Format

Send to

Choose Destination
See comment in PubMed Commons below
J Nat Sci. 2015 Aug;1(8). pii: e160.

ELECTRICAL INSTABILITY DUE TO REGIONAL INCREASE IN EXTRACELLULAR POTASSIUM ION CONCENTRATION.

Author information

1
Department of Physics, Oakland University, Rochester, Michigan.

Abstract

INTRODUCTION:

Ventricular tachycardia and ventricular fibrillation are the two most dangerous arrhythmias. Both are related to reentrant electrical activity in the ventricles. Many studies of arrhythmias consider a homogeneous sheet of cardiac tissue. Since normal ventricular myocardium is inhomogeneous and inhomogeneities play an important role in the induction of reentry, we investigate the effect of a localized inhomogeniety developed at the border between normal and ischemic region.

METHODS:

We used the bidomain model to represent the electrical properties of cardiac tissue and a modified version of the dynamic Luo-Rudy (LRd) model to represent the active properties of the membrane. To investigate the effect of a localized inhomogeneity, the extracellular potassium [K]e concentration is raised to 10 mM from normal [K]e (4 mM) on the right half of the tissue.

RESULTS AND DISCUSSION:

A train of cathodal stimuli are applied from the lower left corner of the tissue with different basic cycle lengths (BCL). At certain BCL, the spatial heterogeneity created with regional elevation of [K]e can lead to action potential instability (alternans) in the normal and border regions, and 2:1 conduction block in the ischemic region. We observed the reentry when local heterogeneity in [K]e is changed from 10 to 12 mM on the right half of the virtual ventricular myocardium sheet.

CONCLUSION:

Electrical alternans occur during high heart rates and are observed in patients suffering from ventricular tachycardia. It is an early indication of left ventricular systolic impairment. This study will help to evaluate alternans as a predictor and guide for antiarrhythmic therapy.

KEYWORDS:

Arrhythmias; Luo-Rudy Model; alternans; bidomain model

PMID:
28795153
PMCID:
PMC5546303
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for PubMed Central
    Loading ...
    Support Center