A 2-year-old neutered male Golden Retriever was referred to the Veterinary Medical Teaching Hospital at Texas A&M University for evaluation of an arrhythmia that was ausculted during routine physical examination. No clinical signs of heart disease, such as cough, syncope, or exercise intolerance, were reported. Vaccination status was current, and the dog was receiving heartworm preventative regularly. Physical examination revealed an energetic dog despite auscultable rhythm abnormalities. An irregular rhythm with a heart rate of 120 beats/min and occasional premature beats was detected. Femoral pulses were strong bilaterally, but deficits occurred during brief bursts of tachycardia. No murmur was ausculted, and lung sounds were considered normal bilaterally.
Diagnostic evaluations included ECG, echocardiography, thoracic radiography, serum biochemical analyses, assessment of serum thyroid hormone concentrations, and determination of serum immunofluorescent antibody titer to rule out possible trypanosomiasis. Results of thoracic radiography were unremarkable, and echocardiographic findings confirmed no abnormalities in cardiac structure and function. Serum biochemical findings included mild hypernatremia and hyperchloremia suggestive of dehydration. Results of serum thyroid hormone concentration assessments (ie, free thyroxine determined via equilibrium dialysis and thyroid-stimulating hormone) were within reference limits. The dog was seronegative for Trypanosoma cruzi. Electrocardiography was performed.
ECG Interpretation
Multiple ECG tracings were acquired at the initial evaluation to assess the complexity of the arrhythmia (Figures 1–3). A sinus arrhythmia with a heart rate of approximately 100 beats/min and brief paroxysms of supraventricular tachycardia (SVT) was detected. Sinus beats maintained a constant PR interval (100 milliseconds) with apparently normal P and QRS wave morphologies. Supraventricular premature depolarizations occurred at the beginning of each burst of SVT and had P′ waves that were taller than the P waves of the sinus beats (0.3 mV vs 0.1 mV). This change in P wave morphology suggested that the beats with P′ waves did not originate from the sinus node. Paroxysms of narrow QRS complex SVT with varying degrees of conduction were recorded; these events were comprised of no more than 5 beats, beginning with a supraventricular premature depolarization and terminating abruptly (Figures 1 and 2). During the paroxysmal SVT, the QRS complexes had variable R wave height (electrical alternans) and a ventricular response rate that ranged from 140 to 200 beats/min. The P′R intervals were prolonged (160 to 220 milliseconds; Figures 1 and 2). In certain portions of the ECG traces, the P′ wave was closer to the preceding R wave, a finding consistent with short–RP′-interval SVT such as occurs with atrioventricular (AV) reentrant tachycardia that is conducted via an accessory pathway. In some of the bursts of SVT, P′ waves occurred without conducted QRS complexes, which is consistent with second-degree AV block type II. In some instances, the P′-P′ intervals occurred at a rapid rate of up to 375 beats/min and did not conduct QRS complexes (Figure 3). A ladder diagram was constructed to evaluate the possible mechanism of SVT (Figure 2).
Lead II ECG trace obtained at the initial evaluation of a dog with a nonclinical arrhythmia. A sinus arrhythmia with a heart rate of approximately 100 beats/min and supraventricular premature depolarizations are present (asterisks). The second premature depolarization is followed by a brief paroxysm of supraventricular tachycardia (SVT) that abruptly ends in second-degree atrioventricular (AV) block. The supraventricular premature depolarizations have P′ waves that are taller than the P′ waves of the sinus beats. The P′R intervals are prolonged and the RaP intervals are short. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 232, 12; 10.2460/javma.232.12.1807
Lead II ECG trace obtained at the initial evaluation of a dog with a nonclinical arrhythmia. A sinus arrhythmia with a heart rate of approximately 100 beats/min and supraventricular premature depolarizations are present (asterisks). The second premature depolarization is followed by a brief paroxysm of supraventricular tachycardia (SVT) that abruptly ends in second-degree atrioventricular (AV) block. The supraventricular premature depolarizations have P′ waves that are taller than the P′ waves of the sinus beats. The P′R intervals are prolonged and the RaP intervals are short. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 232, 12; 10.2460/javma.232.12.1807
Lead II ECG trace obtained at the initial evaluation of a dog with a nonclinical arrhythmia. A sinus arrhythmia with a heart rate of approximately 100 beats/min and supraventricular premature depolarizations are present (asterisks). The second premature depolarization is followed by a brief paroxysm of supraventricular tachycardia (SVT) that abruptly ends in second-degree atrioventricular (AV) block. The supraventricular premature depolarizations have P′ waves that are taller than the P′ waves of the sinus beats. The P′R intervals are prolonged and the RaP intervals are short. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 232, 12; 10.2460/javma.232.12.1807
Lead II ECG trace obtained at the initial evaluation from the same dog as in Figure 1. Notice the underlying sinus arrhythmia with a paroxysm of SVT that is initiated by a supraventricular premature depolarization and ends abruptly without evidence of AV block. A ladder diagram displays the possible mechanism for the SVT via an accessory pathway. Vertical lines in the ladder diagram mark the beginning of the P waves (atrial [A] level) and QRS complexes (ventricular [V] level); connecting lines between the vertical lines indicate AV conduction (AV level). H = Normal pathway. K = Accessory pathway. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 232, 12; 10.2460/javma.232.12.1807
Lead II ECG trace obtained at the initial evaluation from the same dog as in Figure 1. Notice the underlying sinus arrhythmia with a paroxysm of SVT that is initiated by a supraventricular premature depolarization and ends abruptly without evidence of AV block. A ladder diagram displays the possible mechanism for the SVT via an accessory pathway. Vertical lines in the ladder diagram mark the beginning of the P waves (atrial [A] level) and QRS complexes (ventricular [V] level); connecting lines between the vertical lines indicate AV conduction (AV level). H = Normal pathway. K = Accessory pathway. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 232, 12; 10.2460/javma.232.12.1807
Lead II ECG trace obtained at the initial evaluation from the same dog as in Figure 1. Notice the underlying sinus arrhythmia with a paroxysm of SVT that is initiated by a supraventricular premature depolarization and ends abruptly without evidence of AV block. A ladder diagram displays the possible mechanism for the SVT via an accessory pathway. Vertical lines in the ladder diagram mark the beginning of the P waves (atrial [A] level) and QRS complexes (ventricular [V] level); connecting lines between the vertical lines indicate AV conduction (AV level). H = Normal pathway. K = Accessory pathway. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 232, 12; 10.2460/javma.232.12.1807
Lead II ECG trace obtained at the initial examination of the same dog as in Figure 1. Notice the sinus arrhythmia and burst of SVT with an atrial rate that ranges from 300 to 375 beats/min without conducted QRS complexes (consistent with second-degree AV block). Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 232, 12; 10.2460/javma.232.12.1807
Lead II ECG trace obtained at the initial examination of the same dog as in Figure 1. Notice the sinus arrhythmia and burst of SVT with an atrial rate that ranges from 300 to 375 beats/min without conducted QRS complexes (consistent with second-degree AV block). Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 232, 12; 10.2460/javma.232.12.1807
Lead II ECG trace obtained at the initial examination of the same dog as in Figure 1. Notice the sinus arrhythmia and burst of SVT with an atrial rate that ranges from 300 to 375 beats/min without conducted QRS complexes (consistent with second-degree AV block). Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 232, 12; 10.2460/javma.232.12.1807
Although there was no evidence of ventricular myocardial dysfunction in the dog of this report, Holter monitoring was performed over a 24-hour period to evaluate the extent of the arrhythmias. During that monitoring, 10 paroxysms of SVT were recorded, the longest duration of which was 5 beats. Because of the lack of sustained SVT, clinical signs, or obvious underlying cardiac disease, antiarrhythmic medication was not prescribed. A surveillance plan was recommended; after 6 months, a recheck evaluation was planned including follow-up echocardiography and Holter monitoring, assuming that clinical signs of exercise intolerance, weakness, or collapse did not develop in the interim.
Discussion
Supraventricular tachycardia is a broad term for tachyarrhythmias that originate within the atria or AV junction above the bundle of His.1 Supraventricular tachycardia that has an episodic nature is described as paroxysmal. The most common mechanism for SVT is reentry, which is further classified by the location of the reentrant circuit (ie, sinus nodal, intra-atrial, AV nodal, and atrioventricular reentry).2 Other mechanisms include triggered activity (ie, atrial tachycardia such as that associated with digitalis toxicosis) and enhanced automaticity (ie, atrial and junctional tachycardia).1–3 Atrioventricular nodal reentrant tachycardia is the most common SVT diagnosed in humans; however, AV reentrant tachycardia via an accessory pathway and atrial tachycardia appear to be more frequently detected in dogs.1,2,4 If atrial tachycardia occurs at rapid rates with 1 to 1 conduction and prolongation of the PR interval, an accessory pathway should be considered.5 Electrophysiologic examinations are often required to definitively diagnose the mechanism of SVT1,6,7; however, features detected on surface ECG traces may provide enough information to refine the diagnosis. These features include the presence of P′ waves, short or long RP′ intervals, abrupt onset and offset of the SVT, the presence of AV block, and initiation by a supraventricular premature depolarization.1 Short–RP′-interval SVTs have long P′R intervals and include AV nodal reentrant tachycardia and AV reentrant tachycardia. Atrioventricular nodal reentrant tachycardia is often characterized by an absence of P waves or retrograde P waves in lead II ECG traces.1 Atrioventricular reentrant tachycardia occurs via an accessory pathway that connects the atrial and ventricular myocardia. In dogs, the most common accessory pathways are right sided and do not have evidence of pre-excitation.8 Supraventricular premature depolarizations may block at the accessory pathway, yet conduct through the AV node and reenter the accessory pathway retrograde to perpetuate a circus movement. In the dog of this report, the SVT had a short RP′ interval, was initiated with a supraventricular premature depolarization, had abrupt offset, and was occasionally terminated with AV block, which suggested that an accessory pathway may have been present. The mechanism of reentry was evaluated by use of a ladder diagram. Atrial tachycardia occurs more often in the presence of underlying atrial disease or in association with digitalis toxicosis.3 A common finding in SVT is QRS alternans, which is often rate dependent and not related to the underlying mechanism of SVT.9
Causes of SVT in humans and dogs include atrial disease (eg, increased atrial pressure or wall stress in congenital and acquired cardiac disease), infectious or inflammatory diseases (including infection with T cruzi [Chagas disease]), electrolyte imbalance (hypokalemia), endocrinopathies (eg, hypothyroidism and pheochromocytoma), neoplasia, toxins (digitalis), or high-level adrenergic stimulation and exercise.10,11 Supraventricular tachycardias may develop in the absence of structural heart disease2; however, tachycardia-induced myocardial dysfunction may result with sustained SVT.1 In young to middle-aged dogs without structural heart disease, an accessory pathway should be suspected.3
Vagal maneuvers and IV administration of drug treatments may aid in uncovering the mechanism or terminating the SVT.7,12 Because of the brief bursts of SVT in the dog of this report, vagal maneuvers and drug manipulation of the rhythm were not performed. Treatment for SVT involves the use of antiarrhythmic medications and, in some instances, transvenous catheter ablation.1,12 Long-term treatment may not be required for every patient, and treatment duration should be based on clinical signs along with a thorough evaluation of the risks and benefits of treatment.2
References
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Shenasa H, Curry P, Shenasa M. Atrial arrhythmias: clinical concepts and advances in mechanism and management. In: Mandel WJ, ed. Cardiac arrhythmias: their mechanisms, diagnosis, and management. 3rd ed. Philadelphia: JB Lippincott Co, 1995;327–367.
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Meurs KM, Anthony MA, Slater M, et al. Chronic Trypanosoma cruzi infection in dogs: 11 cases (1987–1996). J Am Vet Med Assoc 1998;213:497–500.
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