What are electrolytes and why are they important for our health. How do electrolyte imbalances affect our body. What are the key electrolytes measured in an electrolyte panel. How can we maintain proper electrolyte balance in our daily lives.

The Crucial Role of Electrolytes in Human Health

Electrolytes are minerals dissolved in our blood and other bodily fluids that carry an electric charge. These charged particles play a vital role in maintaining various bodily functions, including muscle contractions, nerve signaling, and fluid balance. The most significant electrolytes in our body include sodium, potassium, chloride, magnesium, calcium, phosphate, and bicarbonate.

Our bodies obtain electrolytes primarily through the food we eat and the fluids we drink. However, electrolyte levels can become imbalanced due to various factors, leading to either high or low concentrations. These imbalances can disrupt normal bodily functions and, in severe cases, lead to life-threatening complications.

Sodium: The Extracellular Fluid Regulator

Sodium is a critical electrolyte found predominantly in the extracellular fluid. It plays a crucial role in:

• Maintaining extracellular fluid volume
• Regulating cell membrane potential
• Facilitating active transport across cell membranes

The kidneys are primarily responsible for sodium regulation. Most sodium reabsorption occurs in the proximal tubule, with additional reabsorption taking place in the distal convoluted tubule. This process is controlled by the hormone aldosterone.

Sodium Imbalances and Their Effects

Hyponatremia, characterized by serum sodium levels below 135 mmol/L, is the most common electrolyte disorder. It can lead to various neurological symptoms, including:

• Headaches
• Confusion
• Nausea
• Delirium

Conversely, hypernatremia occurs when serum sodium levels exceed 145 mmol/L. Symptoms may include:

• Tachypnea (rapid breathing)
• Difficulty sleeping
• Restlessness

It’s important to note that rapid correction of sodium imbalances can lead to severe complications such as cerebral edema and osmotic demyelination syndrome (ODS). Factors like chronic alcohol misuse and malnutrition can increase the risk of developing ODS.

Potassium: The Intracellular Ion Powerhouse

Potassium is primarily an intracellular ion, meaning it’s found in higher concentrations inside cells rather than in the extracellular fluid. The sodium-potassium adenosine triphosphatase (Na+/K+-ATPase) pump plays a crucial role in maintaining the balance between sodium and potassium levels.

In the kidneys, potassium undergoes a complex process of filtration, reabsorption, and secretion:

1. Filtration occurs at the glomerulus
2. Reabsorption takes place in the proximal convoluted tubule and thick ascending loop of Henle
3. Secretion happens in the distal convoluted tubule, stimulated by aldosterone

Potassium Imbalances and Their Consequences

Hypokalemia, defined as serum potassium levels below 3.6 mmol/L, can cause:

• Weakness
• Fatigue
• Muscle twitching

In severe cases, hypokalemic paralysis may occur, resulting in generalized body weakness. This condition can be either familial or sporadic.

Hyperkalemia, characterized by serum potassium levels above 5.5 mmol/L, can lead to:

• Cardiac arrhythmias
• Muscle cramps
• Muscle weakness
• Rhabdomyolysis (breakdown of muscle tissue)
• Myoglobinuria (presence of myoglobin in urine)

Calcium: The Multifunctional Mineral

Calcium plays numerous vital roles in the body, including:

• Skeletal mineralization
• Muscle contraction
• Nerve impulse transmission
• Blood clotting
• Hormone secretion

The primary source of calcium is our diet. Calcium absorption in the intestine is largely controlled by the active form of vitamin D (1,25-dihydroxy vitamin D3). Parathyroid hormone regulates calcium secretion in the kidneys’ distal tubule, while calcitonin acts on bone cells to increase blood calcium levels.

Calcium Imbalances and Their Implications

Hypocalcemia is diagnosed when corrected serum total calcium levels fall below 8.8 mg/dL. This condition can result from:

• Vitamin D deficiency
• Hypoparathyroidism

Hypercalcemia occurs when corrected serum total calcium levels exceed 10.7 mg/dL. Common causes include:

• Primary hyperparathyroidism
• Malignancy-associated humoral hypercalcemia (often due to PTHrP secretion)

Bicarbonate: The Body’s pH Regulator

Bicarbonate levels in the blood are closely tied to the body’s acid-base status. The kidneys play a primary role in regulating bicarbonate concentration and maintaining acid-base balance through two main mechanisms:

1. Reabsorption of filtered bicarbonate
2. Generation of new bicarbonate through net acid excretion (via titrable acid and ammonia excretion)

Bicarbonate imbalances can occur due to various factors:

• Diarrhea often leads to bicarbonate loss, disrupting acid-base regulation
• Kidney disorders can result in excess bicarbonate accumulation in the body

Magnesium: The Overlooked Electrolyte

Magnesium, often underappreciated, is a crucial electrolyte involved in numerous physiological processes. It plays a vital role in:

• Energy production
• Protein synthesis
• Muscle and nerve function
• Blood glucose control
• Blood pressure regulation

Magnesium homeostasis is primarily maintained by the kidneys, which can increase or decrease magnesium excretion based on the body’s needs. Dietary sources of magnesium include green leafy vegetables, nuts, seeds, and whole grains.

Magnesium Imbalances and Their Effects

Hypomagnesemia, or low blood magnesium levels, can lead to:

• Muscle weakness and cramps
• Fatigue
• Irregular heartbeat
• Seizures (in severe cases)

Hypermagnesemia, while less common, can cause:

• Nausea and vomiting
• Lethargy
• Muscle weakness
• Cardiac conduction abnormalities

The Importance of Electrolyte Balance in Clinical Practice

Understanding electrolyte balance is crucial for healthcare providers in diagnosing and treating various medical conditions. Electrolyte imbalances can be both a cause and a consequence of many diseases, making their assessment an essential part of patient care.

Are electrolyte panels routinely performed in clinical settings? Yes, electrolyte panels are commonly ordered as part of basic metabolic panels or comprehensive metabolic panels. These tests provide valuable information about a patient’s:

• Hydration status
• Kidney function
• Acid-base balance
• Overall metabolic health

When interpreting electrolyte panel results, healthcare providers must consider various factors, including:

1. The patient’s medical history
2. Current medications
3. Recent dietary habits
4. Presence of any underlying medical conditions

Maintaining Electrolyte Balance in Daily Life

While electrolyte imbalances often require medical intervention, there are steps individuals can take to maintain proper electrolyte balance in their daily lives:

• Stay hydrated by drinking adequate amounts of water
• Consume a balanced diet rich in fruits, vegetables, and whole grains
• Replace fluids and electrolytes lost during intense physical activity or in hot weather
• Be aware of medications that may affect electrolyte levels
• Limit alcohol consumption, as it can disrupt electrolyte balance

Can certain foods help maintain electrolyte balance? Indeed, many foods are naturally rich in electrolytes:

• Bananas and sweet potatoes (high in potassium)
• Leafy greens like spinach and kale (rich in magnesium and calcium)
• Yogurt and milk (good sources of calcium)
• Nuts and seeds (contain magnesium and phosphorus)
• Coconut water (natural source of multiple electrolytes)

Electrolyte Imbalances in Special Populations

Certain groups of people may be more susceptible to electrolyte imbalances:

1. Athletes: Intense physical activity can lead to significant electrolyte losses through sweat
2. Elderly individuals: Age-related changes in kidney function can affect electrolyte regulation
3. Patients with chronic diseases: Conditions like diabetes, heart failure, and kidney disease can disrupt electrolyte balance
4. Individuals on certain medications: Diuretics, laxatives, and some antibiotics can affect electrolyte levels

How can these at-risk groups protect themselves from electrolyte imbalances? Here are some strategies:

• Regular monitoring of electrolyte levels through blood tests
• Proper hydration and nutrition tailored to individual needs
• Use of electrolyte-rich sports drinks during intense exercise (for athletes)
• Careful medication management under healthcare provider supervision
• Awareness of symptoms that may indicate electrolyte imbalances

The Future of Electrolyte Management in Medicine

As our understanding of electrolyte physiology continues to grow, new approaches to managing electrolyte imbalances are emerging. Some exciting developments include:

• Point-of-care testing for rapid electrolyte assessment
• Personalized electrolyte replacement strategies based on genetic profiles
• Advanced monitoring systems for continuous electrolyte tracking in critically ill patients
• Novel pharmaceutical formulations for more effective electrolyte supplementation

What role will technology play in future electrolyte management? Advancements in technology are likely to revolutionize how we monitor and manage electrolyte balance:

1. Wearable devices that can track electrolyte levels in real-time
2. Artificial intelligence algorithms to predict and prevent electrolyte imbalances
3. Telemedicine platforms for remote electrolyte monitoring and management
4. Smart hydration systems that automatically adjust fluid and electrolyte intake based on individual needs

As research in this field progresses, our ability to maintain optimal electrolyte balance and prevent related health complications will undoubtedly improve, leading to better overall health outcomes for patients across various medical specialties.

Electrolytes – StatPearls – NCBI Bookshelf

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]

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 increase the 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 by 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 losses 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.

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.

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.

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]

• 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

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• Comment on this article.

References

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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]

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Buffington MA, Abreo K. Hyponatremia: A Review. J Intensive Care Med. 2016 May;31(4):223-36. [PubMed: 25592330]

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Ambati R, Kho LK, Prentice D, Thompson A. Osmotic demyelination syndrome: novel risk factors and proposed pathophysiology. Intern Med J. 2022 Jun 19; [PubMed: 35717664]

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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]

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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]

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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]

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Viera AJ, Wouk N. Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician. 2015 Sep 15;92(6):487-95. [PubMed: 26371733]

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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]

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Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ. 2008 Jun 07;336(7656):1298-302. [PMC free article: PMC2413335] [PubMed: 18535072]

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Turner JJO. Hypercalcaemia – presentation and management . Clin Med (Lond). 2017 Jun;17(3):270-273. [PMC free article: PMC6297576] [PubMed: 28572230]

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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]

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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]

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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]

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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]

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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]

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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]

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Boden SD, Kaplan FS. Calcium homeostasis. Orthop Clin North Am. 1990 Jan;21(1):31-42. [PubMed: 2404236]

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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]

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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]

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Agus ZS. Mechanisms and causes of hypomagnesemia. Curr Opin Nephrol Hypertens. 2016 Jul;25(4):301-7. [PubMed: 27219040]

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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.

Electrolytes – StatPearls – NCBI Bookshelf

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]

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 increase the 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 by 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 losses 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.

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.

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.

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]

• 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]

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Buffington MA, Abreo K. Hyponatremia: A Review. J Intensive Care Med. 2016 May;31(4):223-36. [PubMed: 25592330]

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Ambati R, Kho LK, Prentice D, Thompson A. Osmotic demyelination syndrome: novel risk factors and proposed pathophysiology. Intern Med J. 2022 Jun 19; [PubMed: 35717664]

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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]

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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]

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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]

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Viera AJ, Wouk N. Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician. 2015 Sep 15;92(6):487-95. [PubMed: 26371733]

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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]

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Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ. 2008 Jun 07;336(7656):1298-302. [PMC free article: PMC2413335] [PubMed: 18535072]

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Turner JJO. Hypercalcaemia – presentation and management . Clin Med (Lond). 2017 Jun;17(3):270-273. [PMC free article: PMC6297576] [PubMed: 28572230]

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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]

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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]

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Jahnen-Dechent W, Ketteler M. Magnesium basics. Clin Kidney J. 2012 Feb;5(Suppl 1):i3-i14. [PMC free article: PMC4455825] [PubMed: 26069819]

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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]

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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]

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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]

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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]

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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.

Theory of electrolytic dissociation (TED) – what is it? Key points and examples

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A solution of sodium chloride conducts electricity well, but when dry, salt crystals do not conduct electricity. Why? This question is answered by the theory of electrolytic dissociation, which we will now consider. It was first described by the Swedish scientist Svante Arrhenius. Electrolytic dissociation is studied as part of a chemistry course for 9Class.

What is electrolytic dissociation

As you know, electric current is a directed movement of free electrons or ions, ie charged particles. In electrolyte solutions that conduct current, free ions are responsible for this.

In 1882, the Swedish chemist S. Arrhenius, while studying the properties of electrolyte solutions, noticed that they contain more particles than were in the dry matter. For example, in a solution of sodium chloride, there are 2 moles of particles, while dry NaCl contains only 1 mole.

This allowed the scientist to conclude that when such substances are dissolved in water, free ions appear in them. Thus, the foundations of the theory of electrolytic dissociation (TED) were laid – in chemistry it became one of the most important discoveries.

Electrolytic dissociation is the process by which electrolyte molecules react with water or another solvent and break down into ions. It may be reversible or irreversible. The reverse process is called molarization.

Electrolyte solutions become conductive through dissociation. Svante Arrhenius could not explain why different substances differ greatly in electrical conductivity, but D. I. Mendeleev did this. He described in detail the process of decomposition of an electrolyte into ions, which is explained by its interaction with water molecules (or other solvent).

Electrolytic dissociation scheme: KA ⇄ K ⁺ (cation) + A ^– (anion).

Dissociation equation using sodium chloride as an example: NaCl ⇄ Na ⁺ + Cl ^– .

Speak correctly 🤓

Sometimes you can come across the expression “electrical dissociation theory”, but you shouldn’t say that. In this case, one might think that the disintegration of molecules into ions is due to the action of an electric current. In fact, the dissociation process does not depend on whether current is currently passing through the solution or not. All that is needed is the contact of the electrolyte with water (solvent).

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Mechanism of electrolytic dissociation

When in contact with water or other solvents, all substances with an ionic bond are subject to dissociation. Substances with a covalent polar bond can also decompose into ions, which, under the action of water, becomes ionic, and then collapses.

It is convenient to consider the mechanism of electrolyte dissociation using sodium chloride NaCl as an example. Its crystal lattice is formed by sodium cations Na ⁺ and chlorine anions Cl ^– , which are held together by ionic bonding. When dissolved in water, each crystal of sodium chloride is surrounded by its molecules.

Note that water molecules are dipoles. At one end they carry hydrogen atoms with a partial positive charge, and at the other end they carry oxygen atoms with a partial negative charge. Accordingly, oxygen atoms are attracted to sodium cations, and hydrogen atoms are attracted to chlorine anions. This electrostatic attraction weakens and eventually breaks the ionic bond between sodium and chloride. A substance dissociates into ions.

After the decomposition of sodium chloride, the resulting Na ⁺ and Cl ^– ions surround water molecules, creating a hydration shell . Ions with such a shell are called hydrated.

If another solvent, such as ethanol, was used instead of water, its molecules form a solvation shell . In this case, the ions are called solvated.

The scheme conveys the essence of the electrolytic dissociation process:

Electrolytes and non-electrolytes

Although electrolytic dissociation occurs independently of the action of an electric current, there is a connection between these phenomena. The higher the ability of a substance to decompose into ions when interacting with a solvent, the better it conducts electricity. According to this criterion, the famous physico-chemist M. Faraday singled out electrolytes and non-electrolytes.

Electrolytes are substances that, after dissociation into ions in solutions and melts, conduct an electric current. Usually in their molecules there are ionic or polar covalent bonds.

Non-electrolytes are substances that do not decompose into ions in solutions and melts, and therefore do not have conductivity in dissolved form. They are characterized by covalent non-polar or weakly polar bonds.

Degree of dissociation

Depending on how many molecules have dissociated into ions, the substance can be a strong or weak electrolyte. This indicator is called the degree of dissociation, it is measured from 0 to 1 or as a percentage.

The degree of dissociation is the ratio of the number of moles of a substance decomposed into ions to the initial number of moles.

or .

If all 100% of the electrolyte decomposes into ions in solution, .

By strength, electrolytes are divided into the following groups:

• weak – ;

• medium – ;

• strong — .

Important!

Molecules of strong electrolytes irreversibly decompose into ions, so the sign = must be put in the equations. Reactions with weak electrolytes are reversible, so the sign ⇄ is put.

Stepwise dissociation

In some cases, substances are split into ions in several stages or steps. For example, such a reaction is typical for basic and acidic salts, polybasic acids. Stepwise dissociation can include two or more stages, with the ion concentration at the first stage always higher than at the subsequent ones.

Example 1

Phosphoric acid dissociates in 3 steps. On the first of them, the maximum concentration of dihydrophosphate ions is observed, and on the last one, the minimum amount of phosphate ions remains (dissociation almost does not occur). This acid is not a strong electrolyte, so the reaction is reversible.

1. H ₃ PO ₄ 3

2. H ₂ PO ₄ ^– ⇄ H ⁺ + HPO

3. HPO ₄ ^2- ⇄ H ⁺ + PO ₄ ^3-

Summary equation: H ₃ PO ₄ ⇄ 3H ⁺ + PO ₄ ^3- .

Example 2

The acid salt Ca(HCO ₃ ) ₂ dissociates in 3 steps. Because it is a strong electrolyte, the reaction is irreversible in the first step. At the second stage, a weak acid residue HCO ₃ ^– and a weak electrolyte decompose into ions, so the reaction is reversible.

1. Ca(HCO ₃ ) ₂ = Ca ²⁺ + 2HCO

2. HCO ₃ ^– ⇄ H ⁺ + CO ₃ ^2-

3. H ⁺ + H ₂ O = H ₃ O ⁺

Summary equation: Ca(HCO ₃ ) ₂ + 2H ₂ O = Ca ²⁺ + 2H CO ₃ ^2- .

How different groups of substances dissociate

Dissociation of acids

Leads to the formation of hydrogen cations H ⁺ and negatively charged acid residues:

HCl = H ⁺ + Cl ^–

H ₂ SO ₄ = 2H 024 + SO ₄ ^2-

HNO ₂ ⇄ H ₊ + NO ^2-

Polybasic acids dissociate stepwise:

1. AlOHCl AlOH ²⁺ + 2Cl ^–

2. AlOH ²⁺ ⇄ Al ³⁺ + OH ^–

Base dissociation

Occurs with the formation of hydroxyl groups OH ^– and positively charged metal ions. Strong electrolytes in solutions dissociate completely, while weak electrolytes dissociate stepwise and reversibly.

Strong bases:

NaOH = Na ⁺ + OH 0010 Cu(ON) ₂ ⇄ CuOH ⁺ + OH ^–

Dissociation of salts

Leads to the formation of metal cations (or ammonium cation) and negatively charged acid residues.

Medium salts completely decompose in solutions in one step.

Na ₃ PO ₄ = 3Na + PO ₄ ^3-

Acid salts decompose stepwise. At the first stage, metal cations are separated, and at the second stage, hydrogen cations.

1. KHSO ₄ = K ⁺ + HSO ₄ ^–

2. HSO ₄ ^– ⇄ H ⁺ + SO ₄ ^2-

Basic salts also dissociate in two steps. At the first, acid residues are separated, followed by hydroxyl groups OH ^– .

1. MgOHBr = MgOH ⁺ + Br ^–

2. MgOH ⁺ ⇄ Mg ²⁺ + OH ^–

Molecular, complete and abbreviated ionic equations

Molecular equations can be used to show the composition of a substance by decomposing it into molecules. The complete ionic equations reflect the dissociation reaction, i.e., the splitting of molecules into ions. But in this form, only strong electrolytes are painted.

Do not decompose into ions:

• weak electrolytes;

• precipitation;

• gases.

Consider the example of the interaction between lead nitrate and sulfuric acid.

Molecular equation: Pb(NO ₃ ) ₂ + H ₂ SO ₄ → 2HNO ₃ + PbSO 901 31 4 ↓

Lead sulfate PbSO _{4 9We will not decompose 0132 into ions, since it is a weak electrolyte.}

Full ionic equation: Pb ²⁺ + 2NO ₃ ^– + 2H ⁺ + SO ₄ ^2- → 2H ⁺ + 2NO ₃ ^– + PbSO ₄ ↓

It is very easy to reduce this expression – you need to remove the same ions from both parts that have not changed during the reaction.

Abbreviated ionic equation: Pb ²⁺ + SO ₄ ^2- → PbSO ₄ ↓

are the formulas of the formed cations and anions. Between them we put the sign = if it is a strong electrolyte, or the sign ⇄ – if it is medium or weak. After that, you need to put down the coefficients in front of the ions and check the sum of cations and anions (it is always equal to 0).

Fundamentals of the theory of electrolytic dissociation

So, we figured out what dissociation is in chemistry, and now we will repeat the key points:

• When interacting with water or other solvents in electrolytes, the chemical bond between particles is broken and they decompose into ions – electrolytic dissociation occurs.

• Under the action of an electric current, cations move to a positively charged electrode, anions – to a negatively charged one. The electrolyte solution is conductive.

• The degree of dissociation depends on the type of electrolyte and on external conditions. For strong electrolytes, it is irreversible; for weak electrolytes, it is a reversible reaction.

• The chemical properties of electrolytes correspond to the properties of the ions formed during dissociation.

Self-test questions

1. How do electrolytes differ from non-electrolytes? Give examples of both substances.

2. According to the theory of dissociation, what causes the decomposition of electrolytes into ions?

3. What is the degree of dissociation and how is it measured?

4. When does the electrolytic dissociation of acids occur in steps?

5. Under what conditions is the = sign put in the dissociation equation, and under what conditions is the ⇄ sign?

6. Which components of an ionic equation cannot be decomposed into ions?

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Electrolytic dissociation of electrolytes in aqueous solutions

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About electrolytes

What is electrolytic dissociation?

It sounds abstruse, but in fact there is nothing terrible or complicated in this definition.

Electrolytic dissociation – the decomposition of some substance (electrolyte) into ions (charged particles).

Electrolyte is a substance that, when released into water, will decompose into ions, that is, dissociate, and conduct current in melts and solutions.

It is important to remember that some electrolytes are able to break down into ions well (they are called strong ), and some are almost not able to do this (they are called weak ). In this, ions are like athletes: one can squeeze out more than 50 times in a minute (break up into many ions), and the other barely squeezes out ten (almost no ions). People will quickly define the first as strong, and the second, alas, as weak.

It is easiest to remember first those who are classified as strong electrolytes, then all the rest will be weak.

Which classes of substances are classified as electrolytes?

1. Salts.
2. Bases.
3. Acids.

We memorize by the first letters that make up the code word “SOK”.

About solutions

Dissolution of is a physical and chemical process in which particles interact with each other.

What is a solution? Solution is a homogeneous system consisting of two or more components. For example: air (consists of different gases), oil (a mixture of liquid hydrocarbons), vinegar (a solution of acetic acid in water).

There are also supersaturated solutions , in which more substance is dissolved than the maximum possible. Therefore, they are very unstable.

What else is important to know about solutions – they have a certain concentration.

Concentration of a solution is the amount of a substance that is in a unit volume or mass of a solution.

• Electrolytic dissociation – decomposition of some substance (electrolyte) into ions (charged particles).
• Electrolyte is a substance that, when released into water, will decompose into ions, that is, dissociate, and conduct current in melts and solutions.
• Three classes of substances are classified as electrolytes: salts, bases and acids.