Hypoxia, Hypocapnia and Spirometry at Altitude

Pollard, Andrew J.; Barry, PW; Mason, Nicholas; Collier, David; Pollard, R.C.; Pollard, P. F. A.; Martín, Isabel Hierro; Fraser, Robert S.; Miller, Martin; Milledge, J. S.

doi:10.1042/cs0920593

Cited by 32 publications

(22 citation statements)

References 20 publications

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“…On returning to Base Camp after 6days, or more, climbing at 5000m or higher, the median A M S score was 0 (range 0-5), mean oxygen saturation 83.4% (range 76-90%) and mean capillary carbon dioxide tension 3.33 kPa (range 2.51-4.15 kPa). FEVI and PEF were a mean (95% confidence intervals) 4% (1.7-6.3%) and 26.4% (21.9-30.9%) higher than at sea level, similar to the results of a parallel study undertaken during the expedition [14]. The general linear model showed that although a higher AMS score on arrival at 5300m was associated with a greater reduction in cough threshold (F = 6.52, P < O.OOl), overall the reduction in cough threshold between sea level and arrival at 5300 m was not statistically significant.…”

Section: Citric Acid Cough Challenge (Figs 1-3)supporting

confidence: 73%

Cough Frequency and Cough-Receptor Sensitivity are Increased in Man at Altitude

et al. 1997

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1. Travellers to high altitude often complain of paroxysmal cough, which has not been previously investigated. We recorded overnight cough frequency and cough-receptor sensitivity to inhaled citric acid in a group of climbers travelling to 5300 m or higher. 2. Cough frequency, monitored in ten subjects, increased from a median of 0 coughs at sea level (range 0-1) to 5 coughs at 5000 m (range 0-13) and to over 60 coughs in subjects ascending to 7000 m. Citric acid cough threshold, measured in 42 subjects, was unchanged on arrival at 5300 m compared with sea level (geometric mean difference 1.26, 95% confidence intervals 0.84-1.89, P = 0.25), but was significantly reduced after 6 days, or more, at altitude compared with sea level (geometric mean difference 2.2, 95% confidence intervals 1.54-3.15, P = 0.0002). Cough threshold was not related to symptoms of acute mountain sickness, oxygen saturation, carbon dioxide tension or lung function. 3. These results indicate an increase in cough and cough-receptor sensitivity after some days at altitude. This may be due to respiratory tract damage from breathing cold dry air at increased ventilatory rates. Other explanations, such as sub-clinical pulmonary oedema or an effect on the cough centre of acclimatization to altitude, cannot be excluded.

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Section: Citric Acid Cough Challenge (Figs 1-3)supporting

confidence: 73%

Cough Frequency and Cough-Receptor Sensitivity are Increased in Man at Altitude

et al. 1997

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“…In accordance to previous observations, there was no correlation between the magnitude and direction of changes in FEF 25-75 and arterial oxygen saturation (Mason et al 2000;Pollard et al 1997). The individual variability may be explained by the magnitude of bronchoconstriction versus bronchodilation triggered by the ascent to altitude as well as the hypoxia or hypobaria-induced effect on lung fluid accumulation and clearance.…”

Section: Discussionsupporting

confidence: 92%

Variability in pulmonary function following rapid altitude ascent to the Amundsen–Scott South Pole station

et al. 2011

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The impact of acute altitude exposure on pulmonary function is variable. A large inter-individual variability in the changes in forced expiratory flows (FEFs) is reported with acute exposure to altitude, which is suggested to represent an interaction between several factors influencing bronchial tone such as changes in gas density, catecholamine stimulation, and mild interstitial edema. This study examined the association between FEF variability, acute mountain sickness (AMS) and various blood markers affecting bronchial tone (endothelin-1, vascular endothelial growth factor (VEGF), catecholamines, angiotensin II) in 102 individuals rapidly transported to the South Pole (2835 m). The mean FEF between 25 and 75% (FEF(25-75)) and blood markers were recorded at sea level and after the second night at altitude. AMS was assessed using Lake Louise questionnaires. FEF(25-75) increased by an average of 12% with changes ranging from -26 to +59% from sea level to altitude. On the second day, AMS incidence was 36% and was higher in individuals with increases in FEF(25-75) (41 vs. 22%, P = 0.05). Ascent to altitude induced an increase in endothelin-1 levels, with greater levels observed in individuals with decreased FEF(25-75). Epinephrine levels increased with ascent to altitude and the response was six times larger in individuals with decreased FEF(25-75). Greater levels of endothelin-1 in individuals with decreased FEF(25-75) suggest a response consistent with pulmonary hypertension and/or mild interstitial edema, while epinephrine may be upregulated in these individuals to clear lung fluid through stimulation of β(2)-adrenergic receptors.

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“…P revious investigations reported reduced forced vital capacity (FVC) [1][2][3][4][5][6][7][8][9][10][11][12] and reduced forced expiratory volume in 1 s (FEV1) [3,7,9,10,12], as well as increased closing volume (CV) [4,12,13], during the first days after ascent to altitudes of 2,800-5,300 m. These findings were interpreted as being consistent with pulmonary interstitial fluid accumulation or subclinical high-altitude pulmonary oedema (HAPE). However, there are several other factors that could also account for or contribute to the observed changes.…”

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confidence: 64%

No evidence for interstitial lung oedema by extensive pulmonary function testing at 4,559 m

Dehnert¹,

Luks²,

Schendler

et al. 2009

Eur Respir J

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The aim of the present study was to better understand previously reported changes in lung function at high altitude.Comprehensive pulmonary function testing utilising body plethysmography and assessment of changes in closing volume were carried out at sea level and repeatedly over 2 days at high altitude (4,559 m) in 34 mountaineers.In subjects without high-altitude pulmonary oedema (HAPE), there was no significant difference in total lung capacity, forced vital capacity, closing volume and lung compliance between low and high altitude, whereas lung diffusing capacity for carbon monoxide increased at high altitude. Bronchoconstriction at high altitude could be excluded as the cause of changes in closing volume because there was no difference in airway resistance and bronchodilator responsiveness to salbutamol. There were no significant differences in these parameters between mountaineers with and without acute mountain sickness. Mild alveolar oedema on radiographs in HAPE was associated only with minor decreases in forced vital capacity, diffusing capacity and lung compliance and minor increases in closing volume.Comprehensive lung function testing provided no evidence of interstitial pulmonary oedema in mountaineers without HAPE during the first 2 days at 4,559 m. Data obtained in mountaineers with early mild HAPE suggest that these methods may not be sensitive enough for the detection of interstitial pulmonary fluid accumulation.

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Hypoxia, Hypocapnia and Spirometry at Altitude

Cited by 32 publications

References 20 publications

Cough Frequency and Cough-Receptor Sensitivity are Increased in Man at Altitude

Cough Frequency and Cough-Receptor Sensitivity are Increased in Man at Altitude

Variability in pulmonary function following rapid altitude ascent to the Amundsen–Scott South Pole station

No evidence for interstitial lung oedema by extensive pulmonary function testing at 4,559 m

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