ECG of the Month

Julia R. Treseder Department of Clinical Sciences, College of Veterinary Medicine, Auburn University, Auburn, AL 36849.

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SeungWoo Jung Department of Clinical Sciences, College of Veterinary Medicine, Auburn University, Auburn, AL 36849.

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An 11-year-old 4.4-kg (9.7-lb) spayed female Miniature Schnauzer was evaluated at the Wilford and Kate Bailey Small Animal Teaching Hospital at Auburn University for pacemaker implantation. A diagnosis of sick sinus syndrome had been made for the dog 7 months prior to the evaluation by a board-certified cardiologist. The dog had been managed medically with theophylline at a dosage of 11.9 mg/kg (5.4 mg/lb), PO, every 12 hours. The dog was having syncopal episodes associated with exercise, heat, or excitement. These syncopal episodes initially improved with theophylline treatment. However, 5 months after diagnosis, the dog's syncopal episodes increased in frequency, and administration of hyoscyamine (3.9 μg/kg [1.8 μg/lb]), PO, q 8 h) was initiated. In the week prior to the evaluation, the dog's syncopal episodes increased dramatically in frequency up to multiple times each day. The theophylline dosage was increased to 35.7 mg/kg (16.2 mg/lb), PO, every 12 hours, but no improvement was noted. The dog had no other pertinent medical history.

At the evaluation, the dog was bright, alert, and mentally appropriate. Cardiac auscultation revealed a left apical systolic murmur (grade 4/6) with bradyarrhythmias. Bilaterally, femoral arterial pulses were considered normal. A CBC, serum biochemical analysis, and assessment of serum concentrations of thyroid hormones were performed as part of the preanesthetic assessment. Results of these tests indicated that the dog had mild anemia (RBC count, 5.19 × 106 cells/μL [reference interval, 6.02 × 106 cells/μL to 8.64 × 106 cells/μL]; Hct, 37.7% [reference interval, 38.7% to 59.2%]; mean corpuscular hemoglobin, 29.3 pg [reference interval, 20.4 to 25.7 pg]) and high serum alkaline phosphatase activity (169 U/L; reference interval, 14 to 152 U/L). Serum concentrations of thyroxine, free thyroxine, and thyroid-stimulating hormone were within reference intervals. To assess the dog's candidacy for pacemaker implantation, echocardiography was performed. Echocardiography revealed mild tricuspid and mitral valve regurgitation with mild left atrial enlargement, consistent with early myxomatous mitral and tricuspid valve degeneration. Electrocardiography was also performed (Figure 1). The dog had multiple syncopal episodes while hospitalized prior to pacemaker placement.

ECG Interpretation

The ECG examination at the time of evaluation for pacemaker implantation revealed irregular rhythms and a heart rate that varied from 30 to 200 beats/min (bradycardia-tachycardia syndrome). Frequent episodes of sustained supraventricular tachycardia (SVT) with negative P waves in lead II terminated by sinus arrest (overdrive suppression) for a period of 1.5 seconds were noted. The period of sinus arrest was followed by normal sinus beats (narrow QRS complexes preceded by positive P waves in lead II) and then by resumption of SVT at a rate of 200 beats/min (Figure 1).

Figure 1—
Figure 1—

Baseline lead II ECG tracing obtained from a dog with sick sinus syndrome in which bradycardia-tachycardia syndrome was subsequently detected. A supraventricular tachycardia (SVT) is characterized by negative P waves (arrowheads) and a heart rate of 200 beats/min, followed by a period of sinus arrest of approximately 1.5 seconds' duration (overdrive suppression). Two normal sinus beats (arrows) occur after sinus arrest, followed by an atrial premature complex (asterisk) and resumption of SVT, indicating that the ectopic atrial focus in this dog resumed dominant pacemaker activity. Paper speed = 50 mm/s; 5 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 248, 7; 10.2460/javma.248.7.762

Another ECG examination was performed 5 minutes after IV administration of atropine (0.04 mg/kg [0.018 mg/lb]). Sustained SVT with a rate of 200 beats/min and no periods of sinus arrest or rhythm of sinus origin were evident over an interval of several minutes (Figure 2). A full response to the atropine response test is considered to be a sustained heart rate > 140 beats/min.1 Although the dog's heart rate after atropine administration was 200 beats/min, the rhythm was not sinus in origin. Because atropine failed to restore normal sinus nodal rhythm and function, this was considered a lack of response.

Figure 2—
Figure 2—

Lead II ECG tracing obtained from the dog in Figure 1 five minutes after IV administration of atropine (0.04 mg/kg [0.018 mg/lb]). Sustained SVT with a heart rate of 200 beats/min is evident; ectopic p waves (arrowheads) are present. Although no periods of sinus arrest occur, there is a failure of restoration of a normal sinus rhythm and function. This is consistent with sinus nodal disease. Paper speed = 50 mm/s; 5 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 248, 7; 10.2460/javma.248.7.762

On the day following admission, the dog was anesthetized and a ventricular-paced, ventricular-sensed, inhibitory, and rate-responsive bipolar pacemaker was implanted into the right ventricle via the right jugular vein under fluoroscopic guidance. Intraoperative evaluation with a pacing system analyzer confirmed adequate sensing, low capture threshold, and appropriate lead impedance. The rate response function was programmed at 80 to 180 beats/min, and the refractory period was set at 250 milliseconds.

An ECG examination and pacemaker interrogation were performed 24 hours after pacemaker implantation. The ECG examination revealed normal pacemaker function with pacing spikes, followed by wide QRS complexes that were positive in leads I, II, III, and aVF and negative in lead aVR, consistent with paced beats originating from the right ventricle (Figure 3). A histogram of heart rate data collected during a 24-hour period indicated that 74% of total beats were sensed (indicating spontaneous rhythm of the patient) and 26% were paced. Of all sensed spontaneous beats, 43% were at a rate of 180 to 260 beats/min (paroxysmal SVT related to bradycardia-tachycardia syndrome).

Figure 3—
Figure 3—

Lead II ECG tracing obtained from the dog in Figure 1 after pacemaker implantation. The pacemaker is set in ventricular-paced, ventricular-sensed, inhibitory, and rate-responsive mode with a base rate of 80 beats/min. A run of supraventricular tachycardia is followed by a period of sinus arrest with right ventricular-origin paced beats (stars). A normal sinus complex is present after the second paced beat. Paper speed = 50 mm/s; 5 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 248, 7; 10.2460/javma.248.7.762

Follow-up pacemaker interrogation performed 9 weeks after pacemaker placement revealed apparently normal pacemaker function and a marked improvement in the frequency of ectopic supraventricular arrhythmias; < 3% of sensed spontaneous beats recorded occurred at a rate of 180 to 220 beats/min.

Discussion

The sinus node acts as the primary cardiac pacemaker and represents a sickle-shaped area of grossly and histologically distinct tissue located at the junction of the cranial vena cava with the right atrium and extending along the crista terminalis toward the caudal vena cava.2 Sick sinus syndrome is a common cause of clinically apparent bradyarrhythmia and can be a result of intrinsic sinus node dysfunction or extrinsic causes. Intrinsic sinus node dysfunction occurs in aging humans and certain dog breeds (notably, Miniature Schnauzer and West Highland White Terrier but also reported for Dachshund, Cocker Spaniel, Pug, Boxer, and Bull Terrier).3–5 Paroxysmal supraventricular tachyarrhythmias often occur in conjunction with bradyarrhythmias, the so-called bradycardia-tachycardia syndrome, which was first identified in humans and dogs with sinus node dysfunction decades ago.6–8 Although the etiopathogenesis of sick sinus syndrome is unclear, possible causes include mutations in cardiac ion channels or structural proteins, calcium channel dysfunction, and fibrosis of the sinoatrial node.5 In particular, dogs with bradycardia-tachycardia syndrome and chronic degenerative valvular disease develop fibrous tissue that interrupts the contiguity of the sinus node and atrial myocardium.9 Sclerotic changes in the intramural coronary arteries supplying the sinus node have been detected in dogs with sick sinus syndrome, which may also contribute to pathological changes in the sinus node.9 Clinical signs of sick sinus syndrome in dogs include episodic weakness, syncope, and exercise intolerance secondary to profound bradycardia, periods of sinus arrest, and sometimes paroxysmal SVT.

In humans, electrophysiological studies are performed to characterize sinus nodal recovery time (the time required for the sinus node to resume activity after cessation of atrial pacing) and sinoatrial conduction time, which can provide evidence of sinus node dysfunction.10 Electrophysiological and electroanatomic mapping studies have also revealed that humans with sinus node dysfunction have widespread atrial conduction abnormalities and increased right atrial refractoriness.11 In dogs, sick sinus syndrome is frequently associated with more generalized conduction disturbances, including atrial tachyarrhythmias and atrioventricular block.4,5,12 Atrial pacing has been shown to induce sinus node dysfunction because of exit block; this may suggest that sinoatrial exit block, as opposed to pacemaker cell dysfunction, has a major role in bradycardia-tachycardia syndrome.13 Electrophysiological testing of dogs is not a routine procedure; therefore, there are limited data regarding the extent to which sinus node impulse formation and sinoatrial conduction abnormalities contribute to naturally occurring sinus nodal disease.

In the dog of this report, an initial positive response to oral administration of theophylline was followed by worsening clinical signs despite an increase in theophylline dosage and the addition of oral treatment with an anticholinergic agent. This might be attributable to a decline in sinus node function and increasing refractoriness to sympathetic stimulation, with an ectopic atrial focus assuming primary pacemaker function. Although a focal atrial tachycardia is considered most likely, other SVTs (including those involving the atrioventricular junction) cannot be excluded on the basis of the surface ECG. Frequent periods of sinus arrest may have occurred secondary to overdrive suppression temporarily preventing spontaneous depolarization.14 If attributable to overdrive suppression, the bradycardia may have responded to management of the SVT alone (eg, with administration of a β-adrenoreceptor blocker or digoxin); however, given the risk of worsening bradyarrhythmias,5 pharmacological treatment of the tachycardia was withheld until after pacemaker implantation, at which time the tachycardia was largely resolved. Sustained SVT was noted after atropine administration, suggesting ectopic atrial activity was substantially influenced by autonomic tone. Dogs affected with sinus nodal disease can have variable responses to anticholinergics administered both parenterally and orally.15

Autonomic tone has an important role not only in the normal modulation of heart rate and rhythm via the sinus node, but also in the context of sinus node dysfunction. Ablation of the cranial sinus node pacemakers results in a pacemaker location more caudally along the crista terminalis. This reduces the response to adrenergic receptor stimulation.16 In dogs after excision of the sinus node or after experimental embolization of the sinus nodal artery, ectopic atrial rhythms develop within hours to days.17,18 In both situations, administration of parasympatholytics or exercise had an impact on heart rate and rhythm.

Rapid atrial pacing in dogs results in structural and electrophysiological remodeling of the atria.19,20 Atrial remodeling is also evident in humans with sinus node dysfunction, even in the absence of atrial arrhythmias.11 Restoration of a normal mean heart rate with artificial pacing in the dog of this report may have resulted in partial resolution of atrial conduction disturbances and normalization of mean heart rate.

Although sick sinus syndrome is characterized by a negative response to atropine, the elimination of sinus arrests by atropine is not considered diagnostic of a benign arrhythmia.14 If a relationship is established between clinical signs and ECG abnormalities, pacemaker implantation is indicated. The complete resolution of clinical signs after pacemaker implantation in the dog of this report supported the conclusion that the syncopal episodes were not solely vagally induced and that artificial pacing improved atrial electrophysiological remodeling associated with bradycardia-tachycardia syndrome.

References

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