Abstract
Calcium is a critical intracellular messenger and regulator of cell function. Calcium is essential for excitation–contraction coupling in muscle, neurotransmission, cell division, hormonal release, phagocytosis, chemotaxis, and numerous other activities. Although these functions are usually beneficial, calcium also regulates processes that can injure and kill cells such as digestive enzyme activation, cytokine release, free radical production, inhibition of ATP synthesis, and vasoconstriction. Thus, calcium is truly a double-edged sword.
Keywords
- Parathyroid Gland
- Primary Hyperparathyroidism
- Chronic Granulomatous Disease
- Digestive Enzyme Activation
- Calcium Gluconate
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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References
Zivin JR, Gooley T, Zager RA, et al. Hypocalcemia: a pervasive metabolic abnormality in the critically ill. Am J Kidney Dis. 2001;37:689–698.
Lind L, Carlstedt F, Rastad J, et al. Hypocalcemia and parathyroid hormone secretion in critically ill patients. Crit Care Med. 2000;28:93–99.
Zaloga GP, Chernow B. The multifactorial basis for hypocalcemia during sepsis. Studies of the parathyroid hormone–vitamin D axis. Ann Intern Med. 1987;107:36–41.
Lee P, Eisman JA, Center JR. Vitamin D deficiency in critically ill patients. N Engl J Med. 2009;360:1912–1913.
Todd JC, III, Mollitt DL. Effect of sepsis on erythrocyte intracellular calcium homeostasis. Crit Care Med. 1995;23:459–465.
Sayeed MM, Zhu M, Maitra SR, et al. Alterations in cellular calcium and magnesium during circulatory/septic shock. Magnesium. 1989;8:179–189.
Malcolm DS, Zaloga GP, Holaday JW. Calcium administration increases the mortality of endotoxic shock in rats. Crit Care Med. 1989;17:900–903.
Zaloga GP, Sager A, Black KW, et al. Low dose calcium administration increases mortality during septic peritonitis in rats. Circ Shock. 1992; 37:226–229.
Cuschieri J, Gourlay D, Garcia I, et al. Slow channel calcium inhibition blocks proinflammatory gene signaling and reduces macrophage responsiveness. J Trauma. 2002;52:434–442.
Lee HC, Hardman JM, Lum BK. Effects of nicardipine in rats subjected to endotoxic shock. Gen Pharmacol. 1992;23:71–74.
Szabo C, Hasko G, Nemeth ZH, et al. Calcium entry blockers increase interleukin-10 production in endotoxemia. Shock. 1997;7:304–307.
Sirmagul B, Kilic FS, Tunc O, et al. Effects of verapamil and nifedipine on different parameters in lipopolysaccharide-induced septic shock. Heart Vessels. 2006;21:162–168.
Mustafa SB, Olson MS. Effects of calcium channel antagonists on LPS-induced hepatic iNOS expression. Am J Physiol. 1999;277:G351–G360.
Forsythe RM, Wessel CB, Billiar TR, et al. Parenteral calcium for intensive care unit patients. Cochrane Database Syst Rev. 2008;CD006163.
Carlstedt F, Lind L. Hypocalcemic syndromes. Crit Care Clin. 2001;17:139–153.
Zaloga GP. Hypocalcemia in critically ill patients. Crit Care Med. 1992;20:251–262.
Lang RM, Fellner SK, Neumann A, et al. Left ventricular contractility varies directly with blood ionized calcium. Ann Intern Med. 1988;108:524–529.
Vincent JL, Bredas P, Jankowski S, et al. Correction of hypocalcaemia in the critically ill: what is the haemodynamic benefit? Intensive Care Med. 1995;21:838–841.
Ariyan CE, Sosa JA. Assessment and management of patients with abnormal calcium. Crit Care Med. 2004;32:S146-S154.
Stewart AF. Clinical practice. Hypercalcemia associated with cancer. N Engl J Med. 2005;352:373–379.
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Marik, P.E. (2010). Hypo- and Hypercalcemia. In: Handbook of Evidence-Based Critical Care. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-5923-2_41
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DOI: https://doi.org/10.1007/978-1-4419-5923-2_41
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