Theories of Defibrillation

In 1899 when Prevost and Battelli7 discovered that large electric shocks could defibrillate the fibrillating myocardium, they posed the first theory of defibrillation, which was based on the "incapacitation" effects on the myocardium of strong electric shocks. It was not until 1939 that Gurvich and Yuniev proposed the first stimulatory theory of defibrillation.48 They postulated directly stimulating and exciting the myocardium achieved defibrillation.

The stimulatory theory of defibrillation was later refined into the critical mass hypothesis in which experimentalists as well as theorists proposed that a critical mass of the myocardium (75-90%) needs to be directly defibrillated in order to fully terminate fibrillation.49-51 This theory stated that the remaining fibrillating areas not affected by the shock would self-terminate.

In 1967 Fabiato and colleagues52 demonstrated the first correlation between shock-induced fibrillation and defibrillation in a mechanism they called the "threshold of synchronous response." This idea was later extended by Chen and co-workers53 into the now well-known "upper limit of vulnerability" hypothesis. This hypothesis states that the shock must terminate all wavefronts of fibrillation and that, in order to be successful, the shock must produce a sufficient voltage gradient (above the upper limit of vulnerability [ULV]) everywhere in the myocardium as not to reinduce fibrillation. This correlation was subsequently demonstrated in several experimental studies54'55 and in humans.56'57

Although the concept of stimulus-induced reentry had been laid down decades earlier by Wiener and Rosenblueth,58 Frazier and colleagues59 were the first to obtain experimental evidence of this mechanism in 1989 in what they called the "stimulus-induced critical point" mechanism. Frazier et al. demonstrated that the chirality of reentry could be predicted based on the direction of the preshock repolarization gradient and the voltage gradient of the applied shock. After its discovery, the critical point mechanism was held responsible for reinduction of fibrillation after a failed defibrillation shock.60'61

In 1998 Dillon and Kwaku62 proposed the "progressive depolarization" hypothesis of defibrillation and shock-induced fibrillation. This theory expanded on the critical mass, threshold of synchronous response, and ULV hypotheses but with a different interpretation of the supporting experimental evidence. The progressive depolarization hypothesis states that: "(1) Progressively stronger shocks depolarize, (2) Progressively more refractory myocardium, to (3) Progressively prevent postshock wavefronts, and (4) Prolong and synchronize post-shock repolarization, in a (5) Progressively larger volume of ventricle, to (6) Progressively decrease the probability of fibrillation after the shock." Thus, this theory is based on the prolongation of repolarization and refractory periods to effectively eliminate the excitable gap and terminate fibrillation.

However, contrary to this hypothesis, theoretical and experimental evidence supports the creation of virtual electrodes of opposite polarity in response to an applied stim-ulus.44'45'63-66 Although the shock may prolong repolarization in some regions of the myocardium, it may be shortened in others. Thus, the virtual electrode mechanism casts doubt on all of the previously outlined theories of defibrillation, as these theories only account for the "stimulatory" response of defibrillation shocks. An alternative theory that accounts for both shock-induced excitation and deexcitation is the virtual electrode hypothesis of defibrillation.66-68

0 0

Post a comment