Calcium salts, such as calcium chloride and calcium gluconate, antagonize cardiac toxicity by increasing the threshold potential and reestablishing cardiac excitability but have no direct effect on potassium levels. Calcium administration shifts the threshold potential shifts to a less negative value (that is, from –75 mV to –65 mV), so that the initial difference between resting and threshold potentials of 15 mV can be restored. Calcium therapy forhyperkalemia is contraindicated in the setting of digoxin toxicity because calcium can potentiate the toxic effects of this drug.