Terminal electrocardiographic patterns in experimental anoxia, coronary occlusion, and hemorrhagic shock

Electrocardiographic records of dog hearts at the stage of termination of effective pumping in experiments upon generalized anoxia, coronary occlusion, and hemorrhagic shock have been collected and studied. In nineteen general anoxia experiments from which terminal electrocardiograms are available, pacemaker stoppage or cessation of A-V conduction was the first gross manifestation of cardiac failure detectable in electrocardiograms in each case except one. Ventricular fibrillation occurred prior to stoppage in one. Of these nineteen animals, there were twelve with intact chests and seven with chests open for study upon the heart muscle. In a larger series of anoxic dogs with open chests and direct observation of the heart, making a total of more than sixty animals, there have been no further deaths by ventricular fibrillation, all hearts having stopped via pacemaker and conduction failure. The frequency with which pacemaker failure preceded conduction failure, and vice versa, was approximately equal in the nineteen experiments with terminal records. In occlusion of the anterior descending coronary artery there were twenty-five fibrillations during fifty occlusion trials, and four additional fibrillations upon releases of the occluding clamp. Fibrillation occurred, therefore, in fifty per cent of the occlusions, or fifty-eight per cent of trials if fibrillations upon release are included. In nine hemorrhagic shock experiments seven hearts failed by pacemaker stoppage, another probably did also, and one stopped via ventricular fibrillation. The experimental conditions which produce a gradual overall diminution in the functional capacity of the cardiac tissues without predisposition to ectopic ventricular systoles produced failure of the pacemaker or of A-V conduction, but very rarely induced ventricular fibrillation. The experimental condition (coronary occlusion) which predisposes to trains of ectopic ventricular systoles produced a high percentage of ventricular fibrillations. The reasons are discussed. Observations in a few representative clinical papers are reviewed and compared with the experimental observations. Considerable agreement with the experimental patterns and with the conclusion stated in the preceding paragraph was found.