later define the exact nature of the chrono- 

 tropic disturbances in this disease, whose 

 complicated pathology at times forms a de- 

 cided obstacle to the interpretation of cer- 

 tain symptoms. 



As regards the bradycardias of sinus 

 origin we cannot escape the same lack of 

 decision in attempting to interpret their 

 mechanism. Do they indicate extracardiac 

 influences in the form of deficient stimuli 

 of ti.e endocrine organs on the nervous ap- 

 paratus that regulates the chronotropic func- 

 tion of the organ ? Or do they rather indic- 

 ate a disturbance of cardiac origin and 

 manifest the weakness of the altered mus- 

 cle? It should be emphasized that in these 

 cases of bradycardia, as in the former case, 

 the insufficiency of the organ becomes ap- 

 preciable in all of its symptoms, which in 

 a way may give a basis for the last hypo- 

 thesis ; far be it from us, however, to argue 

 on this subject which should be reserved 

 for later explanations. But we must refer to 

 its predominance in males and this is an 

 important factor to be considered in the nec- 

 essary pathologic interpretation. Usually 

 these bradycardias, as well as the tachycar- 

 dias, are accompanied by extrasystolic con- 

 tractions; cases exist, however, in which 

 they constitute the only anomaly of rhythm. 



The slowness of the pulse is yery var- 

 iable, oscillating in the vicinity of fifty beats 

 per minute and is rarely seen below that 

 figure. 



Now let us pass to consider the arrhy- 

 thmias that are indubitably related to the 

 lesion of the myocardium. In the multiplicity 

 of their varieties and in the frequence with 

 which they are seen in nearly all of the clin- 

 ical cases, these express a pathologic con- 

 dition that belongs exclusively tothisjdisease 

 and they show the greatest curiosities in this 

 new chapter of human pathology. 



2. Alterations of conductibility. — The 

 most curious and most characteristic aspect 

 of the cardiac affection is that furnished by 

 the alterations of conductibility, seen in all 

 its phases of evolution from its slightest 



grades, which are manifest by simple delay 

 in the conduction of the contractile stimulus 

 from the node of Keith to the ventricle, up 

 to complete block with independence of the 

 sino-auricular and ventricular rhythms. 



The number of clinical cases with this 

 symptom that has already been verified is 

 considerable, and we may say with all cer- 

 tainty that the knowledge of American tryp- 

 anosomiasis in this particular has opened 

 a new field in cardiac physiopathology with 

 valuable indications, in which to the abun- 

 dant concrete facts there is added the appre- 

 ciable advantage of a known etiologic unity. 

 In other diseases these alterations have been 

 found; in none, however, with the frequency 

 here recorded or with the manifold aspects 

 and stages of development that can be en- 

 countered in trypanosomiasis. To such an 

 extent is this true that we might character- 

 ize this entity as the disease par excellence 

 of alterations of rhythm and especially of 

 slow pulse. 



We have found these alterations in all 

 epochs in life, including even children of 

 eight years of age, and here they do not 

 constitute an appanage of advanced years, 

 as is the rule, but depend exclusively upon 

 lesions of the primitive cardiac bundles 

 These regions are attacked by the diffuse 

 pathologic processes characteristic of tryp- 

 anosomiasis as much as the rest of the 

 muscle ; however, perhaps on account of 

 their anatomic differentiation and greater 

 functional importance there seems to be in 

 these regions a preponderance of those pro- 

 cesses which are manifest in the alterations 

 of rhythm that we are discussing, and in 

 others associated also with anomalies of 

 the primitive bundles. 



In the beginning the alteration is shown 

 by the increase of the spaces ac and PR. 

 which indicates the delay in the passage of 

 the contractile wave through the normal 

 paths of propagation. The increase of ac in 

 many of our tracings reaches 0.6 and in 

 rare cases has exceeded that time. The car- 

 diogram and the radial tracing are some- 

 times regular; in the majority of the patient 



