High altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes above 2,500 meters. Risk factors include a rapid rate of ascent, a history of HAPE, respiratory infections, cold conditions, and certain cardiopulmonary abnormalities. The pathophysiology involves patchy pulmonary hypoxic vasoconstriction leading to overperfusion in some lung areas and increased capillary pressure, causing fluid to accumulate in the alveoli. Exercise and cold can also increase pulmonary pressures and contribute to HAPE. Prompt descent is needed to treat HAPE, as it remains a major cause of high-altitude related death.

1. HIGH ALTITUDE PULMONORY
EDEMA (HAPE)

2. LEARNING OBJECTIVES
•High altitude pulmonary edema (HAPE)
Risk factors
Pathophysiology

3. High Altitude Pulmonary Edema(HAPE)
• High-altitude pulmonary edema (HAPE) is a life-threatening form of non-
cardiogenic pulmonary edema.
• Occurs in otherwise healthy people at altitudes typically above 2,500 meters (8,200 ft).
• Cases have also been reported between 1,500–2,500 meters or 4,900–8,200 feet in
more vulnerable subjects.
• Classically, HAPE occurs in persons normally living at low altitude who travel to an
altitude above 2,500 meters (8,200 feet).
• Re-entry HAPE is also an entity that has been described in persons who normally live at
high altitude but who develop pulmonary edema after returning from a stay at low
altitude. It is severe presentation of altitude sickness.
• HAPE remains the major cause of death related to high-altitude.

4. Risk factors
• Rapid rate of ascent
• A history of HAPE
• Respiratory tract infections
• Excessively cold environmental conditions
• Men are more susceptible than women
• People with abnormalities of the
cardiopulmonary circulation leading to
pulmonary hypertension. For e.g. Mitral
stenosis, Primary pulmonary hypertension.
• Patent foramen ovale has also been shown to
increase the risk of HAPE

5. Pathophysiology
• HAPE is characterized by patchy pulmonary
hypoxic vasoconstriction that leads to
overperfusion in some areas.
• This in turn to increased pulmonary capillary
pressure (>18 mmHg) and capillary “stress”
failure.
• The exact mechanism for this hypoxic
vasoconstriction is unknown.
• Endothelial dysfunction due to hypoxia may play
a role by impairing the release of nitric oxide.
• Exercise and cold lead to increased pulmonary
intravascular pressure and may cause HAPE

6. • Hypoxia triggered increase in sympathetic
drive may lead to pulmonary
venoconstriction and extravasation into
the alveoli.
• Inflammatory processes such as those
elicited by a viral respiratory infection are
shown to cause HAPE.
• impaired transepithelial clearance of
sodium and water from the alveoli.

7. References
• Harrisons Principles of Internal Medicine, Volume 1. 21st edition.
P3623-3626.
• https://www.uptodate.com/contents/high-altitude-pulmonary-
edema#H2

8. Acknowledgement
• I gratefully acknowledge my teachers Dr. Mukesh Bairwa and Dr. Bimlesh
for their valuable guidance, suggestions and support in preparing this
presentation.