A 58-year-old man with chronic obstructive pulmonary disease (COPD) presents to the emergency department with acute dyspnea and altered mental status. His wife reports he has been increasingly somnolent over the past 3 days. On examination, he is cyanotic and has pursed-lip breathing. Arterial blood gas analysis shows: pH 7.28, PaCO₂ 72 mmHg, HCO₃⁻ 32 mEq/L, PaO₂ 48 mmHg. What is the primary acid-base disturbance?

Explanation

## Acid-Base Interpretation ### Step 1: Identify the pH - pH = 7.28 → **Acidemia** (normal: 7.35–7.45) ### Step 2: Determine the primary process - **PaCO₂ = 72 mmHg** (elevated; normal: 35–45) → respiratory component is causing acidemia - **HCO₃⁻ = 32 mEq/L** (elevated; normal: 22–26) → metabolic component is **compensatory** ### Step 3: Assess appropriateness of compensation Using **Winter's formula** for expected respiratory compensation in metabolic acidosis (not applicable here since pH is low due to respiratory cause): For respiratory acidosis, the kidney compensates by retaining HCO₃⁻. An HCO₃⁻ of 32 is appropriately elevated for a PaCO₂ of 72, indicating the kidneys are attempting to buffer the acidosis. **Key Point:** - The **primary disturbance is respiratory acidosis** (elevated PaCO₂ causing low pH) - The **secondary (compensatory) response is metabolic** (kidneys increase HCO₃⁻ reabsorption) - This is consistent with acute-on-chronic COPD exacerbation: acute CO₂ retention superimposed on chronic respiratory disease ### Clinical Correlation **High-Yield:** In COPD exacerbations, hypercapnia (elevated PaCO₂) with altered mental status indicates **CO₂ narcosis** — a medical emergency requiring urgent respiratory support (non-invasive ventilation or intubation). **Clinical Pearl:** The presence of both acidemia (pH 7.28) AND elevated HCO₃⁻ (32) is pathognomonic for **respiratory acidosis with metabolic compensation**. If only metabolic acidosis were present, HCO₃⁻ would be LOW, not high.