By MRCSA in MRCS Part A — 04 Jul 2026

37 ELECTROLYTE IMBALANCES

👩‍⚕️ Electrolyte questions are exam gold. The Part A examiner does not care that you can recite a textbook — they care that you can spot the ECG, name the cation, choose the first-line fluid and avoid killing the patient with rapid correction. Learn the patterns below cold.

Why electrolytes matter

Cells run on gradients. The Na⁺/K⁺ ATPase pumps 3 Na⁺ out and 2 K⁺ in, generating a resting membrane potential of around −70 mV. Calcium is the trigger for muscle contraction and clotting. Magnesium is the cofactor that holds the whole system together. Disturb any of these and you get the three exam-favourite manifestations: arrhythmia, neuromuscular irritability, and altered consciousness.

Sodium

Normal range: 135–145 mmol/L. Sodium disorders are almost always water problems — the patient has too much or too little water relative to sodium, not too much or too little salt.

Hyponatraemia

First classify the type, then classify the volume status. The two-step approach is what examiners reward.

Step 1 — Is it true hyponatraemia?

Type	Serum osmolality	Cause
True (hypotonic)	Low	Genuine water excess or sodium loss
Pseudohyponatraemia	Normal	Lab artefact from high lipids or paraproteins
Translocational	High	Osmotic pull of water from cells (e.g. hyperglycaemia, mannitol)

Step 2 — What is the volume status of the patient?

Volume status	Mechanism	Classic causes
Hypovolaemic	Loss of Na⁺ and water, water loss less	D&V, diuretics, Addison's, salt-losing nephropathy, burns
Euvolaemic	Pure water excess	SIADH, hypothyroidism, glucocorticoid deficiency, primary polydipsia
Hypervolaemic	Water excess > Na⁺ excess	Heart failure, cirrhosis, nephrotic syndrome, renal failure

SIADH is the high-yield euvolaemic cause. Diagnosis requires: low serum sodium, low serum osmolality (<275), inappropriately concentrated urine (osmolality >100), urinary sodium >20 mmol/L, and clinical euvolaemia with normal thyroid, adrenal and renal function. Classic surgical causes are small cell lung carcinoma (ectopic ADH), head injury, post-operative pain/opiates, SSRIs and carbamazepine.

➡ Symptoms depend on rate of fall, not absolute level. Acute drops cause cerebral oedema — headache, nausea, confusion, seizures, coma.

Correction — the cardinal rule:

> Pearl: Correct chronic hyponatraemia by no more than 8–10 mmol/L in 24 hours. Faster correction shrinks brain cells abruptly and causes central pontine myelinolysis (osmotic demyelination) — a devastating, usually irreversible pseudobulbar palsy and quadriparesis.

Hypernatraemia

Almost always a water problem, not a sodium problem. The patient cannot access or retain free water.

Mechanism	Examples
Pure water loss	Diabetes insipidus (cranial or nephrogenic), insensible loss, fever
Hypotonic fluid loss	Osmotic diuresis (hyperglycaemia), D&V, sweating
Sodium gain (rare)	Hypertonic saline, iatrogenic NaHCO₃, salt poisoning

Classic Part A scenario: elderly nursing-home patient, dehydrated, sodium 160. Correct slowly — rapid lowering causes cerebral oedema.

Potassium

Normal range: 3.5–5.0 mmol/L. Cardiac membrane stability hangs on this number.

Hyperkalaemia

Mechanism	Causes
Reduced excretion	AKI, CKD, ACE-i/ARB, K⁺-sparing diuretics, Addison's
Cellular shift out	Acidosis (DKA), tissue breakdown (rhabdomyolysis, tumour lysis, burns), insulin deficiency
Increased intake	Massive transfusion (stored blood leaks K⁺), iatrogenic
Spurious	Haemolysed sample, tight tourniquet, delayed processing

ECG progression (memorise):

➡ Tall tented T waves (earliest, V2–V4) → short QT → prolonged PR → flat P waves → wide QRS → sine wave → VF/asystole.

Management ladder:

1. Calcium gluconate 10% 10 ml IV — stabilises the myocardial membrane within minutes. Does not lower K⁺. Use if any ECG changes or K⁺ >6.5.

2. Insulin (10 units Actrapid) + 50 ml 50% dextrose — drives K⁺ intracellularly, onset 15–30 min.

3. Salbutamol nebuliser (10–20 mg) — β₂ agonist drives K⁺ into cells. Synergistic with insulin.

4. Sodium bicarbonate — only if significant acidosis.

5. Calcium resonium (oral or PR) or patiromer — actually removes K⁺ from the body but slow.

6. Haemodialysis — definitive if refractory or anuric.

👩‍⚕️ Calcium stabilises, insulin/salbutamol/bicarbonate shift, resonium/dialysis remove. Examiners love this distinction.

Hypokalaemia

Mechanism	Causes
GI loss	Vomiting, diarrhoea, fistulae, NG suction, villous adenoma
Renal loss	Loop and thiazide diuretics, hyperaldosteronism, Cushing's, Bartter/Gitelman
Shift into cells	Insulin, β₂ agonists, alkalosis, refeeding syndrome
Inadequate intake	Alcoholism, anorexia

ECG progression:

➡ Flat T waves (earliest) → ST depression → U waves in V2–V4 (classic) → T inversion → prominent P → prolonged PR → VT/VF/Torsade de Pointes.

Remember: low Mg²⁺ causes refractory hypokalaemia. You will never correct the potassium until you replace the magnesium.

> Pearl: Vomiting depletes K⁺ partly through GI loss but mostly through the renal response to the resulting metabolic alkalosis (paradoxical aciduria). This is why severe vomiting causes profound hypokalaemia even though gastric fluid is not particularly K⁺ rich.

Calcium

Half of plasma calcium is bound to albumin. Always correct for albumin:

> Corrected Ca²⁺ = Measured Ca²⁺ + 0.02 × (40 − albumin)

Acidosis frees ionised Ca²⁺ from albumin; alkalosis (e.g. hyperventilation) binds more — which is why anxious hyperventilating patients get perioral tingling.

Hypercalcaemia

Memorise: "bones, stones, abdominal groans, psychic moans" plus polyuria/polydipsia (nephrogenic DI from impaired ADH response) and a short QT.

Causes — 90% are two diagnoses:

Cause	Mechanism	Clue
Primary hyperparathyroidism	Parathyroid adenoma → autonomous PTH	Outpatient, often asymptomatic, ↑Ca, ↑PTH, ↓PO₄
Malignancy	PTHrP (squamous lung, renal, breast), osteolytic bone mets, myeloma	Inpatient, unwell, ↑Ca, ↓PTH (suppressed)

Others: sarcoidosis (granulomatous 1α-hydroxylation of vitamin D), thiazides, thyrotoxicosis, milk-alkali, immobilisation, familial hypocalciuric hypercalcaemia.

Management ladder (corrected Ca²⁺ >3.0 or symptomatic):

1. ECG and rhythm monitoring.

2. Aggressive IV 0.9% saline 3–6 L over 24 h — first line. Restores GFR and promotes calciuresis.

3. Calcitonin — onset hours, tachyphylaxis within 48 h, useful bridge.

4. IV bisphosphonate (pamidronate or zoledronate) — onset 24–48 h, lasts weeks.

5. Dexamethasone — for haematological malignancy, myeloma or granulomatous disease.

6. Haemodialysis — refractory or renal failure.

Hypocalcaemia

Symptoms reflect increased neuromuscular excitability because low ionised Ca²⁺ lowers the threshold for nerve firing.

Signs:

- Perioral and fingertip paraesthesia — earliest.

- Chvostek sign — tap facial nerve anterior to the tragus → ipsilateral facial twitch. Present in ~10% of normocalcaemic adults, so sensitive but not specific.

- Trousseau sign — BP cuff above systolic for 3 minutes → carpal spasm (main d'accoucheur). More specific.

- Severe: tetany, laryngospasm, seizures, prolonged QT, Torsade.

Causes (surgical favourites):

Cause	Mechanism
Post-thyroidectomy	Inadvertent parathyroid injury/devascularisation — perioral tingling within hours
Acute pancreatitis	Fat saponification — free fatty acids chelate Ca²⁺
Massive transfusion	Citrate anticoagulant chelates ionised Ca²⁺
Vitamin D deficiency / CKD	Reduced absorption and 1,25-vitamin D synthesis
Hypoparathyroidism	Surgical, autoimmune, DiGeorge
Hypomagnesaemia	Impairs PTH secretion and end-organ response — refractory until Mg replaced

Magnesium

Normal 0.7–1.0 mmol/L. The forgotten cation. Low Mg²⁺ causes refractory hypokalaemia and refractory hypocalcaemia because Mg is required for both renal K⁺ retention and PTH secretion/action. Always check Mg in any patient with persistently low K⁺ or Ca²⁺. Causes: diuretics, PPIs, alcoholism, refeeding, diarrhoea, malabsorption.

Phosphate and refeeding syndrome

Refeeding syndrome occurs when a malnourished patient is fed (orally, enterally or via TPN) after a prolonged starvation. Carbohydrate triggers an insulin surge which drives phosphate, potassium and magnesium intracellularly. Result:

> Refeeding triad: ↓PO₄³⁻ (hallmark) + ↓K⁺ + ↓Mg²⁺ — plus thiamine depletion.

High-risk patients: BMI <16, weight loss >15% in 3–6 months, little intake for >10 days, anorexia nervosa, post-bariatric surgery, prolonged TPN, oncology.

Prevention: identify risk, give thiamine before feeding (to prevent Wernicke's), start at 50% of energy requirements, monitor and replace electrolytes daily.

[Image: MCQs banner]

Test yourself

An ECG shows flat P waves, inverted T waves, and a prolonged PR interval. Which electrolyte disturbance is most likely?

((Hypokalaemia::☑️ Flat/inverted T, prolonged PR and U waves are the classic hypokalaemia triad.))
((Hyperkalaemia::Causes tall tented T waves and a wide QRS, not flat P with T inversion.))
((Hypocalcaemia::Prolongs QT — does not flatten T or prolong PR.))
((Hyponatraemia::No characteristic ECG signature.))
((Hypomagnesaemia::Mimics hypokalaemia but is not the classic association for this triad.))

👩‍⚕️ Hypo = flat and U. Hyper = tall and wide.

Which ECG change is most characteristic of hypokalaemia?

((Widened QRS::Feature of hyperkalaemia.))
((ST depression::Occurs but is non-specific.))
((Flat T waves::Earliest change but not the most recognisable.))
((T wave inversion::A later, less distinctive finding.))
((U waves in V2–V3::☑️ U waves in V2–V4 are the signature hypokalaemia finding.))

A patient with Cushing's disease has routine bloods taken. Which electrolyte abnormality is most likely?

((Hypokalaemia::☑️ Cortisol cross-activates mineralocorticoid receptors → Na⁺ retention and K⁺ loss.))
((Hyperkalaemia::Opposite — cortisol promotes K⁺ excretion.))
((Hypernatraemia::Sodium is retained but water follows, so frank hypernatraemia is uncommon.))
((Hypocalcaemia::Not a feature of Cushing's.))
((Hypomagnesaemia::Not the primary disturbance.))

👩‍⚕️ Cushing's → hypokalaemic metabolic alkalosis.

A patient with a large villous adenoma of the rectum presents with weakness. Which electrolyte disturbance is most likely?

((Hyperkalaemia::Villous adenomas leak K⁺, they do not retain it.))
((Hypernatraemia::Mucous secretion is not sodium-rich.))
((Hypokalaemia::☑️ Villous adenomas secrete K⁺- and HCO₃⁻-rich mucus — McKittrick–Wheelock syndrome.))
((Hypocalcaemia::Not a recognised association.))
((Hypomagnesaemia::Not the primary loss.))

👩‍⚕️ McKittrick–Wheelock: secretory rectal adenoma causing severe hypokalaemia and AKI.

A patient with atrial fibrillation has had profuse diarrhoea for 5 days. What is the most likely cause of the arrhythmia?

((Dehydration::Volume depletion alone rarely triggers AF.))
((Hyponatraemia::Does not characteristically cause AF.))
((Hypokalaemia::☑️ GI K⁺ loss predisposes to atrial and ventricular arrhythmia.))
((Hypocalcaemia::Causes prolonged QT, not AF.))
((Sepsis::Possible but the direct electrolyte link is the expected answer.))

A patient in DKA has creatinine 400 and glucose 42 mmol/L. Which electrolyte abnormality is most likely on initial bloods?

((Hypokalaemia::Total body K⁺ is depleted but initial serum K⁺ is high.))
((Hyperkalaemia::☑️ Acidosis and insulin deficiency drive K⁺ out of cells; renal failure prevents excretion.))
((Hypernatraemia::Sodium is variable due to osmotic shifts.))
((Hypocalcaemia::Not the primary concern.))
((Hyperphosphataemia::May occur with renal failure but is not the key danger.))

👩‍⚕️ DKA trap: high serum K⁺, depleted total body K⁺ — it crashes once insulin starts. Always check K⁺ before insulin.

An ECG shows flattened P waves and widened QRS complexes. Which electrolyte abnormality is the most likely cause?

((Hypokalaemia::Causes flat T and U waves, not wide QRS.))
((Hyperkalaemia::☑️ Sequence is tall T → flat P → wide QRS → sine wave.))
((Hypocalcaemia::Prolongs QT.))
((Hypomagnesaemia::Can prolong QT but does not widen QRS.))
((Hypernatraemia::No specific ECG signature.))

An elderly woman presents with an osteoporotic vertebral crush fracture. What is the expected calcium finding?

((Hypercalcaemia::Suggests hyperparathyroidism or malignancy, not osteoporosis.))
((Hypocalcaemia::Osteoporosis is structural, not a homeostasis disorder.))
((Normocalcaemia::☑️ All biochemistry is normal in pure osteoporosis.))
((Raised ALP::Suggests Paget's or bone metastases, not osteoporosis.))
((Hypophosphataemia::Suggests osteomalacia.))

👩‍⚕️ Normal bloods distinguish osteoporosis from osteomalacia (low Ca, low PO₄, high ALP) and Paget's (high ALP only).

A patient with acute pancreatitis develops weakness and paraesthesia. Which electrolyte abnormality is most likely?

((Hyperkalaemia::Not a typical complication.))
((Hypokalaemia::Possible with vomiting, but paraesthesia points to calcium.))
((Hypocalcaemia::☑️ Fat saponification chelates Ca²⁺ — a Glasgow score criterion.))
((Hyponatraemia::Does not cause paraesthesia.))
((Hypomagnesaemia::May coexist but hypocalcaemia is the classic link.))

A patient presents with carpopedal spasm and tetany. Which electrolyte abnormality is most likely?

((Hypokalaemia::Causes weakness and arrhythmias, not tetany.))
((Hypocalcaemia::☑️ Low ionised Ca²⁺ raises neuromuscular excitability → tetany and laryngospasm.))
((Hyponatraemia::Causes confusion and seizures.))
((Hyperkalaemia::Causes cardiac conduction defects.))
((Hypomagnesaemia::Can cause tetany but hypocalcaemia is the expected answer.))

An ECG shows a prolonged QT interval. Which electrolyte abnormality is the most likely cause?

((Hyperkalaemia::Shortens QT early then widens QRS.))
((Hypocalcaemia::☑️ Delays repolarisation — predisposes to Torsade de Pointes.))
((Hypokalaemia::Can prolong QT but the single-best answer is hypocalcaemia.))
((Hypermagnesaemia::Causes bradycardia and heart block.))
((Hypercalcaemia::Shortens QT — the opposite.))

A patient develops perioral tingling 12 hours after total thyroidectomy. What is the most likely cause?

((Recurrent laryngeal nerve injury::Causes hoarseness, not tingling.))
((Superior laryngeal nerve injury::Causes voice fatigue.))
((Hypocalcaemia::☑️ Parathyroid injury or devascularisation — perioral tingling is the earliest sign.))
((Wound haematoma::Causes neck swelling and airway compromise.))
((Hypothyroidism::Develops over weeks, not hours.))

👩‍⚕️ Always check calcium post-thyroidectomy. Tingling lips and fingertips precede tetany.

A patient develops hypocalcaemia after a massive blood transfusion. What is the mechanism?

((Dilution::Does not explain the degree of fall.))
((Citrate toxicity::☑️ Stored blood citrate chelates ionised Ca²⁺ when liver clearance is overwhelmed.))
((Hypothermia::Impairs coagulation but does not bind Ca²⁺.))
((Hyperkalaemia::Stored blood leaks K⁺ — a separate problem.))
((TRALI::Immunological lung injury, not a calcium disorder.))

A patient has a corrected calcium of 3.6 mmol/L. What is the most important initial management step?

((IV pamidronate::Effective but takes 24–48 h.))
((Oral alendronate::Not used acutely.))
((Dexamethasone::Reserved for haematological/granulomatous causes.))
((Calcitonin::Useful adjunct but saline comes first.))
((0.9% saline 3–6 L over 24 h::☑️ Restores GFR and drives calciuresis — always first line.))

A patient with metastatic breast cancer presents with confusion and nausea. What is the most likely biochemical abnormality?

((Hyponatraemia::Possible but less likely than hypercalcaemia with bone mets.))
((Hypercalcaemia::☑️ Osteolytic mets and PTHrP — "bones, stones, groans, psychic moans".))
((Hyperkalaemia::Not a paraneoplastic feature.))
((Raised urea::Secondary, not primary.))
((Brain metastases::Not a biochemical abnormality.))

A patient with squamous cell carcinoma of the lung presents with polyuria and polydipsia. What is the underlying mechanism?

((Small cell carcinoma::Causes SIADH (hyponatraemia), not hypercalcaemia.))
((Adenocarcinoma::Not classically PTHrP-secreting.))
((PTHrP secretion::☑️ Squamous lung cancer secretes PTHrP → hypercalcaemia → nephrogenic DI → polyuria.))
((Large cell carcinoma::Not a classic PTHrP secretor.))
((Mesothelioma::Not associated with PTHrP.))

👩‍⚕️ Squamous = PTHrP (hypercalcaemia). Small cell = SIADH or ectopic ACTH.

Which clinical sign is most specific for hypocalcaemia?

((Chvostek sign::Sensitive but present in ~10% of normocalcaemic adults.))
((Trousseau sign::☑️ Carpal spasm after 3 min BP cuff inflation — more specific.))
((Carpopedal spasm::A symptom, not a specific bedside test.))
((Hyperreflexia::Non-specific.))
((Laryngospasm::Severe manifestation, not a diagnostic sign.))

A patient on TPN 10 days after total gastrectomy develops confusion and weakness. Which electrolyte abnormality is most likely?

((Hypokalaemia::Part of the triad but not the hallmark.))
((Hypomagnesaemia::Coexists but not the defining abnormality.))
((Hypophosphataemia::☑️ Hallmark of refeeding syndrome — insulin drives PO₄³⁻ intracellularly.))
((Hyperglycaemia::Can occur but does not explain weakness.))
((Hyponatraemia::Not a refeeding feature.))

👩‍⚕️ Refeeding triad: ↓PO₄ + ↓K⁺ + ↓Mg²⁺. Give thiamine before feeding.

A 70-year-old is admitted with sodium 118 mmol/L after a chest infection. Which is the most important rule of correction?

((Correct to normal within 12 hours::Far too fast — risks osmotic demyelination.))
((Raise serum Na⁺ by no more than 8–10 mmol/L in 24 hours::☑️ Prevents central pontine myelinolysis.))
((Restrict fluid to 250 ml/day::Excessive restriction risks AKI.))
((Give 3% hypertonic saline as a bolus to all::Reserved for severe symptomatic hyponatraemia only.))
((Stop all maintenance fluids::Inadequate management plan.))

The resting membrane potential of a cell is primarily maintained by which ion?

((Na⁺::Influx causes depolarisation, not the resting potential.))
((Ca²⁺::Drives excitation–contraction coupling.))
((Cl⁻::Modulatory role only.))
((K⁺::☑️ Leak channels and the Na⁺/K⁺ ATPase set the −70 mV resting potential.))
((Mg²⁺::Enzyme cofactor, not a primary determinant.))

Revision summary

- Sodium 135–145. Hyponatraemia: classify osmolality (true/pseudo/translocational) then volume (hypo/eu/hyper). SIADH = euvolaemic, urine osm >100, urine Na >20. Correct ≤ 8–10 mmol/L per 24 h or risk central pontine myelinolysis.

- Potassium 3.5–5.0. Hyperkalaemia ECG: tall T → flat P → wide QRS → sine wave. Management: calcium gluconate (stabilise) → insulin+dextrose, salbutamol, bicarbonate (shift) → resonium, dialysis (remove). Hypokalaemia ECG: flat T, U waves V2–V4, prolonged QT, Torsade.

- Calcium. Corrected = measured + 0.02 × (40 − albumin). Hyperca²⁺ = primary hyperparathyroidism (outpatient) or malignancy (PTHrP, mets, myeloma). First line: IV saline 3–6 L / 24 h, then bisphosphonate. Hypoca²⁺: post-thyroidectomy, pancreatitis, citrated transfusion. Trousseau more specific than Chvostek.

- Magnesium. Low Mg → refractory low K⁺ and low Ca²⁺. Always replace Mg first.

- Refeeding triad: ↓PO₄³⁻ (hallmark), ↓K⁺, ↓Mg²⁺. Give thiamine before feeding. Start at 50% energy.

- DKA trap: high serum K⁺, depleted total body — crashes with insulin.

- Cancer pairs: squamous lung → PTHrP/hypercalcaemia; small cell → SIADH/hyponatraemia.