Hemodynamic and inotropic effects of antiarrhythmic drugs used to treat paroxysmal supraventricular arrhythmias

Abstract

Episodes of sustained paroxysmal supraventricular tachycardias can be terminated by antiarrhythmic drugs given intravenously. The cardiodepressive effects of these drugs are an important limitation of this therapeutic procedure. The dose-dependent circulatory and myocardial effects of the nucleoside adenosine (0.5, 2.0, 5.0 mg/kg/minute) and the class I antiarrhythmic drug ajmaline (1.0, 2.0, 4.0 mg/kg) were investigated in 73 open-chest rats. Hemodynamic measurements in the intact circulation and isovolumic registrations (peak isovolumic left ventricular systolic pressure and peak isovolumic dP/dt_max) were compared with saline controls. Adenosine has a short-lasting, negative, chronotropic effect that causes a dose-dependent reduction of cardiac output (−34%, −54%, −65% vs control). The peak isovolumic left ventricular systolic pressure (LVSP) is not changed significantly by adenosine (−6%, −4%, +5% vs control). The negative chronotropic effect of ajmaline with consecutive reduction of cardiac output is less pronounced (cardiac output: −18%, −20%, −38% vs control). The highest dose of ajmaline causes a significant reduction of peak isovolumic LVSP (−2%, −1%, −7% vs control). Adenosine has an impressive negative chronotropic effect with a consequent marked decrease of cardiac output. The reduction of cardiac output by adenosine is more pronounced compared with ajmaline. Nevertheless, adenosine has—in contrast to ajmaline—no cardiodepressive effects in vivo.