Introduction
A 10-year-old 39.3-kg sexually intact male Labrador Retriever was referred to a veterinary medical teaching hospital for investigation of pericardial ef-fusion and ascites. Seven days prior to referral, the dog was presented to a primary care practice because of reduced exercise capacity, abdominal distension, weight loss, and a dry cough. During that clinical examination, the dog had a heart rate of 120 beats/min; pulses were synchronous with the heartbeat and had a regular rhythm. Other diagnostic findings at that time were eosinophilic peritoneal effusion and mild regenerative anemia. On reexamination 24 hours prior to referral, low-volume pericardial effusion was identified.
At the referral evaluation, the dog was bright and responsive with a heart rate of 170 beats/min and an irregular rhythm. There was variable femoral pulse quality, including pulse deficits. Hematologic assessments revealed resolution of the previously diagnosed mild anemia. Serum cardiac troponin I concentration was 0.267 ng/mL (reference interval, < 0.15 ng/mL), indicating recent or ongoing mild myocardial injury. Serum biochemical analysis findings and C-reactive protein concentration were unremarkable. Results of infectious disease screening (for infection with Borrelia burgdorferi, Anaplasma phagocytophilum, Anaplasma platys, Dirofilaria immitis, Ehrlichia canis, Ehrlichia ewingii, or Bartonella henselae) were negative. Doppler echocardiography revealed mild pericardial effusion with no cardiac tamponade. No structural cardiac disease or evidence of cardiac neoplasia was observed.
The dog underwent full-body CT, which revealed mild thoracic and abdominal lymphadenopathy; findings from cytologic examination of lymph node aspirate specimens were consistent with reactive lymph-adenopathy. Pericardiocentesis was performed under sedation (opioid administration was avoided), and 20 mL of hemorrhagic fluid (PCV, 7%) was obtained; results of cytologic and microbiologic examination of the fluid sample were not consistent with infectious or neoplastic processes. Prior to CT, a 6-lead ECG recording (Figure 1) was obtained with the dog in right lateral recumbency.
Six-lead ECG recording obtained from a 10-year-old 39.3-kg dog that was evaluated because of pericardial effusion and ascites. Atrial fibrillation is present (mean ventricular rate, 160 beats/min). The fibrillation waves are present with variable amplitude and morphology and without an isoelectric line between consecutive waves. The duration of the QRS complexes (0.06 seconds) is within reference limits, but there are irregular R-R intervals. Electrical alternans is evident. A single, notched ventricular premature complex is present with left bundle branch block morphology. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 259, 6; 10.2460/javma.259.6.605
ECG Interpretation
The initial surface ECG revealed an irregular rhythm with a mean ventricular response rate of 160 beats/min (Figure 1). The P waves were absent and had been replaced by coarse fibrillation waves with amplitudes ranging from 0.05 to 0.1 mV and durations ranging from 0.02 to 0.08 seconds. The QRS complexes had a duration of 0.06 seconds (reference range, ≤ 0.06 seconds) and variable R-wave amplitude (0.2 to 0.8 mV; reference range, < 3.0 mV), consistent with conduction electrical alternans. Mean electrical axis appeared normal (+60°; reference range, +40° to +100°). Findings were consistent with atrial fibrillation (AF). Occasionally, wide, notched QRS complexes of left bundle branch block morphology (duration, 0.14 seconds) were noted, which were compatible with ventricular premature complexes. Aberrant conduction was excluded on the basis of the absence of a typical sequence of a long R-R interval followed by a short R-R interval before the complexes.1
Given the sudden onset and absence of cardiac structural disease, lidocaine hydrochloridea (2 mg/ kg, IV) was administered. After a second bolus (2 mg/ kg, IV), the rhythm became regular with a mean ventricular rate of 240 beats/min (Figure 2). No P waves were observed, but flutter waves (F waves) were evident at a rate of 440 beats/min. The atrioventricular conduction ratio of F waves to QRS complexes was 2:1. The findings were consistent with typical atrial flutter. The rhythm then became irregular again with a mean ventricular rate of 165 beats/min. There was rapid atrial depolarization at 465 beats/min with variable morphology of what was suspected to be F waves and irregular atrioventricular conduction (Figure 3), suggestive of type II Wells atrial flutter. However, return to AF or development of atrial fibrillatory conduction could not be completely excluded on the basis of the surface ECG traces. This rhythm lasted for 4 seconds, and the dog then converted to sinus rhythm with a heart rate of 120 beats/min and variable P-wave amplitude consistent with wandering pacemaker. A negative P' was noted after the conversion that might have represented a junctional ectopic beat, arising from the lower portion of the right atrium.2 The PR interval was otherwise consistent at 0.12 seconds (reference range, 0.06 to 0.13 seconds).
Six-lead ECG recording obtained from a 10-year-old 39.3-kg dog that was evaluated because of pericardial effusion and ascites. This ECG was taken following a second IV bolus of lidocaine (total dose, 4 mg of lidocaine/kg), just before conversion from atrial fibrillation to sinus rhythm. Notice the typical atrial flutter with a ventricular rate of 240 beats/min and atrial rate of 440 beats/min. The flutter waves have a sawtooth appearance with a fixed 2:1 atrioventricular conduction preceding every QRS complex. The QRS complexes have normal duration (0.06 seconds) but variable amplitude. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 259, 6; 10.2460/javma.259.6.605
Six-lead ECG recording obtained from a 10-year-old 39.3 kg dog that was evaluated because of pericardial effusion and ascites. This ECG was taken during and following conversion from atrial flutter to sinus rhythm. A—The typical atrial flutter degenerates to type II Wells atrial flutter (first upward arrow) with a mean ventricular rate of 165 beats/min and rapid atrial depolarization of 465 beats/min with variable atrial flutter wave morphology. This rhythm lasted for 4 seconds. B—Notice the conversion of atrial flutter to sinus rhythm (second upward arrow) with a mean ventricular rate of 120 beats/min. A negative P' occurs after conversion, suggestive of junctional ectopic beat (downward arrow). Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 259, 6; 10.2460/javma.259.6.605
Discussion
The dog of the present report had sudden-onset AF. Atrial fibrillation is a relatively common, irregular supraventricular tachyarrhythmia characterized by rapid and uncoordinated atrial activity with loss of atrial contraction.3 Large fibrillation waves have been associated with atrial enlargement or recent onset of arrhythmia,4 as suspected in this case, considering recent normal examination findings at the primary care clinic. Electrical alternans was also identified, which can be associated with rapid supraventricular tachyarrhythmias4 and cases of pericardial effusion.5
Atrial fibrillation typically develops in dogs with primary structural cardiac disease secondary to atrial enlargement3 but can be identified at a low ventricular response rate in large to giant-breed dogs with structurally normal hearts; in the latter situation, the condition is sometimes termed lone AF.6 Less frequently, dogs may develop AF as a result of high vagal tone that is induced either pharmacologically (administration of opioids or pentobarbital) or after syncopal episodes.7,8 Direct vagal nerve stimulation, acetylcholine infusion, and α-chloralose anesthesia have been reported to create a favorable environment for the induction and maintenance of AF.9,10 Vagally mediated AF is initiated and maintained through the effects of parasympathetic stimulation on the atrial action potential duration, thereby shortening the action potentials and increasing the heterogeneity of refractoriness of atrial tissue.10,11 It is unclear whether a vagal component was associated with the onset of AF in the dog of the present report, but it remained a possibility because of the presence of concurrent disease processes.
Atrial fibrillation has also been associated with pericardial disease. Acute pericarditis has been historically reported to be accompanied by transient AF.12–14 Humans who undergo posterior pericardiectomy may develop AF in conjunction with pericar-dial effusion,15 and pericardiocentesis converts AF to sinus rhythm in most of those cases.15,16 However, the dog of the present report was considered cardiovascularly stable with no cardiac tamponade, so medical conversion was prioritized. In the veterinary medical literature, there is 1 case report17 of a Golden Retriever with pleural and pericardial effusions that developed AF following pericardiocentesis; successful conversion of AF to sinus rhythm followed after administration of procainamide. In the dog of the present report, whether the pericardial effusion was acute in origin or whether there was a relationship with the peritoneal effusion diagnosed at initial presentation could not be determined.
The sudden-onset AF and clinical suspicion of its possible vagal mediation determined the choice of initial treatment with lidocaine. Lidocaine is not considered the typical treatment option for supraventricular tachyarrhythmias but is used as a first-line treatment for rapid ventricular tachyarrhythmias because it shortens the action potential duration.18 It has been proposed that at higher doses, lidocaine transiently prolongs the atrial effective refractory period.19 In dogs, lidocaine administration has been effective in converting vagally mediated AF to sinus rhythm.9,20,21 However, the underlying electro-physiologic mechanism of lidocaine-sensitive atrial tachyarrhythmias is still unclear.22 Other drugs, such as ranolazine, sotalol, amiodarone, procainamide, pilsicainide, and flecainide, have also been shown to be effective.17,23–26 For the case described in the present report, a total dose of 4 mg of lidocaine/kg was successful in restoring sinus rhythm within a 10-minute interval. However, before converting to sinus rhythm, the dog developed atrial flutter. Atrial flutter is a group of uncommon complex supraventricular, macro-reentrant tachycardias that are characterized by a rapid series of atrial depolarizations.27 There are 3 known types of atrial flutter distinguished by the localization and direction of the macro-reentrant circuit.27 The most common is typical or cavotricuspid isthmus-dependent atrial flutter,27 which developed in the dog of the present report. There is a known bidirectional relationship between AF and typical atrial flutter.28 Specifically, AF induces the formation of a functional line of impulse block, often occurring in the right atrium between the cranial and caudal vena cavae, which enables initiation of atrial flutter. If a functional line of block is not present, atrial flutter does not develop because the block is necessary to prevent short-circuiting of the atrial flutter re-entrant circuit. On the other hand, atrial flutter of sufficiently short cycle duration can induce fibrillatory conduction, which then can manifest as AF.28,29 In human medicine, class Ia and Ic sodium channel blockers, together with amiodarone, are commonly used to suppress AF, and those drugs can promote sustained atrial flutter by inducing a functional line of impulse block.28 To our knowledge, this is the first reported instance of this effect in a dog following lidocaine injection.
Before conversion to sinus rhythm in the dog of the present report, the rhythm changed to an irregular rhythm for 4 seconds. It was speculated that the atrial flutter degenerated to type II Wells atrial flutter with an atrial depolarization rate of 465 beats/ min and an irregular ventricular rate. This unstable type of atrial flutter is typically characterized by a sudden onset and termination with rapid atrial depolarization rates exceeding 450 beats/min; it usually occurs in the presence of high vagal tone and can often transition between AF, atrial flutter, and sinus rhythm.4 An alternative explanation was that atrial flutter may have degenerated into high-rate AF or atrial fibrillatory conduction, just before conversion to sinus rhythm. Atrial fibrillatory conduction occurs when a portion of the atrial myocardium is unable to respond in a 1:1 manner to rapid impulses originating from another part of the atrium. On comparison of the ECG traces obtained from the dog before and after lidocaine administration, the F waves, rapid atrial depolarization, variable F-F intervals, and absence of an isoelectric line between consecutive F waves were more supportive of type II Wells atrial flutter. Additionally, atrial fibrillatory conduction has been reported to promote AF,28 which did not happen in the dog of the present report given that it returned rapidly to sinus rhythm at a heart rate of 120 beats/ min. Sinus rhythm was maintained for 48 hours, and the dog was discharged from the hospital the next day. On reexamination 15 days later, ECG revealed sustained sinus rhythm with occasional ventricular premature complexes.
Footnotes
Hameln Pharmaceuticals, Gloucester, UK.
References
- 1. ↑
Wellens HJ, Durrer D. Supraventricular tachycardia with left aberrant conduction due to retrograde invasion into the left bundle branch. Circulation 1968;38:474–479.
- 2. ↑
Waldo AL, Vitikainen KJ, Hoffman BF. The sequence of retrograde atrial activation in the canine heart. Correlation with positive and negative retrograde P waves. Circ Res 1975;37:156–163.
- 3. ↑
Guglielmini C, Chetboul V, Pietra M, et al. Influence of left atrial enlargement and body weight on the development of atrial fibrillation: retrospective study on 205 dogs. Vet J 2000;160:235–241.
- 4. ↑
Santilli R, Moïse NS, Pariaut R, et al. Supraventricular tachycardias. In: Santilli R, Moïse NS, Pariaut R, eds, et al.Electro-cardiography of the dog and cat: diagnosis of arrhythmias. 2nd ed. Milano, Italy: Edra S.p.A., 2018;160–201.
- 5. ↑
Usher BW, Popp RL, Houston FS. Electrical alternans: mechanism in pericardial effusion. Am Heart J 1972;83:459–463.
- 6. ↑
Takemura N, Nakagawa K, Hirose H. Lone atrial fibrillation in a dog. J Vet Med Sci 2002;64:1057–1059.
- 7. ↑
Pariaut R, Moïse SN, Koetje BD, et al. Evaluation of atrial fibrillation induced during anesthesia with fentanyl and pentobarbital in German Shepherd Dogs with inherited arrhythmias. Am J Vet Res 2008;69:1434–1445.
- 8. ↑
Porteiro Vázquez DM, Perego M, Santos L, et al. Paroxysmal atrial fibrillation in seven dogs with presumed neurally-mediated syncope. J Vet Cardiol 2016;18:1–9.
- 9. ↑
David D, Lang RM, Neumann A, et al. Parasympathetically modulated antiarrhythmic action of lidocaine in atrial fibrillation. Am Heart J 1990;119:1061–1068.
- 10. ↑
Liu L, Nattel S. Differing sympathetic and vagal effects on atrial fibrillation in dogs: role of refractoriness heterogeneity. Am J Physiol 1997;273:E805–816.
- 11. ↑
Wang Z, Feng J, Nattel S. Idiopathic atrial fibrillation in dogs: electrophysiologic determinants and mechanisms of antiarrhythmic action of flecainide. J Am Coll Cardiol 1995;26:277–286.
- 12. ↑
Imazio M, Lazaros G, Picardi E, et al. Incidence and prognostic significance of new onset atrial fibrillation/flutter in acute pericarditis. Heart 2015;101:1463–1467.
- 13.
Syed FF, Ntsekhe M, Wiysonge CS, et al. Atrial fibrillation as a consequence of tuberculous pericardial effusion. Int J Cardiol 2012;158:152–154.
- 14. ↑
Ristić AD, Maisch B, Hufnagel G, et al. Arrhythmias in acute pericarditis. An endomyocardial biopsy study. Herz 2000;25:729–733.
- 15. ↑
Gudbjartsson T, Helgadottir S, Sigurdsson MI, et al. New-onset postoperative atrial fibrillation after heart surgery. Acta Anaesthesiol Scand 2020;64:145–155.
- 16. ↑
Chidambaram M, Akhtár MJ, al-Nozha M, et al. Relationship of atrial fibrillation to significant pericardial effusion in valve-replacement patients. Thorac Cardiovasc Surg 1992;40:70–73.
- 17. ↑
Fries R, Saunders AB. Use of procainamide for conversion of acute onset AF following pericardiocentesis in a dog. J Am Anim Hosp Assoc 2012;48:429–433.
- 18. ↑
Tamargo J, Delpon E. Pharmacological bases of antiarrhythmic therapy. In: Zipes DP, Jalife J, Stevenson WG, eds. Cardiac electrophysiology: from cell to bedside. 7th ed. Philadelphia: Elsevier Inc, 2018;513–524.
- 19. ↑
Wijffels MCEF, Kirchhof CJHJ, Dorland R, et al. Atrial fibrillation begets atrial fibrillation: a study in awake chronically instrumented goats. Circulation 1995;92:1954–1968.
- 20. ↑
Moïse NS, Pariaut R, Gelzer ARM, et al. Cardioversion with lidocaine of vagally associated atrial fibrillation in two dogs. J Vet Cardiol 2005;7:143–148.
- 21. ↑
Pariaut R, Moïse NS, Koetje BD, et al. Lidocaine converts acute vagally associated atrial fibrillation to sinus rhythm in German Shepherd Dogs with inherited arrhythmias. J Vet Intern Med 2008;22:1274–1282.
- 22. ↑
Chiale PA, Faivelis L, Garro HA, et al. Distinct pharmacologic substrate in lidocaine-sensitive, repetitive atrial tachycardia. J Cardiovasc Pharmacol Ther 2012;17:146–152.
- 23. ↑
Burashnikov A, Di Diego JM, Zygmunt AC, et al. Atrium-selective sodium channel block as a strategy for suppression of atrial fibrillation: differences in sodium channel inactivation between atria and ventricles and the role of ranolazine. Circulation 2007;116:1449–1457.
- 24.
Yeşil M, Bayata S, Postaci N, et al. Cardioversion with sotalol in selected patients with vagally and adrenergically mediated paroxysmal atrial fibrillation. Angiology 1999;50:729–733.
- 25.
Oyama MA, Prosek R. Acute conversion of atrial fibrillation in two dogs by intravenous amiodarone administration. J Vet Intern Med 2006;20:1224–1227.
- 26. ↑
Hayashi H, Fujiki A, Tani M, et al. Different effects of class Ic and III antiarrhythmic drugs on vagotonic atrial fibrillation in the canine heart. J Cardiovasc Pharmacol 1998;31:101–107.
- 27. ↑
Saoudi N, Cosio F, Waldo A, et al. Classification of atrial flutter and regular atrial tachycardia according to electrophysio-logical mechanisms and anatomical bases: a statement from a Joint Expert Group from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. J Cardiovasc Electrophysiol 2001;12:852–866.
- 28. ↑
Waldo AL, Feld GK. Inter-relationships of atrial fibrillation and atrial flutter mechanisms and clinical implications. J Am Coll Cardiol 2008;51:779–786.
- 29. ↑
Waldo AL. Mechanisms of atrial flutter and atrial fibrillation: distinct entities or two sides of a coin? Cardiovasc Res 2002;54:217–229.
