Abstract
To review calcium regulation, causes of hypocalcemia during critical illness, clinical features and treatment of hypocalcemia, hemodynamic effects of calcium administration, calcium-catecholamine interactions, and the role of calcium in ischemic injury. Representative articles from the medical literature are used to support the discussion of selected aspects of calcium metabolism which are important to the practice of critical care medicine. Results from both animal and human investigations and both in vitro and in vivo studies are discussed. Circulating calcium levels are best measured using ionized calcium electrodes. Ionized hypocalcemia is common in critically ill patients and usually results from impaired parathyroid hormone secretion or action, impaired vitamin D synthesis or action, or calcium chelation/precipitation. Ionized hypocalcemia most commonly presents as cardiovascular or neuromuscular insufficiency. Mild ionized hypocalcemia (greater than 0.8 mmol/L) is usually asymptomatic and frequently does not require treatment. Moderate-to-severe ionized hypocalcemia is best treated with iv calcium in the critically ill patient. The majority of studies report no increase in cardiac output but a significant increase in BP after iv calcium administration. When administered with beta-adrenergic agonists, calcium frequently impairs their cardiovascular actions. Intracellular calcium dysregulation is common during ischemic and shock states. Agents which increase intracellular calcium may be harmful during cellular ischemia. Alterations in calcium regulation and calcium concentrations are common during critical illness. Optimal management of altered calcium concentrations requires an understanding of the pathophysiology behind these alterations.
Published Version
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