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Tachyarrhythmias can arise from three different mechanisms. First, increased automaticity from more rapid phase 4 depolarization can cause
arrhythmias. Second, in certain conditions, spontaneous depolarizations during phase 3 (early afterdepolarizations; EAD) or phase 4 (late
afterdepolarizations; DAD) can repetitively reach threshold and cause tachycardia. This appears to be the mechanism of the polymorphic ventricular
tachycardia (torsades de pointes) observed in some patients taking procainamide or quinidine and the arrhythmias associated with digoxin toxicity. Third,
the most common mechanism for tachyarrhythmia is reentry. In reentry, two parallel pathways with different conduction properties exist (perhaps at the
border zone of a myocardial infarction or a region of myocardial ischemia). The electrical impulse normally travels down the fast pathway and the slow
Source: Cardiovascular Disorders: Heart Disease, Pathophysiology of Disease: An Introduction to Clinical Medicine, 7e
pathway (shaded region), but at the point where the two pathways converge the impulse traveling down the slow pathway is blocked since the tissue is
Citation:
Hammer
GD, McPhee
Pathophysiology
of Disease:
Anwhen
Introduction
to Clinical
Available
at: occur in the fast
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13,
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pathway, and the impulse will travel down the slow pathway (shaded region) (b). After traveling through the slow pathway the impulse can then enter the
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fast pathway Copyright
in retrograde
fashion
(which because
of the
recovered excitability), and then reenter the slow pathway to start a continuous loop of
activation, or reentrant circuit (c).