ECG of the Month

Risa M. Roland Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853

Search for other papers by Risa M. Roland in
Current site
Google Scholar
PubMed
Close
 DVM
and
Amara H. Estrada Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853

Search for other papers by Amara H. Estrada in
Current site
Google Scholar
PubMed
Close
 DVM, DACVIM

A 7-year-old spayed female American domestic short-hair cat was evaluated at the Cornell University Hospital for Animals because of a history of sudden onset of recumbency, unresponsiveness, ptyalism, and shallow breathing. On physical examination, mucous membranes were pale and the cat was hypothermic (rectal temperature, 35.7°C [96.2°F]). Indirect systolic blood pressure was undetectable by use of an ultrasonic Doppler flow detector.a Thoracic auscultation revealed a heart rate > 300 beats/min and no abnormal lung sounds bilaterally. Electrocardiography was performed to assess the tachycardia (Figure 1). A venous catheter was placed, and supportive care was initiated, including warming and IV administration of fluids. Shortly after the initial ECG was completed, repeat auscultation of the thorax revealed a much slower heart rate and another ECG was recorded (Figure 2). Routine clinicopathologic analyses were performed, and findings were unremarkable with the exception of mild hyperglycemia and mildly high serum activities of alanine aminotransferase, aspartate aminotransferase, and γ-glutamyltranspeptidase. Results of thyroid hormone assessments were within reference limits. Echocardiography revealed a structurally normal heart, and the heart rate remained at 180 to 200 beats/min during the entire procedure.

Figure 1—
Figure 1—

Lead II ECG trace obtained from a cat during an episode of tachycardia. A supraventricular tachycardia is present with a heart rate of approximately 333 beats/min. Questionable p' waves (arrows) with a short Rp' interval are identified. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 228, 10; 10.2460/javma.228.10.1500

Figure 2—
Figure 2—

Electrocardiographic traces obtained from the cat in Figure 1 during sinus rhythm. Notice the p waves (arrows). There is a shortened PR interval and a slurred upstroke of the QRS complex consistent with ventricular preexcitation. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 228, 10; 10.2460/javma.228.10.1500

ECG Interpretations

Evaluation of the initial ECG revealed a supraventricular tachycardia and heart rate of approximately 333 beats/min (Figure 1). Questionable p' waves with a short Rp' interval were identified during the tachycardia. Examination of the second ECG, after the heart rate had slowed, revealed a shortened PR interval (40 milliseconds) and a wide QRS complex (60 milliseconds) with a visible delta wave (Figure 2). This ECG trace was characteristic of sinus rhythm with ventricular preexcitation (heart rate, 188 beats/min).

Discussion

Ventricular preexcitation is a rare arrhythmia in cats. It has been associated with congenital and acquired cardiac disease, including hypertrophic cardiomyopathy and hyperthyroidism.1,2 It can also be idiopathic, without evidence of underlying structural cardiac disease, as in the cat of this report.1 Ventricular preexcitation occurs as a result of the presence of aberrant myocardial tissue, which creates an accessory electrical pathway from the atria to the ventricles that is independent of the normal atrioventricular (AV) conduction pathway.3 Accessory pathways (APs) may be completely independent of the normal cardiac conduction pathways (ie, outside the AV node and Bundle of His) or may incorporate some area of the normal conduction pathways.1,4 Some APs connect the AV node directly to the ventricular muscle.4 The degree of shortening of the PR interval and presence or absence of a delta wave depend on the location of the AP and its proximity to the AV node.

Bypass tracts may or may not conduct in the anterograde direction. If antegrade conduction is present, preexcitation is detected on the surface ECG. This is identified by a short PR interval and a delta wave (slurring of the onset of the QRS complex). The short PR interval occurs as the ventricular myocardium is depolarized faster than the normal conduction pathway because the bypass tract does not have a conduction delay.1,4,5 Depolarization of the ventricle by the bypass tract impulse produces the delta wave. The delta wave occurs because the ventricular depolarization did not occur via the normal, fast His-Purkinje system.1,3,6 The resultant QRS complex is a fusion of the early excitation from the bypass tract with the ventricular depolarization from the normal conduction pathway.1,3 If the sinus impulse conducts through the AV node and the AP is not used, preexcitation does not occur and the ECG trace appears normal. Some APs can conduct only in a retrograde direction and thus are not associated with evidence of preexcitation on the surface ECG. These are called concealed APs (ie, no atrial impulses are capable of reaching the ventricles via the bypass tract)4; their presence can be deduced only when there is no preexcitation during sinus rhythm.

Accessory pathways resulting in ventricular preexcitation become clinically important only if they result in reentrant supraventricular tachycardia and the Wolff-Parkinson-White syndrome (characterized by weakness, syncope, secondary valvular dysfunction, and systolic and diastolic dysfunction).4,5 Atrioventricular reentrant tachycardia can be precipitated by both atrial premature and ventricular premature beats (Figure 3). An atrial premature beat may find the AP refractory and conduct through the normal conduction pathway. On ventricular depolarization, the AP is no longer refractory and is capable of conducting a retrograde impulse to the atria. The depolarizing wave front in the atria can then reach the AV node again and conduct anterograde, thus completing a reentrant cycle.1,3,4 Alternatively, a ventricular premature beat may find the normal AV conduction pathway refractory but depolarize the atria via retrograde conduction through the AP. The atria may then complete the reentrant cycle by conduction via the normal AV conduction pathway. This type of reentrant tachycardia is termed orthodromic reciprocating tachycardia.4,7 Tachycardias can also develop via the reverse circuit (termed antidromic reciprocating tachycardia). In humans, this is much less common than orthodromic reciprocating tachycardia and, to our knowledge, has not yet been reported in cats.4,8 As with orthodromic reciprocating tachycardia, antidromic reciprocating tachycardia can be precipitated by both atrial premature and ventricular premature beats. An atrial premature beat may find the AV node refractory and conduct anterograde through the AP. On ventricular depolarization, the AV node is no longer refractory and is capable of conducting a retrograde impulse to the atria.4 Alternatively, a ventricular premature beat may find the AP conduction pathway refractory and depolarize the atria via retrograde conduction through the AV node. The atria may then complete the reentrant cycle by conduction via the AP. This type of tachycardia is associated with wide QRS complexes because the initial ventricular impulse occurs outside of the normal conduction system (ie, in the AP).9 Thus, it is often difficult to differentiate antidromic reciprocating tachycardia from ventricular tachycardia.

Figure 3—
Figure 3—

Schematic illustrating an atrial premature complex (APC) and a ventricular premature complex (VPC) initiating a reentrant tachycardia (ie, orthodromic reciprocating tachycardia). A—An APC occurs but the acessory pathway (AP) is refractory (dotted line). However, the atrioventricular (AV) node is able to conduct, albeit slowly; conduction occurs through the AV node (solid line). By the time the impulse reaches the ventricles, the AP is no longer refractory and is capable of conducting a retrograde impulse to the atria. The depolarizing wave front in the atria can then reach the AV node again and conduct anterograde to complete a reentrant cycle. B—Alternatively, the normal AV conduction pathway may be refractory to a ventricular premature beat (dotted line), but that beat may depolarize the atria via retrograde conduction through the AP (solid line). The atria may then complete the reentrant cycle by conduction via the normal AV conduction pathway. SA = Sinoatrial node.

Citation: Journal of the American Veterinary Medical Association 228, 10; 10.2460/javma.228.10.1500

Treatment for ventricular preexcitation and resultant orthodromic or antidromic reciprocating AV tachycardia is intended to interrupt the tachycardia and prevent its recurrence.4 Type 1A antiarrhythmic agents (eg, quinidine and procainamide) are used to increase the length of the refractory period of the AP.1,4,7,10 Calciumchannel blockers (eg, diltiazem) and β-adrenergic receptor blockers (eg, propranolol and atenolol) can be used to slow conduction and lengthen the refractory period of the AV node.1,4,7,10 Additionally, β-adrenergic receptor blockers may directly affect the AP during increased sympathetic tone and resultant tachycardia events.4 Type IC antiarrhythmic drugs (eg, flecainide and propafenone) may also be administered. Drugs of this class increase both the conduction and refractory times of the AV node as well as increase the conduction time and refractory time of the anterograde and retrograde APs.4,7 Class III antiarrhythmic agents (eg, amiodarone) lengthen the refractory period of the AP and AV node and suppress premature depolarizations that may incite the tachyarrhythmia.1,4,7 Alternatively, transvenous catheter ablation of the bypass tract by use of radiofrequency energy has been used at a few veterinary centers. This procedure causes thermal destruction of the bypass tract, which essentially cures the tachyarrhythmia.10 This procedure has been used in dogs11,12 but, to the authors' knowledge, has yet to be used in a cat.

The prognosis for recovery from clinical signs of orthodromic or antidromic reciprocating atrioventricular tachycardia is good if the episodes of tachycardia can be well controlled. The cat of this report was sent home, and the owner was instructed to administer treatment with atenolol (a selective β1-adrenergic receptor blocker). Two weeks later, the cat underwent a repeat ECG evaluation. The heart rate was 150 beats/min, and the ECG trace again included evidence of ventricular preexcitation. At home, the owner had assessed the cat's heart rate at several consistent intervals (immediately before and 4 and 8 hours after atenolol administration) and had not detected episodes of tachycardia during the 2-week period. All recorded heart rates were < 160 beats/min. No episodes of weakness, collapse, or other clinical signs had been noted by the owner. Five and a half weeks later, the cat was examined by staff of the emergency service. An ECG revealed a supraventricular tachyarrhythmia. The rhythm converted to a normal sinus rhythm without intervention within 2 hours. A Holter monitor was offered to the owner to assess the frequency of the arrhythmia and efficacy of treatment. The owner declined the use of the Holter monitor, and 1 week later, administration of atenolol was discontinued and oral treatment with diltiazem (a calcium channel blocker) was initiated. After this visit, the cat was lost to follow-up.

a.

Ultrasonic Doppler flow detector, Parks Medical Electronics Inc, Aloha, Ore.

References

  • 1

    Hill BL, Tilley LP. Ventricular preexcition in seven dogs and nine cats. J Am Vet Med Assoc 1985;187:10261031.

  • 2

    Peterson ME, Keene B, Ferguson DC, et al. Electrocardiographic findings in 45 cats with hyperthyroidism. J Am Vet Med Assoc 1982;180:934937.

    • Search Google Scholar
    • Export Citation
  • 3

    Kittleson MD. Drugs used in treatment of arrhythmias (dysrhythmias). In: Kittleson MD, Kienle RD, eds. Small animal cardiovascular medicine. St Louis: CV Mosby Co, 1998;466469.

    • Search Google Scholar
    • Export Citation
  • 4

    Atkins CE, Wright KN. Supraventricular tachycardia associated with accessory atrioventricular pathways in dogs. In: Bonagura JD, ed. Kirk's current veterinary therapy XII. Philadelphia: WB Saunders Co, 1995;807813.

    • Search Google Scholar
    • Export Citation
  • 5

    Miller MS, Tilley LP, Smith FWK, et al. Electrocardiography. In: Fox PR, Sisson D, Moïse NS, eds. Textbook of canine and feline cardiology. 2nd ed. Philadelphia: WB Saunders Co, 1999;8687.

    • Search Google Scholar
    • Export Citation
  • 6

    Marriott HJ, Conover MB. Narrow QRS paroxysmal supraventricular tachycardia. In: Marriott HJ, Conover MB, eds. Advanced concepts in arrhythmias. 3rd ed. St Louis: CV Mosby Co, 1998;162.

    • Search Google Scholar
    • Export Citation
  • 7

    Atkins CE, Kanter R, Wright K, et al. Orthodromic reciprocating tachycardia and heart failure in a dog with concealed posteroseptal accessory pathway. J Vet Intern Med 1995;9:4349.

    • Search Google Scholar
    • Export Citation
  • 8

    Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Braunwald E, ed. Heart disease. 5th ed. Philadelphia: WB Saunders Co, 1997;670.

    • Search Google Scholar
    • Export Citation
  • 9

    Marriott HJ, Conover MB. The other broads. In: Marriott HJ, Conover MB, eds. Advanced concepts in arrhythmias. 3rd ed. St Louis: CV Mosby Co, 1998;269272.

    • Search Google Scholar
    • Export Citation
  • 10

    Wright KN. Assessment and treatment of supraventricular tachyarrhythmias. In: Bonagura JD, ed. Kirk's current veterinary therapy XIII. Philadelphia: WB Saunders Co, 2000;726730.

    • Search Google Scholar
    • Export Citation
  • 11

    Scherlag BJ, Wang X, Nakagawa H, et al. Radiofrequency ablation of a concealed accessory pathway as treatment for incessant supraventricular tachycardia in a dog. J Am Vet Med Assoc 1993;203:11471152.

    • Search Google Scholar
    • Export Citation
  • 12

    Langberg J, Griffin JC, Herre JM, et al. Catheter ablation of accessory pathways using radiofrequency energy in the canine coronary sinus. J Am Coll Cardiol 1989;13:491496.

    • Search Google Scholar
    • Export Citation
  • Figure 1—

    Lead II ECG trace obtained from a cat during an episode of tachycardia. A supraventricular tachycardia is present with a heart rate of approximately 333 beats/min. Questionable p' waves (arrows) with a short Rp' interval are identified. Paper speed = 50 mm/s; 1 cm = 1 mV.

  • Figure 2—

    Electrocardiographic traces obtained from the cat in Figure 1 during sinus rhythm. Notice the p waves (arrows). There is a shortened PR interval and a slurred upstroke of the QRS complex consistent with ventricular preexcitation. Paper speed = 50 mm/s; 1 cm = 1 mV.

  • Figure 3—

    Schematic illustrating an atrial premature complex (APC) and a ventricular premature complex (VPC) initiating a reentrant tachycardia (ie, orthodromic reciprocating tachycardia). A—An APC occurs but the acessory pathway (AP) is refractory (dotted line). However, the atrioventricular (AV) node is able to conduct, albeit slowly; conduction occurs through the AV node (solid line). By the time the impulse reaches the ventricles, the AP is no longer refractory and is capable of conducting a retrograde impulse to the atria. The depolarizing wave front in the atria can then reach the AV node again and conduct anterograde to complete a reentrant cycle. B—Alternatively, the normal AV conduction pathway may be refractory to a ventricular premature beat (dotted line), but that beat may depolarize the atria via retrograde conduction through the AP (solid line). The atria may then complete the reentrant cycle by conduction via the normal AV conduction pathway. SA = Sinoatrial node.

  • 1

    Hill BL, Tilley LP. Ventricular preexcition in seven dogs and nine cats. J Am Vet Med Assoc 1985;187:10261031.

  • 2

    Peterson ME, Keene B, Ferguson DC, et al. Electrocardiographic findings in 45 cats with hyperthyroidism. J Am Vet Med Assoc 1982;180:934937.

    • Search Google Scholar
    • Export Citation
  • 3

    Kittleson MD. Drugs used in treatment of arrhythmias (dysrhythmias). In: Kittleson MD, Kienle RD, eds. Small animal cardiovascular medicine. St Louis: CV Mosby Co, 1998;466469.

    • Search Google Scholar
    • Export Citation
  • 4

    Atkins CE, Wright KN. Supraventricular tachycardia associated with accessory atrioventricular pathways in dogs. In: Bonagura JD, ed. Kirk's current veterinary therapy XII. Philadelphia: WB Saunders Co, 1995;807813.

    • Search Google Scholar
    • Export Citation
  • 5

    Miller MS, Tilley LP, Smith FWK, et al. Electrocardiography. In: Fox PR, Sisson D, Moïse NS, eds. Textbook of canine and feline cardiology. 2nd ed. Philadelphia: WB Saunders Co, 1999;8687.

    • Search Google Scholar
    • Export Citation
  • 6

    Marriott HJ, Conover MB. Narrow QRS paroxysmal supraventricular tachycardia. In: Marriott HJ, Conover MB, eds. Advanced concepts in arrhythmias. 3rd ed. St Louis: CV Mosby Co, 1998;162.

    • Search Google Scholar
    • Export Citation
  • 7

    Atkins CE, Kanter R, Wright K, et al. Orthodromic reciprocating tachycardia and heart failure in a dog with concealed posteroseptal accessory pathway. J Vet Intern Med 1995;9:4349.

    • Search Google Scholar
    • Export Citation
  • 8

    Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Braunwald E, ed. Heart disease. 5th ed. Philadelphia: WB Saunders Co, 1997;670.

    • Search Google Scholar
    • Export Citation
  • 9

    Marriott HJ, Conover MB. The other broads. In: Marriott HJ, Conover MB, eds. Advanced concepts in arrhythmias. 3rd ed. St Louis: CV Mosby Co, 1998;269272.

    • Search Google Scholar
    • Export Citation
  • 10

    Wright KN. Assessment and treatment of supraventricular tachyarrhythmias. In: Bonagura JD, ed. Kirk's current veterinary therapy XIII. Philadelphia: WB Saunders Co, 2000;726730.

    • Search Google Scholar
    • Export Citation
  • 11

    Scherlag BJ, Wang X, Nakagawa H, et al. Radiofrequency ablation of a concealed accessory pathway as treatment for incessant supraventricular tachycardia in a dog. J Am Vet Med Assoc 1993;203:11471152.

    • Search Google Scholar
    • Export Citation
  • 12

    Langberg J, Griffin JC, Herre JM, et al. Catheter ablation of accessory pathways using radiofrequency energy in the canine coronary sinus. J Am Coll Cardiol 1989;13:491496.

    • Search Google Scholar
    • Export Citation

Advertisement