An Analysis of Arrhythmias Induced by Ouabain in Intact Dogs

Abstract

The results of this study show that ouabain administration quite often causes idioventricular automaticity to undergo an initial depression and a subsequent enhancement. When the electrocardiogram shows normal sinus rhythm these changes in ventricular automaticity can be unmasked by vagal stimulation which causes either sinus arrest or atrioventricular block. On occasion, the depression of idioventricular automaticity is permanent; if ouabain produces complete atrioventricular block at this time, ventricular arrest ensues. When, on the contrary, the automaticity of Purkinje fibers is progressively enhanced, a stage is reached in which the idioventricular rhythm becomes faster than the sinus rhythm. Eventually the basic ventricular rhythm exhibits pauses during which electrocardio-graphic complexes of different form become apparent. The second class of arrhythmias comprises extrasystoles which may or may not show a constant coupling to sinus beats but which are characterized by a dependence on an initiating beat. It was demonstrated in this investigation that these extra beats appear during slow intravenous administration of ouabain and that they disappear not only on suppression but also on slowing of the sinus rhythm. Furthermore, it was shown that bigeminal rhythm may be transformed into extrasystoles occurring after every second sinus beat by means of vagal stimulation which slows the sinus rate. If, however, the heart was driven at faster rate, several extrasystoles followed one atrial beat. At a more advanced stage of ouabain intoxication these extrasystoles lose their fixed relationship with the sinus beat and runs of self-sustaining tachycardia appear. Such runs of ventricular tachycardia are unaffected by vagal stimulation but have a tendency to subside, spontaneously, and start anew after another initiating sinus beat. If vagal stimulation inhibits the initiating beat, the run of tachycardia also is suppressed. At an advanced stage of intoxication, however, when polymorphic ventricular complexes are present, vagal stimulation no longer produces any apparent effects. Finally, this investigation has shown that, during vagal stimulation which produces sinus arrest or A-V block, atrial fibrillation can be initiated by retrograde transmission of ventricular escape beats even though atrial escape beats are ineffective in eliciting the same phenomenon.