The role of conductivity discontinuities in design of cardiac debrillation

<p>Fibrillation is an erratic electrical state of the heart, of rapid twitching rather than&nbsp;organized contractions. Ventricular brillation is fatal if not treated promptly. The&nbsp;standard treatment, debrillation, is a strong electrical shock to reinitialize the elec-trical dynamics and allow a normal heart beat. Both the normal and the brillatory&nbsp;electrical dynamics of the heart are organized into moving wave fronts of changing electrical signals, especially in the transmembrane voltage, which is the potential dif-ference between the cardiac cellular interior and the intracellular region of the heart.<br />
In a normal heart beat, the wave front motion is from bottom to top and is accom-panied by the release of Ca ions to induce contractions and pump the blood. In a&nbsp;brillatory state, these wave fronts are organized into rotating scroll waves, with a&nbsp;centerline known as a lament. Treatment requires altering the electrical state of the heart through an externally applied electrical shock, in a manner that precludes the&nbsp;existence of the laments and scroll waves. Detailed mechanisms for the success of&nbsp;this treatment are partially understood, and involve local shock-induced changes in<br />
the transmembrane potential, known as virtual electrode alterations. These trans-membrane alterations are located at boundaries of the cardiac tissue, including blood vessels and the heart chamber wall, where discontinuities in electrical conductivity&nbsp;occur. The primary focus of this paper is the debrillation shock and the subsequent&nbsp;electrical phenomena it induces. Six partially overlapping causal factors for debril-lation success are identied from the literature. We present evidence in favor of veof these and against one of them. A major conclusion is that a dynamically growing<br />
wave front, starting at the heart surface appears to play a primary role during deb-rillation by critically reducing the volume required to sustain the dynamic motion of&nbsp;scroll waves; in contrast, virtual electrode occurring at boundaries of small, isolated&nbsp;blood vessels only cause minor e ects. As a consequence, we suggest that the size&nbsp;of the heart (specically, the surface to volume ratio) is an important debrillation&nbsp;variable.</p>

<p>Fibrillation is an erratic state of the electrical signals in the heart, character-<br />
ized by twitching rather than organized contractions. It is fatal if not treated<br />
promptly. It is a common cause of cardiac arrest, with 350,000 out of hospital US&nbsp;occurrences annually. The recommended treatment is a strong electrical shock,&nbsp;to reset the cardiac electrical activity, and allow resumption of a normal heart&nbsp;beat. The imperfect understanding of debrillation mechanisms and the high di-mensionality of its parameter space are obstacles to optimization of debrillation treatment protocols. This work focuses on virtual electrodes, which are charges&nbsp;occurring at cardiac boundaries, (e. g. cardiac and blood vessel surfaces), due to<br />
shock induced alterations in the transmembrane potential. They are of primary&nbsp;importance for debrillation. We present evidence that a dynamically growing&nbsp;wave front, starting at the heart surface, and aided by the dynamics of the fib-rillation scroll waves to be more important than small, isolated blood vessels in&nbsp;terminating brillation. This conclusion is important for multiple reasons. It&nbsp;sheds light on mechanisms of virtual electrode formation and debrillation. It&nbsp;allows a prioritization of experimental, simulation and modeling focus, It places&nbsp;more emphasis on larger experimental animals for assessing novel low strength&nbsp;debrillation strategies.</p>