Dr. Thotakura and Dr. Barnett are both cardiology fellows, Dr. Stafford is an internal medicine resident, and Dr. Slicker is an interventional cardiology fellow, all at Baylor Scott & White Hospital in Temple, Texas. Dr. Kramer is chief of cardiology and Dr. Gupta is director, cardiac catheterization laboratory, both at Central Texas Veterans Health Care System in Temple. Dr. Kramer is associate professor of medicine and Dr. Gupta is assistant professor of medicine, both at Texas A&M Health Science Center in Temple.
Author disclosures The authors report no actual or potential conflicts of interest with regard to this article.
Disclaimer The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.
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.
