Abstract
The relationship between the action of acetyl strophanthidin and pacemaker stimuli was studied experimentally. In all animals, single pacemaker impulses were able to induce repetitive firing immediately before the appearance of the glycoside-induced tachycardia, as well as up to 30 minutes after its disappearance. This phenomenon was seen with impulses falling in any part of diastole, as well as in the responsive portion of systole. Hence, vulnerability could be ruled out as the underlying mechanism. The intensities required for repetition were as low as control threshold values. It appears that electrical stimuli with intensities in the range of those used in commercially available pacemakers can unmask concealed digitalis toxicity. It is possible that this peculiar type of sensitivity to pacemaker stimuli in digitalized animals could be due to a loss of cellular potassium induced by the electrical discharge.
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