Transcript Slide ()

A. Possible mechanism of proarrhythmia in the anatomic model of reentry. (1a) Nonviable reentrant loop due to bidirectional block (shaded area). (1b)
Instance where a drug slows conduction velocity without significantly prolonging the refractory period. The impulse is now able to reenter the area of
unidirectional block (shaded area) because slowed conduction through the contralateral limb allows recovery of the block. A new reentrant tachycardia
may result. (2a) Nonviable reentrant loop due to a lack of a unidirectional block. (2b) Instance where a drug prolongs the refractory period without
significantly slowing conduction velocity. The impulse moving antegrade meets refractory tissue (shaded area) allowing for unidirectional block. A new
reentrant tachycardia may result. B. Mechanism of reentry and proarrhythmia. (a) Functionally determined (leading circle) reentrant circuit. This model
Source: Chapter 25. The Arrhythmias, Pharmacotherapy: A Pathophysiologic Approach, 8e
should be contrasted with anatomic reentry; here the circuit is not fixed (it does not necessarily move around an anatomic obstacle) and there is no
Citation:
DiPiro
JT, Talbert
Yee GC, Matzke
GR, (b)
Wells
BG, Posey
L. Pharmacotherapy:
A Pathophysiologic
8e; 2011 Available
excitable gap.
All tissue
inside
is held RL,
continuously
refractory.
Instance
where
a drug prolongs the
refractory periodApproach,
without significantly
slowing
at:
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Accessed:
April
01,
2017
conduction velocity. The tachycardia may terminate or slow in rate as shown as a consequence of a greater circuit length. The dashed lines represent the
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Education.
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original reentrant
circuit©prior
drug treatment.
(c) Instance
where
a drug slows conduction velocity without significantly prolonging the refractory period
(i.e., class Ic antiarrhythmic drugs) and accelerates the tachycardia. The tachycardia rate may increase (proarrhythmia) as shown as a consequence of a