Title: Alterations of Ventricular Depolarization in Myocarditis and Cardiomyopathy
Abstract: Depolarization implies changes of the resting membrane potential in a living cell mediated through cation flux. Myocardial cells exhibit a slow diastolic depolarization, which, when reaching threshold potential, initiates the action potential through rapid depolarization. The action potential consists of the rapid depolarization and the phase of repolarization. The question whether myocarditis and cardiomyopathy may influence slow diastolic depolarization, as well as the phases 0 and 1 of the action potential has principally been answered: myocardial disease is apt to influence the physiologic process of de- and repolarisation within all structures of the heart, atrial or ventricular myocardium, sinus node or the specific structures of impulse conduction. Various causes have been discussed. For example alteration of the normal cation flux may be induced in areas of inflammatory infiltration. Myocardial changes induced through lithium therapy have to be considered as a model [1]: lithium acts like sodium in the myocardial cell. It enters the cell and is accumulated there. Quite opposite to sodium, the lithium efflux is slower and is not accompanied by potassium influx as seen with sodium. As a consequence intracellular sodium and potassium concentrations are altered and thereby depolarization of the cell membrane undergoes changes. Disturbances of depolarization will consequently alter impulse formation and conduction. This will result in all kinds of rhythm disturbances as well as in alterations of the configuration of the P-wave and the QRS complex.
Publication Year: 1983
Publication Date: 1983-01-01
Language: en
Type: book-chapter
Indexed In: ['crossref']
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