MECHANISM OF AURICULAR FLUTTER AND FIBRILLATION

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Abstract
Topical application or subepicardial injn. of aconitine (0.05 cc. of a 0.05% soln. of aconitine crystals) into the head of the sinus node induced auricular fibrillation after vageetomy in 27 adult dogs. Cooling the Bite of injn. changed the fibrillation activity to flutter and then resulted in auricular paralysis. Fibrillation recurred on warming. In some instances the flutter resulting from cooling was of low rate with long auricular pauses between the cycle, with records resembling auricular paroxysmal tachycardia with A-V block. Alternation of cycle length during flutter was frequently present. Normal sinus rhythm was re-established by local appln. of K or quinidine. It is assumed that auricular flutter and auricular fibrillation are the result of rapid stimulus formation in one center with the appearance of islets of refractory tissue in the auricles (previously postulated by Lewis) forcing the excitation wave to take a circuitous path. Although vagal stimulation inhibits auricular activity in sinus tachycardia and certain types of auricular paroxysmal tachycardia, it increases the rate of auricular activity in the aconitine-induced irregularities. It is speculated that stimuli which are inhibited by vagal stimulation are rhythmically formed while auricular fibrillation and flutter and the aconitine irregularities are the result of continuous stimulation. The auricular response in the latter would then depend on the refractory period of auricular tissue and the changes induced by vagal stimulation would be the result of a shortening of the refractory phase induced by vagal stimulation.
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