Tramadol, a weak opioid agonist, is the most likely cause of this patient's respiratory findings. She has primary respiratory acidosis characterized by an elevation in PCO₂, a decrease in pH, and a slight increase in bicarbonate. This patient has laboratory findings that suggest an acute onset. For each 10 mm Hg (1.3 kPa) increase in PCO₂, serum bicarbonate increases acutely by 1.0 to 2.0 mEq/L (1.0-2.0 mmol/L) due to the extracellular-to-intracellular shift of hydrogen ions as an immediate compensatory mechanism. Later, renal compensation leads to increased bicarbonate generation, and, after 24 to 48 hours, leads to an increase in serum bicarbonate of 3.0 to 4.0 mEq/L (3.0-4.0 mmol/L) for every 10 mm Hg (1.3 kPa) increase in PCO₂. Primary respiratory acidosis is due to decreased effective ventilation, often noted with opioid overdose, leading to hypercapnia and retention of hydrogen ions. Respiratory acidosis can also result from intrinsic lung pathology or from processes that impede ventilation.

The early phase of acetaminophen overdose is often not associated with any acid-base abnormality. After 72 to 96 hours, patients will often develop an increased anion gap metabolic acidosis related to lactic acidosis. This patient's anion gap is only 11 with no evidence of a metabolic acidosis, making acetaminophen overdose an unlikely cause of her acid-base disorder.

Although decreased respiratory drive can occur in the setting of salicylate intoxication in the later stages, it is more commonly associated with a mixed acid-base abnormality, including an increased anion gap acidosis and respiratory alkalosis, making this an unlikely diagnosis for this patient.

NSAID overdose typically presents with azotemia and hyperkalemia in addition to an increased anion gap metabolic acidosis (primarily a lactic acidosis), making this diagnosis unlikely in this patient.