scholarly journals The Hen or the Egg: Impaired Alveolar Oxygen Diffusion and Acute High-altitude Illness?

2019 ◽  
Vol 20 (17) ◽  
pp. 4105 ◽  
Author(s):  
Heimo Mairbäurl ◽  
Christoph Dehnert ◽  
Franziska Macholz ◽  
Daniel Dankl ◽  
Mahdi Sareban ◽  
...  
Keyword(s):  
High Altitude ◽  
Acute Mountain Sickness ◽  
Gas Diffusion ◽  
Alveolar Wall ◽  
Factors Affecting ◽  
Alveolar Epithelial ◽  
Arterial Blood ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Illness ◽  
Alveolar Oxygen

Individuals ascending rapidly to altitudes >2500 m may develop symptoms of acute mountain sickness (AMS) within a few hours of arrival and/or high-altitude pulmonary edema (HAPE), which occurs typically during the first three days after reaching altitudes above 3000–3500 m. Both diseases have distinct pathologies, but both present with a pronounced decrease in oxygen saturation of hemoglobin in arterial blood (SO2). This raises the question of mechanisms impairing the diffusion of oxygen (O2) across the alveolar wall and whether the higher degree of hypoxemia is in causal relationship with developing the respective symptoms. In an attempt to answer these questions this article will review factors affecting alveolar gas diffusion, such as alveolar ventilation, the alveolar-to-arterial O2-gradient, and balance between filtration of fluid into the alveolar space and its clearance, and relate them to the respective disease. The resultant analysis reveals that in both AMS and HAPE the main pathophysiologic mechanisms are activated before aggravated decrease in SO2 occurs, indicating that impaired alveolar epithelial function and the resultant diffusion limitation for oxygen may rather be a consequence, not the primary cause, of these altitude-related illnesses.

Enhanced fibrin formation in high-altitude pulmonary edema

1987 ◽  
Vol 63 (2) ◽  
pp. 752-757 ◽  
Author(s):  
P. Bartsch ◽  
U. Waber ◽  
A. Haeberli ◽  
M. Maggiorini ◽  
S. Kriemler ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Blood Coagulation ◽  
Acute Mountain Sickness ◽  
Edema Formation ◽  
Mean Values ◽  
Fibrin Formation ◽  
Arterial Blood ◽  
High Altitude Pulmonary Edema

Blood coagulation, fibrinolysis, and arterial blood gases were examined in 66 nonacclimatized mountaineers at 4,557 m. Subjects were classified according to a clinical score as healthy (n = 25), having mild acute mountain sickness (AMS) (n = 24), showing severe AMS (n = 13), and suffering from high-altitude pulmonary edema (HAPE) (n = 4). Coagulation times, euglobulin lysis time, and fibrin(ogen) fragment E were normal in all groups without significant changes. Fibrinopeptide A (FPA), a molecular marker of in vivo fibrin formation, was elevated in HAPE to 4.2 +/- 2.7 ng/ml (P less than 0.0001) compared with the other groups showing mean values between 1.6 +/- 0.4 and 1.8 +/- 0.7 ng/ml. FPA was normal in one patient with HAPE, however. Severe AMS was accompanied by a significant decrease in arterial PO2 due to an increase in alveolar-arterial O2 difference, whereas arterial PCO2 did not change significantly. We conclude that activation of blood coagulation is not involved in the pathogenesis of AMS and the impairment of gas exchange in this disease. Fibrin generation occurring in HAPE is probably an epiphenomenon of edema formation.

Pharmacotherapy for Altitude-Related Illness

2003 ◽  
Vol 16 (1) ◽  
pp. 68-75 ◽  
Author(s):  
Allan Ellsworth
Keyword(s):  
High Altitude ◽  
Alcohol Intake ◽  
Acute Mountain Sickness ◽  
The United States ◽  
Recreational Sports ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Cerebral Edema ◽  
Mountain Sickness ◽  
High Altitude Illness ◽  
The Brain

Altitude-related illness is a frequent cause of morbidity and occasional mortality among recreational sports travelers in the United States and throughout the world. High-altitude illness describes the cerebral and pulmonary syndromes (acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema) that can occur in unacclimatized persons ascending too rapidly to high altitude. The pathogenesis of these syndromes is primarily hypobaric hypoxia that causes compensatory changes in the brain and lungs, resulting in hyperperfusion of microvascular beds, increased capillary pressure, and a microvascular leak with resulting edema and a characteristic constellation of symptoms. Prevention and treatment involve education about rate of ascent; diet; alcohol intake; physical activity; oxygen; hyperbaric chambers; and pharmacotherapy, including acetazolamide, dexamethasone, nifedipine, and salmeterol in selected circumstances.

scholarly journals Acute high-altitude illness: updated principles ofpathophysiology, prevention, and treatment

2020 ◽  
Vol 71 (11-12) ◽  
pp. 267-274
Author(s):  
MM Berger ◽  
LM Schiefer ◽  
G Treff ◽  
M Sareban ◽  
ER Swenson ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Cerebral Edema ◽  
Acute Mountain Sickness ◽  
High Altitude Pulmonary Edema ◽  
Prevention And Treatment ◽  
High Altitude Cerebral Edema ◽  
Mountain Sickness ◽  
High Altitude Illness ◽  
Cardinal Symptom

The interest in trekking and mountaineering is increasing, and growing numbers of individuals are travelling to high altitude. Following ascent to high altitude, individuals are at risk of developing one of the three forms of acute high-altitude illness: acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). The cardinal symptom of AMS is headache that occurs with an increase in altitude. Additional symptoms are anorexia, nausea, vomiting, dizziness, and fatigue. HACE is characterized by truncal ataxia and decreased consciousness that generally but not always are preceded by worsening AMS. The typical features of HAPE are a loss of stamina, dyspnea, and dry cough on exertion, followed by dyspnea at rest, rales, cyanosis, cough, and pink, frothy sputum. These diseases can develop at any time from several hours to 5 days following ascent to altitudes above 2,500-3,000 m. Whereas AMS is usually self-limited, HACE and HAPE represent life-threatening emergencies that require timely intervention. For each disease, we review the clinical features, epidemiology and the current understanding of their pathophysiology. We then review the primary pharmacological and non-pharmacological approaches to the management of each form of acute altitude illness and provide practical recommendations for both prevention and treatment. The essential principles for advising travellers prior to high-altitude exposure are summarized. Key Words: Acute Mountain Sickness, High Altitude Cerebral Edema, High Altitude Pulmonary Edema, Hypoxia

scholarly journals HIGH-ALTITUDE ILLNESS

2015 ◽  
Vol 4 (2) ◽  
Author(s):  
Dwitya Elvira
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Cerebral Edema ◽  
Acute Mountain Sickness ◽  
High Mountain ◽  
Extreme Sports ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Cerebral Edema ◽  
Mountain Sickness ◽  
High Altitude Illness

AbstrakHigh-altitude illness (HAI) merupakan sekumpulan gejala paru dan otak yang terjadi pada orang yang baru pertama kali mendaki ke ketinggian. HAI terdiri dari acute mountain sickness (AMS), high-altitude cerebral edema (HACE) dan high-altitude pulmonary edema (HAPE). Tujuan tinjauan pustaka ini adalah agar dokter dan wisatawan memahami risiko, tanda, gejala, dan pengobatan high-altitude illness. Perhatian banyak diberikan terhadap penyakit ini seiring dengan meningkatnya popularitas olahraga ekstrim (mendaki gunung tinggi, ski dan snowboarding) dan adanya kemudahan serta ketersediaan perjalanan sehingga jutaan orang dapat terpapar bahaya HAI. Di Pherice, Nepal (ketinggian 4343 m), 43% pendaki mengalami gejala AMS. Pada studi yang dilakukan pada tempat wisata di resort ski Colorado, Honigman menggambarkan kejadian AMS 22% pada ketinggian 1850 m sampai 2750 m, sementara Dean menunjukkan 42% memiliki gejala pada ketinggian 3000 m. Aklimatisasi merupakan salah satu tindakan pencegahan yang dapat dilakukan sebelum pendakian, selain beberapa pengobatan seperti asetazolamid, dexamethasone, phosopodiestrase inhibitor, dan ginko biloba.Kata kunci: high-altitude illness, acute mountain sickness, edema cerebral, pulmonary edema AbstractHigh-altitude illness (HAI) is symptoms of lung and brain that occurs in people who first climb to altitude. HAI includes acute mountain sickness (AMS), high-altitude cerebral edema (HACE) and high altitude pulmonary edema (HAPE). The objective of this review was to understand the risks, signs, symptoms, and treatment of high-altitude illness. The attention was given to this disease due to the rising popularity of extreme sports (high mountain climbing, skiing and snowboarding) and the ease and availability of the current travelling, almost each year, millions of people could be exposed to the danger of HAI. In Pherice, Nepal (altitude 4343 m), 43% of climbers have symptoms of AMS. Furthermore, in a study conducted at sites in Colorado ski resort, Honigman describe AMS incidence of 22% at an altitude of 1850 m to 2750 m, while Dean showed that 42% had symptoms at an altitude of 3000 m. Acclimatization is one of the prevention that can be done before the climbing, in the addition of several treatment such as acetazolamide, dexamethasone, phospodiestrase inhibitor and gingko biloba.Keywords: high-altitude illness, acute mountain sickness, edema cerebral, pulmonary edema

scholarly journals The Oxygen Transport Triad in High-Altitude Pulmonary Edema: A Perspective from the High Andes

2021 ◽  
Vol 18 (14) ◽  
pp. 7619
Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Oxygen Transport ◽  
Acute Mountain Sickness ◽  
Breath Holding ◽  
Acid Base Balance ◽  
Initial Exposure ◽  
High Altitude Pulmonary Edema ◽  
Tolerance To Hypoxia ◽  
Dynamic Pump

Acute high-altitude illnesses are of great concern for physicians and people traveling to high altitude. Our recent article “Acute Mountain Sickness, High-Altitude Pulmonary Edema and High-Altitude Cerebral Edema, a View from the High Andes” was questioned by some sea-level high-altitude experts. As a result of this, we answer some observations and further explain our opinion on these diseases. High-Altitude Pulmonary Edema (HAPE) can be better understood through the Oxygen Transport Triad, which involves the pneumo-dynamic pump (ventilation), the hemo-dynamic pump (heart and circulation), and hemoglobin. The two pumps are the first physiologic response upon initial exposure to hypobaric hypoxia. Hemoglobin is the balancing energy-saving time-evolving equilibrating factor. The acid-base balance must be adequately interpreted using the high-altitude Van Slyke correction factors. Pulse-oximetry measurements during breath-holding at high altitude allow for the evaluation of high altitude diseases. The Tolerance to Hypoxia Formula shows that, paradoxically, the higher the altitude, the more tolerance to hypoxia. In order to survive, all organisms adapt physiologically and optimally to the high-altitude environment, and there cannot be any “loss of adaptation”. A favorable evolution in HAPE and pulmonary hypertension can result from the oxygen treatment along with other measures.

Association of variants m.T16172C and m.T16519C in whole mtDNA sequences with high altitude pulmonary edema in Han Chinese lowlanders

2021 ◽  
Author(s):  
Yan Wang ◽  
Xuewen Huang ◽  
Fujun Peng ◽  
Huiling Han ◽  
Yanan Gu ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Sequence Data ◽  
Nuclear Genome ◽  
Han Chinese ◽  
Mtdna Sequences ◽  
Reactive Protein ◽  
Arterial Blood ◽  
High Altitude Pulmonary Edema ◽  
Systolic Arterial Blood Pressure

Abstract Background: High altitude pulmonary edema (HAPE) is a hypoxia-induced non-cardiogenic pulmonary edema that typically occurred in un-acclimatized lowlanders, which inevitably leads to life-threatening consequences. Apart from multiple factors involved, the genetic factors also play an important role in the pathogenesis of HAPE. So far, researchers put more energy into the nuclear genome and HAPE, and ignored the relationship between the mitochondrion DNA (mtDNA) variants and HAPE susceptibility. Methods: We recruited a total of 366 individuals including 181 HAPE patients and 185 healthy or non-HAPE populations through two times. The first time, 49 HAPE patients and 58 non-HAPE cases were performed through whole mtDNA sequences to search the mutations and haplogroups, which were associated with the HAPE. The second time, 132 HAPE patients and 127 non-HAPE subjects were collected to apply of verifying these variants and haplogroups of mtDNA with routine PCR method. Results: We analyzed and summarized the clinical characteristics and sequence data for 49 HAPE patients and 58 non-HAPE cases. We found that a series of routine blood indexes including systolic arterial blood pressure (SBP), heart rate (HR), white blood cell (WBC) and C-reactive protein (CRP) in HAPE group presented higher and displayed the significant differences compared with those in non-HAPE group. Though the average numbers of variants in different regions and groups samples were not statistically significant (P > 0.05), the mutation densities of different region in the internal group shown the significant differences. Then we found that two mutations (T16172C and T16519C) associated with the HAPE susceptibility, and the T16172C mutation increased the risk of HAPE, and the T16519C mutation decreased the HAPE rating. Furthermore, the two mutations were demonstrated with 132 HAPE cases and 127 non-HAPE individuals. Unfortunately, all the haplogroups were not associated with the HAPE haplogroups.Conclusions: We provided the evidence of differences in mtDNA polymorphism frequencies between HAPE and non-HAPE Han Chinese. Genotypes of mtDNA 16172C and 16519C were correlated with HAPE susceptibility, which indicated that the role in mitochondrial genome in the pathogenesis of HAPE.

Blood rheology in acute mountain sickness and high-altitude pulmonary edema

1991 ◽  
Vol 71 (3) ◽  
pp. 934-938 ◽  
Author(s):  
W. H. Reinhart ◽  
B. Kayser ◽  
A. Singh ◽  
U. Waber ◽  
O. Oelz ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Blood Rheology ◽  
Plasma Viscosity ◽  
Erythrocyte Deformability ◽  
Erythrocyte Aggregation ◽  
High Altitude Pulmonary Edema ◽  
Mountain Sickness ◽  
Low Altitude

The role of blood rheology in the pathogenesis of acute mountain sickness and high-altitude pulmonary edema was investigated. Twenty-three volunteers, 12 with a history of high-altitude pulmonary edema, were studied at low altitude (490 m) and at 2 h and 18 h after arrival at 4,559 m. Eight subjects remained healthy, seven developed acute mountain sickness, and eight developed high-altitude pulmonary edema. Hematocrit, whole blood viscosity, plasma viscosity, erythrocyte aggregation, and erythrocyte deformability (filtration) were measured. Plasma viscosity and erythrocyte deformability remained unaffected. The hematocrit level was lower 2 h after the arrival at high altitude and higher after 18 h compared with low altitude. The whole blood viscosity changed accordingly. The erythrocyte aggregation was about doubled 18 h after the arrival compared with low-altitude values, which reflects the acute phase reaction. There were, however, no significant differences in any rheological parameters between healthy individuals and subjects with acute mountain sickness or high-altitude pulmonary edema, either before or during the illness. We conclude that rheological abnormalities can be excluded as an initiating event in the development of acute mountain sickness and high-altitude pulmonary edema.

scholarly journals Acute Lung Edema as a Presentation of Severe Acute Reentry High-Altitude Illness in a Pediatric Patient

2020 ◽  
Vol 2020 ◽  
pp. 1-3
Author(s):  
Alfredo Merino-Luna ◽  
Julio Vizcarra-Anaya
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Pediatric Patient ◽  
Lung Edema ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Illness ◽  
The City ◽  
Determining Factor

Acute high-altitude pulmonary edema (HAPE) is a pathology involving multifactorial triggers that are associated with ascents to altitudes over 2,500 meters above sea level (m). Here, we report two pediatric cases of reentry HAPE, from the city of Huaraz, Peru, located at 3,052 m. The characteristics of both cases were similar, wherein acclimatization to sea level and a subsequent return to the city of origin occurred, and we speculate that it was caused by activation of predisposing factors to HAPE. The diagnosis and management associated with pulmonary hypertension became a determining factor for therapy.

Sign in / Sign up

Export Citation Format

Share Document