A 15-year-old girl is brought to the emergency department after a suicide attempt. The patient has a history of depression, and 12 hours ago she ingested 30 tablets of one of her father's medications. He has a history of hypertension and coronary artery disease. The patient has no other medical conditions and does not use alcohol or illicit drugs. Upon arrival, she has nausea, upper abdominal discomfort, and ringing in the ears. Temperature is 38.1 C (100.5 F), blood pressure is 120/76 mm Hg, pulse is 115/min, and respirations are 26/min. Physical examination is otherwise unremarkable. Which of the following sets of findings are most likely to be observed on arterial blood gas analysis in this patient?
This patient has tinnitus, fever, tachypnea, nausea, and gastrointestinal irritation after a medication overdose. This scenario is highly suggestive of salicylate intoxication (eg, due to aspirin that her father takes for coronary artery disease). Acute salicylate toxicity usually presents with a mixed acid-base disturbance.
Primary respiratory alkalosis develops shortly after ingestion because salicylates directly stimulate the medullary respiratory center, resulting in increased ventilation and low PaCO2 (<40 mm Hg).
Primary anion gap metabolic acidosis develops after several hours because toxic salicylate levels inhibit oxidative phosphorylation. This results in the accumulation of unmeasured organic acids (eg, ketoacids, lactate) in the blood, which causes low serum HCO3− (<24 mEq/L) and increases the anion gap.
The mixed disturbance can be recognized by inappropriate compensation for one of the primary disturbances. Using Winters' formula for the values in the correct answer, expected compensation for serum HCO3− of 14 mEq/L is PaCO2 of ~29 mm Hg (14 × 1.5 + 8 ± 2 = 29 ± 2); the actual PaCO2 of 23 mm Hg is lower and indicates a concomitant primary respiratory alkalosis. Working in the other direction, there should be minimal metabolic compensation for respiratory alkalosis (ie, minimal decrease in HCO3−) in the acute setting; therefore, the significantly decreased serum HCO3− of 14 mEq/L indicates a concomitant primary metabolic acidosis.
(Choice A) Low pH (<7.35) with low HCO3− and low PaCO2 is consistent with primary metabolic acidosis with respiratory compensation. PaCO2 of 27 mm Hg is appropriate compensation for HCO3− of 12 mEq/L (12 × 1.5 + 8 ± 2 = 26 ± 2), indicating the absence of an additional primary disturbance. Acute salicylate toxicity rarely presents with an isolated primary metabolic acidosis unless there is coingestion of a respiratory depressant (eg, opioids) that prevents the primary increase in respiratory drive.
(Choice B) Low pH with high PaCO2 is consistent with respiratory acidosis. Minimal increase in serum HCO3− above 24 mEq/L (minimal metabolic compensation) indicates the respiratory acidosis is acute, as would be expected with an acute opioid overdose.
(Choice C) These values are within normal limits and indicate an absence of acid-base disturbance.
(Choice E) pH within the normal range with high PaCO2 and high HCO3− is consistent with a mixed primary respiratory acidosis and primary metabolic alkalosis, which would be expected with an opioid overdose in a patient who also had severe vomiting.
Educational objective:
Acute salicylate intoxication should be suspected in patients with the triad of tinnitus, fever, and tachypnea. It usually causes a mixed primary respiratory alkalosis and primary metabolic acidosis with arterial pH often within the normal range.