A 20-year-old 407-kg (895-lb) Appaloosa gelding was evaluated at a veterinary teaching hospital because of tachycardia and tachypnea. Seven hours prior, the horse was inappetent and lethargic and had bilateral jugular venous pulsation. There was no known toxin exposure. The horse was treated with flunixin meglumine and referred for evaluation.
Physical examination revealed dull mentation, dark pink mucous membranes with a prolonged capillary refill time, moderate tachypnea (respiratory rate, 46 breaths/min), severe tachycardia (heart rate, 120 beats/min), bilateral jugular pulsations to the level of the ramus of the mandible, and hypokinetic digital and facial arterial pulse quality. Gastrointestinal borborygmi were absent.
A CBC, serum biochemical analysis, and venous blood gas assessment revealed erythrocytosis (Hct, 50.6%; reference range, 26.6% to 42.2%), hyperglycemia (151 mg/dL; reference range, 73 to 113 mg/dL), high creatinine concentration (2.9 mg/dL; reference range, 1.0 to 1.7 mg/dL), hyperphosphatemia (5.9 mg/dL; reference range, 2.1 to 4.1 mg/dL), hypocalcemia (10.7 mg/dL; reference range, 11 to 13.2 mg/dL), hypochloremia (94 mmol/L; reference range, 98 to 103 mmol/L), high anion gap (29.6 mEq/L; reference range, 10 to 15.2 mEq/L), and hyperlactatemia (7.4 mmol/L; reference range, < 2 mmol/L). Abdominal ultrasonography revealed mild intestinal hypomotility. Echocardiography revealed mild mitral and tricuspid valve regurgitation, mild aortic valve thickening, normal systolic function, and volume underloading. Cardiac troponin I (cTnI) concentration was considered undetectable (< 0.2 ng/mL; reference range, < 0.2 mg/mL). The results of ELISAs to detect antibodies against Streptococcus equi M protein and against equine herpesvirus-1 were 1:800 and 1:160, respectively. The results of equine influenza A hemagglutination inhibition testing were positive (H7N7, 1:10; H3N8 [KY], 1:160; and H3N8 [Miami], 1:40). Base-apex ECG was performed.
ECG Interpretation
The base-apex ECG revealed wide-complex tachycardia consistent with sustained ventricular tachycardia at a rate of 140 beats/min (Figure 1). Initial treatment included IV administration of lidocaine hydrochloride (bolus of 1.5 mg/kg followed by continuous rate infusion of 0.05 mg/kg/min [0.023 mg/lb/min]), magnesium sulfate (25 g over a 25-minute period), and lactated Ringer solution supplemented with calcium gluconate (50 mL/kg/d [22.7 mL/lb/d]) and intranasal administration of oxygen (10 L/min).
Initial base-apex lead ECG recording obtained from a 20-year-old 407-kg (895-lb) horse that was evaluated because of tachycardia and tachypnea. Seven hours prior, the horse was inappetent and lethargic and had bilateral jugular venous pulsations. The heart rate is 140 beats/min, and the QRS complexes are wide and bizarre. There are no discernible P waves. The rhythm was interpreted as ventricular tachycardia. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.714
Initial base-apex lead ECG recording obtained from a 20-year-old 407-kg (895-lb) horse that was evaluated because of tachycardia and tachypnea. Seven hours prior, the horse was inappetent and lethargic and had bilateral jugular venous pulsations. The heart rate is 140 beats/min, and the QRS complexes are wide and bizarre. There are no discernible P waves. The rhythm was interpreted as ventricular tachycardia. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.714
Initial base-apex lead ECG recording obtained from a 20-year-old 407-kg (895-lb) horse that was evaluated because of tachycardia and tachypnea. Seven hours prior, the horse was inappetent and lethargic and had bilateral jugular venous pulsations. The heart rate is 140 beats/min, and the QRS complexes are wide and bizarre. There are no discernible P waves. The rhythm was interpreted as ventricular tachycardia. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.714
The heart rate and rhythm remained unchanged after several hours, although the serum concentrations of electrolytes normalized and the concentrations of lactate and creatinine decreased (2.0 mmol/L and 2.2 mg/dL, respectively). Intravenous administration of lidocaine was continued (0.05 mg/kg/min) overnight (approx 23 hours total). On day 2 of hospitalization, the horse developed inspiratory wheezes, crackles, and ventral midline edema. Fluid therapy was discontinued, and 3 individual boluses of furosemide were administered (1.2 mg/kg/bolus [0.55 mg/lb/bolus], IV) over a period of 5 hours. Magnesium sulfate (25 g, IV) was administered again with no change in the heart rate or rhythm. Assessment of serum cTnI concentration was repeated and remained undetectable (< 0.2 ng/mL). The wide-complex tachycardia continued at a rate of 140 beats/min without interruption since hospital admission.
On the second afternoon of hospitalization, procainamide hydrochloride was administered IV (20 mg/kg [9.1 mg/lb] over a 20-minute period), and the rhythm converted to sinus tachycardia with a rate of 60 beats/min at 30 minutes after completion of the infusion (Figure 2). Rate slowing and rhythm conversion allowed detection of notched P waves with a consistent PR interval (440 milliseconds; reference range,1 220 to 560 milliseconds), demonstrating an association with the widened QRS complexes. The consistent PR relationship indicated that the tachycardia was supraventricular with aberrant ventricular conduction. Lidocaine treatment was discontinued, and sotalol hydrochloride administration (1 mg/kg [0.45 mg/lb], PO, q 12 h) was initiated. Sinus rhythm remained, and the rate progressively slowed to 50 beats/min. The horse was treated with furosemide (1.2 mg/kg, IV, q 12 h) for an additional 48 hours until resolution of the peripheral edema and tachypnea.
Base-apex lead ECG recording obtained from the horse in Figure 1 at the time of conversion (A) and 10 minutes after conversion (B) to sinus rhythm (heart rate, 50 beats/min) following a single dose of procainamide hydrochloride (20 mg/kg [9.1 mg/lb], IV). At the slower heart rate, notched P waves can be seen (arrowheads). The QRS complexes remain wide, consistent with aberrant ventricular conduction. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.714
Base-apex lead ECG recording obtained from the horse in Figure 1 at the time of conversion (A) and 10 minutes after conversion (B) to sinus rhythm (heart rate, 50 beats/min) following a single dose of procainamide hydrochloride (20 mg/kg [9.1 mg/lb], IV). At the slower heart rate, notched P waves can be seen (arrowheads). The QRS complexes remain wide, consistent with aberrant ventricular conduction. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.714
Base-apex lead ECG recording obtained from the horse in Figure 1 at the time of conversion (A) and 10 minutes after conversion (B) to sinus rhythm (heart rate, 50 beats/min) following a single dose of procainamide hydrochloride (20 mg/kg [9.1 mg/lb], IV). At the slower heart rate, notched P waves can be seen (arrowheads). The QRS complexes remain wide, consistent with aberrant ventricular conduction. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.714
The horse remained in sinus rhythm, and the duration of the widened QRS complexes decreased to 210 milliseconds (Figure 3) throughout the next 4 days of hospitalization. Auscultation during sinus rhythm revealed a grade 3/6 left basilar diastolic murmur. Repeated echocardiography revealed mild aortic valve insufficiency, mild pulmonic valve insufficiency, and a small, hyperechoic focus at the tip of the anterior papillary muscle. The left ventricle remained volume underloaded, most likely secondary to furosemide administration, although hypertrophic cardiomyopathy or infiltrative disease could not be ruled out.
Base-apex lead ECG recording obtained from the horse in Figure 1 three days after conversion to sinus rhythm following the single dose of procainamide. The heart rate remains mildly elevated (50 beats/min), but sinus rhythm persists. The duration of the QRS complexes has further decreased to 210 milliseconds (arrow), and the P waves have a clearly recognizable notched morphology (arrowheads). Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.714
Base-apex lead ECG recording obtained from the horse in Figure 1 three days after conversion to sinus rhythm following the single dose of procainamide. The heart rate remains mildly elevated (50 beats/min), but sinus rhythm persists. The duration of the QRS complexes has further decreased to 210 milliseconds (arrow), and the P waves have a clearly recognizable notched morphology (arrowheads). Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.714
Base-apex lead ECG recording obtained from the horse in Figure 1 three days after conversion to sinus rhythm following the single dose of procainamide. The heart rate remains mildly elevated (50 beats/min), but sinus rhythm persists. The duration of the QRS complexes has further decreased to 210 milliseconds (arrow), and the P waves have a clearly recognizable notched morphology (arrowheads). Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 6; 10.2460/javma.253.6.714
The horse was discharged from the hospital after 6 days; the predischarge ECG recording indicated the persistence of sinus rhythm (heart rate, 50 beats/min) and mild QRS complex widening (210 milliseconds; reference range,2 ≤ 140 milliseconds). Sotalol (1 mg/kg, PO, q 12 h) was continued, and recheck ECG, echocardiography, and assessment of circulating antiviral antibody titers were recommended 2 weeks after discharge. The horse was not returned for follow-up evaluation. A second episode of recumbency occurred 6 months after discharge from the hospital, and the horse's condition improved after short-term sotalol treatment. Approximately 105 days after the second episode, the referring veterinarian reported that the horse had been doing well since this event without any cardiac medications.
Discussion
Differentiation of ventricular tachycardia from wide-complex supraventricular tachycardia can be challenging in patients with fast heart rates because P waves may be buried in the preceding T waves. In the horse of the present report, the tachyarrhythmia was initially interpreted as ventricular tachycardia; however, there was no response to IV treatment with lidocaine or magnesium. Treatment with procainamide converted the tachyarrhythmia to sinus rhythm and revealed an association between P waves and the widened QRS complexes. Although supraventricular tachyarrhythmias in horses have been reported,1,3,4 there are no publications describing wide-complex supraventricular tachycardia, to the authors' knowledge. The cause of the QRS complex widening in the case described in the present report was unknown; however, the QRS complex duration progressively decreased to a near-normal value during hospitalization. The extensive group B Purkinje system of equids should preclude a ventricular conduction delay that would be detectable on surface ECG tracings,5 so we presumed there was considerable injury to these conduction fibers. This horse appeared to have had a reversible ventricular conduction disturbance associated with supraventricular tachycardia.
The underlying cause of the arrhythmia in the horse of the present report was not determined. Arrhythmias in horses can be attributable to primary cardiac disease, acute infectious disease, or physiologic imbalances.1 The horse of the present report had several serum electrolyte abnormalities at the time of the referral evaluation, but correction of those abnormalities with fluid therapy did not resolve the tachyarrhythmia. Notable structural cardiac disease was not identified echocardiographically, and primary gastrointestinal disease was an unlikely cause of the arrhythmia given the lack of clinical signs referent to the gastrointestinal tract. Results of assessments of serum antibodies against S equi M protein and equine herpesvirus-1 and equine influenza A hemagglutination inhibition testing were consistent with prior vaccination or exposure. Testing of convalescent serum antibody titers was recommended but not performed; thus, an acute viral infection could not be excluded. The repeated lack of an increase in serum cTnI concentration did not support active myocardial injury, which was unexpected because of the sustained tachycardia, focal papillary muscle hyperechogenicity, and ventricular conduction disturbance. Autoantibodies against cTnI have been identified in humans and mice and can falsely decrease measured circulating cTnI concentration.6,7 This phenomenon has not been studied in horses, but is a potential explanation for the apparently normal serum cTnI concentration in the horse of the present report. It is also possible that there was no major cardiomyocyte damage.
Procainamide, a class Ia antiarrhythmic agent, affects sodium and potassium channels to prolong the effective refractory period, decrease automaticity, and slow conduction.8 The active metabolite of procainamide, N-acetylprocainamide, also affects cardiac potassium channels to further prolong the action potential duration and the effective refractory period. The pharmacokinetics of procainamide has been studied in horses, and the drug has been used to treat supraventricular tachycardia in this species.9,10 The half-life of procainamide is 3.5 hours, whereas the half-life of N-acetylprocainamide is 6.3 hours; this allows procainamide to have lasting effects after administration in horses.9 In humans, N-acetylprocainamide can accumulate with procainamide redosing, causing either increased therapeutic or toxic blood concentrations. This has not been investigated in horses but should be considered when treatment with procainamide is repeated.9 For the horse of the present report, repeated procainamide administration was unnecessary. Treatment with sotalol, a nonselective β-adrenergic receptor blocker and class III antiarrhythmic agent, was selected to reduce the risk of arrhythmia recurrence. Sotalol decreases sympathetic tone and prolongs repolarization and the effective refractory period. The sotalol dosage for this horse was based on prior research findings that oral bioavailability of the drug in horses was 48% with no adverse effects when given orally at a dose of 1 mg/kg twice daily.11
Successful conversion of wide-complex supraventricular tachycardia was achieved after a single dose of procainamide in the horse of the present report. The associated conduction aberrancy that masked the supraventricular aspect of the tachycardia has not previously been reported for horses, to the authors' knowledge. Although the QRS complex widening resolved during hospitalization, the recurrence of clinical signs after discontinuation of sotalol treatment suggested that the substrate for arrhythmogenesis persisted in this horse.
Acknowledgments
No third-party funding or support was received in connection with this study or the writing or publication of the manuscript. The authors declare that there were no conflicts of interest.
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