84 



for the presence of a similar mechanism in the occurrence 

 of fibrillation and sudden death (apart from chloroform) 

 during or shortly after muscular effort — granted a condition 

 of abnormal susceptibility in the ventricular muscle. 



In addition to chloroform there are various other toxic 

 agencies capable of establishing the hypersensitive state. 

 Referring to drugs, it is well known from experimental 

 evidence (adduced by Cushny and others) that bodies of the 

 digitalis series have a powerful influence in this direction — 

 as also have barium salts, etc. — and when pushed to 

 extremity kill by causing fibrillation. A whole series of 

 chemical substances might be cited as having well defined 

 effects in this direction. And some abnormal metabolic 

 products may well exercise a similar influence in this respect 

 on the cardiac muscle. The development of the hypersensi- 

 tive condition is not necessarily attended by any recognizable 

 structural alteration. A prominent part in the setting up 

 of abnormal susceptibility to fibrillation must be assigned to 

 defective coronary blood supply. 



Some Effects of Experimental Coronary Obstruction. 



It is unnecessary to recall in detail the long series of 

 experimental investigations at the hands of many workers 

 which have demonstrated the frequent occurrence of fibrilla- 

 tion as a result of ligation of a coronary artery or one of 

 its larger branches. The evidence available leaves little, if 

 any, room for doubt that death from sudden coronary 

 obstruction in man is due to fibrillation ; the clinical features 

 of many recorded cases are very significant, taken in con- 

 junction with the very definite facts established by experi- 

 ment in animals. The reason of the difference between non- 

 fatal and suddenly fatal coronary obstruction is usually to 

 be found in the non-occurrence or occurrence of ventricular 

 fibrillation in the different cases. 



It has been found experimentally that coronary occlusion, 

 if suflBicient to prove fatal, may do so in more than one way : 

 (1) it may kill rapidly (minutes) from acute ischaemia 

 causing ventricular fibrillation, or (2) failing this, it leads 

 to damaged nutrition with degenerative changes (anaemic 

 necrosis, fibrosis, etc.) ; these changes, apart from leading 

 in rare instances to rupture of the heart, naturally diminish 

 the contractile efl&ciency in degrees varying according to 

 the severity of the anaemia and its distribution. iRecovery 

 may occur and life be prolonged indefinitely; or death may 

 be suddenly caused by the supervention of fibrillation. It is 

 easy to understand how altered functional relations in the 

 tissues of the damaged area may lend themselves under 

 certain conditions to the decisive upset of the normal rela- 

 tions of refractory period and conduction time in the ven- 

 tricular walls. It remains to be seen whether the tendency 

 to fibrillation after coronary ligation is dependent mainly 

 on the conditions induced in the Purkinje system or in the 

 ordinary myocardium or in both of these. 



