[Effects of the autonomic nervous system in supraventricular arrhythmia]

Influences of the autonomic nervous system may cause modifications of the initiation, continuation and discontinuation of supraventricular rhythm disturbances. Whether or not clinically relevant bradycardia syndromes (such as the hypersensitive carotid sinus syndrome and the sick sinus syndrome) also may exist primarily on a functional basis, remains to be proven. Organic pathology, whether it is clinically apparent or not, probably provides the basis for the activation of influences on the autonomic nervous system. In atrial fibrillation and atrial flutter the influence of the autonomic nervous system is apparent in a form of the vagotonically and sympathotonically evoked paroxysms. In the case of persistent atrial fibrillation vagal and sympathotonically transmitted changes in the AV-dromotropy determine the mode of heart rate. Junctional re-entry tachycardias and re-entry tachycardias under the influence of accessory pathways, are potentially triggered by mechanisms, as transmitted by the autonomic nervous system. Furthermore, such autonomic influences are responsible for changes in the conducting velocity and the refractory properties, as produced by parallel conducting pathways. Hemodynamic changes themselves, which are induced at the very beginning of the tachycardia, may activate other electrophysiological mechanisms and thereby cause a modification in the type of tachycardia in question.