A 17-year-old Boston Terrier was evaluated because of a loud heart murmur detected during auscultation by a veterinarian. The dog did not have clinical signs of illness. The only physical examination abnormality was a loud systolic heart murmur without precordial thrill that was loudest over the apex on the left when the dog was auscultated in a standing position. The murmur was consistent with mitral valve regurgitation.
Echocardiographic findings confirmed the presence of myxomatous mitral valve degeneration. The mitral leaflets were thickened, and the cranial leaflet had prolapsed behind the caudal leaflet. Color-flow Doppler ultrasonographic examination of the heart confirmed mitral valve regurgitation. The left atrium and left ventricle were moderately dilated. The right heart chambers were neither dilated nor hypertrophied. An ECG examination was performed (Figure 1).
Sections of ECG tracings obtained from leads I and II during a 6-lead ECG examination of a 17-year-old dog that had no clinical signs. A loud systolic heart murmur, without precordial thrill, that was loudest over the left apex was noted when the dog was auscultated in standing position. A—The lead I tracing indicates a sinus rhythm with aberrant conduction in the form of a right bundle branch block. Deep S waves were present in leads I, II, III, aVF, V2, and V4 (data not shown). The mean electrical axis in the frontal plane was shifted to the right. B—This portion of the lead II tracing contains 3 sinus beats with normal conduction (narrow qR waves) among the aberrantly conducted beats. The P-P intervals vary only slightly. C—This portion of the lead II tracing reveals sinus rhythm with normal conduction except for an atrial premature contraction that is conducted aberrantly (Ashman phenomenon) with a right bundle branch block pattern. Notice the fused T-P wave preceding the premature beat. The premature atrial depolarization reset the sinoatrial node with a slight pause. Paper speed = 25 mm/s; 1 cm = 1 m V.
Citation: Journal of the American Veterinary Medical Association 246, 9; 10.2460/javma.246.9.962
ECG Interpretation
Electrocardiography revealed a predominantly normal sinus rhythm with a rate of approximately 150 beats/min (Figure 1). There was an intermittent intraventricular conduction disturbance consistent with right bundle branch block. During a period of normal conduction, a supraventricular premature contraction occurred with aberrant conduction, also with a right bundle branch block pattern. The P′ wave was fused with the preceding T wave. The P′ wave had positive polarity in the lead 2 tracing (also in tracings from leads 1, 3, and AVF [data not shown]) with a normal PR (Pq) interval (0.09 seconds; reference range, 0.06 to 0.13 seconds), indicating that the premature beat was probably atrial in origin. An atrial premature contraction with aberrant conduction was consistent with the Ashman phenomenon.1–3
The Ashman phenomenon is an example of aberrancy caused by the physiologic changes in the refractory period of the conduction system. When a short cycle duration (cycle duration equals the R-R interval) follows a longer cycle duration, such as with an atrial premature contraction, there is the possibility of aberrant conduction in the ventricular conduction fibers.1–3 With normal heart rates, aberrant conduction is readily discerned from ventricular ectopic activity by the presence of a preceding P′ wave detected during ECG examination. However, when aberrancy occurs during rapid sinus tachycardia or atrial tachycardia, the rhythm may appear ominous (as what may be termed a sheep in wolf's clothing). When a dog is nervous during an ECG examination, it may appear to have a ventricular rhythm with a high heart rate (Figure 2). However, during a subsequent evaluation recorded some hours later when the heart rate is considerably slower, the same dog may appear to have a sinus rhythm with aberrant conduction in the form of a right bundle branch block. A supraventricular rhythm with aberrant conduction might be confused for ventricular tachycardia if the P waves are fused with the preceding T waves. In a clinical scenario such as that, the differential diagnosis would be ventricular tachycardia or accelerated ventricular rhythm versus sinus tachycardia with aberrant conduction.
Representative lead II tracings obtained from a nervous 12-year-old dog with a systolic heart murmur consistent with mitral valve regurgitation. The dog had echocardiographic confirmation of mitral valve regurgitation with left atrial and left ventricular enlargement. A—During the initial ECG examination, the dog's heart rate is approximately 188 beats/min. P waves are not visible, and the rhythm appears to be ventricular in origin. The dog was administered a lidocaine bolus, but the heart rate and rhythm did not change. B—A follow-up ECG examination was performed after the dog became calm (approx 1. 5 hours after the initial evaluation). The dog has a sinus rhythm at approximately 112 beats/min. There is aberrant ventricular conduction in the form of a right bundle branch block. Notice that the inscription of ventricular activation (QRS waveform) in this panel is nearly identical to that in panel A. Panel A may represent sinus tachycardia with aberrant ventricular conduction masquerading as a ventricular rhythm. If so, the PR (Pq) interval is prolonged given that the PR (Pq) segment is long enough to allow P waves to be visible in the down strokes of the T waves. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 246, 9; 10.2460/javma.246.9.962
Discussion
The refractory periods of the His-Purkinje system are rate dependent, and as the rate increases, the refractory period of the His-Purkinje system and cardiac muscle decreases.1,2 The refractory period is directly related to previous cycle durations, so that relatively longer cycle durations are associated with longer recovery times and shorter cycle durations are associated with shorter recovery times. When an abrupt cycle of short duration follows a cycle of longer duration, aberrant ventricular depolarization may occur. This aberrant depolarization usually takes the form of a right bundle branch block because the refractory period of the right bundle is slightly longer than that of the left bundle.3
Intermittent intraventricular conduction disturbances may be heart rate dependent or may be unrelated to changes in heart rate. Regardless, aberrant conduction results from incomplete repolarization of the His-Purkinje system at the time it is entered by a supraventricular impulse.1 In our experience, intermittent or unstable intraventricular conduction disturbances are usually rate dependent and associated with older dogs with heart disease. The cycle duration in the dog of the present report was consistently 380 milliseconds, and both normal and aberrant ventricular activations were recorded. Functional aberrancy is dependent on an abrupt change from a long cycle duration to a short cycle duration. Functional aberrancy, often referred to as the Ashman phenomenon in people, can occur with atrial premature contractions.3 The intermittent right bundle branch block in the dog of this report probably was associated with a repolarization abnormality that predisposed the dog to aberrancy when an atrial premature contraction occurred. When aberrant conduction is present with sinus tachycardia or atrial tachycardia, it may be confused for ventricular tachycardia and inappropriate treatment might then be administered.
References
1. Denes P, Wu D, Dhingra R. The effect of cycle lengths on cardiac refractory lengths in man. Circulation 1974; 49: 32–38.
2. Denker ST, Gilber CG, Shenasa M, et al. An electrocardiographic-electrophysiologic correlation of aberrant ventricular conduction in man. J Electrocardiol 1983; 16: 269–275.
3. Chenevert M and Lewis RJ. Ashman's phenomenon—a source of nonsustained wide-complex tachycardia: case report and discussion. J Emerg Med 1992; 10: 179–183.
