THE CIRCULATION OF THE BLOOD 679 



His," as it is called, was further worked out by Tawara (1906), and it is almost 

 universally accepted now that the transmission of excitation in the mammalian 

 heart takes place by means of this muscular bundle. Kent (1893 and 1914) 

 describes another conducting path between the right auricle and the external 

 wall of the right ventricle ; but it is doubtful whether this has any functional 

 importance under normal conditions. 



The existence of nerve fibres in the heart muscle is sufficiently accounted for 

 by the vagus and sympathetic supply. Whether there is any kind of transmission 

 by a nerve network seems very questionable ; the heart beat is certainly not 

 initiated by periodic discharges of ganglion cells, and if a nerve network plays any 

 part in the transmission of excitation, it must be one of that kind whose existence 

 has never been proved in the higher animals (see pages 472-473 above). It must 

 be, in fact, able to conduct equally in all directions. Beats can be obtained by 

 stimulation at any point of the heart muscle, and auricular beats can be brought 

 about by backward transmission from the ventricle. 



As was shown by Gaskell, the automatic rate of each chamber, when it is 

 beating by itself, is slower than that of the chamber preceding it in the cardiac 

 cycle. Thus, in the frog and tortoise, the rate of the sinus is the quickest, that of 

 the bulbus slowest, the order being sinus, auricle, ventricle, bulbus. The sinus is 

 therefore the "pace-maker." In the mammalian heart there is no separate sinus. 

 Where is then the "pace-maker"? An excellent account of the history of the 

 work on this question will be found in the paper by Thos. Lewis (1913, 3). The 

 main facts only can be given here. Keith and Flack (1907) found traces of sinus 

 tissue in certain parts of the auricle, especially at the junction of the superior 

 vena cava with the right auricle. At this point there is a collection of peculiar 

 muscular tissue in intimate relation with the nerves entering the heart. The 

 clearest proof that the normal beat arises in this " Keith-Flack node " has been 

 given by Thos. Lewis (1910). The principle of the method used is simple, 

 depending merely on the fact that muscle in excitation is electrically negative to 

 that at rest. By taking a series of photographs, with the string galvanometer, of 

 the electrical effects from electrodes placed on various points of the auricle, it was 

 shown that the normal beat actually commences in this sino-auricular node. This 

 place was found to become electrically negative before any other place. From it 

 the excitation spreads in all directions. Confirmatory evidence that the beat 

 takes its origin here is afforded by the effect of warming and cooling the node, 

 which is to affect greatly the rate of the whole heart, whereas similar results 

 cannot be obtained from any other part. There is also other evidence, although 

 less conclusive. The work of Sansum (1912), on the shortened compensatory 

 pause after extra-systoles, shows that the sino-auricular or Keith-Flack node 

 behaves like the sinus of the frog. 



When the sino-auricular node is put out of action in any way, the beats are 

 initiated by a point in the auriculo- ventricular bundle of His. They are transmitted 

 from this point in both directions, so that simultaneous contraction of auricle and 

 ventricle results. The rate of discharge of this node is, normally, slower than that 

 of the Keith-Flack node, so that the latter sets the pace. Some observations by 

 Cushny (1912) suggest that there is an additional cause for the subordination of 

 the auriculo- ventricular node. If the bundle of His be cut across on the auricular 

 side of its node, the ventricle is cut off from the impulses arriving from the auricle. 

 But it does not at once develop its own rhythm, and Cushny brings evidence to 

 show that the node is normally kept in a state of diminished excitability, owing 

 to fatigue, by the impulses reaching it from the auricle. A similar state can, 

 in fact, be induced by artificial stimulation of the auriculo-ventricular node, and 

 is not due to inhibition. 



We must suppose that these nodes discharge when they have stored up some- 

 thing to a sufficiently high degree, and that, after a discharge, they are incapable 

 of further discharge until a fresh quantity has been formed. The experiments 

 of Gaskell on the effects of clamping the auriculo-ventricular junction seem to 

 show that the local effect of the clamp is to depress the rate at which the capacity 

 of the tissue to contract is recovered. When the clamp is gradually closed, at 



