Introduction

An 11-year-old 13-kg (28.6-lb) castrated male Standard Schnauzer was presented to the cardiology service at Oregon State University Veterinary Teaching Hospital for potential pacemaker implantation because of recent syncopal episodes. A diagnosis of sinus node dysfunction had previously been made for the dog on the basis of analysis of 24-hour Holter monitoring data. On physical examination, a grade 2/6 left apical systolic murmur and an irregular, tachycardic rhythm were ausculted. The femoral arterial pulses were variable in strength, and jugular venous distension was observed. The dog was noted to be blind bilaterally, which had been previously documented, and had intermittent, transient episodes of nystagmus and circling during the evaluation. Clinicopathologic analyses revealed evidence of mixed hepatopathy (serum alkaline phosphatase activity, 1,335 U/L [reference interval, 10 to 84 U/L]; serum alanine aminotransferase activity, 154 U/L [reference interval, 5 to 65 U/L]) with no azotemia. Plasma cardiac troponin I concentration was 0.2 ng/mL (reference interval, < 0.2 ng/mL). Echocardiography revealed degenerative mitral and tricuspid valve disease, biventricular eccentric hypertrophy with normal systolic function, severe biatrial enlargement, and moderate pulmonary hypertension. Thoracic radiography revealed moderate generalized cardiomegaly with caudal vena caval distension and mild pleural effusion. The dog underwent abdominal ultrasonography, which revealed mild peritoneal effusion and hepatomegaly with mildly increased hepatic echogenicity. Electrocardiography was also performed.

ECG Interpretation

The initial 6-lead ECG recording (Figure 1) indicated that the dog had organized atrial activation with a rate of approximately 600 beats/min and variable AV nodal conduction with a mean ventricular response rate of approximately 140 beats/min. Sawtooth or flutter F waves were present with variable morphology and an inconsistent F-F interval. The F waves were positive in leads II, III, and aVF. These changes were consistent with functional atrial flutter, historically referred to as type II Wells atrial flutter.^1,2,3,4

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Initial 6-lead ECG tracings obtained from an 11-year-old dog with a history of syncope. These tracings were obtained at the time of diagnosis of sinus node dysfunction and right-sided congestive heart failure. The underlying rhythm is atrial flutter. Notice the atrial rhythm with positive F waves in leads II, III, and aVF and a very rapid atrial rate (approx 600 beats/min), consistent with functional reentry atrial flutter. The QRS complexes are narrow, and there is variable atrioventricular conduction present. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 258, 4; 10.2460/javma.258.4.375

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The dog was hospitalized overnight, and right-sided congestive heart failure was treated with furosemide (1.9 mg/kg [0.86 mg/lb], PO, q 12 h) and pimobendan (0.28 mg/kg [0.13 mg/lb], PO, q 12 h). Ventricular response rate control with digoxin (0.0024 mg/kg [0.0011 mg/lb], PO, q 12 h) was also initiated. Overnight telemetry revealed an improved ventricular response rate of 100 to 120 beats/min. Pacemaker implantation was discussed with the owners the following morning, but medical rhythm management was elected. The dog was discharged from the hospital, and the owners were instructed to administer the previously initiated treatments along with enalapril maleate (0.38 mg/kg [0.17 mg/lb], PO, q 24 h).

The dog was returned to the hospital 2 days later following multiple syncopal episodes, vomiting, and diarrhea. A regular heart rate (120 beats/min) with fair femoral arterial pulses, which were synchronous with the heartbeat, and mild dehydration were noted during examination of the dog. Repeated serum biochemical analyses revealed moderate azotemia (BUN concentration, 101 mg/dL [reference interval, 10 to 30 mg/dL]; creatinine concentration, 2.9 mg/dL [reference interval, 1.0 to 2.0 mg/dL]), hyperphosphatemia (12.5 mg/dL; reference interval, 3.0 to 7.0 mg/dL), hyperalbuminemia (4.2 g/dL; reference interval, 2.3 to 4.0 g/dL), and static hepatopathy. Serum potassium concentration was within reference limits. Brief ultrasonographic scans of the abdomen and thorax did not reveal any cavitary effusion. Repeated ECG revealed sinus rhythm with occasional periods of sinus arrest terminated by ventricular escape beats and infrequent supraventricular premature ectopic beats. The result of an atropine response test was negative.

The dog was hospitalized for percutaneous placement of a temporary transvenous pacemaker. Fluid resuscitation was performed to correct dehydration, and a urinary catheter was placed to monitor hydration status. The following morning, results of serum biochemical analyses indicated improvement of azotemia (BUN concentration, 65 mg/dL; creatinine concentration, 1.2 mg/dL) with normalization of phosphorus concentration (4.8 mg/dL). An epicardial pacemaker was surgically placed at the left ventricular apex. An epicardial system was selected because the severe right ventricular eccentric hypertrophy caused concern for lead dislodgement or lead perforation through the myocardium associated with endocardial implantation. The dog recovered from the procedure uneventfully and was discharged from the hospital the following day. At this time, the dog continued to receive pimobendan at the previous dosage in addition to antimicrobials and analgesics; treatments with furosemide, enalapril, and digoxin were discontinued.

Two months after epicardial pacemaker implantation, the dog had recurrent syncopal episodes and was taken to a different veterinary specialty center. Electrocardiography performed at this time revealed atrial flutter with 2:1 conduction and a rapid ventricular response rate (200 to 240 beats/min). Administration of digoxin (0.0024 mg/kg, PO, q 12 h) and diltiazem (1.15 mg/kg [0.52 mg/lb], PO, q 8 h) was initiated for rate control. Shortly thereafter, the dog was again evaluated at our hospital, where an irregular, tachycardic rhythm (heart rate, 180 beats/min) was identified. An ECG recording (Figure 2) showed atrial flutter with an atrial rate of 600 beats/min and variable atrioventricular nodal conduction with ventricular paced beats at 100 beats/min. The paced beats each appeared as a pacing spike followed by a wide QRS complex of right bundle branch morphology, indicative of a left ventricular origin of the impulse generated from the epicardial pacemaker. This ECG tracing was consistent with recurrent functional atrial flutter with variable atrioventricular node conduction and paced ventricular depolarizations.

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Subsequent ECG tracings of leads I, II, and III obtained from the same dog after placement of an artificial epicardial pacemaker at the left ventricular apex. These tracings were obtained following recurrent syncopal events. At the time of this recording, the dog was being treated with digoxin and diltiazem for rate control of previously diagnosed atrial flutter. The underlying rhythm at this time is atrial flutter. The flutter F waves are positive in leads II and III with a rapid atrial rate (600 beats/min), consistent with recurrent functional reentry atrial flutter with variable atrioventricular conduction. Pacemaker spikes (asterisks) generated by the epicardial pacemaker are visible. A wide and bizarre QRS complex follows each spike, representing ventricular depolarization. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 258, 4; 10.2460/javma.258.4.375

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Discussion

In dogs, atrial flutter is an uncommon supraventricular tachyarrhythmia that is characterized by replacement of sinus P waves with flutter waves that represent atrial depolarization and repolarization. The flutter waves represent the continuous activation of the atria; the waves commonly have the same morphology, cycle duration, and polarity.^4,5,6 The atrial rate is usually > 300 beats/min but can exceed 500 beats/min, depending on the type of atrial flutter.²

The driving mechanism in atrial flutter is a macroreentrant circuit in either atrium. Atrial flutter can be associated with atrial enlargement or may occur in the absence of structural heart disease. Atrial flutters are categorized on the basis of the presence or absence of an anatomic substrate for slowed conduction and its location, when present. Both typical atrial flutter and atypical atrial flutter have an anatomic area of slowed conduction that promotes reentry and have historically been termed type 1 Wells atrial flutter. In instances of typical atrial flutter, the location of the slowed conduction is the cavotricuspid isthmus. The circuit can rotate in a counterclockwise (typical) or clockwise (reverse typical) direction,^7,8 with counterclockwise rotation being the most common direction in humans and dogs.^{1,2,9, 10, 11, 12} Atypical atrial flutter has a noncavotricuspid isthmus region of slowed conduction.¹³ In dogs, the 2 sites of atypical atrial flutter that have been described are the right septal wall and the right atrial free wall. In humans, right atrial free wall–related flutter is commonly associated with atriotomy.^2,4,9 The anatomic substrate of both typical and atypical atrial flutter causes a fixed cycle duration of the macroreentrant circuit, resulting in identical F waves with regular F-F intervals for both rhythms. Generally, typical atrial flutter has positive F waves with a negative cusp in the inferior ECG leads (leads II, III, and aVF), an atrial rate of 300 to 500 beats/min, and a sawtooth pattern of atrial activation. Atypical atrial flutter usually has positive F waves in the inferior leads, an atrial rate of approximately 280 beats/min, and an isoelectric line between consecutive F waves.^2,12

Functional atrial flutter (or type II Wells atrial flutter) is related to altered electrophysiologic properties promoting reentry rather than an anatomic substrate.^14,15 A proposed mechanism of functional atrial flutter is elevated parasympathetic tone, which shortens the atrial action potential duration and the atrial effective refractory period. These changes are predominantly modulated through activation of the acetylcholine-activated, inward-rectifying potassium (I_KACh) current, leading to increased potassium ion efflux during phase 3 repolarization. Acetylcholine also inhibits the L-type calcium ion (I_CaL) current, thereby depressing calcium ion influx during phase 2 repolarization.^16,17,18 The ECG features of functional atrial flutter are F waves with variable morphology that are usually positive in the inferior leads (II, III, and aVF), with very rapid atrial rates (> 500 beats/min) and variable F-F intervals.² Functional reentry atrial flutter is an unstable rhythm, which may devolve into atrial fibrillation or return to typical atrial flutter or sinus rhythm.¹²

For the dog of the present report, functional atrial flutter was suspected because of its rapid atrial rate of approximately 600 beats/min, variable F-wave morphology with differing F-F intervals, and positive F waves in leads II, III, and aVF. The rhythm was also unstable; the dog converted to sinus rhythm prior to returning to atrial flutter, consistent with the described instability of functional atrial flutter. We hypothesized that underlying neurologic disease, evidenced by intermittent periods of circling and nystagmus, resulted in elevated parasympathetic tone and intermittent functional atrial flutter.

Treatment of atrial flutter is directed at conversion to sinus rhythm or controlling the ventricular response rate. The most common treatment of atrial flutter in veterinary medicine is slowing the ventricular response rate by administration of β-adrenergic receptor blockers, calcium channel blockers, or digoxin.¹⁹ Pharmacological cardioversion induced with antiarrhythmic drugs (class Ia, Ic, III, or IV) can be considered.^6,7,20,21 Electrical cardioversion may also be used to simultaneously depolarize all vulnerable cardiac myocytes and disrupt the reentry circuit.²² In human medicine, the gold-standard treatment of typical atrial flutter is radiofrequency catheter ablation, which has success rates of 90% to 100%.^8,10,23,24 In veterinary medicine, 2 dogs with typical atrial flutter were treated successfully with radiofrequency catheter ablation, resulting in confirmed resolution of this arrhythmia in both dogs.²⁵ Radiofrequency catheter ablation has also been used in the treatment of atypical atrial flutter in a small number of dogs; in 1 case series, 3 of 5 dogs had successful resolution of the arrhythmia, whereas 1 dog had recurrence of atypical atrial flutter and 1 dog developed atrial fibrillation.²⁶ Although that was a small study, the results parallel the reported lower success rates of radiofrequency catheter ablation of atypical atrial flutters in humans.²⁷