Ventricular fibrillation in the human heart results in global myocardial ischaemia. The aim of this study was to examine how ischaemia modulates the stability and period of re-entry in a computational model of human ventricular tissue. 2D tissue sheets were simulated using the monodomain equation with cellular electrophysiology described by the Ten Tusscher 2006 model. We modeled ischaemia by elevating [K⁺]_o, reducing GCa_L, and activating the ATP dependent K⁺ current. These changes acted to prolong the refractory period of tissue, to reduce conduction velocity, and to flatten restitution. In simulated normal tissue, re-entry had a period of between 230 and 300 ms, whereas in simulated ischaemic tissue the period was prolonged to around 400 ms. Elevating [K⁺]_o to 8.0 mM converted unstable re-entry to stable re-entry. The mechanisms that sustain fibrillation in normal and globally ischaemic human ventricular tissue are likely to be different.