Bradley J Roth1, Salil G Patel. 1. Department of Physics, Oakland University, Rochester, Michigan 48309, USA. roth@oakland.edu
Abstract
INTRODUCTION: Anodal excitation of cardiac tissue occurs by two mechanisms: "make" and "break." Anodal strength-interval curves are divided into two sections, with break excitation occurring at short intervals and make at long intervals. Our goal is to determine how an elevated extracellular potassium ion concentration, [K]o, affects the mechanism of anodal excitation and influences the anodal strength-interval curve. METHODS AND RESULTS: Computer simulations of unipolar stimulation were performed using the bidomain model, with membrane kinetics governed by the Luo-Rudy model. The diastolic threshold for anodal stimulation first decreased and then increased with increasing [K]o, reaching a minimum value at [K]o = 12 mM. The mechanism for diastolic anodal excitation was make for all [K]o values except 13.3 mM, in which case it was break. For low [K]o (4 and 8 mM) the break section of the anodal strength-interval contained a "dip," but for high [K]o (12 and 13 mM), the dip disappeared. CONCLUSION: High [K]o predisposes cardiac tissue to break excitation, which is thought to play an important role in reentry induction and defibrillation. Because fibrillation raises extracellular [K]o levels, break excitation may play a more important role in defibrillation than is suggested by simulations and experiments using normal [K]o values.
INTRODUCTION: Anodal excitation of cardiac tissue occurs by two mechanisms: "make" and "break." Anodal strength-interval curves are divided into two sections, with break excitation occurring at short intervals and make at long intervals. Our goal is to determine how an elevated extracellular potassium ion concentration, [K]o, affects the mechanism of anodal excitation and influences the anodal strength-interval curve. METHODS AND RESULTS: Computer simulations of unipolar stimulation were performed using the bidomain model, with membrane kinetics governed by the Luo-Rudy model. The diastolic threshold for anodal stimulation first decreased and then increased with increasing [K]o, reaching a minimum value at [K]o = 12 mM. The mechanism for diastolic anodal excitation was make for all [K]o values except 13.3 mM, in which case it was break. For low [K]o (4 and 8 mM) the break section of the anodal strength-interval contained a "dip," but for high [K]o (12 and 13 mM), the dip disappeared. CONCLUSION: High [K]o predisposes cardiac tissue to break excitation, which is thought to play an important role in reentry induction and defibrillation. Because fibrillation raises extracellular [K]o levels, break excitation may play a more important role in defibrillation than is suggested by simulations and experiments using normal [K]o values.