scholarly journals Physiology and Medicine at High Altitude: The Exposure and the Stress

2018 ◽  
Vol 3 (3) ◽  
pp. 203 ◽  
Author(s):  
Anil Gurtoo
Keyword(s):  
High Altitude ◽  
Acute Mountain Sickness ◽  
Hemoglobin Concentration ◽  
Barometric Pressure ◽  
Extreme Environment ◽  
Incidence Rates ◽  
Oxygen Requirement ◽  
Classic Model ◽  
Mountain Sickness ◽  
High Altitude Illness

<p>Increase in altitude causes decrease in atmospheric barometric pressure that results in decrease of inspired<br />partial pressure of oxygen, a source for stress and pose a challenge to climbers/trekkers or persons posted on<br />high altitude areas. This review discusses about the high altitude sickness, their incidence rates, pathophysiology<br />and the classic model of acclimatisation, which explains about how oxygen requirement in extreme environment<br />is achieved by complex interplay among pulmonary, hematological and cardiovascular processes. The acute<br />high altitude illness (AHAI) is basically composed of two syndromes: cerebral and pulmonary that can afflict<br />un-acclimatised climbers/trekkers. The cerebral syndrome includes acute mountain sickness (AMS) and high<br />altitude cerebral oedema (HACO) and pulmonary syndrome typically refers to high altitude pulmonary oedema<br />(HAPO). The core physiological purpose, according to the classic model is centered upon the optimisation of<br />increased delivery of oxygen to the cells through a coherent response involving increased ventilation, cardiac<br />output and hemoglobin concentration with aim to increase the oxygen flux across the oxygen cascade, which<br />will help in preventing the development of majority of high altitude illness.</p>

Adaptations to High-Altitude Hypoxia

2021 ◽  
Author(s):  
Cynthia M. Beall ◽  
Kingman P. Strohl
Keyword(s):  
High Altitude ◽  
Oxygen Delivery ◽  
Hemoglobin Concentration ◽  
Barometric Pressure ◽  
Ambient Air ◽  
Extreme Environment ◽  
Indigenous Populations ◽  
East African ◽  
Short Term

Biological anthropologists aim to explain the hows and whys of human biological variation using the concepts of evolution and adaptation. High-altitude environments provide informative natural laboratories with the unique stress of hypobaric hypoxia, which is less than usual oxygen in the ambient air arising from lower barometric pressure. Indigenous populations have adapted biologically to their extreme environment with acclimatization, developmental adaptation, and genetic adaptation. People have used the East African and Tibetan Plateaus above 3,000 m for at least 30,000 years and the Andean Plateau for at least 12,000 years. Ancient DNA shows evidence that the ancestors of modern highlanders have used all three high-altitude areas for at least 3,000 years. It is necessary to examine the differences in biological processes involved in oxygen exchange, transport, and use among these populations. Such an approach compares oxygen delivery traits reported for East African Amhara, Tibetans, and Andean highlanders with one another and with short-term visitors and long-term upward migrants in the early or later stages of acclimatization to hypoxia. Tibetan and Andean highlanders provide most of the data and differ quantitatively in biological characteristics. The best supported difference is the unelevated hemoglobin concentration of Tibetans and Amhara compared with Andean highlanders as well as short- and long-term upward migrants. Moreover, among Tibetans, several features of oxygen transfer and oxygen delivery resemble those of short-term acclimatization, while several features of Andean highlanders resemble the long-term responses. Genes and molecules of the oxygen homeostasis pathways contribute to some of the differences.

Acclimatization at high altitude in gradual and acute induction

1995 ◽  
Vol 79 (2) ◽  
pp. 487-492 ◽  
Author(s):  
S. S. Purkayastha ◽  
U. S. Ray ◽  
B. S. Arora ◽  
P. C. Chhabra ◽  
L. Thakur ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Time Course ◽  
Physiological Responses ◽  
Acute Mountain Sickness ◽  
Blood Gases ◽  
Blood Gas ◽  
Mountain Sickness ◽  
High Altitude Illness ◽  
In Transit

The study assessed physiological responses to induction to high altitude first to 3,500 m and then to 4,200 m and compared the time course of altitude acclimatization in two groups of male volunteers. The acutely inducted group was transported by aircraft (AI) to 3,500 m in 1 h, whereas the gradually inducted group was transported by road (RI) in 4 days. Baseline recordings of basal cardiovascular, respiratory, and blood gas variables were monitored at sea level as well as at 3,500 m on days 1, 3, 5, and 7. Blood gases were measured on day 10 also. After 15 days at 3,500 m, the subjects were inducted to 4,200 m by road, and measurements were repeated on days 1, 3, and 5, except blood gas variables, which were done on day 10 only. Acute mountain sickness symptoms were recorded throughout. The responses of RI were stable by day 3 of induction at 3,500 m, whereas it took 5 days for AI. Four days in transit for RI appear equivalent to 2 days at 3,500 m for AI. Acclimatization schedules of 3 and 5 days, respectively, for RI and AI are essential to avoid malacclimatization and/or high-altitude illness. Both groups took 3 days at 4,200 m to attain stability for achieving acclimatization.

Cerebral spinal fluid dynamics: effect of hypoxia and implications for high-altitude illness

2016 ◽  
Vol 120 (2) ◽  
pp. 251-262 ◽  
Author(s):  
Justin S. Lawley ◽  
Benjamin D. Levine ◽  
Michael A. Williams ◽  
Jon Malm ◽  
Anders Eklund ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
High Altitude ◽  
Cerebral Spinal Fluid ◽  
Acute Mountain Sickness ◽  
Spinal Fluid ◽  
Brain Swelling ◽  
Mountain Sickness ◽  
High Altitude Illness ◽  
Brain Water

The pathophysiology of acute mountain sickness and high-altitude cerebral edema, the cerebral forms of high-altitude illness, remain uncertain and controversial. Persistently elevated or pathological fluctuations in intracranial pressure are thought to cause symptoms similar to those reported by individuals suffering cerebral forms of high-altitude illness. This review first focuses on the basic physiology of the craniospinal system, including a detailed discussion of the long-term and dynamic regulation of intracranial pressure. Thereafter, we critically examine the available literature, based primarily on invasive pressure monitoring, that suggests intracranial pressure is acutely elevated at altitude due to brain swelling and/or elevated sagittal sinus pressure, but normalizes over time. We hypothesize that fluctuations in intracranial pressure occur around a slightly elevated or normal mean intracranial pressure, in conjunction with oscillations in arterial Po2 and arterial blood pressure. Then these modest fluctuations in intracranial pressure, in concert with direct vascular stretch due to dilatation and/or increased blood pressure transmission, activate the trigeminal vascular system and cause symptoms of acute mountain sickness. Elevated brain water (vasogenic edema) may be due to breakdown of the blood-brain barrier. However, new information suggests cerebral spinal fluid flux into the brain may be an important factor. Regardless of the source (or mechanisms responsible) for the excess brain water, brain swelling occurs, and a “tight fit” brain would be a major risk factor to produce symptoms; activities that produce large changes in brain volume and cause fluctuations in blood pressure are likely contributing factors.

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 Acute Mountain Sickness Following Incremental Trekking to High Altitude: Correlation With Plasma Vascular Endothelial Growth Factor Levels and the Possible Effects of Dexamethasone and Acclimatization Following Re-exposure

2021 ◽  
Vol 12 ◽  
Author(s):  
Craig Winter ◽  
Tracy Bjorkman ◽  
Stephanie Miller ◽  
Paul Nichols ◽  
John Cardinal ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Vascular Endothelial ◽  
Mountain Sickness ◽  
High Altitude Illness ◽  
Exercise Induced ◽  
Endothelial Growth Factor ◽  
Vegf Level

Purpose: The recognition and treatment of high-altitude illness (HAI) is increasingly important in global emergency medicine. High altitude related hypobaric hypoxia can lead to acute mountain sickness (AMS), which may relate to increased expression of vascular endothelial growth factor (VEGF), and subsequent blood-brain barrier (BBB) compromise. This study aimed to establish the relationship between AMS and changes in plasma VEGF levels during a high-altitude ascent. VEGF level changes with dexamethasone, a commonly used AMS medication, may provide additional insight into AMS.Methods: Twelve healthy volunteers ascended Mt Fuji (3,700 m) and blood samples were obtained at distinct altitudes for VEGF analysis. Oxygen saturation (SPO2) measurements were also documented at the same time-point. Six out of the 12 study participants were prescribed dexamethasone for a second ascent performed 48 h later, and blood was again collected to establish VEGF levels.Results: Four key VEGF observations could be made based on the data collected: (i) the baseline VEGF levels between the two ascents trended upwards; (ii) those deemed to have AMS in the first ascent had increased VEGF levels (23.8–30.3 pg/ml), which decreased otherwise (23.8–30.3 pg/ml); (iii) first ascent AMS participants had higher VEGF level variability for the second ascent, and similar to those not treated with dexamethasone; and (iv) for the second ascent dexamethasone participants had similar VEGF levels to non-AMS first ascent participants, and the variability was lower than for first ascent AMS and non-dexamethasone participants. SPO2 changes were unremarkable, other than reducing by around 5% irrespective of whether measurement was taken for the first or second ascent.Conclusion: First ascent findings suggest a hallmark of AMS could be elevated VEGF levels. The lack of an exercise-induced VEGF level change strengthened the notion that elevated plasma VEGF was brain-derived, and related to AMS.

Optic nerve oedema at high altitude occurs independent of acute mountain sickness

2018 ◽  
Vol 103 (5) ◽  
pp. 692-698 ◽  
Author(s):  
Andreas Schatz ◽  
Vanessa Guggenberger ◽  
M Dominik Fischer ◽  
Kai Schommer ◽  
Karl Ulrich Bartz-Schmidt ◽  
...  
Keyword(s):  
Optic Nerve ◽  
High Altitude ◽  
Optic Disc ◽  
Acute Mountain Sickness ◽  
Optic Nerve Sheath Diameter ◽  
Future Research ◽  
Oedema Formation ◽  
Altitude Exposure ◽  
Mountain Sickness ◽  
High Altitude Illness

Background/aimsThe study aims to investigate changes in the optic nerve sheath diameter (ONSD) at high altitude and to assess correlation to optic disc oedema (ODE) and acute mountain sickness (AMS). This investigation is part of the Tübingen High Altitude Ophthalmology study.MethodsFourteen volunteers ascended to 4559 m for 4 days before returning to low altitude. Ultrasonography of ONSD, quantification of optic disc parameters using a scanning laser ophthalmoscope and fluorescein angiography were performed at 341 m and at high altitude. Pearson’s coefficient was used to correlate changes in ONSD with the optic disc and AMS. Assessment of AMS was performed using the Lake Louise (LL) and AMS-cerebral (AMS-C) scores of the Environmental Symptom Questionnaire-III. All volunteers were clinically monitored for heart rate (HR) and oxygen saturation (SpO2).ResultsThe mean ONSD at high altitude (4.6±0.3 mm, p<0.05) was significantly increased compared with baseline (3.8±0.4 mm) and remained enlarged throughout high-altitude exposure. This change in ONSD did not correlate with AMS (AMS-C, r=0.26, p=0.37; LL, r=0.21, p=0.48) and high-altitude headache (r=0.54, p=0.046), or clinical parameters of SpO2 (r=0.11, p=0.72) and HR (r=0.22, p=0.44). Increased ONSD did not correlate with altered key stereometric parameters of the optic disc describing ODE at high altitude (r<0.1, p>0.5).ConclusionHigh-altitude exposure leads to marked oedema formation of the optic nerve independent of AMS. Increased ONSD and ODE reflect hypoxia-driven oedema formation of the optic nerve at high altitude, providing important pathophysiological insight into high-altitude illness development and for future research.

scholarly journals Exercise exacerbates acute mountain sickness at simulated high altitude

2000 ◽  
Vol 88 (2) ◽  
pp. 581-585 ◽  
Author(s):  
R. C. Roach ◽  
D. Maes ◽  
D. Sandoval ◽  
R. A. Robergs ◽  
M. Icenogle ◽  
...  
Keyword(s):  
High Altitude ◽  
Minute Ventilation ◽  
Arterial Oxygen Saturation ◽  
Acute Mountain Sickness ◽  
Urine Volume ◽  
Barometric Pressure ◽  
Arterial Oxygen ◽  
Simulated High Altitude ◽  
Mountain Sickness ◽  
Exercise Induced

.—We hypothesized that exercise would cause greater severity and incidence of acute mountain sickness (AMS) in the early hours of exposure to altitude. After passive ascent to simulated high altitude in a decompression chamber [barometric pressure = 429 Torr, ∼4,800 m (J. B. West, J. Appl. Physiol. 81: 1850–1854, 1996)], seven men exercised (Ex) at 50% of their altitude-specific maximal workload four times for 30 min in the first 6 h of a 10-h exposure. On another day they completed the same protocol but were sedentary (Sed). Measurements included an AMS symptom score, resting minute ventilation (V˙e), pulmonary function, arterial oxygen saturation ([Formula: see text]), fluid input, and urine volume. Symptoms of AMS were worse in Ex than Sed, with peak AMS scores of 4.4 ± 1.0 and 1.3 ± 0.4 in Ex and Sed, respectively ( P < 0.01); but restingV˙e and[Formula: see text] were not different between trials. However, [Formula: see text] during the exercise bouts in Ex was at 76.3 ± 1.7%, lower than during either Sed or at rest in Ex (81.4 ± 1.8 and 82.2 ± 2.6%, respectively, P< 0.01). Fluid intake-urine volume shifted to slightly positive values in Ex at 3–6 h ( P = 0.06). The mechanism(s) responsible for the rise in severity and incidence of AMS in Ex may be sought in the observed exercise-induced exaggeration of arterial hypoxemia, in the minor fluid shift, or in a combination of these factors.

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

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