This study investigates the effect of cycle length (BCL) on arrhythmogenicity in hypokalaemic Langendorff-perfused murine hearts. The clinically established proarrhythmic effect of bradycardia and the antiarrhythmic effect of lidocaine were reproduced in these hearts paced over a range of BCLs (80–180 ms). Action potential durations (APD90s), transmural conduction times, and ventricular effective refractory periods (VERPs) were measured during programmed electrical stimulation. A novel graphical analysis of epicardial and endocardial relationships between APD90 and VERP yielded predictions that precisely matched the arrhythmogenic findings across all BCLs studied. In normokalaemic hearts, these relationships were described by straight lines with gradients not significantly different from unity, subtending constant critical angles. Hypokalaemia shifted all points to the left of these reference lines, increasing the critical angles at BCLs where arrhythmic activity was observed. Lidocaine treatment disrupted these linear relationships and decreased the critical angles, confirming its antiarrhythmic effect. This study extends previous analyses by generalizing the relationship between arrhythmogenicity and transmural repolarization gradients to a range of BCLs, providing a more sensitive indication of lidocaine's effect than considering transmural repolarization gradients alone.This study investigates the effect of cycle length (BCL) on arrhythmogenicity in hypokalaemic Langendorff-perfused murine hearts. The clinically established proarrhythmic effect of bradycardia and the antiarrhythmic effect of lidocaine were reproduced in these hearts paced over a range of BCLs (80–180 ms). Action potential durations (APD90s), transmural conduction times, and ventricular effective refractory periods (VERPs) were measured during programmed electrical stimulation. A novel graphical analysis of epicardial and endocardial relationships between APD90 and VERP yielded predictions that precisely matched the arrhythmogenic findings across all BCLs studied. In normokalaemic hearts, these relationships were described by straight lines with gradients not significantly different from unity, subtending constant critical angles. Hypokalaemia shifted all points to the left of these reference lines, increasing the critical angles at BCLs where arrhythmic activity was observed. Lidocaine treatment disrupted these linear relationships and decreased the critical angles, confirming its antiarrhythmic effect. This study extends previous analyses by generalizing the relationship between arrhythmogenicity and transmural repolarization gradients to a range of BCLs, providing a more sensitive indication of lidocaine's effect than considering transmural repolarization gradients alone.