Delayed after depolarization

Exercise-induced ventricular tachycardia in persons without overt cardiac disease is an example of delayed after-depolarizations and is characterized by an increase in intracellular ionized calcium. This type of arrhythmia is known to often respond well to which of the following combinations ... 

Two forms of abnormal activity, early (top) and delayed after depolarizations (bottom). In both cases, abnormal depolarizations arise during or after a normally evoked action potential. They are therefore often referred to as "triggered" automaticity that is, they require a normal action potential for their initiation. 

Prophylaxis in reentrant nodal and atrial tachycardias—not Wolff-Parkinson-White syndrome (WPW). Avoid in VT, as may progress to VF. In digitalis toxicity, can 4 delayed after-depolarization. 

APD, action potential duration ARVD/C, arrhythmogenic right ventricular dysplasia/cardiomyopathy CM, cardiomyocyte CPVT, catecholaminergic polymorphic ventricular tachycardia DAD, delayed after depolarizations DCM, dilated cardiomyopathy EAD, early after depolarization HCM, hypertrophic cardiomyopathy 1 rectifier potassium current 1, sodium current MEA, multielectrode array TNNT2, troponin T type 2. 

An animal study of the mechanism of bupivacaine-induced dysrhythmias has shown that bupivacaine facilitates early after-depolarization in rabbit sinoatrial nodal cells by blocking the delayed rectifier potassium current (11). 

Triggered automaticity is also a possible mechanism for abnormal impulse generation. Briefly, triggered automaticity refers to transient membrane depolarizations that occur during repolarization (early after-depolarizations [EADs]) or after repolarization (delayed afterdepolarizations [DADs]) but prior to phase 4 of the action potential. After-depolarizations may be related to abnormal calcium and sodium influx during or just after full cellular repolarization. Experimentally, early after-depolarizations may be precipitated by hypokalemia, type la antiarrhythmic drugs, or slow stimulation rates— any factor that blocks the ion channels (e.g., potassium) responsible... 

Administration of magnesium sulfate is currently recommended as immediate first-line treatment for torsades (Zipes et al. 2006). While the mechanism of action is uncertain, magnesium may reduce the amplitude of early after-depolarizations by inhibiting the late influx of calcium ions via L-type calcium channels that are associated with delayed ventricular repolarization. Consequently, early afterdepolarizations are less likely to reach threshold potential and provoke or sustain torsades (Kaye and O Sullivan 2002). 

There have been few reports on the effects of temperature on brain ion homeostasis after ischemia. However, there appears to be a consensus that hypothermia does not prevent AD associated with either global or focal ischemia, although it has been reported that the onset of AD may be delayed (32-34). It has also been reported that mild hypothermia reduces the number of SD-like depolarizations associated with focal ischemia (34). The frequency of SD-like depolarizations has been associated with the degree of damage after focal ischemia (35,36). It is possible that the same occurs following TBI. 

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