Purpose: 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.
Design: 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.
Subjects: Results from both animal and human investigations and both in vitro and in vivo studies are discussed.
Results: 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.
Conclusions: 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.