Arrhythmias of ventricular origin have a greatest risk of sudden death. Understanding the mechanism of arrhythmia formation and their treatment methods is not always easy. Physiological modelling help us to understand the cardiac electrophysiology and the mechanisms underlying arrhythmogenesis and arrhythmia maintenance. Electrophysiological model of the heart helps to understand the root cause of a heart disease at the cellular level and gives us a better chance of improving treatment methods and prolonging a person’s life. Biophysical models have the ability to study the propagation of electrical impulse in a two/three dimensional tissue grid, which is difficult through experiments. These models also help us to investigate the changes in ionic currents due to mutation in ion channels and to study the mechanism of arrhythmias in a tissue grid. The biophysical model given by Ten Tusscher et al. in 2004 (TNNP model) and in 2006 (TP06) are considered as more realistic models for human ventricular cells because they are based on experimental data. Therefore, TNNP and TP06 models are used for the simulation study. A study on sodium and potassium ion channel dysfunction that leads to channelopathies was conducted. Sodium ion channel (NaV1.5) dysfunction is possible due to number of mutations. SCN5A L812Q is one among them. A simulation study on effect of SCN5A L812Q gene mutation in epicardial cell and tissue were conducted. Cells and tissue grids of three genotypes, the Wild Type (WT), heterozygous mutated (L812Q/WT) and homozygous mutated (L812Q) conditions were considered for the study. Studies on vulnerable intervals for the formation of arrhythmias in two-dimensional tissue grids such as figure-of-8 reentries and spiral wave reentry are conducted. Wave break is observed in homozygous (L812Q) mutated tissue grids that relate to ventricular fibrillation. Similarly, there are a large number of mutations that lead to potassium ion channel dysfunction. Compound heterozygous KCNQ1 A300T/P535T is one among them and it leads to sudden death. The possible genotypes are Wild Type, heterozygous A300T (A300T/WT), homozygous A300T (A300T), heterozygous P535T (WT/P535T), homozygous P535T (P535T) and compound heterozygous (A300T/P535T) mutations. Therefore, the effects of above-mentioned mutations on SCN5A gene and KCNQ1 gene are studied and the results obtained can be translated clinically.