ECG of the Month

Michelle M. Vereb From the Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608

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Darcy B. Adin From the Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608

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Monica L. Tschosik Upstate Vet Emergency and Specialty Care, Greenville, SC 29607.

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A 7-year-old 26.8-kg (59-lb) neutered male Golden Retriever was presented for recheck assessment of left-sided congestive heart failure. The dog had undergone combined cutting and high-pressure balloon valvuloplasty for severe subvalvular stenosis (pressure gradient, 170 mm Hg) at 6 months of age and had received atenolol (0.47 mg/kg [0.21 mg/lb], PO, q 12 h) since the time of diagnosis. The procedure reduced the pressure gradient to 70 mm Hg and improved the dog's exercise tolerance. The dog was reevaluated 6 years after valvuloplasty because of signs of congestive heart failure. Electrocardiography revealed atrial fibrillation (AF) with a rapid rate of 220 beats/min. The dog had echocardiographic evidence of pleural effusion, severe left atrial enlargement (left atrial-to-aortic diameter ratio, 2.72), left ventricular enlargement with systolic dysfunction (normalized left ventricular diastolic and systolic diameters, 1.88 and 1.29, respectively), and severe subvalvular aortic stenosis (pressure gradient, 91 mm Hg). The dog was treated with thoracocentesis, pimobendan (0.29 mg/ kg [0.13 mg/lb], PO, q 8 h), furosemide (2.3 mg/kg [1.05 mg/lb], PO, q 8 h), immediate-release diltiazem hydrochloride (2.0 mg/kg [0.91 mg/lb], PO, q 8 h), digoxin (0.0048 mg/kg [0.002 mg/lb], PO, q 12 h), and enalapril maleate (0.38 mg/kg [0.17 mg/lb], PO q 12 h). Three months later, the dog was rechecked and was doing well clinically. At that time, mild pleural effusion was present, serum biochemical findings were within reference intervals, and serum digoxin concentration at 7 hours after administration was 2.0 ng/mL (therapeutic range, 1.0 to 2.0 ng/mL). Electrocardiography was repeated to assess heart rate control.

ECG Interpretation

In a 6-lead ECG recording (Figure 1), the rhythm was irregular and lacked distinct P waves, confirming the continued presence of AF; the mean ventricular response rate was 147 beats/min (instantaneous rate, 50 to 250 beats/min). The mean electrical axis was normal at +60°, and a left ventricular enlargement pattern was noted (R-wave amplitude, 3.2 mV; QRS-complex duration, 0.07 seconds). The R-wave amplitude slightly and directly varied with the preceding R-R interval, consistent with the Brody effect.1 The rate control was considered adequate on the basis of these ECG findings, but 24-hour Holter monitoring of the dog was not performed.

Figure 1
Figure 1

Six-lead ECG tracings obtained from of a 7-year-old Golden Retriever with congestive heart failure secondary to long-standing, severe subvalvular aortic stenosis; the stenosis had been previously treated with combined cutting and high-pressure balloon valvuloplasty. Atrial fibrillation is present, and there is a single wide and bizarre QRS complex with right bundle branch block morphology (asterisk). Subtle variation in R-wave amplitude in relation to the preceding R-R interval is consistent with the Brody effect. Paper speed = 50 mm/s; 0.5 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 259, 4; 10.2460/javma.259.4.368

Intermittent wide and bizarre QRS complexes with right bundle branch block (RBBB) morphology were consistently observed when a long R-R interval (0.88 to 1.20 seconds) was followed by a short R-R interval (0.32 to 0.36 seconds; Figure 2). Differential diagnoses for these complexes included supraventricular complexes with Ashman phenomenon and ventricular premature complexes (VPCs). A relatively constant coupling interval (0.32 to 0.36 seconds) could have been supportive of a ventricular beat origin; however, because these complexes occurred immediately following a long-short R-R cycle and lacked an obvious compensatory pause, Ashman phenomenon was considered most likely.

Figure 2
Figure 2

Lead II ECG tracing obtained from the dog during the same examination indicating intermittent aberrant ventricular conduction (asterisks) in the presence of AF, following long-short R-R cycles. This is consistent with the Ashman phenomenon. Paper speed = 25 mm/s; 0.5 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 259, 4; 10.2460/javma.259.4.368

Discussion

Ashman phenomenon is a form of tachycardia-dependent (phase 3) aberrancy that occurs when a relatively long R-R cycle is immediately followed by a relatively short R-R cycle.2,3 In this scenario, the depolarization from the short R-R cycle reaches conduction tissues (eg, the atrioventricular node, bundle branches, or Purkinje fibers) before they are fully repolarized, resulting in prolonged conduction.3 The refractory period varies depending on the type of conduction tissue,3,4 but the relative refractory period overall shortens at faster rates and lengthens at slower rates.3,5,6 Therefore, the relative refractory period of a long R-R cycle is prolonged and incomplete by the time a short R-R depolarization arrives. Blocking of this impulse in the conduction tissues results in slowed conduction between myocardial cells throughout the ventricles, resulting in a wide and bizarre QRS complex morphology.3,5 The degree of aberrancy is directly related to the duration of the preceding cycle because of the direct relationship between the cycle duration and refractory period.7 In people, Ashman phenomenon most often occurs with an RBBB morphology because the refractory period of the right bundle branch is longer than that of the left bundle branch.3,8

Differentiation of aberrancy from ventricular ectopy can be difficult in cases of AF because P waves are absent. Atrial fibrillation prevents identification of atrioventricular dissociation, a defining characteristic of ventricular ectopy.2,8,9 Correct identification of the beat origin is important because treatment and prognostic implications for Ashman phenomenon and VPCs differ.10 Treatment of ventricular ectopy focuses on rhythm control, whereas specific treatment for Ashman phenomenon is not indicated apart from AF rate control.10 Because ventricular arrhythmias can occur concurrently with AF as a consequence of underlying structural disease or digoxin toxicosis,11 there is potential for Ashman phenomenon to remain unrecognized, leading to unnecessary administration of antiarrhythmic medication. Although the dog of the present report did not have clinical signs of digoxin toxicosis, its serum digoxin concentration was at the upper limit of the reported therapeutic range. For this dog, the potential effect of the circulating digoxin concentration on the ECG findings was unknown.

A diagnosis of Ashman phenomenon is most commonly made by evaluating surface ECG tracings for characteristics that differentiate it from VPCs. Gulamhusein et al8 reported that VPCs in people more commonly have a left bundle branch block morphology (although any morphology is possible), whereas aberrantly conducted beats usually have an RBBB morphology as a result of the longer refractory period of the right bundle branch.8 For the dog of the present report, ECG revealed abnormally conducted complexes with RBBB morphology, supportive of Ashman phenomenon; however, the usefulness of this criterion for a diagnosis of Ashman phenomenon has not been explored in dogs. The dog's underlying heart disease could have predisposed the animal to VPCs of left ventricular origin and RBBB morphology; thus, in this case, the presence of abnormally conducted complexes with RBBB morphology was not a helpful differentiating characteristic. Twelve-lead ECG provides additional information with which to differentiate Ashman phenomenon from VPCs2,8; unfortunately, tracings from thoracic leads were not recorded for this dog. If thoracic lead recordings had been available, concordance of the findings from limb leads with those of the left-sided thoracic leads would have supported Ashman phenomenon, whereas discordance of the findings would have supported VPCs.2,8 The duration of the pause after an abnormal beat can also help to differentiate Ashman phenomenon from VPCs. Unlike beats conducted with aberrancy, ventricular ectopic beats are usually followed by a compensatory pause as a result of retrograde impulse conduction into the atrioventricular node.8,9,11 Although determination of the compensatory pause duration in the presence of AF may not be possible on the surface ECG recordings because of the effect of concealed atrioventricular nodal conduction of AF wavelets on cycle duration,2 the presence of compensatory pauses with VPCs and concurrent AF has been electrophysiologically confirmed in people.11 Further, a postectopic-beat pause that exceeds the mean of 10 normally conducted beats preceding the wide QRS complex during AF is consistent with a compensatory pause of a VPC.8 On the ECG tracings for the dog of the present report, only 6 normally conducted beats preceded the wide beats, but the R-R interval after the wide complex was shorter than the mean R-R interval for these 6 beats. The absence of long pauses after the wide QRS complexes in dog's ECG recordings was inconsistent with a ventricular origin.

Differentiation between Ashman phenomenon and VPCs may be further complicated by the appearance of multiple, consecutive, aberrantly conducted beats that simulate ventricular tachycardia.2,3 Repeated depolarization before completion of the relative refractory period of the conduction tissue results in repeated aberrancy, a phenomenon known as linking.2,3 In people, Ashman phenomenon with linking is confirmed when vagal maneuvers slow the rate of supraventricular rhythms and sometimes resolve aberrancy, outcomes that would not occur in cases of ventricular ectopy.4,12 In support of this method for diagnosis confirmation, increased sympathetic tone during exercise has been shown to increase the occurrence of Ashman phenomenon in horses with AF.13 Consecutive, wide QRS complexes were not observed in the ECG tracings obtained from the dog of the present report.

Whereas Ashman phenomenon has been extensively studied in people, there are only a few reports1420 regarding this tachycardia-dependent aberrancy in companion animals. The ECG tracings obtained from the dog of the present report were unique because abnormally conducted complexes with RBBB morphology in the presence of AF were detected, which is a common presentation of Ashman phenomenon in humans but not described for dogs, to our knowledge.

Although surface ECG findings are helpful in making a presumptive diagnosis of Ashman phenomenon, bundle of His ECG recordings are required to definitively differentiate between Ashman phenomenon and VPCs.8 The ECG diagnosis of Ashman phenomenon for the dog of the present report was presumptive, and we could not rule out the possibility that the wide beats represented ventricular ectopy. Despite the limitations and challenges of surface ECG diagnosis, the recognition of Ashman phenomenon in patients is clinically important and should be suspected when a long-short pattern of R-R cycle duration terminates in a wide QRS complex.

References

  • 1.

    Saelinger CA, Estrada AH, Maisenbacher HW. ECG of the Month. Exaggerated sinus arrhythmia and wandering pacemaker. J Am Vet Med Assoc 2008;233:231233.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2.

    Santilli R, Moise NS, Pariaut R, et al. Supraventricular tachycardias, ventricular arrhythmias, and conduction disorders. In: Santilli R, Moise NS, Pariaut R, et al. eds. Electrocardiography of the dog and cat: diagnosis of arrhythmias. 2nd ed. Milano, Italy: Edra SpA, 2018;174179, 231234, 286289.

    • Search Google Scholar
    • Export Citation
  • 3.

    Gouaux JL, Ashman R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am Heart J 1947;34:366373.

  • 4.

    Goldman DS, Damato AN. “The anti-Ashman maneuver”: a bedside method for distinguishing aberrancy from ventricular ectopy. Clin Cardiol 1992;15:5052.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Fisch C. Electrocardiography of arrhythmias: from deductive analysis to laboratory confirmation–twenty-five years of progress. J Am Coll Cardiol 1983;1:306316.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Fisch C. Aberration: seventy five years after Sir Thomas Lewis. Br Heart J 1983;50:297302.

  • 7.

    Longo D, Baranchuk A. Ashman phenomenon dynamicity during atrial fibrillation: the critical role of the long cycles. J Atr Fibrillation 2017;10:1656.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8.

    Gulamhusein S, Yee R, Ko PT, et al. Electrocardiographic criteria for differentiating aberrancy and ventricular extrasystole in chronic atrial fibrillation: validation by intracardiac recordings. J Electrocardiol 1985;18:4150.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9.

    Langendorf R. Aberrant ventricular conduction. Am Heart J 1951;41:700707.

  • 10.

    Singla V, Singh B, Singh Y, et al. Ashman phenomenon: a physiological aberration. BMJ Case Rep 2013;2013.

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    Pritchett EL, Smith WM, Klein GJ, et al. The “compensatory pause” of atrial fibrillation. Circulation 1980;62:10211025.

  • 12.

    Lown B, Levine SA. The carotid sinus. Clinical value of its stimulation. Circulation 1961;23:766789.

  • 13.

    Verheyen T, Decloedt A, van der Vekens N, et al. Ventricular response during lungeing exercise in horses with lone atrial fibrillation. Equine Vet J 2013;45:309314.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Chong AC, Minors SL. ECG of the Month. J Am Vet Med Assoc 2020;256:174175.

  • 15.

    Martel-Arquette A, Tjostheim SS, Miller J, et al. Aortocavitary fistula secondary to vegetative endocarditis in a rabbit. J Vet Cardiol 2019;21:4956.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 16.

    Murphy LA, Nakamura RK. ECG of the Month. J Am Vet Med Assoc 2019;254:470471.

  • 17.

    Nakamura RK, Zimmerman SA. ECG of the Month. Second-degree atrioventricular block in a cat. J Am Vet Med Assoc 2012;241:433434.

  • 18.

    Summerfield N, Estrada A. Ladder diagrams for atrial flutter and atrial fibrillation. J Vet Cardiol 2005;7:131135.

  • 19.

    Thomason JD, Thomason SS, Fallaw T, et al. ECG of the Month. Loud systolic heart murmur consistent with mitral valve regurgitation. J Am Vet Med Assoc 2015;246:962964.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Zarin JA, Quinn RL. ECG of the Month. J Am Vet Med Assoc 2019;254:11591161.

  • Figure 1

    Six-lead ECG tracings obtained from of a 7-year-old Golden Retriever with congestive heart failure secondary to long-standing, severe subvalvular aortic stenosis; the stenosis had been previously treated with combined cutting and high-pressure balloon valvuloplasty. Atrial fibrillation is present, and there is a single wide and bizarre QRS complex with right bundle branch block morphology (asterisk). Subtle variation in R-wave amplitude in relation to the preceding R-R interval is consistent with the Brody effect. Paper speed = 50 mm/s; 0.5 cm = 1 mV.

  • Figure 2

    Lead II ECG tracing obtained from the dog during the same examination indicating intermittent aberrant ventricular conduction (asterisks) in the presence of AF, following long-short R-R cycles. This is consistent with the Ashman phenomenon. Paper speed = 25 mm/s; 0.5 cm = 1 mV.

  • 1.

    Saelinger CA, Estrada AH, Maisenbacher HW. ECG of the Month. Exaggerated sinus arrhythmia and wandering pacemaker. J Am Vet Med Assoc 2008;233:231233.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2.

    Santilli R, Moise NS, Pariaut R, et al. Supraventricular tachycardias, ventricular arrhythmias, and conduction disorders. In: Santilli R, Moise NS, Pariaut R, et al. eds. Electrocardiography of the dog and cat: diagnosis of arrhythmias. 2nd ed. Milano, Italy: Edra SpA, 2018;174179, 231234, 286289.

    • Search Google Scholar
    • Export Citation
  • 3.

    Gouaux JL, Ashman R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am Heart J 1947;34:366373.

  • 4.

    Goldman DS, Damato AN. “The anti-Ashman maneuver”: a bedside method for distinguishing aberrancy from ventricular ectopy. Clin Cardiol 1992;15:5052.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Fisch C. Electrocardiography of arrhythmias: from deductive analysis to laboratory confirmation–twenty-five years of progress. J Am Coll Cardiol 1983;1:306316.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Fisch C. Aberration: seventy five years after Sir Thomas Lewis. Br Heart J 1983;50:297302.

  • 7.

    Longo D, Baranchuk A. Ashman phenomenon dynamicity during atrial fibrillation: the critical role of the long cycles. J Atr Fibrillation 2017;10:1656.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8.

    Gulamhusein S, Yee R, Ko PT, et al. Electrocardiographic criteria for differentiating aberrancy and ventricular extrasystole in chronic atrial fibrillation: validation by intracardiac recordings. J Electrocardiol 1985;18:4150.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9.

    Langendorf R. Aberrant ventricular conduction. Am Heart J 1951;41:700707.

  • 10.

    Singla V, Singh B, Singh Y, et al. Ashman phenomenon: a physiological aberration. BMJ Case Rep 2013;2013.

  • 11.

    Pritchett EL, Smith WM, Klein GJ, et al. The “compensatory pause” of atrial fibrillation. Circulation 1980;62:10211025.

  • 12.

    Lown B, Levine SA. The carotid sinus. Clinical value of its stimulation. Circulation 1961;23:766789.

  • 13.

    Verheyen T, Decloedt A, van der Vekens N, et al. Ventricular response during lungeing exercise in horses with lone atrial fibrillation. Equine Vet J 2013;45:309314.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Chong AC, Minors SL. ECG of the Month. J Am Vet Med Assoc 2020;256:174175.

  • 15.

    Martel-Arquette A, Tjostheim SS, Miller J, et al. Aortocavitary fistula secondary to vegetative endocarditis in a rabbit. J Vet Cardiol 2019;21:4956.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 16.

    Murphy LA, Nakamura RK. ECG of the Month. J Am Vet Med Assoc 2019;254:470471.

  • 17.

    Nakamura RK, Zimmerman SA. ECG of the Month. Second-degree atrioventricular block in a cat. J Am Vet Med Assoc 2012;241:433434.

  • 18.

    Summerfield N, Estrada A. Ladder diagrams for atrial flutter and atrial fibrillation. J Vet Cardiol 2005;7:131135.

  • 19.

    Thomason JD, Thomason SS, Fallaw T, et al. ECG of the Month. Loud systolic heart murmur consistent with mitral valve regurgitation. J Am Vet Med Assoc 2015;246:962964.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Zarin JA, Quinn RL. ECG of the Month. J Am Vet Med Assoc 2019;254:11591161.

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