Introduction

A 12-year-old 37.3-kg neutered male Boxer presented with a 3-day history of seizures and vomiting. On physical examination, no murmur was auscultated; however, the patient was tachycardic and thus an ECG was performed (Figure 1).

Six-lead ECG recording from a 12-year-old Boxer with tachycardia. There is a regular rhythm with a heart rate of 173 beats/min. The QRS complexes are narrow, and there are small, negative P waves (arrows) buried in the ST segment of every QRS complex, suggesting a junctional tachycardia originating from the distal atrioventricular bundle of the atrioventricular node and a 1:1 ventriculoatrial conduction. The P wave and QRS complex morphologies remained constant throughout the ECG recordings. Paper speed = 50 mm/s; 5 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 260, 14; 10.2460/javma.21.02.0079

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Six-lead ECG recording from a 12-year-old Boxer with tachycardia. There is a regular rhythm with a heart rate of 173 beats/min. The QRS complexes are narrow, and there are small, negative P waves (arrows) buried in the ST segment of every QRS complex, suggesting a junctional tachycardia originating from the distal atrioventricular bundle of the atrioventricular node and a 1:1 ventriculoatrial conduction. The P wave and QRS complex morphologies remained constant throughout the ECG recordings. Paper speed = 50 mm/s; 5 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 260, 14; 10.2460/javma.21.02.0079

• Download Figure
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Six-lead ECG recording from a 12-year-old Boxer with tachycardia. There is a regular rhythm with a heart rate of 173 beats/min. The QRS complexes are narrow, and there are small, negative P waves (arrows) buried in the ST segment of every QRS complex, suggesting a junctional tachycardia originating from the distal atrioventricular bundle of the atrioventricular node and a 1:1 ventriculoatrial conduction. The P wave and QRS complex morphologies remained constant throughout the ECG recordings. Paper speed = 50 mm/s; 5 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 260, 14; 10.2460/javma.21.02.0079

• Download Figure
• Download figure as PowerPoint slide

ECG Interpretation

A 6-lead ECG recording revealed a regular rhythm with a heart rate of 173 beats/min. The P wave and QRS complex morphologies remained constant throughout the recording. The P waves had negative deflections and were buried in the ST segments in leads II, III, and aVF. There was a regular R-R interval, and the QRS complexes were tall and narrow, suggesting a supraventricular origin for the arrhythmia and normal His bundle ventricular activation. A P wave could be found within every QRS complex, suggesting 1:1 ventriculoatrial conduction. The diagnosis was focal junctional tachycardia.

Discussion

Supraventricular tachycardia is a broad term that includes various rapid rhythm abnormalities with the focus of the heart beats above the ventricles.¹ This arrhythmia can be broadly classified into atrial or junctional tachyarrhythmias depending on whether they are initiated and maintained in atrial tissue or the atrioventricular node, respectively.¹ On ECG recordings, supraventricular tachycardias usually appear to have regular and narrow QRS complexes with regular R-R intervals and can be further categorized according to the RP interval.¹ This interval represents the time between ventricular activation (ie, the R wave in the QRS complex) and atrial activation (ie, the P wave) and differs depending on the origin of the abnormal rhythm.¹ A supraventricular tachycardia is classified as short RP′ supraventricular tachycardia if P′ waves appear closer to the preceding QRS complex than the subsequent QRS.^1,2 On the other hand, if P′ waves are further from the preceding QRS complex than the subsequent QRS, the supraventricular tachycardia is classified as long RP′ supraventricular tachycardia.^1,2 Generally, atrial tachyarrhythmias are associated with long RP′ intervals and junctional tachyarrhythmias are associated with short RP′ intervals.^1,2

If ectopic beats arise from the junctional area and have a depolarization rate greater than the maximum inherent rate of atrioventricular nodal tissue (60 beats/min), the arrhythmia is described as junctional tachycardia.^1–3 The atrioventricular node is anatomically divided into the proximal atrioventricular bundle, compact node, and distal atrioventricular bundle, and all 3 areas contain cells capable of spontaneous depolarization.³ On an ECG recording, the position of the P wave in relation to the QRS complex will change depending on the source within the atrioventricular node of the ectopic beats. Ectopic beats originating in the atrionodal bundle or proximal atrioventricular bundle must travel through the compact node before activating the ventricles and have a normal physiologic delay as they traverse.³ Thus, impulses reach the atria before the ventricles and P waves will appear before the QRS complexes with a normal or short PR interval.³ Ectopic beats originating from the compact node result in simultaneous atrial and ventricular activation and produce P waves that are hidden within the QRS complexes.³ Finally, ectopic beats originating from the distal atrioventricular bundle will result in P waves within the descending R or ST segment.³ This is due to quick activation of the ventricles and a concurrent delayed impulse as it crosses the compact node to reach atrial tissue.³

The deflection of the P′ wave on an ECG recording and its mean electrical axis are other useful indicators when attempting to identify arrythmias of junctional origin. Negative P′ waves in leads II, III, and aVF and positive P′ waves in leads aVL and aVR with a P′ electrical axis between –80° and –100° suggest the presence of impulses traveling in a retrograde manner from the atrioventricular node toward the atria, as is typically seen with junctional tachycardia.³

The dog of the present report had a focal junctional tachycardia with 1:1 ventriculoatrial conduction. The origin of the tachyarrhythmia was likely within the atrioventricular node or distal atrioventricular bundle, in that P waves were absent before each QRS complex and instead buried in the ST segment. The P waves were also negatively deflected and found within every QRS complex, suggesting retrograde atrial activation and 1:1 ventriculoatrial conduction, respectively. Focal junctional tachycardia has been reported in dogs, with Labrador Retrievers overrepresented, and is said to be associated with isorhythmic atrioventricular dissociation and periods of 1:1 ventriculoatrial conduction.⁴

Incessant forms of junctional tachycardia can induce cardiomyopathy and must be treated efficiently and appropriately.^1–3 If extracardiac diseases are causing the arrhythmia, efforts should be focused on managing them and correcting any underlying abnormalities such as electrolyte disturbances.^2,3 Drug treatment includes class I, II, and III antiarrhythmics, with sotalol anecdotally associated with the best results.³ Calcium channel blockers may also help decrease enhanced automaticity that originates above the compact node.³ Furthermore, radiocatheter ablation with artificial pacing has been described to manage atrial and junctional tachycardias in dogs.³

For the dog of the present report, results of a CBC were unremarkable, and a serum biochemical profile revealed only mildly high hepatic enzyme activities. Thoracic radiography revealed mild generalized cardiomegaly; consequently, treatment with diltiazem (1.2 mg/kg, PO, q 8 h) was initiated. At a recheck examination 1 week later, a surface ECG indicated that the focal junctional tachycardia was controlled. However, the dog continued to have seizures and was ultimately euthanized 1 month later.