Calcium gluconate treats hypermagnesemia through direct antagonism of magnesium at the site of action (e.g., at the neuromuscular junction). This toxicity is due to magnesium’s effect on blocking calcium and potassium channels, both extracellularly and intracellularly. Magnesium toxicity can present in several ways, including diminished deep tendon reflexes, cardiopulmonary arrest, and respiratory depression. Īcute magnesium toxicity is rare and typically seen in patients being given magnesium sulfate to prevent eclampsia in the obstetric setting. However, dialysis is the most efficacious means of potassium excretion, particularly in patients with renal disease. However, though calcium protects myocytes from potassium, it does not resolve the issue of hyperkalemia, for which other medications are typically administered, such as insulin and dextrose or sodium bicarbonate, which shifts potassium into cells and sodium polystyrene sulfate, which increases potassium excretion through stool. Calcium supplementation decreases the threshold to restore the transmembrane voltage gradient. Elevated potassium levels destabilize cardiac membranes by increasing the threshold potential of cardiac myocytes.

Calcium should promptly be administered to any patient presenting with hyperkalemia with EKG changes, indicating a hyperkalemic emergency. The role of calcium gluconate in treating hyperkalemia is to stabilize cardiac cell membranes. Įlevations of extracellular potassium can cause cardiac arrhythmias, which can progress to cardiac arrest and death. Empirically, calcium gluconate is used when the cause of cardiac arrest is due to hyperkalemia or hypermagnesemia. There is no sufficient evidence to indicate empiric usage of calcium gluconate in hypocalcemia or hypercalcemia during cardiac arrest, as it is rare for calcium abnormalities to cause cardiac arrest.

Hypomagnesemia causes hypocalcemia by impairing parathyroid hormone secretion and renal resistance to parathyroid hormone, leading to decreased renal reabsorption of calcium. In severe hypocalcemia with seizures, laryngospasm, hypotension, or tetany, patients should receive emergent parenteral calcium gluconate to replenish calcium levels until severe and life-threatening abnormalities resolve. It is essential to check magnesium levels during calcium repletion as hypomagnesemia is a crucial cause of hypocalcemia. Hypocalcemia treatment initially focuses on symptomatic treatment rather than normalizing serum calcium. EKG abnormalities of hypocalcemia, such as QT prolongation, typically respond to IV calcium gluconate, returning the QT interval to baseline. On EKG, hypocalcemia presents with prolonged QT interval, but its significance is undetermined as it is rare for calcium derangements to be the etiology of cardiac arrest. Physical examination findings include hyperreflexia, carpopedal spasm, Trousseau sign, and Chvostek sign. Symptoms include circumoral paresthesias, muscle cramps, myalgias, dysphagia, depression, confusion, irritability, seizures, tetany, laryngospasm, and hypotension. Clinical manifestations of hypocalcemia depend on the severity of serum calcium levels and the rate of decline, with hypocalcemic crisis symptoms manifesting at an ionized calcium concentration of 2.8 mg/dL (0.7 mmol/L). The remaining 10% of calcium is complexed with anions to form calcium salts. Approximately 40% of circulating calcium is bound to protein (e.g., albumin), whereas about 50% of circulating calcium is in a physiologically active form. The majority of calcium in the body resides in bone, with only 1% of total body stores exchanged with extracellular fluid. Hypocalcemia occurs in 15 to 88% of hospitalized adult patients, depending on the measurement method (serum or ionized calcium). Calcium gluconate is a calcium salt used to directly replete serum calcium levels in cases of hypocalcemia through IV administration.

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