In a patient with serum glucose 400 mg/dL, sodium 144 mEq/L, chloride 113 mEq/L, pH 7.38, partial pressure of carbon dioxide (pCO₂) (value not shown), and bicarbonate (HCO₃⁻) 11 mEq/L, what is the acid‑base disturbance?

Acid-Base Interpretation: Mixed Metabolic Acidosis and Respiratory Alkalosis

This patient has a primary disorder combining metabolic acidosis and respiratory alkalosis (answer d). The pH of 7.38 is deceptively normal because two opposing primary processes are offsetting each other—not because compensation has normalized the pH.

Diagnostic Reasoning

The key to this diagnosis is recognizing that a bicarbonate of 11 mEq/L is severely abnormal and cannot represent simple compensation. 1

Why This Is NOT Simple Compensation

• In pure metabolic acidosis with HCO₃⁻ of 11 mEq/L, the expected compensatory pCO₂ would be approximately 24-26 mmHg (using Winter's formula: expected pCO₂ = 1.5 × [HCO₃⁻] + 8 ± 2). 2
• If the actual pCO₂ is significantly lower than 24 mmHg, this indicates a concurrent primary respiratory alkalosis driving down the CO₂ beyond what metabolic compensation alone would achieve. 1
• The near-normal pH (7.38) with such a low bicarbonate strongly suggests two primary processes canceling each other out. 3

Calculating the Anion Gap

• Anion gap = Na⁺ - (Cl⁻ + HCO₃⁻) = 144 - (113 + 11) = 20 mEq/L, which is elevated (normal 10-12 mEq/L). 1, 2
• The elevated anion gap with glucose of 400 mg/dL points toward diabetic ketoacidosis as the source of the metabolic acidosis. 4, 5

Why This Is Diabetic Ketoacidosis (But Not ONLY DKA)

While this patient clearly has DKA based on the hyperglycemia and high anion gap metabolic acidosis, answer (e) is incomplete because it fails to account for the respiratory component. 4

• DKA diagnostic criteria include glucose >250 mg/dL, pH <7.3, and bicarbonate <15 mEq/L with positive ketones. 4, 5
• However, this patient's pH is 7.38, not <7.3, because a concurrent respiratory alkalosis is elevating the pH above what DKA alone would produce. 4, 1
• The bicarbonate of 11 mEq/L indicates moderate-to-severe DKA (moderate DKA: HCO₃⁻ 10-15 mEq/L; severe DKA: HCO₃⁻ <10 mEq/L). 4

Clinical Implications

This mixed disorder is common in DKA patients who are hyperventilating excessively—either from Kussmaul respirations that overshoot the expected compensation, or from concurrent processes like sepsis, pain, or anxiety. 5, 2

Management Priorities

• Treat the underlying DKA with insulin therapy (0.1 units/kg/h continuous IV infusion after a priming dose) and aggressive fluid resuscitation (15-20 mL/kg/h isotonic saline in the first hour). 4
• Monitor venous pH and anion gap every 2-4 hours to track resolution; arterial blood gases are generally unnecessary once the diagnosis is established. 4, 1
• Bicarbonate therapy is NOT indicated in this patient because the pH is 7.38 (>7.0); bicarbonate may be beneficial only when pH <6.9. 4, 6
• Add potassium supplementation (20-30 mEq/L to IV fluids) once serum K⁺ is confirmed >3.3 mEq/L, as insulin therapy and alkalinization will drive potassium intracellularly. 4

Common Pitfalls

• Do not assume the near-normal pH means "no acid-base imbalance" (answer a is wrong)—a bicarbonate of 11 mEq/L is never normal. 1
• Do not misinterpret this as simple metabolic acidosis with respiratory compensation (answer b is wrong)—the degree of hyperventilation exceeds expected compensation. 1, 2
• Do not diagnose respiratory alkalosis with metabolic compensation (answer c is wrong)—the primary problem is the high anion gap acidosis from DKA, not primary hyperventilation. 1
• Recognize that resolution criteria for DKA include glucose <200 mg/dL, bicarbonate ≥18 mEq/L, and venous pH ≥7.3—this patient has not yet met these targets. 4