A 15-year-old 20.1-kg (44.2-lb) neutered male Springer Spaniel was reevaluated because of progressive stridorous panting with activity, an occasional cough or gag, and worsening anorexia as well as for routine pacemaker interrogation. A previous diagnosis of high-grade second-degree atrioventricular (AV) block and early myxomatous mitral valve disease had been made when the dog was 10 years old. At that time, the dog underwent transvenous pacemaker implantationa set in ventricular-pacing, ventricular-sensing, inhibition-response, and rate-adaptive (VVIR) mode with a minimum response rate of 60 beats/min and maximum rate of 150 beats/min. The dog was also treated with enalapril maleate (0.5 mg/kg [0.23 mg/lb], PO, q 12 h).
Eight months earlier during a routine yearly examination, early laryngeal paralysis was suspected on the basis of characteristic laryngeal stridor. Serum biochemical analysis, performed 10 days prior to the examination during which laryngeal paralysis was suspected, had revealed high activities of alanine aminotransferase (836 U/L; reference range, 12 to 118 U/L) and alkaline phosphatase (767 U/L; reference range, 5 to 131 U/L), findings that were considered secondary to administration of ketoconazole for a previous cutaneous fungal infection. Abdominal ultrasonography at that time revealed no important abnormalities.
At the same time as when laryngeal paralysis was suspected, the dog had undergone an echocardiographic examination; results indicated progressive myxomatous mitral valve disease with progressive borderline severe secondary left atrial chamber dilation and moderate eccentric left ventricular chamber dilation. Medical management was adjusted to include administration of spironolactone (0.93 mg/kg [0.42 mg/lb], PO, q 12 h). The primary care veterinarian was also treating the dog with S-adenosylmethionine, tylosin tartrate, omeprazole, doxycycline, and cyanocobalamin of unknown dosages. Pacemaker interrogation and ECG revealed a normally functioning pacemaker with 74% paced beats and 26% sensed beats, lead impedance of 358 Ω, battery life that was estimated at 2.25 to 2.75 years, sensing threshold of 8.1 to < 10.0 mV, and a capture threshold of 0.75 V at 0.5 milliseconds. The lower and upper rates had previously been programmed to 60 beats/min and 150 beats/min.
At the reevaluation, the dog had a slightly irregular rhythm and a grade 5/6 systolic murmur over the mitral valve region; ausculted lung sounds were considered normal, and pulses were strong and synchronous. No stridor was noted on the physical examination. The dog's body condition score was 5/9. Moderate dental disease was present. Abdominal palpation revealed no notable findings. Serum biochemical analysis performed by the primary care veterinarian 2 weeks earlier revealed high activities of alanine aminotransferase (426 U/L) and alkaline phosphatase (265 U/L). Results of a CBC indicated that the dog had a hemoglobin concentration of 9.9 g/dL (reference range, 12.1 to 20.3 g/dL), RBC count of 4.3 × 106 cells/μL (reference range, 4.8 × 106 cells/μL to 9.3 × 106 cells/μL), Hct of 30% (reference range, 36% to 60%), and platelet count of 134 × 103 platelets/μL (reference range, 170 × 103 platelets/μL to 400 × 103 platelets/μL), although platelet clumping was present. Echocardiography revealed stable borderline severe myxomatous mitral valve disease, subjectively improved degree of mitral valve regurgitation, stable left atrial chamber dilation, and compensated left ventricular systolic function. On pacemaker interrogation, there were 91.54% sensed beats and 9.46% paced beats. A 6-lead ECG was performed (Figure 1).
ECG Interpretation
The recording (Figure 1) revealed atrial flutter (AFL) with a regular atrial rate of 520 beats/min and an irregular ventricular response rate of 80 beats/min. Approximately 8 paced beats/min were recorded, 1 of which appeared as a pacing spike followed by a wide and bizarre QRS complex of left bundle branch configuration indicating a right ventricular origin of the impulse generated from the pacemaker,1 which was consistent with the previously implanted ventricular pacemaker. The remainder of the QRS complexes appeared normal in morphology. The conduction ratio (Figure 2) was 10:1 (ie, 10 F waves/QRS complex).2
Six-lead ECG tracings obtained from a dog with an artificial pacemaker implanted in the right ventricle that was evaluated because of progressive stridorous panting with activity, an occasional cough or gag, and worsening anorexia and for routine pacemaker interrogation. Atrial flutter characterized by regular F waves resulting from macroreentry circuits within the atria was diagnosed. Notice a negative deflection of the F waves in leads II, III, and aVF and biphasic F waves in leads I and aVL, which indicate a counterclockwise macroreentry circuit. A single pacemaker spike generated from the artificial pacemaker is visible (SP). A wide and bizarre QRS complex follows the spike, representing ventricular activation. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 9; 10.2460/javma.253.9.1121
Lead–2 ECG tracing and ladder diagram for the dog in Figure 1. In the ladder diagram, the upper zone represents atrial activation (zone A), the middle zone represents atrioventricular conduction (zone AV), and the lower zone represents ventricular activation (zone V). A single paced beat is generated (P) by the artificial pacemaker implanted in the right ventricle. Electrical impulses within zone A originate with a regular cycle frequency and are represented by the vertical lines in zone A. The dots in zone A represent the same ectopic focus within the atria. The impulses may be blocked at different regions of zone AV, represented by differing AV conduction depths on the ladder diagram. The vertical lines in zone V represent the conduction of the electrical impulses from the AV node to the ventricles, which is responsible for the QRS complexes observed. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 9; 10.2460/javma.253.9.1121
An undulating pattern or a series of sawtooth-shaped flutter waves (F waves) is created when there is a macroreentrant circuit rotating around the tricuspid annulus in the right atrium. The F waves represent the fast, recurrent atrial activation.1,3 Negatively deflected F waves in leads II, III, and aVF, along with low-amplitude or relatively flat, biphasic F waves in leads I and aVL, are consistent with typical or counterclockwise AFL.1,4
Discussion
Atrial flutter is a relatively uncommon arrhythmia in dogs, which is characterized by rapid and regular intervals of depolarization of the atria that have a sawtooth appearance on the ECG tracing. These sawtooth waves are called F waves. The rate of the atrial rhythm usually varies from 300 to 500 beats/min.1,5 The atrial rate of depolarization is rapid, and the conduction ability of the AV node is exceeded, which results in a functional AV block.
Flutter waves represent sequential depolarization and repolarization of the atria. The F waves typically have the same morphology, polarity, and cycle length because they are coursing through the same pathway within the atria and around the tricuspid annulus with each reentry loop.5,6 Flutter waves that appear to be completely blocked may actually penetrate to different levels of the AV node. This phenomenon is known as concealed conduction.5 For an impulse to reach the ventricle, it must reach the AV node when all levels of the node are nonrefractory. This occurs at highly variable intervals and may explain irregular ventricular response rates, such as that detected in the dog of the present report.
In AFL, the ventricular rhythm and rate depend on the atrial rate and state of AV conduction; AV conduction is influenced largely by autonomic tone. Atrial flutter usually has some degree of physiologic AV conduction block because of the high atrial rate and relative refractoriness of the AV node.5 For the dog of the present report, the original diagnosis was high-grade second-degree AV blockade, indicating that the AV node was able to intermittently propagate an electrical current. With the development of a high atrial rate, increased AV nodal propagation occurred, resulting in a higher ventricular response rate and maintenance of adequate cardiac output. In this dog, there were also periods of a slower ventricular response rate (less than the programmed lower rate of the pacemaker), which generated a paced beat.
Atrial flutter can be classified as either type I (typical) or type II (atypical). Type I is generated from the right atrium and can be further characterized as typical (also called counterclockwise) or reverse typical (clockwise). Typical AFL is associated with the appearance of positive F waves in lead V1, negative F waves in lead V6, and negative F waves in leads II, III, and aVF, and it travels in a counterclockwise pathway. Reverse typical AFL is associated with the appearance of negative F waves in lead V1, positive F waves in lead V6, and positive F waves in leads II, III, and aVF.6–10 Reverse typical AFL moves in a clockwise fashion through the atria in a pathway that involves a small strip of tissue (the cavotricuspid isthmus) between the cranial vena cava and the tricuspid annulus.4,6,7,11,12
Atypical flutter is difficult to distinguish from atrial tachycardia because the sawtooth-shaped F waves are not seen.13 Type II AFL is less extensively studied and much less common than type I. Type II AFL is typically characterized by atrial rates that are faster than those associated with type I AFL.14 Type II AFL can arise from either the right or left atrium and has no consistent ECG characteristics.10 This has been called isthmus-independent flutter, whereas type I AFL is isthmus dependent.6
In humans, the rate of AFL development in men is 2.5 times that in women. The risk of AFL is also higher in humans with heart failure (3.5 times the risk in humans without heart failure) and those with chronic obstructive pulmonary disease (1.9 times the risk in humans without the disease).15 The dog of the present report had mild pulmonary hypertension at the time of several of its echocardiographic examinations, but the condition was not sufficiently severe to require treatment. It is unknown whether pulmonary hypertension or the suspected laryngeal paralysis was a potentially contributing factor to the dog's arrhythmia. Other risk factors for AFL in humans include treatment with antiarrhythmic medications, thyrotoxicosis, pulmonary embolism, prior cardiac surgery, or prior atrial ablation.11 One study16 factored periodontal disease into an assessment of the risk of AFL and determined that there is an increased risk of both atrial fibrillation or AFL in humans with periodontal disease. It is certainly feasible to suspect this may be similar in canids, which tend to have worse dental hygiene than humans. In canids, atrial enlargement is the most common cause of this arrhythmia. Other causes are ruptured chordae tendineae, quinidine treatment for atrial fibrillation, atrial septal defect, tricuspid valve dysplasia, chronic mitral valvular fibrosis, and ventricular preexcitation.13 Treatment of AFL is focused on either its conversion to normal sinus rhythm or controlling the ventricular response rate of the AFL. Most commonly in clinical practice, the treatment of AFL aims to control the ventricular response rate. If the ventricular rate is normal and allows adequate cardiac output, then pharmacological rate control may not be indicated.1,11 If a high ventricular rate is present, the treatment of AFL should focus on rate control of the ventricular response. This is performed by blocking AV nodal conduction with administration of calcium channel blockers or β-adrenergic receptor blockers, potentially in combination with digoxin.12 Treatment with digoxin alone is not an effective management strategy for AFL.17 Because of the controlled ventricular rate from the previously diagnosed AV block and implanted pacemaker in the dog of the present report, no additional treatment was necessary. Ocular or carotid pressure massage can be performed as a potential emergency measure to slow conduction through the AV node in patients with a fast ventricular rate and hemodynamic decompensation.5,7 For the dog of the present report, spironolactone administration was discontinued not for reasons related to its cardiac status, but rather to attempt to improve episodes of diminished appetite.
Although pharmacological intervention has an 80% success rate for conversion of AFL to sinus rhythm, the long-term recurrence rate of AFL is high.3 Low-energy precordial shock, or cardioversion, should be considered when drug administration is not effective and the affected animal is in critical condition.13 General anesthesia with intubation is required prior to receiving a transthoracic electrical shock and could be contraindicated in some patients.17 Complications of cardioversion are largely dose dependent. However, the electrical shock dose for this particular arrhythmia tends to be lower than that required for other arrhythmias.
In humans, radiofrequency catheter ablation is a safe and effective first-line treatment of type I AFL. Ablation, which targets the cavotricuspid isthmus, is the most widely accepted and successful treatment for AFL.3 Radiofrequency catheter ablation of the cavotricuspid isthmus is relatively safe; however, complications including heart block, cardiac perforation, tamponade, and thromboembolic events have been noted in approximately 2.5% to 3.0% of humans undergoing this procedure.3,18 The risk of thromboembolic events may be greater for patients with depressed left ventricular function, mitral valve disease, or left atrial enlargement with spontaneous contrast on echocardiograms.3
Atrial flutter is generally an unstable rhythm that often degenerates into atrial fibrillation or spontaneously converts back to normal sinus rhythm.13 In the dog of the present report, the initial cause of AFL was undetermined; however, it was suspected to be related to a combination of marked atrial enlargement and high vagal tone. Increases in vagal tone to atrial cells result in differential effects on the effective refractory period, thereby favoring a macroreentry phenomenon, which is a necessary condition for the development of AFL.14
Acknowledgments
The authors declare that there were no conflicts of interest or financial disclosures.
Footnotes
Victory DR Model 5810 generator, St. Jude Medical Inc, Saint Paul, Minn.
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