Introduction

A 10-year-old 28.5-kg spayed female Boxer was presented to Animal Referral Centre for evaluation of ventricular arrhythmias. Polymorphic ventricular tachycardia had first been diagnosed 2 years earlier, when the dog was presented to an emergency clinic with suspected pancreatitis. Results of echocardiography and hematologic and serum biochemical testing performed at that time were unremarkable. The dog was started on sotalol (80 mg, PO, q 12 h).

The dog recovered from pancreatitis and remained clinically well until 2 years later, when 2 episodes of collapse occurred. A 24-hour Holter recording showed a mean heart rate of 45 beats/min (minimum, 31 beats/min; maximum, 64 beats/min). The P waves could not be seen on the Holter recording owing to baseline artifact. There was evidence of continuing ventricular ectopy, with ventricular couplets occurring at a rate of 180 beats/min. The collapse episodes were presumed to be secondary to severe bradycardia, and the dog was switched from sotalol to mexiletine (150 mg, PO, q 8 h). No further collapse episodes were witnessed, and during a reassessment 1 month later, the heart rate was 80 beats/min. Continuation of mexiletine and cardiac referral were advised.

At presentation, the dog was bright, alert, and responsive and was reported to be clinically well with good exercise tolerance. The heart rate was 80 beats/min with a regular rhythm. The femoral pulses were strong and synchronous. Echocardiographic examination revealed no abnormal structures, cardiac dimensions, or cardiac function. However, a simultaneous ECG performed during the echocardiographic examination showed multiple nonconducted P′ waves. A 6-lead ECG was obtained (Figure 1).

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Six-lead ECG recording of a 10-year-old Boxer with a history of ventricular arrhythmias; the dog was receiving mexiletine at the time of the recording. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 260, 12; 10.2460/javma.20.10.0589

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ECG Interpretation

There were 2 slightly different P wave morphologies. The P waves (amplitude, 0.15 mV; duration, 50 milliseconds) of the first morphology were considered sinus in origin and had a mean electrical axis of +90°. These P waves were positive in leads II, III, and aVF and maximally negative in lead aVR and were always associated with a QRS complex, with a fixed PQ interval of 160 milliseconds, consistent with first-degree atrioventricular block. These sinus P waves occurred at a P-P interval of 750 milliseconds (atrial rate, 80 beats/min). The QRS complexes that followed the sinus P waves were of prolonged duration (100 milliseconds) and had right axis deviation (mean electrical axis, –90°), consistent with right bundle branch block morphology.

The second P wave morphology was similar to the morphology of the sinus P waves, but these P′ waves had a slightly smaller amplitude (amplitude, 0.12 mV; duration, 50 milliseconds). The mean electrical axis of the P′ waves was +90°, suggesting an upper right atrial origin. The P′ waves occurred independently of QRS complexes and occasionally were superimposed on a QRS complex, T wave, or P wave. The interectopic P′-P′ interval was irregular and ranged from 240 to 340 milliseconds, equating to an atrial rate of 170 to 250 beats/min. None of the P′ waves were conducted to the ventricles during the 5-minute ECG recording, and the ectopic P′ waves had no effect on the sinus P-P and R-R intervals, consistent with atrial dissociation (Figure 2).

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Ladder diagram showing atrial dissociation. The 2 independent atrial rhythms are annotated in different colors (black for sinus P waves and red for ectopic P′ waves). The P′-P′ intervals (red) show slight irregularity. Two single P′′ waves (green) are seen, representing superimposed P and P′ waves. The P′′ wave is not a fusion wave because the 2 wavefronts do not meet, as defined by atrial dissociation.

Citation: Journal of the American Veterinary Medical Association 260, 12; 10.2460/javma.20.10.0589

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Because atrial dissociation is considered a benign arrhythmia and the dog was clinically well, no change in treatment was advised. Follow-up 24-hour Holter monitoring was recommended to review the ventricular arrhythmias, but this was declined. Repeated cardiac assessment in 6 to 12 months was advised.

Discussion

Atrial dissociation (AD) is a rare supraventricular arrhythmia characterized by the coexistence of 2 independent atrial rhythms.^1–3 Typically, one of the rhythms is sinus and the other is a unilateral ectopic atrial rhythm confined to 1 portion of the atrium. The ectopic atrial rhythm is protected from the electrical influence of the surrounding myocardial tissue (entrance block) and does not propagate to the ventricles (exit block). Thus, the 2 rhythms do not interfere with each other. The P′-P′ interval in AD is not perfectly regular.

Atrial parasystole (AP) is another type of ectopic atrial rhythm characterized by the presence of an abnormal atrial focus that can occur alongside a sinus rhythm. Atrial parasystole can display entrance block, but, in contrast with AD, P′ waves can be conducted to the ventricles as long as they reach the myocardium when it is in an excitable state.¹ The P′-P′ intervals during AP can vary but are multiples of a common denominator. Because the ectopic atrial rhythm in the dog of the present report appeared to display exit block and the P′-P′ intervals were irregular, we believed the dog was more likely to have had AD than AP.

The underlying mechanism of AD is complete inter- or intra-atrial block, confining the ectopic atrial rhythm to a single atrium (left or right) or a single portion of 1 atrium. The lack of dyssynchrony between left and right atrial contractions observed on echocardiography may suggest that an intra-atrial block was more likely in our case; however, an electrophysiological study would be needed to confirm this suspicion.

The cause of AD in this dog was unknown. In humans, AD has been documented with ischemic heart injury and cardiac surgery but can also be incidental.⁴ In dogs, it is often documented incidentally, although it has been described in 1 dog with high vagal tone.^2,3,5 We speculated the AD in this case was incidental, although the influence of mexiletine on conduction system properties should be considered. Unfortunately, ECG recordings obtained prior to initiation of mexiletine were not available for review, and discontinuing mexiletine was not recommended owing to the history of polymorphic ventricular tachycardia and the fact that the patient was clinically well and AD is considered benign.^2,3

Other differential diagnoses for the ECG appearance include pseudoatrial dissociation, whereby P′ waves are in fact an artifact caused by rhythmic movement of the animal. This was thought to be unlikely because the dog was still during the ECG recording and the P′ waves were not associated with breathing. Frequent, nonconducted atrial premature complexes were also possible but considered less likely because they usually have a fixed P-P′ interval, which was not observed in this dog, and none of the P′ waves were conducted to the ventricle, as would be expected with atrial premature complexes.

In summary, we report a Boxer with AD without any clinical signs. Atrial dissociation should be considered in the differential diagnoses when there are 2 independent atrial rhythms.