3. on the duration of the refractory stage of the ventricle. 
Since the excitation reaches the ventricle almost always too late 
the experiment will generally be more successful during the post- 
compensatory systole, of which the refractory stage has been lengthened. 
Another favourable factor consists in the fact that during the post- 
compensatory systole the rate of the conduction of the excitation is 
increased, which facilitates otir endeavours to make the excitation 
reach the ventricle at the right moment. 
There are still more obstacles in the way of this experiment. I 
said before that the auricles should be excited as early as possible 
in the excitable period for the experiment to succeed. Now just 
then either auricular tibrillation or “gehäufte” auricular extra-systoles — 
arise') repeatedly after a shock, anyhow when the metabolic con- 
dition of the auricles is sufficiently bad. 
In these two cases the ventricle does not display any fibrillation, 
but quite another aspect, which we purpose to describe in another 
paper. If our experiment is to succeed the extra-stimulus must, there 
fore, be followed by asingle auricular systole. The excitation reaching 
the ventricle after this, can cause it to fibrillate. 
Now, since, in the suspended frog’s heart, the metabolic condition 
of the ventricle is impaired much sooner than that of the auricles, 
the ventricle will reach a condition in which it may be made to 
fibrillate, much sooner than the auricles. Consequently an early shock 
applied in this period to the auricles will yield an extrasystole ; 
when after this the excitation reaches the ventricle directly after the 
conclusion of the refractory stage, this chamber will begin to fibrillate. 
I must lay stress on the fact that a chamber can be brought to 
fibrillation through an excitation wave. This fact seems to me to be of 
some clinical significance, because when the human heart-beat is 
accelerated through a sudden bodily exercise i.e. when impulses are 
sent out at a quickened tempo from the pace-maker of the heart 
(sino-auricular node of Kerita-FLUcK), we can conceive an impulse 
to reach the auricles or the ventricle suddenly, directly after the 
conclusion of the refractory stage. The chamber concerned then may 
suddenly begin to fibrillate. 
From this and the first communication it is obvious, that the 
metabolic condition of the chamber concerned is decisive for the 
origin and the continuance of fibrillation, which can reveal itself 
only when this metabolic condition has been sufficiently impaired. 
My new experimental data can also throw more light upon the 
1) To be discussed in a subsequent publication. 
