The pathophysiology of hypercalcemia-induced AV nodal conduction system disease is unknown. Calcium deposition in AV nodes of elderly patients has been associated with paroxysmal 2:1 AV block.8 It could be postulated that elevated serum calcium levels predispose to calcium deposition in cardiac conduction tissue, leading to progressive dysfunction. Although this theory may be applicable in a chronic setting, the mechanism in an acute setting likely relates to elevated serum levels of calcium that causes an alteration in electrochemical gradients. These elevated serum levels also increase intracellular calcium. This rise may result in increased calmodulin activation on the intracellular portion of the myocyte cell membrane and consequent enhanced sodium channel activation, which may then inhibit AV nodal conduction.13
Conclusion
Physicians should be aware that severe hypercalcemia can cause significant conduction system alterations, including complete AV block. A short QTc interval is typical, but a prolonged QTc interval also may be seen. While temporary support with a transvenous pacemaker may be needed, the conduction system abnormality is expected to resolve by treatment of the underlying hypercalcemia.