Treatment of atrial fibrillation in horses: new perspectives.

Abstract

Forty-one horses were treated for atrial fibrillation (AF) with 22 mg/kg quinidine sulfate via nasogastric tube every 2 hours until conversion to sinus rhythm, a cumulative dose of 88 to 132 mg/kg had been administered in 2-hour increments, or the horse had adverse or toxic effects from the drug. Treatment intervals were prolonged to every 6 hours if conversion had not occurred. Digoxin was administered before treatment if the horse had a fractional shortening < or = 27% (3 horses), was prone to tachycardia (resting heart rate > or = 60 beats/min) (1 horse), or had a previous history of sustained tachycardia of over 100 beats/min during prior conversion (3 horses). Digoxin was administered during day 1 of quinidine sulfate treatment if the horse developed a sustained tachycardia of over 100 beats/min during treatment (11 horses) or on day 2 if conversion had not occurred (7 horses). Plasma quinidine concentrations within 1 hour of conversion of AF to sinus rhythm ranged from 1.7 to 7.5 micrograms/mL (mean, 4.05 +/- 1.6) and ranged from 1.7 to 4.7 micrograms/mL in 97% of horses. Most horses (92%) with plasma quinidine concentrations > 5 micrograms/mL exhibited an adverse or toxic effect of quinidine sulfate (clinical or electrocardiographic). There was no statistical association between plasma quinidine concentrations and sustained tachycardia (> 100 beats/min), diarrhea, or colic. Ataxia and upper respiratory tract stridor were significantly associated with plasma quinidine concentrations. In most instances (98%) conversion did not occur while toxic or adverse effects of quinidine sulfate were present or when plasma quinidine concentrations were > 5 micrograms/mL.