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Bryan D. Eason Departments of Veterinary Medicine and Surgery (Eason, Leach) and Equine Medicine and Surgery (Messer), College of Veterinary Medicine, University of Missouri, Columbia, MO 65211.

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Stacey B. Leach Departments of Veterinary Medicine and Surgery (Eason, Leach) and Equine Medicine and Surgery (Messer), College of Veterinary Medicine, University of Missouri, Columbia, MO 65211.

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Nat T. Messer IV Departments of Veterinary Medicine and Surgery (Eason, Leach) and Equine Medicine and Surgery (Messer), College of Veterinary Medicine, University of Missouri, Columbia, MO 65211.

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A 3-year-old 392-kg (862-lb) Rocky Mountain filly with a 5-day history of hypoalbuminemia and facial edema that progressed to ventral edema was referred to the University of Missouri Veterinary Medical Teaching Hospital for further diagnostic testing and evaluation. At the initial referral evaluation, the horse was alert and responsive; heart rate was 44 beats/min, respiratory rate was 40 breaths/min, and rectal temperature was 37.8°C (100.0°F). Mild ataxia in the hind limbs was evident. A CBC and plasma biochemical analysis revealed a stress leukogram and profound panhypoproteinemia (albumin concentration, < 1.5 g/dL [reference range, 3.5 to 4.4 g/dL]; total protein concentration, 3.5 g/dL [reference range, 6.3 to 8.1 g/dL]). Ultrasonographic examination of the abdomen revealed marked peritoneal effusion; gastrointestinal tract motility and small intestinal wall thickness were considered normal. An echocardiographic evaluation was performed the day after initial evaluation to determine whether there was a cardiogenic cause of the edema and effusion. The left ventricular wall measurements appeared normal, but the chamber dimensions were decreased in systole (4.24 cm; reference range, 6.7 to 8.1 cm)1 and diastole (8.05 cm; reference range, 11.2 to 12.6 cm).1 Mild pulmonic and aortic valve regurgitation was also noted. The appearance of the aortic valve was consistent with mild chronic myxomatous degeneration; however, endocarditis could not be ruled out. Mild pericardial and pleural effusions were detected. Given the lack of evidence of major structural heart disease, additional diagnostic testing was pursued. Following cardiac examination, abdominocentesis was performed and approximately 16 L of serosanguineous fluid was removed. Results of fluid analysis were consistent with septic suppurative peritonitis. A sample of the fluid was submitted for bacterial culture. Two days after the referral evaluation and subsequent hospitalization, the horse's resting heart rate was 100 beats/min.

ECG Interpretation

Following auscultation of a tachyarrhythmia, a standard bipolar 3-lead surface ECG recording was obtained, which revealed sustained narrow QRS complex tachycardia with a regular rhythm and a rate of 100 beats/min (Figure 1). The QRS complexes were uniform in appearance; complex duration was 0.12 seconds (reference range, ≤ 0.16 seconds),2 and ST segment elevation was evident in leads I and II. P waves were visible and occasionally buried within the QRS complexes and T waves, which confirmed atrioventricular (AV) dissociation. The atrial rate was approximately 38 to 44 beats/min. Given the presence of AV dissociation, a diagnosis of ventricular tachycardia or junctional tachycardia was considered most likely.

Figure 1—
Figure 1—

Three-lead ECG tracings acquired from a horse that was evaluated because of a 5-day history of hypoalbuminemia and facial edema that progressed to ventral edema. Notice the narrow-complex tachycardia (QRS complex duration, 0.12 seconds) with a right bundle branch block morphology (left ventricular origin) and positively deflected T waves in lead II. Nonconducted P waves (black arrows) are occasionally buried within the QRS complexes, ST segments, and T waves, confirming atrioventricular dissociation. The atrial rate is approximately 40 beats/min, and the ventricular rate is approximately 100 beats/min. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 243, 2; 10.2460/javma.243.2.208

A peripheral blood sample was collected for assessment of plasma electrolyte and cardiac troponin I (cTnI) concentrations. Detected abnormalities included hypokalemia (2.4 mEq/L; reference range, 3.3 to 4.6 mEq/L), hypomagnesemia (0.9 mg/dL; reference range, 1.2 to 2.1 mg/dL), hypocalcemia (9.0 mg/dL; reference range, 11.5 to 13.1 mg/dL), and a high cTnI concentration (3.71 ng/mL; reference range, ≤ 0.06 ng/mL). Following fluid therapy with a balanced crystalloid solution and IV administration of supplemental calcium, magnesium, phosphorous, and potassium, the plasma calcium concentration remained low (9.4 mg/dL) but the hypokalemia and hypomagnesemia resolved. The hypocalcemia was attributed to the profound hypoalbuminemia. Despite resolution of the electrolyte derangements, the tachyarrhythmia persisted. Anti-arrhythmic treatment was then considered.

A total of 3 boluses of lidocaine hydrochloride (0.5 mg/kg [0.23 mg/lb]) were administered IV over a period of 1 hour. Conversion to a sinus rhythm was temporarily successful following administration of each bolus. Three-lead ECG tracings were obtained during administration of lidocaine (Figure 2) and revealed narrow complex tachycardia with AV dissociation. Sinus capture complexes occurred transiently thereafter (instantaneous heart rate, 43 beats/min), before the rhythm returned to narrow complex tachycardia. The QRS complex and T-wave morphologies for the sinus-originated complexes were markedly different from those for the complexes recorded during the periods of tachycardia. After the third bolus, conversion to a sinus rhythm occurred and a lidocaine constant rate infusion (0.005 mg/kg/min [0.0023 mg/lb/min]) was initiated. The constant rate infusion was discontinued after 5 days because of clinical improvement, resolution of the tachyarrhythmia, and loss of venous access as a result of jugular vein thrombosis induced by the presence of the IV catheter.

Figure 2—
Figure 2—

Three-lead ECG tracings acquired following IV administration of a third bolus of lidocaine hydrochloride to the horse in Figure 1. Narrow-complex ventricular tachycardia is evident in the first 6 complexes. The rhythm temporarily converts to a sinus rhythm before returning to ventricular tachycardia. The QRS complex and T-wave morphologies of the sinus-originated complexes are distinctly different from the morphologies of the complexes recorded during the tachycardia. The sinus-capture complexes and response to lidocaine confirm that the tachycardia is ventricular in nature. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 243, 2; 10.2460/javma.243.2.208

While results of bacterial culture of the peritoneal fluid sample were pending, broad-spectrum antimicrobials (gentamicin, 6.6 mg/kg [3.0 mg/lb], q 24 h; penicillin G potassium, 22,000 U/kg [10,000 U/lb], q 6 h) were administered to the horse IV. Oral administration of enrofloxacin (7.5 mg/kg [3.4 mg/lb], q 24 h) was initiated when bacterial culture of the peritoneal fluid sample yielded growth of enrofloxacin-susceptible Escherichia coli. The horse was discharged from the hospital after 17 days, and the owner was instructed to restrict its activity for the next 6 weeks. Plasma cTnI concentration was reassessed on the day before hospital discharge, and the value was within the reference range. Twelve months after the referral evaluation, the horse was reported to be healthy by the referring veterinarian.

Discussion

In horses, ventricular arrhythmias are much less common than supraventricular arrhythmias and are more suggestive of cardiac disease.3 However, ventricular tachycardia in association with a number of systemic and cardiovascular disorders, such as hypoxia, electrolyte abnormalities, fever, sepsis, acidosis, endotoxemia, uremia, and endocarditis of the mitral or aortic valves, has been reported.4,5 The ausculted heart rhythm may be regular or irregular depending on whether the ventricular tachycardia is monomorphic or polymorphic, respectively.4 Given the relatively narrow QRS complex morphology evident in the ECG recordings, the exact nature of the tachyarrhythmia in the horse of the present report was difficult to determine. However, the variability in the P-Q interval, the absence of a P wave preceding some QRS complexes, and the presence of P waves within other complexes aided in confirmation of AV dissociation. Furthermore, the presence of AV dissociation made a junctional or ventricular tachycardia most likely. The response to lidocaine and the morphology of the QRS complexes and T waves of the sinus-originated complexes confirmed the diagnosis of ventricular tachycardia. It is known that the QRS complex duration may be within reference range in horses with ventricular tachycardia.6,7

The cause of the arrhythmia in the horse of the present report could not be determined. Electrolyte derangements were unlikely to be the inciting cause because normalization of plasma electrolyte concentrations did not resolve the tachyarrhythmia. Primary cardiac disease seemed unlikely given the unremarkable echocardiographic findings obtained 1 day prior to the development of the arrhythmia. However, the echocardiographic appearance of the aortic valve warrants some discussion. Although the changes to the aortic valve were more consistent with myxomatous degeneration, endocarditis could not be ruled out. Bacteriologic cultures of blood samples were indicated but, unfortunately, not performed. Arrhythmias associated with endocarditis are common in veterinary species and may include atrial and ventricular premature complexes, paroxysmal and sustained tachycardia, bundle branch block, and first-, second-, and third-degree AV block. The prevalence of arrhythmias in dogs with endocarditis may be as high as 50% to 75%.8 In horses, ventricular premature complexes and atrial fibrillation are the most common arrhythmias associated with endocarditis, but endocarditis-related ventricular tachycardia has been reported.9

Endotoxemia was considered the most likely cause of the arrhythmia in the horse of the present report given the presence of septic suppurative peritoneal effusion. Acute abdominal disease has been associated with myocardial injury in horses.10 The underlying cause for the peritoneal effusion in this horse was never determined. In a recent study,11 healthy horses given an IV infusion of endotoxin developed arrhythmias and had increases in body temperature, heart rate, blood pressure, and plasma cTnI concentrations. It was noted that plasma cTnI concentration significantly increased prior to development of cardiac arrhythmias, and most horses in the study had an increase in ventricular ectopy.11 Unfortunately, plasma cTnI concentrations in the horse of the present report were not measured prior to development of the arrhythmia, and it is not possible to rule out tachycardia alone as a cause for the high plasma cTnI concentration. Tachycardia increases myocardial oxygen demand and reduces oxygen supply by shortening diastolic filling times, thereby potentially leading to myocardial ischemia and increased plasma cTnI concentration.12

Ventricular arrhythmias pose an increased risk of sudden death. Suspicion of ventricular tachycardia based on physical examination findings is possible, but confirmation should be made with an ECG evaluation. Irregular jugular pulsation, or cannon A waves, may be associated with ventricular tachycardia and occurs when the atria contract against a closed AV valve, leading to reflux of blood in the jugular veins. Additionally, intermittently loud first heart sounds (bruit de canon) may be heard because the timing of atrial contraction relative to ventricular contraction is variable. Distinction of supraventricular tachycardia from ventricular tachycardia can be difficult in cases where P waves are not apparent on an ECG tracing. In the horse of the present report, clear dysynchrony of the atria and ventricles was readily apparent in the ECG recordings, thereby aiding in diagnosis. Atrioventricular dissociation in the setting of ventricular tachycardia is attributable to interference from 2 independently depolarizing foci and is not a result of abnormal AV nodal conduction, as is the case with complete heart block. Interference dissociation can occur when there is rapid repetitive depolarization of a ventricular focus with absent retrograde AV conduction to the atria. Sinus-conducted impulses fail to conduct in an antegrade direction because the AV node is refractory from the repetitive partial depolarization from the ventricular focus.13 Continuous ECG monitoring during treatment can also be beneficial, as indicated by the fact that a return to sustained tachycardia was captured following 2 normal sinus complexes on the second ECG tracing obtained from the horse of the present report. Although lidocaine was used as a first line of treatment in this horse, other antiarrhythmic drugs such as quinidine, procainamide, or propafenone could have been considered. Quinidine is frequently used to treat both supraventricular and ventricular tachyarrhythmias; however, the adverse effects of the drug (ie, hypotension, negative inotropy, ataxia, colic, and diarrhea) make its use less desirable.14 Because of its infrequency in horses, a diagnosis of ventricular tachycardia should prompt further evaluation for an underlying cause, although primary cardiac disease must also be considered.

References

  • 1. Reef VB. Equine diagnostic ultrasound. Philadelphia: WB Saunders Co, 1998; 215272.

  • 2. van Loon G, Patteson M. Electrophysiology and arrhythmogenesis. In: Marr CM, Bowen M, eds. Cardiology of the horse. 2nd ed. Edinburgh: Elsevier Ltd, 2010;5973.

    • Search Google Scholar
    • Export Citation
  • 3. McGuirk SM, Muir WW. Diagnosis and treatment of cardiac arrhythmias. Vet Clin North Am Equine Pract 1985; 1: 353370.

  • 4. Reef VB, Marr CM. Dysrhythmias: assessment and medical management. In: Marr CM, Bowen M, eds. Cardiology of the horse. 2nd ed. Edinburgh: Elsevier Ltd, 2010;159178.

    • Search Google Scholar
    • Export Citation
  • 5. Traub-Dargatz JL, Schlipf JW Jr & Boon J, et al. Ventricular tachycardia and myocardial dysfunction in a horse. J Am Vet Med Assoc 1994; 205: 15691573.

    • Search Google Scholar
    • Export Citation
  • 6. Reimer JM, Reef VB, Sweener RW. Ventricular arrhythmias in horses: 21 cases (1984–1989). J Am Vet Med Assoc 1992; 201: 12371243.

  • 7. Stern JA, Doreste YR & Barnett S, et al. Resolution of sustained narrow complex ventricular tachycardia and tachycardia-induced cardiomyopathy in a Quarter Horse following quinidine therapy. J Vet Cardiol 2012; 14: 445451.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8. Miller MW, Fox PR, Saunders AB. Pathologic and clinical features of infectious endocarditis. J Vet Cardiol 2004; 6: 3543.

  • 9. Porter SR, van Galen G & Sandersen C, et al. Vegetative endocarditis in equids (1994–2006). J Vet Intern Med 2008; 22: 14111416.

  • 10. Nath LC, Anderson GA & Hinchcliff KW, et al. Clinicopathologic evidence of myocardial injury in horses with acute abdominal disease. J Am Vet Med Assoc 2012; 241: 12021208.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11. Nostell K, Brojer J & Hoglund K, et al. Cardiac troponin I and the occurrence of cardiac arrhythmias in horses with experimentally induced endotoxaemia. Vet J 2012; 192: 171175.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12. de Gennaro L, Brunetti ND & Cuculo A, et al. Increased troponin levels in nonischemic cardiac conditions and noncardiac diseases. J Interv Cardiol 2008; 21: 129139.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13. Kittleson M. Diagnosis and treatment of arrhythmias (dysrhythmias). In: Kittleson M, Kienle R, eds. Small animal cardiovascular medicine. St Louis: Mosby Inc, 1998; 449494.

    • Search Google Scholar
    • Export Citation
  • 14. Mogg TD. Equine cardiac disease: clinical pharmacology and therapeutics. Vet Clin North Am Equine Pract 1999; 15: 523534.

Contributor Notes

Address correspondence to Dr. Leach (leachsb@missouri.edu).
  • Figure 1—

    Three-lead ECG tracings acquired from a horse that was evaluated because of a 5-day history of hypoalbuminemia and facial edema that progressed to ventral edema. Notice the narrow-complex tachycardia (QRS complex duration, 0.12 seconds) with a right bundle branch block morphology (left ventricular origin) and positively deflected T waves in lead II. Nonconducted P waves (black arrows) are occasionally buried within the QRS complexes, ST segments, and T waves, confirming atrioventricular dissociation. The atrial rate is approximately 40 beats/min, and the ventricular rate is approximately 100 beats/min. Paper speed = 25 mm/s; 1 cm = 1 mV.

  • Figure 2—

    Three-lead ECG tracings acquired following IV administration of a third bolus of lidocaine hydrochloride to the horse in Figure 1. Narrow-complex ventricular tachycardia is evident in the first 6 complexes. The rhythm temporarily converts to a sinus rhythm before returning to ventricular tachycardia. The QRS complex and T-wave morphologies of the sinus-originated complexes are distinctly different from the morphologies of the complexes recorded during the tachycardia. The sinus-capture complexes and response to lidocaine confirm that the tachycardia is ventricular in nature. Paper speed = 25 mm/s; 1 cm = 1 mV.

  • 1. Reef VB. Equine diagnostic ultrasound. Philadelphia: WB Saunders Co, 1998; 215272.

  • 2. van Loon G, Patteson M. Electrophysiology and arrhythmogenesis. In: Marr CM, Bowen M, eds. Cardiology of the horse. 2nd ed. Edinburgh: Elsevier Ltd, 2010;5973.

    • Search Google Scholar
    • Export Citation
  • 3. McGuirk SM, Muir WW. Diagnosis and treatment of cardiac arrhythmias. Vet Clin North Am Equine Pract 1985; 1: 353370.

  • 4. Reef VB, Marr CM. Dysrhythmias: assessment and medical management. In: Marr CM, Bowen M, eds. Cardiology of the horse. 2nd ed. Edinburgh: Elsevier Ltd, 2010;159178.

    • Search Google Scholar
    • Export Citation
  • 5. Traub-Dargatz JL, Schlipf JW Jr & Boon J, et al. Ventricular tachycardia and myocardial dysfunction in a horse. J Am Vet Med Assoc 1994; 205: 15691573.

    • Search Google Scholar
    • Export Citation
  • 6. Reimer JM, Reef VB, Sweener RW. Ventricular arrhythmias in horses: 21 cases (1984–1989). J Am Vet Med Assoc 1992; 201: 12371243.

  • 7. Stern JA, Doreste YR & Barnett S, et al. Resolution of sustained narrow complex ventricular tachycardia and tachycardia-induced cardiomyopathy in a Quarter Horse following quinidine therapy. J Vet Cardiol 2012; 14: 445451.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8. Miller MW, Fox PR, Saunders AB. Pathologic and clinical features of infectious endocarditis. J Vet Cardiol 2004; 6: 3543.

  • 9. Porter SR, van Galen G & Sandersen C, et al. Vegetative endocarditis in equids (1994–2006). J Vet Intern Med 2008; 22: 14111416.

  • 10. Nath LC, Anderson GA & Hinchcliff KW, et al. Clinicopathologic evidence of myocardial injury in horses with acute abdominal disease. J Am Vet Med Assoc 2012; 241: 12021208.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11. Nostell K, Brojer J & Hoglund K, et al. Cardiac troponin I and the occurrence of cardiac arrhythmias in horses with experimentally induced endotoxaemia. Vet J 2012; 192: 171175.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12. de Gennaro L, Brunetti ND & Cuculo A, et al. Increased troponin levels in nonischemic cardiac conditions and noncardiac diseases. J Interv Cardiol 2008; 21: 129139.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13. Kittleson M. Diagnosis and treatment of arrhythmias (dysrhythmias). In: Kittleson M, Kienle R, eds. Small animal cardiovascular medicine. St Louis: Mosby Inc, 1998; 449494.

    • Search Google Scholar
    • Export Citation
  • 14. Mogg TD. Equine cardiac disease: clinical pharmacology and therapeutics. Vet Clin North Am Equine Pract 1999; 15: 523534.

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