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High altitude pulmonary edema: hemodynamic aspects

¹Division of Cardiovascular Medicine, VA Palo Alto Health Care System, USA.

International Journal of Sports Medicine

|January 1, 1997

Summary

High altitude pulmonary edema (HAPE) is caused by pulmonary circulation issues, not heart failure. Hypoxic vasoconstriction leads to increased pulmonary artery pressure and capillary leakage, causing HAPE.

Area of Science:

Cardiovascular Physiology
Pulmonary Medicine
Altitude Sickness Research

Background:

Hemodynamic studies over 30 years ago shifted focus from left ventricular failure to pulmonary circulation in high altitude pulmonary edema (HAPE).
Acute HAPE stages show normal pulmonary artery wedge pressure but elevated pulmonary artery pressure, low cardiac output, and severe arterial unsaturation.

Purpose of the Study:

To elucidate the hemodynamic mechanisms underlying high altitude pulmonary edema (HAPE).
To investigate the role of hypoxic pulmonary vasoconstriction and capillary injury in HAPE pathogenesis.

Main Methods:

Analysis of hemodynamic and physiological data from patients with acute high altitude pulmonary edema (HAPE).
Review of supporting animal and clinical studies, including cases of pulmonary embolism and arterial interventions.

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Main Results:

Elevated pulmonary arteriolar resistance and non-uniform hypoxic pulmonary vasoconstriction were observed.
Overperfusion of patent vessels led to increased pulmonary artery pressure transmission to capillaries, causing injury and leakage.
Thrombi in pulmonary vessels may contribute to severe HAPE cases.

Conclusions:

Hypoxic pulmonary vasoconstriction is a primary driver of HAPE, leading to increased pulmonary artery pressure and capillary stress.
Capillary injury and increased permeability, exacerbated by flow and pressure, are crucial for edema formation in HAPE.
The understanding of HAPE mechanisms is supported by diverse physiological, animal, and clinical evidence.