Abstract
The complex of ventricular disorders that follows exposure to either epinephrine or hydrocarbon-epinephrine administration evolves from two principal actions working in concert. These are depression of nodal pacemaker areas and enhanced extranodal automaticity.
When epinephrine is given alone, reflex vagal activation depresses only the S-A node. In this way A-V nodal rhythms and ventricular tachycardias develop. Ventricular fibrillation does not occur.
The action of epinephrine to increase automaticity is not, by itself, adequate to initiate ventricular rhythms. This is revealed by the fact that epinephrine, in the absence of vagal activity, as in the atropinized cat, will not disturb the regular sinus rhythm.
If the depressant action of the vagus is replaced by less specific depressants such as hydrocarbon vapors, epinephrine will initiate arrhythmias even in the atropinized animal.
When strong depression of dominant pacemaker sites is achieved through hydrocarbon inhalation, the enhancement of myocardial automaticity by epinephrine goes undominated and ominous multifocal or fibrillatory rhythms develop.
Footnotes
- Received January 3, 1955.
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