Acid-Base Disorders — Advanced

This ABG shows primary metabolic acidosis (low HCO3- and acid pH). Expected respiratory compensation for metabolic acidosis can be estimated by Winter's formula: expected PaCO2 ≈ 1.5 × [HCO3-] + 8 ± 2. For HCO3- = 12 mmol/L, expected PaCO2 ≈ 1.5×12 + 8 = 26 ± 2 mmHg. The measured PaCO2 is 40 mmHg, markedly higher than expected, indicating inadequate respiratory compensation consistent with a superimposed respiratory acidosis (i.e. mixed metabolic and respiratory acidosis). Option A is incorrect because the PaCO2 is not adequately reduced. Option C is wrong since primary respiratory acidosis would have elevated PaCO2 as the primary disturbance and compensatory HCO3- rise; here HCO3- is low. Option D is incorrect because the HCO3- is low (acidosis), not high. Option E is false because the measured PaCO2 is far from the expected compensatory value.

Anion gap (AG) = Na+ − (Cl- + HCO3-) = 140 − (80 + 10) = 50 mmol/L → markedly raised (normal ~8–14 depending on lab). Delta AG = AG − normal AG (use ~12) ≈ 50 − 12 = 38. Delta HCO3- = normal HCO3- (24) − measured HCO3- (10) = 14. Delta ratio = 38 / 14 ≈ 2.7. A delta ratio >2 suggests that the increase in AG is disproportionately large relative to the fall in HCO3-, implying a concurrent metabolic alkalosis or a pre-existing elevated bicarbonate state (e.g. chronic metabolic alkalosis) that blunts the fall in HCO3-. Option A is wrong (AG is high). Option B (combined high AG + normal AG acidosis) corresponds to delta ratio ~0.8–1, not >2. Option C would have delta ratio ~1–2. Option E is unrelated. Therefore the best conclusion is a high AG metabolic acidosis with coexisting metabolic alkalosis or pre-existing raised bicarbonate.

The pH is near normal despite markedly elevated PaCO2 and elevated HCO3-, consistent with chronic respiratory acidosis with renal metabolic compensation. In chronic respiratory acidosis, renal retention of HCO3- increases (~3.5–4 mmol/L for each 10 mmHg increase in PaCO2 after chronicity) so a PaCO2 of 68 mmHg (≈28 mmHg above normal 40) would predict a substantial HCO3- rise, as seen. Option B is wrong because acute respiratory acidosis would have little HCO3- compensation and more pronounced acidemia. Option C is incorrect because HCO3- is elevated, not low. Option D is unlikely: metabolic alkalosis would cause elevated HCO3- but would not explain the very high PaCO2 unless hypoventilation coexisted; clinical context of stable COPD supports chronic compensation. Option E is the opposite direction.

Features: normal anion gap metabolic acidosis with hypokalaemia and an inappropriately high urine pH (>5.5) despite systemic acidaemia suggests impaired distal urinary acidification — distal (type 1) RTA. Proximal RTA (type 2) typically presents with bicarbonate wasting, hypokalaemia, but once HCO3- is depleted the urine can be acidified (urine pH <5.5), so urine pH of 6.0 is less consistent with proximal RTA. Type 4 RTA is characterised by hyperkalaemia due to hypoaldosteronism; the patient is hypokalaemic, so option 2 is wrong. DKA (option 3) gives high anion gap metabolic acidosis and hyperglycaemia. Diarrhoea (option 4) causes normal AG metabolic acidosis with low urinary ammonium chloride excretion and typically low urine pH (acidic), and history would point to GI losses. Therefore distal (type 1) RTA is the best fit.

Large-volume 0.9% saline can cause a dilutional (hyperchloraemic) normal anion gap metabolic acidosis by increasing serum chloride and reducing strong ion difference. The first-line response is to stop the offending chloride-rich fluid and, if ongoing fluid resuscitation is needed, switch to a balanced crystalloid (e.g. Plasma-Lyte or similar) which has lower chloride and is less acidifying; reassess acid–base. Routine immediate intravenous sodium bicarbonate is usually unnecessary for moderate hyperchloraemic acidosis and may cause volume/Na overload and overshoot alkalosis. Loop diuretics (option B) are not an appropriate immediate treatment in a volume-resuscitated postoperative patient and may worsen electrolyte derangements. Hyperventilation (option D) treats respiratory alkalosis, not a metabolic acidosis cause. Mineralocorticoid therapy (option E) is not indicated.

This is metabolic alkalosis due to vomiting with contraction alkalosis and hypokalaemia likely. First-line management is to correct the precipitant: restore intravascular volume with isotonic saline and replace potassium (as K+ repletion helps correct alkalosis by allowing renal H+ secretion). Option A (giving bicarbonate) would worsen the alkalosis. Option C (acetazolamide) can be useful for chloride-resistant metabolic alkalosis (often with fluid overload), but it is not appropriate before volume and potassium are corrected and is contraindicated if intravascular depletion exists. Option D (intubation/hyperventilation) would worsen alkalosis by reducing PaCO2 (this patient already has elevated PaCO2 as compensation). Option E (IV calcium) is for severe hypocalcaemic signs, not a routine treatment for metabolic alkalosis per se.

Rapid correction of acidosis during haemodialysis using high-bicarbonate dialysate can cause alkalosis and increase protein binding of calcium, lowering ionised (active) calcium and precipitating signs of hypocalcaemia (tetany, twitching). The immediate treatment is IV calcium (e.g. calcium gluconate) to relieve symptoms and stabilise neuromuscular excitability. Option A incorrectly attributes citrate chelation—citrate is used in regional anticoagulation, not typical dialysate; immediate management in either case would still be IV calcium, but the scenario describes post-dialysis alkalosis rather than citrate toxicity. Option B (hypokalaemia) can occur but neuromuscular irritability with tetany is more typical of low ionised calcium; empiric IV K+ without checking could be harmful. Option D is incorrect—uriaemic tetany is less likely immediately post-dialysis and would not be managed by escalating dialysis. Option E is not relevant.

In DKA total body potassium is depleted despite normal or high serum K+. With a serum K+ of 5.6 mmol/L, it is appropriate to start insulin to treat the ketoacidosis while monitoring potassium closely; insulin will drive potassium intracellularly and serum K+ will fall, necessitating replacement as it declines. Holding insulin until potassium is much lower (option B) is only required when serum K+ is already low (commonly cited threshold is <3.3 mmol/L) because treating with insulin would provoke severe hypokalaemia; that threshold-based management is reflected in guidelines. Routine aggressive potassium replacement irrespective of level (option C) risks hyperkalaemia. Insulin bolus only (option D) is not standard; continuous insulin infusion is preferred. Oral potassium (option E) is inadequate in the acute setting. Hence option A is correct.

Albumin is a major unmeasured anion; hypoalbuminaemia lowers the measured anion gap and may mask a high anion gap metabolic acidosis. A commonly used correction is to add about 2.5 mmol/L to the AG for every 10 g/L decrease in albumin from normal (~40 g/L). Here albumin is 20 g/L (a fall of 20 g/L), so add ≈2.5×2 = 5 mmol/L: corrected AG = 12 + 5 = 17 mmol/L, which suggests a high anion gap metabolic acidosis. Option A is false because albumin affects AG. Option B has the direction reversed (it says subtract). Option D is not the standard correction method. Option E is incorrect—corrected AG is clinically useful to unmask hidden high AG acidosis.

The Stewart approach emphasises that plasma pH is determined by three independent variables: PaCO2, strong ion difference (SID) and total weak acid concentration (predominantly albumin). Infusion of large volumes of 0.9% saline increases serum chloride disproportionately relative to sodium, reducing SID (Na+ − Cl-), which drives metabolic acidosis without increasing the anion gap (i.e. normal AG hyperchloraemic acidosis). Option E correctly identifies the mechanism. Option A describes respiratory rather than metabolic disturbance. Option B (decreased albumin) would cause an alkalinising effect by reducing weak acids. Option C increases the anion gap (high AG acidosis), not the normal AG hyperchloraemic acidosis. Option D is incorrect physiologically.