53D 
2 on the duration of the refractory stage of the ventricle. 
Only when these relations are such that the excitation reaches 
the ventricle directly after the conclusion of the refractory stage, 
will the ventricle begin to fibrillate. 
Usually the excitation reaches the ventricle after an auricular 
extrasystole too late for a ventricular fibrillation. To make the 
experiment succeed better one might lengthen the refractory stage 
by poisons (digitalis, veratrin, ete), through which the excitation 
might reach the ventricle after an auricular extrasystole more 
directly after conclusion of the refractory stage. However, as ap- 
peared from my first communication, it is just after digitalis poisoning 
that the lengthening of the refractory stage hinders the prolongation 
of fibrillation. 
We, therefore, abandon this artifice. I have now succeeded in 
modifying the relations in the non-poisoned bled frog’s heart in such 
a way that the experiment succeeds better. It is well known that 
the duration of the post-compensatory systole is longer than that of 
the periodic systoles. This longer duration coincides with a longer 
duration of the refractory stage, so that when in the commence- 
ment of the post-compensatory systole I administer an induction 
shock to the auricles as early as possible in the excitable period, 
the experiment may meet with a better success. Thus through 2z- 
direct stimulation I could indeed bring the ventricle to fibrillation 
with greater ease. This is instanced in fig. 2. In fig. 2a the auricles 
receive an induction-shock at the first deflection of the signal, which 
causes. on extrasystole of these chambers followed by a premature 
ventricular systole. Now the stimulus’ is repeated after the next 
auricular systole and this as early as possible in the excitable period. 
An extrasystole of the auricles ensues. 
The excitation conducted after this to the ventricle, makes the 
ventricle fibrillate for some time, during which the auricular curve 
displays some anomalies, caused no doubt by intercurrent retrogade 
_ excitations running from the ventricle to the auricles to be oecasion- 
ally incited to an extrasystole. At the fourth deflection of the signal 
the auricles are again stimulated during a post-compensatory systole, 
but now the stimulus affects the auricles a little later than the preceding 
time. Subsequently a brief fibrillation originates (we might also call 
this two extrasystoles — it is wise not to draw a sharp boundary 
line between the two deviations). 
The curves of fig. 26 were registered with an interval of some 
heart-periods after those of fig. 2¢. Here an induction shock affects 
the auricles at the second deflection of the signal, but this time rather 
