Acute myocardial ischaemia is associated with fatal cardiac arrhythmogenesis. In this study we computed the effects of the ischaemia induced changes of cellular ionic and metabolic conditions on ventricular electrophysiology – transmural heterogeneity, excitation conduction patterns, and characteristics of ECG. The Luo-Rudy dynamical model (LRd) of electrical action potential (AP) of guinea-pig ventricular myocytes was modified to incorporate the ischaemia induced changes on cellular membrane ionic currents and intra- and extra-cellular K+ ion concentrations [1]. These changes include (1) the elevation of the extra-cellular K+ concentration ([K+]o was set to 12 mM); (2) intra-cellular and extra-cellular acidosis (pH was set to 6.5) that reduces the maximal conductance of the L-type Ca2+ and Na+ channels by 25% respectively. A depolarising shift of the Na+ channel kinetics (by 3.4 mV) and a decrease in [K+]i (set to 125 mM) caused by extra-cellular acidosis were also included; 3) activation of IK(ATP) current produced by a decrease in [ATP]i (set to 3.0 mM) associated with anoxia and metabolic blockade. The modified cell model was then incorporated into a one-dimensional partial differential equation (PDE) model of transmural ventricular strand that incorporates the regional differences of electrical AP and sensitivity of IK(ATP) to [ATP]i. Transmural heterogeneity was quantified by the dispersions of APD90 and cell membrane potentials under normal and ischaemia conditions. Characteristics of computed pseudo-ECG, such as the width of QRS complex, QT time interval and the width and amplitude of the T-wave were also quantified. Simulations of ischaemia-induced changes on cellular ion channel kinetics and metabolic condition abbreviate ventricular AP with greater effects on epicardial (EPI) and midmyocardial (MID) cells than the endocardial (ENDO) cell. This attenuated rather than augmented the transmural dispersions of measured APD90 and cell membrane potentials. There was a significant increase in the width of the QRS complex in the computed pseudo-ECG (changed from 18 ms in normal to 34 ms in ischaemia conditions), which indicated a dramatic slowing down of transmural ventricular excitation conduction. Ischaemia shortened the QT time interval (changed from 153 ms in normal to 98 ms in ischaemia conditions) and the width of the T-wave. The measured time interval between the peak of the T-wave (Tp) and the end of the T-wave (Te) decreased from 34 ms in normal condition to 22 ms in ischaemia condition. Under our simulation conditions global acute myocardial ischaemia does not augment the transmural heterogeneity of ventricular electrophysiology, but does lead to a shortened QT interval.