ECG of the Month

Amy L. Johnson Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

Search for other papers by Amy L. Johnson in
Current site
Google Scholar
PubMed
Close
 DVM, DACVIM
,
Sophy A. Jesty Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

Search for other papers by Sophy A. Jesty in
Current site
Google Scholar
PubMed
Close
 DVM, DACVIM
,
Anna R. M. Gelzer Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

Search for other papers by Anna R. M. Gelzer in
Current site
Google Scholar
PubMed
Close
 DMV, DACVIM
,
Thomas J. Divers Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

Search for other papers by Thomas J. Divers in
Current site
Google Scholar
PubMed
Close
 DVM, DACVIM, DACVECC
, and
Marc S. Kraus Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

Search for other papers by Marc S. Kraus in
Current site
Google Scholar
PubMed
Close
 DVM, DACVIM

A 10-year-old 533-kg (1,172.6-lb) Warmblood gelding was evaluated after being found recumbent in a pasture with a fever (39.1°C [102.4°F]), loose feces, and tachycardia (rate unknown). On evaluation (day 1) at the university veterinary hospital, the horse was sweating profusely, agitated, and ambulatory but weak. Frequently, the horse postured and strained as if to urinate, but voided only small amounts of urine. Severe tachycardia (180 to 200 beats/min; reference range, 28 to 40 beats/min) with pounding heart sounds and a regular rhythm, prominent jugular pulses, and tachypnea (88 breaths/min; reference range, 8 to 20 breaths/min) were detected. Mucous membranes were dark pink with petechiae, and gastrointestinal tract sounds were severely diminished. Initial hematologic abnormalities included mild neutrophilia (9,000 cells/μL; reference range, 3,000 to 7,000 cells/μL) and lymphopenia (1,100 cells/μL; reference range, 1,800 to 5,000 cells/μL), severe thrombocytopenia (8,000 platelets/μL; reference range, 100,000 to 600,000 platelets/μL), and high PCV (55%; reference range, 31% to 47%). Serum biochemical analyses revealed high creatinine concentration (3.5 mg/dL; reference range, 0.4 to 2.2 mg/dL). The horse was treated with hypertonic saline (7.5% NaCl) solution (4 mL/kg [1.8 mg/lb], IV), isotonic crystalloid fluids (60 mL/kg/d [27 mL/lb/d], IV), magnesium sulfate (25 g in 1 L of 0.9% NaCl, IV, administered during a 15-minute period [3.33 mg/kg/min {1.5 mg/lb/min}]), lidocaine (0.6 mg/kg [0.27 mg/lb], IV, administered during a 15-minute period), and dexamethasone (0.06 mg/kg [0.027 mg/lb], IV, once).

ECG Interpretation

At the initial evaluation, ECG revealed sustained monomorphic ventricular tachycardia (200 beats/min; Figure 1). Concurrent atrial fibrillation could not be confirmed or refuted on the basis of the ECG tracing. One hour later, after treatment with magnesium sulfate, the horse's clinical condition and ECG findings remained unchanged. Two hours after the initial ECG evaluation was performed and after treatment with lidocaine, atrial fibrillation (60 to 68 beats/min; Figure 2) was detected. After development of atrial fibrillation and a considerable decrease in heart rate, the horse immediately appeared to relax and began eating hay. No additional antiarrhythmic drugs were administered during the initial treatment period.

Figure 1—
Figure 1—

Inverted base apex lead ECG trace obtained during the initial evaluation of a horse that was found recumbent with a fever, loose feces, and tachycardia. Notice the rapid sustained ventricular tachycardia (heart rate, 200 beats/min). Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 231, 5; 10.2460/javma.231.5.706

Figure 2—
Figure 2—

Inverted base apex lead ECG trace obtained from the horse in Figure 1 approximately 2 hours after admission (following treatment with magnesium and lidocaine). Notice the supraventricular rhythm (heart rate, approx 65 beats/min) with irregularly irregular R-R intervals and absence of identifiable P waves. The baseline between QRS complexes is undulating with small F waves, which is indicative of rapid activation of the atria from atrial fibrillation. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 231, 5; 10.2460/javma.231.5.706

Approximately 8 hours after admission, ECG evaluation revealed sinus tachycardia with frequent ventricular premature depolarizations (Figure 3). Repeated hematologic assessments revealed leukopenia (3,300 WBCs/μL; reference range, 5,500 to 12,500 WBCs/μL) and worsening thrombocytopenia (5,000 platelets/μL). The horse was treated with a higher dose of dexamethasone (0.14 mg/kg [0.06 mg/lb], IV, once) and with enrofloxacin (7.5 mg/kg [3.4 mg/lb], IV, q 24 h). The horse remained in sinus tachycardia for approximately 12 hours, at which time ECG findings included atrioventricular dissociation and a rapid idioventricular rhythm. The idioventricular rhythm persisted for approximately 4 hours, and then the horse again developed atrial fibrillation with frequent ventricular premature depolarizations (singlets, couplets, and triplets; Figure 4).

Figure 3—
Figure 3—

Inverted base apex lead ECG trace obtained from the horse in Figure 1 approximately 8 hours after admission to the hospital. Sinus tachycardia is evident (heart rate, 70 beats/min), and there are occasional ventricular premature beats (arrow). Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 231, 5; 10.2460/javma.231.5.706

Figure 4—
Figure 4—

Base apex lead ECG trace obtained from the horse in Figure 1 approximately 24 hours after admission to the hospital. Notice atrial fibrillation with occasional ventricular premature depolarizations (couplet and a single ventricular premature contraction [S]). Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 231, 5; 10.2460/javma.231.5.706

On day 3, more extensive clinicopathologic services were available. The horse had mild anemia (Hct, 30%; reference range, 31% to 47%), mild neutrophilia (8,300 cells/μL; reference range, 2,700 to 6,600 cells/μL), severe lymphopenia (300 cells/μL; reference range, 1,600 to 6,600 cells/μL), and thrombocytopenia (52,000 platelets/μL; reference range, 98,000 to 246,000 platelets/μL); serum concentrations of urea nitrogen (37 mg/dL; reference range, 9 to 20 mg/dL) and creatinine (3 mg/dL; reference range, 0.9 to 1.8 mg/dL) were high. Serum activities of aspartate aminotransferase (1,109 U/L; reference range, 212 to 426 U/L), sorbitol dehydrogenase (130 U/L; reference range, 2 to 11 U/L), alkaline phosphatase (318 U/L; reference range, 75 to 220 U/L), γ-glutamyltransferase (76 U/L; reference range, 8 to 33 U/L), and creatine kinase (852 U/L; reference range, 93 to 348 U/L) were high. Coagulation assays revealed clotting times and antithrombin III activity that were within reference limits. Echocardiography revealed a globoid, dilated left ventricle with poor systolic function and a mildly dilated left atrium. Fractional shortening was low (19%; reference range, 33% to 43%). Mild regurgitation of the tricuspid, mitral, and aortic valves was evident. No vegetative valvular lesions were present.

From days 3 through 8, atrial fibrillation persisted; the horse's heart rate ranged from 60 to 80 beats/min. The frequency of ventricular premature beats decreased notably during that period. On day 3, dexamethasone treatment was decreased to 0.12 mg/kg (0.05 mg/lb), IV, once daily and continued for a total of 3 days. On day 6, the horse developed signs of acute, severe laminitis and dexamethasone treatment was stopped. Phenylbutazone (4 mg/kg, IV) and pentoxifylline (8.4 mg/kg [3.8 mg/lb], PO) were administered twice daily, and supportive foot treatments (eg, ice immersion and application of sole support pads) were initiated. Fluid therapy was discontinued. By day 7, the signs of laminitis had resolved and the horse had no residual lameness. On day 9, ECG findings indicated that the horse had converted to sinus rhythm (48 to 60 beats/min). By day 10, all serum enzyme abnormalities had resolved or were decreasing toward reference ranges, with the exception of creatinine concentration, which remained high. Administrations of enrofloxacin, phenylbutazone, and pentoxifylline were discontinued on day 12.

During the course of the horse's visit, an extensive search for infection or neoplasia, including rectal examination, thoracic and abdominal ultrasonography, thoracic radiography, and cytologic evaluation of peritoneal fluid samples, failed to reveal any abnormalities. Serologic testing for viral (equine herpesvirus–1 and –4, equine influenza virus, equine arteritis virus, and equine rhinovirus–1 and –2), bacterial (Streptococcus equi subsp equi), and rickettsial (Neorickettsia risticii and Anaplasma phagocytophilium) infections was also pursued, but all results were negative or attributed to vaccination. Two plasma samples (collected 12 and 36 hours after admission) were tested for anti-platelet antibodies; results were within reference limits. At admission, serum cardiac troponin I (cTnI) concentration was high (0.98 ng/mL; reference range, 0.01 to 0.11 ng/mL); at approximately 8 hours after admission, serum cTnI concentration was much higher (30.74 ng/mL). Assessments of serum samples obtained on days 3, 4, and 13 revealed progressive decreases toward reference range (26.06, 8.13, and 0.21 ng/mL, respectively). The horse was discharged from the hospital on day 13, and the owners were given instructions to provide stall rest; no further medications were prescribed. Eight months after discharge, the horse was reportedly doing well at home.

Discussion

Ventricular tachycardia in horses has been associated with myocardial disease, electrolyte or acid-base imbalances, autonomic imbalances, systemic disease, and drug administration.1,2 Causes of myocardial disease resulting in ventricular tachycardia include viral or bacterial infection, parasite migration, metabolic insults, pericarditis or endocarditis, toxins (especially monensin), trauma, infarcts, and myocardial ischemiahypoxia.3 In the horse of this report, the arrhythmias and poor cardiac function that developed in the absence of septicemia, endotoxemia, or other severe systemic disease suggested a primary myocardial disease, such as myocarditis.

Serum cardiac troponin I concentrations were assessed in the horse of this report, and findings also supported primary myocardial disease. In horses, results of preliminary studies4,5 have indicated that assessment of cTnI concentration appears to be a sensitive and specific means of evaluating myocardial damage. In the horse of this report, serum cTnI concentrations were markedly high in multiple samples. However, the cause of the myocardial damage in the horse of this report was not determined. There was no evidence of neoplastic or systemic disease, and although a toxic etiology was considered, that was not confirmed. The horse was kept at a private farm with 3 other horses, none of which had any clinical signs. The 4 horses were pastured together, with no travel history for > 1 year. No recent changes in feed, management, or weather conditions were reported. Monensin exposure was considered unlikely because no other horses were affected and no new feed had been purchased. The horse was not ridden regularly and had not been ausculted by a veterinarian for at least 1 year prior to the examination at the hospital; thus, subclinical cardiac abnormalities (such as preexisting atrial fibrillation) could not be ruled out. However, the horse's relatively rapid recovery with supportive care and dexamethasone treatment suggested an acute problem rather than a chronic heart condition. Furthermore, if atrial fibrillation had been present before this episode of illness, the horse likely would not have converted to sinus rhythm. The severe thrombocytopenia was also difficult to explain because anti-platelet antibody assessments yielded results within reference range. Unfortunately, the samples were collected after the first dose of dexamethasone had been administered, which may have influenced the results. Coagulation assays did not identify any abnormalities, thereby ruling out disseminated intravascular coagulation as a cause of thrombocytopenia. The thrombocytopenia improved rapidly and there was no evidence of blood loss, indicative of adequate bone marrow production and no source of excessive platelet consumption. Therefore, an immune-mediated problem was considered the most likely explanation for the thrombocytopenia and, possibly, also for the myocarditis.

The horse of this report had signs of cardiovascular collapse and rapid ventricular tachycardia, necessitating rapid intervention with antiarrhythmic drugs. After the ventricular tachycardia ceased and the horse developed atrial fibrillation, no additional antiarrhythmic medications were administered because of the decreased heart rate. The horse continued to improve during the following week and eventually converted to sinus rhythm. It is unknown whether a single factor (time, stall rest, glucocorticoid administration, or other supportive treatment) resulted in the clinical improvement; the most likely scenario is that a combination of factors contributed to the positive outcome.

References

  • 1.

    Bonagura JD, Miller MS. Junctional and ventricular arrhythmias. J Equine Vet Sci 1985;5:347350.

  • 2.

    Reimer JM, Reef VB, Sweeney RW. Ventricular arrhythmias in horses: 21 cases (1984–1989). J Am Vet Med Assoc 1992;201:12371243.

  • 3.

    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
  • 4.

    Cornelisse CJ, SchottHC II & Olivier NB, et al. Concentration of cardiac troponin I in a horse with a ruptured aortic regurgitation jet lesion and ventricular tachycardia. J Am Vet Med Assoc 2000;217:231235.

    • Search Google Scholar
    • Export Citation
  • 5.

    Schwarzwald CC, Hardy J, Buccellato M. High cardiac troponin I serum concentration in a horse with multiform ventricular tachycardia and myocardial necrosis. J Vet Intern Med 2003;17:364368.

    • Search Google Scholar
    • Export Citation
All Time Past Year Past 30 Days
Abstract Views 80 0 0
Full Text Views 634 561 7
PDF Downloads 118 54 1
Advertisement