Biomedical subjects

K Skouibine

Publications and source records attributed to K Skouibine.

7 recordsLinked to original sources

PubMed2000

A numerically efficient model for simulation of defibrillation in an active bidomain sheet of myocardium.

Presented here is an efficient algorithm for solving the bidomain equations describing myocardial tissue with active membrane kinetics. An analysis of the accuracy shows advantages of this numerical technique over other simple and therefore popular approaches. The modular structure of the algorithm provides the critical flexibility needed in simulation studies: fiber orientation and membrane kinetics can be easily modified. The computational tool described here is designed specifically to simulate cardiac defibrillation, i. e., to allow modeling of strong electric shocks applied to the myocardium extracellularly. Accordingly, the algorithm presented also incorporates modifications of the membrane model to handle the high transmembrane voltages created in the immediate vicinity of the defibrillation electrodes.

Algorithms↗

PubMed2000

Termination of spiral waves with biphasic shocks: role of virtual electrode polarization.

INTRODUCTION: This simulation study seeks to extend the virtual electrode polarization (VEP) theory for defibrillation to explain the success and failure of biphasic shocks. The goals of the study are to (1) provide insight into why optimal biphasic shocks have a lower voltage defibrillation threshold than monophasic shocks, (2) examine the mechanisms of biphasic shock failure and to determine whether they differ from those of monophasic shocks, and (3) study how the timing of biphasic shock delivery to a spiral wave affects voltage defibrillation threshold. METHODS AND RESULTS: A spiral wave is initiated in a bidomain representation of a 2-cm x 2-cm sheet of ventricular myocardium. The model incorporates nonuniform fiber curvature, membrane kinetics suitable for high-strength shocks, and electroporation. A spatially uniform extracellular field is delivered by line electrodes. The shock establishes VEP that dictates the postshock activity in the tissue. Our results demonstrate that the second phase of biphasic shocks leaves the tissue with substantially smaller postshock excitable gap, thus eliminating the majority of the substrate for reinitiation of reentrant activity. Further, the occurrence of break excitations for weaker biphasic shocks indicates that the mechanisms for biphasic shock failure are more complex than for monophasic shocks. Biphasic voltage defibrillation thresholds range from 8 to 16 V/cm, depending on the position of the spiral wave. An increase in the amount of preshock excitable gap leads to an increase in voltage defibrillation threshold. CONCLUSION: This study demonstrates the importance of VEP and its interaction with preshock activity in the success and failure of biphasic defibrillation shocks.

Computer Simulation↗

PubMed2000

Success and failure of the defibrillation shock: insights from a simulation study.

INTRODUCTION: This simulation study presents a further inquiry into the mechanisms by which a strong electric shock fails to halt life-threatening cardiac arrhythmias. METHODS AND RESULTS: The research uses a model of the defibrillation process that represents a sheet of myocardium as a bidomain. The tissue consists of nonuniformly curved fibers in which spiral wave reentry is initiated. Monophasic defibrillation shocks are delivered via two line electrodes that occupy opposite tissue boundaries. In some simulation experiments, the polarity of the shock is reversed. Electrical activity in the sheet is compared for failed and successful shocks under controlled conditions. The maps of transmembrane potential and activation times calculated during and after the shock demonstrate that weak shocks fail to terminate the reentrant activity via two major mechanisms. As compared with strong shocks, weak shocks result in (1) smaller extension of refractoriness in the areas depolarized by the shock, and (2) slower or incomplete activation of the excitable gap created by deexcitation of the negatively polarized areas. In its turn, mechanism 2 is associated with one or more of the following events: (a) lack of some break excitations, (b) latency in the occurrence of the break excitations, and (c) slower propagation through deexcited areas. Reversal of shock polarity results in a change of the extent of the regions of deexcitation, and thus, in a change in defibrillation threshold. CONCLUSION: The results of this study indicate the paramount importance of shock-induced deexcitation in both defibrillation and postshock arrhythmogenesis.

Electric Countershock↗

PubMed2000

Increasing the computational efficiency of a bidomain model of defibrillation using a time-dependent activating function.

Realistic simulations of the effects of strong shocks on cardiac muscle require solving the bidomain model, a continuum representation of cardiac tissue by a system of two reaction-diffusion equations. For two- and three-dimensional problems, the computations tend to take a prohibitively long time. This study develops a computationally efficient and accurate approximation of the bidomain model: a "reduced bidomain" model. The approximation is based on the fact that during a strong shock, the extracellular field in the muscle changes only slightly and, therefore, can be approximated by an activating function, following the concept introduced by Rattay (Rattay, F. Analysis of models for external stimulation of axons. IEEE Trans. Biomed. Eng. 33:974-977, 1986). The activating function used here is time-dependent and is computed using an iterative algorithm. The results show that in two spatial dimensions, the "reduced bidomain" model, as implemented in this study, cuts the computational cost by two orders of magnitude while preserving most properties of the "full bidomain" model. It faithfully represents the spatial pattern and the temporal development of the muscle polarization. Consequently, relative errors in the "defibrillation" threshold, the strength of the weakest shock that terminates all electrical activity within 100 ms, are below 10%.

Action Potentials↗

PubMed1999

Extension of refractoriness in a model of cardiac defibrillation.

This simulation study presents an inquiry into the mechanisms by which a strong electric shock halts life-threatening cardiac arrhythmias. It examines the "extension of refractoriness" hypothesis for defibrillation which postulates that the shock induces an extension of the refractory period of cardiac cells thus blocking propagating waves of arrhythmia and fibrillation. The present study uses a model of the defibrillation process that represents a sheet of myocardium as a biodomain with unequal anisotropy ratios. The tissue consists of curved fibers in which spiral wave reentry is initiated. The defibrillation shock is delivered via two line electrodes that occupy opposite tissue boundaries. Simulation results demonstrate that a large-scale region of depolarization is induced throughout most of the tissue. This depolarization extends the refractoriness of the cells in the region. In addition, new wavefronts are generated from the regions of induced hyperpolarization that further restrict the spiral wave pathway and cause its termination.

Anisotropy↗

PubMed1998

Modeling defibrillation: effects of fiber curvature.

The goal of this modeling study is to demonstrate extinguishing of a spiral wave reentry in a sheet of myocardium that incorporates curved fibers. The tissue is represented as a homogeneous bidomain with unequal anisotropy ratios. The spiral wave is initiated via cross-field stimulation of the bidomain sheet. The defibrillation shock is delivered via two line electrodes that occupy opposite tissue boundaries. Simulation results demonstrate that large-scale regions of depolarization are induced under the cathode as well as at locations in the vicinity of the anode. For high shock strengths, the new wavefronts generated from the regions of induced depolarization restrict the spiral wave pathway and render the tissue too refractory to further maintain the reentry. Weak shocks leave large portions of the sheet unaffected allowing the spiral wave to find recovered tissue and thus survive.

Anisotropy↗

PubMed1998

Virtual electrode effects in defibrillation.

This modeling study demonstrates that a re-entrant activity in a sheet of myocardium can be extinguished by a defibrillation shock delivered via extracellular point-source electrodes which establish spatially non-uniform applied field. The tissue is represented as a homogeneous bidomain with unequal anisotropy ratios in the cardiac conductivities. Spiral wave re-entry is initiated in the bidomain sheet following an S1-S2 stimulation protocol. The results indicate that the point-source defibrillation shock establishes large-scale changes in transmembrane potential in the tissue (virtual electrodes) that are 'superimposed' over regions of various degrees of membrane refractoriness in the myocardium. The close proximity of large-scale shock-induced regions of alternating membrane polarity is central to the ability of the shock to terminate the spiral wave. The new wavefronts generated following anode/cathode break phenomena restrict the spiral wave and render the tissue too refractory to further maintain the re-entry. In contrast, shocks delivered via line electrodes establish, in close proximity to the electrode, changes in transmembrane potential that are of same-sign polarity. These shocks are incapable of terminating the re-entrant activation.

Anisotropy↗