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Justin D. Thomason Department of Veterinary Clinical Sciences, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK 74078.

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Tiffany L. Fallaw Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA 30602.

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Clay A. Calvert Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA 30602.

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A 10-year-old 12.7-kg (27.9-lb) neutered male Miniature Schnauzer was referred to the University of Georgia Veterinary Teaching Hospital for evaluation of episodic weakness and syncope of 9 months' duration. The dog had no other pertinent medical history. The referring veterinarian made a diagnosis of sick sinus syndrome on the basis of a static ECG assessment. The ECG trace revealed sinoatrial arrest, junctional escape beats, and atrial premature contractions. The heart rate range was 35 to 145 beats/min. The veterinarian performed an atropine response test by administering atropine (0.044 mg/kg [0.02 mg/lb], IV, once). The heart rate and rhythm improved within 5 minutes, and the effects persisted for at least 30 minutes. Treatment with hyoscyamine sulfate elixira (0.005 mg/kg [0.0023 mg/lb], PO, q 8 h) was initiated. Subsequently, the episodes of weakness and syncope became less frequent and less protracted. However, after approximately 8 months, the clinical signs progressed to daily episodes of weakness and syncope; the duration of these episodes varied from a few to 45 seconds. The dog was referred to the University of Georgia for evaluation and possible pacemaker implantation.

At the hospital, physical examination revealed signs of depressed mentation and slow, irregular heart rate and rhythm. Sinus bradycardia, sinoatrial arrest, and first- and second-degree heart block were present, consistent with sick sinus syndrome. The heart rate range was 45 to 55 beats/min.

A CBC, serum biochemical analyses, and urinalysis revealed no abnormalities. Echocardiography revealed evidence of mild bilateral myxomatous degeneration of the atrioventricular (AV) valves. Measurements of both atria and ventricles were at the upper limits of the reference ranges. Findings of color-flow Doppler imaging confirmed mild mitral valve and tricuspid valve regurgitation.

One day following admission, the dog was anesthetized, and with fluoroscopic guidance, a ventricular-paced, ventricular-sensed, ventricular-inhibited, rateresponsive (VVIR) bipolar pacemakerb was implanted transvenously via the right jugular vein. Active fixation of the lead in the right ventricular apex was uncomplicated, and intraoperative evaluation with a program system analyzer confirmed a low capture threshold, an adequate voltage (strength)-duration safety margin, proper lead impedance, and good sensing. A refractory period of 240 milliseconds was programmed. The rate-responsive feature was turned on, and the rate range was set at 60 to 180 beats/min. The morning following implantation, follow-up static ECG was performed (Figure 1).

Figure 1—
Figure 1—

Six-lead ECG recordings obtained the day following pacemaker implantation in a 10-year-old Miniature Schnauzer with sick sinus syndrome. Notice the low-voltage pacing stimulation artifacts immediately preceding each P wave (arrow). The P-wave duration is excessive, and the PR interval is prolonged. The P-wave polarities are negative in leads III and aVF, positive in leads I and aVL, and mostly isoelectric in leads II and aVR. These polarities are consistent with atrial depolarization originating in the tricuspid valve orifice and progressing cranially and to the left. Each P wave is followed by a qR wave of normal appearance in leads I, II, and aVF indicating supraventricular origin. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 233, 9; 10.2460/javma.233.9.1406

ECG Interpretation

The morning after pacemaker implantation, the dog appeared normal. Examination of the ECG trace obtained at that time revealed that the dog's heart rate was regular at 90 beats/min (Figure 1). However, the ECG trace contained small pacing spikes (consistent with bipolar pacing), which were immediately followed by wide P waves that were positive in leads 1 and aVL, negative in leads 3 and aVF, and nearly isoelectric in leads 2 and aVR. At 180 milliseconds following each pacing spike, supraventricular qR waves were recorded via leads 1, 2, and aVF. The P-wave mean electrical axis in the frontal plane was directed cranial and to the left, which was consistent with an origin near the tricuspid valve. The ECG interpretation was that the lead had dislodged and was pacing from the right atrium with 1:1 AV nodal conduction. Echocardiography was performed and confirmed that the tip of the electrode was in the tricuspid valve orifice, adjacent to the septal leaflet. Thoracic radiographic findings were consistent with this conclusion.

The dog was again anesthetized and with fluoroscopic guidance, the lead was reimplanted in the apex of the right ventricle. The following day, an ECG was performed (Figure 2). Pacing appeared to be generally appropriate, and pacemaker-driven ventricular depolarizations were properly sensed. At times, however, during pacing at 360-millisecond intervals, the R-R intervals became suddenly prolonged (to 540 milliseconds) for several successive beats before returning to durations of 360 milliseconds. During the beats accompanied by prolonged R-R intervals, the interval from the peak of the T waves to the subsequent pacing spikes was 360 milliseconds. T waves were being sensed whereupon the next pacing cycle (360 milliseconds) was then initiated. At other times, pacing occurred continuously at 540-millisecond intervals (ie, at 360 milliseconds following the peak of each T wave) except when interrupted by sinus node–driven ventricular depolarizations (Figure 3). The paced beat following each of those sinus beats occurred at 360 milliseconds. The problem was diagnosed as oversensing of T waves. By use of the program system analyzer, sensing was reduced and the problem was resolved.

Figure 2—
Figure 2—

Lead III ECG trace obtained from the dog in Figure 1 the day following reimplantation of the dislodged pacemaker lead in the apex of the right ventricle. Notice that the R-R interval suddenly becomes prolonged from 360 milliseconds (normal pacing) to 540 milliseconds for 4 beats and then returns to 360 milliseconds. The stimulation artifacts are evident at intervals of 360 milliseconds after the peaks of the T waves. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 233, 9; 10.2460/javma.233.9.1406

Figure 3—
Figure 3—

Lead II ECG trace obtained from the dog in Figure 1 the day following reimplantation of the dislodged pacemaker lead in the apex of the right ventricle. Pacing is occurring continuously at 540-millisecond intervals at this time, most likely the result of T wave oversensing, and is interrupted by a sinus beat with a coupling interval of 500 milliseconds (320 milliseconds after the peak of the T wave). Following the sinus beat, the next paced beat occurs at 360 milliseconds because the lower voltage of the sinus-beat T wave was not sensed. Oversensing then continues with pacing at 540-millisecond intervals (360-millisecond intervals between oversensed T wave peaks and subsequent paced beats). Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 233, 9; 10.2460/javma.233.9.1406

Discussion

Sick sinus syndrome is a common abnormality of middle-aged to old Miniature Schnauzers.1 The clinical signs typically include episodic weakness and syncope of variable frequency and severity. Sick sinus syndrome most likely has a genetic basis because most affected dogs are Miniature Schnauzers and American Cocker Spaniels. Sinoatrial arrest, an abnormality of impulse formation, is a consistent finding on long-term ambulatory ECG (Holter) recordings of affected dogs and is often detected on static ECG recordings following recent episodes of syncope. Syncope and episodic weakness become apparent during protracted sinoatrial arrest when the AV nodal escape rhythm fails to develop in time to prevent hypoxia. In this syndrome, sinoatrial arrest, sinus bradycardia, and first- and second-degree AV block are typically interrupted by supraventricular premature contractions and tachycardia, junctional escape beats and rhythm, and ventricular escape beats. Often, some of the manifestations of this syndrome are not detected via static ECG assessments.

Sick sinus syndrome is considered a benign or at least nonlethal condition that may or may not require treatment. Dogs with clinical signs are most effectively treated with pacemaker implantation, but this is not always feasible. Some dogs respond well to IV administration of atropine, but others respond poorly, briefly, or not at all. Dogs that respond appropriately to atropine can be treated orally with anticholinergic drugs such as hyoscyamine sulfate. The hyoscyamine sulfate elixir (0.125 mg of hyoscyamine sulfate/5 mL) is easily dispensed in amounts appropriate for administration to small-breed dogs (dosages ranging from 0.003 to 0.005 mg/kg [0.0014 to 0.0023 mg/lb], PO, q 8 h). Dosage adjustments required to meet a patient's needs can be readily achieved. Adverse effects of anticholinergic drugs include dryness of the mouth; mydriasis; lethargy; anorexia, gastric distention, and ileus (and other gastrointestinal tract problems); and urine retention. With proper dosing and monitoring, adverse effects are usually minimal. Theophylline is occasionally of benefit but, in general, is less effective than anticholinergic treatment. The combination of an anticholinergic agent and theophylline can be administered to dogs that respond inadequately to the former as monotherapy. Nonetheless, pacemaker implantation is the treatment of choice, especially when medical treatment fails.

Pacemaker implantation is a practical, cost-efficient, and highly effective treatment for many dogs with severe abnormalities of impulse formation or conduction.2 The most common indication for pacemaker implantation is high-grade (advanced) AV block, usually complete heart block. The second-most common indication in dogs is sick sinus syndrome. Most pacemakers implanted in affected dogs are demand, singlechamber, ventricular-pacing, ventricular-sensing, and inhibited pacemakers.2,3 Inhibition refers to the sensing function of the electrode wherein normal beats, ventricular escape beats, and ventricular premature contractions are sensed and pacing is inhibited for a userselected refractory period; thus, the pacemaker will not stimulate the ventricle during its vulnerable period (ie, during the relative refractory period). Such stimulation could induce ventricular tachycardia or ventricular fibrillation. These pacemakers may have a rate-responsive feature that is turned on or off as determined by the clinician on the basis of the patient's lifestyle and exercise requirement (ie, user selected). When turned on, a motion sensor bonded to the inside of the pulse generator detects motion (a nonphysiologic function) or lack thereof and the heart rate can then respond within a user-selected maximum range of 60 to 180 beats/min. The sensitivity of the motion sensor, response delay, and rates of heart rate increase and decrease are determined by the clinician.

Two potential complications of pacemaker implantation2,3 occurred in the dog of this report. The first was lead dislodgement. Interestingly, rather than losing capture of the rhythm, which is the typical result of lead dislodgment, the electrode lodged in the tricuspid valve orifice and continued to pace from the right atrium. Because AV block was absent, the dog did not develop clinical signs. The second problem, which also did not result in clinical signs, was oversensing of T waves. If the sensing function is programmed to be highly sensitive (ie, set to sense low-voltage endocardial potentials) and if the endocardial T-wave voltages are relatively high, then these sensed T waves will inhibit pacing and reset the pacing cycle. Oversensing of T waves was not a major problem in the dog of this report but was corrected after the program system analyzer was used to reduce the sensitivity. Care was taken not to reduce the sensitivity to the point that ventricular depolarizations would not be sensed.

a.

Levsin, Schwarz Pharma Inc, Milwaukee, Wis.

b.

Medtronic Inc, Minneapolis, Minn.

References

  • 1.

    Moise NS. Diagnosis and management of canine arrhythmias. In: Fox PW, Sisson D, Moise NS, eds. Textbook of canine and feline cardiology. 2nd ed. Philadelphia: WB Saunders Co, 1999;331385.

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    • Export Citation
  • 2.

    Moise NS. Pacemaker therapy. In: Fox PW, Sisson D, Moise NS, eds. Textbook of canine and feline cardiology. 2nd ed. Philadelphia: WB Saunders Co, 1999;400425.

    • Search Google Scholar
    • Export Citation
  • 3.

    Oyama MA, Sisson DD, Lehmkuhl LB. Practices and outcome of artificial cardiac pacing in 154 dogs. J Vet Intern Med 2001;15:229239.

  • Figure 1—

    Six-lead ECG recordings obtained the day following pacemaker implantation in a 10-year-old Miniature Schnauzer with sick sinus syndrome. Notice the low-voltage pacing stimulation artifacts immediately preceding each P wave (arrow). The P-wave duration is excessive, and the PR interval is prolonged. The P-wave polarities are negative in leads III and aVF, positive in leads I and aVL, and mostly isoelectric in leads II and aVR. These polarities are consistent with atrial depolarization originating in the tricuspid valve orifice and progressing cranially and to the left. Each P wave is followed by a qR wave of normal appearance in leads I, II, and aVF indicating supraventricular origin. Paper speed = 50 mm/s; 1 cm = 1 mV.

  • Figure 2—

    Lead III ECG trace obtained from the dog in Figure 1 the day following reimplantation of the dislodged pacemaker lead in the apex of the right ventricle. Notice that the R-R interval suddenly becomes prolonged from 360 milliseconds (normal pacing) to 540 milliseconds for 4 beats and then returns to 360 milliseconds. The stimulation artifacts are evident at intervals of 360 milliseconds after the peaks of the T waves. Paper speed = 50 mm/s; 1 cm = 1 mV.

  • Figure 3—

    Lead II ECG trace obtained from the dog in Figure 1 the day following reimplantation of the dislodged pacemaker lead in the apex of the right ventricle. Pacing is occurring continuously at 540-millisecond intervals at this time, most likely the result of T wave oversensing, and is interrupted by a sinus beat with a coupling interval of 500 milliseconds (320 milliseconds after the peak of the T wave). Following the sinus beat, the next paced beat occurs at 360 milliseconds because the lower voltage of the sinus-beat T wave was not sensed. Oversensing then continues with pacing at 540-millisecond intervals (360-millisecond intervals between oversensed T wave peaks and subsequent paced beats). Paper speed = 50 mm/s; 1 cm = 1 mV.

  • 1.

    Moise NS. Diagnosis and management of canine arrhythmias. In: Fox PW, Sisson D, Moise NS, eds. Textbook of canine and feline cardiology. 2nd ed. Philadelphia: WB Saunders Co, 1999;331385.

    • Search Google Scholar
    • Export Citation
  • 2.

    Moise NS. Pacemaker therapy. In: Fox PW, Sisson D, Moise NS, eds. Textbook of canine and feline cardiology. 2nd ed. Philadelphia: WB Saunders Co, 1999;400425.

    • Search Google Scholar
    • Export Citation
  • 3.

    Oyama MA, Sisson DD, Lehmkuhl LB. Practices and outcome of artificial cardiac pacing in 154 dogs. J Vet Intern Med 2001;15:229239.

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