StatPearls [Internet].
Persevering with Schooling Exercise
Calcium gluconate is a medicine used within the administration of hypocalcemia, cardiac arrest and cardiotoxicity as a result of hyperkalemia or hypermagnesemia. It’s categorized as a calcium salt. This exercise outlines the indications, motion, and contraindications for calcium gluconate as a useful agent within the administration of hypocalcemia, cardiac arrest, cardiotoxicity as a result of hyperkalemia or hypermagnesemia and different problems as relevant. This exercise will spotlight the mechanism of motion, antagonistic occasions, and different key components (e.g., off-label makes use of, dosing, pharmacodynamics, monitoring, related interactions). The exercise is pertinent for members of the healthcare staff who’re engaged within the administration of hypocalcemia, cardiac arrest, cardiotoxicity as a result of hyperkalemia or hypermagnesemia and associated circumstances.
Goals:Assessment the mechanism of motion and administration of calcium gluconate as a therapy.Determine indications the place calcium gluconate has a medical function.Summarize the dosing parameters for calcium gluconate remedy.Define interprofessional staff methods for enhancing care coordination and communication when utilizing calcium gluconate in relevant medical eventualities.Earn persevering with schooling credit (CME/CE) on this matter.
Indications
Calcium gluconate is the calcium salt of gluconic acid. Gluconic acid is an oxidation product of glucose. There’s 93 mg of elemental calcium in a ten ml ampoule of 10% calcium gluconate. As compared, there may be 272 mg of elemental calcium in a ten mL of 10% resolution of calcium chloride, one other calcium salt. Calcium gluconate is usually most well-liked over calcium chloride as a result of decrease the chance of tissue necrosis if the fluid is extravasated.[1]
Calcium gluconate is usually administered intravenously (IV) or orally within the therapy of hypocalcemia, cardiac arrest, or cardiotoxicity as a result of hyperkalemia or hypermagnesemia.[1][2] Calcium gluconate has additionally been used off-label within the administration of β-blocker toxicity, calcium-channel blocker (CCB) toxicity, magnesium toxicity, and hydrofluoric acid burns.[2][3][4][5]
Mechanism of Motion – “calcium gluconate iv”
Hypocalcemia
Calcium gluconate is a calcium salt that’s used to instantly replete serum calcium ranges in circumstances of hypocalcemia by means of IV administration. Hypocalcemia happens in 15 to 88% of hospitalized grownup sufferers, relying on the strategy of measurement (serum or ionized calcium). Nearly all of calcium within the physique resides in bone, with only one% of whole physique shops exchanging with extracellular fluid. Roughly 40% of circulating calcium is sure to protein (e.g., albumin), whereas roughly 50% of circulating calcium is in a physiologically lively kind. The rest 10% of calcium is complexed with anions to kind calcium salts. Scientific manifestations of hypocalcemia depend upon the severity of serum calcium ranges and the speed of decline, with hypocalcemic disaster signs manifesting at an ionized calcium focus of two.8 mg/dL (0.7 mmol/L).[6] Signs embrace circumoral paresthesias, muscle cramps, myalgias, dysphagia, melancholy, confusion, irritability, seizures, tetany, laryngospasm, and hypotension. Bodily examination findings embrace hyperreflexia, carpopedal spasm, Trousseau signal, and Chvostek signal. On EKG, hypocalcemia presents with extended QT interval, however the significance of that is undetermined as it’s uncommon for calcium derangements to be the etiology of cardiac arrest. EKG abnormalities of hypocalcemia, resembling QT prolongation, usually reply to IV calcium gluconate, returning the QT interval to baseline.[1][2][7]
The therapy of hypocalcemia initially focuses on symptomatic therapy fairly than normalizing serum calcium. In extreme hypocalcemia with seizures, laryngospasm, hypotension, or tetany, sufferers ought to obtain emergent parenteral calcium gluconate to replenish calcium ranges till extreme and life-threatening abnormalities resolve. It’s important to test magnesium ranges throughout calcium repletion as hypomagnesemia is a vital explanation for hypocalcemia. Hypomagnesemia causes hypocalcemia by means of impairment of parathyroid hormone secretion and renal resistance to parathyroid hormone, resulting in decreased renal reabsorption of calcium.[1][8]
There isn’t any adequate proof to point empiric utilization of calcium gluconate in hypocalcemia or hypercalcemia throughout cardiac arrest, as it’s uncommon for calcium abnormalities to trigger cardiac arrest. Empirically, calcium gluconate is used when the reason for cardiac arrest is because of hyperkalemia or hypermagnesemia.[2]
Hyperkalemia
Elevations of extracellular potassium could cause cardiac arrhythmias, which may progress to cardiac arrest and dying. The function of calcium gluconate in treating hyperkalemia is to stabilize cardiac cell membranes. Calcium ought to promptly be administered to any affected person presenting with hyperkalemia with EKG adjustments, indicating a hyperkalemic emergency. Elevated potassium ranges destabilize cardiac membranes by growing the brink potential of cardiac myocytes. Calcium supplementation decreases the brink to revive the transmembrane voltage gradient. Nonetheless, although calcium protects myocytes from potassium, it doesn’t resolve the problem of hyperkalemia, for which different medicines are usually administered, resembling insulin and dextrose or sodium bicarbonate, which shifts potassium into cells; and sodium polystyrene sulfate, which will increase potassium excretion by means of stool. Nonetheless, dialysis is probably the most efficacious technique of potassium excretion, notably in sufferers with renal illness.[2][9]
Hypermagnesemia
Acute magnesium toxicity is uncommon, and usually seen within the obstetric setting in sufferers being given magnesium sulfate for the prevention of eclampsia. Magnesium toxicity can current in a number of methods, together with diminished deep tendon reflexes, cardiopulmonary arrest, and respiratory melancholy. This toxicity is because of magnesium’s impact on blocking calcium and potassium channels, each extracellularly and intracellularly. Calcium gluconate treats hypermagnesemia by means of direct antagonism of magnesium on the website of motion (e.g., on the neuromuscular junction).[5][10]
Hydrofluoric Acid Burns
Within the therapy of hydrofluoric acid burns, calcium is a mainstay of therapy that features by binding to fluoride ions, successfully neutralizing them to forestall additional toxicity. Moreover, fluoride could cause hypocalcemia, presumably because of the formation of fluorapatite (Ca(PO)F) salt, thus reducing ranges of free calcium inside the serum. Calcium gluconate instantly replenishes ionized calcium ranges inside the blood in circumstances of fluoride-induced hypocalcemia.[11][12]
Beta-blocker and Calcium Channel Blocker Toxicity
Calcium could also be helpful in beta-blocker overdose in sufferers with shock refractory to different measures. The calcium impact in beta-blocker toxicity seems to be because of the function of calcium in growing cardiac inotropy as the inflow of calcium into the cardiac cell contributes to the contraction of myofibrils.[13]
Calcium gluconate additionally performs a task within the therapy of CCB toxicity. CCB toxicity causes hypotension, bradycardia, and a lower in cardiac contractility. The reasoning behind calcium’s mechanism in opposition to CCB toxicity is to overwhelm the calcium receptors to antagonize the CCB competitively. Thus, restoring cardiac contractility, which, together with IV fluids, can ameliorate the hypotensive signs of CCB toxicity.[3]
Administration
The varied dosing models and conversion components of calcium gluconate are potential sources of medicine errors. Dose data is given as calcium gluconate salt or compounds except offered in any other case. 10% means there are 10 grams of calcium gluconate in 100 mL of the solvent, water. In 10 mL of 10% calcium gluconate, there may be 1 g calcium gluconate salt or compound which incorporates 93 mg elemental calcium, which is 4.65 mEq, which is 2.33 mmol. As a result of calcium has a valence of +2, the milliequivalents are twice the millimoles. 1 mL of 10% calcium gluconate incorporates 9.3 mg of elemental calcium.
Hypocalcemia
The emergency therapy of hypocalcemia focuses primarily on reversing signs fairly than correcting serum calcium ranges. Repeat measurements of serum calcium ought to be checked 4-6 hours after calcium therapy. Moreover, the affected person ought to be assessed for hypomagnesemia as low magnesium ranges could cause decreased serum calcium ranges.[1]
Remedy of hypocalcemia utilizing calcium gluconate contains the next [1]:
Extreme symptomatic hypocalcemia (seizure, laryngospasm, tetany): 1 to 2 grams of calcium gluconate ought to be administered in 10 minutes and repeated in 10 to 60 minutes till signs resolve. Roughly 100 to 200 mg of elemental calcium (in case of calcium gluconate: 93 mg elemental calcium in 1 gram of calcium gluconate) ought to be infused over a interval of 10 minutes to deal with symptomatic hypocalcemia. Rhythm monitoring with an EKG is advisable throughout intravenous calcium bolus (IV push over 10 minutes) administration. 10 to twenty mL of 10% calcium gluconate diluted in 50 to 100 mL dextrose or regular saline intravenously over 10 minutes is advisable.[14] For persistent signs, the bolus might be repeated after 10-60 minutes till signs resolve. After this, observe the steps for average to extreme hypocalcemia. Sufferers mustn’t obtain bicarbonate or phosphate throughout calcium administration.
Average to extreme hypocalcemia (ionized calcium <4 mg/dL) with out seizure or tetany: An infusion of roughly 100 mg/hr of elemental calcium might be given to adults over a number of hours. 4 g calcium gluconate IV over 4 hours, which corresponds to 1 gram of calcium gluconate (one ampoule, 10 mL of 10% calcium gluconate) for every hour. Sufferers with persistent hypocalcemia can obtain a steady infusion of 5 to twenty mg/kg/hour of calcium gluconate. For instance, one ampoule of 10% calcium gluconate in 90 mL of regular saline or 5% dextrose at 100 mL per hour will ship 10 mg/kg/hr in a 100 kg particular person. Ten ampoules of 10% calcium gluconate in 900 mL of regular saline or 5% dextrose can even ship 10 mg/kg/hr in a 100 kg particular person. Primarily based on the affected person’s weight, supposed fluid supply, and desired IV fee, the clinician can alter the infusion parameters. Gentle hypocalcemia (ionized calcium above 4 to five mg/dL): 1 to 2 g calcium gluconate IV over 2 hours. Oral calcium could also be given to asymptomatic sufferers. Hyperkalemia Calcium gluconate is given as a ten% resolution, 15 to 30 mL IV over 2 to five minutes to stabilize cardiac cell membranes within the therapy of hyperkalemia.[2] The everyday onset of motion of calcium gluconate is 3 minutes, and the period of motion is 20 to 60 minutes. EKG findings of hyperkalemia ought to enhance on this time; nonetheless, in circumstances the place EKG findings persist or worsen, one other dose of calcium gluconate ought to be administered.[9]
Hypermagnesemia Cardiac toxicity as a result of hypermagnesemia ought to obtain therapy with the equal routine as hyperkalemia: 10% resolution, 15 to 30 mL IV over 2 to five minutes throughout cardiac arrest as a result of hypermagnesemia. In any other case, the standard dosage of calcium gluconate is 1 to 2 g, elemental calcium roughly 100 to 200 mg (about 10 to twenty mL) over 5 to 10 minutes in symptomatic hypermagnesemia in these with renal impairment awaiting dialysis.[2] Hydrofluoric Acid Burns Calcium gluconate can be utilized as a 2.5% gel within the therapy of hydrofluoric burns. This gel might be made with 25 mL of 10% calcium gluconate with 75 mL of glycerol (glycerine) and hydroxyethylcellulose gel. The gel is to be utilized liberally and massaged into the burn space for 30 to 60 minutes with reapplication as mandatory. For persistent ache in burns, 5% calcium gluconate resolution might be injected subcutaneously with a 27-gauge needle 0.5 cm away from the burn border into the encircling unaffected space beneath and into the burn space (0.5mL/cm^2 of burn floor space). This injection will not be for use on the digits. For extreme hydrofluoric acid burns and unrelenting ache regardless of aggressive therapy, intraarterial use of calcium gluconate might be utilized. On this case, 10 to fifteen mL of 10% calcium gluconate might be added to 40 mL of Ringer’s lactate and delivered over 3 hours into the artery that provides the burned space. Inhalation damage can have therapy with 2.5% calcium gluconate administered by way of nebulizer.[12][15] Beta-blocker and Calcium Channel Blocker Toxicity Calcium gluconate is a viable possibility in circumstances of beta-blocker overdose with shock refractory to different measures. A ten% calcium gluconate resolution ought to be administered as 0.6 to 1.2 mL/kg (60 to 120 mg/kg) IV over 5 to 10 minutes, repeated as wanted each 10 to twenty minutes for 3 to 4 occasions and adopted by a steady infusion of 0.65 mL/kg/hr.[2] When treating calcium channel blocker toxicity, a dose of calcium gluconate might be given as a bolus or steady infusion. Bolus dosing is 0.6 mL/kg (60 mg/kg) of 10% calcium gluconate resolution,repeated as wanted each 10-20 minutes for 3 to 4 occasions and adopted by a steady infusion of 0.6 to 1.5 mL/kg/hr (60 to 150 mg/kg/hr). All through the method, ionized calcium ranges require monitoring to attain a calcium stage two occasions the conventional. It's value noting that calcium supplementation is an adjunct to different therapies resembling glucagon, atropine, and hyperinsulinemia/euglycemia remedy within the therapy of CCB toxicity.[3]Hostile Results
Hostile results of calcium gluconate embrace syncope, bradycardia, and paresthesias.
One of many most regarding antagonistic results of calcium gluconate is extravasation from intravenous websites. Calcium can induce tissue necrosis by means of calcium-induced vasoconstriction of capillaries and intracellular fluid retention, resulting in deep tissue harm and late-onset calcifications. For extravasation damage therapy, cease the infusion after which gently aspirate the extravasated fluid. In early or acute calcium extravasation, a hyaluronidase antidote is an possibility along with chilly, dry compresses and elevation of the extremity. Between 1 and 1.7 mL of hyaluronidase could also be given intradermally into the border of the extravasated space as 5 separate injections. Injection into the catheter that prompted the infiltration can also be applicable.[16]