Log in / Register Soon
Official Education Partner of the Delhi Medicos Premier League — free question bank for every player and college
Q4 LONG ANSWER 10M ★ High-yield

Classify the acid–base disorders. Describe their causes, compensation and the use of the anion gap.

Biochemistry · 1st Professional — Pre-Clinical

Normal Values

ParameterNormal range
Arterial pH7.35–7.45
PCO235–45 mmHg
HCO3−22–26 mEq/L
PO280–100 mmHg
Base excess−2 to +2 mEq/L
Anion gap8–16 mEq/L

Henderson–Hasselbalch: pH = 6.1 + log ([HCO3−] ÷ 0.03 × pCO2)The ratio of bicarbonate to carbonic acid is normally 20 : 1.

  • The kidney controls the numerator (bicarbonate); the lung controls the denominator (pCO2). Every acid–base disorder is a disturbance of one, compensated by the other

The Four Primary Disorders

DisorderPrimary changePHCompensationSpeed
Metabolic acidosis↓ HCO3↓↓ pCO2 (hyperventilation)Minutes to hours
Metabolic alkalosis↑ HCO3↑↑ pCO2 (hypoventilation)Hours; limited
Respiratory acidosis↑ pCO2↓↑ HCO3 (renal)Days
Respiratory alkalosis↓ pCO2↑↓ HCO3 (renal)Days
  • Compensation never fully corrects the pH — if the pH is normal with abnormal values, suspect a mixed disorder
  • Respiratory compensation is fast; renal compensation is slow but far more powerful

Metabolic Acidosis and the Anion Gap

Anion gap = Na+ − (Cl− + HCO3−); normal 8–16 mEq/L. It represents the unmeasured anions, chiefly albumin.

High anion gap (added acid)Normal anion gap (bicarbonate lost)
MethanolDiarrhoea — the commonest
UraemiaRenal tubular acidosis
Diabetic ketoacidosisPancreatic or biliary fistula
ParaldehydeAcetazolamide
Isoniazid, IronUreteric diversion
Lactic acidosisExcess saline (hyperchloraemic)
Ethylene glycol—
Salicylates—
  • Mnemonic mudpiles for the raised gap causes
  • Normal anion gap acidosis is also called hyperchloraemic — chloride rises to replace the lost bicarbonate
  • The gap must be corrected for albumin — add 2.5 mEq/L for every 1 g/dL that albumin falls below 4

Causes of the Other Disorders

DisorderCauses
Metabolic alkalosisVomiting, nasogastric suction, diuretics, hyperaldosteronism, excess alkali, hypokalaemia
Respiratory acidosisCOPD, respiratory depression (opioids, anaesthesia), neuromuscular disease, airway obstruction, severe asthma
Respiratory alkalosisAnxiety and hyperventilation, high altitude, fever, sepsis, early salicylate poisoning, hepatic failure, pregnancy

Approach to Interpretation

  • 1. Look at the pH — acidaemia or alkalaemia? → 2.
  • Which value explains it — HCO3 (metabolic) or pCO2 (respiratory)? → 3.
  • Is compensation appropriate? Use the expected formulas → 4.
  • If metabolic acidosis, calculate the anion gap → 5.
  • If the gap is raised, check the delta ratio for a second disorder → 6.
  • Interpret alongside the clinical picture
  • Winter formula for metabolic acidosis: expected pCO2 = 1.5 × HCO3 + 8 ± 2. A higher value means a coexisting respiratory acidosis; a lower one, a respiratory alkalosis

Clinical Consequences

  • Acidosis — Kussmaul breathing, reduced myocardial contractility, vasodilatation, arrhythmias, hyperkalaemia, insulin resistance, confusion
  • Alkalosis — tetany (ionised calcium falls), paraesthesiae, confusion, hypokalaemia, arrhythmias; the oxygen dissociation curve shifts left
  • Acidosis raises serum potassium by shifting it out of cells; alkalosis lowers it — a link that must be remembered when correcting either

Compensation Formulas

Primary disorderExpected compensation
Metabolic acidosisPCO2 = 1.5 × HCO3 + 8 ± 2 (Winter)
Metabolic alkalosisPCO2 rises 0.7 mmHg per 1 mEq/L rise in HCO3
Acute respiratory acidosisHCO3 rises 1 mEq/L per 10 mmHg rise in pCO2
Chronic respiratory acidosisHCO3 rises 3.5 mEq/L per 10 mmHg
Acute respiratory alkalosisHCO3 falls 2 mEq/L per 10 mmHg fall
Chronic respiratory alkalosisHCO3 falls 5 mEq/L per 10 mmHg fall

Applied Aspects

  • Salicylate poisoning gives a mixed picture — direct stimulation of the respiratory centre causes respiratory alkalosis, while uncoupling and lactate cause metabolic acidosis. A normal pH here is ominous
  • Treat the cause, not the number — bicarbonate in lactic acidosis and DKA is reserved for severe acidaemia, and may worsen intracellular pH
  • Correcting acidosis unmasks hypokalaemia and can precipitate arrhythmia; potassium must be replaced alongside
  • In chronic COPD the bicarbonate is high from renal compensation; giving too much oxygen removes the hypoxic drive and worsens CO2 retention
  • Venous blood gases suffice for pH and bicarbonate in most non-respiratory situations, sparing an arterial puncture

All questions in Clinical & Applied Biochemistry

  1. Q1Classify the liver function tests. Describe the biochemical findings in the three types of jaundice. ★
  2. Q2Classify the renal function tests. Describe the assessment of glomerular filtration rate and the tests of tubular function. ★
  3. Q3Describe the biosynthesis of haem and its regulation. Classify the porphyrias and add a note on lead poisoning. ★
  4. Q4Classify the acid–base disorders. Describe their causes, compensation and the use of the anion gap. ★
  5. Q5Describe the formation, transport, conjugation and excretion of bilirubin. Classify jaundice and add a note on neonatal jaundice. ★
  6. SN1Classify the tumour markers with their clinical applications and limitations. ★
  7. SN2Describe the normal composition of cerebrospinal fluid and the changes in meningitis. ★
  8. SN3Describe the thyroid function tests and their interpretation. ★
  9. SN4Describe quality control in the clinical biochemistry laboratory. ★
  10. SN5Describe automation in the clinical biochemistry laboratory with its advantages and limitations.
  11. SN6Describe the principles and applications of therapeutic drug monitoring.
  12. SN7Describe the principles of biochemical screening with examples in the newborn and in pregnancy. ★

Every Biochemistry chapter →

Scroll to Top