J Exp Med. 1912 Sep 01;16(3):291-302. doi: 10.1084/jem.16.3.291.
The Journal of experimental medicine
G C Robinson
PMID: 19867574 PMCID: PMC2124962 DOI: 10.1084/jem.16.3.291
In four of the seven cases the ventricles remained active from one and a half to eighteen minutes after the electrocardiograms failed to show evidence of auricular activity. In two cases the auricles outlasted the ventricles and in one case only did the auricles and ventricles stop apparently at the same time. Complete dissociation occurred three times. Some delay in the conduction time was seen in five of the seven cases. In two cases the auricles ceased to beat before evidence of impaired conduction appeared. There was always marked slowing; the slowest independent ventricular rates varied from 13.6 to 47.0. The slowest rates at which the auricles beat regularly varied from 20 to 65 per minute. There was never evidence of auricular fibrillation, although in two cases the electrocardiograms give fairly conclusive evidence that ventricular fibrillation occurred. The ventricles reëstablished a regular rhythm after a short period of ventricular fibrillation in one case, while in the other but one ventricular contraction occurred after the appearance of fibrillation. Characteristic changes in the ventricular complex of the electrocardiograms occurred in all the records. They consisted of a gradual fusion of the R- and T-waves, forming, when the fusion was complete, a large rounded or peaked wave. In some cases the identity of the two waves was not entirely lost. In spite of the marked change in shape of the ventricular complexes, there was often but little change in their duration. In some cases the ventricular systole was shortened at the end, while in others it was prolonged. The change in the form of the ventricular electrical complex indicates that the course of the stimulus and the manner of the contraction of the muscle were abnormal. The fact that the R-wave became gradually prolonged suggests that the conduction of the stimulus through the ventricular walls became delayed as the heart died. The fact that after death there is a continuation of cardiac muscular activity sufficient to cause a difference in electrical potential between the two sides of the body does not necessarily mean that a ventricular systole in the sense of muscular shortening takes place. It has been observed experimentally that well defined electrical complexes may be caused by cardiac activity which cannot be seen or recorded graphically. As the duration of the ventricular complexes characteristic of the dying heart usually does not differ markedly from the duration of the complexes before clinical death, it seems probable that the entire musculature of the ventricles participates in the contraction; as definite shortening, or at least a marked change in duration, would be expected if only a part of the ventricular musculature participated in the activity which produced the complex.
