Electrophysiological mechanisms for ventricular arrhythmias.
The proposed mechanisms for ventricular arrhythmias include reentry, reflection, enhanced and abnormal automaticity, afterpotential triggering, and repolarization re-excitation. The original model for re-entrant excitation, the ring model, has been augmented by newer models applicable to three-dimensional propagation in the cardiac syncytium, the "leading circle" and the "figure of eight." Heterogeneous refractory properties are important for slow conduction, unidirectional block, and formation of a barrier. Abnormal cellular properties such as depressed excitatory current and cell uncoupling contribute to slow conduction and block. Tachyarrhythmias can result from enhanced normal automaticity or abnormal automaticity in which the pacemaker currents differ. Excess calcium loading and depression of repolarizing currents have been identified as important factors in the induction of after depolarizations, which may play a role in ventricular arrhythmias related to cardiac glycosides, in certain stages of ischemia, and in the long QT syndromes.
Lazzara
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Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City.
D000200:Action Potentials; D015220:Calcium Channels; D004562:Electrocardiography; D004594:Electrophysiology; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular; D015222:Sodium Channels; D013610:Tachycardia / Q000209:etiology / Q000503:physiopathology*
D015220:Calcium Channels; D015222:Sodium Channels