Respiratory Muscle Strength May Explain Hypoxia-Induced Decrease in Vital Capacity

Deboeck, Ga L; Moraine, J. J.; Naeije, Robert

doi:10.1249/01.mss.0000162687.18387.97

Cited by 30 publications

(32 citation statements)

References 28 publications

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“…Reductions in inspiratory muscle force have been reported previously in hypobaric and normobaric hypoxia and have been correlated with reductions in FVC [19]. The reasons for the fall in FVC and TLC are most likely a combination of reduced lung compliance due to interstitial fluid accumulation and inspiratory muscle weakness as suggested by the reduced SNIP preceding HAPE (table 2) [1], [2].…”

Section: Discussionsupporting

confidence: 56%

Lung Function and Breathing Pattern in Subjects Developing High Altitude Pulmonary Edema

et al. 2012

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IntroductionThe purpose of the study was to comprehensively evaluate physiologic changes associated with development of high altitude pulmonary edema (HAPE). We tested whether changes in pulmonary function and breathing pattern would herald clinically overt HAPE at an early stage.MethodsIn 18 mountaineers, spirometry, diffusing capacity, nitrogen washout, nocturnal ventilation and pulse oximetry were recorded at 490 m and during 3 days after rapid ascent to 4559 m. Findings were compared among subjects developing HAPE and those remaining well (controls).ResultsIn 8 subjects subsequently developing radiographically documented HAPE at 4559 m, median FVC declined to 82% of low altitude baseline while closing volume increased to 164% of baseline (P<0.05, both instances). In 10 controls, FVC decreased slightly (to 93% baseline, P<0.05) but significantly less than in subjects with HAPE and closing volume remained unchanged. Sniff nasal pressure was reduced in both subjects with and without subsequent HAPE. During nights at 4559 m, mean nocturnal oxygen saturation dropped to lower values while minute ventilation, the number of periodic breathing cycles and heart rate were higher (60%; 8.6 L/min; 97 cycles/h; 94 beats/min, respectively) in subjects subsequently developing HAPE than in controls (73%; 5.1 L/min; 48 cycles/h; 79 beats/min; P<0.05 vs. HAPE, all instances).ConclusionThe results comprehensively represent the pattern of physiologic alterations that precede overt HAPE. The changes in lung function are consistent with reduced lung compliance and impaired gas exchange. Pronounced nocturnal hypoxemia, ventilatory control instability and sympathetic stimulation are further signs of subsequent overt HAPE.RegistrationClinicalTrials.gov identifier: NCT00274430

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Section: Discussionsupporting

confidence: 56%

Lung Function and Breathing Pattern in Subjects Developing High Altitude Pulmonary Edema

et al. 2012

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“…Similar variable results have been reported regarding respiratory muscle strength. DEBOECK et al [29] reported decreased maximum inspiratory and expiratory pressures at a simulated altitude of 4,267 m, while FORTE et al [34] showed no change in these variables at 4,300 m. The reasons for all of these conflicting results may relate to various methodological differences between the studies such as the altitude reached, the speed of ascent, and other elements of the research programme which might have altered the observed results. Unfortunately, with all of these disparities between the various studies, it is difficult to determine which are the more valid outcomes.…”

Section: Pulmonary Mechanicsmentioning

confidence: 99%

“…This change occurs within the first day and persists over time at high altitude [27,28]. Various mechanisms have been proposed to explain this change including pulmonary vascular engorgement, mild interstitial oedema [28], increased abdominal distension [26] and decreased respiratory muscle strength [29]. In contrast, total lung capacity (TLC) is increased at altitude [25,30], suggesting that residual volume is increased as well.…”

Section: Pulmonary Mechanicsmentioning

confidence: 99%

Travel to high altitude with pre-existing lung disease

Luks

Swenson²

2007

Eur Respir J

107

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The pathophysiology of high-altitude illnesses has been well studied in normal individuals, but little is known about the risks of high-altitude travel in patients with pre-existing lung disease. Although it would seem self-evident that any patient with lung disease might not do well at high altitude, the type and severity of disease will determine the likelihood of difficulty in a high-altitude environment. The present review examines whether these individuals are at risk of developing one of the main forms of acute or chronic high-altitude illness and whether the underlying lung disease itself will get worse at high elevations. Several groups of pulmonary disorders are considered, including obstructive, restrictive, vascular, control of ventilation, pleural and neuromuscular diseases. Attempts will be made to classify the risks faced by each of these groups at high altitude and to provide recommendations regarding evaluation prior to high-altitude travel, advice for or against taking such excursions, and effective prophylactic measures.

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“…However, as with thoracic gas compression, few investigators have addressed the issue of air‐density dependence on FEFs obtained at high altitude (Deboeck et al. ; Basu et al. ; Fasano et al.…”

Section: Introductionmentioning

confidence: 99%

The influence of thoracic gas compression and airflow density dependence on the assessment of pulmonary function at high altitude

et al. 2018

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The purpose of this report was to illustrate how thoracic gas compression (TGC) artifact, and differences in air density, may together conflate the interpretation of changes in the forced expiratory flows (FEFs) at high altitude (>2400 m). Twenty‐four adults (10 women; 44 ± 15 year) with normal baseline pulmonary function (>90% predicted) completed a 12‐day sojourn at Mt. Kilimanjaro. Participants were assessed at Moshi (Day 0, 853 m) and at Barafu Camp (Day 9, 4837 m). Typical maximal expiratory flow‐volume (MEFV) curves were obtained in accordance with ATS/ERS guidelines, and were either: (1) left unadjusted; (2) adjusted for TGC by constructing a “maximal perimeter” MEFV curve; or (3) adjusted for both TGC and differences in air density between altitudes. Forced vital capacity (FVC) was lower at Barafu compared with Moshi camp (5.19 ± 1.29 L vs. 5.40 ± 1.45 L, P < 0.05). Unadjusted data indicated no difference in the mid‐expiratory flows (FEF 25–75%) between altitudes (∆ + 0.03 ± 0.53 L sec−1; ∆ + 1.2 ± 11.9%). Conversely, TGC‐adjusted data revealed that FEF 25–75% was significantly improved by sojourning at high altitude (∆ + 0.58 ± 0.78 L sec−1; ∆ + 12.9 ± 16.5%, P < 0.05). Finally, when data were adjusted for TGC and air density, FEFs were “less than expected” due to the lower air density at Barafu compared with Moshi camp (∆–0.54 ± 0.68 L sec−1; ∆–10.9 ± 13.0%, P < 0.05), indicating a mild obstructive defect had developed on ascent to high altitude. These findings clearly demonstrate the influence that TGC artifact, and differences in air density, bear on flow‐volume data; consequently, it is imperative that future investigators adjust for, or at least acknowledge, these confounding factors when comparing FEFs between altitudes.

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Respiratory Muscle Strength May Explain Hypoxia-Induced Decrease in Vital Capacity

Abstract: We conclude that a decrease in respiratory muscle strength may contribute to the decrease in FVC observed at high altitude.

Cited by 30 publications

References 28 publications

Lung Function and Breathing Pattern in Subjects Developing High Altitude Pulmonary Edema

Lung Function and Breathing Pattern in Subjects Developing High Altitude Pulmonary Edema

Travel to high altitude with pre-existing lung disease

The influence of thoracic gas compression and airflow density dependence on the assessment of pulmonary function at high altitude

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