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Electrolyte Tests

Electrolyte Tests


Electrolytes are positively and negatively charged molecules, called ions, that are found within cells, between cells, in the bloodstream, and in other fluids throughout the body. Electrolytes with a positive charge include sodium, potassium, calcium, and magnesium; the negative ions are chloride, bicarbonate, and phosphate. The concentrations of these ions in the bloodstream remain fairly constant throughout the day in a healthy person. Changes in the concentration of one or more of these ions can occur during various acute and chronic disease states and can lead to serious consequences.


Tests that measure the concentration of electrolytes are useful in the emergency room and to obtain clues for the diagnosis of specific diseases. Electrolyte tests are used for diagnosing dietary deficiencies, excess loss of nutrients due to urination, vomiting, and diarrhea, or abnormal shifts in the location of an electrolyte within the body. When an abnormal electrolyte value is detected, the physician may either act to immediately correct the imbalance directly (in the case of an emergency) or run further tests to determine the underlying cause of the abnormal electrolyte value. Electrolyte disturbances can occur with malfunctioning of the kidney (renal failure), infections that produce severe and continual diarrhea or vomiting, drugs that cause loss of electrolytes in the urine (diuretics), poisoning due to accidental consumption of electrolytes, or diseases involving hormones that regulate electrolyte concentrations.


Electrolyte tests are performed from routine blood tests. The techniques are simple, automated, and fairly uniform throughout the United States. During the preparation of blood plasma or serum, health workers must take care not to break the red blood cells, especially when testing for serum potassium. Because the concentration of potassium within red blood cells is much higher than in the surrounding plasma or serum, broken cells would cause falsely elevated potassium levels.


Electrolyte tests are typically conducted on blood plasma or serum, urine, and diarrheal fluids. Electrolytes can be classified in at least five different ways. One way is that some electrolytes tend to exist mostly inside cells, or are intracellular, while others tend to be outside cells, or are extracellular. Potassium, phosphate, and magnesium occur at much greater levels inside the cell than outside, while sodium and chloride occur at much greater levels extracellularly. A second classification distinguishes those electrolytes that participate directly in the transmission of nerve impulses and those that do not. Sodium, potassium, and calcium are the important electrolytes involved in nerve impulses, and disorders affecting them are most closely associated with neurological disorders. A third classification focuses on electrolytes that are able to form a tight union, or complex, with one another. Calcium and phosphate have the greatest tendency to form complexes with each other. Disorders that cause an increase in either plasma calcium or phosphate can result in the deposit of calcium-phosphate crystals in the soft tissues of the body. A fourth classification concerns those electrolytes that influence the acidity or alkalinity of the bloodstream, also known as the pH. The pH of the bloodstream is normally in the range of 7.35-7.45. A decrease below this range is called acidosis, while a pH above this range is called alkalosis. The electrolytes most closely associated with the pH of the bloodstream are bicarbonate, chloride, and phosphate.


All electrolyte tests can be performed on plasma or serum. Plasma is prepared by withdrawing a blood sample and placing it in a test tube containing a chemical that prevents blood from clotting (an anticoagulant). Serum is prepared by withdrawing a blood sample, placing it in a test tube, and allowing it to clot. The blood spontaneously clots within a minute of withdrawing the blood from a vein. The serum or plasma is then rapidly spun with a centrifuge in order to remove the blood cells or clot.

Normal results

Electrolyte concentrations are similar whether measured in serum or plasma. Values can be expressed in terms of weight per unit volume (mg/ deciliter; mg/dL) or in the number of molecules in a volume, or molarity (moles or millimoles/liter; M or mM). The range of normal values sometimes varies slightly between different age groups, for males and females, and between different analytical laboratories.

The normal level of serum sodium is in the range of 136-145 mM. The normal levels of serum potassium are 3.5-5.0 mM. Note that sodium occurs at a much higher concentration than potassium. The normal concentration of total serum calcium (bound calcium plus free calcium) is in the range of 8.8-10.4 mg/dL. About 40% of the total calcium in the plasma is loosely bound to proteins; this calcium is referred to as bound calcium. The normal range of free calcium is 4.8-5.2 mg/dL. The normal concentration of serum magnesium is in the range of 2.0-3.0 mg/dL.

The normal concentration range of chloride is 350-375 mg/dL or 98-106 mM. The normal level of phosphate, as expressed as the concentration of phosphorus, is 2.0-4.3 mg/dL. Bicarbonate is an electrolyte that is freely and spontaneously interconvertable with carbonic acid and carbon dioxide. The normal concentration of carbonic acid (H2CO3) is about 1.35 mM. The normal concentration of bicarbonate (HCO3) is about 27 mM. The concentration of total carbon dioxide is the sum of carbonic acid and bicarbonate; this sum is normally in the range of 26-28 mM. The ratio of bicarbonate/carbonic acid is more significant than the actual concentrations of these two forms of carbon dioxide. Its normal value is 27/1.35 (equivalent to 20/1).

Abnormal results

Positively charged electrolytes

High serum sodium levels (hypernatremia ) occur at sodium concentrations over 145 mM, with severe hypernatremia over 152 mM. Hypernatremia is usually caused by diseases that cause excessive urination. In these cases, water is lost, but sodium is still retained in the body. The symptoms include confusion and can lead to convulsions and coma. Low serum sodium levels (hyponatremia ) are below 130 mM, with severe hyponatremia at or below 125 mM. Hyponatremia often occurs with severe diarrhea, with losses of both water and sodium, but with sodium loss exceeding water loss. Hyponatremia provokes clinical problems only if serum sodium falls below 125 mM, especially if this has occurred rapidly. The symptoms can be as mild as tiredness but may lead to convulsions and coma.

High serum potassium (hyperkalemia ) occurs at potassium levels above 5.0 mM; it is considered severe over 8.0 mM. Hyperkalemia is relatively uncommon, but sometimes occurs in patients with kidney failure who take potassium supplements. Hyperkalemia can result in abnormal beating of the heart (cardiac arrhythmias ). Low serum potassium (hypokalemia ) occurs when serum potassium falls below 3.0 mM. It can result from low dietary potassium, as during starvation or in patients with anorexia nervosa; from excessive losses via the kidneys, as caused by diuretic drugs; or by diseases of the adrenal or pituitary glands. Mild hypokalemia causes muscle weakness, while severe hypokalemia can cause paralysis, the inability to breathe, and cardiac arrhythmias.

High levels of calcium ions (hypercalcemia ) occur at free calcium ion concentrations over 5.2 mg/dL or total serum calcium above 10.4 mg/dL. Hypercalcemia usually occurs when the body dissolves bone at an abnormally fast rate, increasing both serum calcium and serum phosphate. Sudden hypercalcemia can cause vomiting and coma, while prolonged and moderate hypercalcemia results in the deposit of calcium phosphate crystals in the kidneys and eye. Hypocalcemia occurs when serum free calcium ions fall below 4.4 mg/dL, or when total serum calcium falls below 8.8 mg/dL. Hypocalcemia can result from hypoparathyroidism (low parathyroid hormone), from failure to produce 1,25-dihydroxyvitamin D, from low levels of plasma magnesium, and from phosphate poisoning (the phosphate enters the bloodstream and forms a complex with the free serum calcium). Hypocalcemia can cause depression and muscle spasms.

Hypermagnesemia occurs at serum magnesium levels over 25 mM (60 mg/dL). Hypermagnesemia is rare but can occur with the excessive consumption of magnesium salts. Hypomagnesemia occurs when serum magnesium levels fall below 0.8 mM, and can result from poor nutrition. Chronic alcoholism is the most common cause of hypomagnesemia, in part because of poor diet. Magnesium levels below 0.5 mM (1.2 mg/dL) cause serum calcium levels to decline. Some of the symptoms of hypomagnesemia, including twitching and convulsions, actually result from the concurrent hypocalcemia. Hypomagnesemia can also result in hypokalemia and thereby cause cardiac arrhythmias.

Negatively charged electrolytes

Serum chloride levels sometimes increase to abnormal levels as an undesirable side effect of medical treatment with sodium chloride or ammonium chloride. The toxicity of chloride results not from the chloride itself, but from the fact that the chloride occurs as the acid, hydrogen chloride (more commonly known as hydrochloric acid, or HCl). An overdose of chloride may cause the accumulation of hydrochloric acid in the bloodstream, with consequent acidosis. Renal tubular acidosis, one of many kidney diseases, involves the failure to release acid into the urine. The acidosis produces weakness, headache, nausea, and cardiac arrest. Low plasma chloride leads to the opposite situation: a decline in the acid content of the bloodstream. This is known as alkalization of the bloodstream, or alkalosis. Hydrochloric acid, originally from extracellular fluids, can be lost by vomiting. At its most severe, alkalosis results in paralysis (tetany).

Hyperphosphatemia occurs at serum phosphate levels above 5 mg/dL. It can result from the failure of the kidneys to excrete phosphate into the urine, causing phosphate to accumulate in the bloodstream. Hyperphosphatemia can also be caused by the impaired action of parathyroid hormone and by phosphate poisoning. Severe hyperphosphatemia can cause paralysis, convulsions, and cardiac arrest. These symptoms result because the phosphate, occurring in elevated levels, complexes with free serum calcium, resulting in hypocalcemia. Tests for heart function (an electrocardiogram) and parathyroid hormone levels are used in the diagnosis of hyperphosphatemia. Hypophosphatemia occurs if serum phosphorus falls to 2.0 mg/dL or lower. It often results from a shift of inorganic phosphate from the bloodstream to various organs and tissues. This shift can be caused by a rise in pH (alkalization) of the bloodstream, which can occur during hyperventilation, a reaction in various disease states. A shift in phosphate to intracellular tissues may draw calcium away from the bloodstream via the formation of insoluble calcium phosphate crystals within cells, with consequent hypocalcemia. Thus, tests for abnormalities in phosphate metabolism also involve tests for serum calcium.

Bicarbonate metabolism involves several compounds. When dietary starches, sugars, and fats are broken down for energy production, carbon dioxide is created. Much of this carbon dioxide (CO2) spontaneously converts to carbonic acid (H2CO3), and some of the carbonic acid spontaneously converts to bicarbonate (HCO3) plus a hydrogen ion (H). Eventually, almost every molecule of carbon dioxide produced in the body, whether in the form of carbon dioxide, carbonic acid, or bicarbonate, must convert back to carbon dioxide in order to leave via the lungs during normal breathing.

If one holds one's breath, carbon dioxide cannot escape from the lungs, but continues to be generated within the body. This results in an increase in production of carbonic acid. A portion of the carbonic acid breaks apart (dissociates), causing an increase in hydrogen ions in the plasma, with a resulting acidosis. Tests for serum bicarbonate levels are accompanied by tests for acidosis (pH test). Conversely, when one breathes too rapidly (hyperventilation), the carbon dioxide is drawn off from the bloodstream and expelled in the breath at an increased rate. This results in an increase in the rate of combination of bicarbonate with hydrogen ions, resulting in alkalosis. Acidosis and alkalosis can be produced by means other than by altering the rate of breathing. The carbonic acid and bicarbonate in the bloodstream minimize (or buffer) any trend to acidosis or alkalosis. Tests for bicarbonate are generally accompanied by tests for blood pH and possibly tests for kidney malfunction, abnormal hormone function, or gastrointestinal disorders.



Fried, L. F., and P. M. Palevsky. "Hyponatremia and hypernatremia." Medical Clinics of North America 81 (1997): 585-609.

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Electrolyte Tests

Electrolyte tests


Electrolytes are positively and negatively charged molecules called ions, that are found within the body's cells and extracellular fluids, including blood plasma. A test for electrolytes includes the measurement of sodium, potassium, chloride, and bicarbonate. These ions are measured to assess renal (kidney), endocrine (glandular), and acid-base function, and are components of both renal function and comprehensive metabolic biochemistry profiles. Other important electrolytes routinely measured in serum or plasma include calcium and phosphorus. These are measured together because they are both affected by bone and parathyroid diseases, and often move in opposing directions. Magnesium is another electrolyte that is routinely measured. Like calcium, it will cause tetany (uncontrolled muscle contractions) when levels are too low in the extracellular fluids.


Tests that measure the concentration of electrolytes are needed for both the diagnosis and management of renal, endocrine, acid-base, water balance, and many other conditions. Their importance lies in part with the serious consequences that follow from the relatively small changes that diseases or abnormal conditions may cause. For example, the reference range for potassium is 3.6-5.0 mmol/l. Potassium is often a STAT (needed immediately) test because values below 3.0 mmol/l are associated with arrhythmia (irregular heartbeat), tachycardia (rapid heartbeat), and cardiac arrest, and values above 6.0 mmol/L are associated with bradycardia (slow heartbeat) and heart failure. Abnormal potassium cannot be treated without reference to bicarbonate, which is a measure of the buffering capacity of the plasma. Sodium bicarbonate and dissolved carbon dioxide act together to resist changes in blood pH. For example, an increased plasma bicarbonate indicates a condition called metabolic alkalosis, which results in blood pH that is too high. This may cause hydrogen ions to shift from the cells into the extracellular fluid in exchange for potassium. As potassium moves into the cells, the plasma concentration falls. The low plasma potassium, called hypokalemia, should not be treated by administration of potassium, but by identifying and eliminating the cause of the alkalosis. Administration of potassium would result in hyperkalemia when the acid-base disturbance is corrected. Sodium measurements are very useful in differentiating the cause of an abnormal potassium result. Conditions such as the overuse of diuretics (drugs that promote lower blood pressure) often result in low levels of both sodium and potassium. On the other hand, Cushing's disease (adrenocortical over-activity) and Addison's disease (adrenocortical under-activity) drive the sodium and potassium in opposing directions. Chloride levels will follow sodium levels except in the case of acid-base imbalances, in which chloride may move in the opposing direction of bicarbonate. In short, diagnosis and management of a patient with an electrolyte disturbance is best served by measuring all four electrolytes.


Sodium is the principal extracellular cation and potassium the principal intracellular cation. A cation is an ion with a positive charge. An anion is an ion with a negative charge. Sodium levels are directly related to the osmotic pressure of the plasma. In fact, since an anion is always associated with sodium (usually chloride or bicarbonate), the plasma osmolality (total dissolved solute concentration) can be estimated. Since water will often follow sodium by diffusion, loss of sodium leads to dehydration and retention of sodium leads to edema. Conditions that promote increased sodium, called hypernatremia, do so without promoting an equivalent gain in water. Such conditions include diabetes insipidus (water loss by the kidneys), Cushing's disease, and hyperaldosteronism (increased sodium reabsorption). Many other conditions, such as congestive heart failure, cirrhosis of the liver, and renal disease result in renal retention of sodium, but an equivalent amount of water is retained as well. This results in a condition called total body sodium excess, which causes hypertension and edema, but not an elevated serum sodium concentration. Low serum sodium, called hyponatremia, may result from Addison's disease, excessive diuretic therapy, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), burns, diarrhea, vomiting, and cystic fibrosis. In fact, the diagnosis of cystic fibrosis is made by demonstrating an elevated chloride concentration (greater than 60 mmol/l) in sweat.

Potassium is the electrolyte used as a hallmark sign of renal failure. Like sodium, potassium is freely filtered by the kidney. However, in the distal tubule sodium is reabsorbed and potassium is secreted. In renal failure, the combination of decreased filtration and decreased secretion combine to cause increased plasma potassium. Hyperkalemia is the most significant and life-threatening complication of renal failure. Hyperkalemia is also commonly caused by hemolytic anemia (release from hemolysed red blood cells), diabetes insipidus, Addison's disease, and digitalis toxicity. Frequent causes of low serum potassium include alkalosis, diarrhea and vomiting, excessive use of thiazide diuretics, Cushing's disease, intravenous fluid administration, and SIADH.

Calcium and phosphorus are measured together because they are both likely to be abnormal in bone and parathyroid disease states. Parathyroid hormone causes resorption of these minerals from bone. However, it promotes intestinal absorption and renal reabsorption of calcium and renal excretion of phosphorus. In hyperparathyroidism, serum calcium will be increased and phosphorus will be decreased. In hypoparathyroidism and renal disease, serum calcium will be low but phosphorus will be high. In vitamin D dependent rickets (VDDR), both calcium and phosphorus will be low; however, calcium is normal while phosphorus is low in vitamin D resistant rickets (VDRR). Differential diagnosis of an abnormal serum calcium is aided by the measurement of ionized calcium (i.e., calcium not bound by protein). Approximately 45% of the calcium in blood is bound to protein, 45% is ionized, and 10% is complexed to anions in the form of undissociated salts. Only the ionized calcium is physiologically active, and the level of ionized calcium is regulated by parathyroid hormone (PTH) via negative feedback (high ionized calcium inhibits secretion of PTH). While hypoparathyroidism, VDDR, renal failure, hypoalbuminemia, hypovitaminosis D, and other conditions may cause low total calcium, only hypoparathyroidism (and alkalosis) will result in low ionized calcium. Conversely, while hyperparathyroidism, malignancies (those that secrete parathyroid hormone-related protein), multiple myeloma, antacids, hyperproteinemia, dehydration, and hypervitaminosis D cause an elevated total calcium, only hyperparathyroidism, malignancy, and acidosis cause an elevated ionized calcium.

Serum magnesium levels may be increased by hemolytic anemia, renal failure, Addison's disease, hyperparathyroidism, and magnesium-based antacids. Chronic alcoholism is the most common cause of a low serum magnesium owing to poor nutrition. Serum magnesium is also decreased in diarrhea, hypoparathyroidism, pancreatitis, Cushing's disease, and with excessive diuretic use. Low magnesium can be caused by a number of antibiotics and other drugs and by administration of intravenous solutions. Magnesium is needed for secretion of parathyroid hormone, and therefore, a low serum magnesium can induce hypocalcemia. Magnesium deficiency is very common in regions where the water supply does not contain sufficient magnesium salts. Magnesium acts as a calcium channel blocker, and when cellular magnesium is low, high intracellular calcium results. This leads to hypertension, tachycardia, and tetany. Unfortunately serum total magnesium levels do not correlate well with intracellular magnesium levels, and serum measurement is not very sensitive for detecting chronic deficiency because of compensatory contributions from bone. Ionized magnesium levels are better correlated with intracellular levels because the ionized form can move freely between the cells and extracellular fluids.

Measurement of electrolytes

Electrolytes are measured by a process known as potentiometry. This method measures the voltage that develops between the inner and outer surfaces of an ion selective electrode. The electrode (membrane) is made of a material that is selectively permeable to the ion being measured. This potential is measured by comparing it to the potential of a reference electrode. Since the potential of the reference electrode is held constant, the difference in voltage between the two electrodes is attributed to the concentration of ion in the sample.


Electrolyte tests are performed on whole blood, plasma, or serum, usually collected from a vein or capillary.

Special procedures are followed when collecting a sweat sample for electrolyte analysis. This procedure, called pilocarpine iontophoresis, uses electric current applied to the arm of the patient (usually an infant) in order to convey the pilocarpine to the sweat glands where it will stimulate sweating. Care must be taken to ensure that the collection device (macroduct tubing or gauze) does not become contaminated and that the patient's parent or guardian understands the need for the electrical equipment employed.


Usually no special preparation is necessary by the patient. Samples for calcium and phosphorus and for magnesium should be collected following an eight-hour fast.


Discomfort or bruising may occur at the puncture site, or the person may feel dizzy or faint. Pressure to the puncture site until the bleeding stops reduces bruising. Applying warm packs to the puncture site relieves discomfort.


Minor temporary discomfort may occur with any blood test, but there are no complications specific to electrolyte testing.

Normal results

Electrolyte concentrations are similar whether measured in serum or plasma. Values are expressed as mmol/L for sodium, potassium, chloride, and bicarbonate. Magnesium results are often reported as milliequivalents per liter (meq/L) or in mg/dL. Total calcium is usually reported in mg/dL and ionized calcium in mmol/L. Since severe electrolyte disturbances can be associated with life-threatening consequences such as heart failure, shock, coma, or tetany, alert values are used to warn physicians of impending crisis. Typical reference ranges and alert values are cited below:

  • serum or plasma sodium: 135145 mmol/l; alert levels: less than 120 mmol/l and greater than 160 mmol/l
  • serum potassium: 3.65.4 mmol/l (plasma, 3.65.0 mmol/l); alert levels: less than 3.0 mmol/l and greater than 6.0 mmol/l
  • serum or plasma chloride: 98108 mmol/l
  • sweat chloride: 460 mmol/l
  • serum or plasma bicarbonate: 1824 mmol/l (as total carbon dioxide, 2226 mmol/l); alert levels: less than 10 mmol/l and greater than 40 mmol/l
  • serum calcium: 8.510.5 mg/dl (2.02.5 mmol/l); alert levels: less than 6.0 mg/dl and greater than 13.0 mg/dl
  • ionized calcium: 1.01.3 mmol/l
  • serum inorganic phosphorus: 2.34.7 mg/dl (children, 4.07.0 mg/dl); alert level: less than 1.0 mg/dl
  • serum magnesium: 1.83.0 mg/dl (1.22.0 meq/l or 0.51.0 mmol/l)
  • ionized magnesium: 0.530.67 mmol/l
  • osmolality (calculated) 280300 mosm/kg



henry, j. b. clinical diagnosis and management of laboratory methods. 20th ed. philadelphia: w. b. saunders company, 2001.

tierney, lawrence m., stephen j. mcphee, and maxine a. papadakis. current medical diagnosis and treatment 2001. 40th ed. new york: lange medical books/mcgraw-hill, 2001.

wallach, jacques. interpretation of diagnostic tests. 7th ed. philadelphia: lippincott williams & wilkins, 2000.


medline plus. "electrolytes." october 18, 2001 [cited april 4, 2003]. <>.

national institutes of health. [cited april 5, 2003]. <>.

Erika J. Norris Mark A. Best, M.D.

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