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Artykuły w czasopismach na temat "Acute mountain sickness"

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Borowska, Emilia, Emilia Harasim i Katarzyna Van Damme -Ostapowicz. "Acute mountain sickness". Archives of Physiotherapy and Global Researches 18, nr 1 (1.12.2014): 19–22. http://dx.doi.org/10.15442/apgr.18.1.21.

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Pigman, Edwin C. "Acute Mountain Sickness". Sports Medicine 12, nr 2 (sierpień 1991): 71–79. http://dx.doi.org/10.2165/00007256-199112020-00001.

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Tassan Din, Chiara, i Massimo Pesenti Campagnoni. "Acute mountain sickness". Emergency Care Journal 2, nr 4 (9.08.2006): 6. http://dx.doi.org/10.4081/ecj.2006.4.6.

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McNeil, Edward L. "Acute Mountain Sickness". Journal of the Royal Society of Medicine 89, nr 6 (czerwiec 1996): 359–60. http://dx.doi.org/10.1177/014107689608900625.

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Goodman, Benny. "Acute mountain sickness". Practice Nursing 14, nr 8 (sierpień 2003): 374–77. http://dx.doi.org/10.12968/pnur.2003.14.8.11465.

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Murdoch, David R. "Acute Mountain Sickness". Journal of the Royal Society of Medicine 89, nr 12 (grudzień 1996): 728. http://dx.doi.org/10.1177/014107689608901238.

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Jin, Jill. "Acute Mountain Sickness". JAMA 318, nr 18 (14.11.2017): 1840. http://dx.doi.org/10.1001/jama.2017.16077.

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Murdoch, David R., i Andrew J. Pollard. "Acute Mountain Sickness". Journal of Travel Medicine 4, nr 2 (1.06.1997): 90–93. http://dx.doi.org/10.1111/j.1708-8305.1997.tb00786.x.

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Johnson, T. Scott, i Paul B. Rock. "Acute Mountain Sickness". New England Journal of Medicine 319, nr 13 (29.09.1988): 841–45. http://dx.doi.org/10.1056/nejm198809293191306.

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Wright, A. D., i R. F. Fletcher. "Acute mountain sickness." Postgraduate Medical Journal 63, nr 737 (1.03.1987): 163–64. http://dx.doi.org/10.1136/pgmj.63.737.163.

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Rozprawy doktorskie na temat "Acute mountain sickness"

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Hieronymus, Mathias. "THE EFFECTS OF CARDIORESPIRATORY FITNESS ON SYMPTOMS OF ACUTE MOUNTAIN SICKNESS". Miami University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=miami1249835075.

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Wang, Pei. "Genetic association studies of the susceptibility to acute mountain sickness". Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44545.

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Purpose: Acute mountain sickness (AMS) is the most common and most benign altitude illness. The main symptoms (i.e. headache, nausea, fatigue, dizziness, and disturbed sleep) appear in 6 – 12 h after rapid ascent (usually to above 2500 m) and often subside after 4 – 5 days without further ascent. The etiology is unclear and may be partially due to an innate susceptibility, which could be genetic. The studies described in this thesis focused on genetic predisposition to AMS susceptibility in Nepalese. Given that ancestral background of Nepalese is strongly influenced by its neighbouring populations (e.g. Tibetan and Indian) who may have different levels of AMS susceptibility, due to differing in evolutionary history, population stratification was assessed. Methods: Two hundred and thirty five Nepalese who permanently live below 1800 m were recruited in 2005 (n = 103) and 2008 (n = 132) while attending a religious festival at Gosainkunda (4380 m). Subjects were assigned to the AMS+ and AMS- groups based on clinical diagnosis performed by physicians and using Lake Louise Scoring (LLS) system. Twenty polymorphisms in five candidate genes (ACE, AGTR1, BDKRB2, ADRB2, and NOS3) that encode important components of vascular and pulmonary physiological pathways were investigated. Allele and genotype frequencies at the polymorphic loci were compared between the AMS+ and AMS- groups. Population stratification was assessed by comparing allele and genotype frequencies of fifteen ancestry informative markers and estimating Tibetan and South Asian genetic contributions to Nepalese subjects. Results: No significant difference in allele and genotype frequencies of 19 polymorphisms was found between the AMS+ and AMS- groups. An association was found between the alleles of the NOS3G⁸⁹⁴T polymorphism (rs1799983) in NOS3 and AMS in the 2005 cohort as well as in native Andean highlanders (Quechua) collected in the late 1990s; however, the association was not replicated in the 2008 Nepalese cohort. No population stratification was found in the Nepalese cohorts. Conclusion: Genetic predisposition to AMS in Nepalese was not shown strongly influenced by either alleles in the genes investigated in the studies described in this thesis or by ancestry (South Asian or Tibetan).
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Knott, Jonathan R. "Arterial Oxygen Saturation as a Predictor of Acute Mountain Sickness and Summit Success among Mountianeers". DigitalCommons@USU, 2010. https://digitalcommons.usu.edu/etd/674.

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The purpose of this study was to determine if arterial oxygen saturation (SaO2), as measured by a finger pulse oximeter upon rapid arrival to 4260 m, could be predictive of acute mountain sickness (AMS) or summit success on a climb to 5640 m. In total 73 climbers volunteered to participate in the study. After excluding those taking drugs to counteract the effects of AMS and those with missing data, 48 participants (45 male, 3 female) remained. Climbers were transported from 2650 m to the Piedra Grande hut at 4260 m on Pico de Orizaba within 2 hr. After a median time of 10 ± 13 hr at the hut, they climbed toward the summit (5640 m) and returned with a median trip time of 13.3 ± 4.8 hr. The Lake Louise Self-assessment Questionnaire (LLSA) for AMS, heart rate, and SaO2 from a finger pulse oximeter was collected upon arrival at the hut, repeated immediately before the climbers departed for their summit attempts, and immediately upon their return. The presence of AMS was defined as a LLSA score ≥ 3 with a headache and at least one other symptom. Fifty-nine percent of the participants successfully reached the summit. Average SaO2 for all participants at 4260 m prior to their departure for the summit was 84.2 ± 3.8%. Sixty percent of the participants met the criteria for AMS during their ascent. There was not a significant difference (p = .90) in SaO2 between those who experienced AMS (SaO2 = 84.3 ± 3.3%) and those who did not (SaO2 = 84.2 ± 4.2%) during the ascent. Neither was there a significant difference (p = .18) in SaO2 between those who reached the summit (84.8 ± 3.7%) and those who did not (83.3 ± 4.0%). Arterial oxygen saturation does not appear to be predictive of AMS or summit success.
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Nybäck, Linn. "Spirometry before high altitude exposure: a way to predict an individual risk of developing acute mountain sickness". Thesis, Mittuniversitetet, Institutionen för hälsovetenskap, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:miun:diva-22182.

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MacInnis, Martin J. "Understanding the variable human response to hypoxia : physiological, genetic, and epidemiological investigations of acute mountain sickness susceptibility". Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/50106.

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High-altitude (and simulated high-altitude) environments can be extraordinarily stressful for low-altitude organisms because of the reduced oxygen availability (i.e. hypoxia). Humans, who live primarily at low altitude, can adjust physiologically (i.e., acclimatise or acclimate) to hypoxic environments; however, the human acclimatisation response to hypoxia is highly variable, evident from the differential susceptibility to acute altitude illnesses, such as acute mountain sickness (AMS). For my dissertation, I attempted to identify some of the physiological, genetic, and epidemiological variables that could explain the variation in hypoxia tolerance. I conducted (i) two studies using a normobaric hypoxia chamber at the University of British Columbia; (ii) two field studies in a mountainous region of the Nepalese Himalaya; and (iii) two meta-anaylyses. The most important findings of my dissertation are that (i) oxygen saturation (SPO₂) and heart rate (HR) were not strong markers of AMS susceptibility in laboratory or field settings; (ii) a low fraction of exhaled nitric oxide (FENO) was associated with increased susceptibility to AMS in the laboratory but not in the field; (iii) physiological responses (FENO, SPO₂, HR, blood pressure) to hypoxia were repeatable on two normobaric hypoxia exposures; (iv) AMS severity was lower on the second of two identical normobaric hypoxia exposures (but headache severity was similar); (v) in a large Nepalese sample, age, sex, ascent rate, and preventative strategies were associated with AMS susceptibility; (vi) the severity of AMS was similar in brothers; (vii) there were biogeographical differences in AMS susceptibility in the Nepalese sample; (viii) polymorphisms of the FAM149A gene were associated with AMS severity; (ix) AMS history was a poor predictor of future AMS outcomes; and (x) sleep quality was weakly related to other AMS symptoms. In conclusion, this dissertation demonstates that the measured physiological variables (FENO, SPO₂, HR, blood pressure) were not associated with AMS status, that a genetic basis to the variation in AMS susceptibility is likely, and that the Lake Louise Score definition of AMS should be amended. Our understanding of acute altitude tolerance in humans may be aided by the redefinition of AMS.
Education, Faculty of
Kinesiology, School of
Graduate
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Evans, Kevin Andrew. "Hypoxia and vascular nitric oxide bioavailability : implications for the pathophysiology of high-altitude illness". Thesis, University of South Wales, 2009. https://pure.southwales.ac.uk/en/studentthesis/hypoxia-and-vascular-nitric-oxide-bioavailability(3cd64bcd-5fb9-4209-a6f3-ab219e906a17).html.

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Introduction: Nitric oxide (NO) is an integral molecule implicated in the control of vascular function. It has been suggested that vascular dysfunction may lead to the development of acute mountain sickness (AMS), high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE), though data to date remains scarce. Therefore, there is a clear need for further work to address the role of NO in the pathogenesis of high-altitude illness. Aims: There were two primary aims of the current work: (1) To examine whether hypoxia mediated changes in systemic NO metabolism are related to the development of AMS and sub-clinical pulmonary oedema and (2) to examine whether hypoxia mediated changes in the trans-cerebral exchange kinetics of NO metabolites are related to the development of AMS and headache. Hypothesis: We hypothesise that hypoxia will be associated with an increase in reactive oxygen species (ROS) formation, resulting in a decrease in vascular NO bioavailability (O2•- + NO → ONOO•-, k = 109 M.s-1). The reduction in NO will lead to vascular dysfunction and impaired oxygen (O2) delivery. Subsequent hypoxaemia will result in pulmonary vascular vasoconstriction and the development of sub-clinical pulmonary oedema within and mild brain swelling. Symptoms and reductions in NO bioavailability will be more pronounced in those who develop AMS since they are typically more hypoxaemic. Alternatively, a hypoxia mediated increase in NO, during vasodilatation, specifically across the cerebral circulation, may activate the trigminovascular system resulting in headache and by consequence, AMS. Methods: Study 1 – AMS symptoms, systemic venous NO concentration and nasal potential difference (NPD), used as a surrogate biomarker of extravascular lung oedema, were quantified in normoxia, after a 6hr passive exposure to 12% oxygen (O2) and immediately following a hypoxic maximal exercise challenge (≈6.5 hrs). Final measurements were 2 obtained two hours into (hypoxic) recovery. Study 2 – AMS, radial arterial and internal jugular venous NO metabolite concentrations and global cerebral blood flow (CBF), using the Kety-Schmidt technique, were assessed in normoxia and after a 9hr passive exposure to 12.9% O2. AMS was diagnosed if subjects presented with a combined Lake Louise score of ≥5 points and an Environmental Symptoms Questionnaire – Cerebral score of ≥0.7 points. Results: Hypoxia was associated with a reduction in total plasma NO, primarily due to a reduction in nitrate (NO3•) and a compensatory increase in red blood cell (RBC)-bound NO(P < 0.05 vs. normoxia) in both studies. Study 1 – Exercise reduced plasma nitrite (NO2•) (P< 0.05 vs. normoxia) whereas RBC-bound NO did not change. NO was not different in those who developed AMS (AMS+) compared to those who remained comparatively more healthy (AMS-) (P < 0.05). NPD was not affected by hypoxia or exercise and was not different between AMS+ and AMS- (P > 0.05). Study 2 – Hypoxia decreased arterial concentration of total plasma NO due primarily to a reduction in NO2•- and nitrate (NO3•-). Hypoxia did not alter the cerebral metabolism of RSNO, whereas the formation of RBC-bound NO increased. Discussion: These findings suggest that alterations in systemic or trans-cerebral NO metabolism are not implicated in the pathophysiology of AMS or sub-clinical pulmonary oedema. However, hypoxia was associated with an overall reduction in the total NO pool (NOx), whereas, selected alterations in more vasoactive NO metabolites were observed. Reductions in the partial pressure of O2 (pO2) were thought to be a key regulator in these changes. Overall net increases in RBC NO and corresponding reductions in plasma NO2• in the face of no alterations in NOx indicates that rather than being simply consumed, NO is reapportioned to other NO metabolites and this may be implicated in the pathophysiology of AMS.
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Johnson, Pamela Lesley. "Sleep and Breathing at High Altitude". University of Sydney, 2008. http://hdl.handle.net/2123/3531.

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Doctor of Philosphy (PhD)
This thesis describes the work carried out during four treks, each over 10-11 days, from 1400m to 5000m in the Nepal Himalaya and further work performed during several two-night sojourns at the Barcroft Laboratory at 3800m on White Mountain in California, USA. Nineteen volunteers were studied during the treks in Nepal and seven volunteers were studied at White Mountain. All subjects were normal, healthy individuals who had not travelled to altitudes higher than 1000m in the previous twelve months. The aims of this research were to examine the effects on sleep, and the ventilatory patterns during sleep, of incremental increases in altitude by employing portable polysomnography to measure and record physiological signals. A further aim of this research was to examine the relationship between the ventilatory responses to hypoxia and hypercapnia, measured at sea level, and the development of periodic breathing during sleep at high altitude. In the final part of this thesis the possibility of preventing and treating Acute Mountain Sickness with non-invasive positive pressure ventilation while sleeping at high altitude was tested. Chapter 1 describes the background information on sleep, and breathing during sleep, at high altitudes. Most of these studies were performed in hypobaric chambers to simulate various high altitudes. One study measured sleep at high altitude after trekking, but there are no studies which systematically measure sleep and breathing throughout the whole trek. Breathing during sleep at high altitude and the physiological elements of the control of breathing (under normal/sea level conditions and under the hypobaric, hypoxic conditions present at high altitude) are described in this Chapter. The occurrence of Acute Mountain Sickness (AMS) in subjects who travel form near sea level to altitudes above 3000m is common but its pathophysiology not well understood. The background research into AMS and its treatment and prevention are also covered in Chapter 1. Chapter 2 describes the equipment and methods used in this research, including the polysomnographic equipment used to record sleep and breathing at sea level and the high altitude locations, the portable blood gas analyser used in Nepal and the equipment and methodology used to measure each individual’s ventilatory response to hypoxia and hypercapnia at sea level before ascent to the high altitude locations. Chapter 3 reports the findings on the changes to sleep at high altitude, with particular focus on changes in the amounts of total sleep, the duration of each sleep stage and its percentage of total sleep, and the number and causes of arousals from sleep that occurred during sleep at increasing altitudes. The lightest stage of sleep, Stage 1 non-rapid eye movement (NREM) sleep, was increased, as expected with increases in altitude, while the deeper stages of sleep (Stages 3 and 4 NREM sleep, also called slow wave sleep), were decreased. The increase in Stage 1 NREM in this research is in agreement with all previous findings. However, slow wave sleep, although decreased, was present in most of our subjects at all altitudes in Nepal; this finding is in contrast to most previous work, which has found a very marked reduction, even absence, of slow wave sleep at high altitude. Surprisingly, unlike experimental animal studies of chronic hypoxia, REM sleep was well maintained at all altitudes. Stage 2 NREM and REM sleep, total sleep time, sleep efficiency and spontaneous arousals were maintained at near sea level values. The total arousal index was increased with increasing altitude and this was due to the increasing severity of periodic breathing as altitude increased. An interesting finding of this research was that fewer than half the periodic breathing apneas and hypopneas resulted in arousal from sleep. There was a minor degree of upper airway obstruction in some subjects at sea level but this was almost resolved by 3500m. Chapter 4 reports the findings on the effects on breathing during sleep of the progressive increase of altitude, in particular the occurrence of periodic breathing. This Chapter also reports the results of changes to arterial blood gases as subjects ascended to higher altitudes. As expected, arterial blood gases were markedly altered at even the lowest altitude in Nepal (1400m) and this change became more pronounced at each new, higher altitude. Most subjects developed periodic breathing at high altitude but there was a wide variability between subjects as well as variability in the degree of periodic breathing that individual subjects developed at different altitudes. Some subjects developed periodic breathing at even the lowest altitude and this increased with increasing altitude; other subjects developed periodic breathing at one or two altitudes, while four subjects did not develop periodic breathing at any altitude. Ventilatory responses to hypoxia and hypercapnia, measured at sea level before departure to high altitude, was not significantly related to the development of periodic breathing when the group was analysed as a whole. However, when the subjects were grouped according to the steepness of their ventilatory response slopes, there was a pattern of higher amounts of periodic breathing in subjects with steeper ventilatory responses. Chapter 5 reports the findings of an experimental study carried out in the University of California, San Diego, Barcroft Laboratory on White Mountain in California. Seven subjects drove from sea level to 3800m in one day and stayed at this altitude for two nights. On one of the nights the subjects slept using a non-invasive positive pressure device via a face mask and this was found to significantly improve the sleeping oxyhemoglobin saturation. The use of the device was also found to eliminate the symptoms of Acute Mountain Sickness, as measured by the Lake Louise scoring system. This finding appears to confirm the hypothesis that lower oxygen saturation, particularly during sleep, is strongly correlated to the development of Acute Mountain Sickness and may represent a new treatment and prevention strategy for this very common high altitude disorder.
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Nespoulet, Hugo. "Oxygénation en conditions hypoxiques : rôle de la chémosensibilité sur la tolérance à l'altitude, plasticité et amélioration par pression positive expiratoire". Thesis, Grenoble, 2011. http://www.theses.fr/2011GRENS041/document.

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A l'éveil comme au cours du sommeil, en plaine comme en haute altitude, le maintien d'une oxygénation artérielle stable et élevée est un marqueur essentiel d'une bonne réponse physiologique de l'organisme. L'intolérance à l'altitude regroupe des pathologies graves voire fatales dont le développement est en lien direct avec le taux d'oxygénation artériel des sujets. D'autre part, en plaine, la prévalence élevée du syndrome d'apnées obstructives du sommeil (SAOS) incite les chercheurs au développement de modèles d'études spécifiques, permettant d'investiguer les conséquences du principal stimulus du SAOS : l'hypoxie intermittente. La chémosensibilité pourrait avoir un impact important dans ces deux pathologies, ayant pour rôle le maintien des gaz du sang à des valeurs normales, en adaptant la ventilation aux conditions externes ou internes à l'organisme.Les objectifs de ce travail étaient de comprendre l'impact de la chémosensibilité (avec d'autres mécanismes décrits dans la littérature) sur l'oxygénation et la tolérance à l'altitude, d'étudier les effets de la résistance expiratoire sur l'amélioration de l'oxygénation, ainsi que les conséquences de l'hypoxie intermittente chronique sur la plasticité du chémoréflexe.Il en ressort que la chémosensibilité périphérique à l'hypoxie a un impact majeur sur le développement de l'intolérance à l'altitude. Cela semble en outre être un facteur prédictif de la survenue de ces pathologies. En hypoxie, une amélioration efficace de l'oxygénation a été obtenue par l'utilisation d'une résistance expiratoire calibrée à 10 cm H2O permettant l'amélioration de la diffusion alvéolo-capillaire. L'exposition à l'hypoxie intermittente chronique nocturne a provoqué une fragmentation du sommeil ainsi qu'une intensification de la chémosensibilité à l'hypoxie et à l'hypercapnie.Ainsi, une altération de la réponse des corps carotidiens à l'hypoxémie participerait au développement du mal aigu des montagnes et de ses complications, tout en facilitant sa prédiction avant ascension. L'utilisation d'une résistance expiratoire pourrait permettre de combler la désaturation exagérée retrouvée chez les sujets sensibles à l'altitude lors d'un séjour en haute montagne. Il apparaît également que la chémosensiblité périphérique et centrale (CO2 et O2) fasse preuve d'une plasticité importante en réponse à l'hypoxie intermittente nocturne chez des sujets sains
At awakening and during sleep, at sea level or in high altitude, maintaining a high level in arterial blood oxygenation is a marker for an adaptated physiological response external and internal factors.High altitude illness encompasses pathologies, that sometimes could be fatal, and which seems to be correlated with the level of arterial oxygenation in hypoxia.Secondly, at sea level and in general population, the high prevalence of obstructive sleep apnea syndrome (OSAS) encourage scientists to develop new models for studying consequences of the main OSAS' stimulus: intermittent hypoxia.Chemosensitivity could play an important role in those two different diseases, with regulation of blood gases and homeostasis by controlling ventilation.Our objectives was to investigate (1) impact of chemosensitivity on blood oxygenation and tolerance to high altitude, comparatively to other physiological factors commonly involved, (2) effects of using positive expiratory pressure in order to improve oxygenation in hypoxia, and (3) consequences of chronic exposure to nocturnal intermittent hypoxia on chemoreflexe plasticity.We found that peripheral chemoresponse to hypoxia play a crucial role in high altitude illness development. Moreover, this variable seems to be a predictive factor for those diseases. In hypoxic conditions, using a positive expiratory pressure (10 cmH2O) lead to a significant improve in arterial oxygenation, by increasing pulmonary diffusion. Finally, nocturnal intermittent hypoxia induced significant sleep disturbances and major changes in chemoresponse to hypoxia and hypercapnia
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Kao, Wei-Chun, i 高偉君. "Acute Mountain Sickness and Oxygen Saturation among Jade Mountain Climbers of Taiwan". Thesis, 2003. http://ndltd.ncl.edu.tw/handle/04993094368813127675.

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碩士
國立臺灣大學
預防醫學研究所
91
Background As number of trekkers for high-altitude mountain have increased over the past decade, an increase of occurrence of acute mountain sickness (AMS) would be expected. The association between SaO2 and AMS by different altitude was never reported before in Taiwan. Objective The aim of this study was to estimate prevalence rate by different altitude, to elucidate the association between SaO2 and AMS, and finally to develop predictive model for AMS. Methods A total of 26 mountaineers on the pursuit of peak of Jade Mountain between fifteenth November and seventeenth November, 2002 were used as our study subjects. A prospective study design was devised to collect basic characteristics, SaO2 and questionnaire related to AMS. The level of SaO2 was measured nine times at different huts and seal-level with oximeter. We used Lake Louise AMS questionnaire for defining AMS. There are two definitions for AMS. The first type, AMS-1 was defined as having headache together with one of clinical symptoms. The second type, AMS-2 was defined as having three or more clinical symptoms. Those who had symptoms but did not meet the criteria of AMS were referred to as high altitude related symptoms (HARS). At least one of high altitude symptoms occurred was defined as high altitude syndrome (HAS). Predictive models using SaO2 at hut 1 or SaO2 at previous hut as predictor were developed by using logistic regression model. Results At hut 1 (2659m), no HAS and AMS cases were found. At hut 2 (3402m), the prevalence rates of HAS, AMS-1 and AMS-2 were 15.4%, 7.7%, and 7.7%, respectively. The prevalence rates were 65.4%%, 26.9%%, and 30.8% while trekkers climbed to the summit of Jade mountain. The overall prevalence rates were 80.8%, 34.6% and 38.5% for HAS, AMS-1, and AMS-2, respectively, from hut 1 to the summit. The decline in SaO2 at the summit was more remarkable in the HAS group than the normal (p=0.03). The difference in the decline of SaO2 between the AMS-1 group and the control group was borderline statistical significance (p=0.07). No remarkable difference was found between the AMS-2 and the normal group. The differences in the decline of SaO2 were even more pronounced on the descent of hut 2 for the HAS group (p < 0.01) and the AMS-1 group (p=0.03) but not so remarkable for the AMS-2 group (p=0.13). Predictive model using SaO2 at previous hut can significantly account for occurrence of HAS, AMS-1 and AMS-2. Conclusions The association between SaO2 and HAS or AMS by different altitudes was demonstrated. Both the predictive models using SaO2 at baseline or SaO2 at previous hut were also developed. These predictive models may be useful for reducing AMS.
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Lee, Mao-Lung, i 李茂榮. "A Study of Acute Mountain Sickness Emergency Care in Tibet Tourism". Thesis, 2017. http://ndltd.ncl.edu.tw/handle/16094147441472543896.

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碩士
萬能科技大學
經營管理研究所在職專班
105
The biggest, sometimes fatal, risk for travelling in Tibet is altitude sickness (a.k.a. acute mountain sickness, AMS). When it occurs, the patient not only has to be sent to hospital immediately, but also need to be observed to see if returning to lower altitude areas is necessary. This paper focuses on the risk management for AMS, including setting up a SOP to deal with AMS situation, and prevention measures to reduce the impact of AMS. After all, human life is beyond value. If travelling in Tibet is always threatened by high-risk danger and potential physical impairment, the tourism market will eventually shrink under the shadow. The observation on high altitude (above 2,000 meters) tourism groups indicates that tourists will have different symptoms and severity level of AMS along with the rising of altitude and decreasing of air pressure and oxygen amount. Climate and temperature are also contributing factors to AMS severity. Among those tourists, about 40% have light reaction in the beginning, and 35% of the patients are reported to have reduced symptoms after given medical treatment. However, approximate 5% of them will turn out to suffer from more severe AMS symptoms, including Pulmonary edema (HAPE) or Cerebral edema (HACE), due to lacking of or delayed medical care. And approximate 2% of those severe patients, the symptoms were combined with multiple-organ dysfunctions. At this critical moment, if the patient continues to stay in high altitude area, the medical treatment will be in vain, the possibility to incur multiple organ dysfunction syndromes (MODS) becomes much higher, which leads to a life-threatening situation. In consideration of this, this paper studies how to incorporate current medical and rescue resource system, in order to establish an “AMS Emergency and Medical Assistance Center” in Tibet. This center will be based on local medical staff that has rich experience on AMS medical and caring treatment in Tibet and equipped with private transport vehicles, in order to coordinate and assist overseas rescue organization for transporting patients. And with communication facility, they will be able to conduct distant consultation on medical and nursing to shorten rescue time. AMS should be taken more seriously at the onset of slight symptom and the passenger needs treatments in time. If the symptoms progress to severe situation, the patient needs to be transported to lower altitude areas. The medical process relies on the cooperation and support from associated organizations to enable overall supporting system: The first issue to address is how to require the support from the emergency unit of local hospitals and the agreement of doctors, in order to provide necessary assistance in discharging and transporting the patient to low altitude area, under the supervision of accompanying doctors and nurses along the way. For expense which might incur, there should be an agreement with insurance companies to activate their medical assistance service for overseas emergency medical transport. In the meanwhile, build a bridge between overseas rescue company (also called SOS company) in charge and the transporting company, for the latter to take over the arrangement of a charter flight. The charter flight will carry a professional medical team (doctors and nurses) with necessary medical equipment to provide treatments and transport service for the patient. The paper suggests a model of Emergency and Medical Assistance Center containing the following aspects: Build up an emergency medical and care system Look for local clinics and professional physician for cooperation Build up a reporting platform for emergency medical assistance Purchase an well-equipped ambulance Set up a long-distances communication facility and provide training to emergency medical assistance staff UIA (Union International Assistance) Coordinate with Tibetan tourists for them to be insured by the same insurance company for process convenience. Cope with the exclusive terms of insurance policy Promote a stationed charter flight for medical purpose at Lhasa airport. Make and print manuals of “SOP for medical and emergency assistance during travel”Promote security education for “High Plateau travelling precautions and AMS prevention” Tibetan Travel Emergency and Medical Assistance Center is implemented in the following sequence: Build up an Emergency and Medical Assistance Center. Examine passenger’s physical condition against AMS.Promote the consultancy service of associate doctors or nurses while travelling.Build up a reporting platform for emergency assistance.Establish a coordinating center for long-distance medical treatments.Promote the service system for medical transport of critically-ill patients to low altitude areas. Through the study of a series of documents and local medical culture, experience sharing from first-aid doctors and medical professionals, in-depth interviews with senior travel agents and tour group leads, this paper aims to build up a medical assistance model for AMS, and enable an working model for overseas medical transport system. With the study of this paper, we hope to facilitate the establishment and management of Emergency and Medical Assistance Center, in order to benefit the tourism in high altitude areas such as Taiwan and Tibet, ensuring the travelers to start their journey with a happy mood, and come back home safe and sound. We believe the Overseas Assistance model and Emergency and Medical Assistance Center developed by this paper will be highly welcome by travel agents who share the tourism business in high altitude areas. With the system provided in this paper, high altitude tourism might greets its era with low (or zero) risk.
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Książki na temat "Acute mountain sickness"

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Grissom, Colin Kerst. Acetazolamide in the treatment of acute mountain sickness: Clinical efficacy and effect on gas exchange. [New Haven :bs.n.], 1990.

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Martin, Daniel S., i Michael P. W. Grocott. Pathophysiology and management of altitude-related disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0350.

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Streszczenie:
Acute high-altitude related illnesses include acute mountain sickness (AMS), high altitude pulmonary oedema (HAPO) and high altitude cerebral oedema (HACO). AMS is characterized by headache, lack of appetite, poor sleep, lethargy, and fatigue. AMS is a common, generally benign, self-limiting condition if managed with rest, no ascent, and symptomatic treatment. Descent is indicated in severe cases. HACO and HAPO are rare, but serious conditions that should be considered life-threatening medical emergencies. HACO is characterized by the presence of neurological signs (including confusion) at altitude, commonly in the presence of headache. HAPO is characterized by breathlessness and signs of respiratory distress at altitude, particularly accompanying exercise. Management of HACO and HAPO involves urgent descent, supplemental oxygen (cylinder, concentrator, or portable hyperbaric chamber) if available, and specific treatment with dexamethasone (HACO) or nifedipine (HAPO). Slow controlled ascent (adequate acclimatization) is the best prophylaxis against the acute high-altitude-related illnesses. Acetazolamide is an effective prophylaxis against AMS.
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Nussbaumer-Ochsner, Yvonne, i Konrad E. Bloch. Sleep at high altitude and during space travel. Redaktorzy Sudhansu Chokroverty, Luigi Ferini-Strambi i Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0054.

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This chapter summarizes data on sleep–wake disturbances in humans at high altitude and in space. High altitude exposure is associated with periodic breathing and a trend toward reduced slow-wave sleep and sleep efficiency in healthy individuals. Some subjects are affected by altitude-related illness (eg, acute and chronic mountain sickness, high-altitude cerebral and pulmonary edema). Several drugs are available to prevent and treat these conditions. Data about the effects of microgravity on sleep are limited and do not allow the drawing of firm conclusions. Microgravity and physical and psychological factors are responsible for sleep–wake disturbances during space travel. Space missions are associated with sleep restriction and disruption and circadian rhythm disturbances encouraging use of sleep medication. An unexplained and unexpected finding is the improvement in upper airway obstructive breathing events and snoring during space flight.
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Części książek na temat "Acute mountain sickness"

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Oette, Mark, Marvin J. Stone, Hendrik P. N. Scholl, Peter Charbel Issa, Monika Fleckenstein, Steffen Schmitz-Valckenberg, Frank G. Holz i in. "Mountain Sickness, Acute". W Encyclopedia of Molecular Mechanisms of Disease, 1351–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_3228.

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Böning, Dieter, Michael I. Lindinger, Damian M. Bailey, Istvan Berczi, Kameljit Kalsi, José González-Alonso, David J. Dyck i in. "Acute Mountain Sickness". W Encyclopedia of Exercise Medicine in Health and Disease, 8–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4.

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Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling i in. "Acute Mountain Sickness". W Encyclopedia of Molecular Mechanisms of Disease, 30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9013.

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Oelz, O. "Prophylaxis and Treatment of Acute Mountain Sickness". W Travel Medicine, 450–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73772-5_99.

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Vann, Richard D., Neal W. Pollock, Carl F. Pieper, David R. Murdoch, Stephen R. Muza, Michael J. Natoli i Luke Y. Wang. "Epidemiological Modeling of Acute Mountain Sickness (AMS)". W Advances in Experimental Medicine and Biology, 355–58. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-8997-0_25.

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Hackett, Peter H. "High Altitude Cerebral Edema and Acute Mountain Sickness". W Advances in Experimental Medicine and Biology, 23–45. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4711-2_2.

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Kumar, Kushal, Kalpana Kumari Barwal i Sunil Kumar Hota. "Pathophysiology and Management of Acute Mountain Sickness (AMS)". W The Therapeutic Properties of Medicinal Plants, 167–84. Series statement: Innovations in plant science for better health: from soil to fork: Apple Academic Press, 2019. http://dx.doi.org/10.1201/9780429265204-8.

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Bärtsch, Peter, i Damian Miles Bailey. "Acute Mountain Sickness and High Altitude Cerebral Oedema". W High Altitude, 379–403. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8772-2_20.

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Mathew Kinsey, C., i Robert Roach. "Role of Cerebral Blood Volume in Acute Mountain Sickness". W Advances in Experimental Medicine and Biology, 151–59. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-8997-0_11.

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Naeije, Robert, i Aurelie van Osta. "Altered Autoregulation Of Cerebral Blood Flow In Hypoxia: Relevance To The Pathophysiology Of Acute Mountain Sickness". W Problems of High Altitude Medicine and Biology, 211–20. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-6300-8_15.

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Streszczenia konferencji na temat "Acute mountain sickness"

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Yan, Tzu-Hao, Hsing-Fang Tsai, Sih-Yin Lu, Ching-Shuen Chen, Shih-Tsang Tang i Jiun-Hung Lin. "Portable oximeter for acute mountain sickness". W 2010 International Conference on Electronics and Information Engineering (ICEIE 2010). IEEE, 2010. http://dx.doi.org/10.1109/iceie.2010.5559839.

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Côrte, Ana Carolina, Roberto Nahon, Breno Schor, Felipe Hardt i Rodrigo Sasson. "357 Can ibuprofen prevent acute mountain sickness in moderate altitude?" W IOC World Conference on Prevention of Injury & Illness in Sport 2021. BMJ Publishing Group Ltd and British Association of Sport and Exercise Medicine, 2021. http://dx.doi.org/10.1136/bjsports-2021-ioc.324.

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Liu, Zeng Fang, Xing Jia Wei, Fang Fang Liu i Dian Jun Lu. "Evaluation Model of Acute Mountain Sickness Based on item Response Theory". W 2019 10th International Conference on Information Technology in Medicine and Education (ITME). IEEE, 2019. http://dx.doi.org/10.1109/itme.2019.00039.

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Furian, Michael, Maamed Mademilov, Ainura Abdraeva, Mona Lichtblau, Ulan Sheraliev, Nuriddin H. Marazhapov, Aline Buergin i in. "Acetazolamide for Preventing Acute Mountain Sickness in Healthy Older than 40 years. RCT". W ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa749.

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Gopal, Muralikrishna, i Thomas E. Aldrich. "Prediction Of Acute Mountain Sickness (AMS) Based On Pulse Oximetry Measurements During Mt. Kilimanjaro Ascent". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4787.

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Vinnikov, Denis, Paul Blanc, Nurlan Brimkulov i Craig Steinmaus. "LATE-BREAKING ABSTRACT: Meta-analysis of the risk of acute mountain sickness from cigarette smoking". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa2910.

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Chen, Jing, Yuan Tian, Guangbo Zhang, Zhengtao Cao, Lingling Zhu i Dawei Shi. "IoT-enabled Intelligent Dynamic Risk Assessment of Acute Mountain Sickness Based on Data from Wearable Devices". W 2021 4th IEEE International Conference on Industrial Cyber-Physical Systems (ICPS). IEEE, 2021. http://dx.doi.org/10.1109/icps49255.2021.9468233.

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Hamzah, Azham Afzanizam, Abdul Hafidz Hj Omar, Anuar Suun i Dayang Hjh Tiawa Awang Hj Hamid. "ACUTE MOUNTAIN SICKNESS PREDICTION USING PERIPHERAL CAPILLARY OXYGEN SATURATION (SPO2) DEVICE AND LAKE LOUIS SELF-ASSESMENT AMONG MALAYSIAN EVEREST CLIMBERS". W Movement, Health and Exercise 2014 Conference. Universiti Malaysia Pahang, 2014. http://dx.doi.org/10.15282/mohe.2014.sms.083.

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Luo, Xiaomin, Lei Wang i Lei Yang. "Influence of Induced Altitude Acclimatization on Development of Acute Mountain Sickness Associated with a Subsequent Rapid Ascent to High Altitude". W 2016 IEEE 16th International Conference on Bioinformatics and Bioengineering (BIBE). IEEE, 2016. http://dx.doi.org/10.1109/bibe.2016.41.

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Raporty organizacyjne na temat "Acute mountain sickness"

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Giorgio Manferdelli, Giorgio Manferdelli. Can people be screened for acute mountain sickness susceptibility? Experiment, marzec 2019. http://dx.doi.org/10.18258/13160.

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Muza, S. R., D. Kaminsky, C. S. Fulco, L. E. Banderet i A. Cymerman. Cysteinyl Leukotriene Blockade Does Not Prevent Acute Mountain Sickness. Fort Belvoir, VA: Defense Technical Information Center, maj 2004. http://dx.doi.org/10.21236/ada423394.

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Roach, Robert. Prediction of Acute Mountain Sickness using a Blood-Based Test. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2013. http://dx.doi.org/10.21236/ada612856.

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Roach, Robert. Prediction of Acute Mountain Sickness using a Blood-Based Test. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2015. http://dx.doi.org/10.21236/ada624167.

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Muza, Stephen R., Paul B. Rock, Timothy Lyons, Charles S. Fulco i Beth A. Beidleman. Susceptibility to Acute Mountain Sickness: Relationship to Pre-Ascent Resting Ventilation. Fort Belvoir, VA: Defense Technical Information Center, maj 2000. http://dx.doi.org/10.21236/ada377573.

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Lovering, Andrew T. Prediction of Susceptibility to Acute Mountain Sickness Using Hypoxia-Induced Intrapulmonary Arteriovenous Shunt and Intracardiac Shunt Fractions. Fort Belvoir, VA: Defense Technical Information Center, październik 2012. http://dx.doi.org/10.21236/ada612590.

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Lovering, Andrew. Prediction of Susceptibility to Acute Mountain Sickness Using Hypoxia-Induced Intrapulmonary Arteriovenous Shunt and Intracardiac Shunt Fractions. Fort Belvoir, VA: Defense Technical Information Center, październik 2013. http://dx.doi.org/10.21236/ada612591.

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Fulco, Charles S., Laurie A. Trad, Vincent A. Forte, Gonzalez Jr., Iwanyk Julio i Eugene J. The Use of Hypoxic and Carbon Dioxide Sensitivity Tests of Predict the Incidence and Severity of Acute Mountain Sickness in Soldiers Exposed to an Elevation of 3800 Meters. Fort Belvoir, VA: Defense Technical Information Center, luty 1991. http://dx.doi.org/10.21236/ada241792.

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