Annalisa Cogo

Pulmonary extravascular fluid accumulation in recreational climbers: a prospective study

BACKGROUND High altitude pulmonary oedema (HAPE) that is severe enough to require urgent medical care is infrequent. We hypothesised that subclinical HAPE is far more frequent than suspected during even modest climbs of average effort. METHODS We assessed 262 consecutive climbers of Monte Rosa (4559 m), before ascent and about 24 h later on the summit 1 h after arriving, by clinical examination, electrocardiography, oximetry, spirometry, carbon monoxide transfer, and closing volume. A chest radiograph was taken at altitude. FINDINGS Only one climber was evacuated for HAPE, but 40 (15%) of 262 climbers had chest rales or interstitial oedema on radiograph after ascent. Of 37 of these climbers, 34 (92%) showed increased closing volume. Of the 197 climbers without oedema, 146 (74%) had an increase in closing volume at altitude. With no change in vital capacity, forced expiratory volume in 1 s and forced expiratory flow at 25-75% of forced vital capacity increased slightly at altitude, without evidence of oedema. If we assume that an increased closing volume at altitude indicates increased pulmonary extravascular fluid, our data suggest that three of every four healthy, recreational climbers have mild subclinical HAPE shortly after a modest climb. INTERPRETATION The risk of HAPE might not be confined to a small group of genetically susceptible people, but likely exists for most climbers if the rate of ascent and degree of physical effort are great enough, especially if lung size is normal or low.

Bronchial Asthma and Airway Hyperresponsiveness at High Altitude

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.

High altitude exposure reduces bronchial responsiveness to hypo-osmolar aerosol in lowland asthmatics

It is well-known that many patients with asthma undergo clinical improvement during a stay at high altitude. At high altitude, the atmospheric and climatic conditions (such as hypoxia, cold and dry air inhalation) could modify the bronchial responsiveness in asthmatics. Our study was designed to assess the difference in bronchial responsiveness to hypotonic aerosol between sea level and high altitudes in nonresident asthmatic subjects. The results were obtained during two mountaineering expeditions above 4,000 m i.e. at 4,559 m on Mt Rosa, Italy; and at 5,050 m near the Mt Everest base camp in Nepal. Eleven mild asthmatics performed standard bronchial challenges with ultrasonically nebulized distilled water (5 min inhalation, delivery 2 mL-min-1) at sea level and after staying at least 72 h at the above mentioned altitudes. The decrease in forced expiratory volume in one second (FEV1) from baseline was used as index of bronchial response. There was no significant difference in pre-challenge FEV1 between sea level and high altitude in either study. However, the bronchoconstriction response to ultrasonically nebulized distilled water was significantly reduced at high altitude in both studies. At sea level the mean FEV1 decrease was 22.2% (range 15-35%), whereas as the maximal altitude it was 6.7% (range 2-11%). Our results indicate that there is a reduction in bronchial responsiveness to hypoosmolar aerosol at high altitude. This suggests that atmospheric and climatic conditions, or physiological adaptations, via mediators such as atrial natriuretic peptide, are beneficial to patients with asthma at high altitude.

Hypoxic ventilatory response in successful extreme altitude climbers

A very high ventilatory response to hypoxia is believed necessary to reach extreme altitude without oxygen. Alternatively, the excessive ventilation could be counterproductive by exhausting the ventilatory reserve early on. To test these alternatives, 11 elite climbers (2004 Everest-K2 Italian Expedition) were evaluated as follows: 1) at sea level, and 2) at 5,200 m, after 15 days of acclimatisation at altitude. Resting oxygen saturation, minute ventilation, breathing rate, hypoxic ventilatory response, maximal voluntary ventilation, ventilatory reserve (at oxygen saturation = 70%) and two indices of ventilatory efficiency were measured. Everest and K2 summits were reached 29 and 61 days, respectively, after the last measurement. Five climbers summited without oxygen, the other six did not, or succeeded with oxygen (two climbers). At sea level, all data were similar. At 5,200 m, the five summiters without oxygen showed lower resting minute ventilation, breathing rate and ventilatory response to hypoxia, and higher ventilatory reserve and ventilatory efficiency, compared to the other climbers. Thus, the more successful climbers had smaller responses to hypoxia during acclimatisation to 5,200 m, but, as a result, had greater available reserve for the summit. A less sensitive hypoxic response and a greater ventilatory efficiency might increase ventilatory reserve and allow sustainable ventilation in the extreme hypoxia at the summit.

Efficacy and tolerability of yoga breathing in patients with chronic obstructive pulmonary disease: a pilot study.

PURPOSE Yoga-derived breathing has been reported to improve gas exchange in patients with chronic heart failure and in participants exposed to high-altitude hypoxia. We investigated the tolerability and effect of yoga breathing on ventilatory pattern and oxygenation in patients with chronic obstructive pulmonary disease (COPD). METHODS Patients with COPD (N = 11, 3 women) without previous yoga practice and taking only short-acting β2-adrenergic blocking drugs were enrolled. Ventilatory pattern and oxygen saturation were monitored by means of inductive plethysmography during 30-minute spontaneous breathing at rest (sb) and during a 30-minute yoga lesson (y). During the yoga lesson, the patients were requested to mobilize in sequence the diaphragm, lower chest, and upper chest adopting a slower and deeper breathing. We evaluated oxygen saturation (SaO2%), tidal volume (VT), minute ventilation (E), respiratory rate (i>f), inspiratory time, total breath time, fractional inspiratory time, an index of thoracoabdominal coordination, and an index of rapid shallow breathing. Changes in dyspnea during the yoga lesson were assessed with the Borg scale. RESULTS During the yoga lesson, data showed the adoption of a deeper and slower breathing pattern (VTsb L 0.54[0.04], VTy L 0.74[0.08], P = .01; i>fsb 20.8[1.3], i>fy 13.8[0.2], P = .001) and a significant improvement in SaO2% with no change in E (SaO2%sb 91.5%[1.13], SaO2%y 93.5%[0.99], P = .02; Esb L/min 11.2[1.1], Ey L/min 10.2[0.9]). All the participants reported to be comfortable during the yoga lesson, with no increase in dyspnea index. CONCLUSION We conclude that short-term training in yoga is well tolerated and induces favorable respiratory changes in patients with COPD.

Respiratory Function at Different Altitudes

For the evaluation of a respiratory test at high altitude, several factors must be taken into account: the decreased barometric pressure, the decreased density of air and the degree of acclimatization which is related to the altitude and to the length of exposure. Several studies have shown a reduction in forced vital capacity (FVC) at high altitude and using simulated conditions, mainly related to an increase in pulmonary blood volume and development of interstitial edema. To assess the daily spirometric patterns during ascending to high altitudes we studied 17 healthy subjects at both Capanna Regina Margherita on the Italian Alps (4,559 m) and the Pyramid Laboratory in Nepal (5,050 m). Respiratory function tests were performed every day. Peak expiratory flow values significantly increased. The mean percent increase was 15% at 3,200 and 3,600 m and 26% at 4,559 m. FVC and MEF25 values showed a significant decrease (p < 0.005) during the first days above 3,500 m and improved only after several days spent above this altitude. For each subject the maximal reductions in FVC and maximal expiratory flow (MEF) at 25% of FVC however were found on different days. In our opinion, these data support the hypothesis that at high altitude the respiratory function can be affected by the presence of an increased pulmonary blood volume and/or the development of interstitial edema. The observed changes in forced expiration curves at high altitude seem to reflect the degree of acclimatization that is related to the individual susceptibility, to the altitude reached and to the duration of the exposure. These changes are transient and resolve after returning to sea level.

Airway responses to methacholine and exercise at high altitude in healthy lowlanders

Peribronchial edema has been proposed as a mechanism enhancing airway responses to constrictor stimuli. Acute exposure to altitude in nonacclimatized lowlanders leads to subclinical interstitial pulmonary edema that lasts for several days after ascent, as suggested by changes in lung mechanics. We, therefore, investigated whether changes in lung mechanics consistent with fluid accumulation at high altitude within the lungs are associated with changes in airway responses to methacholine or exercise. Fourteen healthy subjects were studied at 4,559 and at 120 m above sea level. At high altitude, both static and dynamic lung compliances and respiratory reactance at 5 Hz significantly decreased, suggestive of interstitial pulmonary edema. Resting minute ventilation significantly increased by approximately 30%. Compared with sea level, inhalation of methacholine at high altitude caused a similar reduction of partial forced expiratory flow but less reduction of maximal forced expiratory flow, less increments of pulmonary resistance and respiratory resistance at 5 Hz, and similar effects of deep breath on pulmonary and respiratory resistance. During maximal incremental exercise at high altitude, partial forced expiratory flow gradually increased with the increase in minute ventilation similarly to sea level but both achieved higher values at peak exercise. In conclusion, airway responsiveness to methacholine at high altitude is well preserved despite the occurrence of interstitial pulmonary edema. We suggest that this may be the result of the increase in resting minute ventilation opposing the effects and/or the development of airway smooth muscle force, reduced gas density, and well preserved airway-to-parenchyma interdependence.

Respiratory and leg muscles perceived exertion during exercise at altitude.

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.

Comparison of a visual analogue scale and Lake Louise symptom scores for acute mountain sickness

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.

Periodic Breathing, Arterial Oxyhemoglobin Saturation, and Heart Rate during Sleep at High Altitude

The aim of this study was to investigate the effects of acclimatization to high altitude on periodic breathing (PB), arterial oxygen saturation (Sao(2)), and heart rate (HR). Nine male elite climbers, age 24-52 years underwent overnight cardiorespiratory monitoring at sea level and at Everest North Base Camp (5180 m), during the first (BC1) and the tenth (BC2) nights. PB was commonplace in all subjects at high altitude. PB cycle duration increased (p<0.0001) from BC1 (21.7±1.9 s) to BC2 (26.7±2.1 s). Mean Sao(2) from BC1 to BC2, significantly increased during wakefulness (77.4±3.4% vs. 82.5±2.8%; p<0.001) and during sleep regular breathing (73.3±3.8% vs. 77.8±2.9%; p=0.022). During PB, mean higher Sao(2) was 75.3±3.6% at BC1 and 82.4±2.9% at BC2 (p<0.001); mean lower Sao(2) was 68.2±4.0% at BC1 and 74.5±4.3% at BC2 (p<0.01). During PB, mean higher HR was 72.4±8.8 b/min at BC1 and 63.3±6.0 b/min at BC2 (p<0.0002); mean lower HR were 53.6±7.5% at BC1 and 43.6±7.3% at BC2 (p<0.0001). The mean Sao(2) during PB compared with Sao(2) at night without PB was unchanged. Acclimatization to high altitude resulted in an overall increase in Sao(2) along with an increase in the PB cycle duration and a decrease in HR.