Electrolytes are essential for basic life functioning, such as maintaining electrical neutrality in cells, generating and conducting action potentials in the nerves and muscles. Sodium, potassium, and chloride are the significant electrolytes along with magnesium, calcium, phosphate, and bicarbonates. Electrolytes come from our food and fluids. 

These electrolytes can have an imbalance, leading to either high or low levels. High or low levels of electrolytes disrupt normal bodily functions and can lead to even life-threatening complications. This article reviews the basic physiology of electrolytes and their abnormalities, and the consequences of electrolyte imbalance.  


Sodium, which is an osmotically active cation, is one of the most important electrolytes in the extracellular fluid. It is responsible for maintaining the extracellular fluid volume, and also for regulation of the membrane potential of cells. Sodium is exchanged along with potassium across cell membranes as part of active transport. 

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 takes place via sodium-chloride symporters, which are by the action of the hormone aldosterone.[1]

Among the electrolyte disorders, hyponatremia is the most frequent. Diagnosis is when the serum sodium level is less than 135 mmol/L. Hyponatremia has neurological manifestations. Patients may present with headaches, confusion, nausea, delirium. Hypernatremia presents when the serum sodium levels are greater than145 mmol/L. Symptoms of hypernatremia include tachypnea, sleeping difficulty, and feeling restless. Rapid sodium corrections can have serious consequences like cerebral edema and osmotic demyelination syndrome. 


Potassium is mainly an intracellular ion. The sodium-potassium adenosine triphosphatase pump has the primary responsibility 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. The reabsorption of potassium takes place at the proximal convoluted tubule and thick ascending loop of Henle.[2] Potassium secretion occurs at the distal convoluted tubule. Aldosterone increases potassium secretion.[3] Potassium channels and potassium-chloride cotransporters at the apical membrane also secrete potassium.[2]

Potassium disorders are related to cardiac arrhythmias. Hypokalemia occurs when serum potassium levels under 3.6 mmol/L—weakness, fatigue, and muscle twitching present in hypokalemia. Hyperkalemia occurs when the serum potassium levels are above 5.5 mmol/L, which can result in arrhythmias. Muscle cramps, muscle weakness, rhabdomyolysis, myoglobinuria are presenting signs and symptoms in hyperkalemia.[4]


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. It is mostly present in the extracellular fluid. Absorption of calcium in the intestine is primarily under the control of 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 kidneys.[5] 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, and the diagnosis is 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.[6] 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.[7] 


The acid-base status of the blood drives bicarbonate levels. The kidneys predominantly regulate bicarbonate concentration and are responsible for maintaining the acid-base balance. Kidneys reabsorb the filtered bicarbonate and also generate new bicarbonate by net acid excretion, which occurs by excretion of both titrable acid and ammonia. Diarrhea usually results in loss of bicarbonate, thus causing an imbalance in acid-base regulation.[8] 


Magnesium is an intracellular cation. Magnesium is mainly involved in ATP metabolism, contraction and relaxation of muscles, proper neurological functioning, and neurotransmitter release. When muscle contracts, calcium re-uptake by the calcium-activated ATPase of the sarcoplasmic reticulum is brought about by magnesium.[9] Hypomagnesemia occurs when the serum magnesium levels are less under 1.46 mg/dl. It can present with alcohol use disorder and gastrointestinal and renal losses—ventricular arrhythmias, which include torsades de pointes seen in hypomagnesemia. 


Chloride is an anion found predominantly in the extracellular fluid. The kidneys predominantly regulate serum chloride levels. Most of the chloride, which is filtered by the glomerulus, is reabsorbed by both proximal and distal tubules (majorly by proximal tubule) by both active and passive transport.[10] 

Hyperchloremia can occur due to gastrointestinal bicarbonate loss. Hypochloremia presents in gastrointestinal losses like vomiting or excess water gain like congestive heart failure. 


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 adenosine triphosphate(ATPs) and nucleotides. Phosphate is regulated simultaneously with calcium by Vitamin D3, PTH, and calcitonin. The kidneys are the primary avenue of phosphorus excretion. 

Phosphorus imbalance may result due to three processes: dietary intake, gastrointestinal disorders, and excretion by the kidneys.[11]

Specimen Collection

A blood specimen for electrolytes use lithium heparin tubes, plus the standard phlebotomy equipment and personnel, as with any blood draw.[12]


Blood collected in lithium heparin tubes then goes to the laboratory for evaluation of serum electrolytes.[12]


Indications to order serum electrolyte panel are numerous. Some of which include:

  1. As a part of routine blood investigations  
  2. For in-patients and ICU patients, the monitoring of serum electrolytes often occurs daily or more frequently as they can be affected by the medications, fluid therapy, diet changes, and illnesses.
  3. Any illness that can cause electrolyte derangement- malnutrition, gastrointestinal disorders, cardiac disorders, kidney dysfunction, endocrine disorders, circulatory disorders, lung disorders, acid-base imbalance
  4. Arrhythmias, cardiac arrest
  5. Use of diuretics or any medications that can interfere with fluid and electrolyte homeostasis

Potential Diagnosis

Measurement of electrolytes will help the clinicians in the diagnosis of a medical condition, the effectiveness of treatment, and the potential side effect of medications. Examples include: 

  1. A patient with heart failure receiving diuretics needs a workup for potassium, bicarbonate, magnesium as diuretics can exert adverse effects on electrolyte balance.
  2. A patient that presents with weakness needs a basic electrolyte workup, as an electrolyte imbalance, especially in sodium and potassium levels, can lead to fatigue

Normal and Critical Findings

Laboratory Values: 

Serum Sodium: 

Normal Range: 135 to 145 mmol/L  

Mild-moderate Hyponatremia: 125 to 135 mmol/L, Severe: less than 125 mmol/L

Hypernatremia: Mild-moderate: 145 to 160 mmol/L, Severe: over 160 mmol/L

Serum Potassium:

Normal Range: 3.6 to 5.5 mmol/L 

Hypokalemia: Mild Hypokalemia under 3.6 mmol/L, Moderate: 2.5 mmol/L, Severe : greater than 2.5 mmol/L

Hyperkalemia: Mild hyperkalemia: 5 to 5.5 mmol/L, Moderate- 5.5 to 6.5, Severe: 6.5 to 7 mmol/L

Serum Calcium: 

Normal Range: 8.8 to 10.7 mg/dl

Hypercalcemia: greater than 10.7 mg/dl , Severe: over 11.5 mg/dl 

Hypocalcemia: less than 8.8 mg/dl

Serum Magnesium: 

Normal Range: 1.46 to 2.68 mg/dl 

Hypomagnesemia: under 1.46 mg/dl

Hypermagenesemia: over 2.68


Normal Range: 23 to 30 mmol/L

It increases or decreases depending on the acid-base status.


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

Hypomagnesemia can lead to hypocalcemia as it interferes with the action of parathormone. 

Administration of intravenous insulin is associated with a spurious decrease in potassium levels as insulin shifts potassium intracellularly.[13]

Most of the calcium remains bound to proteins, out of which albumin-bound calcium comprises about 80%. Therefore, a patient with hypoalbuminemia, as seen in liver cirrhosis, the nephrotic syndrome will demonstrate low calcium levels vs. the actual values.[14]


Both hyponatremia and hypernatremia, as well as hypomagnesemia, can lead to neurological consequences such as seizure disorders. 

Hypokalemia and hyperkalemia, as well as hypocalcemia, are more responsible for arrhythmias. 

Bicarbonate imbalance can lead to metabolic acidosis or alkalosis.

Patient Safety and Education

A piece of valuable advice to the patients would be to take the medications exactly as prescribed by the clinicians to avoid electrolyte imbalance as a consequence of not taking the prescribed dose. 

One should call for immediate medical help when the patient feels weak, has muscle ache, or has altered consciousness.  

Clinical Significance

Some of the common causes of electrolyte disorders seen in clinical practices are:

  • Hyponatremia: low dietary sodium intake, primary polydipsia, SIADH, congestive heart failure, hepatic cirrhosis, failure of adrenal glands, hyperglycemia, dyslipidemia
  • Hypernatremia: unreplaced fluid loss through the skin and gastrointestinal tract, osmotic diuresis, hypertonic saline administration
  • Hypokalemia: hyperaldosteronism, loop diuretics 
  • Hyperkalemia: increase release from cells as in metabolic acidosis, insulin deficiency, beta-blocker or decreased potassium excretion as in acute or chronic kidney disease, aldosterone deficiency or resistance
  • Hypercalcemia: malignancy, hyperparathyroidism, chronic granulomatous disease
  • Hypocalcemia: acute pancreatitis, parathyroid hormone deficiency after thyroidectomy, neck dissection, resistance to parathormone, hypomagnesemia, sepsis 
  • Hypermagnesemia: increase oral magnesium intake
  • Hypomagnesemia: renal losses as in diuretics, alcohol use disorder, or GI losses as in diarrhea
  • Bicarbonate level: increases in primary metabolic alkalosis or compensation to primary respiratory acidosis - decreases in primary metabolic acidosis or compensation to primary respiratory alkalosis.
  • Hyperchloremia: normal saline infusion
  • Hypochloremia: GI loss as in diarrhea, renal losses with diuretics
  • Hypophosphatemia: refeeding syndrome, vitamin D deficiency, hyperparathyroidism
  • Hyperphosphatemia: hypoparathyroidism, chronic kidney disease

Article Details

Article Author

Isha Shrimanker

Article Editor:

Sandeep Bhattarai


7/25/2022 11:05:56 PM



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