The lungs play a pivotal role in adaptation to high altitude. The increase in ventilation and the rise in pulmonary artery pressure are the first features of lung response to hypoxic exposure. At high altitude the lungs can also be affected by high-altitude pulmonary oedema, a severe form of acute mountain sickness. In healthy subjects the ascent to high altitude is also associated with alterations in lung function, which have been in part interpreted as an effect of extra vascular lung fluid accumulation. The patterns of respiratory function changes at high altitude are discussed, taking into account the body fluid movement and the increase in endothelial permeability induced by hypoxic exposure. As the problem of “respiratory” patients at high altitude is very important, a short summary of the guidelines for altitude exposure of asthmatic and COPD patients is reported at the end of the chapter.

The aim of this paper is to review how preexisting pulmonary diseases can be affected by altitude exposure. Obstructive (asthma and chronic obstructive pulmonary disease or COPD) and restrictive (interstitial pulmonary fibrosis), as well as pulmonary vascular diseases, will be considered, and the goal will be to provide insight and tools to clinicians to optimize the medical condition and thus the life-style of these patients. The underlying pathophysiologies and the effect of hypobaric hypoxia on these diseases will be reviewed such that techniques to assess patients will be appropriate. Therapeutic interventions, including the use of supplemental oxygen, in light of the underlying pathologic processes, will also be discussed.

This article examines the possibility of traveling to altitude for patients suffering from bronchial asthma. The mountain environment, the adaptations of the respiratory system to high altitude, the underlying pathophysiologies of asthma, and the recommendations for patients, according to altitude, are discussed. In summary, staying at low altitude has a significant beneficial effect for asthmatic patients, due to the reduction of airway inflammation and the lower response to bronchoconstrictor stimuli; for staying at moderate altitude, there is conflicting information and no clinical data; at high altitude, the environment seems beneficial for well-controlled asthmatics, but intense exercise and upper airway infections (frequent during trekking) can be additional risks and should be avoided. Further, in remote areas health facilities are often difficult to reach.

Introduction INTERSTITIAL EDEMA is the first appearance of water accumulation in the lung and has been reported to affect a large majority of otherwise healthy climbers during acute exposure to high altitude. In the following, we will review the hypoxia-induced changes of the main mechanisms implicated in the regulation of lung fluid homeostasis, the changes induced in lung physiology by interstitial fluid accumulation, and the diagnostic tools available to demonstrate the presence of interstitial edema at high altitude

It was the aim of the study to assess the maximal pressure generated by the inspiratory muscles (MIP) during exposure to different levels of altitude (i.e., hypobaric hypoxia). Eight lowlanders (2 females and 6 males), aged 27 - 46 years, participated in the study. After being evaluated at sea level, the subjects spent seven days at altitudes of more than 3000 metres. On the first day, they rode in a cable car from 1200 to 3200 metres and performed the first test after 45 - 60 minutes rest; they then walked for two hours to a mountain refuge at 3600 metres, where they spent three nights (days 2 - 3); on day 4, they walked for four hours over a glacier to reach Capanna Regina Margherita (4559 m), where they spent days 5 - 7. MIP, flow-volume curve and SpO (2) % were measured at each altitude, and acute mountain sickness (Lake Louise score) was recorded. Increasing altitude led to a significant decrease in resting SpO (2) % (from 98 % to 80 %) and MIP (from 134 to 111 cmH (2)O) (baseline to day 4: p < 0.05); there was an improvement in SpO (2) % and a slight increase in MIP during the subsequent days at the same altitude. Expiratory (but not inspiratory) flows increased, and forced vital capacity and FEF (75) decreased at higher altitudes. We conclude that exposure to high altitude hypoxia reduces the strength of the respiratory muscles, as demonstrated by the reduction in MIP and the lack of an increase in peak inspiratory flows. This reduction is more marked during the first days of exposure to the same altitude, and tends to recover during the acclimatisation process.

The mountain climate can modify respiratory function and bronchial responsiveness of asthmatic subjects. Hypoxia, hyperventilation of cold and dry air and physical exertion may worsen asthma or enhance bronchial hyperresponsiveness while a reduction in pollen and pollution may play an important role in reducing bronchial inflammation. At moderate altitude (1,500-2,500 m), the main effect is the absence of allergen and pollutants. We studied bronchial hyperresponsiveness to both hyposmolar aerosol and methacholine at sea level (SL) and at high altitude (HA; 5,050 m) in 11 adult subjects (23-48 years old, 8 atopic, 3 nonatopic) affected by mild asthma. Basal FEV1 at SL and HA were not different (p = 0.09), whereas the decrease in FEV1 induced by the challenge was significantly higher at SL than at HA. (1) Hyposmolar aerosol: at SL the mean FEV1 decreased by 28% from 4.32 to 3.11 liters; at 5,050 m by 7.2% from 4.41 to 4.1 liters (p < 0.001). (2) Methacholine challenge: at SL PD20-FEV1 was 700 micrograms and at HA > 1,600 micrograms (p < 0.005). In 3 asthmatic and 5 nonasthmatic subjects plasma levels of cortisol were also measured. The mean value at SL was 265 nmol and 601 nmol at HA (p < 0.005). We suppose that the reduction in bronchial response might be mainly related to the protective role carried out by the higher levels of cortisol and, as already known, catecholamines.

We tested the hypothesis that the individual ventilatory adaptation to high altitude (HA, 5050 m) may influence renal water excretion in response to water loading. In 8 healthy humans (33+/-4 S.D. years) we studied, at sea level (SL) and at HA, resting ventilation (VE), arterial oxygen saturation (SpO2), urinary output after water loading (WL, 20 mL/kg), and total body water (TBW). Ventilatory response to HA was defined as the difference in resting VE over SpO2 (DeltaVE/DeltaSpO2) from SL to HA. At HA, a significant increase in urinary volume after the first hour from WL (%WLt0-60) was observed. Significant correlations were found between DeltaVE/DeltaSpO2 versus %WLt0-60 at HA and versus changes in TBW, from SL to HA. In conclusion, in healthy subjects the ventilatory response to HA influences water balance and correlates with kidney response to WL. A higher ventilatory response at HA, allowing a more efficient water renal handling, is likely to be a protective mechanisms from altitude illness.

The oxygen saturation values reported in the high altitude literature are usually taken during a few minutes of measurement either at rest or during exercise. We aimed to investigate the daily hypoxic profile by monitoring oxygen saturation for 24h in 8 lowlanders (4 females, ages 26 to 59) during trekking from Lukla (2850m) to the Pyramid Laboratory (5050m). Oxygen saturation was measured (1) daily at each altitude (sm), (2) for 24-h during ascent to 3500m, 4200m, and on day 1 at 5050m (lm), and (3) during a standardized exercise (em). Results: (1) the sm and lm values were 90.9% (±0.5) and 86.4% (±1.1) at 3500m; 85.2%(±1.1), and 80% (±1.9) at 4200m; 83.8%(±1) and 77% (±1.7) at 5050m (p<0.05); (2) the daily time spent with oxygen saturation <90% was 56.5% at 3500m, 81% at 4200m, and 95.5% at 5050m; (3) during exercise, oxygen saturation decreased by 10.58%, 13.43%, and 11.24% at 3500, 4200, and 5050?m, respectively. In conclusion, our data show that the level of hypoxemia during trekking at altitude is more severe than expected on the basis of a short evaluation at rest and should be taken into account.

Assessment of the presence and severity of acute mountain sickness (AMS) is based on subjective reporting of the sensation of symptoms. The Lake Louise symptom scoring system (LLS) uses categorical variables to rate the intensity of AMS-related symptoms (headache, gastrointestinal distress, dizziness, fatigue, sleep quality) on 4-point ordinal scales; the sum of the answers is the LLS self-score (range 0–15). Recent publications indicate a potential for a visual analogue scale (VAS) to quantify AMS. We tested the hypothesis that overall and single-item VAS and LLS scores scale linearly. We asked 14 unacclimatized male subjects [age 41 (14), mean (SD) yr; height 176 (3)?cm; weight 75 (9)?kg] who spent 2 days at 3647?m and 4 days at 4560?m to fill out LLS questionnaires, with a VAS for each item (i) and a VAS for the overall (o) sensation of AMS, twice a day (n?=?172). Even though correlated (r?=?0.84), the relationship between LLS(o) and VAS(o) was distorted, showing a threshold effect for LLS(o) scores below 5, with most VAS(o) scores on one side of the identity line. Similar threshold effects were seen for the LLS(i) and VAS(i) scores. These findings indicate nonlinear scaling characteristics that render difficult a direct comparison of studies done with either VAS or LLS alone

We compared the rate of perceived exertion for respiratory (RPE,resp) and leg (RPE,legs) muscles, using a 10-point Borg scale, to their specific power outputs in 10 healthy male subjects during incremental cycle exercise at sea level (SL) and high altitude (HA, 4559 m). Respiratory power output was calculated from breath-by-breath esophageal pressure and chest wall volume changes. At HA ventilation was increased at any leg power output by ? 54%. However, for any given ventilation, breathing pattern was unchanged in terms of tidal volume, respiratory rate and operational volumes of the different chest wall compartments. RPE,resp scaled uniquely with total respiratory power output, irrespectively of SL or HA, while RPE,legs for any leg power output was exacerbated at HA. With increasing respective power outputs, the rate of change of RPE,resp exponentially decreased, while that of RPE,legs increased. We conclude that RPE,resp uniquely relates to respiratory power output, while RPE,legs varies depending on muscle metabolic conditions.