A 17-year-old 513-kg (1,129-lb) gray Holsteiner gelding was presented for evaluation of lethargy of indeterminate duration. On examination, the horse was markedly lethargic with dull attitude and exercise intolerance when walking. It was thin (body condition score, 3/9). Mucous membranes were pink and moist with a capillary refill time < 2 seconds. Heart rate was 28 beats/min, respiratory rate was 20 breaths/min, and rectal temperature was 37.6°C (99.8°F). Cardiac auscultation revealed a grade 3/6 left-sided, apical, systolic murmur as well as an irregularly irregular arrhythmia. Frequent pauses with presumptive S4 heart sounds were auscultated. Gastrointestinal sounds and digital pulses were considered normal. Normal bronchovesicular sounds were noted during a rebreathing examination. A neurologic examination revealed lethargy with no cranial nerve abnormalities. Gait analysis revealed that the horse had weakness during walking along a straight line and bilateral pelvic limb circumduction that was worse for the left pelvic limb. The remainder of the gait analysis was truncated because of grade 4/5 lameness of the right thoracic limb. Cardiac auscultation before and after the lameness evaluation did not reveal changes in the arrhythmia.
A definitive cause of the lethargy and weakness could not be immediately determined. The primary differential diagnoses were cardiac disease, systemic illness (eg, neoplasia), neurologic disease, and narcolepsy or sleep deprivation; the evident lameness (musculoskeletal pain) was considered less likely. Additional diagnostic evaluation was performed. Thoracoabdominal ultrasonography revealed a moderate amount of free, hypoechoic peritoneal fluid. Abdominocentesis yielded clear, yellow-tinged, protein-poor transudate. Transrectal abdominal palpation revealed no abnormalities. Targeted clinicopathologic analyses to screen for liver disease revealed that plasma ammonia and sorbitol dehydrogenase concentrations were within reference intervals. Plasma ionized calcium concentration was high (1.96 mmol/L; reference range, 1.38 to 1.60 mmol/L). A CBC, serum biochemical profile, and assessment of serum cardiac troponin I concentration were recommended but declined by the owner in favor of these tests being performed at the local veterinary clinic. Owing to the cardiac abnormalities noted on physical examination of the horse, cardiac evaluation was pursued and included ECG, Holter recording, and echocardiography. An exercising ECG could not be undertaken because of the hor s e's la meness.
ECG Interpretation
Base-apex ECG revealed an underlying sinus arrhythmia conducted with second-degree atrioventricular (AV) block (Figure 1). The mean atrial rate was 35 beats/min, and the mean ventricular rate was 25 beats/min. Atrioventricular conduction varied from 1:1 to 3:1, and conducted P waves were observed with PR intervals that progressively shortened in successive impulses until the P wave was blocked. This pattern of a progressively shortened PR interval in successive impulses until impulse blockade occurred was frequently observed, and this was best described as a reverse Wenckebach pattern. Duration of the PR intervals ranged from 400 to 680 milliseconds (reference range, 220 to 560 milliseconds). Duration of the QRS complexes was 60 milliseconds (reference range, < 140 milliseconds), consistent with a normal ventricular depolarization.
Portions of a base-apex lead ECG recording obtained from a 17-year-old 513-kg (1,129-lb) horse that was evaluated because of lethargy, weakness, and a heart murmur. Notice the sinus origin P waves (asterisks) with an atrioventricular (AV) conduction range of 1:1 to 3:1. Progressively decreasing PR interval duration is observed during times of 1:1 AV conduction, known as a reverse Wenckebach pattern, which terminates with 1 blocked P wave (A) or 2 blocked P waves (B). Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 257, 5; 10.2460/javma.257.5.489
The horse also underwent echocardiography to assess cardiac health. The left ventricular size and function were considered normal. The cause of the heart murmur was identified as systolic, mild mitral valve degeneration and regurgitation. Diastolic mitral and tricuspid valve regurgitation was observed during times of second-degree AV block. The left atrium appeared to be normal in size. Trivial aortic valve insufficiency was also observed. The right side of the heart was subjectively normal in size and in function, and there was no evidence of pulmonary hypertension. A 24-hour Holter recording was then performed to further characterize the arrhythmia. This revealed frequent periods of second-degree AV block throughout the recording, with observed AV conduction rates of 2:1, 3:1, and 4:1. The periods of AV block resulted in ventricular heart rates as low as 9 beats/min, with pauses between ventricular beats that were commonly of 5 or 6 seconds’ duration. There were also periods of 1:1 AV conduction with an appropriate sinus rate for a duration of several minutes.
On the basis of physical examination and diagnostic test findings, the bradyarrhythmia was considered the likely cause of the horse's lethargy and weakness. Transvenous permanent pacemaker implantation was recommended, but additional evaluation and treatment were declined by the owner. No additional follow-up information was available. Owing to its risk of sudden cardiac death, the horse was classified as unsafe to ride, and it was recommended that only adults who had been informed of the risk for sudden collapse take care of the horse.
Discussion
For the horse of the present report, the likely cause of lethargy and weakness was considered to be the documented bradyarrhythmia. Horses frequently develop cardiac arrhythmias, and most are considered physiologic and related to high vagal tone. However, pathological arrhythmias are also identified, which may be a cause of poor performance with certain risks for the horse and rider. Exercise will usually eradicate vagally induced arrhythmias and can be used as a simple test to make a presumptive diagnosis of a vagal arrhythmia. For pathological arrhythmias, underlying cardiac disease, such as acquired valvular disease, congenital deformations, myocardial damage, pericarditis, and endocarditis, should be excluded as a cause; similarly, noncardiac disease such as electrolyte and acid-base disturbances, hypoxemia, endotoxemia, and toxic causes should be excluded.1
In horses, increased vagal tone results in a delay in conduction through the AV node much more commonly than it causes sinus bradycardia; thus, first-degree AV block and second-degree AV block type I are considered the most common arrhythmias in horses.2 Atrioventricular blocks can be classified as delayed impulse conduction toward the ventricles (first-degree block), intermittently blocked conduction (second-degree block), or complete absence of conduction (third-degree block). With second-degree AV block, some atrial impulses fail to reach the ventricles, which therefore do not depolarize. Two types of second-degree AV block can be distinguished: Mobitz type I (or Wenckebach periodicity) and Mobitz type II.3 Second-degree AV block type I describes a repeating pattern of progressive lengthening of PR intervals until there is a lack of conduction through the AV node, usually observed as 3:2 or 4:3 AV conduction. Second-degree AV block type II describes a fixed PR interval before and after the blocked P wave with a variable number of blocked P waves, and this arrhythmia may be more commonly associated with myocardial disease at the His-Purkinje level. The Wenckebach phenomenon observed in second-degree AV block type I is associated with increased vagal tone and conduction fatigue and block at the AV nodal level,4 and this arrhythmia typically resolves with stimulation or exercise.1 In the horse of the present report, limited exercise performed during the lameness evaluation and the perceived associated musculoskeletal pain did not abolish the arrhythmia.
Seldomly, a reverse Wenckebach pattern occurs when the first conducted P wave after the block has a longer PR interval than that of the subsequent conducted beat. Subsequent conducted beats have progressively shorter PR intervals, and the first conducted beat after the blocked P wave may have a slightly wider ventricular complex, compared with that of the subsequent complex.4,5 Disease in the proximal portion of the His-Purkinje system is present in humans with reverse Wenckebach periodicity.4 The affected His-Purkinje system may have differences in speeds of conduction in the left posterior fascicle, compared with those in the left anterior or right bundle branch, and this pattern of conduction accounts for an initially prolonged PR interval followed by shortened PR intervals. Once conduction fatigue occurs, there is a blocked P wave, which allows phase 4 (ie, bradycardia-dependent) depolarization of the His-Purkinje system to occur in only a portion of the His-Purkinje system and enables this cycle to repeat.4 When the phase 4 depolarization occurs in all of the His-Purkinje system, paroxysmal AV block occurs.4 This rare arrhythmia may result in syncope, which is a clinical indication for permanent cardiac pacing because this arrhythmia is not associated with vagal tone. In the human medical literature, possible causes of reverse Wenckebach periodicity include toxic effects of potassium and digitalis and myocardial disease.4,6 In the horse of the present report, the reverse Wenckebach pattern persisted after exercise and there was paroxysmal AV block characterized by consecutive blocked P waves, both of which were consistent with disease of the His-Purkinje system.
In horses, successive P waves that are blocked lead to long pauses between ventricular contractions and may result in a decrease in blood pressure and syncope.3 Affected horses usually have severe exercise intolerance and may collapse.7 Possible causes of successive blocked P waves include electrolyte imbalances, digitalis toxicosis, and myocardial disease (inflammatory or degenerative) involving the specialized conduction system. Structural abnormalities affecting conduction through the AV node and major conduction pathways are considered rare in horses. Affected horses have a slow heart rate, and on auscultation, S1 and S2 are regularly spaced with an audible S4 preceding each S1. A complete cardiovascular examination, serum biochemical profile, and CBC should be performed for all affected horses to attempt to determine the underlying cause of the dysrhythmia. Appropriate treatment should be instituted as soon as possible to prevent progression of the conduction disturbance to complete AV block. Pacemaker implantation is recommended when the dysrhythmia cannot be controlled.2,6
The major concern regarding the horse of this report was possible collapse and sudden death, because the Holter monitoring recorded very low ventricular heart rates with notably long pauses between ventricular beats. To the authors’ knowledge, this is the first report of a horse with reverse Wenckebach periodicity and lethargy and weakness as suspected consequences.
Acknowledgments
The authors thank Dr. Daniel K. Newhard for his collaboration and expertise.
The horse of this report was evaluated at the J. T. Vaughan Large Animal Teaching Hospital, Auburn University, Auburn, Ala.
References
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3. Verheyen T, Decloedt A, De Clercq D, et al. Electrocardiography in horses, part 2: how to read the equine ECG. Vlaams Diergen Tijds 2010;79:337–344.
4. Zahid M, Arora S. Reverse Wenckebach “pseudo-supernormal” conduction or paroxysmal atrioventricular block. J Cardiovasc Dis Res 2012;3:225–227.
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7. Durando MM. Cardiovascular causes of poor performance and exercise intolerance and assessment of safety in the equine athlete. Vet Clin North Am Equine Pract 2019;35:175–190.
