TREATMENT OF ATRIAL-FIBRILLATION IN HORSES - NEW PERSPECTIVES

Forty-one horses were treated for atrial fibrillation (AF) with 22 mg/ kg quinidine sulfate via nasogastric tube every 2 hours until conversi on to sinus rhythm, a cumulative dose of 88 to 132 mg/kg had been admi nistered in 2-hour increments, or the horse had adverse or toxic effec ts from the drug, Treatment intervals were prolonged to every 6 hours if conversion had not occurred. Digoxin was administered before treatm ent if the horse had a fractional shortening less than or equal to 27% (3 horses), was prone to tachycardia (resting heart rate greater than or equal to 60 beats/min) (1 horse), or had a previous history of sus tained tachycardia of over 100 beats/min during prior conversion (3 ho rses). Digoxin was administered during day 1 of quinidine sulfate trea tment if the horse developed a sustained tachycardia of over 100 beats /min during treatment (1 1 horses) or on day 2 if conversion had not o ccurred (7 horses). Plasma quinidine concentrations within 1 hour of c onversion of AF to sinus rhythm ranged from 1.7 to 7.5 mu g/mL (mean, 4.05 +/- 1.6) and ranged from 1.7 to 4.7 mu g/mL in 97% of horses. Mos t horses (92%) with plasma quinidine concentrations >5 mu g/mL exhibit ed an adverse or toxic effect of quinidine sulfate (clinical or electr ocardiographic). There was no statistical association between plasma q uinidine concentrations and sustained tachycardia (>100 beats/min), di arrhea, or colic. Ataxia and upper respiratory tract strider were sign ificantly associated with plasma quinidine concentrations. In most ins tances (98%) conversion did not occur while toxic or adverse effects o f quinidine sulfate were present or when plasma quinidine concentratio ns were >5 mu g/mL.