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Antoni H. Pathophysiologie der Herzrhythmusstörungen. [Pathophysiology of cardiac arrhythmias]. Z Kardiol. 1992;81:111-7
Antoni, H. (1992). Pathophysiologie der Herzrhythmusstörungen. [Pathophysiology of cardiac arrhythmias]. Zeitschrift fur Kardiologie, 81111-7.
Antoni, H. "Pathophysiologie der Herzrhythmusstörungen." [Pathophysiology of cardiac arrhythmias]. Zeitschrift fur Kardiologie vol. 81 (1992): 111-7.
Antoni H. Pathophysiologie der Herzrhythmusstörungen. [Pathophysiology of cardiac arrhythmias]. Z Kardiol. 1992;81:111-7. German. PMID: 1290287.
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Z Kardiol. 1992;81:111-7.

[Pathophysiology of cardiac arrhythmias].

Zeitschrift fur Kardiologie

[Article in German]
H Antoni

Affiliations

  1. Physiologisches Institut der Universität Freiburg.

PMID: 1290287

Abstract

Cardiac arrhythmias are ambiguous symptoms. Intracardiac as well as extracardiac alterations may be responsible. There is little direct information from the ECG concerning their pathophysiological mechanism. Bradycardic as well as tachycardic arrhythmias can be the result of two different fundamental disturbances: alterations of impulse formation (automaticity) or alterations of impulse conduction. Either one of these, or both of them acting together, may be responsible for the arrhythmia. Tachycardias due to disturbances of impulse formation may be brought about by enhanced firing of regular pacemakers (sino-atrial node, av-node, ventricular conduction system), by abnormal automaticity occurring in ordinary atrial or ventricular myocardium, or by triggered activity due to early or delayed afterdepolarizations. Bradycardic disturbances of impulse formation are primarily concerned with sino-atrial nodal function. Bradycardic conduction disturbances mainly impair sinoatrial or atrioventricular propagation causing partial or total conduction block. Tachyarrhythmias due to disturbances of conduction are generated by re-entry of excitatory waves either along anatomically preformed pathways or around functional obstacles (refractory zones) with excitable gaps being more or less pronounced. On the cellular level, altered activities of ionic channels or transport systems play a significant part. Such changes are caused by: alterations of electrolyte composition (potassium, sodium, calcium), acidosis or alkalosis, autonomic and hormonal influences, membrane active metabolites (long-chain acylcarnitine, lysophosphatidylcholine), drugs (class I and III antiarrhythmics, cardiac glycosides) and poisons. In disturbances of conduction other aspects like geometry of pathways or cable properties (anisotropic conduction, coupling resistances between cells) are of particular significance.(ABSTRACT TRUNCATED AT 250 WORDS)

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