THE EFFECTS OF MYOCARDIAL ISCHEMIA ON THE FIBRILLATION THRESHOLD—THE MECHANISM OF SPONTANEOUS VENTRICULAR FIBRILLATION FOLLOWING CORONARY OCCLUSION

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Abstract
Alternate detns. of the fibrillation threshold of ventricles with a normal blood supply and during brief coronary occlusion were repeatedly made on the same animal. Rectilinear shocks 0.01 to 0.02 second in duration were applied to an identical area of the left ventricle. The milliampere value of a shock which, when applied during the vulnerable phase, induced fibrillation, served as the quantitative measure of the fibrillation threshold. Significant reduction in the current strength required to fibrillate was noted during coronary occlusion, e.g., a decrease from 13.9 to 3 M.A. in 1 expt. The vulnerable period of the ischemic region does not bear a normal relation to the ventricular pressure curve because the contraction of fibers in the ischemic area does not contribute to the pressure elevation and because the form and duration of the pressure curve are altered. Consequently, stimuli coinciding with the descending limb fibrillate, but those which fall on the horizontal portion of the pressure curve are ineffective in this respect. The observations of Tennant and Wiggers that the ischemic area no longer shortens but stretches during systole cannot be interpreted as a complete failure of the effort of contraction, but rather that the strength of effort is insufficient to overcome the stretching force of rising intraventricular pressure. When this force is removed during fibrillation, contractile waves are able to manifest themselves again. Since ischemia reduces the fibrillation threshold to artificial stimuli and also causes formation of ectopic centers, the theory is put forward that spontaneous fibrillation during cpronary occlusion is precipitated because such ectopic stimuli now become of threshold value for the hyperirritable myocardium and any one is capable of inducing fibrillation when it falls either during the vulnerable period of a normal beat or that of a premature beat excited from another ectopic center.

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