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.

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

2021 ◽  
Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Oxygen Transport ◽  
Arterial Oxygen ◽  
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. 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 increased hemoglobin at high altitude reduces the percentage of dissolved oxygen in the arterial oxygen content with respect to sea level. At high altitude, 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. All organisms adapt physiologically and optimally to a high-altitude environment to survive. Reduction of pulmonary hypertension in HAPE through oxygen administration results in a favorable outcome.

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 Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema: An enhanced view from the High Andes

2021 ◽  
Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Cerebral Edema ◽  
Acute Mountain Sickness ◽  
Point Of View ◽  
La Paz ◽  
Mountain Climbing ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Cerebral Edema ◽  
Mountain Sickness

Background: Travelling to high altitude for entertainment or work is sometimes associated with acute high altitude pathologies. In the past, scientific literature from the lowlander point of view was mostly based on mountain climbing. Nowadays, altitude descent and evacuation are not mandatory in populated highland cities. Methods: We present how to diagnose and treat acute high altitude pathologies based on 50 years of high altitude physiology and medical practice in hypobaric hypoxic diseases in La Paz, Bolivia (3,600m; 11,811ft), at the High Altitude Pulmonary and Pathology Institute (HAPPI – IPPA) altitudeclinic.com.Results: Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema are all medical conditions faced by some travelers. These can occasionally present after flights to high altitude cities, both in lowlanders or high-altitude residents during re-entry, particularly after spending more than 20 days at sea level.Conclusions: Acute high altitude ascent diseases can be adequately diagnosed and treated without altitude descent. Traveling to high altitude should not be feared as it has many benefits;

scholarly journals Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema: A view from the High Andes

2021 ◽  
Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Cerebral Edema ◽  
Acute Mountain Sickness ◽  
Healthy Children ◽  
Number Of Children ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Cerebral Edema ◽  
Potential Risks ◽  
Mountain Sickness

Healthy children and those with pre-existing conditions traveling to high altitude may experience diverse physiologic changes. Individuals who are not acclimatized and ascend rapidly are at risk of developing acute high altitude illnesses (HAI), which may occur within a few hours after arrival at high altitudes, being acute mountain sickness (AMS) the most common. In very few cases, serious complications may occur, including High Altitude Pulmonary Edema (HAPE) and very rarely High Altitude Cerebral Edema (HACE). Moreover, the number of children and adolescents traveling on commercial aircrafts is growing and this poses a need for their treating physicians to be aware of the potential risks of hypoxia while air traveling. In this article we present 50 years of medical practice at high altitude treating these pathologies succesfully with no casualties.

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.

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

Sign in / Sign up

Export Citation Format

Share Document