Patchy Vasoconstriction Versus Inflammation: A Debate in the Pathogenesis of High Altitude Pulmonary Edema
| Autor: | Jeevan Gautam, Nusrat Jahan, Amer Alaref, Rajan Sharma Kandel, Rohi Mishra, Abdallah Hassan |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Orthopnea
medicine.medical_specialty Pulmonology Inflammation 030204 cardiovascular system & hematology 03 medical and health sciences 0302 clinical medicine Internal medicine medicine.artery Hypoxic pulmonary vasoconstriction High-altitude pulmonary edema Internal Medicine Pathology medicine genetics pathophysiology Altitude sickness business.industry patchy vasoconstriction General Engineering altitude sickness medicine.disease Pathophysiology Blood pressure inflammation Pulmonary artery Cardiology high altitude pulmonary edema medicine.symptom business 030217 neurology & neurosurgery |
| Zdroj: | Cureus |
| ISSN: | 2168-8184 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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