Experimental studies on auricular flutter and auricular fibrillation

Injection of aconitine into the region of the head of the sinus node causes auricular tachycardia with a rate between 200 and 400 per minute. Often auricular fibrillation appears spontaneously or follows vagus stimulation. The change of the auricular tachycardia into fibrillation and vice versa, which was ofter registered, shows that the auricular tachycardia is auricular flutter and not “paroxysmal auricular tachycardia”.Cooling of the focus of injection immediately abolishes the fibrillation which reappears when the cooling is interrupted. These results cannot be explained by the circus movement theory of Lewis. They can only be explained by assuming that auricular flutter and fibrillation are initiated by rapid impulse formation in a single center. As the impulses thus formed move into the larger mass of auricular muscle, islands of refractory tissue appear, which cause a weaving and interweaving of the contraction process that is characteristic of fibrillation.The increase of auricular rate during vagus stimulation in the presence of auricular flutter is caused by a direct action of the vagus on the center of stimulus formation. Shortening of the refractory phase increases the rate of stimulus formation.When flutter originates in the auricular appendices the increase in rate during vagus stimulation is greater than when it originates in the area of the sinus node. The vagus effect on the refractory phase seems to be less pronounced on specific tissue than on auricular muscle.