Correct Answer: D. Metabolic acidosis
This patient presents with metabolic acidosis secondary to hyperglycemia (350 mg/dL) with clinical signs of DKA (diabetic ketoacidosis). The discriminating ABG findings are: pH 7.2 (normal 7.35–7.45, indicating acidemia), HCO₃⁻ 10 mEq/L (normal 22–26, severely low), and pCO₂ 30 mmHg (normal 35–45, appropriately low). The low pCO₂ reflects appropriate respiratory compensation for metabolic acidosis—the respiratory system is hyperventilating to blow off CO₂ and raise pH. This is Kussmaul respiration, clinically evident as tachypnea. The mental confusion and tachypnea in the setting of severe hyperglycemia, low pH, and low HCO₃⁻ are classic for DKA, a medical emergency in India where diabetes prevalence is rising (IDF 2021: ~77 million Indians with diabetes). The primary disorder is metabolic acidosis; respiratory compensation is secondary and appropriate. Using the Winter formula: expected pCO₂ = 1.5 × HCO₃⁻ + (8 ± 2) = 1.5 × 10 + 8 ± 2 = 23 ± 2 = 21–25 mmHg. The observed pCO₂ of 30 is slightly higher than expected, suggesting a concurrent mild respiratory acidosis component, but the PRIMARY abnormality remains metabolic acidosis with appropriate (though slightly inadequate) respiratory compensation.
Why the other options are wrong
A. Respiratory acidosis — This is wrong because respiratory acidosis requires elevated pCO₂ (>45 mmHg) with low pH. Here, pCO₂ is 30 (LOW), not high. The low pCO₂ indicates the lungs are hyperventilating appropriately to compensate for metabolic acidosis, not causing it. Respiratory acidosis would be a secondary concern only if pCO₂ were rising despite metabolic acidosis—not the case here. B. Respiratory alkalosis — This is wrong because respiratory alkalosis requires elevated pH (>7.45) with low pCO₂. Although pCO₂ is low (30), the pH is 7.2 (acidemia, not alkalemia). The low pCO₂ is a compensatory response to metabolic acidosis, not the primary disorder. NBE may trap students who see 'low pCO₂' and reflexively choose respiratory alkalosis without checking the pH. C. Metabolic alkalosis — This is wrong because metabolic alkalosis requires elevated HCO₃⁻ (>26 mEq/L) with elevated pH (>7.45). Here, HCO₃⁻ is severely low at 10 (normal 22–26), and pH is 7.2 (acidemia). The clinical picture of hyperglycemia, Kussmaul respiration, and mental confusion is entirely inconsistent with alkalosis. This option may trap students unfamiliar with DKA presentation.
High-Yield Facts
- Metabolic acidosis is defined as pH <7.35 with HCO₃⁻ <22 mEq/L; DKA is a life-threatening cause in uncontrolled diabetes.
- Kussmaul respiration (deep, rapid breathing) is the clinical hallmark of metabolic acidosis—the body hyperventilates to blow off CO₂ and raise pH.
- Winter formula (expected pCO₂ = 1.5 × HCO₃⁻ ± 8 ± 2) helps identify concurrent respiratory disorders; deviation suggests dual pathology.
- DKA mortality in India remains 5–10% despite insulin availability, often due to delayed diagnosis and inadequate fluid/electrolyte management in rural settings.
- Anion gap in DKA is elevated (>12 mEq/L) due to accumulation of ketoacids (β-hydroxybutyrate, acetoacetate); calculate as Na⁺ − (Cl⁻ + HCO₃⁻).
Mnemonics
ABG Interpretation: pH First
- 1.Check pH (acidemia vs alkalemia). 2. Check HCO₃⁻ and pCO₂ direction. 3. If pH ↓ and HCO₃⁻ ↓ → metabolic acidosis. 4. Check pCO₂ for appropriate compensation. Use this in every ABG question—it prevents confusion between primary and compensatory disorders.
DKA Triad Hyperglycemia (>250 mg/dL), Ketoacidosis (pH <7.3, HCO₃⁻ <15), Kussmaul respiration (tachypnea). Remember: DKA = Diabetes + Ketones + Kussmaul. Helps recall the clinical constellation in exam stress.
NBE Trap
NBE pairs low pCO₂ with respiratory alkalosis to trap students who confuse compensatory hyperventilation with primary respiratory pathology. Always check pH first—low pCO₂ with low pH = metabolic acidosis with respiratory compensation, not respiratory alkalosis.
Clinical Pearl
In Indian emergency departments, DKA is often the first presentation of undiagnosed Type 2 diabetes in middle-aged men, especially in rural areas with poor glycemic screening. Recognition of Kussmaul respiration + confusion + hyperglycemia should trigger immediate ABG and serum ketones; delay in insulin and fluid therapy increases mortality risk significantly.
_Reference: Harrison Ch. 297 (Acid-Base Disorders); KD Tripathi Ch. 12 (Endocrine Pharmacology—DKA management); Park's Textbook of Preventive and Social Medicine (Diabetes epidemiology in India)_