We document full exposure of the electrocardiographic hyperkalemia signs brought about by exogenous epinephrine in a patient on long-term beta-blockade treatment in whom spironolactone-induced hyperkalemia developed. We propose that the stimulated adrenergic receptor promoted re-expression of two main potassium channels (I(Kr), I(Ks)) involved in ventricular repolarization, modifying the ECG waveform. The effects of hyperkalemia could be aggravated in the presence of beta-adrenergic blockade.