Recent studies suggest that atrial fibrillation (AF) is maintained by fibrillatory conduction emanating from a small number of high-frequency reentrant sources (rotors). Our goal was to study the ionic correlates of a rotor during simulated chronic AF conditions. We utilized a two-dimensional (2-D), homogeneous, isotropic sheet (5×5cm²) of human atrial cells to create a chronic AF substrate, which was able to sustain a stable rotor (dominant frequency ∼5.7Hz, rosette-like tip meander ∼2.6cm). Doubling the magnitude of the inward rectifier K⁺ current (I_K1) increased rotor frequency (∼8.4Hz), and reduced tip meander (∼1.7cm). This rotor stabilization was due to a shortening of the action potential duration and an enhanced cardiac excitability. The latter was caused by a hyperpolarization of the diastolic membrane potential, which increased the availability of the Na⁺ current (I_Na). The rotor was terminated by reducing the maximum conductance (by 90%) of the atrial-specific ultrarapid delayed rectifier K⁺ current (I_Kur), or the transient outward K⁺ current (I_to), but not the fast or slow delayed rectifier K⁺ currents (I_Kr/I_Ks). Importantly, blockade of I_Kur/I_to prolonged the atrial action potential at the plateau, but not at the terminal phase of repolarization, which led to random tip meander and wavebreak, resulting in rotor termination. Altering the rectification profile of I_K1 also slowed down or abolished reentrant activity. In combination, these simulation results provide novel insights into the ionic bases of a sustained rotor in a 2-D chronic AF substrate.