Clinical focus: Interpreting electrolytes is an emergency skill: verify the sample, identify the dominant water/solute problem, assess symptoms and ECG, correct dangerous abnormalities at a safe rate, and always search for the cause. Reference ranges vary by laboratory, age, pregnancy and method. Treat the patient and trend—not an isolated number.
Learning objectives
- Interpret sodium, potassium, chloride, bicarbonate, calcium, magnesium and phosphate in relation to water balance, kidney function and acid–base status.
- Use serum osmolality, urine osmolality and urine sodium to classify hyponatraemia and hypernatraemia.
- Recognise ECG and neuromuscular dangers of potassium, calcium and magnesium abnormalities.
- Calculate corrected sodium, corrected calcium, anion gap, delta gap and effective osmolality.
- Choose safe emergency priorities, infusion principles, monitoring and escalation for severe electrolyte disorders.
1. First principles and pre-analytical safety
Electrolytes are charged particles that determine extracellular tonicity, nerve and muscle excitability, cardiac conduction, fluid distribution, enzyme activity and acid–base balance. A result can be misleading when blood is drawn from an IV line, the sample is haemolysed, prolonged tourniquet time causes stasis, the patient is receiving a concentrated infusion, or the analyzer method differs.
- Repeat an unexpected critical result from a clean venous sample, but do not delay ECG monitoring and treatment when symptoms or an ECG-toxic result are present.
- Check glucose, urea/creatinine, albumin, blood gas, phosphate, magnesium, medication list, fluid balance and recent vomiting/diarrhoea or diuretic use.
- Ask what the patient’s baseline was and how rapidly the abnormality developed. Rate of change often predicts symptoms better than the absolute number.
- Look at the ECG for potassium, calcium and magnesium toxicity. A normal ECG does not guarantee safety.
| Common adult reference interval (approximate) | Typical range | Main role |
|---|---|---|
| Sodium (Na+) | 135–145 mmol/L | Extracellular tonicity and water balance. |
| Potassium (K+) | 3.5–5.0 mmol/L | Resting membrane potential and cardiac conduction. |
| Chloride (Cl−) | 98–106 mmol/L | Electroneutrality and acid–base balance. |
| Total CO2/bicarbonate | 22–29 mmol/L | Metabolic component of acid–base status. |
| Total calcium | 2.15–2.55 mmol/L (8.5–10.5 mg/dL) | Neuromuscular, cardiac and bone function. |
| Magnesium | 0.70–1.00 mmol/L (1.7–2.4 mg/dL) | ATP reactions, neuromuscular and potassium/calcium handling. |
| Phosphate | 0.80–1.50 mmol/L (2.5–4.5 mg/dL) | ATP, bone, cell membranes and oxygen delivery. |
2. Sodium: water balance and tonicity
Serum sodium mainly reflects the ratio of body water to exchangeable sodium and potassium, not total-body sodium alone. Always ask: is the abnormality hypotonic, isotonic or hypertonic, and is the patient hypovolaemic, euvolaemic or hypervolaemic?
Hyponatraemia (Na <135 mmol/L)
| Step | Interpretation |
|---|---|
| 1. Confirm and check glucose | Exclude sample error and hyperglycaemia-related translocation. Severe symptoms include seizure, coma, severe confusion, vomiting or respiratory arrest. |
| 2. Measure serum osmolality | Hypotonic (<275 mOsm/kg) is the common true hyponatraemia; isotonic suggests pseudohyponatraemia; hypertonic suggests glucose or another effective osmole. |
| 3. If hypotonic, measure urine osmolality | ≤100 mOsm/kg suggests excess water intake or low solute intake; >100 means antidiuretic hormone (ADH) is active. |
| 4. Measure urine sodium and examine volume status | Low urine sodium often supports hypovolaemia (unless diuretics/CKD); higher urine sodium may occur in SIADH, adrenal insufficiency, renal salt loss or diuretic use. |
Causes: hypovolaemic losses (diarrhoea, vomiting, burns, diuretics), SIADH from pulmonary/CNS disease or drugs, adrenal insufficiency, hypothyroidism, heart failure, cirrhosis, nephrotic syndrome, advanced kidney disease, primary polydipsia and low-solute intake.
Severe symptomatic hyponatraemia
- ABC, seizure precautions, ECG and frequent sodium checks. Stop hypotonic fluids and offending drugs; obtain glucose, serum/urine osmolality and urine sodium, but do not delay rescue therapy.
- A common adult emergency regimen is 3% hypertonic saline 100 mL IV over 10 minutes, repeated up to two more times if severe symptoms persist (some protocols use 150 mL over 20 minutes). Aim for an initial rise of about 4–6 mmol/L, then stop boluses.
- Limit correction to generally ≤8 mmol/L in 24 hours in high-risk patients (and not more than about 10–12 mmol/L in 24 hours or 18 mmol/L in 48 hours under local guidance). High-risk patients include alcoholism, malnutrition, liver disease, hypokalaemia and very low sodium.
- If overcorrection occurs, stop active correction and seek expert help; desmopressin and free water (for example D5W) may be used to re-lower sodium under monitored protocol.
Never give routine isotonic saline to presumed SIADH without assessment: it may worsen hyponatraemia. Treat hypovolaemic hyponatraemia with cautious isotonic crystalloid, adrenal insufficiency with steroid replacement, and SIADH with fluid restriction and cause-specific therapy.
Hypernatraemia (Na >145 mmol/L)
Hypernatraemia is usually water deficit (impaired access/thirst, fever, osmotic diuresis, diabetes insipidus, diarrhoea or burns), less often sodium gain. Assess chronicity, neurological symptoms, volume status, urine volume and urine osmolality.
- Shock requires isotonic crystalloid first to restore circulation; replace the remaining free-water deficit with oral/enteral water, IV dextrose 5% or hypotonic fluid as appropriate.
- For chronic or unknown-duration hypernatraemia, lower sodium slowly—often ≤0.5 mmol/L/hour and ≤10–12 mmol/L/day—to reduce cerebral oedema risk. Acute sodium loading may be corrected more rapidly with specialist guidance.
- Very dilute urine despite hypernatraemia suggests diabetes insipidus; distinguish central from nephrogenic causes and involve endocrinology.
Free-water deficit (L) ≈ TBW × [(current Na/desired Na) − 1]. Estimate TBW as about 0.6 × weight (kg) in a young adult male, 0.5 in an adult female, and lower in older adults; reassess frequently because ongoing losses and renal function alter the calculation.
3. Potassium: the immediate cardiac electrolyte
Hypokalaemia (K <3.5 mmol/L)
Common causes are gastrointestinal loss, loop/thiazide diuretics, renal tubular losses, hyperaldosteronism, insulin or beta-agonist shift, alkalosis and low magnesium. Ask whether the loss is renal or extrarenal and correct magnesium if low.
| Severity | Clinical approach |
|---|---|
| 3.0–3.4 mmol/L | Oral potassium replacement and cause treatment if stable; review drugs and repeat level. |
| 2.5–2.9 mmol/L or symptoms | Urgent ECG, oral/IV replacement depending on tolerance, renal function and monitoring capacity. |
| <2.5 mmol/L, ECG changes, paralysis or arrhythmia | Monitored emergency replacement, usually IV potassium chloride; senior/critical-care input. |
Typical adult IV replacement is 10 mmol/hour through a peripheral line; higher rates (up to 20 mmol/hour, occasionally more in critical care) require continuous ECG and local protocol. Never give potassium as an IV bolus. Check the level every 2–4 hours during aggressive replacement. Oral potassium is safer when the gut works. Insulin, beta-agonists and bicarbonate may worsen the shift.
Hyperkalaemia (usually K ≥5.5 mmol/L)
First exclude pseudohyperkalaemia from haemolysis, fist clenching, thrombocytosis or delayed processing, but obtain an ECG immediately and treat a compatible clinical emergency without waiting for repeat confirmation. Causes include AKI/CKD, hypoaldosteronism, ACE inhibitors/ARBs, potassium-sparing diuretics, NSAIDs, trimethoprim, tissue breakdown, acidosis and insulin deficiency.
| Emergency sequence | Purpose and common adult examples |
|---|---|
| Protect the heart | If ECG changes or severe hyperkalaemia: 10% calcium gluconate 10 mL IV over 2–5 minutes (or local calcium chloride protocol in arrest/central access). Repeat ECG and dose if changes persist; calcium does not lower potassium. |
| Shift potassium intracellularly | Regular insulin 10 units IV with 25 g glucose (adjust for pre-treatment glucose and hypoglycaemia risk); nebulised salbutamol 10–20 mg may be adjunctive. Check glucose repeatedly. |
| Correct severe acidosis when indicated | Sodium bicarbonate is not routine potassium therapy; consider only in significant metabolic acidosis under senior guidance. |
| Remove potassium | Loop diuretic if producing urine and volume status permits, potassium binder according to local formulary, and urgent dialysis for refractory or life-threatening hyperkalaemia/renal failure. |
Repeat potassium and ECG after treatment, monitor for rebound (especially with renal failure or sulfonylurea/ACE inhibitor exposure), stop potassium-containing fluids and review all medicines.
4. Chloride and bicarbonate: read acid–base together
Chloride usually moves with sodium. High chloride can accompany saline-related hyperchloraemic acidosis; low chloride occurs with vomiting, gastric suction, diuretics or dilution. Bicarbonate on a chemistry panel is a metabolic estimate and should be confirmed with a blood gas when the patient is unwell.
Anion gap (AG) = Na+ − (Cl− + HCO3−). Typical reference range is approximately 8–12 mmol/L without potassium, but use the laboratory’s range. Correct for albumin because low albumin lowers the expected gap:
Corrected AG ≈ measured AG + 2.5 × (4.0 − albumin in g/dL).
| Pattern | Examples | Next questions |
|---|---|---|
| High AG metabolic acidosis | Lactic acidosis, ketoacidosis, renal failure, toxins (methanol, ethylene glycol, salicylate) | Check lactate, ketones, renal function, toxicology, glucose and clinical perfusion. |
| Normal AG (hyperchloraemic) acidosis | Diarrhoea, renal tubular acidosis, large-volume normal saline | Check potassium, urine pH, GI loss and medication history. |
| Metabolic alkalosis | Vomiting, gastric suction, diuretics, mineralocorticoid excess | Assess volume, urine chloride, potassium and magnesium. |
| Low bicarbonate with respiratory compensation | Metabolic acidosis from many causes | Use Winter’s expected pCO2 ≈ 1.5 × HCO3 + 8 ±2. |
Delta gap: compare (AG − normal AG) with (normal HCO3 − measured HCO3). A much larger AG rise than bicarbonate fall suggests a concurrent metabolic alkalosis; a smaller rise suggests additional normal-gap acidosis.
5. Calcium: total, ionised and albumin
Only ionised calcium is biologically active. Total calcium falls with low albumin even when ionised calcium is normal; alkalosis lowers ionised calcium and can cause tetany without changing total calcium.
Corrected total calcium (mg/dL) ≈ measured calcium + 0.8 × (4.0 − albumin g/dL). This approximation is unreliable in critical illness, severe pH changes, kidney disease or paraproteinaemia—measure ionised calcium when symptoms or treatment decisions are urgent.
| Abnormality | Clues and causes | Emergency priorities |
|---|---|---|
| Hypocalcaemia | Perioral tingling, cramps, tetany, seizures, prolonged QT; low PTH, vitamin D deficiency, CKD, pancreatitis, sepsis, citrate from massive transfusion, hypomagnesaemia | Symptomatic/QT-prolonged: 10% calcium gluconate 10–20 mL IV slowly with ECG, repeat as needed; correct magnesium and cause. |
| Hypercalcaemia | “Stones, bones, groans, psychiatric overtones”; primary hyperparathyroidism, malignancy, vitamin D, thiazides, immobilisation | IV isotonic saline if not contraindicated, stop causes, monitor ECG/renal function; severe or refractory disease needs specialist therapy (calcitonin/bisphosphonate/denosumab as appropriate). |
6. Magnesium
Hypomagnesaemia causes tremor, weakness, seizures, QT prolongation, torsades and refractory hypokalaemia or hypocalcaemia. Causes include diarrhoea, alcohol use, malnutrition, PPIs, aminoglycosides, amphotericin, cisplatin and diuretics. Replace magnesium before or alongside potassium when both are low.
- Stable mild deficiency: oral magnesium is preferred but may cause diarrhoea.
- Severe symptoms, arrhythmia or very low magnesium: IV magnesium sulfate under ECG and renal monitoring. A common adult emergency dose is 2 g (8 mmol) IV over 10–20 minutes; slower replacement or infusion may follow local protocol.
- Reduce dose and monitor closely in renal failure. Hypermagnesaemia (often from renal failure or magnesium-containing laxatives/antacids) causes reduced reflexes, hypotension, bradycardia and respiratory depression; stop magnesium, provide support, give IV calcium for toxicity and consider dialysis.
7. Phosphate
Phosphate is needed for ATP, 2,3-DPG and bone. Low phosphate occurs with refeeding, alcohol use, DKA treatment, respiratory alkalosis, hyperparathyroidism and malabsorption; severe deficiency can cause weakness, rhabdomyolysis, haemolysis and respiratory failure. High phosphate occurs in CKD, tumour lysis, rhabdomyolysis and hypoparathyroidism.
Replace severe or symptomatic hypophosphataemia using local oral or IV phosphate formulation and renal function. IV phosphate can cause hypocalcaemia, metastatic calcification and dangerous potassium shifts; choose potassium- or sodium-phosphate according to serum potassium and monitor calcium, phosphate and renal function.
8. Osmolality and fluid status
Calculated serum osmolality ≈ 2 × Na + glucose (mmol/L) + urea (mmol/L). Effective osmolality (tonicity) excludes urea: 2 × Na + glucose. A measured–calculated difference is the osmolar gap; a high gap suggests unmeasured osmoles such as toxic alcohols, ketones or mannitol.
| Volume state | Electrolyte clues | Clinical examination |
|---|---|---|
| Hypovolaemia | Often sodium loss or concentration; urea/creatinine may rise, urine sodium often low | Postural dizziness, tachycardia, dry mucosa, reduced JVP, oliguria. |
| Euvolaemia | SIADH, endocrine disease or primary polydipsia may have normal renal function and no oedema | Neither convincing dehydration nor oedema; examine carefully. |
| Hypervolaemia | Heart failure, cirrhosis, nephrotic syndrome or CKD; dilutional sodium abnormality | Oedema, raised JVP, crackles, ascites or weight gain. |
9. Medication and disease patterns
| Drug or condition | Typical electrolyte effects |
|---|---|
| Loop diuretic | Low K, Na, Mg and Ca; metabolic alkalosis. |
| Thiazide | Hyponatraemia, low K and Mg; may raise calcium. |
| ACE inhibitor/ARB, spironolactone, trimethoprim, NSAID | Hyperkalaemia, especially with CKD or dehydration. |
| Insulin, beta-agonist, alkalosis | Shift potassium into cells; serum K may fall rapidly. |
| SSRIs, carbamazepine, oxcarbazepine, MDMA | SIADH/hyponatraemia. |
| Diarrhoea | Low bicarbonate, potassium and magnesium; normal-gap acidosis. |
| Vomiting/gastric suction | Low chloride, potassium and hydrogen; metabolic alkalosis. |
| Massive transfusion | Citrate-related low ionised calcium, potassium shifts, acid–base change and hypothermia. |
10. A practical emergency algorithm
- Confirm: repeat critical value, check haemolysis/line contamination and compare baseline.
- Stabilise: ABC, cardiac monitor/ECG, IV access, seizure precautions and bedside glucose.
- Classify the problem: sodium/tonicity and volume, potassium/cardiac risk, calcium/magnesium neuromuscular risk, acid–base and renal function.
- Calculate: corrected sodium for hyperglycaemia, osmolality, anion gap corrected for albumin, corrected calcium and delta gap when relevant.
- Treat dangerous abnormalities at a controlled rate: cardiac calcium before potassium-shifting therapy, hypertonic saline for severe symptomatic hyponatraemia, isotonic fluid for shock, and monitored replacement for potassium/magnesium/calcium deficits.
- Search for cause: drugs, GI losses, endocrine disease, renal failure, sepsis, burns, toxins, endocrine crisis and nutritional/refeeding risk.
- Trend: repeat results at a frequency proportional to severity and treatment; document target, maximum correction and escalation plan.
11. Worked cases
Case 1: hyperglycaemic hyponatraemia
Sodium is 126 mmol/L and glucose 30 mmol/L. Corrected sodium will be higher than measured because water has shifted into the extracellular space. Measure osmolality and treat the hyperglycaemia and volume state; do not assume primary hypotonic SIADH or give hypertonic saline without assessing symptoms and tonicity.
Case 2: hyperkalaemia with a normal ECG
Potassium is 6.8 mmol/L in a patient with AKI. Repeat a non-haemolysed sample, obtain continuous monitoring and ECG, and treat severe hyperkalaemia according to protocol even if the first ECG is normal. ECG changes may be absent despite life-threatening potassium.
Case 3: severe hyponatraemia after excess water intake
A person has a seizure and sodium 112 mmol/L, serum osmolality 250 mOsm/kg and urine osmolality 70 mOsm/kg. This is severe symptomatic hypotonic hyponatraemia with suppressed ADH. Give monitored 3% saline boluses to raise sodium by about 4–6 mmol/L, then prevent overcorrection and treat the cause.
Case 4: low calcium after transfusion
Following a major haemorrhage, a patient develops hypotension and prolonged QT with low ionised calcium. Citrate toxicity is likely. Give calcium under ECG monitoring, correct hypothermia/acidosis and continue to monitor ionised calcium during transfusion.
12. Quick self-test
- What three questions classify hypotonic hyponatraemia after checking serum osmolality?
- Why is a normal ECG not sufficient reassurance in hyperkalaemia?
- What is the formula for the anion gap?
- Which electrolyte should be corrected when hypokalaemia is refractory?
- What is the maximum safe correction principle for chronic hyponatraemia?
Answers
- Urine osmolality, urine sodium and clinical volume status (with medication/endocrine context).
- Severe potassium toxicity can occur with initially nondiagnostic ECG findings; the ECG can evolve quickly.
- AG = Na − (Cl + HCO3), corrected for low albumin when appropriate.
- Magnesium.
- Correct slowly, generally no more than about 8 mmol/L in 24 hours in high-risk patients, with local protocol and close monitoring.
Key take-home points
- Always verify the sample and assess symptoms, ECG, rate of change, glucose, renal function and volume status.
- Sodium is primarily a water/tonicity problem; potassium, calcium and magnesium can be immediate cardiac or neuromuscular emergencies.
- Corrected values and formulas are estimates—use them to guide, not replace, clinical assessment.
- Correct chronic sodium abnormalities slowly; rapid correction can cause osmotic demyelination or cerebral oedema.
- In hyperkalaemia, protect the heart first, shift potassium second, remove potassium third, and monitor for rebound.
References and further reading
- MedlinePlus: Electrolyte panel
- MedlinePlus: Fluid and electrolyte balance
- MedlinePlus: Basic metabolic panel
- MedlinePlus: Anion gap blood test
- NCBI Bookshelf: Hyperkalaemia
- MedlinePlus: Low blood sodium
- MedlinePlus: Magnesium blood test
- MedlinePlus: Phosphate blood test
Educational note: Emergency doses are adult examples, not a substitute for current local protocols. Use weight-, pregnancy-, paediatric- and renal-function-specific guidance, continuous monitoring and senior/critical-care consultation when indicated.
