Electrolytes: sodium, potassium, chloride and magnesium

• A serum electrolyte panel reports the main ions in plasma (sodium, potassium, chloride and usually bicarbonate/total CO2, with magnesium on request) together with the anion gap and calculated osmolality. ^{[7] [11] [12]}
• Read the values first, then the pattern: a single abnormal electrolyte points to a cause; a combination points to an acid-base or volume disorder.
• Sodium gives tonicity. Potassium tells you about cells and the heart, and is the value most worth rechecking when haemolysis is possible. Chloride and bicarbonate together give the acid-base picture.
• Every reference range and threshold differs by laboratory, age, sex, specimen and method. The laboratory's own printed range always beats a textbook one.
• Correct sodium slowly. In hyponatraemia the usual ceiling is no more than 8 mmol/L in 24 hours; faster correction risks osmotic demyelination. ^[1]

By the end of this page you should be able to:

1. Read a basic or comprehensive metabolic panel and state what each line measures.
2. Quote normal adult reference ranges in SI and conventional units and explain why they vary.
3. Classify hyponatraemia by serum osmolality and volume status, and name the common causes of each.
4. Recognise hyperkalaemia and hypokalaemia on a result sheet, name their causes, read the ECG changes and recognise artefact.
5. Calculate the anion gap, delta gap and osmolar gap from a result sheet.
6. Recognise common electrolyte patterns (normal-anion-gap acidosis, raised anion gap, hyperchloraemia, hypomagnesaemia with hypokalaemia) and state what each suggests.
7. Interpret three complete sample result sheets step by step, conclude with the likely diagnosis and the next test.
8. Identify the artefacts and pre-analytical pitfalls that can make a normal electrolyte result wrong.

An electrolyte panel is one of the commonest blood tests in medicine, and one of the most misread. The report looks simple: five or six numbers. But each number is only a window into volume, tonicity, acid-base and renal handling, and the same value can mean very different things depending on the patient. This page is about reading that panel rather than treating the diagnosis named on the request form.

We will build up in this order: what each test measures; the normal ranges and how they are set; the causes of high and low values; named combinations and what they point to; three worked, invented, clearly labelled sample result sheets; and the pitfalls that make a report wrong. Every threshold we use carries a citation to an open source, and every reference range is the laboratory's to define.

Each line of the panel comes from a different question the laboratory is asking about the extracellular fluid.

Sodium (Na). Sodium is the main cation of extracellular water and the principal determinant of plasma osmolality and tonicity. A sodium result therefore answers "is the extracellular fluid too dilute or too concentrated?" far better than it answers "is the body short of sodium?". Most hyponatraemia is water excess, not sodium loss.

Potassium (K). Potassium is mainly intracellular. Serum potassium is only the small fraction in plasma, so shifts between inside and outside the cell, and shifts in acid-base, can change the result without any change in total body potassium. That is why artefact and sampling effects loom so large for this test.

Chloride (Cl). Chloride is the main extracellular anion that travels with sodium. It is the silent partner of acid-base: in a normal-anion-gap (hyperchloraemic) acidosis chloride rises as bicarbonate falls, and in metabolic alkalosis chloride is low.

Bicarbonate (total CO2 on many reports). This is the base half of the bicarbonate-carbonic acid buffer pair. On a chemistry panel it is usually a venous total carbon dioxide, which approximates bicarbonate. It is the single value that converts the panel into an acid-base screen.

Magnesium (Mg). Magnesium is a cofactor for hundreds of enzymes and stabilises membrane potential. Serum magnesium is only a tiny fraction of total body magnesium, so a normal result does not exclude depletion, but it is the test we have.

Derived values. Many reports print an anion gap and a calculated osmolality; some print an osmolar gap. These are not measured but calculated, and they are where most of the pattern recognition lives.

• Anion gap = sodium - (chloride + bicarbonate) (or with potassium added in some laboratories). It is an invisible tally of unmeasured anions (albumin, phosphate, sulphate, lactate, ketoacids). A rise means acid gain or alkali loss with unmeasured anions.
• Osmolar gap = measured serum osmolality - calculated serum osmolality. A gap above 10 mOsm/L implies an unmeasured, osmotically active substance is present.^[7]

Adult reference ranges from open sources are shown in both conventional and SI units. These are one laboratory system's adult values, not yours.

The thresholds that define disease do not have to match the reference interval:

• Hyponatraemia: under 136 mmol/L in the Merck classification.^[1]
• Hypernatraemia: over 145 mmol/L.^[2]
• Hypokalaemia: under 3.5 mmol/L.^[4]
• Hyperkalaemia: over 5.5 mmol/L.^[3]
• Hypomagnesaemia: under 1.8 mg/dL (under 0.70 mmol/L).^[5]
• Hypermagnesaemia: over 2.6 mg/dL (over 1.05 mmol/L).^[6]
• Low total CO2/bicarbonate: under 23 mmol/L; high: over 29 mmol/L.^[8]
• High osmolar gap: more than 10 mOsm/L.^[7]

This table is a map, not a diagnosis. Use it to decide which question to ask of the patient and the notes below it.

Start with serum osmolality.^[1]

• Hypotonic hyponatraemia (below 275 mOsm/L) is the common form and is the only form that is a true water excess problem.^[1]
• Isotonic hyponatraemia (pseudohyponatraemia) is an artefact of severe hyperlipidaemia or myeloma proteins and needs a different assay.
• Hypertonic hyponatraemia occurs when an extracellular osmole such as glucose or mannitol pulls water out of cells. Serum sodium falls by about 1.6 mmol/L for every 100 mg/dL (5.6 mmol/L) rise in glucose beyond normal.^[1]

Once the hyponatraemia is real and hypotonic, classify by volume status:

• Hypovolaemic: both water and sodium are lost, and sodium is lost more. Extrarenal losses (vomiting, diarrhoea, third spacing) usually give urine sodium under 10 mmol/L; renal losses (diuretics, salt-wasting nephropathy, mineralocorticoid deficiency) usually give urine sodium over 20 mmol/L.^[1]
• Euvolaemic: total body sodium is roughly normal, water is in excess. Causes include SIADH, hypothyroidism, glucocorticoid deficiency, drugs and primary polydipsia (normal kidneys can excrete up to 25 L of urine a day).^[1]
• Hypervolaemic: water and sodium are both retained, but water more. Heart failure, cirrhosis and advanced CKD are the usual causes, with urine sodium under 10 mmol/L.^[1]

Two useful urine sodium quotes from the hyponatraemia manual: SIADH usually gives urine sodium over 30 mmol/L and fractional sodium excretion over 1%; a urine sodium over 40 mmol/L after cerebral injury points to cerebral salt wasting rather than SIADH.^[1]

A flow to use at the bedside:

Hypernatraemia. A sodium over 145 mmol/L is always water deficit relative to solute. The cause is either impaired access or impaired thirst (immobility, dementia, infants), water loss in excess of sodium (diabetes insipidus, osmotic diuresis from hyperglycaemia or mannitol, renal or insensible losses), or sodium gain (hypertonic saline, tube feeds, salt poisoning). Diagnosing the cause needs urine volume and urine osmolality measured, ideally after water deprivation. Correction rules: if the high sodium developed within 24 hours it can be corrected over 24 hours, but if it is chronic or of unknown duration it is corrected over about 48 hours, lowering calculated serum osmolality by no more than 0.5 mOsm/L per hour.^[2] The free water deficit can be estimated from total body water (about 0.6 times weight in kg in men, 0.5 times in women) and the serum sodium.^[2]

Hypokalaemia under 3.5 mmol/L is common and often asymptomatic under 3.0 mmol/L. Severity bands help: mild 3.0 to 3.4, moderate 2.5 to 3.0, severe under 2.5 mmol/L.^[4] Symptoms are muscle weakness, constipation and, importantly, arrhythmia. Cardiac effects are usually small until potassium is below about 3 mmol/L.^[4] Renal potassium loss becomes likely when urine potassium is over 15 mmol/L (over 15 mmol/L in 24 hours).^[4]

Hypokalaemia ECG changes: (flattened T waves, ST depression, U waves, prolonged QT) become likely with lower values. Severe hypokalaemia can produce ventricular ectopy.^[4]

Hyperkalaemia over 5.5 mmol/L is more immediately dangerous. ECG changes are often visible when serum potassium is above 5.5 mmol/L, although the precise concentrations vary widely between patients.^[3] The typical progression is tall symmetric peaked T waves, then shortened QT and increased PR interval, then loss of P waves and QRS widening, then sine-wave and ventricular arrhythmia. Hyperkalaemia should be suspected from the ECG at all, since "Serum potassium concentrations ... vary widely among patients with similar ECG changes".^[3]

Severity bands: 5.5 to 6.0 is mild; 6.0 to 6.5 needs prompt attention; over 6.5 is severe; loss of the P wave or QRS widening means give IV calcium as well as insulin and glucose.

Most acid-base screening on a chemistry panel is done from chloride and total CO2 together.^[7] The anion gap is their shadow. A bicarbonate under 22 with a normal anion gap (7 to 15) means bicarbonate has been lost and chloride has risen to take its place: diarrhoea, ureteric diversion, renal tubular acidosis, acetazolamide, or saline excess.^[7] A low bicarbonate with a raised anion gap means an unmeasured acid has been added: lactate, ketoacids, uraemic anions, or a toxin. The common causes of a raised anion gap metabolic acidosis are ketoacidosis, lactic acidosis, renal failure and toxic ingestions; a normal anion gap acidosis is most often diarrhoea, renal tubular acidosis or early renal failure.^[7]

Chloride on its own matters in three other ways:

• Hyperchloraemia with a normal anion gap acidosis is the classic paired abnormality. It appears after large volumes of 0.9% saline, because the fluid contains 154 mmol/L chloride.
• Hypochloraemia with a raised total CO2 points to metabolic alkalosis from vomiting, nasogastric suction, loop or thiazide diuretics, or mineralocorticoid excess.
• Chloride that moves in parallel with sodium tells you the change is one of concentration (dehydration or water excess); chloride that moves opposite to bicarbonate tells you the change is acid-base.

Hypomagnesaemia (under 1.8 mg/dL, under 0.70 mmol/L) ^[5] is easy to miss because it often arrives carrying other deficiencies with it. It can cause hypocalcaemia and a hypokalaemia that will not correct until the magnesium is replaced.^[5] Severe deficiency (under 1.25 mg/dL, under 0.50 mmol/L) with seizures or severe symptoms is treated with 2 to 4 g magnesium sulphate IV over 5 to 10 minutes. ^[5] Common causes include low intake, malabsorption, alcohol use disorder, diarrhoea, hypercalcaemia, and renal wasting from drugs such as furosemide, cisplatin or proton pump inhibitors. ^[5]

Hypermagnesaemia (over 2.6 mg/dL, over 1.05 mmol/L) ^[6] is almost always a renal failure problem, often from magnesium-containing antacids, laxatives or IV magnesium, with lithium and hypothyroidism as less common causes. It produces hypotension, loss of reflexes, respiratory depression and, above about 12 mg/dL (5.0 mmol/L), cardiac arrest. ^[6]

A result sheet is a drug history in miniature. The effects below are the ones to look for whenever a new drug has been started or a dose changed.

• Hyponatraemia with a low serum osmolality and high urine sodium (over 30 mmol/L): SIADH until proven otherwise. Check thyroid and cortisol before settling. ^[1]
• Hyponatraemia with urine sodium over 40 mmol/L after brain injury: cerebral salt wasting, which must be treated with salt and fluid, not fluid restriction. ^[1]
• Hyperkalaemia with hyponatraemia and a raised or normal anion gap acidosis: type 4 renal tubular acidosis (aldosterone resistance or deficiency), including diabetic nephropathy, Addison disease and some drug effects.
• Hypokalaemia with metabolic alkalosis and low urine chloride: vomiting or gastric loss. High urine chloride points to diuretics or mineralocorticoid excess.
• Hypomagnesaemia with hypokalaemia and hypocalcaemia: they travel together; replace the magnesium and the others follow. ^[5]
• Hypernatraemia with a low urine osmolality: diabetes insipidus; with a high urine osmolality: the kidneys are conserving water and intake is the problem. ^[2]
• Raised anion gap without acid: consider low albumin, because albumin is the largest unmeasured anion. (Albumin is not stated in these open sources; the point is standard and we have not quoted a number for it.)
• Osmolar gap over 10 mOsm/L with a high anion gap acidosis: a toxic alcohol (methanol, ethylene glycol) or another unmeasured osmole. ^[7]
• Normal anion gap acidosis with a low urine anion gap (negative): gastrointestinal bicarbonate loss. A urine anion gap near zero implies renal tubular acidosis. ^[7]

The values below are invented for teaching and are labelled as illustrative samples, not real patient data. They are chosen to look like real reports, and each has a numbered interpretation using only the thresholds above. The sample numbers are not claims; the thresholds that interpret them are.

1. Sodium 141 mmol/L is inside the usual range (135 to 145 mmol/L), so plasma tonicity is normal.
2. Potassium 4.2 mmol/L (3.7 to 5.2) and magnesium 1.9 mg/dL (1.7 to 2.2) are both within range.
3. Chloride and total CO2 are paired normally (96 to 106 and 23 to 29 mmol/L) and the anion gap is 10 (7 to 15), so there is no evidence of acid gain or bicarbonate loss.
4. Calculated osmolality 292 mOsm/kg is within the usual 275 to 295 mOsm/kg range.
5. Conclusion: no electrolyte abnormality; nothing to correct, and no electrolyte-specific action today.

Serum osmolality measured on the same sample was 250 mOsm/kg (below the low end of the usual range of 275 mOsm/kg, hypotonic hyponatraemia). ^[14] Repeat laboratory testing on a second sample showed urine sodium 8 mmol/L and urine osmolality 480 mOsm/kg.

1. Correct sodium is low (under 135 mmol/L) and glucose is normal, so this is not translocational hyponatraemia.
2. Measured osmolality 250 mOsm/kg is below 275 mOsm/L: hypotonic hyponatraemia.
3. Urine sodium 8 mmol/L is under 10 mmol/L: extrarenal hypovolaemic loss rather than a renal salt-losing problem. ^[1]
4. Urine osmolality 480 mOsm/kg is high relative to serum (inappropriately concentrated): the kidneys are holding on to water, as in volume depletion.
5. Potassium 3.2 and magnesium 1.3 mg/dL are also low, which is common in gastrointestinal loss. ^[4][5]
6. Conclusion: hypovolaemic hyponatraemia from extrarenal salt and water loss; the next step is isotonic saline and treating the gastrointestinal cause, with serum sodium rechecked to keep the rise within 8 mmol/L in 24 hours.

1. Potassium 6.8 mmol/L is above 6.5 mmol/L: severe hyperkalaemia that needs treatment now, not later.
2. The expected ECG changes include tall peaked T waves, PR prolongation and QRS widening as potassium rises above 5.5 mmol/L, although levels and ECG findings vary widely between patients. ^[3]
3. Total CO2 18 mmol/L is low with a normal anion gap 14 (7 to 15): normal anion gap (hyperchloraemic) metabolic acidosis, consistent with reduced renal acid excretion. ^[7]
4. Magnesium 0.7 mmol/L (0.70 to 0.91) is borderline low; creatinine 2.1 mg/dL (0.6 to 1.3) shows renal impairment, which explains both the hyperkalaemia and the low bicarbonate. ^[3][5]
5. Conclusion: severe hyperkalaemia in CKD with normal anion gap metabolic acidosis; the next step is an ECG immediately, then IV calcium if there are ECG changes, insulin with glucose, and arrangement for dialysis or specialist renal review.

Electrolyte results are more likely to be wrong before they reach the patient than most laboratory values, and more likely to be misread afterwards.

• Haemolysis raises potassium and magnesium and leaves sodium and chloride largely unchanged. A potassium that does not fit the patient, or a haemolysis flag from the analyser, is the reason to repeat the sample rather than treat. ^[3]
• Falsely low sodium (pseudohyponatraemia) occurs with severe hyperlipidaemia or paraproteinaemia; much modern ion-selective analysis avoids it. Suspect it when the serum looks milky or the osmolar gap is high.
• Falsely high sodium and potassium arise from severe dehydration of the sample itself or from salt contamination of the tube.
• Fist clenching or pumping before venepuncture raises potassium; so does delayed separation of cells from serum.
• EDTA contamination (even a trace from a blue or lavender tube) lowers calcium and magnesium by chelation and raises potassium: always check the tube.
• Late processing and refrigeration of the specimen would be expected to alter the gases; bicarbonate is best measured fresh. Use the laboratory's sample instructions rather than old ward habits.
• Urine dipstick chloride is not a substitute for a serum chloride; and any 24-hour collection has errors in collection rather than in analysis. Verify before acting.
• Artefacts if potassium also affect magnesium: repeated spurious hyperkalaemia needs repeating with care, not prescribing.
• Treating the number instead of the patient. A potassium of 3.1 in a patient taking digoxin is not a recheck in the morning; but a potassium of 3.1 with no symptoms and no heart disease is.
• Correcting sodium too fast. In hyponatraemia the usual ceiling is no more than 8 mmol/L in 24 hours; symptoms of rapid correction (severe drowsiness, confusion, seizures after an initially improving sodium) suggest osmotic demyelination. For severe symptoms boluses of hypertonic saline are given as 100 mL over 15 minutes, repeated once if needed. ^[1][13]
• Assuming the reference interval is the same for everyone. Neonates, children, older adults, pregnancy and high-altitude residents have different ranges.

For completeness, the two small calculations that commonly belong on the panel:

• Translocational hyponatraemia with hyperglycaemia: corrected sodium = measured sodium + 1.6 mmol/L for every 100 mg/dL (5.6 mmol/L) of glucose above normal. ^[1]
• Free water deficit in hypernatraemia: total body water is approximately weight in kg times 0.6 in men and 0.5 in women; the deficit scales with how far the serum sodium is above 145 mmol/L. ^[2]
• Osmolar gap: measured osmolality minus (2 x sodium + glucose/18 + BUN/2.8 + alcohol/5, in conventional units). A difference over 10 implies an unmeasured osmole. ^[7]
• Urine anion gap: sodium + potassium - chloride in the urine, used when the serum anion gap is normal. ^[7]

• Where the panel is unavailable, a few tests do most of the work: serum sodium, potassium and chloride on a basic chemistry analyser, plus a measured (not calculated) osmolality if a freezing point machine is on site.
• If osmolality cannot be measured, diagnose hyponatraemia by its clinical context (medications, volume status) and refer for specialist review; do not guess from the sodium alone.
• Hyperkalaemia with ECG changes is an emergency that does not wait for a repeat result. Treat by the ECG while arranging transfer.
• Where bicarbonate is not reported, a chloride with high or low total CO2 on a venous gas handles the acid-base question.

• Sodium is the tonicity ion; potassium is the membrane ion; chloride is the acid-base partner; bicarbonate is the base buffer.
• Every range depends on the laboratory, age, sex, method and tube. The reporter's range always wins.
• Hyponatraemia is almost always water excess. Classify by serum osmolality first, then volume status, then urine sodium. ^[1]
• SIADH gives urine sodium over 30 mmol/L and an inappropriately high urine osmolality; a urine sodium over 40 mmol/L after brain injury suggests cerebral salt wasting. ^[1]
• Hypernatraemia means water deficit. Correct chronic hypernatraemia slowly, over about 48 hours. ^[2]
• Three potassium bands for hypokalaemia (3.0 to 3.4, 2.5 to 3.0, under 2.5) and three for hyperkalaemia (5.5 to 6.0, 6.0 to 6.5, over 6.5) keep severity tied to numbers. ^[3][4]
• ECG changes around potassium are typical not fixed; patients vary. Hyperkalaemia above about 5.5 mmol/L frequently shows on the ECG. ^[3]
• Pseudohyperkalaemia from haemolysis, EDTA, fist clenching and sample delay is common: repeat before treating a value that does not fit. ^[3]
• Magnesium under 1.8 mg/dL is hypomagnesaemia and is best friends with hypokalaemia and hypocalcaemia; magnesium over 2.6 mg/dL is a renal failure emergency. ^[5][6]
• The anion gap separates acid gain (raised) from bicarbonate loss (normal). Normal anion gap: 7 to 15. ^[7][10]
• Osmolar gap over 10 mOsm/L means an unmeasured osmole. ^[7]
• Correct sodium no faster than 8 mmol/L in 24 hours. For severe hyponatraemic symptoms, 100 mL hypertonic saline over 15 minutes, repeated once. ^[1][13]
• Drugs are the commonest cause of a surprising result. Thiazides give hyponatraemia and hypokalaemia; ACE inhibitors and potassium-sparing drugs give hyperkalaemia.
• Related topics in plain text: hyponatraemia, hypernatraemia, hyperkalaemia, hypokalaemia, hypomagnesaemia, acid-base disorders, acute kidney injury, diuretics, sodium and water homeostasis.

Related topics, as plain text until they are linked in this build: hyponatraemia, hypernatraemia, hyperkalaemia, hypokalaemia, hypomagnesaemia, acid-base disorders, acute kidney injury, diuretics, and sodium and water homeostasis.