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3.6 Dynamics of Reentry in a Fixed Pathway

Reentry of the cardiac action potential is thought to be the most common mechanism of

clinical arrhythmias, including atrial flutter and fibrillation, and ventricular arrhythmias following
myocardial ischemia or infarction. During normal cardiac excitation, the excitation wave becomes
extinct before the next wave arrives. This behavior results from the refractoriness of cardiac cells
that lasts longer than the excitation period, insuring rhythmic periodicity and repetitive activation
sequence on every beat.

Under pathological conditions, the excitation wave may encounter a zone of conduction
block. It might be forced to rotate around it to reenter the region of pre-block excitation and re-

excite it in a repetitive cyclical fashion. The rotating wavefront can emanate excitation waves that
capture the surrounding tissue, causing an arrhythmia. This mechanism, in which the rotating
action potential plays the role of an “excitatory oscillator” is called reentry or circus movement.
For the reentrant wavefront to encounter an excitable tissue that is no longer refractory in the
pre-block region, the rotation time must be longer than the refractory period. Thus, slow

conduction velocity facilitates reentry. In the space domain, the concept of wavelength was
defined as λ=θT, where θ is conduction velocity and T the refractory period. As long as λ is smaller

than the length of the reentry pathway, an excitable gap exists between the head and tail of the

circulating wave and reentry is stable at a constant cycle length (frequency) of rotation. If λ is
longer than the reentry pathway, the wavefront encounters refractory tissue and reentry cannot
be sustained. When λ is similar in length to the reentry pathway, complex dynamics arise.

In the heart, reentry occurs in three-dimensional space. The reentry pathway can be fixed

or constantly changing. The reentrant action potential may propagate around an inexcitable
obstacle (e.g. naturally occurring orifices) on a fixed anatomical pathway (“anatomical reentry”)
or may reside in a region of the myocardium that is excitable in its entirety (“functional reentry”).

Dynamically, anatomical reentry is the simplest form of reentrant excitation. Many of the funda-
mental concepts and mechanistic insights into reentry were obtained from early experimental
studies in rings of excitable tissue. 231-234 A canine isolated tricuspid ring preparation 235,236,237 was
used to obtain both extracellular and intracellular (microelectrode) recordings from all segments
of the pathway during reentry, relating action potential properties to the dynamics of reentry.

A theoretical equivalent to the experimental ring preparation can be constructed by connecting
“head” and “tail” of the 1-dimensional multicellular fiber model. 222 Reentry is initiated by a
premature stimulus in the vulnerable window of an action potential generated by a primary

stimulus (Figure 3.20).

The duration of the reentrant action potential depends on the frequency of excitation and
the degree of head-tail interaction. Figure 3.21A shows reentrant action potentials in different size
rings, decreasing in size from top row (600 cells) to bottom row (50 cells) of the figure. As ring size