Abstract
Of the several theories which have been advanced to explain auricular and ventricular fibrillation 2 have been very widely accepted. One, advocated by Rothberger 1 and Scherf, 2 is that fibrillation is due to one or several foci sending out impulses at a very rapid rate, resulting in tachysystole which is manifested as fibrillation. The other theory, advanced chiefly by T. Lewis 3 and his coworkers, states that in auricular flutter and fibrillation a single mother wave circulates usually about the orifices of the superior and inferior vena cavae and sends off centrifugal waves into the remainder of the auricular tissue. Lewis and Garrey 4 suggest that auricular and ventricular fibrillation are the same and Lewis assumes that the mechanism in ventricular fibrillation is the same as was shown by him to be the cause of auricular fibrillation.
A series of experiments was performed by us to test the validity of the assumption that ventricular fibrillation is caused either by a single focus or a single mother wave as stated above. Twelve dogs were used, under morphine and sodium barbital anesthesia, and artificial respiration was maintained with the open chest. The heart was exposed and permitted to remain in a cradle made from the pericardium. Two direct non-polarizable leads were fixed to the left ventricle and 2 to the right. These were connected with an electrocardiograph. Ventricular fibrillation was induced by temporary faradic stimulation at the base of the right ventricle.
As soon as the rate of spontaneous fibrillation became somewhat stabilized a control tracing was made from the right and left ventricles, both of which were visibly fibrillating. The 2 ventricles were then quickly and completely severed from each other, care being taken not to displace them, and the records taken quickly again.
Get full access to this article
View all access options for this article.