scholarly journals A hypothesis study on a four-period prevention model for high altitude disease

2018 ◽  
Vol 5 (1) ◽  
Author(s):  
Xian-Sheng Liu ◽  
Xiang-Rong Yang ◽  
Lu Liu ◽  
Xian-Kui Qin ◽  
Yu-Qi Gao
Keyword(s):  
High Altitude ◽  
Prevention Model ◽  
High Altitude Disease

scholarly journals High-altitude Pulmonary Edema in Emergency Department: A Review

2021 ◽  
pp. 113-118
Author(s):  
Hisham Mohammed Sonbul ◽  
Abdu Saleh Alwadani ◽  
Bader Aziz Alharbi ◽  
D. Almaymuni, Saleh Mohammed ◽  
Abdulrazaq Abdulmohsen Alkhalaf ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Supplemental Oxygen ◽  
Severe Form ◽  
Physical Effort ◽  
Disease Etiology ◽  
Salt Consumption ◽  
Pulmonary Vasodilator ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Disease

High altitude pulmonary Edema (HAPE) is a severe form of high-altitude disease that, if left untreated, can result in death in up to half of those who are affected. Lowlanders who rapidly go to elevations more than 2500-3000 m are more likely to develop high altitude pulmonary Edema (HAPE). Individual sensitivity owing to a low hypoxic ventilatory response (HVR), quick pace of climb, male sex, usage of sleep medicine, high salt consumption, chilly ambient temperature, and intense physical effort are all risk factors. HAPE may be totally and quickly reversed if caught early and correctly treated. Slow climb is the most effective technique of prevention. A fall of at least 1000 meters, is the best and most certain treatment choice in HAPE. Supplemental oxygen, portable hyperbaric chambers, and pulmonary vasodilator medications (nifedipine and phosphodiesterase-5 inhibitors) may be beneficial. In this article we’ll be looking at the disease etiology, epidemiology, diagnosis and management.

scholarly journals To compare the incomparable: COVID-19 pneumonia and high-altitude disease

2020 ◽  
Vol 55 (6) ◽  
pp. 2001362 ◽  
Author(s):  
Giacomo Strapazzon ◽  
Matthias P. Hilty ◽  
Pierre Bouzat ◽  
Lorenza Pratali ◽  
Hermann Brugger ◽  
...  
Keyword(s):  
High Altitude ◽  
High Altitude Disease

scholarly journals 293 Use of reaction norms to evaluate high altitude disease susceptibility in Angus sires.

2018 ◽  
Vol 96 (suppl_3) ◽  
pp. 110-111
Author(s):  
M Sánchez-Castro ◽  
T Holt ◽  
M Thomas ◽  
R Enns ◽  
S Speidel
Keyword(s):  
High Altitude ◽  
Disease Susceptibility ◽  
Reaction Norms ◽  
High Altitude Disease

Medical Continuing Education: Reform of Teaching Methods about High Altitude Disease in China

2013 ◽  
Vol 14 (2) ◽  
pp. 181-182 ◽  
Author(s):  
Yongjun Luo ◽  
Qiquan Zhou ◽  
Jianjun Huang ◽  
Rong Luo ◽  
Xiaohong Yang ◽  
...  
Keyword(s):  
Education Reform ◽  
Continuing Education ◽  
High Altitude ◽  
Teaching Methods ◽  
High Altitude Disease

DPOAEs in High Altitude Disease at Mount Everest

2008 ◽  
Vol 139 (2_suppl) ◽  
pp. P54-P54
Author(s):  
Axel Rolf Behnisch ◽  
Gerd Rasp ◽  
Klaus Mees
Keyword(s):  
Oxygen Saturation ◽  
Intracranial Hypertension ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Measurement Data ◽  
Blood Oxygen ◽  
Mount Everest ◽  
Blood Oxygen Saturation ◽  
Distortion Product ◽  
High Altitude Disease

Objective The aim of this study was to measure DPOAEs in climbers on Mount Everest as a criterion for differential diagnosis of high altitude disease. The levels of distortion product otoacoustic emissions (DPOAEs) change at frequencies between 0,75 kHz and 1,5 kH along with intracranial pressure (ICP). DPOAEs are suggested for monitoring ICP changes. Methods In order to determine the etiology of DPOAE-level changes obtained in 6 climbers with severe acute mountain sickness, blood oxygen saturation was measured simultaneously, and a standard request form of Lake-Louis symptoms of high altitude disease was filled in with every DPOAE measurement. Data are presented from DPOAE measurements at frequencies of 1, 1.5, 2, 3 and 4 kHz during an ascent to Mount Everest (8848 m) up to an altitude of 7800 m. Results In all climbers, DPOA levels decreased at 4 kHz and 3 kHz with declining oxygen saturation (SaO2) at high altitude. That has been described in many prior animal studies. On the other hand, DPOAE at 1 kHz showed decreasing levels only with symptoms of high altitude disease (AMS). In one climber with severe symptoms of intracranial hypertension after the ascent to the high camp at 7800 m, decreasing DPOAE levels at 1 kHz were measured in the absence of declining blood oxygen saturation. The most pronounced decline of DPOAEs at 1 kHz was also seen on that occasion. Conclusions DPOAEs are suggested for detection of intracranial hypertension and early detection of high-altitude cerebral edema.

High-altitude pulmonary oedema

ESC CardioMed ◽  
2018 ◽  
pp. 1078-1080
Author(s):  
Samuel Verges ◽  
Patrick Levy
Keyword(s):  
High Altitude ◽  
Pulmonary Oedema ◽  
Acute Mountain Sickness ◽  
Arterial Oxygenation ◽  
Lower Altitude ◽  
Vasodilator Drugs ◽  
Oxygen Administration ◽  
Pulmonary Vasoconstriction ◽  
High Altitude Disease ◽  
Alveolar Capillary

At high altitude, the reduction in arterial oxygenation frequently leads to symptoms of acute mountain sickness. While these symptoms generally resolve spontaneously, high-altitude pulmonary oedema can develop and represents a potentially lethal form of high-altitude disease. High-altitude pulmonary oedema is a non-cardiogenic oedema due to exaggerated pulmonary vasoconstriction and altered alveolar–capillary permeability. In addition to descending to lower altitude, it requires specific emergency cares such as oxygen administration, a hyperbaric bag, and vasodilator drugs.

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