Abstract
Abstract In this particular example the use of calcium therapy in resuscitation resulted in a toxic serum level and was strongly linked to the initiation of VF. A review of current arguments reveals that in the setting of cardiac arrest, calcium administration may be valueless or even hazardous, except in cases of calcium antagonist overdose, hypoparathyroidism, hyperkalemia, or hypocalcemia associated with massive citrated blood transfusion. There are no data yet on which to recommend the use of calcium in patients who have suffered cardiac arrest and who have taken a therapeutic dose of a calcium-channel antagonist. This case illustrates that ventricular fibrillation may result from the rapid induction of excessive calcium levels associated with standard doses of IV calcium chloride. Prospective evaluation is necessary to establish the appropriate dose and indications for the use of calcium chloride in cardiac arrest.
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