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Katherine M. Hogan Angell Animal Medical Center, 350 S Huntington Ave, Boston, MA 02130.

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Rebecca L. Quinn Angell Animal Medical Center, 350 S Huntington Ave, Boston, MA 02130.

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A 4.5-year-old 5.23-kg (11.5-lb) castrated male domestic shorthair cat was referred to the Angell Animal Medical Center for evaluation of a bradyarrhythmia. The cat was adopted 1 year prior and was initially without clinical signs. In the 6-month period preceding the evaluation, the clients reported that the cat had developed intermittent lethargy and exercise intolerance. The cat's normal daily routine consisted of a walk outdoors (distance, 0.4 to 0.8 km [one-quarter to half mile]), and occasional bouts of fatigue during walks and following short periods of activity were noted prior to evaluation. Cardiac auscultation revealed an irregular bradyarrhythmia and a grade II of VI left apical systolic heart murmur. Other physical examination findings were within reference limits. The cat received flea and heartworm preventative on a monthly basis. Blood samples were collected, but no abnormalities were revealed by a CBC, biochemical panel, or thyroid hormone testing. Echocardiography, including Doppler interrogation, revealed apparently normal cardiac structures and blood flow velocities; no discrete cause of the murmur was determined. Electrocardiography was performed with the cat in right lateral recumbency; tracings from leads I, II, III, aVR, aVL, aVF, and V2 were recorded (Figure 1).

ECG Interpretation

The ECG tracings revealed that the cat's atrial heart rate varied from 100 to 230 beats/min (Figure 1). The P-wave morphology was consistent and within reference limits (amplitude, 0.2 mV; duration, 0.03 seconds); consistent PR intervals were not present, and P waves were not associated with QRS complexes. The inconsistency of PR intervals led to the diagnosis of atrioventricular (AV) dissociation. Overall, the P-P intervals were regular (0.46 seconds). However, an early P wave with a shortened P-P interval (0.26 seconds) was detected. The P-P interval (0.38 seconds) following this early P wave was slightly greater than the preceding P-P interval, but then the interval returned to a duration of 0.46 seconds for the remainder of the tracing. This early P wave was considered indicative of a supraventricular discharge or ectopic focus, but may also have been indicative of an abnormal sinoatrial node, as with sick sinus syndrome, sinus arrest, sinoatrial block, or potentially atrial parasystole.1 None of the P waves were conducted.

The ventricular heart rate was also irregular, varying from 60 to 166 beats/min. Multiple QRS complex morphologies were evident in the tracings (Figures 1 and 2). Some QRS complexes appeared narrow and upright, suggesting they were supraventricular or junctional in origin; however, it is also possible that these complexes originated from a location high in the ventricle. There were also intermittent complexes that were suspected to be fusion beats. The remaining QRS complexes were ventricular in origin, originating from specialized conductile tissue of either the left or right ventricle. Often, right ventricular origin complexes were followed by left ventricular origin complexes. The coupling intervals (0.38 to 0.40 seconds) between these complexes were consistent throughout the tracings.

Figure 1—
Figure 1—

Leads II, aVF, and V2 ECG tracings and a Lewis (ladder) diagram from a 6-lead ECG examination of a cat that had developed intermittent lethargy and exercise intolerance over a 6-month period. In the ladder diagram, the upper zone represents atrial activation (A), the middle zone represents AV conduction (AV), and the lower zone represents ventricular activation (V). There are 2 types of QRS complexes present. Most complexes appear AV junctional in origin (thin downward arrows); the others are ventricular in origin (these beats are coupled and appear to arise first from the right, followed by the left, ventricular conduction system [wide downward arrows]). Two other beats (upward arrows) appear to be fusion beats. Overall, the P-P intervals are consistent (0.46 seconds; P waves are marked by stars). However, there is an early P wave (indicated by an asterisk) after a shortened P-P interval (0.26 seconds); the subsequent P-P interval is also shortened (0.38 seconds). These P waves are indicative of ectopic atrial beats. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 246, 8; 10.2460/javma.246.8.843

Figure 2—
Figure 2—

Six-lead (leads I, II, III, aVR, aVL, and aVF) ECG tracing strip obtained within 1 minute after the ECG recording in Figure 1. Notice the AV dissociation with no conduction of P waves. On this section of the tracing, most QRS complexes appear supraventricular in origin (downward arrows), but may also be originating at the high atrioventricular junction. There is 1 fusion beat (upward arrow) present. The P-P intervals are difficult to calculate because many of the P waves (stars) seem to be buried in the QRS complexes. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 246, 8; 10.2460/javma.246.8.843

Discussion

Atrioventricular dissociation is a condition wherein the normal association between atrial and ventricular depolarization no longer exists; the atria and ventricles are driven by 2 independent foci of impulse formation, causing them to beat asynchronously.2,3 This is always the result of a basic abnormality of impulse formation or conduction.3 Atrioventricular dissociation can be caused by depressed sinoatrial node automaticity, which allows normal AV junctional or ventricular automaticity to escape and control the heart rate; increased AV junctional or ventricular automaticity, which causes dissociation by interference as an ectopic focus assumes control of the ventricles while the sinoatrial node continues to activate the atria; or disturbed AV conduction, as occurs with third-degree AV block. The disturbed AV conduction may allow an AV junctional focus or a ventricular focus to control the ventricles. Distinguishing which of the 3 mechanisms is causing AV dissociation in a particular patient is often difficult, and a combination of 2 or all 3 mechanisms may be occurring.

The case described in the present report had features consistent with disturbed AV conduction caused by third-degree AV block, given that consistent PR intervals were not present and P waves were not associated with QRS complexes. Diagnosis of AV dissociation is based on identifying P waves that have variable relationships (preceding, within, and after) to the QRS complexes. In the cat of this report, the ECG revealed a lack of conduction of the P waves as well as the presence of ventricular escape rhythms, suggesting the AV dissociation was consistent with third-degree AV block.4

In the ECG tracings obtained from the cat of the present report, the atrial rate was overall slow and variable followed by intermittent coupled ventricular beats. The variable atrial rate may have been early evidence of concurrent sick sinus syndrome. Sick sinus syndrome is present when the sinus node tissue is diseased or destroyed. When most of the sinus node tissue is destroyed, it loses its ability to automatically produce depolarizations. This can cause conduction failure, leading to exit block or even sinus arrest. Sinus arrest is a common ECG finding associated with sinus node disease in dogs and cats. Sinus arrest, caused by failure to form an impulse, can continue for a short period and be terminated by the sinus node depolarizing again; alternatively, sinus arrest can continue for a longer period such that a subsidiary pacemaker (eg, the AV junction or Purkinje fibers) takes over the heart rhythm. Depolarizations by subsidiary pacemakers that occur after a pause are called escape beats and the slow rhythms are called escape rhythms. When the sinus rate and the discharge rate of the ectopic ventricular pacemaker are similar, the ectopic pacemaker rate may exceed that of the sinoatrial node and capture the cardiac rhythm for a series of beats. Such a ventricular escape rhythm will usually be accompanied by bouts of sinus rhythm, single ventricular escape beats, pairs of ventricular escape beats, and fusion beats. This results in the heart rate being governed by the 2 nodal pacemakers as well as by fusion beats and coupled ventricular beats.5

The origin of ventricular escape beats can be determined on the basis of heart rate and configuration of the QRS complexes. In the case described in the present report, there were many instances in which the QRS complexes appeared to be fusion beats or beats arising from the ventricular conduction system (ie, wider than normal with abnormal-appearing T waves).4 These QRS complexes were multiform (appearing to arise first from the right, followed by the left, ventricular conduction system) and coupled, with a consistent interval between ventricular beats. Multiform ventricular complexes usually have the same coupling intervals because they originate in the same ectopic site but their conduction through the ventricles differs.6 These abnormal QRS complexes in the cat of this report likely represented pairs of ventricular escape beats.

In human and veterinary patients, there are many documented causes of AV dissociation: surgery, general anesthesia, changes in circulating catecholamine concentrations, sinus node disease, digoxin toxicosis, structural heart disease, hyperkalemia, vagal activation, ventricular tachycardia, or ventricular pacing.3,7 In cats, AV dissociation occurs in apparently normal individuals, those with cardiovascular disease or calcium channel blocker toxicosis, or those undergoing anesthesia.4 Any adverse effects are related to ensuing bradycardia, AV dysynchrony, or underlying conditions.7 In cats with third-degree AV block, hyperthyroidism can be linked as an underlying cause.8

In the case described in the present report, infectious disease testing (eg, for serum antibody titers against Toxoplasma spp and rickettsial organisms) and atropine response testing were offered but declined by the clients. Pacemaker implantation was also discussed but declined by the owners because the cat was minimally affected by the arrhythmia. This was considered a reasonable plan, given that at a recheck examination 6 months later, the cat's ECG and echocardiographic findings were unchanged and it was clinically stable without intervention.

For the cat of this report, the primary diagnosis was AV dissociation attributed to disturbed AV conduction in the form of third-degree AV block. Given the cat's slow and variable atrial heart rate, a component of sick sinus syndrome was likely present. Despite the severity of the arrhythmia, the cat remained clinically stable without progression of reported clinical signs 19 months after diagnosis. A clear cause for the arrhythmia could not be identified, and an acquired or congenital conduction system abnormality, such as fibrosis, seemed likely.

References

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  • 2. Harrigan RA, Perron AD, Brady WJ. Atrioventricular dissociation. Am J Emerg Med 2001; 19: 218222.

  • 3. Tilley LP. Analysis of common canine cardiac arrhythmias. AV dissocation. In: Essentials of canine and feline electrocardiography: interpretation and treatment. 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 1992; 392405.

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  • 4. Kittleson MD, Kienle RD. Chapter 27: diagnosis and treatment of arrhythmias (dysrhythmias)—specific arrhythmias. In: Small animal cardiovascular medicine textbook. St Louis: Mosby, 1998; 486.

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  • 5. Detweiler DK. Chapter 35: the dog electrocardiogram: a critical review. In: MacFarlane P, Veitch Lawrie TD, eds. Comprehensive electrocardiology: theory and practice in health and disease. Vol 2. New York: Pergamon Press, 1989; 12681329.

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  • 6. Yanowitz FG. Ventricular arrhythmias in ECG. Learning Center. University of Utah School of Medicine, 2012. Available at: http://ecg.utah.edu/lesson/5-3. Accessed Jan 22, 2015.

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  • 7. Sandesara CM. Atrioventricular dissociation. In: Medscape reference: drugs, diseases, & procedures. 2013. Available at: http://emedicine.medscape.com/article/151715-overview. Accessed Jan 22, 2015.

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  • 8. Tilley LP. Treatment of cardiac arrhythmias and conduction disturbances. In: Tilley LP, Smith FWK, Oyama MA, et al. Manual of canine and feline cardiology. 4th ed. St Louis: Saunders, 2008; 325326.

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