We aimed to evaluate the relative role of membrane and [Ca²⁺]_i dynamics in the formation of early afterdepolarisations (EADs). We analysed the membrane system (i.e. with all intra- and extra-cellular ionic concentrations clamped) of a Luo-Rudy ventricular cell model (LRd00; [1]) using continuation algorithms with the maximal conductance of the slow delayed rectifying K⁺ current (g*_Ks) as the bifurcation parameter (Fig. 1a). A stable equilibrium existed at membrane potential V ≈ -88.5 mV for all g*_Ks. Unstable oscillations states (OS) were found in between 0.105 < g*_Ks < 0.223 mS μF⁻¹, within the physiological range. These OS originated from a subcritical Hopf bifurcation (HB) at g*_Ks ≈ 0.18 mS μF⁻¹. Two equilibria coexisted (bistability) for g*_Ks below the HB. The g*_Ks of a LRd00 epi-: mid-: endocardial cells are 0.433: 0.125: 0.289 mS μF⁻¹ [2]. The LRd00 mid-myocardial membrane model is bistable, whereas the epicardial and endocardial membrane models have a single stable equilibrium. This is confirmed by numerical integration from different initial conditions (Fig. 1b). The addition of [Ca²⁺]_i dynamics to the mid-myocardial membrane restored the model to a single equilibrium (Fig. 1d). Action potentials and EADs in the cell model (Fig. 1c) showed similar plateau and repolarization dynamics as the transients in Fig. 1d. [Ca²⁺]_i dynamics prevents the bistability of the mid-myocardial membrane model, and accounts for the EAD family of waveforms.