  It has become widely accepted that the most dangerous cardiac arrhythmias are
due to re- entrant waves, i.e., electrical wave(s) that re-circulate repeatedly
throughout the tissue at a higher frequency than the waves produced by the
heart's natural pacemaker (sinoatrial node). However, the complicated structure
of cardiac tissue, as well as the complex ionic currents in the cell, has made
it extremely difficult to pinpoint the detailed mechanisms of these
life-threatening reentrant arrhythmias. A simplified ionic model of the cardiac
action potential (AP), which can be fitted to a wide variety of experimentally
and numerically obtained mesoscopic characteristics of cardiac tissue such as
AP shape and restitution of AP duration and conduction velocity, is used to
explain many different mechanisms of spiral wave breakup which in principle can
occur in cardiac tissue. Some, but not all, of these mechanisms have been
observed before using other models; therefore, the purpose of this paper is to
demonstrate them using just one framework model and to explain the different
parameter regimes or physiological properties necessary for each mechanism
(such as high or low excitability, corresponding to normal or ischemic tissue,
spiral tip trajectory types, and tissue structures such as rotational
anisotropy and periodic boundary conditions). Each mechanism is compared with
data from other ionic models or experiments to illustrate that they are not
model-specific phenomena. The fact that many different breakup mechanisms exist
has important implications for antiarrhythmic drug design and for comparisons
of fibrillation experiments using different species, electromechanical
uncoupling drugs, and initiation protocols.
