A quantitative analysis of the effect of cycle length on arrhythmogenicity in hypokalaemic Langendorff-perfused murine hearts was conducted. The study investigated how changes in baseline cycle length (BCL) affect arrhythmogenicity in normokalaemic and hypokalaemic hearts, with and without lidocaine treatment. The results showed that hypokalaemia increased the incidence of arrhythmic activity at longer BCLs but not at shorter BCLs. In normokalaemic hearts, arrhythmic activity was not observed, while in hypokalaemic hearts, arrhythmic activity was observed at longer BCLs. Lidocaine treatment reduced arrhythmic activity and altered the relationship between action potential duration (APD90) and ventricular effective refractory period (VERP). The study used graphical analysis to examine the relationship between APD90 and VERP across different BCLs. It found that in normokalaemic hearts, the relationship between APD90 and VERP was linear and consistent, with a critical angle (θ) of approximately 45 degrees. Hypokalaemia shifted this relationship, increasing θ at longer BCLs where arrhythmic activity was observed. Lidocaine treatment decreased θ, indicating an antiarrhythmic effect. The analysis showed that the relationship between APD90 and VERP was more sensitive to changes in BCL than previous analyses based on transmural repolarization gradients. The study extended previous findings from single BCLs to a range of BCLs, demonstrating that the relationship between APD90 and VERP varied with BCL. The results suggest that the analysis of APD90 and VERP provides a more accurate indication of arrhythmogenicity than previous methods. The findings have implications for understanding arrhythmogenicity in physiological and pharmacological situations, particularly in conditions such as hypokalaemia and congenital long QT syndrome. The study highlights the importance of considering both APD90 and VERP in assessing arrhythmogenicity and the role of BCL in modulating these parameters.A quantitative analysis of the effect of cycle length on arrhythmogenicity in hypokalaemic Langendorff-perfused murine hearts was conducted. The study investigated how changes in baseline cycle length (BCL) affect arrhythmogenicity in normokalaemic and hypokalaemic hearts, with and without lidocaine treatment. The results showed that hypokalaemia increased the incidence of arrhythmic activity at longer BCLs but not at shorter BCLs. In normokalaemic hearts, arrhythmic activity was not observed, while in hypokalaemic hearts, arrhythmic activity was observed at longer BCLs. Lidocaine treatment reduced arrhythmic activity and altered the relationship between action potential duration (APD90) and ventricular effective refractory period (VERP). The study used graphical analysis to examine the relationship between APD90 and VERP across different BCLs. It found that in normokalaemic hearts, the relationship between APD90 and VERP was linear and consistent, with a critical angle (θ) of approximately 45 degrees. Hypokalaemia shifted this relationship, increasing θ at longer BCLs where arrhythmic activity was observed. Lidocaine treatment decreased θ, indicating an antiarrhythmic effect. The analysis showed that the relationship between APD90 and VERP was more sensitive to changes in BCL than previous analyses based on transmural repolarization gradients. The study extended previous findings from single BCLs to a range of BCLs, demonstrating that the relationship between APD90 and VERP varied with BCL. The results suggest that the analysis of APD90 and VERP provides a more accurate indication of arrhythmogenicity than previous methods. The findings have implications for understanding arrhythmogenicity in physiological and pharmacological situations, particularly in conditions such as hypokalaemia and congenital long QT syndrome. The study highlights the importance of considering both APD90 and VERP in assessing arrhythmogenicity and the role of BCL in modulating these parameters.