Calcium chloride (CaCl2) is an ionic form of intravenous calcium repletion with roughly three times more bioavailable calcium than its organic counterpart – calcium gluconate.
The teaching that one needs a functional liver to metabolize calcium gluconate before calcium becomes bioavailable is wrong, as shown in patients undergoing liver transplantation during the anhepatic phase. In addition, there are plenty of cited cases where the extravasation of calcium CHLORIDE from peripheral veins led to injuries (pain, tissue necrosis, etc.) as the medication is a vesicant. So why don’t we use higher doses of calcium gluconate for repletion?
In the OR, my cardiac medication tray is stocked with calcium chloride. In the ICU, crash carts are stocked with calcium chloride. Perhaps the lack of options drives our practices? Or maybe in these acute care settings, the ability to get more “bang for the buck” with a single syringe of calcium chloride is more prudent?
I routinely use calcium chloride (yes, even in large peripheral IVs) to mitigate citrate toxicity from massive transfusions, as an inotrope/vasopressor, and stabilize the myocardial membranes in cases of hyperkalemia. However, if patients are hemodynamically stable with limited access, I’ll consider using calcium gluconate as an alternative.
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