page_title: Afterdepolarization
section_title: Delayed afterdepolarizations
hierarchical_section_title: Afterdepolarization / Delayed afterdepolarizations
caption_attribution_description: English: Cartoon showing mechanisms underlying early afterdepolarisations, delayed afterdepolarisations, and re-entry
context_page_description: Afterdepolarizations are abnormal depolarizations of cardiac myocytes that interrupt phase 2, phase 3, or phase 4 of the cardiac action potential in the electrical conduction system of the heart. Afterdepolarizations may lead to cardiac arrhythmias.
context_section_description: Delayed afterdepolarizations (DADs) begin during phase 4, after repolarization is completed but before another action potential would normally occur via the normal conduction systems of the heart. They are due to elevated cytosolic calcium concentrations, classically seen with digoxin toxicity. The overload of the sarcoplasmic reticulum may cause spontaneous Ca²⁺ release after repolarization, causing the released Ca²⁺ to exit the cell through the 3Na⁺/Ca²⁺-exchanger. This results in a net depolarizing current. The classical feature is Bidirectional ventricular tachycardia. Also seen in catecholaminergic polymorphic ventricular tachycardia (CPVT). Delayed afterdepolarization is also seen in myocardial infarction. Ischemic tissue is partially depolarized due to its high concentration of cations. Partially depolarized tissue fires rapidly resulting in delayed after depolarization.
caption: Cellular mechanisms of early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs).
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