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Disopyramide resembles quinidine electrophysiologically, but its effect on left ventricular function has not been clarified. Twelve awake dogs were instrumented for measurement of cardiac output, left ventricular pressure and its maximal first derivative (dP/dt max), and left atrial and aortic pressures. Disopyramide or quinidine at identical, clinically relevant doses (1 and 5 mg/kg i.v.) was infused over 5 minutes at each level. Peak changes after disopyramide 1 mg/kg included increases in heart rate (34%), mean aortic pressure (24%) and systemic vascular resistance (33%), and decreases in stroke volume (16%) and dP/dt max (19%). With disopyramide at 5 mg/kg these changes were of greater magnitude (e.g., dP/dt -- 36%). Quinidine at both doses caused no changes except a 13% decrease in vascular resistance at 5 mg/kg. Heart rate with disopyramide increased after propranolol (1 mg/kg i.v.), was unchanged after atropine (0.1 mg/kg i.v.), and slowed after propranolol and atropine. Phenoxybenzamine (2 mg/kg i.v.) did not prevent the rise in systemic vascular resistance produced by disopyramide. Thus, disopyramide in clinical dosages exerts opposing direct and indirect effects on cardiac pacemakers and, unlike quinidine, is a potent myocardial depressant and vasoconstrictor in the conscious dog.

Adverse hemodynamic effects of intravenous disopyramide compared with quinidine in conscious dogs.