High-Altitude Pulmonary Edema
High-Altitude Pulmonary Edema (HAPE) FAQs – NEET-SS InfoBits
Basics
1. What is High-Altitude Pulmonary Edema (HAPE)?
A life-threatening non-cardiogenic pulmonary edema caused by hypoxia at high altitude.
2. At what altitude does HAPE usually occur?
Typically above 2500–3000 m.
3. What is the main pathophysiological mechanism of HAPE?
Uneven hypoxic pulmonary vasoconstriction causing pulmonary hypertension and capillary leak.
4. Is HAPE cardiogenic or non-cardiogenic?
It is non-cardiogenic pulmonary edema.
5. What is the pulmonary capillary wedge pressure (PCWP) in HAPE?
Normal, distinguishing it from cardiogenic edema.
Clinical Features
6. When do HAPE symptoms usually appear after ascent?
Typically 2–5 days after rapid ascent.
7. What is the earliest symptom of HAPE?
Dyspnea on exertion.
8. What respiratory symptoms occur in advanced HAPE?
Dyspnea at rest, cough, pink frothy sputum, and severe hypoxemia.
9. What are common examination findings in HAPE?
Tachypnea, tachycardia, crackles, and low oxygen saturation.
10. Which lung region often shows earliest crackles?
Right middle lobe region.
Pathophysiology
11. What vascular response triggers HAPE?
Hypoxic pulmonary vasoconstriction.
12. Why is pulmonary edema patchy in HAPE?
Because pulmonary vasoconstriction is heterogeneous across lung regions.
13. What happens to pulmonary artery pressure in HAPE?
It becomes markedly elevated.
14. What type of fluid accumulates in HAPE?
Protein-rich edema fluid due to capillary stress failure.
15. Does inflammation play a primary role in HAPE?
No, HAPE is primarily hemodynamic rather than inflammatory.
Risk Factors
16. What is the strongest risk factor for HAPE?
Previous history of HAPE.
17. Which ascent pattern increases HAPE risk?
Rapid ascent without acclimatization.
18. Does strenuous exercise increase HAPE risk?
Yes, especially during early altitude exposure.
19. Which environmental factor worsens HAPE risk?
Cold exposure.
20. Are young individuals more susceptible to HAPE?
Yes, particularly young healthy males.
Diagnosis
21. What is the typical chest X-ray finding in HAPE?
Patchy alveolar infiltrates with normal heart size.
22. How does chest CT appear in HAPE?
Patchy ground-glass opacities and consolidation.
23. What oxygen saturation finding suggests HAPE?
Severe hypoxemia disproportionate to altitude.
24. What scoring system is used for high-altitude illness diagnosis?
Lake Louise Scoring System.
25. What distinguishes HAPE from pneumonia radiologically?
HAPE shows patchy infiltrates without consolidation pattern or fever.
Treatment
26. What is the most important treatment for HAPE?
Immediate descent to lower altitude.
27. How much descent is usually recommended?
At least 500–1000 meters.
28. What oxygen saturation should be targeted during treatment?
SpO₂ above 90%.
29. Which drug is first-line pharmacologic therapy?
Nifedipine.
30. Why is nifedipine used in HAPE?
It reduces pulmonary artery pressure by vasodilation.
Advanced Management
31. Which PDE-5 inhibitors can treat HAPE?
Sildenafil or tadalafil.
32. What steroid may be used adjunctively in altitude illness?
Dexamethasone.
33. What portable device can simulate descent?
The Gamow portable hyperbaric bag.
34. Is diuretic therapy routinely recommended in HAPE?
No, because HAPE is not caused by fluid overload.
35. Can mechanical ventilation be required in severe HAPE?
Yes, in life-threatening respiratory failure.
Prevention
36. What is the safest ascent rate above 3000 m?
Increase sleeping altitude ≤500 m per day.
37. How often should rest days be taken during ascent?
Every 3–4 days.
38. Which drug prevents Acute Mountain Sickness but not primarily HAPE?
Acetazolamide.
39. Which drug is recommended for HAPE prophylaxis in susceptible individuals?
Nifedipine sustained release.
40. What is the single most effective preventive strategy for HAPE?
Gradual acclimatization during ascent.
