325 
3 deflections in the mechanogram and in the electrogram. This is 
instanced in Fig. 1 (2"d row of curves at 4). Here we see after the 
electric stimulus 3 small deflections in the suspension-curve (a, 6 
and c) with which electric deflections correspond. Now what does 
this mean? When looking at 2 or 3 deflections, we observe a phe- 
nomenon formerly described by me as deformed ventricular systoles 
and which is known in the literature by the name of ventricular 
peristalsis. Similar deformed systoles also occur after digitalis poison- 
ing'). We illustrate this by a series of curves registered from a 
frog’s heart 25 minutes after a subcutaneous injection in the thigh 
of 14 drops of digitalis dialysate (Fig. 4). The first ventricular curve 
of the figure consists of two parts; first the suspension curve rises 
up to a certain point and at the beginning of the dilatation line a 
second rise begins. This form of the curve owes its origin to the 
circumstance that first a part of the ventricular muscle begins to 
contract; subsequently, owing to the bad metabolic condition the rest 
of the muscle comes into action with a prolonged latent stage; this 
causes a retarded contraction. 
The electrogram. registered at the same time fully confirms this 
statement. The third ventricular curve of the figure presents a break 
in the ascending branch and is, therefore, also deformed. During 
these deformed ventricular systoles the whole muscle is indeed made 
to contract, but in 2 or 3 tempos. The same is the case with the 
brief delirium. After the extra stimulus which affects the ventricle 
at a moment when the recovery of the muscle is still unsatisfactory, 
part of the ventricle begins to contract. The proceeding “Erregung” 
imparts contraction to the following portion only after a long lasting 
latent stage, so that the “Erregung’”’ passes through the ventricie in 
two stages. The brief delirium, then, is nothing but a deformed 
fractionated extrasystole. 
Now upon this basis we can readily conceive the origin of the 
longer fibrillation in our experiments. As set forth heretofore, the 
refractory stage of the contraction, generated at the outset of the 
excitable period, is shortened. This shortening is of great moment 
for the lengthening of the delirium. When the “Erregung”’, after 
an extra-stimulus, has gone through the ventricle in stages, the time 
of such a circulation is lengthened considerably. Now when the 
excitation wave reaches the starting point again, it begins to contract 
again, because the short refractory stage of the preceding contraction 
has already come to a close. Again the “Erregung”’ proceeds through 
1) Arch. Neêrl. de Physiologie. Tom. III, p. 69, 1918. 
