Salicylate Overdose: Reading the Blood Gas, the Anion Gap and the Bicarbonate Strength
A 19-year-old is brought to the emergency department six hours after swallowing about 30 tablets of acetylsalicylic acid (aspirin). He is drowsy but rousable and breathing deeply at 28 breaths per minute. Arterial blood gas at 37 °C: pH 7.25, HCO₃⁻ 12 mmol/L; the analyser also reports a calculated PCO₂. Serum electrolytes: Na⁺ 138 mmol/L, Cl⁻ 100 mmol/L, K⁺ 3.6 mmol/L. The resident knows that the pKa₁ of carbonic acid is 6.1 at body temperature and that Winter's formula (expected PCO₂ = 1.5 × HCO₃⁻ + 8 ± 2) is used to judge whether respiratory compensation is appropriate. She then plans intravenous sodium bicarbonate, using a bicarbonate space of 0.5 × body weight, with the patient weighing 70 kg and a target bicarbonate of 24 mmol/L. The pharmacy stocks 8.4% and 1.4% sodium bicarbonate (molar mass 84 g/mol), and she must choose which strength to run through a peripheral line.
1. Calculate the PCO₂ from the Henderson–Hasselbalch equation and decide whether the respiratory compensation is appropriate.
Read the worked answer
Henderson–Hasselbalch: pH = 6.1 + log([HCO₃⁻] / (0.03 × PCO₂)) 7.25 − 6.1 = 1.15 = log(12 / (0.03 × PCO₂)) 10^1.15 = 14.1, so 0.03 × PCO₂ = 12 / 14.1 = 0.85 PCO₂ ≈ 28 mmHg.
Is that appropriate? Winter's formula: expected PCO₂ = 1.5 × 12 + 8 = 26 mmHg, acceptable range 24–28 mmHg. The measured 28 mmHg sits at the top of that range, so this is appropriate respiratory compensation for a primary metabolic acidosis - not a primary respiratory alkalosis and not a second, independent respiratory disorder.
Interpretation. The low pH with low bicarbonate defines a metabolic acidosis; the fact that the measured PCO₂ matches Winter's prediction means no additional respiratory acid–base process needs to be invoked at this moment. This matters clinically because salicylates often produce an early primary respiratory alkalosis, and a mixed picture is common later; the arithmetic here says the dominant process at six hours is the metabolic acidosis.
2. Calculate the anion gap and the delta ratio. What do they add to the picture, given that the chloride is 100 mmol/L?
Read the worked answer
Anion gap: AG = Na⁺ − (Cl⁻ + HCO₃⁻) = 138 − (100 + 12) = 26 mmol/L. With a reference range of roughly 8–12 mmol/L, this is a high-anion-gap metabolic acidosis, consistent with salicylate plus accumulated lactate and ketones.
Delta ratio: ΔAG / ΔHCO₃⁻ = (26 − 12) / (24 − 12) = 14 / 12 ≈ 1.2.
What this adds.
- The chloride of 100 mmol/L is normal, so this is not a hyperchloraemic (normal-gap) acidosis; no large volume of 0.9% saline had been given at the time of sampling.
- A delta ratio near 1.0 indicates a single high-anion-gap process with bicarbonate falling in proportion to the unmeasured anions. A ratio > 2 would suggest a coexisting metabolic alkalosis or a chronic respiratory acidosis; a ratio < 1 would suggest a coexisting normal-gap acidosis. At 1.2, the simplest reading is a single dominant process.
- The judgement is therefore not 'give bicarbonate and stop thinking' but 'the acidosis is organic-acid driven, so treat the cause (charcoal if within the window, urinary alkalinisation to enhance salicylate excretion, potassium replacement) and use bicarbonate only for a defined threshold'.
3. Compute the bicarbonate deficit for a target of 24 mmol/L, the volume of 8.4% and of 1.4% solution that represents, and the osmolarity of each. Which strength should go through a peripheral line, and how much of the deficit should actually be given?
Read the worked answer
Deficit: (24 − 12) mmol/L × 0.5 × 70 kg = 12 × 35 = 420 mmol.
8.4% solution: 84 g/L ÷ 84 g/mol = 1 mol/L = 1000 mmol/L, i.e. 1 mmol/mL → 420 mL. 1.4% solution: 14 g/L ÷ 84 g/mol = 0.167 mol/L = 167 mmol/L → 420 / 0.167 ≈ 2500 mL.
Osmolarity (NaHCO₃ dissociates into two particles): 8.4% ≈ 2 × 1000 = 2000 mOsm/L, about 6–7 times plasma (≈300 mOsm/L) - strongly hypertonic, veno-irritant, and usually reserved for central access or dilution. 1.4% ≈ 2 × 167 = 334 mOsm/L, close to isotonic and safe peripherally.
Judgement on dose. The 420 mmol figure is a theoretical full correction and is far more than should be given: it is a large fraction of the body's total bicarbonate pool, and rapid full correction risks overshoot alkalosis, hypokalaemia (K⁺ is already 3.6 mmol/L), hypocalcaemic tetany and a paradoxical fall in intracellular and CSF pH as generated CO₂ crosses membranes. The practical aim is to bring pH to about 7.15–7.20, not bicarbonate to 24 mmol/L - typically a fraction of the deficit, given slowly with repeat gases. Therefore: 1.4% peripherally, roughly one-third to one-half of the calculated deficit, titrated against repeat blood gases.