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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019-.
2019 May 3.

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UPMC Pinnacle


Electrolytes are essential for basic life functioning such as maintaining electrical neutrality in the cells, generation, and conduction of 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. A high or a low level of electrolytes disrupts the 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 Sodium, which is an osmotically active anion, is one of the most important electrolytes in the extra-cellular 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 the sodium reabsorption takes place. In the distal convoluted tubule, sodium undergoes reabsorption.  Sodium transport takes place via sodium-chloride symporters which is by the action of the hormone aldosterone.[1] Among the electrolyte disorders, hyponatremia is the most frequent. It is diagnosed when the serum sodium level less than 135 mmol/L. Hyponatremia has neurological manifestations. Patients may present with headache, confusion, nausea, deliriums. Hypernatremia presents when the serum sodium levels 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 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, filtration of potassium takes place at the glomerulus. Reabsorption of potassium takes place at the proximal convoluted tubule and thick ascending loop of Henle.[2] Potassium secretion takes place 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 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 Calcium has a significant physiological role in the body. It is involved in skeletal mineralization, contraction of muscles, transmission of nerve impulse, 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 calcium level in 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]  Bicarbonate 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 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 alcoholism and gastrointestinal and renal losses. Ventricular arrhythmias which include torsades de pointes seen in hypomagnesemia.  Chloride Chloride is an anion found predominantly in the extracellular fluid. The kidneys predominantly regulate serum chloride level. 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 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 vital 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]

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