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  1. Pharmacology

    1. Calcium is a cation that is necessary for the normal functioning of a variety of enzymes and organ systems, including muscle and nerve tissue. Hypocalcemia, or a blockade of the effects of calcium, may cause muscle cramps, tetany, and ventricular fibrillation. Antagonism of calcium-dependent channels results in hypotension, bradycardia, and atrioventricular (AV) block.

    2. Calcium ions rapidly bind to fluoride ions, abolishing their toxic effects.

    3. Calcium can reverse the negative inotropic effects of calcium antagonists; however, depressed automaticity and AV nodal conduction velocity and vasodilation may not respond to calcium administration.

    4. Calcium stabilizes cardiac cell membranes in hyperkalemic states.

  2. Indications

    1. Symptomatic hypocalcemia resulting from intoxication by fluoride, oxalate, or the intravenous anticoagulant citrate.

    2. Hydrofluoric acid exposure (See Hydrogen Fluoride and Hydrofluoric Acid).

    3. Hypotension in the setting of calcium channel antagonist (eg, verapamil) overdose (See Calcium Channel Antagonists).

    4. Severe hyperkalemia with cardiac manifestations (relatively contraindicated in the setting of digitalis toxicity; see Item III.B below).

    5. Symptomatic hypermagnesemia.

  3. Contraindications

    1. Hypercalcemia except in the setting of calcium channel antagonist poisoning, in which hypercalcemia may be desirable.

    2. Although controversial, calcium is relatively contraindicated in the setting of intoxication with cardiac glycosides (may aggravate digitalis-induced ventricular tachydysrhythmias) and should be reserved for life-threatening situations.

    3. Note: Calcium chloride salt should not be used for intradermal, subcutaneous, or intra-arterial injection because it is highly concentrated and may result in further tissue damage.

  4. Adverse effects

    1. Tissue irritation, particularly with calcium chloride salt; extravasation may cause local irritation or necrosis.

    2. Hypercalcemia, especially in patients with diminished renal function.

    3. Hypotension, bradycardia, syncope, and cardiac dysrhythmias caused by rapid intravenous administration.

    4. Neuromuscular weakness.

    5. Constipation caused by orally administered calcium salts.

    6. Use in pregnancy. FDA Category C (indeterminate). This does not preclude its acute, short-term use for a seriously symptomatic patient (See Introduction in Section III).

  5. Drug or laboratory interactions

    1. Inotropic and dysrhythmogenic effects of digitalis may be potentiated by calcium. The use of intravenous calcium in the setting of cardiac glycoside toxicity is not absolutely contraindicated, but indications remain controversial.

    2. A precipitate will form with solutions containing soluble salts of carbonates, phosphates, or sulfates and with various antibiotics.

  6. Dosage and method of administration. Note: A 10% solution of calcium chloride contains three times the amount of calcium ions per milliliter that a 10% solution of calcium gluconate contains. (A 10% solution of calcium chloride contains 27.2 mg/mL of elemental calcium; a 10% solution of calcium gluconate contains 9 mg/mL of elemental calcium.)

    1. Oral fluoride ingestion. Administer calcium-containing antacid (calcium carbonate) orally to complex fluoride ions.

    2. Symptomatic hypocalcemia, hyperkalemia. Give 10% calcium gluconate, 20–30 mL (children: 0.3–0.4 mL/kg), or 10% calcium chloride, 5–10 mL (children: 0.1–0.2 mL/kg), slowly IV. Repeat as needed every 5–10 minutes.

    3. Calcium antagonist poisoning. Start with doses as described above. High-dose calcium therapy has been reported to be effective in some cases of severe calcium channel blocker overdose. Corrected calcium concentrations of approximately 1.5–2 times normal have correlated with improved cardiac function. In the setting of calcium channel antagonist overdose, as much ...

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