ECG of the Month

Nora K. Sheehan 1Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706.

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Sonja S. Tjostheim 1Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706.

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A 5-month-old sexually intact male German Shepherd Dog weighing 23 kg (50.6 lb) was presented for evaluation of persistent tachycardia that had been auscultated at every routine wellness visit performed by the primary care veterinarian. The first auscultation was performed when the dog was 3 months old, and the maximal heart rate recorded by the primary veterinarian was 235 beats/min. Electrocardiography (lead II) performed 1 week prior to the referral evaluation identified a supraventricular tachycardia (SVT) with a rate of 200 to 240 beats/min. Results of a CBC and serum biochemical panel were within reference intervals. The dog was reported to be clinically normal at home with no evidence of weakness, collapse, or apparent exercise intolerance.

At the referral evaluation, the dog was bright, alert, and responsive. Its auscultated heart rate was 260 beats/min, and the heart rhythm was slightly irregular. The femoral pulses were weak but synchronous with the heartbeat. There was no murmur detectable on cardiac auscultation, and no other physical examination abnormalities were identified. Echocardiography was performed, which revealed elongation of the parietal (posterior) mitral valve leaflet with mild septally (anteriorly) directed mitral valve regurgitation, consistent with mild mitral valve dysplasia without evidence of stenosis. The endocardium of the left ventricular walls was diffusely hyperechoic, and there was evidence of severe systolic dysfunction (ejection fraction [determined by the Simpson method of disks], 24%; reference range,1 46.7% to 80.7%). All heart chamber sizes were within reference limits. Trivial pericardial effusion was identified. Thoracic radiography revealed equivocal enlargement of the cardiac silhouette (vertebral heart score, 10.75 vertebrae; reference range,2 9.2 to 10.2 vertebrae) with no specific chamber enlargement. Six-lead ECG was performed.

ECG Interpretation

Electrocardiography revealed incessant narrow QRS-complex (duration, 40 milliseconds; upper reference limit,3 70 milliseconds) tachycardia with an atrial rate of 216 to 230 beats/min (Figure 1). Cycle duration irregularity was present as a result of intermittent second-degree atrioventricular (AV) block (atypical Mobitz type 1) and periods of advanced (ie, high-grade) second-degree AV block with conduction ratios of 3:1 and 4:1 (Figure 2). The polarity of the P' waves was positive in the lead I, II, III, and aVF tracings and maximally negative in the lead aVR tracing. The mean electrical axis of the P' waves was calculated to be +20° (reference range for sinus P waves,3 −18° to +90°). The direction of the vector of atrial depolarization indicated that the P' waves were coming from the more dorsal region of the right atrium (crista terminalis, right auricle, cranial portion of the vena cava, right pulmonary veins, or sinus node). The P'Q interval was variable and occasionally prolonged (100 to 180 milliseconds; reference range,3 60 to 130 milliseconds). There was a long RP' segment, and the RP':P'R ratio, which defines the relationship between the P' wave and QRS complex during narrow QRS-complex tachycardia, was 1.8 (cutoff point for a short RP':P'R ratio,4 0.7). Superimposition of each P' wave on the preceding T wave at faster cycle durations (so-called camel sign) was noted. All of these findings were consistent with a diagnosis of focal atrial tachycardia (FAT) originating from the more dorsal right atrial region.

Figure 1—
Figure 1—

Six-lead ECG tracing obtained at an initial referral evaluation of a 5-month-old German Shepherd Dog that had a history of a persistent tachyarrhythmia. Notice the incessant narrow QRS-complex (duration, 40 milliseconds; upper reference limit, 70 milliseconds) tachycardia with an atrial rate of 216 to 230 beats/min. Each P' wave is superimposed onto the preceding T wave. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 257, 3; 10.2460/javma.257.3.273

Figure 2—
Figure 2—

Lead I, II, and aVF ECG recordings obtained at the initial referral evaluation of the dog in Figure 1. Notice the narrow QRS-complex tachycardia and intermittent second-degree atrioventricular block with 2:1 and 3:1 conduction. The P'Q interval is variable and occasionally prolonged (duration, 120 to 180 milliseconds; reference range, 60 to 130 milliseconds). The P' waves are positive in the lead I, II, and aVF (and lead III [data not shown]) tracings and maximally negative in the lead aVR tracing (data not shown). The mean electrical axis of the P' wave is +20° (reference range for sinus P waves, −18° to +90°). There is evidence of a so-called camel sign formed by superimposition of a P' wave with the preceding T wave (asterisk). These findings are consistent with focal atrial tachycardia originating from the more dorsal right atrial region. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 257, 3; 10.2460/javma.257.3.273

At the referral evaluation and prior to initiation of medical treatment, the dog was fitted with a Holter monitor. The Holter evaluation confirmed incessant FAT. The fastest cycle duration was 226 milliseconds, which corresponded to a heart rate of 265 beats/min, with a P'-P' interval that ranged between 226 and 304 milliseconds. Second-degree AV block was identified with a conduction ratio up to 8:1, which resulted in a period of ventricular asystole of 2.5 seconds' duration. The overall 24-hour mean heart rate was 209 beats/min (range of mean hourly heart rates, 187 to 238 beats/min). Rare periods of underlying sinus rhythm were identified with heart rates of 150 to 170 beats/min.

Treatment of the dog with sotalol at a dosage of 0.86 mg/kg (0.39 mg/lb), PO, every 12 hours was initiated. Sotalol was chosen because of its class II and class III antiarrhythmic effects. The dosage was gradually titrated to a final dosage of 2 mg/kg (0.9 mg/lb), PO, every 12 hours and then adjusted monthly to account for the dog's growth-associated weight gain. A second Holter assessment was recommended 2 weeks following initiation of treatment but was not performed until 11 weeks after the baseline Holter assessment because of the owners' financial constraints. This recheck Holter evaluation revealed persistent incessant FAT. The mean hourly heart rates ranged from 140 to 194 beats/min, and the 24-hour mean heart rate was 168 beats/min. Second-degree AV block was identified with a conduction ratio ranging from 2:1 to 11:1 (Figure 3). The Holter monitoring results indicated that the dog's arrhythmia was inadequately controlled because the ventricular response rate remained rapid. Given the potential for a patient's increased responsiveness to one β-adrenoceptor blocker over another, administration of sotalol was discontinued, and the dog was transitioned to treatment with atenolol (1 mg/kg [0.45 mg/lb], PO, q 12 h).

Figure 3—
Figure 3—

Three-channel ECG tracing from a 24-hour Holter assessment of the dog in Figure 1 following initiation of treatment with sotalol. The rhythm on the left-hand side of the tracing is incessant focal atrial tachycardia conducted 1:1 with an atrial ectopic rate of 320 to 335 milliseconds, corresponding to a heart rate range of 179 to 187 beats/min. This is followed by a period of high-grade second-degree atrioventricular block with 11:1 conduction, which results in a 3.2-second period of ventricular asystole (shown in red). The atrial tachycardia is then conducted at a rate of 2:1, resulting in a ventricular response rate of 94 to 104 beats/min. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 257, 3; 10.2460/javma.257.3.273

A third Holter assessment was not performed until 2 months after this adjustment in treatment because of the owners' financial constraints. This Holter evaluation revealed persistence of incessant FAT with an adequately controlled ventricular response rate (24-hour mean heart rate, 134 beats/min; range of mean hourly heart rates, 108 to 164 beats/min). The fastest recorded heart rate was 202 beats/min. The rate of atrial depolarization was also slower, with the P'-P' interval rate ranging between 328 and 371 milliseconds. No definitive periods of sinus rhythm were identified. The owners reported that the dog's activity level had improved. They declined recheck echocardiography, and 11 months after the third Holter assessment, the owners reported that the dog was doing well and had no clinical signs.

Discussion

Narrow QRS-complex tachycardias are a group of tachyarrhythmias that involve at least 1 supraventricular anatomic structure during rhythm propagation. These rhythms are often referred to as SVTs, although not all SVT rhythms are classified as narrow QRS-complex tachycardias because of the potential for phasic or permanent aberrant ventricular conduction that results in wide QRS complexes.4 Supraventricular tachycardia can be subdivided into rhythms that do and do not rely on the AV node for propagation. Atrioventricular node-dependent rhythms include AV reciprocating tachycardia, AV nodal reentry tachycardia, and permanent junctional reciprocating tachycardia. Other SVT rhythms, such as atrial fibrillation, atrial flutter, and FAT, are not dependent on the AV node for generation of the tachycardic rhythm. Focal atrial tachycardia originates from ectopic foci in atrial tissue. Proposed mechanisms for FAT include increased or abnormal automaticity, triggered electrical activity, or a microreentrant circuit.4–6

In the case described in the present report, features of the 6-lead ECG tracings were used to differentiate between types of SVT. The SVT was identified as an AV node–independent rhythm because there were several instances when atrial depolarization did not result in ventricular depolarization owing to AV nodal block (Figures 2 and 3). An ECG diagnosis of FAT was made on the basis of a narrow complex tachycardia with an atrial rate of 210 to 330 beats/min, an RP':P'R ratio > 0.7, variation in cycle duration, presence of a camel sign, and absence of ventriculoatrial conduction.4,7 Atypical atrial flutter was considered a differential diagnosis; however, it was thought to be less likely because the P' wave rate in this dog was slower than what is typical for dogs with atrial flutter (range, 300 to 450 beats/min).4 Similarly, physiologic sinus tachycardia was considered unlikely given the incessant nature of the rhythm. Inappropriate sinus tachycardia could not be completely excluded but has not been proven to occur in dogs.4 In humans, the documentation of Mobitz type I second-degree AV block is strongly supportive of a diagnosis of FAT when identified in concert with the aforementioned features.4,5,8

The morphology and mean electrical axis of P' waves are essential for determining the likely location of an ectopic focus. For the dog of the present report, the P'-wave morphology was suggestive of an ectopic focus located in the roof of the right atrium. Anatomic structures located in that part of the heart include the sinus node, crista terminalis, right auricle, cranial portion of the vena cava, and right pulmonary veins.9 The P'-wave morphology and mean electrical axis did not help differentiate FAT from sinus tachycardia in this case.

For the dog of the present report, classification of the FAT as incessant was made on the basis of the ambulatory ECG findings, which indicated > 12 hours of sustained SVT in a 24-hour period.4 The mechanism of the arrhythmia could not be determined on the basis of the ECG data; therefore, treatment of the dog with sotalol (a wide-spectrum antiarrhythmic drug) was initially chosen to try to convert FAT to sinus rhythm. The class III effects of the drug would have been beneficial to the dog had the FAT been a result of a microreentry mechanism.4,10 The class II effects of sotalol may be beneficial in the treatment of some FATs that have an automatic mechanism or that are triggered by increased sympathetic tone.10 The negative dromotropic effects of this drug were also deemed beneficial for the dog of the present report because those effects would help slow the ventricular response rate if the FAT did not convert to sinus rhythm. The results from the second Holter evaluation revealed persistence of FAT with a decrease in the mean heart rate and an increase in the frequency of second-degree AV block. As such, the revised treatment goal was to lower the overall mean heart rate by reducing the firing rate of the ectopic focus and by increasing the frequency of Mobitz type I second-degree AV block. A survival benefit has been identified in dogs with atrial fibrillation when an applied heart rate control strategy results in a mean heart rate of < 125 beats/min over 24 hours.11 However, it is unknown whether application of a similar rate control goal strategy in dogs with incessant FAT would result in an improvement in survival time.

For the dog of the present report, repeated Holter assessments identified a superior response to atenolol administration, compared with the response to sotalol administration. Treatment with atenolol resulted in a slower atrial ectopic rate (ie, longer P'-P' interval) as well as a slower ventricular response rate because of an increased frequency of second-degree AV block. The owners reported improvement in the dog's exercise tolerance, which, when combined with the overall lowered mean heart rate and ectopic focus firing rate, suggested a clinical response to treatment.

Confirmation of FAT relies on electrophysiologic studies to differentiate this rhythm from atypical atrial flutter or inappropriate sinus tachycardia. In the case described in the present report, atypical atrial flutter or inappropriate sinus tachycardia was considered less likely given the 6-lead ECG and Holter monitoring findings. Results of an electrophysiologic study may also elucidate the mechanism of the FAT and provide an opportunity for ablation of the ectopic focus. For the dog of the present report, an electrophysiologic study and radiofrequency ablation procedure were recommended but declined by the dog's owners.

At the time of initial diagnosis, the dog's left ventricular systolic function was severely impaired, which was suspected to be related to the persistently elevated heart rate and incessant nature of the arrhythmia. Arrhythmia-induced cardiomyopathy is a potentially reversible cause of systolic dysfunction and cardiac chamber dilation in the face of persistent arrhythmias.12,13 Given this dog's heart rhythm, systolic dysfunction, and hyperechogenicity of the left ventricular endocardium, we could not definitively rule out myocarditis as an underlying cause for both the ectopic rhythm and echocardiographic changes. However, in the absence of overt clinical signs or a history of systemic illness, myocarditis was considered less likely in this dog. If these echocardiographic changes had been solely attributable to an arrhythmia-induced cardiomyopathy, one would have expected normalization of systolic function following improvement in overall heart rate control.13

References

  • 1. Visser LC, Ciccozzi MM, Sintov DJ, et al. Echocardiographic quantitation of left heart size and function in 122 healthy dogs: a prospective study proposing reference intervals and assessing repeatability. J Vet Intern Med 2019;33:19091920.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2. Buchanan JW, Bucheler J. Vertebral scale system to measure canine heart size in radiographs. J Am Vet Med Assoc 1995;206:194199.

  • 3. Santilli RA, Moïse NS, Pariaut R, et al. Formation and interpretation of the electrocardiographic waves. In: Santilli R, Moise NS, Pariaut R, et al, eds. Electrocardiography of the dog and cat. 2nd ed. Trento, Italy: Edra S.p.A., 2018;5256.

    • Search Google Scholar
    • Export Citation
  • 4. Santilli RA, Moïse NS, Pariaut R, et al. Supraventricular tachycardias. In: Santilli R, Moise NS, Pariaut R, et al. Electrocardiography of the dog and cat. 2nd ed. Trento, Italy: Edra S.p.A., 2018;145187.

    • Search Google Scholar
    • Export Citation
  • 5. Rosso R, Kistler PM. Focal atrial tachycardia. Heart 2010;96:181185.

  • 6. Santilli RA, Perego M, Perini A, et al. Electrophysiologic characteristics and topographic distribution of focal atrial tachycardias in dogs. J Vet Intern Med 2010;24:539545.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7. Santilli RA, Perego M, Crosara S, et al. Utility of 12-lead electrocardiogram for differentiating paroxysmal supraventricular tachycardias in dogs. J Vet Intern Med 2008;22:915923.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8. Leonelli F, Bagliani G, Boriani G, et al. Arrhythmias originating in the atria. Card Electrophysiol Clin 2017;9:383409.

  • 9. Santilli RA, Moïse NS, Pariaut R, et al. Supraventricular beats and rhythms. In: Santilli R, Moise NS, Pariaut R, et al, eds. Electrocardiography of the dog and cat. 2nd ed. Trento, Italy: Edra S.p.A., 2018;131144.

    • Search Google Scholar
    • Export Citation
  • 10. Nattel S, Gersh BJ, Opie LG. Antiarrhythmic drugs and strategies. In: Opie LH, Gersh BJ, eds. Drugs for the heart. 8th ed. Philadelphia: Elsevier Saunders, 2013;272331.

    • Search Google Scholar
    • Export Citation
  • 11. Pedro B, Dukes-McEwan J, Oyama MA, et al. Retrospective evaluation of the effect of heart rate on survival in dogs with atrial fibrillation. J Vet Intern Med 2018;32:8692.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12. Foster SF, Hunt GB, Thomas SP, et al. Tachycardia-induced cardiomyopathy in a young Boxer dog with supraventricular tachycardia due to an accessory pathway. Aust Vet J 2006;84:326331.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13. Wright KN. Interventional catheterization for tachyarrhythmias. Vet Clin North Am Small Anim Pract 2004;34:11711185.

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