It was previously demonstrated that transmural electrophysiological heterogeneities can inscribe the ECG T-wave. However, the bifurcated T wave caused by loss of IK1 function is not fully explained by transmural heterogeneities. Since right ventricular (RV) guinea pig myocytes have significantly lower I_K1 than left (LV), we hypothesized that the complex ECG can be inscribed by heterogeneous chamber specific responses to hypokalemia and partial I_K1 blockade. Ratiometric optical action potentials were recorded from the epicardial surface of the RV and LV. BaCl₂ (10 µmol/L) was perfused to partially block I_K1 in isolated guinea pig whole-heart preparations. BaCl₂ or hypokalemia alone significantly increased RV basal (RV_B) action potential duration (APD) by approximately 30% above control compared to LV apical (LV_A) (14%, p<0.05). In the presence of BaCl₂ , 2mmol/L extracellular potassium (hypokalemia) further increased RV_B APD to a greater extent (31%) than LV_A APD (19%, p<0.05) compared to BaCl₂ perfusion alone. Maximal dispersion between RV_B and LV_A APD increased by 105%,(p<0.05) and the QT interval prolonged by 55% (p<0.05) during hypokalemia and BaCl₂ . Hypokalemia and BaCl₂ produced an ECG with a double repolarization wave. The first wave (QT1) corresponded to selective depression of apical LV plateau potentials, while the second wave (QT2) corresponded to the latest repolarizing RV basal myocytes. These data suggest that final repolarization is more sensitive to extracellular potassium changes in regions with reduced I_K1, particularly when I_K1 availability is reduced. Furthermore, underlying I_K1 heterogeneities can potentially contribute to the complex ECG during I_K1 loss of function and hypokalemia.