Vagotonia; a clinical study in vegetative neurology / by Hans Eppinger and Leo Hess. Authorized translation by Walter Max Kraus and Smith Ely Jelliffe.

  • Eppinger, Hans, 1846-1916.
Date:
1917
Catalogue details

Licence: Public Domain Mark

Credit: Vagotonia; a clinical study in vegetative neurology / by Hans Eppinger and Leo Hess. Authorized translation by Walter Max Kraus and Smith Ely Jelliffe. Source: Wellcome Collection.

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    cular node, but it may also act in the region between the auricle and ventricle. ‘The result of this latter is that not every auri-_ cular contraction finds its way into the ventricle, and that the - auricle beats oftener than the ventricle without any incodrdina- tion between the actions of the auricle and ventricle. The char- acteristic of “nervous’’ heart block [omitted ventricular systole of Hering] is that it may be relieved by atropin. The same result may be accomplished by adrenalin. But those bradycardias which are the result of disease of the heart muscle may be bettered by atropin through its beneficial action upon the transmission of impulses of the nodal system, and may show a slight increase of the pulse rate. Now and then, the ‘“block’’ may involve but part of the nodal system, and may show transitorily those types which are demonstrated electrocardiographically when there is disease in one or another part of the nodes of Tawara. An officer, aged 50, has complained for one year of occasional feelings of pressure in the region of the heart, with pains passing outward into the left arm. During all of these attacks, which have become more frequent of late, the patient has sweated profusely, and has vomited in some of them as well. He has observed himself with care, and states that during the attacks his pulse goes from 88 to 50-56. The patient gave a history of lues. He does not seem old. His face is somewhat red, and be perspires readily. Blood pressure varies from 120 to 180. The second aortic sound is accen- tuated. The heart itself is not enlarged. Since the electrocardiographic examination of the patient interested us most, other details will be but super- ficially considered. During a period when the patient was in normal condition [pulse 86], the electrocardiogram was of normal character. In all the three leads, there was a positive R wave, and positive subsequent wave. During an attack in which he experienced the above described feelings of depression— pulse 54—the following was found: The auricular wave remained at the same distance from the R wave. The R wave, which was small before, was now three times as wide. Furthermore, it was noted that at this time the subsequent wave was negative and came directly from the R wave. With the second and third leads, the R wave was negative and the subsequent wave positive. This condition was observed for some length of time [one hour]. It seemed of great interest to us to note that a subcutaneous administration of .ooI gram of atropin relieved the bradycardia and at the same time changed the electrocardiogram to what it was before. There was no gallop rhythm during the bradycardia. Of course all heart diseases cannot be diagnosed in this manner even if atropin does relieve them. There are cases which owe their disturbance to auricular or ventricular extrasystoles. To what degree this condition may be correlated to the physiologic fact that the vagus is a negative inotropic nerve is hard to say. Some physiologists deny that the vagus has an influence upon the caliber of the coronary vessels. Counterbalanced to this view is the fact that adrenalin dilates the coronary vessels not