Development of an endocardial-epicardial gradient of activation rate during electrically induced, sustained ventricular fibrillation in dogs
Electrograms recorded with currently available electrodes become indistinct soon after the onset of ventricular fibrillation (VF); thus, little is known about transmural myocardial depolarization during VF. A plunge electrode system (plunge) was developed that registers discrete deflections during V...
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Veröffentlicht in: | The American journal of cardiology 1985-03, Vol.55 (6), p.813-820 |
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Zusammenfassung: | Electrograms recorded with currently available electrodes become indistinct soon after the onset of ventricular fibrillation (VF); thus, little is known about transmural myocardial depolarization during VF. A plunge electrode system (plunge) was developed that registers discrete deflections during VF. These plunges were used to record for 20 minutes after inducing VF with a single premature shock in 20 open-chest dogs. In the first 6 dogs the epicardium was exposed to room temperature and in 14 dogs transmural temperature was maintained at 38°C. Electrograms recorded with the transmural plunges contained sharp, discrete deflections during early VF in all dogs. Over the next 20 minutes of VF, the rate, regularity of cycle length and discreteness of the deflections in the electrograms decreased with time, first at the epicardial level, then deeper toward the endocardium. In all dogs, however, discrete, regular, rapid deflections persisted in the most subendocardial electrogram throughout the recording period. In 8 dogs, transmural myocardial biopsy samples were taken before fibrillation, and at intervals after the onset of fibrillation. The high-energy phosphate content of the myocardium decreased during VF, with comparable decreases in the epicardial and endocardiai halves. Coronary perfusion was maintained during the first 20 minutes of VF in 6 additional dogs by cardiopulmonary bypass. A gradient of activation rates did not develop on bypass, but did develop within 1 minute of halting bypass. Thus, the endocardial-epicardial gradient of activation rates during VF is caused by ischemia. It is not caused by transmural differences in ischemia, however, as evidenced by the homogeneous transmural decrease in high-energy phosphate compounds during VF, nor is it caused by transmural differences in temperature. These findings suggest that the endocardium plays a dominant role in the maintenance of VF. |
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ISSN: | 0002-9149 1879-1913 |
DOI: | 10.1016/0002-9149(85)90162-6 |