IV-124 Circulation December 13. 2005 Treatment of hypermagnesemia Although total serum albumin is directly related to total Hypermagnesemia is treated with administration of calcium, erum calcium, the ionized calcium is inversely related to which removes magnesium from serum. It is important serum albumin. The lower the serum albumin. the higher the eliminate sources of ongoing magnesium intake. Cardiorespi- portion of the total calcium that is present in ionized form.In ratory support may be needed until magnesium levels are the presence of hypoalbuminemia, although total calcium reduced. Administration of 10% solution of calcium chloride level may be low, the ionized calcium level may be normal (5 to 10 mL [500 to 1000 mg Iv) will often correct lethal Calcium antagonizes the effects of both potassium and arrhythmias. This dose may be repeated if needed. magnesium at the cell membrane. For this reason it is Dialysis is the treatment of choice for severe hypermag- extremely useful for treating the effects of hyperkalemia and nesemia. If renal function is normal and cardiovascular function adequate, IV saline diuresis(administration of IV normal saline and furosemide [1 mg/kgl) can be used to Hypercalcemia increase renal excretion of magnesium until dialysis can be Hypercalcemia is defined as a total serum calcium concen- performed Diuresis can also increase calcium excretion; the tration >10.5 mEq/L(or an elevation in ionized calcium development of hypocalcemia will make signs and symptoms >4.8 mg/dL). Primary hyperparathyroidism and malignancy of hypermagnesemia wor account for >90% of reported cases. 7 In these and most forms of hypercalcemia, release of calcium from the bones Hy hypomagneseMia and intestines is increased, and renal clearance may be Hypomagnesemia, defined as a serum magnesium concentra compromised tion <1.3 mEq/L, is far more common than hypermag Symptoms of hypercalcemia usually develop when the nesemia. Hypomagnesemia usually results from decreased total serum calcium concentration is 212 to 15 mg/dL. bsorption or increased loss of magnesium from either the Neurologic symptoms are depression, weakness, fatigue, and kidneys or intestines(diarrhea). Alterations in thyroid hor- confusion at lower levels. At higher levels patients may mone function and certain medications (eg, pentamidine, experience hallucinations, disorientation, hypotonicity, sei- diuretics, alcohol) can also induce hypomagnesemia. zures, and coma. Hypercalcemia interferes with renal concen Hypomagnesemia interferes with the effects of parathyroid tration of urine; the diuresis can cause dehydration hormone, resulting in hypocalcemia. It may also cause hypokalemia. Symptoms of low serum magnesium are mus- Myocardial contractility may initially increase until the cal- cular tremors and fasciculations, ocular nystagmus, tetany, cium level reaches >15 mg/dL. Above this level myocardial depression occurs. Automaticity is decreased and ventricular de pointes (multifocal ventricular tachycardia). Other possi- systole is shortened. Arrhythmias occur because the refrac- ble symptoms are ataxia, vertigo, seizures, and dysphagia. toxicity and may cause hypertension. In addition, many Treatment of hypomagnesemia patients with hypercalcemia develop hypokalemia. Both of The treatment of hypomagnesemia is determined by its these conditions contribute to cardiac arrhythmias. 8 The QT severity and the patient's clinical status. For severe or interval typically shortens when the serum calcium is >13 ymptomatic hypomagnesemia, give I to 2 g of IV MgSO4 mg/dL, and the PR and QRS intervals are prolonged. Atrio- over 5 to 60 minutes. For torsades de pointes with cardiac ventricular block may develop and progress to complete heart arrest, give I to 2 g of MgSO IV push over 5 to 20 minutes. block and even cardiac arrest when the total serum calcium i If torsades de pointes is intermittent and not associated with >15 to 20 mg/dL. arrest, administer the magnesium over 5 to 60 minutes Iv. If Gastrointestinal symptoms of hypercalcemia include dys izures are present, give 2 g IV MgSO, over 10 minutes. phagia, constipation, peptic ulcers, and pancreatitis. Effects Administration of calcium is usually appropriate because on the kidney include diminished ability to concentrate urine most patients with hypomagnesemia are also hypocalcemic. 16 diuresis, leading to loss of sodium, potassium, magnesium, and phosphate; and a vicious cycle of calcium absorption in Calcium(Catt) the intestines and calcium release from the bones that Calcium is the most abundant mineral in the body. Many worsens hypercalcemia. processes depend on intracellular calcium, such as enzymatic Treatment of hypercalcemia reactions,receptor activation, muscle contraction, cardiac Treatment for hypercalcemia is required if the patient is contractility,and platelet aggregation. Calcium is essential symptomatic( typically a total serum concentration of appl for bone strength and neuromuscular function. Half of all imately >12 mg/dL) or if the calcium level is >15 mg/dL calcium in the ECF is bound to albumin; the other half is in Immediate therapy is directed at restoring intravascular vol- the biologically active, ionized form. Calcium concentration ume and promoting calcium excretion in the urine In patients is normally regulated by parathyroid hormone and vitamin D with adequate cardiovascular and renal function this is Total serum calcium is directly related to the serum accomplished with infusion of 0.9% saline at 300 to 500 albumin concentration. The total serum calcium will increase mL/h(saline diuresis) until any fluid deficit is replaced and 0.8 mg/dL for every I g/dL rise in serum albumin and will fall diuresis occurs (urine output >200 to 300 mL/h). Once 0.8 mg/dL for every I g/dL fall in serum albumin. adequate rehydration has occurred, the saline infusion rate isTreatment of Hypermagnesemia Hypermagnesemia is treated with administration of calcium, which removes magnesium from serum. It is important to eliminate sources of ongoing magnesium intake. Cardiorespi￾ratory support may be needed until magnesium levels are reduced. Administration of 10% solution of calcium chloride (5 to 10 mL [500 to 1000 mg] IV) will often correct lethal arrhythmias. This dose may be repeated if needed. Dialysis is the treatment of choice for severe hypermag￾nesemia. If renal function is normal and cardiovascular function adequate, IV saline diuresis (administration of IV normal saline and furosemide [1 mg/kg]) can be used to increase renal excretion of magnesium until dialysis can be performed. Diuresis can also increase calcium excretion; the development of hypocalcemia will make signs and symptoms of hypermagnesemia worse. Hypomagnesemia Hypomagnesemia, defined as a serum magnesium concentra￾tion 1.3 mEq/L, is far more common than hypermag￾nesemia. Hypomagnesemia usually results from decreased absorption or increased loss of magnesium from either the kidneys or intestines (diarrhea). Alterations in thyroid hor￾mone function and certain medications (eg, pentamidine, diuretics, alcohol) can also induce hypomagnesemia. Hypomagnesemia interferes with the effects of parathyroid hormone, resulting in hypocalcemia. It may also cause hypokalemia. Symptoms of low serum magnesium are mus￾cular tremors and fasciculations, ocular nystagmus, tetany, altered mental state, and cardiac arrhythmias such as torsades de pointes (multifocal ventricular tachycardia). Other possi￾ble symptoms are ataxia, vertigo, seizures, and dysphagia. Treatment of Hypomagnesemia The treatment of hypomagnesemia is determined by its severity and the patient’s clinical status. For severe or symptomatic hypomagnesemia, give 1 to 2 g of IV MgSO4 over 5 to 60 minutes. For torsades de pointes with cardiac arrest, give 1 to 2 g of MgSO4 IV push over 5 to 20 minutes. If torsades de pointes is intermittent and not associated with arrest, administer the magnesium over 5 to 60 minutes IV. If seizures are present, give 2 g IV MgSO4 over 10 minutes. Administration of calcium is usually appropriate because most patients with hypomagnesemia are also hypocalcemic.16 Calcium (Ca

) Calcium is the most abundant mineral in the body. Many processes depend on intracellular calcium, such as enzymatic reactions, receptor activation, muscle contraction, cardiac contractility, and platelet aggregation. Calcium is essential for bone strength and neuromuscular function. Half of all calcium in the ECF is bound to albumin; the other half is in the biologically active, ionized form. Calcium concentration is normally regulated by parathyroid hormone and vitamin D. Total serum calcium is directly related to the serum albumin concentration. The total serum calcium will increase 0.8 mg/dL for every 1 g/dL rise in serum albumin and will fall 0.8 mg/dL for every 1 g/dL fall in serum albumin. Although total serum albumin is directly related to total serum calcium, the ionized calcium is inversely related to serum albumin. The lower the serum albumin, the higher the portion of the total calcium that is present in ionized form. In the presence of hypoalbuminemia, although total calcium level may be low, the ionized calcium level may be normal. Calcium antagonizes the effects of both potassium and magnesium at the cell membrane. For this reason it is extremely useful for treating the effects of hyperkalemia and hypermagnesemia. Hypercalcemia Hypercalcemia is defined as a total serum calcium concen￾tration
10.5 mEq/L (or an elevation in ionized calcium
4.8 mg/dL). Primary hyperparathyroidism and malignancy account for
90% of reported cases.17 In these and most forms of hypercalcemia, release of calcium from the bones and intestines is increased, and renal clearance may be compromised. Symptoms of hypercalcemia usually develop when the total serum calcium concentration is 12 to 15 mg/dL. Neurologic symptoms are depression, weakness, fatigue, and confusion at lower levels. At higher levels patients may experience hallucinations, disorientation, hypotonicity, sei￾zures, and coma. Hypercalcemia interferes with renal concen￾tration of urine; the diuresis can cause dehydration. Cardiovascular symptoms of hypercalcemia are variable. Myocardial contractility may initially increase until the cal￾cium level reaches
15 mg/dL. Above this level myocardial depression occurs. Automaticity is decreased and ventricular systole is shortened. Arrhythmias occur because the refrac￾tory period is shortened. Hypercalcemia can worsen digitalis toxicity and may cause hypertension. In addition, many patients with hypercalcemia develop hypokalemia. Both of these conditions contribute to cardiac arrhythmias.18 The QT interval typically shortens when the serum calcium is
13 mg/dL, and the PR and QRS intervals are prolonged. Atrio￾ventricular block may develop and progress to complete heart block and even cardiac arrest when the total serum calcium is
15 to 20 mg/dL. Gastrointestinal symptoms of hypercalcemia include dys￾phagia, constipation, peptic ulcers, and pancreatitis. Effects on the kidney include diminished ability to concentrate urine; diuresis, leading to loss of sodium, potassium, magnesium, and phosphate; and a vicious cycle of calcium absorption in the intestines and calcium release from the bones that worsens hypercalcemia. Treatment of Hypercalcemia Treatment for hypercalcemia is required if the patient is symptomatic (typically a total serum concentration of approx￾imately
12 mg/dL) or if the calcium level is
15 mg/dL. Immediate therapy is directed at restoring intravascular vol￾ume and promoting calcium excretion in the urine. In patients with adequate cardiovascular and renal function this is accomplished with infusion of 0.9% saline at 300 to 500 mL/h (saline diuresis) until any fluid deficit is replaced and diuresis occurs (urine output 200 to 300 mL/h). Once adequate rehydration has occurred, the saline infusion rate is IV-124 Circulation December 13, 2005