6/10/24, 9:00 PM Electrolytes - StatPearls - NCBI Bookshelf
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Electrolytes
Isha Shrimanker; Sandeep Bhattarai.
Author Information and Affiliations
Last Update: July 24, 2023.
Introduction
Electrolytes are essential for basic life functioning, such as maintaining electrical neutrality in
cells and generating and conducting action potentials in the nerves and muscles. Significant
electrolytes include sodium, potassium, chloride, magnesium, calcium, phosphate, and
bicarbonates. Electrolytes come from our food and fluids.
These electrolytes can be imbalanced, leading to high or low levels. High or low levels of
electrolytes disrupt normal bodily functions and can lead to life-threatening complications. This
article reviews the basic physiology of electrolytes and their abnormalities, and the consequences
of electrolyte imbalance.
Sodium
Sodium, an osmotically active cation, is one of the essential electrolytes in the extracellular fluid.
It is responsible for maintaining the extracellular fluid volume and regulating the membrane
potential of cells. Sodium is exchanged along with potassium across cell membranes as part of
active transport.[1]
Sodium regulation occurs in the kidneys. The proximal tubule is where the majority of sodium
reabsorption takes place. In the distal convoluted tubule, sodium undergoes reabsorption. Sodium
transport occurs via sodium-chloride symporters, controlled by the hormone aldosterone.[2]
Among the electrolyte disorders, hyponatremia is the most frequent. Hyponatremia is diagnosed
when the serum sodium level is less than 135 mmol/L. Hyponatremia has neurological
manifestations.[3] Patients may present with headaches, confusion, nausea, and
delirium. Hypernatremia occurs when serum sodium levels are greater than 145 mmol/L.
Symptoms of hypernatremia include tachypnea, sleeping difficulty, and restlessness. Rapid
sodium corrections can have severe consequences like cerebral edema and osmotic
demyelination syndrome (ODS). Other factors like chronic alcohol misuse disorder and
malnutrition also play a role in the development of ODS.[4]
Potassium
Potassium is mainly an intracellular ion. The sodium-potassium adenosine triphosphatase pump
is primarily responsible for regulating the homeostasis between sodium and potassium, which
pumps out sodium in exchange for potassium, which moves into the cells. In the kidneys, the
filtration of potassium takes place at the glomerulus. Potassium reabsorption occurs at the
proximal convoluted tubule and thick ascending loop of Henle.[5] Potassium secretion occurs at
the distal convoluted tubule. Aldosterone increases potassium secretion.[6] Potassium channels
and potassium-chloride cotransporters at the apical tubular membrane also secrete potassium.[5]
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Potassium derangements may result in cardiac arrhythmias. Hypokalemia occurs when serum
potassium levels are under 3.6 mmol/L. The features of hypokalemia include weakness, fatigue,
and muscle twitching. Hypokalemic paralysis is generalized body weakness that can be either
familial or sporadic.[7] Hyperkalemia occurs when the serum potassium levels are above 5.5
mmol/L, which can result in arrhythmias. Muscle cramps, muscle weakness, rhabdomyolysis,
and myoglobinuria may be presenting signs and symptoms of hyperkalemia.[8]
Calcium
Calcium has a significant physiological role in the body. It is involved in skeletal mineralization,
contraction of muscles, the transmission of nerve impulses, blood clotting, and secretion of
hormones. The diet is the predominant source of calcium. Calcium is a predominately
extracellular cation. Calcium absorption in the intestine is primarily controlled by the hormonally
active form of vitamin D, which is 1,25-dihydroxy vitamin D3. Parathyroid hormone also
regulates calcium secretion in the distal tubule of the kidneys.[9] Calcitonin acts on bone cells to
decrease calcium levels in the blood.
Hypocalcemia diagnosis requires checking the serum albumin level to correct for total calcium.
Hypocalcemia is diagnosed when the corrected serum total calcium levels are less than 8.8
mg/dL, as in vitamin D deficiency or hypoparathyroidism. Checking serum calcium levels is a
recommended test in post-thyroidectomy patients.[10] Hypercalcemia is when corrected serum
total calcium levels exceed 10.7 mg/dL, as seen with primary hyperparathyroidism. Humoral
hypercalcemia presents in malignancy, primarily due to PTHrP secretion.[11]
Bicarbonate
The acid-base status of the blood drives bicarbonate levels. The kidneys predominantly regulate
bicarbonate concentration and maintain the acid-base balance. Kidneys reabsorb the filtered
bicarbonate and generate new bicarbonate by net acid excretion, which occurs through the
excretion of titrable acid and ammonia. Diarrhea usually results in bicarbonate loss, causing an
imbalance in acid-base regulation.[12] Many kidney-related disorders can result in imbalanced
bicarbonate metabolism leading to excess bicarbonate in the body.[13]
Magnesium
Magnesium is an intracellular cation. Magnesium is mainly involved in adenosine triphosphate
(ATP) metabolism, proper functioning of muscles, neurological functioning, and
neurotransmitter release. When muscles contract, calcium re-uptake by the calcium-activated
ATPase of the sarcoplasmic reticulum is brought about by magnesium.[14] Hypomagnesemia
occurs when the serum magnesium levels are less than 1.46 mg/dL. Alcohol use disorder,
gastrointestinal conditions, and excessive renal loss may result in hypomagnesemia. It commonly
presents with ventricular arrhythmias, which include torsades de pointes. Hypomagnesemia may
also result from the use of certain medications, such as omeprazole.[15]
Chloride
Chloride is an anion found predominantly in the extracellular fluid. The kidneys predominantly
regulate serum chloride levels. Most chloride, filtered by the glomerulus, is reabsorbed by both
proximal and distal tubules (majorly by proximal tubule) by both active and passive transport.
[16]
Hyperchloremia can occur due to gastrointestinal bicarbonate loss. Hypochloremia presents
in gastrointestinal losses like vomiting or excess water gain like congestive heart failure.
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Phosphorus
Phosphorus is an extracellular fluid cation. Eighty-five percent of the total body phosphorus is in
the bones and teeth in the form of hydroxyapatite; the soft tissues contain the remaining 15%.
Phosphate plays a crucial role in metabolic pathways. It is a component of many metabolic
intermediates and, most importantly, of ATP and nucleotides. Vitamin D3, PTH, and calcitonin
regulate phosphate simultaneously with calcium. The kidneys are the primary avenue of
phosphorus excretion.
Phosphate imbalance is most commonly due to one of three processes: impaired dietary
intake, gastrointestinal disorders, and deranged renal excretion.[17]
Specimen Collection
A blood specimen for electrolytes uses lithium heparin tubes, plus the standard phlebotomy
equipment and personnel, as with any blood draw.[18]
Procedures
Blood is collected in lithium heparin tubes and then goes to the laboratory to evaluate serum
electrolytes.[18] The collection tubes should not be left for an extended period as cell lysis can
occur, causing the intracellular electrolytes and other contents to come out in the serum.
Indications
Indications to order serum electrolyte panels are numerous. Some indications are:
Routine blood investigations
Routine monitoring of hospitalized patients on medications, receiving fluid therapy,
undergoing dietary changes, or being treated for ongoing illnesses.
Any illness that can cause electrolyte derangements, such as malnutrition, gastrointestinal
disorders, cardiac disorders, kidney dysfunction, endocrine disorders, circulatory disorders,
lung disorders, and acid-base imbalance[19]
Arrhythmias
Cardiac arrest
Use of diuretics or any medications that can interfere with fluid and electrolyte
homeostasis
Potential Diagnosis
Measurement of electrolytes will help clinicians in the diagnosis of a medical condition, the
effectiveness of treatment, and the potential side effect of medications. Examples include:
A patient with heart failure receiving diuretics needs a workup for sodium, potassium,
bicarbonate, and magnesium, as diuretics can exert adverse effects on electrolyte balance.[20]
A patient that presents with weakness needs a basic electrolyte workup, as an electrolyte
imbalance, especially in sodium and potassium levels, can lead to generalized weakness.
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A patient with gastroesophageal reflux disease on long-term proton pump inhibitor therapy
should be monitored for hypomagnesemia.
Normal and Critical Findings
Laboratory Values
Serum Sodium
Normal range: 135 to 145 mmol/L
Mild to moderate hyponatremia: 125 to 135 mmol/L
Severe hyponatremia: less than 125 mmol/L
Mild to moderate hypernatremia: 145 to 160 mmol/L
Severe hypernatremia: greater than 160 mmol/L
Serum Potassium
Normal range: 3.6 to 5.5 mmol/L
Mild hypokalemia: less than 3.6 mmol/L
Moderate hypokalemia: less than 2.5 mmol/L
Severe hypokalemia: less than greater than 2.5 mmol/L
Mild hyperkalemia: 5 to 5.5 mmol/L
Moderate hyperkalemia: 5.5 to 6.5 mmol/L
Severe hyperkalemia: 6.5 to 7 mmol/L
Serum Calcium
Normal range: 8.8 to 10.7 mg/dL
Hypocalcemia: less than 8.8 mg/dL
Mild to moderate hypercalcemia: greater than 10.7 10 11.5 mg/dL
Severe hypercalcemia: greater than 11.5 mg/dL
Serum Magnesium
Normal range: 1.46 to 2.68 mg/dL
Hypomagnesemia: less than 1.46 mg/dL
Hypermagenesemia: greater than 2.68 mg/dL
Bicarbonate
Normal range: 23 to 30 mmol/L
It increases or decreases depending on the acid-base status.
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Phosphorus
Normal range: 3.4 to 4.5 mg/dL
Hypophosphatemia: less than 2.5 mg/dL
Hyperphosphatemia: greater than 4.5 mg/dL
Interfering Factors
Factors such as total protein content, hormones, and total body volume status can biochemically
influence electrolyte levels. Hypomagnesemia can lead to hypocalcemia due to its effects on
parathyroid hormone activity. Intravenous insulin administration is associated with a spurious
decrease in potassium levels as insulin shifts potassium intracellularly.[21]
Most serum calcium is bound to proteins; albumin-bound calcium comprises about 80%.
Therefore, a patient with hypoalbuminemia, as seen in liver cirrhosis or nephrotic syndrome, will
demonstrate artificially abnormal serum calcium levels.[22]
Complications
Hyponatremia, hypernatremia, and hypomagnesemia can lead to neurological consequences such
as seizures.
Hypokalemia and hyperkalemia, as well as hypocalcemia, may cause cardiac arrhythmias.[23]
Bicarbonate imbalance can lead to metabolic acidosis or alkalosis.
Some consequences of potassium, calcium, and magnesium abnormalities are fatigue, lethargy,
and muscle weakness.
Patient Safety and Education
Patients should be counseled to take all medications exactly as prescribed to avoid any potential
adverse effect of electrolyte imbalance. They should also call for immediate medical help if
experiencing generalized weakness, muscle aches, or altered mental status.
Clinical Significance
Some of the common causes of electrolyte disorders seen in clinical practices are:
Hyponatremia: low dietary sodium intake, primary polydipsia, syndrome of
inappropriate antidiuretic hormone secretion (SIADH), heart failure, cirrhosis, adrenal
insufficiency, prolonged hyperglycemia, and severe dyslipidemia.
Hypernatremia: unreplaced fluid loss via the skin or gastrointestinal tract, osmotic diuresis,
or hypertonic saline administration.
Hypokalemia: hyperaldosteronism or the use of loop diuretics.
Hyperkalemia: metabolic acidosis, insulin deficiency, hypoaldosteronism, prolonged beta-
blocker use, or acute or chronic kidney disease.
Hypercalcemia: malignancy, hyperparathyroidism, or chronic granulomatous diseases such
as tuberculosis or sarcoidosis.[24]
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Hypocalcemia: acute pancreatitis, iatrogenic parathyroid dysfunction, resistance to
parathyroid hormone, hypomagnesemia, or sepsis.
Hypermagnesemia: increased oral magnesium intake.
Hypomagnesemia: increased renal losses with diuretics, alcohol use disorder, or
gastrointestinal losses.[25]
Bicarbonate level: increases in primary metabolic alkalosis or compensation to primary
respiratory acidosis and decreases in primary metabolic acidosis or compensation to
primary respiratory alkalosis.
Hyperchloremia: excessive normal saline infusion.
Hypochloremia: increased gastrointestinal or renal losses.
Hypophosphatemia: refeeding syndrome, vitamin D deficiency, or hyperparathyroidism.
[26]
Hyperphosphatemia: hyperparathyroidism or chronic kidney disease.
Review Questions
Access free multiple choice questions on this topic.
Comment on this article.
References
1. Ferrannini E. Sodium-Glucose Co-transporters and Their Inhibition: Clinical Physiology.
Cell Metab. 2017 Jul 05;26(1):27-38. [PubMed: 28506519]
2. Palmer LG, Schnermann J. Integrated control of Na transport along the nephron. Clin J Am
Soc Nephrol. 2015 Apr 07;10(4):676-87. [PMC free article: PMC4386267] [PubMed:
25098598]
3. Buffington MA, Abreo K. Hyponatremia: A Review. J Intensive Care Med. 2016
May;31(4):223-36. [PubMed: 25592330]
4. Ambati R, Kho LK, Prentice D, Thompson A. Osmotic demyelination syndrome: novel risk
factors and proposed pathophysiology. Intern Med J. 2023 Jul;53(7):1154-1162. [PubMed:
35717664]
5. Gumz ML, Rabinowitz L, Wingo CS. An Integrated View of Potassium Homeostasis. N Engl
J Med. 2015 Jul 02;373(1):60-72. [PMC free article: PMC5675534] [PubMed: 26132942]
6. Ellison DH, Terker AS, Gamba G. Potassium and Its Discontents: New Insight, New
Treatments. J Am Soc Nephrol. 2016 Apr;27(4):981-9. [PMC free article: PMC4814195]
[PubMed: 26510885]
7. Stedwell RE, Allen KM, Binder LS. Hypokalemic paralyses: a review of the etiologies,
pathophysiology, presentation, and therapy. Am J Emerg Med. 1992 Mar;10(2):143-8.
[PubMed: 1586409]
8. Viera AJ, Wouk N. Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam
Physician. 2015 Sep 15;92(6):487-95. [PubMed: 26371733]
9. Veldurthy V, Wei R, Oz L, Dhawan P, Jeon YH, Christakos S. Vitamin D, calcium
homeostasis and aging. Bone Res. 2016;4:16041. [PMC free article: PMC5068478]
[PubMed: 27790378]
10.
[Link] 6/8
6/10/24, 9:00 PM Electrolytes - StatPearls - NCBI Bookshelf
Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ. 2008 Jun
07;336(7656):1298-302. [PMC free article: PMC2413335] [PubMed: 18535072]
11. Turner JJO. Hypercalcaemia - presentation and management . Clin Med (Lond). 2017
Jun;17(3):270-273. [PMC free article: PMC6297576] [PubMed: 28572230]
12. Hamm LL, Nakhoul N, Hering-Smith KS. Acid-Base Homeostasis. Clin J Am Soc Nephrol.
2015 Dec 07;10(12):2232-42. [PMC free article: PMC4670772] [PubMed: 26597304]
13. Kraut JA, Madias NE. Adverse Effects of the Metabolic Acidosis of Chronic Kidney
Disease. Adv Chronic Kidney Dis. 2017 Sep;24(5):289-297. [PubMed: 29031355]
14. Jahnen-Dechent W, Ketteler M. Magnesium basics. Clin Kidney J. 2012 Feb;5(Suppl 1):i3-
i14. [PMC free article: PMC4455825] [PubMed: 26069819]
15. Hansen BA, Bruserud Ø. Hypomagnesemia as a potentially life-threatening adverse effect
of omeprazole. Oxf Med Case Reports. 2016 Jul;2016(7):147-9. [PMC free article:
PMC4962887] [PubMed: 27471598]
16. Morrison G. Serum Chloride. In: Walker HK, Hall WD, Hurst JW, editors. Clinical
Methods: The History, Physical, and Laboratory Examinations. 3rd ed. Butterworths;
Boston: 1990. [PubMed: 21250151]
17. Berkelhammer C, Bear RA. A clinical approach to common electrolyte problems: 3.
Hypophosphatemia. Can Med Assoc J. 1984 Jan 01;130(1):17-23. [PMC free article:
PMC1875686] [PubMed: 6418367]
18. Toffaletti J, Ernst P, Hunt P, Abrams B. Dry electrolyte-balanced heparinized syringes
evaluated for determining ionized calcium and other electrolytes in whole blood. Clin
Chem. 1991 Oct;37(10 Pt 1):1730-3. [PubMed: 1914173]
19. Raza M, Kumar S, Ejaz M, Azim D, Azizullah S, Hussain A. Electrolyte Imbalance in
Children With Severe Acute Malnutrition at a Tertiary Care Hospital in Pakistan: A Cross-
Sectional Study. Cureus. 2020 Sep 19;12(9):e10541. [PMC free article: PMC7574973]
[PubMed: 33094080]
20. Cody RJ, Pickworth KK. Approaches to diuretic therapy and electrolyte imbalance in
congestive heart failure. Cardiol Clin. 1994 Feb;12(1):37-50. [PubMed: 8181024]
21. Liamis G, Liberopoulos E, Barkas F, Elisaf M. Spurious electrolyte disorders: a diagnostic
challenge for clinicians. Am J Nephrol. 2013;38(1):50-7. [PubMed: 23817179]
22. Boden SD, Kaplan FS. Calcium homeostasis. Orthop Clin North Am. 1990 Jan;21(1):31-42.
[PubMed: 2404236]
23. Hoppe LK, Muhlack DC, Koenig W, Carr PR, Brenner H, Schöttker B. Association of
Abnormal Serum Potassium Levels with Arrhythmias and Cardiovascular Mortality: a
Systematic Review and Meta-Analysis of Observational Studies. Cardiovasc Drugs Ther.
2018 Apr;32(2):197-212. [PubMed: 29679302]
24. Negri AL, Rosa Diez G, Del Valle E, Piulats E, Greloni G, Quevedo A, Varela F, Diehl M,
Bevione P. Hypercalcemia secondary to granulomatous disease caused by the injection of
methacrylate: a case series. Clin Cases Miner Bone Metab. 2014 Jan;11(1):44-8. [PMC free
article: PMC4064440] [PubMed: 25002879]
25. Agus ZS. Mechanisms and causes of hypomagnesemia. Curr Opin Nephrol Hypertens. 2016
Jul;25(4):301-7. [PubMed: 27219040]
26. Marinella MA. Refeeding syndrome and hypophosphatemia. J Intensive Care Med. 2005
May-Jun;20(3):155-9. [PubMed: 15888903]
Disclosure: Isha Shrimanker declares no relevant financial relationships with ineligible companies.
Disclosure: Sandeep Bhattarai declares no relevant financial relationships with ineligible companies.
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