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
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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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    Atropin can always obliterate the bradycardias resultant upon certain acute infections, as for instance in diphtheria, or in the convalescent stage of febrile angina, mild pneumonia, typhoid, erysipelas, acute articular rheumatism, and scarlet fever. This action implies that the bradycardia is the result of increased tone in the vagus. If this reaction to atropin fails it may be assumed that organic changes exist. The type of bradycardia which is best and longest known is that accompanying increased in- tracranial pressure, as in cases of brain tumor, hydrocephalus, pseudo-tumor of the brain, hematoma of the dura mater, and incipient meningitis. These bradycardias are always referable to cerebral stimulation of the vagus. In these cases there is also an individual variation so that certain cases may be instances of latent vagotonia. ‘The effects of the increase of intracranial pres- sure are well shown by the administration of adrenalin. After an injection of this drug which contracts peripheral vessels but has no apparent effect upon the cerebral vessels, there occurs a flow of blood to the brain followed by an increase of intracranial pressure. This stimulates the vagus center, and causes a pulse characteristic of increased vagal action which may be relieved by atropin or vagotomy. Many drugs acting upon the heart can cause a bradycardia through vagal stimulation. Thus, after very small doses of digitalis its bradycardiac action may be so promi- nent that its entire cardiac action cannot be obtained without simultaneous administration of atropin. This bradycardia from digitalis is usually associated with other symptoms of autonomic stimulation, as for example digestive disturbances and vomiting. Similar idiosyncrasies must be considered if the various results of physostigmin in paroxysmal tachycardia are to be explained. Pilocarpin can hardly be included among the stimulants of the chronotropic functions of the vagus nerve. Vagotonics often give evidence of a great deal of cardiac activ- ity when the precordium is inspected. Closer investigation of this heaving shows that it is not accompanied by increased car- diac action, as occurs in valvular disease, but, as the X-ray exam- ination shows, that there are great variations in the size of the heart in systole and diastole. This symptom is frequent in vago-,; tonia, very frequent in the vagotonic type of Graves’ disease’ [Basedow-thymus], and in the so-called goiter heart [F. Kraus]. In vagotonic bradycardia, the stimulus acts at the sino-auri- sf