With the clinical recognition, that different degrees of fibrillation occur and that these in turn are closely related to a coordinated type of auricular tachyrhythmia (flutter); further, that one type may lapse into another or into a perfectly normal rhythm, the conviction has grown that finer and coarser types of auricular movement may be recognized by the amplitude of the diastolic waves of the electrocardiogram and venous pulse. The present investigation into the cause of these waves has shown that this is not possible. There is no theoretical or experimental reason for the assumption that any fixed relation exists between the amplitude of the electrical variations of the electrocardiogram, which are the resultant of variations accompanying the irregularly spreading excitation wave, and the degree of mass contraction following. The large recurrent waves of the venous pulse, which may with more reason be regarded as related to the size of the auricular mechanical contractions on theoretical grounds, are also shown to be without differential value. The reasons for this may be briefly summarized.

In the first place, the presence of diastolic waves is contingent upon a slow heart rate and long ventricular diastoles. With rapid heart rate their occurrence is prevented by the closely placed systolic variations. It is therefore conceivable that both coarse and fine fibrillation as well as flutter will be without diastolic waves as long as the heart is rapid.

Even in the cases with long beats present their significance must remain doubtful. It is true that in the experiments the waves accompanying coarse fibrillation are as a rule somewhat larger than those occurring during fine fibrillation; waves of considerable size may, however, be present in fine fibrillation. Hence, as long as no calibrated method of recording is possible, it is difficult to draw any inference. It is possible from the same patient to record with the same apparatus diastolic waves of varying amplitude by merely changing the pressure of the receiving tambour.

The chief reason that the amplitude of these waves cannot be regarded as of differential value is found in their origin. Fine fibrillating movements of the auricle do not in themselves produce waves in the jugular. They produce neither pressure variations in the auricle, nor exert any traction upon the veins. The only factor capable of producing jugular waves during fine fibrillation seems to be the traction exerted by the position changes of the ventricle on the auricle and large veins. This may, in a measure, explain why the diastolic waves recorded from the apex and second left interspace of patients often closely correspond with those simultaneously recorded from the jugular. The term "fibrillary waves" commonly applied to the smaller of these variations is evidently poorly chosen when their etiology is considered. The coarser contractions of the auricle during coarse fibrillation also produce no pressure changes within the auricle. They are vigorous enough at times, however, to exert a traction upon the venous walls. Hence, the waves during coarse fibrillation may be regarded as partly of ventricular and partly of auricular origin, or, as is frequently the case, as due to an interference of the two tractions. It is owing to their dual origin that they are more numerous and distinct when recorded from the same animal without changing the position or pressure of the receiving apparatus.

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