Update: High altitude pulmonary edema

Bärtsch, Peter; Swenson, Erik R.; Maggiorini, Marco

doi:10.1007/978-1-4757-3401-0_8

Cited by 42 publications

(20 citation statements)

References 47 publications

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“…The observation that inhaled NO did not completely normalize PAP in HAPE-susceptible individuals, but did so in those resistant to HAPE (5,16), indicates that impaired NO synthesis cannot fully account for the excessive pulmonary vascular reactivity in HAPE-prone subjects. It is likely that additional factors, such as increased sympathetic activity or other vasoconstrictors such as angiotensin II (15), endothelin (93), or arachadonic acid metabolites (98) contribute to the increased PAP in HAPE-susceptible subjects.…”

Section: Mechanisms Accounting For Enhanced Hpvmentioning

confidence: 97%

Physiological aspects of high-altitude pulmonary edema

Bärtsch

Mairbäurl²,

Maggiorini³

et al. 2005

Journal of Applied Physiology

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302

217

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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 hypoxia as a major cause of the excessive hypoxic PAP rise in HAPE-susceptible individuals. Studies using right heart catheterization or BAL in incipient HAPE have demonstrated that edema is caused by an increased microvascular hydrostatic pressure in the presence of normal left atrial pressure, resulting in leakage of large-molecular-weight proteins and erythrocytes across the alveolarcapillary barrier in the absence of any evidence of inflammation. These studies confirm in humans that high capillary pressure induces a high-permeability-type lung edema in the absence of inflammation, a concept first introduced under the term "stress failure." Recent studies using microspheres in swine and magnetic resonance imaging in humans strongly support the concept and primacy of nonuniform hypoxic arteriolar vasoconstriction to explain how hypoxic pulmonary vasoconstriction occurring predominantly at the arteriolar level can cause leakage. This compelling but as yet unproven mechanism predicts that edema occurs in areas of high blood flow due to lesser vasoconstriction. The combination of high flow at higher pressure results in pressures, which exceed the structural and dynamic capacity of the alveolar capillary barrier to maintain normal alveolar fluid balance. pulmonary artery pressure; hypoxic pulmonary vasoconstriction; nitric oxide; inflammation; alveolar fluid clearance; pathophysiology; review CLINICAL PICTUREHigh-altitude pulmonary edema (HAPE) is noncardiogenic pulmonary edema that usually occurs at altitudes above 3,000 m in rapidly ascending nonacclimatized individuals within the first 2-5 days after arrival. It may also occur in high-altitude dwellers who return from sojourns at low altitude. The first medical description of HAPE was published in Peru and recognized the latter form, also called reentry HAPE, as a pulmonary edema associated with electrographic signs of right ventricular overload (67). The first cases of HAPE in unacclimatized lowlanders climbing to high altitude were reported from the Rocky Mountains (53). The two forms very probably share the same pathophysiology.The reader is referred to other reviews (9,41,96,97) for an extensive presentation of the clinical picture. In this review, we point out some particular characteristics that might elucidate the underlying pathophysiology and are revealed by classical and newly evolving pathophysiological concepts.The prevalence of HAPE depends on the degree of susceptibility, the rate of ascent, and the final altitude. At an altitude of 4,500 m, the prevalence may ...

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Section: Mechanisms Accounting For Enhanced Hpvmentioning

confidence: 97%

Physiological aspects of high-altitude pulmonary edema

Bärtsch

Mairbäurl²,

Maggiorini³

et al. 2005

Journal of Applied Physiology

Self Cite

302

217

View full text Add to dashboard Cite

show abstract

“…It has been well demonstrated that hypoxia at high altitude is responsible for an increase in the risk of acute mountain sickness [4,5]. In this regard, Goerre et al [6] reported that the degree of hypoxiainduced acute pulmonary hypertension was associated with increased plasma endothelin-1 (ET-1) levels in healthy mountaineers.…”

Section: Introductionmentioning

confidence: 99%

Vascular reactivity and biomarkers of endothelial function in healthy subjects exposed to acute hypobaric hypoxia

Iglesias

Rosso

Vainstein

et al. 2015

Clinical Biochemistry

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“…1,2 The increased venular tone with increased capillary pressure that follows rapid ascent to high altitude without adequate acclimatization 3 may contribute to force liquid across the endothelial barrier into the interstitial space, which may contribute to respiratory problems in this condition. Because tens of thousands of tourists travel to a variety of high-altitude destinations around the world on a yearly basis, the search for new strategies to prevent and treat high-altitude-induced pulmonary hypertension is now considered a priority.…”

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confidence: 99%

Role of Endothelin-1 in Exposure to High Altitude

et al. 2006

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Background-The degree of pulmonary hypertension in healthy subjects exposed to acute hypobaric hypoxia at high altitude was found to be related to increased plasma endothelin (ET)-1. The aim of the present study was to investigate the effects of ET-1 antagonism on pulmonary hypertension, renal water, and sodium balance under acute and prolonged exposure to high-altitude-associated hypoxia. Methods and Results-In a double-blind fashion, healthy volunteers were randomly assigned to receive bosentan (62.5 mg for 1 day and 125 mg for the following 2 days; nϭ10) or placebo (nϭ10) at sea level and after rapid ascent to high altitude (4559 m). At sea level, bosentan did not induce any significant changes in hemodynamic or renal parameters. At altitude, bosentan induced a significant reduction of systolic pulmonary artery pressure (21Ϯ7 versus 31Ϯ7 mm Hg, PϽ0.03) and a mild increase in arterial oxygen saturation versus placebo after just 1 day of treatment. However, both urinary volume and free water clearance (H 2 OCl/glomerular filtration rate) were significantly reduced versus placebo after 2 days of ET-1 antagonism (1100Ϯ200 versus 1610Ϯ590 mL; Ϫ6.7Ϯ3.5 versus Ϫ1.8Ϯ4.8 mL/min, PϽ0.05 versus placebo for both). Sodium clearance and segmental tubular function were not significantly affected by bosentan administration. Conclusions-The present results indicate that the early beneficial effect of ET-1 antagonism on pulmonary blood pressure is followed by an impairment in volume adaptation. These findings must be considered for the prevention and treatment of acute mountain sickness.

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Update: High altitude pulmonary edema

Cited by 42 publications

References 47 publications

Physiological aspects of high-altitude pulmonary edema

Physiological aspects of high-altitude pulmonary edema

Vascular reactivity and biomarkers of endothelial function in healthy subjects exposed to acute hypobaric hypoxia

Role of Endothelin-1 in Exposure to High Altitude

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