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Sarah E. Achen Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843-4474.

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Ashley B. Saunders Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843-4474.

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Matthew W. Miller Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843-4474.

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10-year-old 20-kg (44-lb) spayed female Brittany was examined by a veterinarian because of acute onset of lethargy and inappetence. Tachycardia was detected on physical examination and confirmed via ECG; in all leads, the QRS complexes were wide. Lidocaine hydrochloride (2 mg/kg [0.9 mg/lb]) was administered IV, which slowed the heart rate slightly. The dog was subsequently transferred to a local emergency clinic for supervision overnight. Because of the incomplete response to lidocaine, the dog was referred to the Veterinary Medical Teaching Hospital at Texas A&M University for further evaluation the following morning.

The dog was bright and alert at the initial evaluation. Thoracic auscultation revealed an irregularly irregular tachyarrhythmia with associated femoral pulse deficits. No murmurs were detected, and bronchovesicular sounds were considered normal. A history of bird hunting, the last episode of which occurred > 1 year earlier, was reported. Vaccination status was current, and the dog was regularly receiving a heartworm preventative.

Diagnostic procedures included thoracic radiography; echocardiography; ECG; systemic blood pressure evaluation; CBC; serum biochemical analyses; titer assessment of serum antibodies against Trypanosoma cruzi via an immunofluorescent antibody test; and measurements of serum concentrations of taurine, thyroid hormones (total thyroxine, free thyroxine [determined via equilibrium dialysis], and thyroid-stimulating hormone), and cardiac troponin I. Findings of thoracic radiography included mild generalized cardiomegaly with a mildly large left atrium, pulmonary venous congestion, and a mild unstructured interstitial pattern in the lungs. Echocardiographic findings included left ventricular internal dimensions indicative of dilatation, left ventricular systolic dysfunction, a mild centrally located jet of mitral valve regurgitation, a moderately large left atrium, and mild low-velocity tricuspid valve regurgitation. The mitral and tricuspid valves appeared normal. Indirect systemic blood pressure measured by use of an oscillometric device was within reference limits. Results of serum biochemical analyses and a CBC were unremarkable. The dog was seronegative for T cruzi; serum taurine and thyroid hormone concentrations were within reference limits. Serum cardiac troponin I concentration was increased at 3.86 ng/mL (reference range, < 0.2 ng/mL).

ECG Interpretation

Electrocardiographic findings during the initial examination included an irregularly irregular wide and bizarre QRS tachycardia, conducted with a right bundle branch block (RBBB) morphology, and all QRS complexes were conducted with an RS complex morphology (Figure 1). Instantaneous heart rates varied from 55 to 188 beats/min. The RS complex appearance varied depending on heart rate. With heart rates < 97 beats/min, the RS complexes were conducted with an RBBB (RS complex duration, 100 milliseconds). More-narrow (40 milliseconds in duration), upright RS complexes occurred at heart rates < 62 beats/min, suggesting more-normal intraventricular conduction. With intermediate heart rates that were ≥ 62 beats/min and ≤ 97 beats/min, the RS complex morphology was more isoelectric and appeared to be transitional between the RBBB morphologic appearance and the narrower, upright morphologic appearance (ie, 60 milliseconds in duration). Infrequent ventricular premature complexes were evident; P waves could not be identified. In an attempt to slow the ventricular rate, procainamide hydrochloride (20 mg/kg [9.1 mg/lb]) was administered IV to effect. Following administration of 11 mg of procain-amide/kg (5 mg/lb), the dog’s heart rate increased to 200 beats/min; administration of procainamide was discontinued. Treatment with amiodarone (15 mg/kg [6.8 mg/lb], PO, q 24 h) for 5 days followed by 10 mg/kg (4.5 mg/lb, PO, q 24 h) was initiated. In addition, the dog was given benazepril (0.25 mg/kg [0.114 mg/lb], PO, q 24 h) as well as pimobendan (0.25 mg/kg, PO, q 12 h) because of systolic dysfunction.

Figure 1—
Figure 1—

Lead II ECG traces obtained from a 10-year-old Brittany that was evaluated because of tachycardia that was unresponsive to treatment with lidocaine hydrochloride. Atrial fibrillation conducted with a right bundle branch block (RBBB) is present. Notice the heart rate–dependent variation in QRS complex morphology: an RBBB is present at higher heart rates (A); a transitional QRS complex morphology appears when the R-R interval is intermediate (960 milliseconds; B); and more-narrow, upright QRS complexes occur when the R-R interval is longer (≥ 1 second; C). There is an absence of P waves. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 232, 5; 10.2460/javma.232.5.684

The dog was returned to the veterinary medical teaching hospital for reevaluation 1 week later. The owner reported dramatic improvement in activity level and appetite, and the dog was bright and alert during the physical examination. Thoracic auscultation revealed a predominantly regular rhythm. Femoral pulse quality was strong, and no pulse deficits were evident. A grade 4/6 left apical systolic murmur was ausculted, and bronchovesicular sounds were considered normal.

Diagnostic evaluations included thoracic radiography, ECG, serum biochemical analyses, and assessment of serum cardiac troponin I concentration. Additionally, a serum sample was submitted to North Carolina State University for serologic assessment of Babesia canis, Bartonella vinsonii, Rickettsia rickettsii, Borrelia burgdorferi, and Ehrlichia canis via immunofluorescent antibody testing; serum N-terminal prohormone brain natriuretic peptide (NT-proBNP) concentration was also evaluated. Findings of thoracic radiography and serum biochemical analyses were unremarkable. Serum cardiac troponin I concentration remained mildly high but had decreased to 0.39 ng/mL. The dog was seronegative for B canis, B vinsonii, R rickettsii, B burgdorferi, and E canis. Serum NT-ProBNP concentration was 8 pmol/L; dogs with heart failure have higher concentrations (≥ 500 pmol/L).a,b

Electrocardiography was performed 1 week following amiodarone administration and revealed conversion to a normal sinus rhythm (mean heart rate, 105 beats/min; Figure 2). In both human and veterinary medicine, conversion of atrial fibrillation to a sinus rhythm after administration of amiodarone has been recorded, and in 1 study,1 the reported conversion rate in dogs reached 35%. Later during the examination, an ECG was repeated and a rate-dependent conduction abnormality similar to that detected when the dog had atrial fibrillation was evident (Figure 3). At lower heart rates (95 to 115 beats/min), RS complexes that were narrow (40 milliseconds in duration) and upright were detected. During bursts of sinus tachycardia (heart rates > 167 beats/min), an RBBB was present. The RS duration during the RBBB was 80 milliseconds. With intermediate heart rates > 136 beats/min, RS complexes were slightly wide (60 milliseconds in duration) and more isoelectric. Regardless of the RS duration, the PR interval remained constant with all morphologies of 100 milliseconds’ duration; however, at higher heart rates, the P waves were not visible because they were integrated into the preceding T waves.

Figure 2—
Figure 2—

Lead II ECG trace obtained from the dog in Figure 1 one week following administration of a loading dose of amiodarone. Notice the conversion to a normal sinus rhythm. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 232, 5; 10.2460/javma.232.5.684

Figure 3—
Figure 3—

Lead II ECG trace obtained the same day as that in Figure 2 representing sinus rhythm with heart rate–dependent RBBB. Notice the presence of an RBBB during high heart rates (critical rate, 167 beats/min; A); isoelectric RS complexes during intermediate heart rates (critical rate, 136 beast/min; B); and normal, narrow, and upright RS complexes at lower heart rates (C). Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 232, 5; 10.2460/javma.232.5.684

One month following the initial examination, the dog was returned for further evaluation. The owners reported that the dog had no clinical signs. Echocardiography was repeated, and findings included normalization of left ventricular internal dimensions and systolic function, mild mitral valve regurgitation with a mildly large left atrium, and no tricuspid valve regurgitation. Electrocardiographic findings included an underlying sinus rhythm with persistence of the rate-dependent RBBB. There were occasional single ventricular premature complexes conducted with multiple forms, including both right and left bundle branch block morphologies. Serum cardiac troponin I concentration had continued to decrease (0.22 ng/mL). Improvement in the arrhythmia, reduction in serum cardiac troponin I concentration, and improvement in left ventricular systolic function suggested ongoing resolution of the dog’s condition.

Discussion

In the dog of this report, no P waves were identified on the initial ECG recording, leading to differential diagnoses of ventricular tachycardia and atrial fibrillation conducted with aberrancy. Procainamide is one of the most effective injectable drug treatments available for conversion of ventricular tachycardia; such treatment is capable of converting atrial fibrillation to a sinus rhythm.2 On the basis of the lack of response to procainamide, a diagnosis of atrial fibrillation conducted with an RBBB was made. The increase in heart rate after administration of procainamide may have been incidental; this change may have developed in response to the vagolytic effects of procain amide or may have represented a reflex sympathetic discharge secondary to negative inotropic and vasodilatory effects of procainamide.2–4 Other supporting factors for the diagnosis of atrial fibrillation included variation of R-R intervals and variation of QRS complex morphology.5, 6 Unlike atrial fibrillation, which is associated with irregularly irregular R-R intervals, ventricular tachycardia typically occurs at a regular rate with identical R-R intervals. In addition, the initial ECG recording obtained from the dog of this report revealed gradations of aberrancy, ranging from a QRS complex appearance that was more normal to that of an RBBB morphology.

In the dog of this report, varying degrees of interventricular conduction abnormalities were associated with changes in its heart rate. Phasic aberrant ventricular conduction is a term used to describe temporary aberrant intraventricular conduction (also termed a ratedependent bundle branch block).5,7 Critical rate is the term used to describe the heart rate at which the bundle branch block occurs as heart rate is increasing or the rate at which it disappears as heart rate is decreasing. The refractory period is always shorter at higher heart rates and slower at lower heart rates, causing the critical rate at which the bundle branch block occurs to be higher than the critical rate at which it disappears.7

There are 3 potential mechanisms for aberrant intraventricular conduction, including stimulation during phase 3 of the action potential, retrograde concealed conduction, and stimulation during phase 4 of Purkinje fiber action potentials.7 Retrograde concealed conduction is associated with ventricular arrhythmias and is unlikely in the dog of this report. Phase 3 aberrancy is tachycardia dependent, and phase 4 aberrancy is bradycardia dependent; therefore, phase 3 aberrancy is the most likely mechanism in this dog. Phase 3 aberrancy is attributable to a premature stimulus that occurs during phase 3 of the action potential, the time at which the resting membrane potential is reduced and conduction time is increased. During phase 3, only some of the fast sodium channels normally used for phase 0 depolarization are available for activation. This causes the action potential to rely more on slow calcium channels, thereby creating slower intraventricular conduction. Phase 3 aberrancy can develop in apparently normal hearts if the premature impulse occurs early, when one of the bundle branches has not fully repolarized. Alternatively, phase 3 aberrancy can develop in disease-affected hearts if electrical systole or the refractory period of the involved fascicle is prolonged and the premature impulses occur very rapidly.7 The latter mechanism is the most likely in the dog of this report.

Phase 3 aberrancy is favored by longer preceding R-R intervals. However, in the case of rapid supraventricular rhythms, it can be maintained. This may be because of unequal refractoriness of the bundle branches. As an impulse travels down the nonrefractory bundle branch, it can retrogradely activate the blocked bundle branch, perpetuating the unequal refractoriness. More-normal-appearing QRS complexes may occur because both bundle branches had sufficient time to repolarize prior to the next impulse.5

In addition to prematurity, unequal refractoriness of the bundle branches also favors phasic aberrant ventricular conduction. Results of several studies5–9 in which aberrant ventricular conduction in humans and dogs was investigated have indicated that the right bundle branch is more susceptible to block, most likely because the right bundle branch has a larger diameter and a longer action potential, compared with that of the left bundle branch.

The resolution of systolic dysfunction in this dog supports a diagnosis of tachycardia-induced myocardial failure. Tachycardia-induced myocardial failure has been induced experimentally in dogs in which implanted pacemakers were paced at a rate > 200 beats/min.10 Tachycardia-induced myocardial failure has also been identified clinically in dogs with sustained supraventricular tachycardia.11 The exact mechanism is unknown, but is most likely attributable to a primary defect in isolated myocyte contractile performance that is secondary to abnormalities in cell architecture and calcium responsiveness.12 The myocardial failure rapidly reverses when the tachycardia is terminated.

In the dog of this report, no definitive cause of the arrhythmia was identified. The high serum cardiac troponin I concentration was suggestive of myocardial cell damage. However, whether that damage was a result of an inflammatory process or tachycardia remains unknown.

a.

Tarnow I, Pederson HD, Kvart C, et al. Natriuretic peptides are elevated in Cavalier King Charles Spaniels with congestive heart failure, but not in dogs with clinically inapparent mitral valve disease (abstr), in Proceedings. 25th Annu Forum Am Coll Vet Intern Med J Vet Intern Med 2007;21:587.

b.

Wess G, Timper N, Hirschberger J. The utility of NT-proBNP to differentiate cardiac and respiratory causes of coughing or dyspnea in dogs (abstr), in Proceedings. 25th Annu Forum Am Coll Vet Intern Med J Vet Intern Med 2007;21:608.

References

  • 1

    Saunders AB, Miller MW, Gordon SG, et al. Oral amiodarone therapy in dogs with atrial fibrillation. J Vet Intern Med 2006;20:921926.

  • 2

    DiMarco JP, Gersh BJ, Opie LH. Antiarrhythmic drugs and strategies. In:Opie LH, Gersh BJ, ed.Drugs for the heart. 6th ed. Philadelphia: Elsevier Inc, 2005;218274.

    • Search Google Scholar
    • Export Citation
  • 3

    Boucher M, Chassaing C, Laborde P, et al. Cardiac anticholinergic effects of procainamide and its N-acetylated metabolite: experimental pharmacological and radioligand binding studies. J Auton Pharmacol 1998;18:8387.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4

    Jordan JL, Mandel WJ. Disorders of sinus rhythm. In:Mandel WJ, ed.Cardiac arrhythmias: their mechanisms, diagnosis, and management. 3rd ed. Philadelphia: JB Lippincott, 1987;245295.

    • Search Google Scholar
    • Export Citation
  • 5

    Schamroth L. Phasic aberrant ventricular conduction. In:Schamroth L, ed.The disorders of cardiac rhythm. 2nd ed. Oxford, England: Blackwell Scientific Publications, 1971;215224.

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    • Export Citation
  • 6

    Wellens HJ, Bär FW, Lie KI. The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med 1978;64:2733.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7

    Marriott HJL, Conover MB. Aberrant ventricular conduction. In:Marriott HJL, Conover MB, ed.Advanced concepts in arrhythmias. 3rd ed. St Louis: CV Mosby Co, 1998;215236.

    • Search Google Scholar
    • Export Citation
  • 8

    Tilley LP. Uncommon complex arrhythmias. In:Tilley LP, ed.Essentials of canine and feline electrocardiography: interpretation and treatment. 3rd ed. Philadelphia: Lea & Febiger, 1992;385416.

    • Search Google Scholar
    • Export Citation
  • 9

    Sandler IA, Marriott HJL. The differential morphology of anomalous ventricular complexes of RBBB-type in lead V; ventricular ectopy versus aberration. Circulation 1965;31:551556.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10

    Wilson JR, Douglas P, Hickey WF, et al. Experimental congestive heart failure produced by rapid ventricular pacing in the dog: cardiac effects. Circulation 1987;75:857867.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11

    Kittleson MD. Primary myocardial disease leading to chronic myocardial failure (dilated cardiomyopathy and related diseases). In:Kittleson MD, Keinle RD, ed.Small animal cardiovascular medicine. Philadelphia: Mosby Inc, 1998;319346.

    • Search Google Scholar
    • Export Citation
  • 12

    Spinale FG, Fulbright M, Mukherjee R, et al. Relation between ventricular and myocyte function with tachycardia-induced cardiomyopathy. Circ Res 1992;71:174187.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • Figure 1—

    Lead II ECG traces obtained from a 10-year-old Brittany that was evaluated because of tachycardia that was unresponsive to treatment with lidocaine hydrochloride. Atrial fibrillation conducted with a right bundle branch block (RBBB) is present. Notice the heart rate–dependent variation in QRS complex morphology: an RBBB is present at higher heart rates (A); a transitional QRS complex morphology appears when the R-R interval is intermediate (960 milliseconds; B); and more-narrow, upright QRS complexes occur when the R-R interval is longer (≥ 1 second; C). There is an absence of P waves. Paper speed = 25 mm/s; 1 cm = 1 mV.

  • Figure 2—

    Lead II ECG trace obtained from the dog in Figure 1 one week following administration of a loading dose of amiodarone. Notice the conversion to a normal sinus rhythm. Paper speed = 25 mm/s; 1 cm = 1 mV.

  • Figure 3—

    Lead II ECG trace obtained the same day as that in Figure 2 representing sinus rhythm with heart rate–dependent RBBB. Notice the presence of an RBBB during high heart rates (critical rate, 167 beats/min; A); isoelectric RS complexes during intermediate heart rates (critical rate, 136 beast/min; B); and normal, narrow, and upright RS complexes at lower heart rates (C). Paper speed = 25 mm/s; 1 cm = 1 mV.

  • 1

    Saunders AB, Miller MW, Gordon SG, et al. Oral amiodarone therapy in dogs with atrial fibrillation. J Vet Intern Med 2006;20:921926.

  • 2

    DiMarco JP, Gersh BJ, Opie LH. Antiarrhythmic drugs and strategies. In:Opie LH, Gersh BJ, ed.Drugs for the heart. 6th ed. Philadelphia: Elsevier Inc, 2005;218274.

    • Search Google Scholar
    • Export Citation
  • 3

    Boucher M, Chassaing C, Laborde P, et al. Cardiac anticholinergic effects of procainamide and its N-acetylated metabolite: experimental pharmacological and radioligand binding studies. J Auton Pharmacol 1998;18:8387.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4

    Jordan JL, Mandel WJ. Disorders of sinus rhythm. In:Mandel WJ, ed.Cardiac arrhythmias: their mechanisms, diagnosis, and management. 3rd ed. Philadelphia: JB Lippincott, 1987;245295.

    • Search Google Scholar
    • Export Citation
  • 5

    Schamroth L. Phasic aberrant ventricular conduction. In:Schamroth L, ed.The disorders of cardiac rhythm. 2nd ed. Oxford, England: Blackwell Scientific Publications, 1971;215224.

    • Search Google Scholar
    • Export Citation
  • 6

    Wellens HJ, Bär FW, Lie KI. The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med 1978;64:2733.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7

    Marriott HJL, Conover MB. Aberrant ventricular conduction. In:Marriott HJL, Conover MB, ed.Advanced concepts in arrhythmias. 3rd ed. St Louis: CV Mosby Co, 1998;215236.

    • Search Google Scholar
    • Export Citation
  • 8

    Tilley LP. Uncommon complex arrhythmias. In:Tilley LP, ed.Essentials of canine and feline electrocardiography: interpretation and treatment. 3rd ed. Philadelphia: Lea & Febiger, 1992;385416.

    • Search Google Scholar
    • Export Citation
  • 9

    Sandler IA, Marriott HJL. The differential morphology of anomalous ventricular complexes of RBBB-type in lead V; ventricular ectopy versus aberration. Circulation 1965;31:551556.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10

    Wilson JR, Douglas P, Hickey WF, et al. Experimental congestive heart failure produced by rapid ventricular pacing in the dog: cardiac effects. Circulation 1987;75:857867.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11

    Kittleson MD. Primary myocardial disease leading to chronic myocardial failure (dilated cardiomyopathy and related diseases). In:Kittleson MD, Keinle RD, ed.Small animal cardiovascular medicine. Philadelphia: Mosby Inc, 1998;319346.

    • Search Google Scholar
    • Export Citation
  • 12

    Spinale FG, Fulbright M, Mukherjee R, et al. Relation between ventricular and myocyte function with tachycardia-induced cardiomyopathy. Circ Res 1992;71:174187.

    • Crossref
    • Search Google Scholar
    • Export Citation

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