The mechanism of sudden cardiac death following acute fluoride intoxication has been thought to result from profound hypocalcemia produced by the precipitation of calcium fluoride salts. In studies of a canine model, the onset of lethal ventricular arrhythmias was temporally more associated with an elevation of serum potassium than with a drop in serum calcium. Fluoride-induced hyperkalemia could not be prevented with glucose, insulin, or bicarbonate. In the erythrocytes, a five-minute exposure to 10 mM NaF caused a 50% increase in extracellular potassium concentrations after 12 hours compared to control erythrocyte suspensions (P less than .001). The total potassium efflux after 12 hours of incubation was linearly related to the log of fluoride contact time (r, 0.886; P less than .001). The treatment of fluoride-induced hyperkalemia may depend on removal of fluoride and potassium.
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