ECG of the Month

Mark W. Harmon Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Columbia, MO 65211.

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Deborah M. Fine Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Columbia, MO 65211.

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 DVM, MS, DACVIM

A 9-year-old 4.4-kg (9.7-lb) castrated male Pomeranian was referred to the University of Missouri Veterinary Medical Teaching Hospital for evaluation of a murmur. The murmur was first ausculted a month earlier by the referring veterinarian during a recheck examination of the dog, which had been previously evaluated because of coughing. The dog had been treated with amoxicillin-clavulanic acida (14.2 mg/kg [6.45 mg/lb], PO, q 12 h) for 2 weeks, and at the recheck examination, the owner reported that coughing had resolved. However, the owner had noticed progressive inappetence and lethargy. Serum biochemical analysis performed at the recheck examination revealed mildly high activities of aspartate aminotransferase (218 U/L; reference range, 15 to 66 U/L) and alanine aminotransferase (200 U/L; reference range, 12 to 118 U/L). No additional physical or clinicopathologic abnormalities were present. The referring veterinarian prescribed treatment with amoxicillin-clavulanic acid for an additional 2 weeks to treat the clinical signs reported by the owner. The dog was then taken to a naturopathic veterinarian for a second opinion and prescribed a variety of homeopathic remedies to support cardiac and hepatic health. Approximately 1 week prior to the cardiographic evaluation, the owner noted a possible syncopal episode. She had found the dog collapsed and unresponsive, but after a few seconds, the dog spontaneously recovered with apparently normal mentation.

On arrival at the veterinary medical teaching hospital, the dog was bright, alert, and responsive. The heart rate was 160 beats/min, and the rhythm was regular. Auscultation revealed grade 4/6 left- and right-sided systolic murmurs that were equally intense over the mitral and tricuspid valves. Femoral pulses were strong and synchronous with the heartbeats. Broncho-vesicular sounds in all lung fields were considered normal. A cough was easily elicited via tracheal palpation. No other abnormalities were detected during physical examination.

Systolic arterial blood pressure, as measured by use of Doppler flow ultrasonography, was 134 mm Hg. Thoracic radiography revealed marked generalized enlargement of the cardiac silhouette relative to the thorax (vertebral heart score, 12.75; reference range, 9.2 to 10.1)1 and moderate left atrial enlargement. The appearance of the pulmonary vasculature was considered normal. There was a moderate diffuse broncho-interstitial pattern that was considered most likely an age-related change. Echocardiography revealed moderate enlargement of the left atrium; the mitral valve was thickened, had areas of prolapse, and appeared hyperechoic relative to a normal mitral valve. Despite marked mitral valve regurgitation, as evidenced by color flow Doppler ultrasonographic imaging, left ventricular measurements were within reference limits. During the echocardiographic examination, a simultaneous ECG revealed paroxysms of supraventricular tachycardia (SVT) with occasional isolated ventricular premature complexes. Further ECG evaluation was performed.

ECG Interpretation

The initial 6-lead ECG tracing revealed sinus tachycardia with a regular rate of 180 beats/min (Figure 1). This rhythm was interrupted by paroxysms of SVT with a ventricular depolarization rate of 250 beats/min. During the paroxysmal tachycardia, the morphology of the QRS complexes was apparently normal (amplitude, 1.1 to 1.4 mV [reference range, < 2.5 mV in small dog breeds2]; duration, 0.04 seconds [reference range, < 0.05 seconds2]), indicative of normal ventricular depolarization through the His-Purkinje conduction system. P' waves were present in the terminal portion of each preceding T wave and were closer to the subsequent R wave than to the preceding R wave, consistent with a long RP' SVT. P wave polarity was positive in leads I, II, III, and aVF, suggesting that the most likely rhythm diagnosis was atrial tachycardia.

Figure 1—
Figure 1—

Six-lead ECG tracing obtained during evaluation of a 9-year-old Pomeranian at a veterinary medical teaching hospital. The dog had been initially examined because of coughing; the owner had subsequently noticed progressive inappetence, lethargy, and a possible syncopal episode, and the referring veterinarian had detected right- and left-sided murmurs during a recheck examination. At this ECG assessment, the ventricular rate of depolarization is 250 beats/min. Positive P' waves are present in the terminal portion of the preceding T waves of the inferior leads (arrows), and the RP' intervals are long. A spontaneously blocked P' wave is present in the T wave of the fifth complex in leads I, II, and III. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 240, 6; 10.2460/javma.240.6.668

A vagal maneuver (bilateral retropulsion of the globes) was performed in an attempt to obtain a more definitive rhythm diagnosis. The maneuver caused second-degree atrioventricular (AV) block and subtle prolongation of the R-R interval before conversion to a sinus arrhythmia with a ventricular depolarization rate of 140 beats/min (Figure 2). Given the brief deceleration in heart rate in response to the vagal maneuver, the arrhythmia was considered most consistent with ectopic atrial automaticity. A ladder diagram was drawn to explain the proposed rhythm diagnosis.

Figure 2—
Figure 2—

Lead II ECG tracing (with accompanying ladder diagram) obtained during a vagal maneuver performed on the dog in Figure 1 to further characterize the atrial tachycardia. Vagal stimulation resulted in a subtle prolongation of the R-R interval and second-degree atrioventricular (AV) block (arrow) before conversion to a sinus arrhythmia. The resultant sinus arrhythmia has a ventricular rate of 140 beats/min. Ectopic atrial automaticity was suspected given the nature of the supraventricular tachycardia and response to vagal stimulation. A ladder diagram illustrates the proposed mechanism. The vertical lines capped by a dot mark the atrial depolarization from an ectopic atrial focus (A level). Notice the progressive prolongation of the P'R interval (indicated by the progressive increase in the slope of the AV level lines; values in milliseconds) and slowing of the heart rate prior to the block and conversion. The number of beats per minute are noted under the ladder diagram. HR = Heart rate. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 240, 6; 10.2460/javma.240.6.668

Discussion

Supraventricular tachyarrhythmias are defined as rapid rhythms that originate within the atria or AV junction near the bundle of His.3 Given the tissue involved in sustaining SVTs, the QRS complex morphology is typically normal.3–6 Identification and evaluation of P' waves is essential in assessing the underlying mechanisms. If the P' wave is closer to the preceding R wave than it is to the subsequent R wave, it is classified as a short RP' SVT. Short RP' SVTs include orthodromic AV reciprocating tachycardia (OAVRT) and AV nodal reentrant tachycardia.3 The P' waves in the dog of this report were closer to the subsequent R wave than they were to the preceding R wave, thereby classifying the arrhythmia as a long RP' SVT. Long RP' SVTs are typically AV node independent and include sinus nodal reentrant tachycardia, automatic atrial tachycardia, and intra-atrial reentrant tachycardia.3,4,6 Another important consideration in distinguishing SVTs is the initiation and termination of the tachycardia. Sudden onset and offset tachycardias are typically secondary to reentry.3,4

Tachyarrhythmias that have periods of acceleration and deceleration are more suggestive of automatic SVTs. The termination of an SVT with a ventricular premature complex is strongly suggestive of AV junctional involvement.3 In humans, 12-lead ECG is routinely performed to evaluate SVTs, and recently, its use in dogs has been validated.6 In the dogs in that validation study,6 positive P waves in leads II, III, and aVF were more consistent with atrial tachycardia than with OAVRT.

In humans, vagal maneuvers such as ocular pressure or carotid sinus massage have diagnostic and therapeutic uses in patients with arrhythmias involving the sinus and AV nodes.3,4 The maneuver-induced elevation in vagal tone results in a slower sinus rate of depolarization and delayed AV nodal conduction. Abrupt response to a vagal maneuver occurs most commonly in patients with OAVRT, AV nodal reentrant tachycardia, and sinus nodal reentrant tachycardia; however, lack of response to a vagal maneuver in dogs does not rule out these rhythm disturbances because these maneuvers may not reliably increase vagal tone in this species.3,4,7 Excessive and prolonged ocular pressure should be avoided to prevent possible retinal detachment.3

Ectopic atrial tachycardia is the result of atrial automaticity in a location other than the sinus node. Characteristic ECG findings are a long RP' SVT with a gradual onset and offset3,4; such findings were evident in the dog of this report. Just prior to termination of the tachycardia, animals often develop first-degree AV block. Vagal maneuvers are not usually effective at terminating ectopic atrial tachycardia because of their independence of the sinoatrial and AV nodes; however, the delayed AV conduction can slow the rate of ventricular response.4 Treatment for these arrhythmias is difficult if abnormal automaticity is present, and rate control is best achieved via administration of a combination of β-adrenergic receptor blockers and calcium channel blockers.3–5

For the dog of this report, atenolol (1.42 mg/kg [0.65 mg/lb], PO, q 24 h) was prescribed to slow AV node conduction. Following administration of the first dose, the owner reported by telephone that the dog appeared disoriented and lethargic. The owner was unable to have the dog evaluated at that time and was therefore instructed to contact the cardiologist prior to administration of the next dose. When the owner evaluated the dog again that evening, she believed that the appetite and attitude of the dog had returned to normal and chose to administer the second dose without consulting the cardiologist. The dog was found dead the following morning. In the absence of findings of an ECG evaluation performed immediately prior to death, it was impossible to determine whether the dog had became excessively bradycardic owing to β-adrenergic receptor blockade or the tachycardia had degenerated into a fatal ventricular arrhythmia.

a.

Clavamox, Pfizer Animal Health, New York, NY.

References

  • 1.

    Buchanan JW, Bücheler J. Vertebral scale system to measure canine heart size in radiographs. J Am Vet Med Assoc 1995; 206:194199.

  • 2.

    Tilley LP. Analysis of canine P-QRS-T deflections. In: Tilley LP, ed. Essentials of canine and feline electrocardiography: interpretation and treatment. 2nd ed. Philadelphia: Lea & Febiger, 1985;58.

    • Search Google Scholar
    • Export Citation
  • 3.

    Wright KN. Assessment and treatment of supraventricular tachyarrhythmias. In: Bonagura JD, ed. Current veterinary therapy XIV. St Louis: Elsevier, 2008;722727.

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    • Export Citation
  • 4.

    Fox PR, Sisson DD, Moise NS. Diagnosis and management of canine arrhythmias. In: Fox PR, Sisson DD, Moise NS, eds. Textbook of canine and feline cardiology: principles and clinical practice. 2nd ed. Philadelphia: Saunders, 1999;332355.

    • Search Google Scholar
    • Export Citation
  • 5.

    Kittleson MD. Diagnosis and treatment of arrhythmias (dysrhythmias). In: Kittleson MD, Kienle RD, eds. Small animal cardiovascular medicine. St Louis: Mosby, 1998;449494.

    • Search Google Scholar
    • Export Citation
  • 6.

    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
  • 7.

    Tilley LP, Smith FWK Jr, Oyama MA, et al, eds. Manual of canine and feline cardiology. 4th ed. St Louis: Saunders, 2008.

  • Figure 1—

    Six-lead ECG tracing obtained during evaluation of a 9-year-old Pomeranian at a veterinary medical teaching hospital. The dog had been initially examined because of coughing; the owner had subsequently noticed progressive inappetence, lethargy, and a possible syncopal episode, and the referring veterinarian had detected right- and left-sided murmurs during a recheck examination. At this ECG assessment, the ventricular rate of depolarization is 250 beats/min. Positive P' waves are present in the terminal portion of the preceding T waves of the inferior leads (arrows), and the RP' intervals are long. A spontaneously blocked P' wave is present in the T wave of the fifth complex in leads I, II, and III. Paper speed = 50 mm/s; 1 cm = 1 mV.

  • Figure 2—

    Lead II ECG tracing (with accompanying ladder diagram) obtained during a vagal maneuver performed on the dog in Figure 1 to further characterize the atrial tachycardia. Vagal stimulation resulted in a subtle prolongation of the R-R interval and second-degree atrioventricular (AV) block (arrow) before conversion to a sinus arrhythmia. The resultant sinus arrhythmia has a ventricular rate of 140 beats/min. Ectopic atrial automaticity was suspected given the nature of the supraventricular tachycardia and response to vagal stimulation. A ladder diagram illustrates the proposed mechanism. The vertical lines capped by a dot mark the atrial depolarization from an ectopic atrial focus (A level). Notice the progressive prolongation of the P'R interval (indicated by the progressive increase in the slope of the AV level lines; values in milliseconds) and slowing of the heart rate prior to the block and conversion. The number of beats per minute are noted under the ladder diagram. HR = Heart rate. Paper speed = 50 mm/s; 1 cm = 1 mV.

  • 1.

    Buchanan JW, Bücheler J. Vertebral scale system to measure canine heart size in radiographs. J Am Vet Med Assoc 1995; 206:194199.

  • 2.

    Tilley LP. Analysis of canine P-QRS-T deflections. In: Tilley LP, ed. Essentials of canine and feline electrocardiography: interpretation and treatment. 2nd ed. Philadelphia: Lea & Febiger, 1985;58.

    • Search Google Scholar
    • Export Citation
  • 3.

    Wright KN. Assessment and treatment of supraventricular tachyarrhythmias. In: Bonagura JD, ed. Current veterinary therapy XIV. St Louis: Elsevier, 2008;722727.

    • Search Google Scholar
    • Export Citation
  • 4.

    Fox PR, Sisson DD, Moise NS. Diagnosis and management of canine arrhythmias. In: Fox PR, Sisson DD, Moise NS, eds. Textbook of canine and feline cardiology: principles and clinical practice. 2nd ed. Philadelphia: Saunders, 1999;332355.

    • Search Google Scholar
    • Export Citation
  • 5.

    Kittleson MD. Diagnosis and treatment of arrhythmias (dysrhythmias). In: Kittleson MD, Kienle RD, eds. Small animal cardiovascular medicine. St Louis: Mosby, 1998;449494.

    • Search Google Scholar
    • Export Citation
  • 6.

    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
  • 7.

    Tilley LP, Smith FWK Jr, Oyama MA, et al, eds. Manual of canine and feline cardiology. 4th ed. St Louis: Saunders, 2008.

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