ECG of the Month

Evan S. Ross 1Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66502.

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Justin D. Thomason 1Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66502.

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A 1-year-old 19-kg (41.8-lb) spayed female Collie that had undergone surgical correction of a partial atrioventricular septal defect (AVSD; ostium primum defect) 6 months earlier underwent a recheck evaluation at a veterinary teaching hospital. After the previous echocardiographic diagnosis of a partial AVSD and a cleft anterior mitral valve leaflet had been made, surgical correction of both the dog's abnormalities had been performed with cardiopulmonary bypass. A right atriotomy was performed to access the partial AVSD. The cleft in the mitral valve leaflet was observed through the septal defect and closed with 4 cruciate sutures. The partial AVSD was repaired with a polytetrafluoroethylene patch. The dog had recovered without complications from surgery. Surface ECG performed at the 2-week and 3-month postoperative recheck evaluations revealed a sinus rhythm with right bundle branch block.

At the time of the 6-month recheck evaluation, the dog had been weaned off all cardiac medications and was clinically well. Salient features detected during cardiologic examination were a grade 3/6 left apical systolic heart murmur and an irregular rhythm with a pulse rate of 120 beats/min with no evident pulse deficits. Echocardiography revealed mild residual left-to-right shunting through the AVSD at the ventral aspect of the polytetrafuoroethylene patch; this degree of shunting was considered to be hemodynamically unimportant. The anterior mitral valve leaflet appeared thickened with tethering to the interventricular septum, which was responsible for moderate mitral valve regurgitation. A 6-lead ECG recording was obtained at this time (Figure 1).

Figure 1—
Figure 1—

Six-lead ECG recording obtained during a recheck evaluation of a dog with a previous history of partial atrioventricular septal defect and cleft mitral valve repair. Notice the positive deflections corresponding to atrial depolarization at a rate of 400 beats/min. These deflections do not have the characteristic features of F waves associated with typical atrial flutter. There is a variable degree of atrioventricular conduction resulting in 2:1 to 5:1 second-degree atrioventricular block. The QRS complexes have right bundle branch block morphology. On the basis of the ECG findings and the dog's history, it is likely that this atypical atrial flutter can be further characterized as incisional atrial reentrant tachycardia. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 256, 3; 10.2460/javma.256.3.306

ECG Interpretation

Electrocardiography (Figure 1) revealed an irregularly irregular rhythm with a calculated mean heart rate of 120 beats/min over the course of the ECG tracing. There were positive deflections in the inferior leads corresponding to atrial depolarization that occurred at a regular interval with an atrial rate of 400 beats/min. These deflections were not consistent with the sawtooth appearance of F waves in typical atrial flutter (AFL). Given the rapid rate of depolarization, these were considered to be F waves moving with clockwise depolarization. The F waves were often embedded within T waves. There was a variable degree of atrioventricular (AV) conduction evident that ranged from 2:1 to 5:1 second-degree AV block. In addition, there was variable AV nodal conduction velocity as evidenced by the changing duration of PR intervals. The QRS complexes were wide (duration, 0.1 seconds) with negative deflections in leads II, III, and aVF, suggestive of right bundle branch block. The rhythm diagnosis was macroreentrant supraventricular tachycardia, consistent with atypical AFL, with physiologic AV block and right bundle branch block. On the basis of the dog's history of AVSD repair, the authors suspected that the AFL could be further characterized as an incisional atrial reentrant tachycardia (IART).

Because of the ECG findings, the dog was treated with sotalol (2.1 mg/kg [0.95 mg/lb], PO, q 12 h). Two weeks after the start of treatment with sotalol, a surface ECG examination was performed by the primary veterinarian, which revealed a regular sinus rhythm with a heart rate of 90 beats/min. The dog was rechecked at the veterinary teaching hospital 3 months after the start of sotalol administration. Six-lead ECG performed at that time revealed a sinus arrhythmia with a calculated mean heart rate of 90 beats/min over the course of the ECG tracing (Figure 2). There was prolongation of the PR interval (duration, 160 milliseconds) consistent with first-degree AV block. The QRS complexes were wide (duration, 0.08 seconds) with right bundle branch block morphology. Holter monitoring of the dog for 24 hours revealed sinus rhythm with first-degree AV block and rare single atrial premature complexes throughout the recording.

Figure 2—
Figure 2—

Lead II ECG tracing obtained from the dog in Figure 1 at 3 months after the start of treatment with sotalol (2.1 mg/kg [0.95 mg/lb], PO, q 12 h). There is an underlying sinus rhythm with right bundle branch block morphology. Notice the absence of rapid atrial depolarizations that were detected previously. Paper speed = 25 mm/s; 1 cm =1 mv.

Citation: Journal of the American Veterinary Medical Association 256, 3; 10.2460/javma.256.3.306

Discussion

Traditionally, atrial tachycardia can be distinguished from AFL on surface ECG recordings.1–3 A newer classification scheme defines atrial tachycardia on the basis of mechanisms determined by electrophysiologic studies. The first type of atrial tachycardia is focal atrial tachycardia, which can be caused by an automatic, triggered, or microreentrant mechanism.1,2 On surface ECG recordings, focal atrial tachycardia typically has a ventricular response rate between 210 and 330 beats/min in dogs. Generally, there are regular R-R intervals with possible periods of irregularities and atrioventricular block. The P’ waves are discrete with a variable axis in the frontal planes, but generally have a superior to inferior orientation.2–4

The second type of atrial tachycardia is macroreentrant atrial tachycardia, commonly referred to as AFL, which is subclassified as typical and atypical AFL. Typical AFL has been identified as a macroreentrant circuit that uses the cavotricuspid isthmus.1 This circuit rotates around the tricuspid valve in a counterclockwise direction, moving up the atrial septum and down the free wall. This results in characteristic findings of negative sawtooth deflections (F waves) in leads II, III, and aVF.1,3 In approximately 10% of human cases, the activation travels in a clockwise direction, which is known as reverse typical AFL. On surface ECG recordings obtained from dogs with reverse typical AFL, F waves appear as broad positive deflections in leads II, III, and aVF because the activation of the interatrial septum occurs in the superior to inferior direction.1–4

Atypical AFL is defined as a macroreentrant circuit that is not dependent on conduction through the cavotricuspid isthmus.1,3,5 In humans, this circuit can be secondary to scarring from previous cardiac surgery or ablation or can be idiopathic in nature. This arrhythmia has undulation of the atrial complexes with a rate > 240 beats/min and usually has a different appearance than typical and reverse typical AFL on surface ECG recordings.1–3,5 There are many potential macroreentrant circuits that can cause atypical AFL.1–6 The mechanism of atypical AFL in a series of 5 dogs determined by use of electrophysiologic mapping and entrainment has been previously described.5

In people undergoing surgical correction of congenital heart defects, there are multiple reasons for postoperative development of arrhythmia. One possible cause is the progression of preexisting atrial substrate abnormalities that developed secondary to cardiac remodeling with long-standing hemodynamic overload.7 In addition, transient arrhythmia can develop in the early postoperative period (days to weeks) because of local irritation of the myocardium.7 The presence of the closure device itself can induce atrial arrhythmias, although this is considered rare in humans.7 Finally, incision into the right atrial free wall can cause scarring that creates regions of abnormal conduction, which allow for the formation of a reentry circuit.1,7–10 Arrhythmias attributable to these types of reentry can cause a type of atypical AFL known as IART in humans. The onset of IART can occur both early and late in the postoperative period following surgical repair of congenital defects.6–8,10 In a series of people who underwent surgical closure of atrial septal defects, postoperative IART developed in 4 of 136 patients, which was the second most common arrhythmia behind atrial fibrillation.8 The patients who developed postoperative IART in that study8 were treated successfully by either radiofrequency catheter ablation or antiarrhythmic medications. Postoperative IART has been reported for 10% to 38% of patients who have undergone surgery for congenital cardiac defects other than atrial septal defects.6–10

On surface ECG recordings, flutter wave morphology is variable in appearance in cases of IART. Flutter waves can be large and mistaken for typical AFL. Alternatively, IART-related flutter waves may be small if there is a short reentry cycle, and those waves can be misclassified as atrial fibrillation.9 Electrophysiologic assessment is required for definitive diagnosis of IART and location of the reentrant circuit, although suspicion of IART can be raised on the basis of surface ECG findings.9

For the dog of the present report, the first ECG recording did not have the characteristics of typical or reverse typical AFL. Given that the dog underwent previous right atriotomy but had no history of arrhythmia prior to the procedure, the authors suspected that the underlying rhythm was likely IART. To the authors’ knowledge, this is the first reported case of suspected IART in a dog, although an electrophysiologic examination of the dog would be required for definitive diagnosis.

Initial treatment of AFL is aimed at controlling the ventricular response rate, which can be achieved with administration of class II, III, and IV antiarrhythmics and digoxin.2,11 Ongoing management of AFL is geared toward maintaining an appropriate ventricular response rate when the flutter is hemodynamically tolerated.2,11 However, for patients in which clinical signs persist despite antiarrhythmic treatment, rhythm control is desirable. In addition, AFL has a risk of degenerating to atrial fibrillation, which may interfere with achieving adequate rate control. Recurrence of AFL following electrical cardioversion is common because the reentrant circuit remains.10,11 In people, radiofrequency catheter ablation provides an alternative solution for AFL and has a reported success rate of 90% to 100%.11 For the dog of the present report, ablation was deemed to be not indicated as a first-line treatment because the animal had no clinical signs and a normal ventricular response rate.

For the dog of the present report, conversion to a sinus rhythm was achieved within 2 weeks after initiation of treatment with sotalol. Sotalol is a class III antiarrhythmic drug with β-adrenergic receptor blocking effects.2 Class III antiarrhythmics cause prolongation of atrial and ventricular refractory periods, which can influence myocardial conduction velocity sufficiently to interfere with reentry circuits.2,11 This can achieve a sinus rhythm in patients with AFL. Sotalol has been used successfully to convert AFL to a sinus rhythm in children who developed IART after surgery for congenital heart disease.12 Through the use of sotalol, AFL was converted to a sinus rhythm in 2 young large-breed dogs that had no evidence of structural heart disease.13 In addition, among 15 dogs with experimentally induced AFL without structural heart disease, IV administration of d-sotalol successfully converted 14 dogs to normal sinus rhythm.14 The biggest concern regarding treatment with class III antiarrhythmics is the potential for QT-interval prolongation and induction of torsades de pointes that can degenerate to ventricular fibrillation.2,11,13 Nevertheless, sotalol administration may help achieve adequate rhythm control in dogs with atypical AFL and suspected IART. Such treatment may help prevent the onset of atrial fibrillation and may be a reasonable option prior to pursuing radiofrequency catheter ablation in certain cases of atypical AFL and IART.

References

  • 1. Saoudi N, Cosio F, Waldo AE, et al. A classification of atrial flutter and regular atrial tachycardia according to electrophysiologic mechanisms and anatomical bases; a Statement from a Joint Expert Group from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Eur Heart J 2001;22:11621182.

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  • 2. Oliveira P. Atrial rhythms. In: Willis R, Oliveira P, Mavropoulou A, eds. Guide to canine and feline electrocardiography. Hoboken, NJ: John Wiley & Sons Inc, 2018;109126.

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  • 3. Supraventricular tachycardias. In: Santilli R, Moïse NS, Pariaut R, et al, eds. Electrocardiography of the dog and cat: diagnosis of arrhythmias. Milano, Italy: Edra, 2018;145187.

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  • 4. Santilli RA, Perego M, Perini A, et al. Radiofrequency catheter ablation of cavo-tricuspid isthmus as treatment of atrial flutter in two dogs. J Vet Cardiol 2010;12:5966.

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  • 5. Santilli RA, Ramera L, Perego M, et al. Radiofrequency catheter ablation of atypical atrial flutter in dogs. J Vet Cardiol 2014;16:917.

  • 6. Cosío FG. Atrial flutter, typical and atypical: a review. Arrhythm Electrophysiol Rev 2017;6:5562.

  • 7. Chubb H, Whitaker J, Williams SE, et al. Pathophysiology and management of arrhythmias associated with atrial septal defect and patent foramen ovale. Arrhythm Electrophysiol Rev 2014;3:168172.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8. Mantovan R, Gatzoulis MA, Pedrocco A, et al. Supraventricular arrhythmia before and after surgical closure of atrial septal defects: spectrum, prognosis and management. Europace 2003;5:133138.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9. Tatarskiy R, Garkina S, Lebedev D. Catheter ablation of incisional atrial tachycardia. J Atr Fibrillation 2016;9:1476.

  • 10. Waldo AL. Treatment of atrial flutter. Heart 2000;84:227232.

  • 11. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2016;67:e27e115.

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    • Search Google Scholar
    • Export Citation
  • 12. Beaufort-Krol GC, Bink-Boelkens MT. Effectiveness of sotalol for atrial flutter in children after surgery for congenital heart disease. Am J Cardiol 1997;79:9294.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13. Armentano RA, Schmidt MK, Maisenbacher HW III. ECG of the Month. Atrial flutter. J Am Vet Med Assoc 2010;236:5153.

  • 14. Feld GK, Venkatesh NA, Singh BN. Pharmacologic conversion and suppression of experimental canine atrial flutter: differing effects of d-sotalol, quinidine, and lidocaine and significance of changes in refractoriness and conduction. Circulation 1986;74:197204.

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Contributor Notes

Address correspondence to Dr. Ross (esross24@vet.k-state.edu).
  • Figure 1—

    Six-lead ECG recording obtained during a recheck evaluation of a dog with a previous history of partial atrioventricular septal defect and cleft mitral valve repair. Notice the positive deflections corresponding to atrial depolarization at a rate of 400 beats/min. These deflections do not have the characteristic features of F waves associated with typical atrial flutter. There is a variable degree of atrioventricular conduction resulting in 2:1 to 5:1 second-degree atrioventricular block. The QRS complexes have right bundle branch block morphology. On the basis of the ECG findings and the dog's history, it is likely that this atypical atrial flutter can be further characterized as incisional atrial reentrant tachycardia. Paper speed = 50 mm/s; 1 cm = 1 mV.

  • Figure 2—

    Lead II ECG tracing obtained from the dog in Figure 1 at 3 months after the start of treatment with sotalol (2.1 mg/kg [0.95 mg/lb], PO, q 12 h). There is an underlying sinus rhythm with right bundle branch block morphology. Notice the absence of rapid atrial depolarizations that were detected previously. Paper speed = 25 mm/s; 1 cm =1 mv.

  • 1. Saoudi N, Cosio F, Waldo AE, et al. A classification of atrial flutter and regular atrial tachycardia according to electrophysiologic mechanisms and anatomical bases; a Statement from a Joint Expert Group from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Eur Heart J 2001;22:11621182.

    • Search Google Scholar
    • Export Citation
  • 2. Oliveira P. Atrial rhythms. In: Willis R, Oliveira P, Mavropoulou A, eds. Guide to canine and feline electrocardiography. Hoboken, NJ: John Wiley & Sons Inc, 2018;109126.

    • Search Google Scholar
    • Export Citation
  • 3. Supraventricular tachycardias. In: Santilli R, Moïse NS, Pariaut R, et al, eds. Electrocardiography of the dog and cat: diagnosis of arrhythmias. Milano, Italy: Edra, 2018;145187.

    • Search Google Scholar
    • Export Citation
  • 4. Santilli RA, Perego M, Perini A, et al. Radiofrequency catheter ablation of cavo-tricuspid isthmus as treatment of atrial flutter in two dogs. J Vet Cardiol 2010;12:5966.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5. Santilli RA, Ramera L, Perego M, et al. Radiofrequency catheter ablation of atypical atrial flutter in dogs. J Vet Cardiol 2014;16:917.

  • 6. Cosío FG. Atrial flutter, typical and atypical: a review. Arrhythm Electrophysiol Rev 2017;6:5562.

  • 7. Chubb H, Whitaker J, Williams SE, et al. Pathophysiology and management of arrhythmias associated with atrial septal defect and patent foramen ovale. Arrhythm Electrophysiol Rev 2014;3:168172.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8. Mantovan R, Gatzoulis MA, Pedrocco A, et al. Supraventricular arrhythmia before and after surgical closure of atrial septal defects: spectrum, prognosis and management. Europace 2003;5:133138.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9. Tatarskiy R, Garkina S, Lebedev D. Catheter ablation of incisional atrial tachycardia. J Atr Fibrillation 2016;9:1476.

  • 10. Waldo AL. Treatment of atrial flutter. Heart 2000;84:227232.

  • 11. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2016;67:e27e115.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12. Beaufort-Krol GC, Bink-Boelkens MT. Effectiveness of sotalol for atrial flutter in children after surgery for congenital heart disease. Am J Cardiol 1997;79:9294.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13. Armentano RA, Schmidt MK, Maisenbacher HW III. ECG of the Month. Atrial flutter. J Am Vet Med Assoc 2010;236:5153.

  • 14. Feld GK, Venkatesh NA, Singh BN. Pharmacologic conversion and suppression of experimental canine atrial flutter: differing effects of d-sotalol, quinidine, and lidocaine and significance of changes in refractoriness and conduction. Circulation 1986;74:197204.

    • Crossref
    • Search Google Scholar
    • Export Citation

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