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Michelle A. Oranges Angell Animal Medical Center, Boston, MA 02130

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Julia R. Lindholm Angell Animal Medical Center, Boston, MA 02130

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Rebecca L. Quinn Angell Animal Medical Center, Boston, MA 02130

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An 8-year-old 46.1-kg (101.4-lb) spayed female Newfoundland underwent a routine physical examination during which tachyarrhythmia (heart rate, 220 beats/min) and asynchronous pulses were detected (day 0). Twelve days earlier, the dog was presented in severe obstructive shock secondary to gastric dilatation-volvulus. The dog underwent emergency surgery, and a 50% gastrectomy, partial splenectomy, and gastropexy were performed. After surgery, the dog was administered 2 packed RBC transfusions and fresh frozen plasma and provided with intensive supportive care. Rare ventricular premature complexes were noted during surgery and the immediate postoperative period. No other rhythm abnormalities were detected. The dog ultimately recovered well and was discharged from the hospital 4 days after surgery; it was returned 4 days later for medical boarding.

At the initial evaluation on day 0, the dog was bright, alert, responsive, and adequately hydrated. The dog's mucous membranes were pink and moist with a normal capillary refill time (< 2 seconds). Aural temperature (38.4°C [101.2°F]) and respiratory rate (18 breaths/min) were within reference limits. Cardiac auscultation revealed tachycardia with an irregular rhythm. No heart murmur was detected. Results of point-of-care clinicopathological analysis of a blood sample were unremarkable, except for mildly high potassium concentration (4.72 mmol/L; reference interval, 3.62 to 4.60 mmol/L) and low glucose concentration (74 mg/dL; reference interval, 75 to 116 mg/dL). Echocardiography revealed mild chronic degenerative mitral valve disease (mild mitral valve regurgitation). Electrocardiography was performed to further evaluate the tachycardia.

ECG Interpretation

A 6-lead ECG examination was performed to evaluate the dog on day 0 (Figure 1). The recording revealed supraventricular tachycardia with an irregular ventricular response rate ranging from 166 to 300 beats/min (mean heart rate, 180 beats/min). P waves were absent and replaced by baseline sawtooth undulations (flutter [F] waves) deflected positively in leads II, III, and aVF. The atrial rate was 500 beats/min with a variable atrioventricular (AV) conduction ratio of 3:1 to 4:1. Such variation in the observed AV conduction ratio is thought to be suggestive of a multilevel block within the AV node.1,2 Once conducted, the QRS complexes appeared normal (QRS complex duration, 0.065 seconds; upper reference limit,3 0.065 seconds in giant-breed dogs) and electrical alternans was evident in lead II (R-wave amplitude, 0.22 to 0.90 mV; upper reference limit,3 3.0 mV). These findings resulted in an ECG diagnosis of reverse typical atrial flutter (AFL) with physiologic second-degree AV block. The variation in R-wave amplitude in this dog was likely attributable to superimposition of F waves and alternating QRS complexes, although electrical alternans has also been shown to be a rate-dependent phenomenon of supraventricular tachycardia.4

Figure 1—
Figure 1—

Initial 6-lead ECG traces obtained from a dog with tachyarrhythmia 12 days after surgery to treat gastric dilatation-volvulus. Supraventricular tachycardia with an irregular ventricular response rate ranging from 166 to 300 beats/min (mean heart rate, 180 beats/min) is identified. P waves are replaced by positively deflected, sawtooth, baseline undulations (flutter [F] waves) that are consistent with a diagnosis of reverse typical atrial flutter (AFL). Paper speed = 20 mm/s; 0.5 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 257, 12; 10.2460/javma.257.12.1235

Treatment with extended-release diltiazem (2.6 mg/kg [1.18 mg/lb], PO, q 12 h) was initiated. The dog was returned for reexamination on day 7. Recheck ECG (Figure 2) revealed reverse typical AFL with physiologic second-degree AV block (ventricular response rate, 190 beats/min) and suspected ventriculophasic variation in the AFL cycle duration (atrial rate, 400 to 500 beats/min).5 Conducted QRS complexes were normal in duration (0.040 seconds) and variable in R-wave amplitude (0.60 to 1.1 mV). The AV conduction ratio ranged from 2:1 to 3:1.

Figure 2—
Figure 2—

Lead II ECG tracing with a corresponding ladder diagram for the dog in Figure 1 seven days after starting twice-daily treatment with extended-release diltiazem. In the ladder diagram, the upper zone represents atrial activation (A), the center zone represents conduction through the atrioventricular (AV) node, and the lower zone represents ventricular activation (V). The ECG findings are consistent with a diagnosis of reverse typical AFL with physiologic second-degree AV block (ventricular response rate, 190 beats/min). The AV conduction ratio ranges from 2:1 to 3:1. In this schematic diagram of the proposed conduction pattern, a ventricular phasic variation in the AFL cycle duration (atrial rate, 400 to 500 beats/min) is also suspected. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 257, 12; 10.2460/javma.257.12.1235

The owner was instructed to change the dog's antiarrhythmic treatment to nonextended-release diltiazem (2 mg/kg [0.91 mg/lb], PO, q 8 h) and return the dog in 1 week for possible cardioversion. On day 17, ECG evaluation revealed an underlying sinus rhythm (mean heart rate, 90 beats/min; Figure 3), frequent atrial premature contractions (P-P’ coupling interval, 320 to 340 milliseconds; instantaneous heart rate [IHR], 176 to 187 beats/min), occasional premature ventricular complexes (R-R’ coupling interval, 280 to 300 milliseconds; IHR, 200 to 214 beats/min), and intermittent paroxysms of atrial tachycardia (IHR, 316 to 375 beats/min). During episodes of atrial tachycardia, the ventricular rate was irregular and ranged from 167 to 230 beats/min. The P waves were wide (duration, 0.06 seconds; upper reference limit,3 0.04 seconds), variably tall (amplitude, 0.2 to 0.5 mV; upper reference limit,3 0.4 mV), and consistent (P-R interval, 0.11 seconds; upper reference limit,3 0.13 seconds). The QRS complexes were normal in duration (0.06 seconds; upper reference limit,3 0.06 seconds) and R-wave amplitude (1.5 mV).

Figure 3—
Figure 3—

Leads II and aVF ECG tracings obtained from the same dog 17 days after the diagnosis of reverse typical AFL was made. The dog was undergoing treatment with extended-release diltiazem. There is an underlying sinus rhythm (mean heart rate, 90 beats/min) with frequent atrial premature contractions, occasional premature ventricular complexes, and intermittent paroxysms of atrial tachycardia. Paper speed = 25 mm/s; 2 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 257, 12; 10.2460/javma.257.12.1235

The dog did not undergo cardioversion. The owner was instructed to continue administration of diltiazem (2 mg/kg, PO, q 8 h) and begin amiodarone (17.5 mg/kg [7.95 mg/lb], PO, q 24 h for 14 days, then 12 mg/kg [5.45 mg/lb], PO, q 24 h for 14 days, then 9.5 mg/kg [4.32 mg/lb], PO, q 24 h for 14 days, and finally 8.3 mg/kg [3.77 mg/lb], PO, q 24 h). Three months after the initial evaluation, recheck Holter monitoring revealed that the dog continued to be well controlled on this combination of amiodarone and diltiazem. The ECG findings included 30 pauses over 2 seconds, with the longest pause being 2.356 seconds; 228 isolated premature ventricular complexes (IHR, 174 to 200 beats/min); and 67 isolated premature atrial complexes (IHR, 142 to 192 beats/min).

No changes were made to the dog's antiarrhythmic medications, and additional Holter monitoring rechecks were performed at 6 months, 14 months, and 16 months after the initial evaluation. The latest recheck Holter findings were indicative of reduced ventricular ectopy and increased supraventricular ectopy; there were 15 pauses over 2 seconds, with the longest pause being 2.289 seconds; 2 isolated premature ventricular complexes (IHR, 121 to 146 beats/min); and 351 isolated premature atrial complexes with 2 atrial couplets (IHR, 196 to 251 beats/min). A CBC, serum biochemical panel, and serum thyroid hormone panel were performed at 2 months, 6 months, and 14 months after the initial evaluation. Leukopenia (5.8 × 103 WBCs/μL; reference interval, 6.0 × 103 to 14.3 × 103 WBCs/μL) characterized by neutropenia (1.9 × 103 neutrophils/μL; reference interval, 3.3 × 103 to 10.1 × 103 neutrophils/μL) was identified at 6 months; these variables improved to borderline normal values at 14 months (4.7 × 103 WBCs/μL and 3.2 × 103 neutrophils/μL). The dog's serum liver enzyme activities were variable; alkaline phosphatase activity remained within the reference interval, whereas alanine aminotransferase activity was 435 U/L (reference interval, 22 to 74 U/L) at 6 months and 86 U/L at 14 months, and aspartate aminotransferase activity was mildly high (62 U/L; reference interval, 14 to 49 U/L) at 6 months. Mild hypercholesterolemia (385 to 417 mg/dL; reference interval, 130 to 339 mg/dL) was noted at all recheck assessments. The dog's serum total thyroid hormone (1.1 to 1.4 μg/dL; reference interval, 0.8 to 4.0 μg/dL) and thyroid-stimulating hormone (0.13 to 0.28 ng/mL; reference interval, 0.00 to 0.60 ng/mL) concentrations remained within reference limits; however, low serum free thyroxine concentration (6.0 ng/mL; reference interval, 7.7 to 47.6 ng/mL) was detected at 14 months. A recheck thyroid hormone panel at 17 months after the initial evaluation was recommended but was ultimately performed at the 25-month point; at that time, serum concentrations of free thyroxine (13.4 ng/mL), total thyroid hormone (1.3 μg/dL), and thyroid-stimulating hormone (0.23 ng/mL) concentrations were within reference limits. Up to the 25-month time point, the owner reported that the dog had remained clinically normal at home, and no changes were made to the dog's treatment.

Discussion

Atrial flutter is an AV node-independent macro-reentrant atrial tachycardia that is common in humans but relatively uncommon in dogs.6–8 Historically, AFL has been an ECG diagnosis. Findings consistent with AFL include narrow QRS complexes, a rapid atrial rate (generally > 240 beats/min; reported rates in humans and dogs include 250 to 300 beats/min and > 300 beats/min, respectively), and altered atrial conduction that appears as regular sawtooth F waves in the absence of an isoelectric baseline.2,9 The ventricular response rate may be regular or irregular.2,6 Because F waves conduct to different levels of the AV node, concealed conduction and a combination of physiologic (integral) and Wenckebach conduction block may occur, resulting in an irregular ventricular response rate.2 Concealed conduction describes the phenomenon in which a nonconducted impulse alters the conduction of the subsequent impulse via the AV node.10,11

Notably, AFL may be present in the absence of expected surface ECG findings.9 Atrial flutter QRS complexes may be wide in cases of aberrant conduction or bundle branch block.6,12 It is also known that atrial rate and the absence of an isoelectric baseline are not reliable indicators of an arrhythmogenic mechanism.9 For clarity, AFL is now defined as typical or atypical. This is a mechanistic distinction that differentiates AFL on the basis of the location of the underlying macroreentrant circuit.9 Typical AFL involves the cavotricuspid isthmus (ie, sub-Eustachian isthmus or tricuspid annulus-Eustachian ridge isthmus) to form a reentry circuit within the right atrium.9,13,14 Atypical AFL arises from a macroreentrant circuit outside of the cavotricuspid isthmus.9,15 Atypical reentrant circuits can form around functional or anatomic substrates within the left or right atrium.9,13 Substrates that slow conduction, thereby accentuating the nonuniform anisotropy (microscopic electrical coupling) of cardiac cells, or that have an altered refractory period may precipitate a reentrant circuit.6,16,17 Incisional scar or atriotomy tachycardia is an example of atypical AFL in humans.9 Spontaneous atypical AFL within the right atrial free wall of humans and dogs has also been documented.15,18

Typical AFL is further defined by the direction of the reentrant circuit. Counterclockwise activation of the atrial myocardium results in negative (inverted) F waves in leads II, III, and aVF, whereas clockwise rotation usually results in positive F waves in those leads.9,13,14,19 Counterclockwise rotation is more common for spontaneous cases of AFL in humans and dogs.9,13 Consequently, clockwise activation is termed reverse typical AFL.14 In both forms of typical AFL, the site of unidirectional block is the same.17

The ECG findings for the dog of the present report appeared most consistent with reverse typical AFL. It was speculated that the trigger for AFL in this dog arose from the trabeculated right atrium rather than the left atrium or septal aspect of the isthmus.14,17 Increased parasympathetic tone may have been a precipitating factor for AFL in this case, given the interplay of gastrointestinal tract disease, anesthesia, and perioperative pain medication administration.20 Acetylcholine reduces the refractory period of atrial myocardial cells, thereby promoting reentry.20,21 Alternatively, lone atrial fibrillation (AF) may have been converted to AFL in this dog. Atrial fibrillation is thought to precede AFL in most instances because AF forms the functional conduction block between the vena cavae that supports the AFL circuit.22 Lone AF can develop secondary to anesthesia or gastrointestinal tract disease.23 Large- and giant-breed dogs, including Newfoundlands, are also predisposed to lone AF, likely owing to their naturally substantial atrial mass.24 Other causes of AFL in dogs include hyperthyroidism and thyrotoxicosis. High total serum thyroxine concentration decreases the refractory period of myocardial cells.25 In humans, common causes of AFL include pulmonary embolism, myocardial infarction, decompensated congestive heart failure, and exacerbation of chronic lower airway disease.7

For the dog of the present report, the diagnosis of reverse typical AFL was not definitive. Neither entrainment nor atrial mapping was performed in this case. These diagnostic tests are required to identify the underlying arrhythmogenic mechanism and definitively diagnose typical versus atypical AFL.9,15 Reverse typical AFL is more difficult to diagnose on the basis of surface ECG findings than is typical AFL.8,14 Definitive diagnosis is pertinent if treatment via targeted ablation of the macroreentrant circuit is to be pursued.

Treatment of AFL is recommended when the rapid ventricular response rate and absent atrial kick result in clinical signs of hemodynamic instability, including episodic weakness, collapse, or exercise intolerance. Treatment may focus on rhythm conversion or rate control. Conversion may be attempted by direct current cardioversion or radiofrequency catheter ablation. Radiofrequency catheter ablation targeting the cavotricuspid isthmus is the first-line approach for rhythm control in humans.13,14 It has been successfully used in a small group of dogs with either typical or atypical AFL.8,18 Antiarrhythmic treatment may also be used to achieve either rhythm conversion or rate control. The ideal antiarrhythmic treatment for conversion is unclear. Historically, digoxin has been the first-line choice for rate control in dogs with AFL or AF.6 High dosages of sotalol, a class III antiarrhythmic, may promote sustained conversion to normal sinus rhythm by prolonging the atrial refractory period.14,26 Amiodarone, another class III antiarrhythmic, has been shown to prevent sustained, surgically induced AFL when administered with silymarin in dogs.27 In that study,27 amiodarone alone prolonged the AFL cycle duration so that it exceeded the right atrial refractory period; however, administration of amiodarone and silymarin resulted in an AFL cycle duration that was shorter than the duration of the right atrial refractory period. To the author's knowledge, this is the first report of conversion with diltiazem treatment alone in a dog. However, AFL is known to be an unstable rhythm in dogs, and it may convert to normal sinus rhythm or AF without any intervention.6

Following conversion of AFL, amiodarone was added to the treatment regimen of the dog of the present report to control the subsequently observed combination of ventricular and supraventricular arrhythmias. Long-term amiodarone administration may be associated with gastrointestinal tract problems (eg, vomiting or decreased appetite), hepatotoxicosis, neutropenia, altered circulating thyroid hormone concentrations or thyroid dysfunction, and bradycardia.28–31 Prolongation of the QT interval with a low risk for torsade de pointes in amiodarone-treated dogs has also been reported.28,32 In turn, recheck clinicopathologic analysis and ECG or Holter monitoring every 3 to 6 months is recommended for dogs undergoing long-term treatment with amiodarone. The dog of the present report was started on a low dose of amiodarone and tolerated the treatment well.

Acknowledgments

The authors have no conflicts of interest or financial disclosures to report.

References

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