Increased QT dispersion (QTd) has been associated with increased risk for ventricular arrhythmias. Pathologic extracellular electrolyte concentrations may result in ventricular arrhythmias. The aim of this study was to evaluate the effect of electrolyte abnormalities on QTd. Ten consecutive patients with isolated electrolyte abnormalities were selected for each of the following groups: hypokalemia, hyperkalemia, hypercalcemia, hypocalcemia, hypomagnesemia, and normal controls. Standard 12-lead electrocardiography was performed for each patient and average QT, JT, and RR intervals were calculated for each lead. Dispersion of QT, JT (JTd), and QTc (QTcd) intervals were calculated as the range between the longest and shortest measurements. Compared with controls, only patients with hypokalemia had a greater QTd (115 ± 31 vs. 49 ± 15 ms), JTd (116 ± 34 vs. 52 ± 12 ms), and QTcd (141 ± 40 vs. 58 ± 1 ms), (P < 0.05). In an experimental substudy, seven rats were maintained on K+ and seven on Mg2+-free diet followed by normal diet. Experimental hypokalemia significantly increased QTd (10 ± 4 to 37 ± 7 ms), and QTcd (32 ± 6 to 79 ± 27 ms) (P < 0.05), whereas hypomagnesemia did not. Restoration of serum potassium resulted in normalization of dispersion (QTd, 14 ± 2; QTcd, 34 ± 6 ms). Hypokalemia increases the dispersion of ventricular repolarization that may be responsible for arrhythmias. Even though hyperkalemia, hypocalcemia, and hypercalcemia are known to affect ventricular repolarization, our study shows that they are not associated with increased dispersion.