Afterdepolarization
From QT interval
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.
Early afterdepolarizations
Early afterdepolarizations (EADs) occur with abnormal depolarization during phase 2 or phase 3, and are caused by an increase in the frequency of abortive action potentials before normal repolarization is completed. Phase 2 may be interrupted due to augmented opening of calcium channels, while phase 3 interruptions are due to the opening of sodium channels. Early afterdepolarizations can result in torsades de pointes, tachycardia, and other arrhythmias.<ref>Cranefield, PF: The Conduction of the Cardiac Impulse. New York, Future Publishing Co. 1975</ref>.
Afterhyperpolarisations can also occur in cortical pyramidal neurons. There, they typically follow an action potential and are mediated by voltage gated sodium or chloride channels. This phenomenon requires potassium channels to close quickly to limit repolarisation. It is responisible for the difference between regular spiking and intrinsically bursting pyramidal neurons. <ref>Nelson Spruston, "Pyramidal Neurons: dendritic structure and synaptic integration", 2008. Nature Reviews. Neuroscience.</ref>
Delayed afterdepolarizations
Delayed afterdepolarizations (DADs), on the other hand, begin during phase 4 - after repolarization is completed, but before another action potential would normally occur. They are due to elevated cytosolic calcium concentrations, as might be seen with digoxin toxicity.<ref name="Katzung">Katzung, B: "Basic & Clinical Pharmacology", chapter 14: "Agents Used in Cardiac Arrhythmias", The McGraw-Hill Companies, 2007, ISBN 978-0-07-145154-6</ref><ref name="Lilly">Lilly, L: "Pathophysiology of Heart Disease", chapter 11: "Mechanisms of Cardiac Arrhthmias", Lippencott, Williams and Wilkens, 2007</ref>
