title: Update: High altitude pulmonary edema.
abstract: Recent high altitude studies with pulmonary artery (PA) catheterization and broncho-alveolar lavage (BAL) in early high altitude pulmonary edema(HAPE) have increased our understanding of the pathogenetic sequence in HAPE. High preceding PA and pulmonary capillary pressures lead to a non-inflammatory leak of the alveolar-capillary barrier with egress of red cells, plasma proteins and fluid into the alveolar space. The mechanisms accounting for an increased capillary pressure remain speculative. The concept that hypoxic pulmonary vasoconstriction (HPV) is uneven so that regions with less vasoconstriction are over-perfused and become edematous remains compelling but unproved. Also uncertain is the role and extent of pulmonary venoconstriction. With disruption of the normal alveolar-capillary barrier, some individuals may later develop a secondary inflammatory reaction. A high incidence of preceding or concurrent respiratory infection in children with HAPE has been used to support a causative role of inflammation in HAPE. However, alternatively even mild HPV may simply lower the threshold at which inflammation-mediated increases in alveolar capillary permeability cause significant fluid flux into the lung. Other major questions to be addressed in future research are: 1.) What is the mechanism of exaggerated hypoxic pulmonary vasoconstriction? Is there a link to primary pulmonary hypertension? Several observations suggest that susceptibility to HAPE is associated with endothelial dysfunction in pulmonary vessels. This has not yet been studied adequately. 2.) What is the nature of the leak? Is there structural damage, i. e. stress failure, or does stretch cause opening of pores? 3.) What is the pathophysiologic significance of a decreased sodium and water clearance across alveolar epithelial cells in hypoxia? 4.) What is the role of exercise? Do HAPE-susceptible individuals develop pulmonary edema when exposed to hypoxia without exercise? Answers to these questions will increase our understanding of the pathophysiology of HAPE and also better focus research on the genetic basis of susceptibility to HAPE.
authors.affiliation: Department of Internal Medicine, University of Heidelberg, Germany.
authors.forename: P
authors.initials: P
authors.lastname: Bärtsch
authors.forename: E R
authors.initials: ER
authors.lastname: Swenson
authors.forename: M
authors.initials: M
authors.lastname: Maggiorini
mesh_terms: D000532:Altitude Sickness / Q000276:immunology / Q000503:physiopathology*; D000818:Animals; D001794:Blood Pressure; D002196:Capillaries / Q000503:physiopathology*; D006801:Humans; D011654:Pulmonary Edema / Q000276:immunology / Q000503:physiopathology*