Hemodynamic and Electrocardiographic Effects of Disopyramide in Patients with Ventricular Arrhythmia

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Abstract
Antiarrhythmic and hemodynamic effects of i.v. disopyramide phosphate (1.7 mg/kg body weight over 2 min) were studied in 9 patients, several in various degrees of cardiac decompensation, with sinus rhythm and persistent ventricular ectopic beats (VEB). In 1 case with primary cardiomyopathy, with < 30 VEB/min, disopyramide (DE) abolished the arrhythmia for 30 min, but precipitated brief dyspnea. Other side-effects were tolerable and mainly attributable to anticholinergic effects of the drug. DE either abolished or significantly reduced the arrhythmia in all cases. For 30 min only 1 patient showed VEB, and in 3 patients no VEB were seen for 3 h. Changes in cardiac output and pulmonary artery (PAP) and central aortic pressures were measured in 8 patients. Negative inotropic effects were indicated in 7 by an increased diastolic PAP/stroke volume ratio and in 7 by a decreased central aortic (dp/dt)max [maximum change of pressure with temperature]. Patients with high control values for diastolic PAP showed marked reductions in cardiac output, stroke volume and stroke work. In predicting myocardial depressant effects of DE, the control values for diastolic PAP seemed to be superior to central venous pressure, cardiac index and systolic time intervals. Mean arterial pressure measured 5 and 10 min after drug administration showed no significant change, indicating that vasoconstrictor reflexes were well preserved, and a pressure level significantly above the control value was reached from the 20th min. DE is potent in suppressing VEBs but exerts negative inotropic effects that may be of clinical importance. The optimal antiarrhythmic dose is probably lower than that used in the present study.