Skip to main content
search

Essential electrolytes

The Anesthesia Guide » Topics » Essential electrolytes

Author:
Kai Knudsen



Updated:
3 April, 2026

Practical overview of electrolyte disorders in perioperative and critical care settings, covering pathophysiology, ECG changes, clinical risks, and evidence-based management strategies.

Content:
  1. Essential Electrolytes Normal Ranges and Clinical Significance
  2. Potassium (K⁺)
  3. Sodium (Na⁺)
  4. Magnesium (Mg²⁺)
  5. Calcium (Ca²⁺)
  6. Important Electrolyte Interactions
  7. ICU Principles
  8. Special Considerations in Anesthesia
  9. Calculate the Anion Gap
  10. Calculate the Osmolal Gap
  11. Hyperkalemia
  12. Hypokalemia
  13. Hyponatremia
  14. Hypophosphatemia

Essential Electrolytes Normal Ranges and Clinical Significance

Potassium (K⁺)

Normal range: 3.5–5.0 mmol/L (mEq/L)

Physiological Role

  • Critical for cardiac electrical activity
  • Skeletal muscle contraction
  • Membrane potential regulation
  • Acid–base balance

Hyperkalemia (>5.5 mmol/L)

ECG findings:

  • Peaked T waves
  • Widened QRS complex
  • AV block
  • Risk of ventricular fibrillation or asystole

Common ICU causes:

  • Renal failure
  • Acidosis
  • Rhabdomyolysis
  • Massive transfusion
  • ACE inhibitors / potassium-sparing diuretics

Emergency treatment:

  1. Calcium (membrane stabilization)
  2. Insulin + glucose
  3. Beta-2 agonists
  4. Bicarbonate (if acidosis present)
  5. Dialysis in refractory cases

Hypokalemia (<3.5 mmol/L)

Risks:

  • Ventricular arrhythmias
  • Increased digoxin sensitivity
  • Muscle weakness
  • Prolonged neuromuscular blockade

Important:

Hypomagnesemia must be corrected for potassium levels to normalize.

Sodium (Na⁺)

Normal range: 135–145 mmol/L

Physiological Role

  • Determines extracellular fluid volume
  • Regulates osmolality
  • Influences intracranial pressure

Hyponatremia

Risks:

  • Cerebral edema
  • Seizures
  • Altered consciousness

Perioperative considerations:

  • Avoid rapid correction (>8–10 mmol/L per day)
  • Risk of osmotic demyelination syndrome

Hypernatremia

Risks:

  • Cellular dehydration
  • CNS dysfunction
  • Increased ICU mortality

Magnesium (Mg²⁺)

Normal range: 1.3–2.1 mEq/L (≈0.7–1.0 mmol/L)

Physiological Role

  • Regulates neuromuscular transmission
  • Stabilizes cardiac excitability
  • Modulates potassium and calcium channels

Hypomagnesemia

Common in ICU:

  • Diuretics
  • Alcohol use disorder
  • Sepsis

Consequences:

  • Torsades de pointes
  • Refractory hypokalemia
  • Cardiac arrhythmias

Treatment:

IV magnesium sulfate

Hypermagnesemia

Causes:

  • Renal failure
  • Excessive therapeutic administration (e.g., eclampsia treatment)

Symptoms:

  • Hypotension
  • Muscle weakness
  • Respiratory depression
  • Prolonged neuromuscular blockade

Calcium (Ca²⁺)

Normal range:
Total calcium: 8.5–10.5 mg/dL
Ionized calcium: ~1.1–1.3 mmol/L

Physiological Role

  • Myocardial contractility
  • Coagulation cascade
  • Neuromuscular stability

Hypocalcemia

Risks:

  • Prolonged QT interval
  • Tetany
  • Hypotension
  • Impaired coagulation

Common in:

  • Massive transfusion (citrate binding)
  • Sepsis

Hypercalcemia

Risks:

  • Shortened QT interval
  • Arrhythmias
  • Confusion

Important Electrolyte Interactions

  • ↓ Mg²⁺ → ↓ K⁺
  • ↓ Mg²⁺ → Increased arrhythmia risk
  • ↑ K⁺ ↔ Acidosis
  • Massive transfusion → ↓ Ca²⁺
  • Lithium and diuretics affect Na⁺ balance

ICU Principles

  1. Interpret electrolytes together with acid–base status
  2. Monitor ECG in potassium disturbances
  3. Always check magnesium in arrhythmias
  4. Monitor ionized calcium during massive transfusion
  5. Rapid correction may be more dangerous than the abnormality itself

Special Considerations in Anesthesia

  • Hyperkalemia + succinylcholine → potentially fatal
  • Hypocalcemia → impaired cardiovascular function
  • Hypomagnesemia → torsades risk
  • Electrolyte disturbances alter neuromuscular blocker response

Calculate the Anion Gap

Anion Gap

Albumin correction: AGcorr = AG + 0.25 x (40 - Alb[g/L])

Calculate the Osmolal Gap

Osmol Gap

Hyperkalemia

Hyperkalemia typically occurs with cell breakdown, metabolic acidosis, acute or chronic kidney failure, critical ischemia, Addison’s disease, or after the intake of potassium or potassium-sparing diuretics. Dehydration and starvation are other conditions that can lead to severe hyperkalemia. With pronounced hyperkalemia, there is a risk of severe cardiac arrhythmias, ventricular fibrillation, and circulatory collapse. Investigation and treatment must address the underlying cause, but with S-Potassium values over 6.0 mmol/L, treatment should be initiated immediately. Below are suggestions for various forms of treatment. When inducing anesthesia in a patient with hyperkalemia, the surgery should be postponed, and hyperkalemia should be corrected preoperatively at values over 5.5 mmol/L, if possible.

Treatment of Hyperkalemia

  • Calcium: With QRS involvement and S-Potassium > 6.0 mmol/L: 10 ml Calcium-Sandoz 9 mg/ml over 1 minute – repeat until ECG normalizes.
  • Intravenous fluid: Dilute plasma volume with NaCl 9 mg/ml 1000-2000 ml.
  • Glucose-insulin drip: 20 E Actrapid/Novorapid in 500 ml 10% Glucose, give 250 ml over 15 minutes. The remainder over 2-3 hours. Monitor P-glucose and blood gases. Effect typically seen after about 15 minutes, often later.
  • Sodium bicarbonate in acidosis: 100 ml IV – gives immediate effect, can be repeated. Lowers potassium by approximately 0.5 mmol/L.
  • Bricanyl (terbutaline – beta2-agonist): 0.5-1 mg IV over 15 minutes. 1 mg mixed in 100 ml NaCl, administered over 30-60 minutes, monitor pulse.
  • Resonium: Sodium polystyrene sulfonate, cation exchanger. 15 g x 3-4. Effect after 1-2 hours, administered rectally or orally.
  • Sodium zirconium cyclosilicate (Lokelma) 10 g x 3
  • Magnesium: 20 mmol IV (use caution with low blood pressure) over 20 minutes.
  • Diuretics
  • Possibly hemodialysis
  •  

Hypokalemia

Definition of hypokalemia: S-Potassium < 3.5 mmol/L.

Symptoms and Findings

Rarely symptomatic until S-Potassium drops below 3.0 mmol/L (related to the increased gradient of membrane potential, i.e., in all muscles)

Symptoms of Hypokalemia

Muscle weakness, reduced tendon reflexes, ileus/subileus, ECG changes (depressed ST-segment, flattened T-wave, and the presence of U-wave), and increased fatigue. Cases with neuromuscular disease, critically ill patients, decreased GFR, and reduced kidney concentration ability with polyuria may be particularly sensitive to hypokalemia.

Causes of Hypokalemia

Renal lossNon-Renal Causes
With HypertensionWith normal blood pressure
Cushing syndromRenal tubular acidosisAlkalosisIntestinal losses
Congenital adrenal hyperplasiaFanconi syndromeLeucemiaDiarrhéa
Primary hyperaldosteronismBartter's syndromFamiliar hypokalemic periodic paralysis Laxatives
Increased amount of reninDiabetic keto acidosisSweatingEnema
Renovascular diseaseAntibioticsAnorexia nervosa
DiureticsEnterocutanous fistula  
Alcoholism
Urinary K > 20 mmol /LUrinary K < 20 mmol /L

Diagnosis and Investigation

Depending on the clinical picture and underlying cause:

  • Blood tests: Hb, Na, K, Cl, creatinine, urea, glucose, acid-base status, CK, renin, cortisol, possibly 17α-OH-progesterone, 11-deoxycortisol, and aldosterone
  • Urine: Urine dipstick (glucose, protein), Na, K, Cl, osmolality.
  • Other: Standard ECG and ECG monitoring with telemetry.

Treatment and Follow-up

Potassium supplementation should primarily be administered orally, but in intensive care settings, potassium is preferably given parenterally with caution. The concentration in intravenous solutions should be up to 40 mmol KCl per 1000 ml solution, typically 20-40 mmol/L. If higher concentrations are desired, the infusion must be labeled and administered via a central venous catheter (CVC). This is to avoid dangerous and rapid infusion of potassium. If necessary, the rate of administration can be increased, but the maximum rate is 0.5 mmol/kg/hour (maximum 20 mmol/hour for an adult patient). In such cases, the infusion must, for safety reasons, be administered through a separate needle/lumen where no other infusion or medications are administered. At high infusion rates, S-Potassium must be monitored with frequent blood tests. Strong potassium solutions are highly irritating to veins, skin, and subcutis, and should be administered via central catheters. Extremities where potassium infusions are administered should not be covered during surgery so that the access site is not concealed during ongoing anesthesia.

Hyponatremia

  • Hyponatremia – diagnostic checklist

    Hyponatremia
  • Assess urine osmolality (U-Osm)
    U-Osm < 100 mOsm/kg Primary polydipsia
    Malnutrition (low solute intake)
    U-Osm > 100 mOsm/kg Assess volume status

    Hypovolemic hyponatremia
    Assess urine sodium (U-Na) U-Na < 30 mmol/L Extrarenal sodium losses
    U-Na > 30 mmol/L Renal sodium losses

    Euvolemic hyponatremia
    U-Na > 30 mmol/L SIADH (etc.)

    Hypervolemic hyponatremia
    Assess urine sodium (U-Na) U-Na < 30 mmol/L Heart failure, etc.
    U-Na > 30 mmol/L Renal failure, etc.


    • Hyponatremia (S-Na <135 mmol/L) is the most common electrolyte disturbance, affecting 15-30% of hospitalized patients. It leads to increased mortality, morbidity, and prolonged hospital stays. Hyponatremia is not primarily a pure sodium deficiency but a relative water excess. When hyponatremia occurs acutely, there is a risk of brain edema as fluid shifts intracellularly when blood osmolality decreases. The brain needs about 48 hours to adapt to the hypotonic environment. Once this has occurred, the risk of brain edema is reduced, but the risk of osmotic demyelination syndrome increases if serum sodium levels rise too quickly. This is because the myelin sheaths that insulate neurons can be damaged during a rapid shift in osmolality. This is the rationale behind the importance of distinguishing acute from chronic hyponatremia before initiating correction.

    Common causes of hyponatremia include SIADH, diuretics, ethanol, hyperglycemia, polydipsia, renal failure, medications, hypotonic fluid administration, and to some extent, physical exercise with excessive water intake.

    Wide variation, from mild, nonspecific symptoms to very severe life-threatening symptoms with brain edema and herniation. Acutely occurring hyponatremia usually presents with more pronounced symptoms, while hyponatremia developing over time may be asymptomatic despite very low serum sodium levels.
    Common symptoms include balance difficulties, cognitive impairment, headache, nausea, vomiting, seizures, altered consciousness, and confusion.

    Investigation

    Differentiating between acute hyponatremia (documented duration < 48 hours). If the duration is unclear, assume the hyponatremia is chronic unless the history clearly suggests otherwise, such as in long-distance running.

    Exclude hyperglycemia as a cause of hyponatremia, as well as other iso/hyperosmolar conditions such as the administration of mannitol, contrast agents, urea, and various alcohols. These conditions have normal or high serum osmolality, and the hyponatremia is secondary.

    Testing for Hyponatremia

    S-Na, S-K, U-Na, U-K, S-Osm, U-Osm, P-glucose, S-creatinine, liver function tests, TSH, free T4, S-cortisol.

    Assess the patient’s volume status according to the diagram below (hypo-, hyper-, or euvolemic?). The diagram also indicates common underlying causes of the different conditions.

    Figure 1. Investigation of Hyponatremia.

    Investigation of Hyponatremia


    Treatment of Hyponatremia

    • Treat the underlying condition.
    • Discontinue medications that may have triggered hyponatremia.
    • In cases of strong clinical suspicion of acute adrenal insufficiency, Addison’s disease, treatment with hydrocortisone (Solu-Cortef) and 0.9% NaCl IV should be initiated.
    • Check other electrolytes and correct if necessary.
    • Correct hyponatremia cautiously.

    Chronic hyponatremia (>48 hours) with mild symptoms should first be investigated, and underlying causes treated. Hyponatremia should be corrected slowly, with a goal to raise sodium by a maximum of 0.5 mmol/L/hour, totaling <8 mmol/L/day. In awake, normovolemic patients, this can be done through fluid restriction. Hypovolemia is treated with 0.9% NaCl, and hypervolemia with loop diuretics. Calculating the infusion rate of 0.9% NaCl is challenging as the formulas do not account for how much sodium is lost through urine, etc. The calculation should, therefore, be seen as a guideline that is adjusted based on testing depending on how the patient responds to the treatment.

    For chronic hypovolemic hyponatremia where slow correction is planned, an initial infusion rate can be calculated as follows:

    • Target S-Na 130 mmol/L
    • Measure current S-Na (mmol/L) and weight V(kg)
    • Calculate body water volume KV (L), women: Weight x 0.5, men: Weight x 0.6
    • Determine the net increase in S-Na (mmol/L); 130 minus current value;
      • If the planned net increase is >8 mmol/L: Calculate the total time (hours) to reach the goal with 0.3 mmol/L/hour.
      • If the planned net increase is <8 mmol/L: Calculate the total time (hours) to reach the goal with 0.5 mmol/L/hour.
    • Calculate total Na requirement (number of mmol); KV(L) x net increase in S-Na
    • Calculate the fluid volume (L) needed; total Na requirement (mmol)/Na concentration (mmol/L) in the infusion solution
    • Calculate the infusion rate (ml/hour); planned fluid volume (ml)/planned number of hours

    Severe symptomatic hyponatremia, such as seizures, must be corrected quickly initially until the severe symptoms subside. Raise S-Sodium initially by 1-2 mmol/L/hour using 0.9% or 3% NaCl IV. When symptoms subside, reduce the correction rate, and the total daily correction should not exceed 8 mmol/L/day.

    If rapid correction is necessary, 3% NaCl 1 ml/kg increases S-Na by about 1 mmol/L.
    Hypertonic 3% NaCl is obtained by adding 160 mmol Na (40 ml Addex Na) to 500 ml 0.9% NaCl. Frequent testing is required if hypertonic saline is given due to the risk of overcorrection.

    It is crucial to closely monitor during correction! Initially every hour, which can be spaced out as the patient stabilizes and the increase occurs at the planned rate. Increased diuresis may indicate reduced ADH release and be a sign of too rapid correction. Reduce the infusion rate and check S-Na.

    Too rapid correction?
    – Slow down the infusion rate or stop
    – Administer sodium-free fluid (glucose, water orally/through a tube)
    – In cases of large diuresis, consider desmopressin (Minirin). NOTE! Be aware of the risk of brain edema!
    – Reversing, i.e., dilution if sodium rises too quickly.

    References

    • Chantzichristos et al, Vårdprogram för hyponatremi, 2012.
    • Spasovski et al, Clinical Practice Guideline on Diagnosis and Treatment of Hyponatremia. Eur J Endocrinol. 2014 Feb 25;170(3):G1-47
    • Verbalis et al, Diagnosis, Evaluation, and treatment of Hyponatremia: Expert panel recommendations. Am Journal of Med 126:S5-S42

    Hypophosphatemia

    Phosphorus is stored in large amounts in the body – it is the second most abundant mineral. About 80% is stored in the skeleton and teeth, 20% in the blood and various body tissues. There are approximately 12 g of phosphorus per kilogram of fat-free tissue. About 85% of phosphorus exists as inorganic calcium phosphate in a 2:1 ratio compared to phosphorus in bone tissue and teeth. Blood plasma contains 3.5 mg of phosphorus per 100 ml, which is about half the amount of calcium present. There are 30–45 mg of phosphorus per 100 ml of whole blood and 3.5 mg per 100 ml of blood plasma. Levels are maintained through reabsorption in the kidneys, and this level is related to the concentrations of calcium and phosphorus in blood plasma, PTH, and vitamin D3.

    Phosphorus is a very important substance for the skeleton and is a part of the structure of cells, even in soft tissues. Phosphorus is also a component of nucleic acids, which form the genetic code in all cells and are therefore important for growth, repair, and maintenance of all body tissues, as well as for protein synthesis. Phosphorus helps calcium attach to the protein matrix in the skeleton. Phosphorus is also a component of ATP (adenosine triphosphate), ADP (adenosine diphosphate), and AMP (adenosine monophosphate). It is necessary for energy production and transport and plays an important role in the phosphorylation of monosaccharides for energy. Phosphorus enables nutrients to pass through cell membranes or to be transported in the blood.

    Symptoms of phosphorus deficiency in the central nervous system may include fatigue, paresthesias, tremor, seizures, muscle weakness, respiratory failure, and paresis. Other symptoms of phosphorus deficiency are vomiting, poor appetite, bone pain, depression, and osteomalacia.

    Serum contains different forms of phosphate, but only inorganic phosphate is measured in the blood, and this serves as the transport form of phosphorus and also acts as a pH buffer.

    Hyperphosphatemia is caused by decreased phosphate excretion, as seen in renal insufficiency, or increased tubular phosphate reabsorption, as in hypoparathyroidism.

    Hypophosphatemia can be caused by

    • Malnutrition, starvation
    • Shift of phosphate from the extracellular to the intracellular space (e.g., during treatment of malnutrition)
    • CRRT treatment
    • Renal losses, e.g., due to tubular defects (familial hypophosphatemia)
    • Decreased intestinal absorption

    The kidneys’ normal response to phosphate depletion is to increase phosphate reabsorption, which means that phosphate excretion in the urine can be practically zero. Most of the filtered phosphate is reabsorbed in the proximal tubule via the sodium-phosphate cotransporter.

    Reference Range for Normal Values

    Men > 50 years0.75 – 1.4 mmol/L
    Men 18 – 50 years0.7 – 1.6 mmol/L
    Women > 18 years0.8 – 1.5 mmol/L

    Symptoms of Hypophosphatemia

    • Fatigue
    • Paresthesias
    • Tremor
    • Muscle weakness
    • Rhabdomyolysis
    • Seizures
    • Coma

    Overt symptoms of hypophosphatemia rarely appear unless phosphate levels are below 0.64 mmol/L.

    Severe symptoms such as muscle weakness and rhabdomyolysis are usually not seen until phosphate levels are below 0.32 mmol/L. There is some evidence that even mild hypophosphatemia may be associated with poorer clinical outcomes. Most patients with hypophosphatemia do not need any treatment other than that given for the underlying cause. For example, hypophosphatemia associated with correction of diabetic ketoacidosis will spontaneously resolve with normal food intake.

    Intravenous phosphate is potentially dangerous as it can precipitate with calcium and cause side effects such as:

    • Hypocalcemia (due to precipitation with calcium)
    • Renal failure (due to precipitation with calcium in the kidneys)
    • Severe arrhythmias

    Treatment of Hypophosphatemia

    Oral phosphate is recommended for patients with S-phosphate levels between 0.32 and 0.63 mmol/L. Administer 30-80 mmol/day divided into 3-4 doses. Check S-phosphate 2-12 hours after the last dose.

    If intravenous treatment is necessary due to severe hypophosphatemia (S-phosphate < 0.32 mmol/L) or if oral treatment is not possible, the following regimen is recommended:

    • For S-phosphate < 0.40 mmol/L, administer 0.5 mmol/kg (maximum 80 mmol) over 8-12 hours
    • For S-phosphate > 0.40 mmol/L, administer 0.2 mmol/kg (maximum 30 mmol) over 6 hours
    • Phosphate should be administered slowly. Maximum 100 mmol over at least 8 hours.

    Higher doses are described but should not be given in cases of concurrent renal failure.

    S-phosphate levels should be monitored every 6 hours during intravenous phosphate administration, and the patient should, if possible, be switched to oral phosphate when S-phosphate exceeds 0.48 mmol/L.

    Dilution and Preparation for Infusion

    Glycophos infusion concentrate 1 mmol/ml. A 20 ml vial contains 20 mmol phosphate and 40 mmol sodium.  Maximum 100 mmol glycophos should be added alone per 1000 ml glucose (5%, 10%, or 20%).

    The daily normal phosphate requirement for adults receiving intravenous nutrition is typically 10-30 mmol. This means that 20 mmol Glycophos can be added to 250 mmol glucose 5% (nothing else added to the same bag). The infusion is administered over at least 8 hours.

     

    Disclaimer:

    The content on AnesthGuide.com is intended for use by medical professionals and is based on practices and guidelines within the Swedish healthcare context.

    While all articles are reviewed by experienced professionals, the information provided may not be error-free or universally applicable.

    Users are advised to always apply their professional judgment and consult relevant local guidelines.

    By using this site, you agree to our Terms of Use.




    Close Menu