A 28-year-old woman at high altitude (4500 m) develops acute mountain sickness with headache, nausea, and mild dyspnea. Her ABG shows: pH 7.48, PaCO₂ 28 mmHg, PaO₂ 55 mmHg, HCO₃⁻ 20 mEq/L, SaO₂ 82%. Vital signs: RR 24/min, HR 110/min, BP 118/82 mmHg. She is conscious and alert. What is the most appropriate immediate management?

Explanation

## Acute Mountain Sickness (AMS) Pathophysiology **Key Point:** At high altitude, barometric pressure and FiO₂ both decrease, causing **hypoxemia** despite normal alveolar ventilation. The body compensates with hyperventilation, which lowers PaCO₂ and creates **respiratory alkalosis**. $$PaO₂ = (P_{atm} - P_{H_2O}) \times FiO₂ - \frac{PaCO_2}{RQ}$$ At 4500 m: P_{atm} ≈ 380 mmHg (vs. 760 at sea level), so even with hyperventilation, PaO₂ drops to 55 mmHg. ## ABG Interpretation | Parameter | Value | Interpretation | |-----------|-------|----------------| | pH | 7.48 | Respiratory alkalosis (hyperventilation response) | | PaCO₂ | 28 mmHg | Low (appropriate for altitude; hyperventilation) | | PaO₂ | 55 mmHg | Hypoxemia (altitude-induced) | | HCO₃⁻ | 20 mEq/L | Low (metabolic compensation) | | SaO₂ | 82% | Mild-moderate hypoxemia | **Clinical Pearl:** This is a **compensatory respiratory alkalosis** — the low PaCO₂ and HCO₃⁻ are the body's normal response to altitude, not pathology. The problem is the underlying **hypoxemia**. ## Mechanism of Acetazolamide ```mermaid flowchart TD A[High altitude → Hypoxemia]:::outcome --> B[Hyperventilation response]:::action B --> C[PaCO₂ falls, pH rises]:::outcome C --> D[Respiratory alkalosis blunts further ventilation]:::urgent D --> E[Acetazolamide blocks carbonic anhydrase]:::action E --> F[Bicarbonate excretion in urine]:::action F --> G[Metabolic acidosis develops]:::outcome G --> H[Acidosis stimulates ventilation]:::action H --> I[PaCO₂ falls further → PaO₂ rises]:::outcome I --> J[Improved oxygenation + acclimatization]:::action ``` **High-Yield:** Acetazolamide **lowers HCO₃⁻** by blocking carbonic anhydrase in the proximal tubule. This creates metabolic acidosis, which **stimulates the respiratory center** to hyperventilate even more, further lowering PaCO₂ and raising PaO₂. It also has a diuretic effect that reduces cerebral edema. ## Management Strategy for AMS **Key Point:** AMS is **mild-to-moderate altitude illness** (alert, conscious, no pulmonary/cerebral edema). Management is: 1. **Acetazolamide** 250 mg BD (prevents progression, accelerates acclimatization) 2. **Descent** to lower altitude (definitive treatment; reduces hypoxemia) 3. Rest and hydration 4. Avoid further ascent until symptoms resolve **Warning:** Do NOT use dexamethasone for AMS alone — it is reserved for **High Altitude Cerebral Edema (HACE)**, which presents with ataxia, confusion, and altered consciousness. This patient is alert and oriented. ## Why Each Distractor Fails | Option | Error | Outcome | |--------|-------|----------| | Supplemental O₂ + stay at altitude | Treats symptom, not cause; delays descent | Continued hypoxemia; risk of HACE/HAPE progression | | Dexamethasone + stay | Wrong drug for AMS; used for HACE/HAPE | Delays appropriate therapy; patient worsens | | Immediate descent alone | Omits acetazolamide; slower symptom relief | Unnecessary suffering; acetazolamide speeds recovery | [cite:Harrison 21e Ch 476; Robbins 10e Ch 4]