ECG Interpretation

The dog was positioned in left lateral recumbency, and a 6-lead ECG recording^a (Figure 1) was obtained. Electrocardiography revealed sinus arrhythmia with intermittent premature wide QRS complexes (duration, 0.07 to 0.08 seconds; duration of sinus beat QRS complexes, 0.05 seconds [reference range, ≤ 0.06 seconds]) with left bundle branch block morphology. The mean heart rate was 132 beats/min. There were occasional wide QRS complexes noted with left bundle branch block morphology. The R-R intervals immediately preceding the wide QRS complexes were relatively shorter, compared with the R-R interval just preceding the sinus beat before the wide QRS complexes. This was consistent with the Ashman phenomenon, which is also known as the long-short phenomenon or phase 3 aberrancy. P waves were associated with the aberrantly conducted atrial premature beats. The PR intervals of the sinus beats were of normal duration (0.12 to 0.13 seconds; reference range, ≤ 0.14 seconds). However, the PR intervals of the Ashman beats were prolonged (0.14 to 0.18 seconds) likely because the premature P waves occurred prior to full atrioventricular node repolarization. The mean electrical axis was normal at + 90 degrees.

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Leads II and III ECG tracings obtained during a 6-lead ECG examination of a 10-year-old dog that had intermittent panting at rest. An intermittent grade 3/6 left apical holosystolic heart murmur had been ausculted, and an irregularly irregular rhythm was also detected. A—There is a sinus arrhythmia with aberrant conduction of atrial premature complexes (Ashman phenomenon) with left bundle branch block morphology. P waves are associated with the Ashman beats (asterisks). The classical paired long-short R-R intervals of the Ashman beats are marked by horizontal lines, and their durations are stated. The PR intervals of the Ashman beats are mildly prolonged (0.14 to 0.18 seconds), likely secondary to a lengthened atrioventricular node refractory period. Paper speed = 50 mm/s; 1 cm = 1 mV. B—Leads II and III ECG tracings obtained 2 minutes later during the 6-lead ECG examination of the dog. Notice the atrial tachycardia with physiologic block; the segment of the lead II tracing denoted by the bar indicates an area where the physiologic block is most obvious. The P-P intervals are variable, and an isoelectric shelf is evident. Some P waves are buried in the ST segment and others are fused with T waves. Intermittent Ashman beats are also present. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 256, 2; 10.2460/javma.256.2.174

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After 2 minutes, ECG revealed continued phase 3 aberrancy with normalization of the QRS complex morphology after subsequent atrial premature complexes (Figure 1). There were multiple P waves without associated QRS complexes. During the atrial tachycardia and at lower atrial rates, an isoelectric shelf was present. Occasionally, P waves were found within the ST segment, and other P waves were fused with T waves. The P-P interval was irregular and ranged from 0.08 to 0.32 seconds. The P-wave morphology was also variable, with amplitudes ranging from 0.1 mV (in association with sinus beats) to 0.2 to 0.3 mV (in association with premature atrial beats). The peak heart rate during atrial tachycardia was 280 beats/min. These findings were indicative of atrial tachycardia with physiologic block.

Discussion

The dog underwent echocardiography, which revealed apparently normal cardiac function and morphology. A lead II ECG recording obtained during the echocardiographic examination revealed brief periods of ventricular tachycardia with evidence of R-on-T phenomenon. Further diagnostic testing involving abdominal ultrasonography, clinicopathologic analyses, and assessment of circulating cardiac troponin I concentration was discussed with and declined by the owner. The dog was discharged from the hospital, and the owner was instructed to administer sotalol (0.52 mg/kg [0.24 mg/lb], PO, q 12 h). The dog was not returned for follow-up evaluation.

Ashman phenomenon, also known as phase 3 aberrancy or long-short phenomenon, was initially described by Gouaux and Ashman¹ in 1947, who identified patients with atrial fibrillation and intermittent wide QRS complexes. These aberrantly conducted atrial premature complexes were consistently preceded by a short R-R interval that followed a long R-R interval. This aberration is linked to the fact that the His-Purkinje refractory period is determined by the R-R interval of the preceding beat. Therefore, a long R-R interval will prolong the refractory period of the following beat. If a shorter R-R cycle follows, then the terminating beat will be conducted aberrantly. These beats tend to conduct with a right bundle branch block morphology owing to the inherently longer refractory period of the right bundle branch, compared with that of the left bundle branch.^2,3 However, the Ashman phenomenon can occur with left bundle branch block morphology when cardiac disease is present.³ For the dog of the present report, atrial premature complexes were conducted with left bundle branch block morphology, consistent with Ashman phenomenon. Although one could argue that these could be a combination of blocked P waves with a ventricular premature complex, it would be highly unlikely for these to occur so frequently and persistently (for this dog, every wide and bizarre QRS had an associated P wave).

The latter ECG recording obtained from the dog of the present report indicated the presence of atrial tachycardia with physiologic block. Although atrial flutter was also a differential diagnosis, atrial flutter typically has a sawtooth F-wave form (ie, no isoelectric shelf), regular P-P intervals, and a very fast atrial rate that typically reaches 340 to 440 beats/min.^4,5 The atrial rate in the ECG recording for this dog was variable, ranging from 188 to 333 beats/min. An important property specific to the AV node is decremental conduction. Decremental conduction is a consequence of the low-amplitude action potentials and high internal resistance of the AV node. Therefore, the more frequently the AV node is stimulated, the slower the conduction. This property of the AV node prevents rapid conduction through the ventricles in cases of supraventricular tachycardia. Because of the high atrial tachycardia rate in the dog of the present report, some of the atrial impulses were physiologically blocked, leading to variable conduction to the ventricles.⁶ Therefore, it was more likely that this dog had atrial tachycardia with physiologic block.

On the basis of the dog's normal echocardiographic findings, it was suspected that the dog had a primary electrical disease that caused both supraventricular and ventricular (as evidenced echocardiographically) arrhythmias. The dog might have had infectious myocarditis, but this was considered unlikely given the lack of infectious agents in the local area and the dog's lack of recent travel history. Occult cardiomyopathy was also possible.