Ashman Phenomenon Research Articles

Aberrant Ventricular Conduction: Revisiting an Old Concept.

The well-defined concept of aberrant ventricular conduction was introduced over 100 years ago and, despite advances in cardiac physiology and electrophysiologic testing, it is still widely misunderstood. Aberrant ventricular conduction is due to physiologic refractoriness of the His-Purkinje system and in most cases does not reflect underlying conduction system disease. Electrophysiologically, aberrant ventricular conduction can manifest with premature atrial ectopics, the Ashman phenomenon with atrial tachyarrhythmias, concealed conduction, echo beats and with the sinus mechanism including rate dependent bundle branch block, bradycardia dependent bundle branch block and early sinus beats. It is important to recognise aberrant ventricular conduction in the context of a broad complex tachycardia, as the differentiation between supraventricular tachyarrhythmias with aberrant ventricular conduction and ventricular tachyarrhythmias carry different therapeutic and prognostic implications. This review will define the ECG footprints of aberrant ventricular conduction to allow accurate ECG interpretation.

EKG eponimi

Eponyms are widely represented in technical, social and natural sciences. Electrocardiography terms, named after the researcher who first described them, have not been summarized in one place until now. Wellens syndrome (Henrick Joan Joost Wellens, Dutch cardiologist) refers to a subgroup of patients with unstable angina who are at risk of developing an anterior myocardial infarction. In 2008, the Dutch cardiologist Robert Jan de Winter described a unique electrocardiographic (ECG) finding for proximal left anterior descending artery occlusion, named de Winter's pattern.Smith-Sgarbossa criteria (Elena Sgarbossa, Stephen Smith) are used to recognize acute myocardial infarction in patients with left bundle branch block. Schamroth's sign (Abraham Leo Schamroth, South African cardiologist) is an indirect ECG finding that indicates chronic obstructive pulmonary disease. Wolff-Parkinson-White syndrome (WPW) was named after the doctors who in 1930. first described the syndrome of short PR interval and abnormal QRS complexes, associated with paroxysmal tachycardia (Louis Wolff, John Parkinson, Paul Dudley White). S1Q3T3 or McGinn-White sign (Sylvester McGinn and Paul White) was first described in 1935. as an ECG finding in support of acute pulmonary heart disease. Second degree AV blocks could be type Wenckebach (Karel Frederik Wenckebach, Dutch anatomist) or type Mobitz (Woldemar Mobitz, Russian-German physician). Ashman's phenomenon (Richard F. Ashman, American physiologist) is a simple ECG manifestation of conduction disturbances, caused by a change in frequency. Bix's rule (Harold Bix) is used to recognize supraventricular tachycardia. Brugada syndrome (Pedro and Josep Brugada) is a congenital channelopathy of sodium channels, with a high risk of sudden cardiac arrest. TP segment's down-sloping in the early stage of pericarditis is called Spodick's sign (David H. Spodick, American cardiologist).

An intriguing case of regular RR and QRS alternans during idiopathic left posterior fascicle ventricular tachycardia

This study represents a case of idiopathic left posterior fascicle ventricular tachycardia (LPF-VT), which is intriguing due to regular alternation of short-long RR intervals and QRS morphology. Transthoracic echocardiogram analysis did not detect any structural heart disease. A baseline electrophysiological study was performed. Intracardiac recording during tachycardia showed V-A dissociation, confirming the final diagnosis of idiopathic LPF-VT. No regularity in the monomorphic VT was recorded. Previous relevant studies suggested that a single focus with two exits in distal branches of the left posterior fascicle or two different foci localized in the Purkinje-myocardial network of the left posterior fascicle can clarify the mechanisms. Our team proposed an additional explanation that combines the physiological refractory period with the Ashman phenomenon in individual reentrant LPF-VT circuit.

A Rare Arrhythmia in a Child with Atrial Fibrillation: Ashman Phenomenon

A Rare Arrhythmia in a Child with Atrial Fibrillation: Ashman Phenomenon

Ashman Phenomenon: Looked but Invisible

Isa Ardahanli* Author Affiliations Department of Cardiology, Bilecik State Hospital, Turkey Received: June 07, 2019 | Published: June 11, 2019 Corresponding author: Isa Ardahanli, Department of Cardiology, Bilecik State Hospital, Bilecik, Turkey DOI: 10.26717/BJSTR.2019.18.003199 Also View In:

Ashman phenomenon dynamicity during atrial fibrillation: the critical role of the long cycles

A case of a patient with Atrial Fibrillation and intermittent wide complex beats. What's the mechanism?

ECG Response: March 25, 2014

ECG Challenge: A 72-year-old man with a history of chronic obstructive pulmonary disease presents with an increase in shortness of breath that began 2 weeks ago after experiencing an upper respiratory infection presenting with a cough productive of yellowish sputum, pleuritic chest pain, and a low grade fever with temperatures of up to 100°. He did not seek medical attention, but because of worsening shortness of breath he presented to the emergency room. On physical examination he has bilateral rhonchous sounds and wheezing. A chest x-ray showed evidence of chronic obstructive pulmonary disease with hyperaeration and fibrous streaking. His O2 saturation was 88% on room air. He was placed on supplemental O2 via a nasal cannula at 4 L/min. He received albuterol therapy via a nebulizer. Shortly after his first treatment he was noted to have a transient increase in heart rate and an ECG was obtained. The first 4 QRS complexes have a …

The Long and Short of It: Ashman's Phenomenon

PRESENTATION Preoperative assessment has been shown to decrease mortality and morbidity, especially in patients with multiple medical problems. One such examination uncovered an interesting finding in the electrocardiogram (ECG) of a 74year-old woman. The patient had a past medical history of chronic obstructive pulmonary disease, hypertension, and paroxysmal atrial fibrillation. She presented to the preoperative clinic for evaluation prior to her right hip replacement surgery. While her functional capacity had been excellent, recently, her activities had been limited due to increased hip pain. She denied any active cardiac symptoms such as chest pain, shortness of breath, or orthopnea. Her regular medications included aspirin and metoprolol. She also used an albuterol inhaler as needed.

IKr blocker dofetilide promotes Ashman phenomenon in patients with atrial fibrillation

IKr blocker dofetilide promotes Ashman phenomenon in patients with atrial fibrillation

Ashman phenomenon

Ashman phenomenon

Sequential Bilateral Bundle Branch Block During Dofetilide, A New Class III Antiarrhythmic Agent, In a Patient with Atrial Fibrillation

The mechanism of wide QRS complex tachycardias during dofetilide infusion was studied in a patient with atrial fibrillation. Endocardial recordings from the intraventricular conduction system showed that dofetilide caused "classic" aberrant conduction (Ashman phenomenon, typical QRS morphology) at high prematurity ratios (preceding interval = 1.78 x coupling interval--290), thus mimicking ventricular ectopy. In addition, there was frequent sequential bilateral bundle branch block, caused by a significant difference in preceding bundle-to-bundle intervals (mean difference +/- 1 SD: 74 +/- 26 msec). The present findings may prove helpful in the clinical assessment of wide QRS complex rhythms after dofetilide and possibly other "pure" Class III antiarrhythmics.

Ashman's phenomenon—a source of nonsustained wide-complex tachycardia: Case report and discussion

The refractory period of the right bundle branch is increased when the R-R interval between the prior two conducted impulses is long. Thus, an impulse that arrives soon after the second of two impulses separated by a long R-R interval may be aberrantly conducted with a right bundle branch block morphology on electrocardiogram. This aberrant conduction is termed “Ashman's phenomenon” and is often responsible for isolated wide QRS complexes in the presence of underlying atrial fibrillation. This process may also produce runs of wide QRS complexes that must be distinguished from nonsustained ventricular tachycardia. A case of such multibeat Ashman's phenomena is presented, and the characteristics used to identify this phenomenon are discussed. A brief review of several recent studies on the differentiation of sustained ventricular tachycardia from supraventricular tachycardia with aberrancy in the setting of a regular underlying rhythm is given as well.

Ashman phenomenon of the T wave

In 1947 Gouaux and Ashman 1 described a patient with atrial fibrillation in whom the sequence of long-short cycle lengths led to QRS aberration of the QRS complex terminating the short cycle. The long cycle causes the action potential 2 and refractory period 3–5 of the next beat to lengthen. The impulse that terminates the short cycle is thus likely to meet relatively refractory ventricular conduction tissue. 6 Such QRS aberration has been referred to as the Ashman phenomenon. Because the form of the T wave is influenced by both the ventricular repolarization process and the ventricular activation sequence, aberrated QRS complexes of the Ashman phenomenon are usually accompanied by T-wave abnormalities. We report here 2 patients in whom T-wave aberration occurred in the absence of QRS aberration, when short ventricular cycles followed beats of relatively longer cycles. This is the first description of the Ashman phenomenon of the T wave without aberration of the corresponding QRS complex.

Mechanisms of Verapamil-Induced Conduction Block in Anomalous Atrioventricular Bypass Tracts

Verapamil, a calcium channel blocking agent, has been demonstrated to have depressive effects on the atrioventricular (AV) node but not anomalous AV bypass tracts. Of 39 patients with AV reciprocating tachycardia utilizing left-sided bypass tracts for retrograde conduction, intravenous infusion of verapamil (0.15 mg/kg) terminated the tachycardia in 31 patients. Verapamil interrupted the tachycardia circuit by inducing retrograde conduction block in the bypass tract rather than the AV node in 5 of these 31 patients. Electrophysiologic studies in these five patients revealed that verapamil-induced conduction block in the bypass tract could be accounted for by two distinctly different mechanisms. In three patients, verapamil induced alternating slow and fast AV nodal conduction resulting in alternating long and short cycle lengths during the tachycardia; consequently, development of the Ashman phenomenon in the bypass tract terminated the tachycardia. In the remaining two patients, the bypass tract exhibited properties similar to those of the AV node; verapamil prolonged the effective refractory period of the bypass tract, thereby terminating the tachycardia. Thus, depending on the functional properties of the bypass tract, verapamil may interrupt an AV reciprocating tachycardia circuit by exerting either a direct or indirect depressive action on the bypass tract.

Electrocardiographic criteria for differentiating aberrancy and ventricular extrasystole in chronic atrial fibrillation: Validation by intracardiac recordings

Many electrocardiographic criteria have been proposed for the differentiation of ventricular extrasystole and supraventricular conduction with aberrancy in atrial fibrillation but the validity of these have not been confirmed by intracardiac studies. We recorded His bundle electrograms in nineteen patients (eleven men, eight women) referred for diagnosis of abnormal QRS complexes in the context of chronic atrial fibrillation. Of 1,068 wide QRS complexes analyzed, 91% proved to be of ventricular origin. Electrocardiographic criteria which were specific for ventricular extrasystole included: left bundle branch block morphology, right bundle branch block morphology with a monophasic R in lead V1 or an RS or QS pattern in lead V6, presence of a "compensatory pause", i.e., compensatory cycle (V2-V3) longer than the average cycle length of ten normally conducted beats preceding the abnormal complex (927 +/- 317 vs 780 +/- 199, mean +/- SD in msec. p less than 0.005), frontal QRS axis of the abnormal complex directed superiorly or to the right and the presence of a "short-long" cycle sequence. Right bundle branch morphology with a triphasic R in lead V1 or QRS pattern in V6 and concordant initial vector in lead V1 or in more than one ECG leads were very specific for supraventricular conduction with aberrancy. Analysis of coupling interval and Ashman's phenomenon, i.e., the long-short cycle sequence, were not specific for supraventricular conduction with aberrancy. We conclude that in digitalis-treated patients with chronic atrial fibrillation the majority of abnormal QRS complexes are of ventricular origin. The diagnosis of ventricular extrasystole or aberrancy can be made using a single ECG lead (V1) and applying a combination of easily applied criteria.

Supraventricular Arrhythmia With Abnormal QRS Complex

Thus far, the discussion of supraventricular arrhythmia with abnormal QRS complex has included preexisting conduction defects, the preexcitation syndrome (Wolff-Parkinson-White syndrome), and functional bundle-branch block due to sudden shortening of cycle length, often combined with prolongation of preceding cycle; the latter is popularly called the "Ashman phenomenon." We will now present examples of other causes of aberrancy for which the mechanistic explanations may not be as clearly delineated as for those entities previously presented. <h3>Aberrancy Occurring at Slow Rates</h3> The contour of QRS complexes which escape after long pauses may differ from the QRS complex inscribed during the normal dominant rhythm; yet, the duration of these escape systoles, which is less than 0.12 seconds, strongly, but not unequivocally, indicates an origin above the bifurcation of the bundle of His (Fig 1 and 2). Basically, four theories exist which attempt to explain the cause of such aberrantly conducted junctional escape beats.

Supraventricular Arrhythmia With Abnormal QRS Complex

Thus far, the discussion of supraventricular arrhythmia with abnormal QRS complex has included preexisting conduction defects, the preexcitation syndrome (Wolff-Parkinson-White syndrome), and functional bundle-branch block due to sudden shortening of cycle length, often combined with prolongation of preceding cycle; the latter is popularly called the "Ashman phenomenon." We will now present examples of other causes of aberrancy for which the mechanistic explanations may not be as clearly delineated as for those entities previously presented. Aberrancy Occurring at Slow Rates The contour of QRS complexes which escape after long pauses may differ from the QRS complex inscribed during the normal dominant rhythm; yet, the duration of these escape systoles, which is less than 0.12 seconds, strongly, but not unequivocally, indicates an origin above the bifurcation of the bundle of His (Fig 1 and 2). Basically, four theories exist which attempt to explain the cause of such aberrantly conducted junctional escape beats.