Physiological aspects of high-altitude pulmonary edema.

  title={Physiological aspects of high-altitude pulmonary edema.},
  author={Peter B{\"a}rtsch and Heimo Mairb{\"a}url and Marco Maggiorini and Erik R. Swenson},
  journal={Journal of applied physiology},
  volume={98 3},
High-altitude pulmonary edema (HAPE) develops in rapidly ascending nonacclimatized healthy individuals at altitudes above 3,000 m. An excessive rise in pulmonary artery pressure (PAP) preceding edema formation is the crucial pathophysiological factor because drugs that lower PAP prevent HAPE. Measurements of nitric oxide (NO) in exhaled air, of nitrites and nitrates in bronchoalveolar lavage (BAL) fluid, and forearm NO-dependent endothelial function all point to a reduced NO availability in… 

Figures and Tables from this paper

High altitude pulmonary edema: A pressure-induced leak

Hypoxic Lung

  • Medicine
  • 2006
The evidence for this chain of events is that high pulmonary arterial pressure precedes HAPE, reduction in pulmonary arterIAL pressure by any means is effective therapy, and HAPE-susceptible people have very strong pulmonary vascular responses to hypoxia and exercise.

High altitude pulmonary edema-clinical features, pathophysiology, prevention and treatment

Slow descent is the most effective method for prevention; in addition, graded ascent and time for acclimatization, low sleeping altitudes, avoidance of alcohol and sleeping pills, and avoidance of exercise are the key to preventing HAPE.

Pulmonary Hypertension in Acute and Chronic High Altitude Maladaptation Disorders

A literature review on the role of pulmonary hypertension in the pathogenesis of acute and chronic high altitude maladaptation disorders and current knowledge regarding potential treatment options is provided.

Exaggerated hypoxic pulmonary vasoconstriction without susceptibility to high altitude pulmonary edema.

An exaggerated HPV cannot be considered a surrogate maker for HAPE-susceptibility although excessively elevated PAP is a hallmark in HAPE, while a normal HPV appears to protect from HAPE in this study.

New insights of aquaporin 5 in the pathogenesis of high altitude pulmonary edema

Deletion of AQP5 slightly increased lung edema and lung injury compared to wildtype mice during HAPE development, which suggested that the AQP 5 plays an important role in HAPE formation induced by high altitude simulation.

Hypoxic Lung Whiteout: Further Clearing but More Questions from on High

The evidence for this chain of events is that high pulmonary arterial pressure precedes HAPE, reduction in pulmonary arterIAL pressure by any means is effective therapy, and HAPE-susceptible people have very strong pulmonary vascular responses to hypoxia and exercise.

Does High Alveolar Fluid Reabsorption Prevent HAPE in Individuals with Exaggerated Pulmonary Hypertension in Hypoxia?

Results show low nasal ion transport in HAPE but higher transport in those individuals with the highest HPV but without HAPE, indicating that in some individuals with high PAsP at high altitude high alveolar fluid reabsorption might protect them from HAPE.



High-Altitude Pulmonary Edema Is Initially Caused by an Increase in Capillary Pressure

HAPE is initially caused by an increase in pulmonary capillary pressure, and the pulmonary transcapillary escape of radiolabeled transferrin increased slightly from low to high altitude in the HAPE-susceptible subjects but remained within the limits of normal and did not differ significantly from the control subjects.

Update: High altitude pulmonary edema.

Questions to be addressed in future research will increase the understanding of the pathophysiology of HAPE and also better focus research on the genetic basis of susceptibility to HAPE.

High-altitude pulmonary edema: from exaggerated pulmonary hypertension to a defect in transepithelial sodium transport.

High-altitude pulmonary edema (HAPE) is a form of lung edema which occurs in otherwise healthy subjects, thereby allowing the study of underlying mechanisms of pulmonary edema in the absence of

Exhaled nitric oxide in high-altitude pulmonary edema: role in the regulation of pulmonary vascular tone and evidence for a role against inflammation.

Reduced exhaled NO may be related to altered pulmonary NO synthesis and/or transport and clearance, and the data in this study could be consistent with the novel concept that in HAPE-prone subjects, a defect in pulmonary epithelial NO synthesis may contribute to exaggerated hypoxic pulmonary vasoconstriction and in turn to pulmonary edema.

Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor.

Early HAPE is characterized by high pulmonary artery pressures that lead to a protein-rich and mildly hemorrhagic edema, with normal levels of leukocytes, cytokines, and eicosanoids, with no differences in BAL fluid total leukocyte counts between resistant and susceptible subjects or between counts taken at low and high altitudes.

Hypoxia decreases exhaled nitric oxide in mountaineers susceptible to high-altitude pulmonary edema.

The data provide the first evidence of decreased pulmonary NO production in HAPE-susceptible subjects during acute hypoxia that may contribute among other factors to their enhanced hypoxic pulmonary vascular response.

The lung at high altitude: bronchoalveolar lavage in acute mountain sickness and pulmonary edema.

It is hypothesized that acute mountain sickness in which gas exchange is impaired to a milder degree is a precursor to HAPE, and BAL with 0.89% NaCl by fiberoptic bronchoscopy was performed on Mt. McKinley to evaluate the cellular and biochemical responses of the lung at high altitude.

Abnormal Circulatory Responses to High Altitude in Subjects with a Previous History of High‐Altitude Pulmonary Edema

In five men with a history of susceptibility to high-altitude pulmonary edema (HAPE), hemodynamics and pulmonary gas exchange were measured at sea level, and again 24 hours following ascent to an

Exaggerated endothelin release in high-altitude pulmonary edema.

These findings suggest that in HAPE-susceptible mountaineers, an augmented release of the potent pulmonary vasoconstrictor peptide endothelin-1 and/or its reduced pulmonary clearance could represent one of the mechanisms contributing to exaggerated pulmonary hypertension at high altitude.

Inhaled nitric oxide for high-altitude pulmonary edema.

The inhalation of nitric oxide improves arterial oxygenation in high-altitude pulmonary edema, and this beneficial effect may be related to its favorable action on the distribution of blood flow in the lungs.