THe acid-base status of aspirin is always in the process of shifting from alkalosis to acidosis over a few hours. So relying on ABG is unreliable (in my opinion) for a quick answer.

Rule of thumb for aspirin toxicity: Fast respirations, tinnitus, kidney damage (increased creatinine).

This question she had a fast respiration rate.

---Not perfect but may help in a quick pinch-----

• Patient who attempted an overdose who has a mixed anion-gap metabolic acidosis (140 – 104 – 6 = 30 > 12) with a significant respiratory alkalosis, most consistent with aspirin/salicylate poisoning

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Calculated anion gap is 140-(104+6) = 30. This patient has a high anion gap metabolic acidosis.

Based on Winter's formula, adequate respiratory compensation would yield a PCO2 of 1.5*6 + 8 ± 2 = 17 ±2. Since this patient's actually PCO2 was lower, she also has a concomitant respiratory alkalosis.

Since salicylates stimulate respiratory drive and are part of the MUDPILES mnemonic, aspirin is the only answer choice that explains the high anion gap metabolic acidosis with respiratory alkalosis.