythmogenic Right Ventricular Dysplasia • Dilated Cardiomyopathy • Hypertrophic Cardiomyopathy Drug Effects on the EKG • Adenosine • β-blockers • Digitalis • Quinidine • Procainamide • Disopyramide • Lidocaine • Tocainide and Mexiletine • Phenytoin • Encainide, Flecainide and Propafenone • Amiodarone • Bretylium • Ca Channel Blockers • Phenothiazines • Tricyclic Antidepressants • Lithium Congenital Heart Disease • Dextrocardia • Atrial Septal Defect • Ventricular Septal Defect • Tetralogy of Fallot • Conjoined Twins or Siamese Twins • Congenital heart block Electrolyte Disturbances • Hyperkalemia • Hypokalemia • Hypercalcemia • Hypocalcemia • Nonspecific Changes Other Heart Diseases • Pericarditis • Myocarditis • Tamponade • Heart Transplantation • Sick Sinus Syndrome • Long QT Syndrome Inherited Disease • Brugada Syndrome Systemic Diseases • CNS Disease • Cardiac Tumors Heart Transplantation • EKG Changes in patient with Heart Transplantation Exogenous Effects • Hypothermia • Chest Trauma • Insect Bites • Electric Injuries
Technical Issues and Potential Errors in Interpretation	Artifacts • Lead Placement Errors • The EKG in a Patient with a Pacemaker • EKG in athletes