Fluids, Electrolytes and Acid–Base for NEET PG Medicine: Hyponatraemia (ICMR), Potassium, Calcium, Anion Gap

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🎯 Exam priority: High. Expect: hyponatraemia by volume status, 3% saline and the 8–10 mmol/L limit, SIADH criteria, potassium ECG changes, pseudohyperkalaemia, Chvostek and Trousseau, hypercalcaemia treatment, magnesium with low potassium, and high vs normal anion gap acidosis.

CBME mapping: GM 23.1–23.12. Hyperkalaemia emergency treatment is also in article 15; DKA acid–base in article 17; renal physiology in Physiology.

Electrolyte disorders, ICMR hyponatraemia approach, SIADH and acid–base. Drawn by TrackNation.

Volume and Sodium

• Volume depletion: reduced skin turgor, dry mucosa, tachycardia, orthostatic hypotension; urine sodium < 10. Severe: IV 0.9% saline or Ringer's lactate.

• Hyponatraemia causes: diuretics (especially thiazides), diarrhoea, heart failure, liver and kidney disease, SIADH. Severe if < 125 mmol/L. Pseudohyponatraemia is caused by glucose or lipids, not a water imbalance.

• SIADH: Na < 135, plasma osmolality < 275, urine osmolality > 100 (often > 300), urine Na > 40, low uric acid. Euvolaemic. Restrict fluid; oral tolvaptan 15 mg on day 1 (ICMR) if Na stays low.

• Hypernatraemia: replace the intravascular volume and the free-water deficit.

Potassium, Calcium, Magnesium

• Hypokalaemia (< 3.5): ST sagging, T-wave depression, prominent U waves. Diuretics are the commonest drug cause; low magnesium increases renal K loss — correct it. Replace with oral KCl (IV if severe).

• Hyperkalaemia (> 5.5): peaked T waves → (> 6.5) wide QRS → sine wave → VF/asystole. A haemolysed sample gives pseudohyperkalaemia.

• Hypocalcaemia: hypoparathyroidism (low Ca, high phosphate), vitamin D deficiency, renal disease. Chvostek (facial twitch on tapping in front of the ear) and Trousseau (carpal spasm with cuff 20 mm Hg above systolic for 3 min); prolonged QTc. Severe: IV 10% calcium gluconate — hazardous with digoxin.

• Hypercalcaemia: commonest causes hyperparathyroidism and cancer; short QTc. IV saline (± furosemide), bisphosphonates (choice in cancer), calcitonin acts fast.

• Hypomagnesaemia: features come from accompanying low K and Ca — tremor, tetany, seizures, arrhythmias; replace magnesium.

Acid–Base

• Acidaemia pH < 7.35; alkalaemia > 7.45. Check compensation for metabolic acidosis with Winters formula.

• High anion gap metabolic acidosis: ketoacidosis, lactic acidosis, CKD, toxins (methanol → formate, ethylene glycol → oxalate, salicylates). Normal anion gap (hyperchloraemic): GI bicarbonate loss (diarrhoea, fistulas) and renal tubular acidosis (types 1, 2, 4). Urinary anion gap = Na + K − Cl helps separate them.

• Bicarbonate therapy is generally safe for normal-gap acidosis; in organic (high-gap) acidosis it is controversial. Severe acidosis: nausea, lethargy, hyperpnoea.

• Metabolic alkalosis: prolonged vomiting, hypovolaemia, diuretics, hypokalaemia.

Traps the Examiner Sets

• Chronic hyponatraemia: ≤ 8–10 mmol/L in 24 h.

• SIADH: urine Na > 40 and urine osm > 100 with low plasma osm.

• Low K that will not correct → check Mg.

• U waves = low K; peaked T = high K; long QT = low Ca; short QT = high Ca.

• Diarrhoea → normal-gap acidosis; vomiting → alkalosis.

Memory Hooks & Shortcuts

Shortcuts to lock in this article's numbers and lists. Each one only re-packages facts proven above.

• 🧠 Sodium: 'Slow and Steady — 8 to 10 a day' — correction limit

• 🧠 'From low to high your pons will die' (correcting low Na too fast) — osmotic demyelination

• 🧠 No pot, no tea, but a U (low K: flat T, U wave) — hypokalaemia ECG

• 🧠 CATs go numb: Chvostek, Arrhythmia (long QT), Tetany, Seizures in low Ca — hypocalcaemia

• 🧠 High-gap 'MUDPILES'-style list: methanol, uraemia, DKA, lactate, ethylene glycol, salicylate — high anion gap

Rapid-Revision Cards

• Hypovolaemic hypoNa

  IV normal saline.

• Hypervolaemic hypoNa

  Treat cause (CCF, cirrhosis, nephrotic).

• Severe acute hypoNa

  3% saline 1–2 mL/kg/h.

• Correction limit

  ≤ 8–10 mmol/L in 24 h.

• Too-fast correction

  Osmotic demyelination.

• 3% saline arithmetic

  513 mmol/L; 1 mL/kg/h ≈ +1 mmol/L/h.

• SIADH

  Posm < 275, Uosm > 100, UNa > 40, low urate.

• SIADH Rx

  Fluid 500–1000 mL/d; tolvaptan.

• Pseudohyponatraemia

  Lipids, glucose.

• Hypernatraemia

  Replace volume + free water.

• Hypokalaemia ECG

  ST sag, T down, U waves.

• Refractory hypoK

  Correct Mg.

• Hyperkalaemia ECG

  Peaked T → wide QRS (> 6.5) → sine wave.

• Pseudohyperkalaemia

  Haemolysed sample.

• Chvostek

  Tap facial nerve → twitch.

• Trousseau

  Cuff 20 above systolic × 3 min → carpal spasm.

• Hypoparathyroidism

  Low Ca, high PO4.

• Calcium & QT

  Low Ca long QT; high Ca short QT.

• Hypercalcaemia causes

  PTH, cancer.

• Hypercalcaemia Rx

  Saline; bisphosphonate; calcitonin fast.

• High AG acidosis

  Ketones, lactate, CKD, methanol, ethylene glycol, salicylate.

• Normal AG acidosis

  Diarrhoea, RTA.

• Urinary AG

  Na + K − Cl.

• Metabolic alkalosis

  Vomiting, diuretics, low K.

Sources

Facts in this article were checked against these documents.

• Standard Treatment Workflow: Approach to Hyponatremia — Indian Council of Medical Research, DHR, 2022 (link)

• MSD Manual Professional: Hyponatremia; Hypernatremia; Hypokalemia; Hyperkalemia; Hypocalcemia; Hypercalcemia; Hypomagnesemia; Acid-Base Disorders; Metabolic Acidosis; Metabolic Alkalosis; Volume Depletion — Merck & Co. (MSD Manuals), reviewed 2025–26 (link)

• Competency Based Undergraduate Curriculum, General Medicine (GM 23) — National Medical Commission, 2024

Test Yourself: Practice Questions

Thirty questions in NEET PG style, most of them clinical vignettes.

Practice Questions (NEET PG pattern)

Original questions written in the style of the exam: +4 for a correct answer, −1 for a wrong one. Every answer was checked against the sources listed above. NEET PG papers are not published by NBEMS, so these are not past-paper questions.

Q1. A patient with diarrhoea has dry mucosa, tachycardia, postural hypotension and Na 128 mmol/L. Per ICMR, treat with

• (a) tolvaptan

• (b) 3% saline bolus

• (c) IV isotonic normal saline

• (d) fluid restriction

Q2. A patient with cirrhosis and ascites has Na 126 mmol/L. The ICMR approach is to

• (a) ignore it

• (b) give 3% saline rapidly

• (c) give normal saline

• (d) treat the underlying disease (hypervolaemic hyponatraemia)

Q3. A patient develops seizures with Na 118 mmol/L that fell within the last 12 hours. Per ICMR,

• (a) start tolvaptan and wait

• (b) give emergency 3% saline 1–2 mL/kg/h until symptoms resolve

• (c) give normal saline slowly

• (d) restrict fluids only

Q4. In chronic hyponatraemia, serum sodium should be raised by no more than

• (a) 20 mmol/L in 24 hours

• (b) 8–10 mmol/L in the first 24 hours

• (c) any amount

• (d) 2 mmol/L in 24 hours

Q5. Overly rapid correction of chronic hyponatraemia can cause

• (a) hyperkalaemia

• (b) cerebral oedema

• (c) osmotic demyelination (central pontine myelinolysis)

• (d) hypoglycaemia

Q6. Per ICMR, infusing 3% saline at 1 mL/kg/h raises serum sodium by about

• (a) 10 mmol/L per hour

• (b) 5 mmol/L per hour

• (c) 0.1 mmol/L per hour

• (d) 1 mmol/L per hour

Q7. A patient has Na 124 mmol/L, plasma osmolality 260, urine osmolality 450, urine Na 60 and low uric acid; he is euvolaemic. The diagnosis is

• (a) pseudohyponatraemia

• (b) psychogenic polydipsia

• (c) SIADH

• (d) hypovolaemic hyponatraemia

Q8. In chronic euvolaemic hyponatraemia, ICMR advises fluid restriction to

• (a) 500–1000 mL per 24 hours

• (b) 3 L per day

• (c) 100 mL per day

• (d) no restriction

Q9. A patient with very high blood lipid levels has a low measured sodium without a true water–sodium imbalance. This is

• (a) cerebral salt wasting

• (b) hypovolaemia

• (c) pseudohyponatraemia

• (d) SIADH

Q10. A common drug cause of hyponatraemia is

• (a) metformin

• (b) thiazide diuretics

• (c) amlodipine

• (d) paracetamol

Q11. The main goal in treating hypernatraemia is

• (a) giving 3% saline

• (b) replacing intravascular volume and the free-water deficit

• (c) giving furosemide alone

• (d) restricting water

Q12. A patient on furosemide has K 2.6 mmol/L. The ECG is most likely to show

• (a) delta waves

• (b) ST sagging, T-wave depression and prominent U waves

• (c) short QT

• (d) peaked T waves

Q13. Hypokalaemia keeps recurring despite potassium replacement. The next electrolyte to check and correct is

• (a) phosphate

• (b) magnesium

• (c) sodium

• (d) chloride

Q14. The earliest ECG change of hyperkalaemia is

• (a) ST elevation in V1–V3

• (b) U waves

• (c) tall, symmetric, peaked T waves

• (d) QT prolongation

Q15. A well patient has K 6.4 mmol/L on a visibly haemolysed blood sample; ECG is normal. The likely explanation is

• (a) Addison crisis

• (b) true hyperkalaemia needing dialysis

• (c) rhabdomyolysis

• (d) pseudohyperkalaemia from haemolysis of the sample

Q16. After thyroid surgery, a patient has perioral tingling; tapping in front of the ear makes the facial muscles twitch. This is

• (a) Trousseau sign

• (b) Babinski sign

• (c) Chvostek sign of hypocalcaemia

• (d) Kernig sign

Q17. Trousseau sign is elicited by

• (a) tapping the facial nerve

• (b) flexing the neck

• (c) inflating a BP cuff 20 mm Hg above systolic for 3 minutes to provoke carpal spasm

• (d) percussing the patella

Q18. Hypoparathyroidism causes

• (a) low calcium with low phosphate

• (b) low calcium with high phosphate

• (c) high calcium with low phosphate

• (d) normal calcium

Q19. Severe hypocalcaemia shows on ECG as

• (a) prolonged QTc

• (b) U waves

• (c) short QTc

• (d) delta waves

Q20. IV calcium for hypocalcaemia must be given especially carefully in a patient taking

• (a) amoxicillin

• (b) metformin

• (c) digoxin

• (d) paracetamol

Q21. The two most common causes of hypercalcaemia are

• (a) thiazides and milk

• (b) hyperparathyroidism and cancer

• (c) vitamin D deficiency and CKD

• (d) sarcoidosis and TB

Q22. A patient with breast cancer has calcium 14 mg/dL. The drug class of choice for cancer-associated hypercalcaemia is

• (a) bisphosphonates

• (b) vitamin D

• (c) thiazides

• (d) calcium supplements

Q23. ECG in severe hypercalcaemia typically shows

• (a) a shortened QTc interval

• (b) U waves

• (c) a prolonged QTc

• (d) low-voltage complexes only

Q24. Clinical features of hypomagnesaemia are largely due to accompanying

• (a) hyperkalaemia

• (b) hypernatraemia

• (c) hypokalaemia and hypocalcaemia

• (d) hyperglycaemia

Q25. Acidaemia is defined as arterial pH below

• (a) 7.20

• (b) 7.35

• (c) 7.45

• (d) 7.00

Q26. In toxic-alcohol poisoning with a high anion gap metabolic acidosis, the correct toxin–acid pair is

• (a) ethylene glycol → formate

• (b) isopropanol → oxalate

• (c) ethanol → lactate only

• (d) methanol → formate

Q27. A normal anion gap (hyperchloraemic) metabolic acidosis is typically caused by

• (a) lactic acidosis

• (b) diabetic ketoacidosis

• (c) salicylate poisoning

• (d) diarrhoea

Q28. The urinary anion gap is calculated as

• (a) Na + K − Cl

• (b) Cl − Na

• (c) Na − (Cl + HCO3)

• (d) K − Cl

Q29. Bicarbonate therapy is generally safe and appropriate in

• (a) DKA routinely

• (b) normal anion gap acidosis from bicarbonate loss

• (c) respiratory acidosis

• (d) lactic acidosis in all cases

Q30. A patient has prolonged vomiting. The expected acid–base disorder is

• (a) normal anion gap acidosis

• (b) high anion gap acidosis

• (c) metabolic alkalosis

• (d) respiratory acidosis

Active Recall

From memory: give the ICMR approach to hyponatraemia by volume status and severity with the correction limit, state SIADH criteria, describe ECG changes of potassium and calcium disorders, Chvostek and Trousseau signs, hypercalcaemia treatment, and classify metabolic acidosis by anion gap with causes and the causes of metabolic alkalosis.