What are the phases of repolarization in the pathophysiology of torsade de pointes?

Updated: Jan 31, 2017
  • Author: Jatin Dave, MD, MPH; Chief Editor: Mikhael F El-Chami, MD  more...
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Repolarization has 3 phases. During the initial upstroke of action potential in a normal cardiac cell, a rapid net influx of positive ions (Na+ and Ca++) occurs, which results in the depolarization of the cell membrane. This is followed by a rapid, transient outward potassium current (Ito), while the influx rate of positive ions (Na+, Ca++) declines. This represents the initial part of the repolarization, or phase 1.

Phase 2 is characterized by the plateau. The positive currents flowing inward and outward become almost equal during this stage.

Phase 3 of repolarization is mediated by activation of the delayed rectifier potassium current (IK) moving outward while the inward positive current decays. If a slow inactivation of the Ca++ and Na+ currents occurs, this inward "window" current can cause single or repetitive depolarization during phases 2 and 3 (ie, EADs). These EADs appear as pathologic U waves on a surface ECG, and, when they reach a threshold, they may trigger ventricular tachyarrhythmias.

These changes in repolarization do not occur in all myocardial cells. The deep endocardial region and midmyocardial layer (composed of M cells) of the ventricle are more prone to prolongation of repolarization and EADs because they have a less-rapid delayed rectifier potassium current (IKr), while other regions might have short or normal cycles. This heterogeneity of repolarization in the myocardial cells promotes the spread of triggered activity, which is initiated by EADs by a reentrant mechanism and currently is thought to be responsible for the maintenance of torsade. [1]

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