A 22-year-old woman is brought to the emergency department 4 hours after intentionally ingesting an unknown quantity of pills. She complains of ringing in her ears, nausea, and diffuse abdominal pain. Her temperature is 37.8°C (100.0°F), blood pressure is 110/70 mm Hg, pulse is 115/min, and respirations are 26/min.
Laboratory studies show:
| Test | Value |
|---|---|
| Serum sodium | 140 mEq/L |
| Serum potassium | 3.5 mEq/L |
| Serum chloride | 104 mEq/L |
| Serum bicarbonate | 14 mEq/L |
| Blood urea nitrogen | 18 mg/dL |
| Serum creatinine | 0.9 mg/dL |
Arterial blood gas analysis on room air:
| Test | Value |
|---|---|
| pH | 7.42 |
| PaCO2 | 22 mm Hg |
| PaO2 | 98 mm Hg |
Which of the following best characterizes this patient's primary acid-base disturbance(s)?
- AHigh anion gap metabolic acidosis with appropriate respiratory compensation
- Mixed high anion gap metabolic acidosis and primary respiratory alkalosisAnswer
- CMixed normal anion gap metabolic acidosis and primary respiratory alkalosis
- DPrimary respiratory alkalosis with appropriate metabolic compensation
- EMixed high anion gap metabolic acidosis and primary metabolic alkalosis
Answer
Mixed high anion gap metabolic acidosis and primary respiratory alkalosis
This patient has a mixed acid-base disorder characteristic of acute salicylate toxicity (indicated by tinnitus, nausea, and hyperventilation). Step 1: The anion gap is , confirming a high anion gap metabolic acidosis. Step 2: To check for appropriate respiratory compensation, Winter's formula is applied: . Step 3: The patient's measured PaCO2 is 22 mm Hg, which is lower than the expected 27-31 mm Hg range. This indicates an excessive respiratory drive beyond what is needed for compensation, signifying an independent primary respiratory alkalosis. Step 4: The delta-delta ratio is , which rules out any additional primary metabolic alkalosis or non-anion gap metabolic acidosis.
Step-by-Step Solution
Key Concept
Patients with salicylate toxicity typically present with a mixed high anion gap metabolic acidosis (due to uncoupling of oxidative phosphorylation) and a primary respiratory alkalosis (due to direct stimulation of the medullary respiratory center).