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known from experiment that in the auricular and ventri- 

 cular muscle, with their complexly arranged bundles of fibres, 

 fibrillation can be propagated across an artificial isthmus, 

 made by incision, connecting portions of the musculature, 

 only as long as the isthmus is of sufficient breadth; in the 

 junctional mechanism, comprising the a-v node with its 

 special properties, and the narrow a-v bundle with its 

 longitudinally arranged fibres terminating in the Purkinje 

 network on the inner surface of the ventricles, the fibrilla- 

 tion process fails to be transmitted (as such) either from 

 auricles to ventricles or from ventricles to auricles. The 

 junctional mechanism, while able to conduct impulses 

 sufficiently fast to give ventricular beats at rates much above 

 those of the normal heart under resting conditions or in 

 moderate exercise, is not able to transmit the vastly more 

 rapid and characteristic series of excitations of fibrillation. 

 It is only under certain very special conditions, where the 

 susceptibility of the ventricles to fibrillation (at relatively 

 slow rates of excitation) is extraordinarily great, that the 

 writer has in rare instances seen any experimental evidence 

 of the possibility of ventricular fibrillation being excited 

 from the auricles by impulses passing through the a-v 

 bundle. The possibility of such occurring under pathological 

 conditions in man is worthy of consideration. 



The Purkinje network formed in the interior of the 

 ventricular walls by the arborizations of the fibres of the 

 A-v bundle form a sort of distributing board over which 

 the normal impulses descending the bundle spread swiftly 

 so as to be delivered almost simultaneously to the myo- 

 cardium at the various parts of the ventricular cavities, 

 bringing about the normal co-ordinated contraction of the 

 ventricular fibres at each beat. Such mode of excitation is 

 obviously unfavourable to the development of the fibrillation 

 mechanism, but the latter might under certain conditions 

 be promoted by an abnormal delivery of irregular and 

 aberrant exciting impulses, dependent on defects in the 

 branches of the bundle or its terminal arborizations, such 

 partially interrupted or distorted impulses impinging upon 

 the myocardium at different points in abnormal fashion — 

 alterations in timing or direction of the impulses as might 

 readily be determined by morbid conditions in some parts of 

 the conducting network. An exaggeration of these func- 

 tional aberrations may easily be favoured by circumstances 

 making an extra call on the heart, such as emotion or mus- 

 cular effort, or by the succeeding phase of reaction with its 

 increase of vagus control and other changes. 



There is some clinical and pathological evidence that 

 points to the operation of such causes, resulting in ven- 

 tricular fibrillation and sudden death in the human subject, 

 though the particular mode of causation indicated above 

 does not seem to have been suggested. Thus Nuzum'* 

 described a case of sudden death in a man, aged 38, who 

 had shown no definite signs of ill health and where there 



