Medicine — Acid–Base and Electrolytes, NMC MBBS licence examination syllabus (Nepal Medical Council).
Acid–base disorders: reading a gas without guessing
Five numbers, five steps, and the answer falls out every time.
Blood gas interpretation has a reputation for being hard, and it is almost entirely undeserved. It feels hard because it is usually taught as a set of patterns to recognise. Recognition fails the moment a patient has two disorders at once — which, in the sick patients where gases actually get taken, is common.
Approached as a fixed sequence of questions, it is mechanical. This chapter builds that sequence, and it insists on one habit that separates people who can read a gas from people who guess: always work through the steps in order, even when the answer looks obvious. The obvious answer is exactly where the second disorder hides.
🩺 Where this lives: A patient with diabetic ketoacidosis arrives, is treated, and looks better — but their repeat gas shows a pH that has barely moved. Reading it stepwise reveals why: the ketoacidosis is resolving, but litres of normal saline have produced a second, hyperchloraemic acidosis on top of it. Pattern recognition sees "still acidotic, treatment failing" and escalates wrongly. The stepwise read sees two disorders and one of them iatrogenic.
The foundation: pH is a ratio
Everything in this topic follows from one equation, and specifically from the fact that pH depends on a ratio rather than on either value alone.
Because pH is a ratio, a normal pH does not mean normal physiology. A patient can have a badly deranged bicarbonate and a badly deranged CO₂ that happen to divide out to a normal number. This is why you never read the pH alone, and why "the gas is normal" is a statement about three values, not one.
Note the asymmetry in speed, because it explains a great deal of what you will see. The lung responds in minutes — a patient with a metabolic acidosis is already hyperventilating by the time you meet them. The kidney takes days. So in an acute respiratory problem there has been no time for renal compensation, and a raised bicarbonate in that setting tells you the process is chronic.
Naming the disorder
There are four primary disorders, and they sit naturally in a two-by-two: the pH tells you which column, and whichever value moved with it tells you which row.
THE NORMAL VALUES — worth knowing cold
pH 7.35 – 7.45
pCO₂ 4.7 – 6.0 kPa (35 – 45 mmHg)
HCO₃⁻ 22 – 26 mmol/L
Base excess −2 to +2
Anion gap 8 – 12 mmol/L
pO₂ > 10.6 kPa on air (80 mmHg)
A NOTE ON WORDING — examiners use it precisely
ACIDAEMIA / ALKALAEMIA describe the BLOOD pH.
ACIDOSIS / ALKALOSIS describe the PROCESS driving it.
A patient can have a metabolic acidOSIS and a respiratory
alkalOSIS at once, with a normal pH and therefore no
acidAEMIA at all. Getting the words right forces you to
think about processes rather than about one number.
The five steps
Step three is where most errors happen, so it is worth stating the compensation rule explicitly rather than leaving it to intuition.
Compensation never fully corrects the pH, and never overshoots it. So if you find a pH that has returned to the middle of the normal range in a patient with an obviously deranged bicarbonate and CO₂, you are not looking at excellent compensation — you are looking at two opposing primary disorders. That is a finding, not a reassurance.
Step four: the anion gap
This is the step most often skipped, and it is the one that turns "metabolic acidosis" — which is a description — into a differential diagnosis.
RAISED ANION GAP — mnemonic: MUDPILES
M Methanol
U Uraemia (renal failure)
D Diabetic ketoacidosis
P Paraldehyde / Propylene glycol
I Isoniazid, Iron
L Lactic acidosis ← by far the commonest in practice
E Ethylene glycol
S Salicylates
NORMAL ANION GAP — mnemonic: HARDUPS, or simply:
Gastrointestinal loss — diarrhoea, high-output stoma
Renal loss — renal tubular acidosis,
carbonic anhydrase inhibitors
Iatrogenic — large-volume normal saline
(hyperchloraemic acidosis)
💡 Exam angle: lactic acidosis is the commonest raised-gap acidosis you will actually meet, and its commonest cause is tissue hypoperfusion — that is, shock. A question giving you a raised anion gap acidosis in a hypotensive, tachycardic patient is testing whether you connect the gas to the circulation rather than treating the number. Meanwhile large-volume saline causing a hyperchloraemic normal-gap acidosis is the classic iatrogenic answer, and it explains a "worsening" acidosis in a patient who is genuinely improving.
Worked interpretations
GAS 1
pH 7.18 pCO₂ 3.2 kPa HCO₃⁻ 9 Na⁺ 138 Cl⁻ 99
Step 1 pH 7.18 → acidaemia.
Step 2 HCO₃⁻ is low (9) and moves WITH the low pH
→ primary METABOLIC ACIDOSIS.
Step 3 pCO₂ is low (3.2), same direction → appropriate
respiratory compensation. Not a second disorder.
Step 4 Anion gap = 138 − (99 + 9) = 30 → RAISED.
Step 5 Check oxygenation separately.
READ: raised anion gap metabolic acidosis with appropriate
respiratory compensation. Now go hunting the acid —
ketones, lactate, toxin.
GAS 2
pH 7.36 pCO₂ 8.9 kPa HCO₃⁻ 36
Step 1 pH 7.36 → just within range. Do NOT stop here.
Step 2 Both values are markedly abnormal, so something
is wrong despite the normal pH. pCO₂ is high and
pH sits at the LOW end → the acidosis is primary.
→ RESPIRATORY ACIDOSIS.
Step 3 HCO₃⁻ is high (36), same direction, and the pH has
nearly normalised → full renal compensation, which
takes DAYS. This is therefore CHRONIC.
READ: chronic respiratory acidosis with full metabolic
compensation — the classic picture in long-standing COPD.
The near-normal pH is the clue to chronicity, not to health.
GAS 3 — the one pattern recognition misses
pH 7.40 pCO₂ 2.9 kPa HCO₃⁻ 14 Na⁺ 140 Cl⁻ 104
Step 1 pH 7.40 → normal. Tempting to stop. Don't.
Step 2 HCO₃⁻ low AND pCO₂ low — both far outside range.
Step 3 Compensation never returns pH to 7.40 exactly, so
this is not one disorder compensated. It is TWO.
Step 4 Anion gap = 140 − (104 + 14) = 22 → RAISED.
READ: a raised-gap metabolic acidosis AND a primary
respiratory alkalosis together — for example sepsis, where
lactate drives the acidosis and tachypnoea independently
drives off CO₂. A "normal" gas in a very sick patient.
Clinical reasoning: four presentations
🔍 Case 1 — the textbook read
PresentationA 19-year-old with polyuria, thirst and vomiting. Deep sighing respiration. Glucose 28 mmol/L, ketones raised. pH 7.10, pCO₂ 2.8, HCO₃⁻ 7.
ReasoningAcidaemic; bicarbonate low and moving with the pH → metabolic acidosis. The low pCO₂ is appropriate compensation — the deep sighing breathing (Kussmaul) is that compensation, visible at the bedside. Ketones give the raised gap.
AnswerDiabetic ketoacidosis. Treat with fluid, insulin and potassium replacement. Do not "correct" the respiratory compensation — it is helping.
🔍 Case 2 — the dangerous reassurance
PresentationA 25-year-old with a severe asthma attack. Initially pCO₂ 3.1 kPa. Forty minutes later, tiring, pCO₂ now 5.4 kPa — within the normal range.
TrapA CO₂ that has "normalised" looks like improvement.
ReasoningA patient in severe asthma should be hyperventilating, so a low pCO₂ is the expected finding. A rising, normal pCO₂ means they can no longer sustain the work of breathing. This is exhaustion, not recovery.
AnswerA normalising pCO₂ in acute severe asthma is a sign of life-threatening asthma and impending respiratory failure. Escalate urgently to critical care.
🔍 Case 3 — two disorders at once
PresentationA 62-year-old with pneumonia and hypotension. pH 7.39, pCO₂ 3.0 kPa, HCO₃⁻ 15, lactate 5.1, Na⁺ 139, Cl⁻ 102.
The distractorThe pH is normal, so the gas looks unremarkable.
ReasoningBoth values are far outside range, and compensation never restores a pH to 7.39 exactly. Anion gap = 139 − (102 + 15) = 22, raised, with a lactate to explain it. The low pCO₂ exceeds what compensation alone would produce — the tachypnoea of pneumonia is a primary respiratory alkalosis.
AnswerRaised-gap lactic acidosis from sepsis, plus a primary respiratory alkalosis. The normal pH conceals a critically ill patient — treat the sepsis.
🔍 Case 4 — the iatrogenic acidosis
PresentationA patient in DKA, six hours into treatment. Ketones have fallen and glucose is controlled, but the acidosis persists: pH 7.28, HCO₃⁻ 16, Na⁺ 140, Cl⁻ 116. Four litres of 0.9% saline have been given.
Key clueThe chloride is high, and the anion gap = 140 − (116 + 16) = 8 — now normal, when it started raised.
ReasoningThe original raised-gap ketoacidosis has resolved. What remains is a normal-gap hyperchloraemic acidosis caused by the resuscitation fluid itself.
AnswerRecognise it as iatrogenic and expected. It resolves as the kidney excretes the chloride load. Escalating insulin for a "persistent acidosis" here would be the wrong response — the gap, not the pH, told you the ketoacidosis was already fixed.
Commonly confused
Confusion
The distinction
Why it matters
Acidaemia vs acidosis
Acidaemia is the blood pH; acidosis is the process
Two opposing processes can give a normal pH and no acidaemia at all.
Compensation vs a second disorder
Compensation never normalises or overshoots the pH
A perfectly normal pH with grossly abnormal values means two primary disorders.
Acute vs chronic respiratory acidosis
Renal compensation takes days, so a raised HCO₃⁻ means chronic
It distinguishes an acute deterioration from a stable chronic state.
Raised vs normal anion gap
Acid added versus bicarbonate lost
They point to entirely different differentials.
Low vs normalising pCO₂ in asthma
Low is expected; normalising means exhaustion
The "reassuring" value is the emergency.
Persistent acidosis in treated DKA
Check whether the GAP has closed
A closed gap means the ketoacidosis is fixed and the rest is saline.
Rapid revision
MUST-KNOW FACTS
1. pH ∝ HCO₃⁻ / pCO₂ — a RATIO, so a normal pH proves nothing alone.
2. Kidney controls HCO₃⁻ (days). Lung controls pCO₂ (minutes).
3. Normal: pH 7.35–7.45 · pCO₂ 4.7–6.0 kPa · HCO₃⁻ 22–26.
4. Acidaemia/alkalaemia = the blood. Acidosis/alkalosis = the process.
5. The value moving the SAME way as the pH is the primary disorder.
6. Compensation moves the other value in the SAME direction.
7. Compensation NEVER fully corrects and never overshoots.
8. A normal pH with grossly abnormal values = TWO primary disorders.
9. Raised HCO₃⁻ in respiratory acidosis = chronic (renal compensation took days).
10. Always calculate the anion gap in a metabolic acidosis.
11. Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻); normal 8–12.
12. Raised gap = acid ADDED (MUDPILES; lactate and ketones commonest).
13. Normal gap = bicarbonate LOST (diarrhoea, RTA, saline).
14. Lactic acidosis usually means hypoperfusion — look at the circulation.
15. Large-volume 0.9% saline causes hyperchloraemic normal-gap acidosis.
16. Kussmaul breathing IS respiratory compensation, visible at the bedside.
17. In DKA, a closed gap means the ketoacidosis has resolved.
18. A normalising pCO₂ in acute severe asthma signals exhaustion — escalate.
19. Vomiting → metabolic alkalosis (loss of gastric acid).
20. Never correct compensation; treat the primary process.
21. Oxygenation is a separate question from acid–base.
22. Work the steps in order every time — the obvious answer hides the second disorder.
💡 Exam angle: the highest-yield threads are (a) the normal pH concealing two disorders, (b) the anion gap naming the cause, (c) chronic versus acute respiratory acidosis from the bicarbonate, (d) the rising pCO₂ in tiring asthma, and (e) hyperchloraemic acidosis after saline. Every one of them is invisible to pattern recognition and obvious to the five steps. That is the whole argument for working them in order.
Syllabus points
The bicarbonate buffer system and why pH is a ratio
Normal values for pH, pCO₂, bicarbonate and anion gap
Acidaemia versus acidosis: getting the wording right
The four primary disorders
The five-step interpretation sequence
Compensation: direction, speed and limits
The anion gap and its differentials
Mixed disorders and the normal-pH trap
Acute versus chronic respiratory acidosis
Iatrogenic hyperchloraemic acidosis
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