Abstract
In a recent paper 1 we reported that a single, short, strong, localized shock applied directly to different regions of the left ventricle of dogs anesthetized by sodium barbital can produce permanent ventricular fibrillation. The same results have since been obtained on dogs under chloralosane and in cats under dial anesthesia. A shock, if strong enough and given during the vulnerable period near the end of ventricular systole, produces one extra-systole followed by about 4 more or less coordinated beats and then by true ventricular fibrillation. If the shock is not quite strong enough or comes a little early in systole, instead of producing ventricular fibrillation, it gives a single premature contraction and only rarely several.
It is important to establish with certainty that these effects are due 10 ventricular excitation by the shock applied during systole rather than to a spread of current to the atria and subsequent ventricular excitation by supraventricular impulses arriving during diastole.
By recording simultaneous electrocardiograms and left ventricular pressure curves the latter possibility can be definitely excluded for the following reasons:
1. The premature electrical variation starts too shortly after the stimulus to allow for the A-V conduction time (Figs. 1-4).
2. The electrical variation has the form of a ventricular premature beat and not that of a ventricular beat due to an auricular impulse (Figs. 1-4).
3. The P-wave occurs after the premature ventricular complex and the spacing of the P-wave remains normal, showing that the auricular rhythm has not been disturbed (Figs. 1, 2-4).
4. The premature contraction when not producing fibrillation is followed by a full compensatory pause which, although possible in case of auricular premature systoles, is a rare occurrence (Fig. 1).
5. A stimulus applied a little too early in ventricular systole to produce an extra contraction never induces premature auricular contraction as it should if it were spreading to the atria.
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