Cardiac glycosides and drugs used in dysrhythmias

Abstract

This chapter discusses cardiac glycosides and drugs used in dysrhythmias. N-Acetylprocainamide prolongs the QT interval, and it is therefore, not surprising that it has been reported to cause polymorphic ventricular tachycardias. In all cases the QT interval was prolonged. Since N-acetylprocainamide is eliminated by the kidneys it accumulates in renal failure, and renal failure was the chief risk factor in the cardiovascular toxicity seen in these cases. The pharmacology, clinical pharmacology, and adverse effects of amiodarone have recently been the subjects of a monograph, and the adverse effects of amiodarone have also been thoroughly reviewed. The short-term antidysrhythmic effect of amiodarone during programmed electrical stimulation has hitherto proved disappointing as a predictor of the subsequent long-term therapeutic efficacy of amiodarone. The mechanism whereby amiodarone enhances the anticoagulant action of warfarin has not previously been formally elucidated, although it has been thought to be due to inhibition of warfarin metabolism. All antidysrhythmic drugs have the potential for causing dysrhythmias, which has been discussed in the chapter.