Fibrillation is an erratic electrical state of the heart, of rapid twitching rather than organized contractions. Ventricular brillation is fatal if not treated promptly. The 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 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.
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 brillatory state, these wave fronts are organized into rotating scroll waves, with a 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 existence of the laments and scroll waves. Detailed mechanisms for the success of this treatment are partially understood, and involve local shock-induced changes in
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 occur. The primary focus of this paper is the debrillation shock and the subsequent 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
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 scroll waves; in contrast, virtual electrode occurring at boundaries of small, isolated blood vessels only cause minor e ects. As a consequence, we suggest that the size of the heart (specically, the surface to volume ratio) is an important debrillation variable.
Fibrillation is an erratic state of the electrical signals in the heart, character-
ized by twitching rather than organized contractions. It is fatal if not treated
promptly. It is a common cause of cardiac arrest, with 350,000 out of hospital US occurrences annually. The recommended treatment is a strong electrical shock, to reset the cardiac electrical activity, and allow resumption of a normal heart 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 occurring at cardiac boundaries, (e. g. cardiac and blood vessel surfaces), due to
shock induced alterations in the transmembrane potential. They are of primary importance for debrillation. We present evidence that a dynamically growing 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 terminating brillation. This conclusion is important for multiple reasons. It sheds light on mechanisms of virtual electrode formation and debrillation. It allows a prioritization of experimental, simulation and modeling focus, It places more emphasis on larger experimental animals for assessing novel low strength debrillation strategies.
Fibrillation is an erratic electrical state of the heart, of rapid twitching rather than organized contractions. Ventricular brillation is fatal if not treated promptly. The 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 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.
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 brillatory state, these wave fronts are organized into rotating scroll waves, with a 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 existence of the laments and scroll waves. Detailed mechanisms for the success of this treatment are partially understood, and involve local shock-induced changes in
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 occur. The primary focus of this paper is the debrillation shock and the subsequent 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
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 scroll waves; in contrast, virtual electrode occurring at boundaries of small, isolated blood vessels only cause minor e ects. As a consequence, we suggest that the size of the heart (specically, the surface to volume ratio) is an important debrillation variable.
Fibrillation is an erratic state of the electrical signals in the heart, character-
ized by twitching rather than organized contractions. It is fatal if not treated
promptly. It is a common cause of cardiac arrest, with 350,000 out of hospital US occurrences annually. The recommended treatment is a strong electrical shock, to reset the cardiac electrical activity, and allow resumption of a normal heart 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 occurring at cardiac boundaries, (e. g. cardiac and blood vessel surfaces), due to
shock induced alterations in the transmembrane potential. They are of primary importance for debrillation. We present evidence that a dynamically growing 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 terminating brillation. This conclusion is important for multiple reasons. It sheds light on mechanisms of virtual electrode formation and debrillation. It allows a prioritization of experimental, simulation and modeling focus, It places more emphasis on larger experimental animals for assessing novel low strength debrillation strategies.