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Summary The principal effects of cardiac glycosides probably can be classified as parasympathomimetic or sympathomimetic. Data from animals and from man suggest that polar cardiac glycosides, such as ouabain and digoxin, possess greater parasympathomimetic (vagal) cardiac effect for a given amount of sympathomimetic (positive inotropic) cardiac effect than do less polar cardiac glycosides, such as digitoxin. Polar glycosides therefore offer some advantage in uncomplicated paroxysmal atrial tachycardia and in uncomplicated atrial flutter and atrial fibrillation when the principal desired effect is reduction in the number of atrial impulses reaching the ventricles or conversion to normal sinus rhythm. Non-polar glycosides offer an advantage when positive inotropicity is desired but when there is some degree of atrioventricular block or when inappropriate sinus bradycardia or anorexia, nausea, or vomiting are present. Ectopic impulse formation when due to cardiac glycosides is a toxic manifestation of excessive sympathomimetic effect, but is aggravated by vagal-induced sinus bradycardia, so that both parasympathomimetic and sympathomimetic capability of cardiac glycosides must be considered when dealing with myocardial electrical instability.

Patients with accelerated atrioventricular conduction are peculiarly prone to paroxysmal atrial tachycardia and atrial fibrillation, which with the conduction anomaly result in very rapid arrhythmias, producing bizarre electrocardiograms. The pseudo bundle branch block causes the development of pseudoventricular complexes and the accelerated atrioventricular conduction gives rise to high ventricular rates that are alarming. These are usually more rapid than the simulated serious ventricular mechanism disorders. The importance of taking the seemingly good general status of the patient into consideration in electrocardiographic interpretation is emphasized. The diagnostic criteria have been set forth with emphasis on the presence of a P wave on every complex in the tachycardia and short runs of definite supraventricular fibrillation with narrow QRS in between the bizarre pseudoventricular runs of complexes. Some of the cases of a paroxysmal ventricular tachycardia and some of the cases of paroxysmal ventricular fibrillation with recovery reported in the literature are probably of this pseudoventricular disorder. The relatively excellent prognosis of the pseudo type is emphasized. However, it must be remembered that, in a rare case, the patient has died suddenly in a paroxysm of tachycardia. The relatively prompt and satisfactory response to procaine amide intravenously has been demonstrated. Some patients seem to be somewhat refractory to quinidine during a paroxysm and digitalization does not effectively slow the ventricular rate in this type of atrial fibrillation and accelerated conduction. The probable pathophysiology of these pseudoventricular paroxysms, tachycardia, or fibrillation have been discussed. The conspicuously high ventricular rates are the result of the accelerated A-V transmission. The clinical axiom follows that the presence of ventricular paroxysmal disorders, regular or irregular, with rates above 240 is presumptive evidence of the presence of accelerated A-V conduction as the fundamental cardiac mechanism disorder in the patient.