ECG of the Month

Romain Pariaut Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Eva M. Oxford Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Roberto A. Santilli Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.
Clinica Veterinaria Malpensa, Viale Marconi 27, Samarate, Varese, 21017, Italy.

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A 3-year-old 5-kg (11-lb) neutered male Chihuahua was referred to a veterinary teaching hospital because of 1 episode of syncope and persistent bradycardia. Previous medical history was incomplete because the dog had recently been rescued from a shelter; however, lethargy had been noted since adoption. Following the syncopal event, a diagnosis of left-sided congestive heart failure and bradycardia was made by a veterinarian on the basis of clinical signs and physical and radiographic examination findings. Treatment with furosemide (12.5 mg, PO, q 12 h), enalapril maleate (1.25 mg, PO, q 12 h), theophylline (25 mg, PO, q 12 h), pimobendan (1.25 mg, PO, q 12 h), and spironolactone (6.25 mg, PO, q 12 h) was initiated. By the time the dog was presented to the Cornell University Hospital for Animals for further evaluation of the persistent bradycardia 4 weeks later, its clinical status had improved. On physical examination, no abnormal heart sounds or murmurs were present and femoral pulses were strong and slow. Results of clinicopathologic testing, including serum electrolyte concentrations, were unremarkable. Echocardiography revealed biatrial enlargement, mild increases in left ventricular and right ventricular end-diastolic dimensions, normal left ventricular systolic function, and mild-to-moderate mitral and tricuspid valve regurgitations. These echocardiographic findings suggested volume overload secondary to chronic bradycardia or primary cardiomyopathy. Interestingly, A waves were absent from the transmitral pulsed-wave Doppler signal, which suggested the absence of left atrial contraction (Figure 1). A 6-lead ECG recording was obtained.

Figure 1—
Figure 1—

Pulsed-wave Doppler tracing of the mitral valve inflow in a 3-year-old Chihuahua that was referred for evaluation because of 1 episode of syncope and bradycardia. The tracing was obtained after 4 weeks of medical treatment, at which time the dog had persistent bradycardia. For this tracing, the sample volume was placed at the tip of the mitral valve leaflets on a left apical 4-chamber view. A single early diastolic wave is recorded, suggesting the absence of atrial contraction.

Citation: Journal of the American Veterinary Medical Association 252, 11; 10.2460/javma.252.11.1350

ECG Interpretation

Electrocardiography revealed a slow and regular rhythm with a rate of 52 beats/min (Figure 2). P waves were absent from the tracing, even after the low-pass filter was adjusted from 40 to 100 Hz. The duration of the QRS complexes was prolonged (approx 80 milliseconds; reference range, < 70 milliseconds), and complex morphology was characterized by a broad S wave in leads I, II, and aVF. The mean electrical axis of ventricular activation was −125° (reference range, +40° to +100°) in the frontal plane, which was consistent with a right bundle branch block pattern. The rate and morphology of the QRS complexes were most consistent with a ventricular escape rhythm. Possible ECG diagnoses included third-degree atrioventricular block with failure to detect small or hidden P waves, atrial fibrillation with third-degree atrioventricular block, atrial standstill, sinus standstill or persistent third-degree sinoatrial block with a ventricular escape rhythm, and sinoventricular rhythm.

Figure 2—
Figure 2—

Six-limb lead ECG recording for the dog in Figure 1. The rhythm is regular, and the heart rate is 52 beats/min. The QRS complex duration is prolonged (approx 80 milliseconds; reference range, < 70 milliseconds), and there is a deep S wave in leads I, II, and aVF. P waves are not visible on the tracing. Paper speed = 50 mm/s; 1 cm = 2 mV.

Citation: Journal of the American Veterinary Medical Association 252, 11; 10.2460/javma.252.11.1350

At that point, pacemaker implantation was indicated for the patient. An electrophysiologic assessment was performed just before pacemaker placement to further characterize the atrial rhythm. The dog was anesthetized, and a quadripolar electrophysiologic cathetera was introduced in the right jugular vein so that its tip was positioned within the right atrium for recording and pacing purposes. The catheter was connected to a dedicated electrophysiology recording systemb to display the signals corresponding to the propagation of electrical impulses within the atria (atrial electrogram) and ventricles (ventricular electrogram). There was, however, no evidence of spontaneous atrial deflection in this dog, confirming that the right atrium was electrically silent. Pacing of the atrium at a rate of 50 beats/min initially failed to capture the right atrial myocardium. However, P waves immediately followed by atrial repolarization (Ta) waves appeared on the ECG tracings when the output of the pacing stimulus was increased to 7 mA (Figure 3). Even during atrial pacing, there was no evidence of atrioventricular conduction, confirming the presence of third-degree atrioventricular block. Worsening of the bradycardia during anesthesia prevented extensive electrophysiologic mapping of all cardiac chambers, and a permanent pacemaker was implanted with a single endocardial lead secured in the right ventricular apex.

Figure 3—
Figure 3—

Results of right intra-atrial mapping for the dog in Figure 1. A—Fluoroscopic lateral view of the heart with a quadripolar electrophysiologic catheter positioned within the right atrium. The dog's head is to the left side of the image. B—During pacing from the 2 distal electrodes (high right atrium distal [HRAd]) of the catheter with a pacing output of 7 mA, atrial electrograms were recorded by the 2 proximal electrodes (high right atrium proximal [HRAp]), and P waves are visible on lead I (upper tracing) of the surface ECG (arrowheads). Each P wave is followed by a Ta wave with low amplitude and opposite polarity that represents atrial repolarization. On the HRAp tracing, the QRS complexes on the surface ECG are recorded as ventricular electrograms (V); atrial electrograms are also recorded (A).

Citation: Journal of the American Veterinary Medical Association 252, 11; 10.2460/javma.252.11.1350

Sinoventricular rhythm was considered unlikely because serum potassium concentration was within reference range and subsequently ruled out by the presence of third-degree atrioventricular block and the ability to pace the atrium. Given the results of the electrophysiologic study, which failed to detect any spontaneous atrial electrical activity, a failure to detect P waves on the surface ECG or a diagnosis of atrial fibrillation with atrioventricular block could also be excluded. Although the rhythm had many features of persistent atrial standstill, it did not fulfill 1 major diagnostic criterion for atrial standstill, namely the absence of response to pacing in the regions of the atrium that are electrically silent. Therefore, the most likely diagnosis was persistent third-degree sinoatrial block or sinus standstill with third-degree atrioventricular block.

Nine months after initial diagnosis, the dog remained stable with appropriate ventricular pacing and no apparent atrial electrical activity detectable by ECG. Left and right atrial dimensions were slightly increased, compared with previous findings, and left ventricular function remained stable. Administration of medications (furosemide, enalapril, spironolactone, and pimobendan) to manage signs of congestive heart failure was continued with no adjustments in dosages.

Discussion

In the presence of sustained bradycardia and an absence of discernable P waves on an ECG recording, it is important to first confirm the absence of atrial depolarization. Low-amplitude P waves can indeed overlap with the QRST complexes. In addition, ECG filter settings should be adjusted to a high cutoff value (usually > 150 Hz) to limit the risk of removing the frequency component of the signal that forms the P wave.1 Atrial fibrillation should also be ruled out whenever ECG evidence of atrial electrical activity is lacking. Fibrillation waves are not always visible on an ECG tracing, and it is particularly challenging to confirm atrial fibrillation when concomitant third-degree atrioventricular block is present because the characteristic irregular ventricular response to supraventricular impulses during atrial fibrillation cannot be used to make the diagnosis. As in the case described in the present report, intracardiac atrial recordings are the best method with which to confirm the absence of fibrillation waves. Another arrhythmia that is important to identify in dogs and cats is sinoventricular rhythm, which frequently accompanies severe hyperkalemia. During sinoventricular rhythm, ventricular electrical activation remains controlled by the sinus pacemaker, but the electrical impulses travel through preferential anatomic or functional internodal pathways between the nodes without propagating to the atrial myocardium, which explains the absence of P waves.2 An increase in ventricular rate with exercise or stress in patients with absent P waves would suggest sinoventricular conduction.3

Prior to the electrophysiologic assessment in the dog of the present report, atrial standstill was considered the most likely diagnosis on the basis of ECG and echocardiographic findings and the dog's age.4,5 Atrial standstill is an absence of atrial electrical and mechanical activity. It is complete or partial.6 Partial atrial standstill indicates that some regions of the atria, sometimes limited to 1 auricle, are still electrically active even when atrial activity is not visible on ECG recordings.7 However, spontaneous depolarization can be detected in these regions via intracardiac recordings, and those regions respond to pacing. Therefore, in addition to the absence of P waves on ECG recordings, a diagnosis of atrial standstill requires not only the absence of spontaneous electrical activity but also no response to high-output intracardiac pacing. In people, atrial pacing with an output as high as 25 mA is used to confirm absence of atrial capture.8 In the case described in the present report, 7-mA stimuli generated an atrial electrogram from a region of the right atrium that appeared electrically silent. It resulted in large-amplitude P waves during pacing, which indicated that a large portion of the atrial myocardium was depolarized by the impulse.

A more likely cause for the absence of P waves in the dog of the present report was a failure of impulse formation within the sinus node (sinus arrest) or impulse propagation from the sinus node to the surrounding atrial myocardium (sinoatrial block). These 2 dysrhythmias cannot be differentiated during an ECG or standard electrophysiologic assessment because that would necessitate recording the electrical activity within the sinus node itself. Typically, periods of sinus arrest and block are interspersed by sinus rhythm, which remains the dominant rhythm. Intermittent sinus arrest is a common feature of sick sinus syndrome. However, on occasion, sinus arrest can persist for extended periods, and sinus node quiescence of 30 days’ duration in people after myocardial infarction has been reported.9 Prolonged sinus arrest is also called sinus standstill. It is commonly associated with a junctional escape rhythm, although a ventricular escape rhythm is possible. In addition, retrograde ventriculo-atrial conduction characterized by P’ waves following QRS complexes is usually present.

Although intracardiac recording was used in addition to ECG for the dog of the present report, some uncertainties remained with regard to the exact pathophysiologic process responsible for the arrhythmia. Some elements suggested that the pathological process was not limited to the sinus node and its periphery. Indeed, cardiac chamber enlargement could not be exclusively attributed to chronic bradycardia because it did not resolve after pacemaker implantation. Moreover, the pacing output required to capture the atrial myocardium was high, compared with values reported for healthy research dogs (typically approx 0.25 mA with epicardial pacing).10 This pacing threshold likely indicated extensive cardiac tissue remodeling. The lesions of atrial standstill typically originate in the upper region of the atria and progressively expand toward the atrioventricular junction.11 In the case described in the present report, intracardiac mapping was limited to the right atrium; therefore, it was unknown whether the electrophysiologic characteristics of the left atrium were comparable.8 Finally, there was complete atrioventricular block indicating that more than 1 component of the conduction system was affected.12

In the dog of the present report, this brady-arrhythmia could have been an unusual manifestation of sick sinus syndrome, which has been shown to infrequently progress to atrial standstill but more commonly progress to atrioventricular block in up to 18% of human patients.13,14 Long-term administration of β-adrenoreceptor blockers, preexisting bundle branch block, and evidence of delayed atrioventricular conduction at the time of pacemaker implantation have been identified as predisposing factors for the development of atrioventricular block.13

Footnotes

a.

Response electrophysiology catheter, 5F, quadripolar, CRD tip, St. Jude Medical, Minnetonka, Minn.

b.

Workmate Claris Recording System, Abbott-St. Jude Medical, Saint Paul, Minn.

References

  • 1. García-Niebla J, Llontop-García P, Valle-Racero JI, et al. Technical mistakes during the acquisition of the electrocardiogram. Ann Noninvasive Electrocardiol 2009;14:389403.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2. Johns SM, Stern JA, Nelson OL. ECG of the month. Hyperkalemia. J Am Vet Med Assoc 2011;238:982984.

  • 3. Amram SS, Vagueiro MC, Pimenta A, et al. Persistent atrial standstill with atrial inexcitability. Pacing Clin Electrophysiol 1978;1:8089.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4. Schmitt KE, Lefbom BK. Long-term management of atrial myopathy in two dogs with single chamber permanent transvenous pacemakers. J Vet Cardiol 2016;18:187193.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5. Thomason JD, Kraus MS, Fallaw TL, et al. Survival of 4 dogs with persistent atrial standstill treated by pacemaker implantation. Can Vet J 2016;57:297298.

    • Search Google Scholar
    • Export Citation
  • 6. Wesselowski S, Abbott J, Borgarelli M, et al. Presumptive partial atrial standstill secondary to atrial cardiomyopathy in a Greyhound. J Vet Cardiol 2017;19:276282.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7. Demiralp E, Kirilmaz A, Cebeci BS, et al. Partial atrial standstill: a case report. J Electrocardiol 2005;38:252255.

  • 8. Talwar KK, Dev V, Chopra P, et al. Persistent atrial standstill—clinical, electrophysiological, and morphological study. Pacing Clin Electrophysiol 1991;14:12741280.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9. Rokseth R, Hatle L. Sinus arrest in acute myocardial infarction. Br Heart J 1971;33:639642.

  • 10. Friedman HS, Wattanasuwan N, Sharafkhaneh A, et al. The comparative effects of drive and test stimulus intensity on myocardial excitability and vulnerability. Pacing Clin Electrophysiol 2000;23:8495.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11. Arimoto T, Sukekawa H, Takayama S, et al. Electroanatomical mapping in partial atrial standstill for visualization of atrial viability and a suitable pacing site. Pacing Clin Electrophysiol 2008;31:509512.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12. Nakazato Y, Nakata Y, Hisaoka T. Clinical and electrophysiological characteristics of atrial standstill. Pacing Clin Electrophysiol 1995;18:12441254.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13. Hosoda J, Ishikawa T, Sumita S, et al. Development of atrioventricular block and diagnostic value of stored electrograms in patients with sick sinus syndrome and implanted pacemaker. Circ J 2015;79:12631268.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14. Sanders P, Kalman JM. Progressive and persistent atrial inexcitability. Pacing Clin Electrophysiol 2006;29:546548.

  • Figure 1—

    Pulsed-wave Doppler tracing of the mitral valve inflow in a 3-year-old Chihuahua that was referred for evaluation because of 1 episode of syncope and bradycardia. The tracing was obtained after 4 weeks of medical treatment, at which time the dog had persistent bradycardia. For this tracing, the sample volume was placed at the tip of the mitral valve leaflets on a left apical 4-chamber view. A single early diastolic wave is recorded, suggesting the absence of atrial contraction.

  • Figure 2—

    Six-limb lead ECG recording for the dog in Figure 1. The rhythm is regular, and the heart rate is 52 beats/min. The QRS complex duration is prolonged (approx 80 milliseconds; reference range, < 70 milliseconds), and there is a deep S wave in leads I, II, and aVF. P waves are not visible on the tracing. Paper speed = 50 mm/s; 1 cm = 2 mV.

  • Figure 3—

    Results of right intra-atrial mapping for the dog in Figure 1. A—Fluoroscopic lateral view of the heart with a quadripolar electrophysiologic catheter positioned within the right atrium. The dog's head is to the left side of the image. B—During pacing from the 2 distal electrodes (high right atrium distal [HRAd]) of the catheter with a pacing output of 7 mA, atrial electrograms were recorded by the 2 proximal electrodes (high right atrium proximal [HRAp]), and P waves are visible on lead I (upper tracing) of the surface ECG (arrowheads). Each P wave is followed by a Ta wave with low amplitude and opposite polarity that represents atrial repolarization. On the HRAp tracing, the QRS complexes on the surface ECG are recorded as ventricular electrograms (V); atrial electrograms are also recorded (A).

  • 1. García-Niebla J, Llontop-García P, Valle-Racero JI, et al. Technical mistakes during the acquisition of the electrocardiogram. Ann Noninvasive Electrocardiol 2009;14:389403.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2. Johns SM, Stern JA, Nelson OL. ECG of the month. Hyperkalemia. J Am Vet Med Assoc 2011;238:982984.

  • 3. Amram SS, Vagueiro MC, Pimenta A, et al. Persistent atrial standstill with atrial inexcitability. Pacing Clin Electrophysiol 1978;1:8089.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4. Schmitt KE, Lefbom BK. Long-term management of atrial myopathy in two dogs with single chamber permanent transvenous pacemakers. J Vet Cardiol 2016;18:187193.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5. Thomason JD, Kraus MS, Fallaw TL, et al. Survival of 4 dogs with persistent atrial standstill treated by pacemaker implantation. Can Vet J 2016;57:297298.

    • Search Google Scholar
    • Export Citation
  • 6. Wesselowski S, Abbott J, Borgarelli M, et al. Presumptive partial atrial standstill secondary to atrial cardiomyopathy in a Greyhound. J Vet Cardiol 2017;19:276282.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7. Demiralp E, Kirilmaz A, Cebeci BS, et al. Partial atrial standstill: a case report. J Electrocardiol 2005;38:252255.

  • 8. Talwar KK, Dev V, Chopra P, et al. Persistent atrial standstill—clinical, electrophysiological, and morphological study. Pacing Clin Electrophysiol 1991;14:12741280.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9. Rokseth R, Hatle L. Sinus arrest in acute myocardial infarction. Br Heart J 1971;33:639642.

  • 10. Friedman HS, Wattanasuwan N, Sharafkhaneh A, et al. The comparative effects of drive and test stimulus intensity on myocardial excitability and vulnerability. Pacing Clin Electrophysiol 2000;23:8495.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11. Arimoto T, Sukekawa H, Takayama S, et al. Electroanatomical mapping in partial atrial standstill for visualization of atrial viability and a suitable pacing site. Pacing Clin Electrophysiol 2008;31:509512.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12. Nakazato Y, Nakata Y, Hisaoka T. Clinical and electrophysiological characteristics of atrial standstill. Pacing Clin Electrophysiol 1995;18:12441254.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13. Hosoda J, Ishikawa T, Sumita S, et al. Development of atrioventricular block and diagnostic value of stored electrograms in patients with sick sinus syndrome and implanted pacemaker. Circ J 2015;79:12631268.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14. Sanders P, Kalman JM. Progressive and persistent atrial inexcitability. Pacing Clin Electrophysiol 2006;29:546548.

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