Abstract
High altitude pulmonary edema (HAPE) occurs in individuals rapidly ascending at altitudes greater than 2,500 m within one week of arrival. HAPE is characterized by orthopnea, breathlessness at rest, cough, and pink frothy sputum. Several mechanisms to describe the pathophysiology of HAPE have been proposed in different kinds of literature where most of the mechanisms are reported to be activated before a drop in oxygen saturation levels. The majority of the current studies favor diffuse hypoxic pulmonary vasoconstriction (HPV) as a pathophysiological basis for HAPE. However, some of the studies described inflammation in the lungs and genetic basis as the pathophysiology of HAPE. So, there is a major disagreement regarding the exact pathophysiology of HAPE in the current literature, which raises a question as to what is the exact pathophysiology of HAPE. So, we reviewed 23 different articles which include clinical trials, review articles, randomized controlled trials (RCTs), and original research published from 2010 to 2020 to find out widely accepted pathophysiology of HAPE. In our study, we found out sympathetic stimulation, reduced nitric oxide (NO) bioavailability, increased endothelin, increased pulmonary artery systolic pressure (PASP) resulting in diffuse HPV, and reduced reabsorption of interstitial fluid to be the most important determinants for the development of HAPE. Similarly, with the evaluation of the role of inflammatory mediators like C-reactive protein (CRP) and interleukin (IL-6), we found out that inflammation in the lungs seems to modulate but not cause the process of development of HAPE. Genetic basis as evidenced by increased transcription of certain gene products seems to be another promising hypoxic change leading to HAPE. However, comprehensive studies are still needed to decipher the pathophysiology of HAPE in greater detail.
Highlights
BackgroundHigh altitude pulmonary edema (HAPE), which is a non-cardiogenic pulmonary edema [1], usually occurs in rapidly ascending non-acclimatized healthy individuals above 2,500 to 3,000 meters [2, 3]
We found out sympathetic stimulation, reduced nitric oxide (NO) bioavailability, increased endothelin, increased pulmonary artery systolic pressure (PASP) resulting in diffuse hypoxic pulmonary vasoconstriction (HPV), and reduced reabsorption of interstitial fluid to be the most important determinants for the development of HAPE
This study suggested that increased vascular resistance and pulmonary artery systolic pressure (PASP) at HA decreases pulmonary NO bioavailability due to free radical formation
Summary
BackgroundHigh altitude pulmonary edema (HAPE), which is a non-cardiogenic pulmonary edema [1], usually occurs in rapidly ascending non-acclimatized healthy individuals above 2,500 to 3,000 meters [2, 3]. Military deployment worldwide in high-altitude (HA) areas and decreased time of acclimatization due to air transport account for the increasing incidence of HAPE [5]. HAPE can develop within hours to days, typically within the first week after arrival at high altitude [3, 6]. It presents with weakness, dyspnea, and dry cough with exertion which progresses to dyspnea at rest, rales, cyanosis, and pink-frothy sputum [7]. HAPE is the most common cause of high-altitude related deaths [8], accounting for up to 50% mortality in untreated conditions [7]. Apart from hypoxia, other factors like ventilatory control, activation of the sympathetic nervous system, endothelial function, reabsorption of sodium, and water from alveolar epithelium likely increase HAPE susceptibility [2]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
