Abstract
Physiological U wave genesis occurs likely secondary to either late repolarisation of Purkinje fibres, or late repolarisation of some myocardial cells and/or delayed after depolarisation of the ventricular wall occurring during ventricular filling. Hypokalaemia has a well-known association with pathological 'U wave' which actually combines with the T wave (TU complex) and results from slowing of phase 3 of the action potential with resultant electrical interaction between the three myocardial layers. U waves usually tend to disappear in the setting of hyperkalaemia. We report an unusual case where hyperkalaemia and discordant U waves coexisted. We believe that this may have occurred as a result of partial clinical adaptation of cardiac myocytes to the long-standing effects of hyperkalaemia as the patient had underlying history of chronic kidney disease. We also discuss the possible mechanisms of the U wave genesis and the importance of different U wave morphologies encountered in the real clinical practice.