Three days of vomiting: reading the blood gas before the surgeon arrives
A 58-year-old man is brought in after three days of repeated vomiting; for weeks he has had early satiety and a feeling of fullness after meals. He looks dehydrated, with dry mucous membranes, a pulse of 112/min and a blood pressure of 100/70 mmHg; urine output has been low. Arterial blood gas on room air: pH 7.49, pCO₂ 46 mmHg, HCO₃⁻ 33 mEq/L. Serum electrolytes: Na⁺ 133, K⁺ 3.0, Cl⁻ 90 mEq/L. A spot urine sample shows a chloride of 8 mEq/L. He takes no diuretics and has no history of heart or kidney disease. The surgical team suspects gastric outlet obstruction and plans nasogastric decompression. The resident asks you to interpret the gases before the next sample is drawn, and specifically whether the potassium needs replacing before saline is started.
1. Characterise the acid–base disorder, calculate the anion gap and decide whether the respiratory compensation is appropriate.
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Primary disorder. pH 7.49 is alkalaemia, and HCO₃⁻ 33 mEq/L is raised, so this is a metabolic alkalosis. pCO₂ 46 mmHg is above the normal 40, i.e. the lungs are retaining CO₂ to compensate - the expected direction.
Anion gap
$$AG = Na^+ - (Cl^- + HCO_3^-) = 133 - (90 + 33) = 10\ \text{mEq/L}$$
A gap of 10 is within the normal range (roughly 8–12). So there is no hidden unmeasured anion and no superimposed metabolic acidosis; the high bicarbonate is a genuine gain of base equivalents, not a compensation for something else.
Adequacy of compensation. For metabolic alkalosis the expected pCO₂ is
$$pCO_2 \approx 0.7 \times HCO_3^- + 21 = 0.7 \times 33 + 21 = 44.1\ \text{mmHg}$$
Measured 46 mmHg is within about 2 mmHg of predicted, so respiratory compensation is appropriate and there is no second respiratory disorder. The picture is a simple, chloride-responsive metabolic alkalosis with hypokalaemia, and the history of vomiting points to loss of gastric HCl as the driver.
2. What does the urine chloride of 8 mEq/L add, and how would the interpretation change if he had been taking a diuretic?
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The urine chloride separates the two common causes of a saline-responsive alkalosis.
- In vomiting or nasogastric suction, the patient is volume-depleted and the filtered chloride load is low, so the tubule reabsorbs chloride avidly. Urine Cl⁻ falls below about 20 mEq/L. The value of 8 mEq/L fits this exactly.
- In current diuretic use (loop or thiazide), the drug blocks sodium chloride reabsorption upstream of the distal chloride-sensitive segment, so despite volume depletion the urine still contains chloride, usually above 20 mEq/L.
So the low urine chloride tells you the alkalosis will respond to saline: give NaCl, restore volume, and the kidney regains the ability to excrete bicarbonate.
Caveats worth stating. The test is only valid at the moment of sampling. After a diuretic is stopped, the pattern reverts to a low urine chloride within a few days, and the history may then be the only clue. Vomiting plus diuretics can therefore give a low value even though both causes are present. The spot value of 8 mEq/L here, with a clear history of vomiting and no diuretic, is reliable.
3. Outline the fluid and electrolyte plan, and name the specific risks of correcting too fast. Why is potassium replacement not optional here?
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Fluids. 0.9% sodium chloride is the correct choice: it supplies the volume and the chloride that the kidney needs to excrete the excess bicarbonate. Normal saline itself has a pH around 5.5 and is acidifying relative to this patient's plasma, which is exactly the direction wanted. Titrate to urine output, pulse and blood pressure; in a 58-year-old, watch for volume overload.
Potassium. K⁺ is 3.0 mEq/L with an alkalosis, which means total body potassium is depleted even though serum K⁺ looks only mildly low. Alkalosis shifts K⁺ into cells in exchange for H⁺, so the serum value understates the deficit, and the alkalosis itself cannot be corrected while potassium remains low, because potassium deficiency increases renal bicarbonate reabsorption and hydrogen excretion. Replace as potassium chloride, not potassium bicarbonate or citrate, since chloride is needed too. Peripheral infusion is limited to about 10 mEq/h with cardiac monitoring above that; check magnesium, because hypomagnesaemia makes hypokalaemia refractory.
Risks of over-rapid correction
- Rapid saline in an older patient can cause pulmonary oedema.
- Rapid potassium can cause arrhythmia and phlebitis.
- Both must be tracked with repeat electrolytes and gases.
Also: do not give bicarbonate, and do not leave the nasogastric tube unclamped without replacing its losses - suction removes more HCl and worsens the alkalosis. Definitive treatment is relieving the obstruction.