Strengthening altitude knowledge: a delphi study to define minimum knowledge of altitude illness for laypersons traveling to high altitude

Introduction: A lack of knowledge among laypersons about the hazards of high-altitude exposure contributes to morbidity and mortality from acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE) among high-altitude travelers. There are guidelines regarding the recognition, prevention, and treatment of acute-altitude illness for experts, but essential knowledge for laypersons traveling to high altitudes has not been defined. We sought expert consensus on the essential knowledge required for people planning to travel to high altitudes. Methods: The Delphi method was used. The panel consisted of two moderators, a core expert group and a plenary expert group. The moderators made a preliminary list of statements defining the desired minimum knowledge for laypersons traveling to high altitudes, based on the relevant literature. These preliminary statements were then reviewed, supplemented, and modified by a core expert group. A list of 33 statements was then presented to a plenary group of experts in successive rounds. Results: It took three rounds to reach a consensus. Of the 10 core experts invited, 7 completed all the rounds. Of the 76 plenary experts, 41 (54%) participated in Round 1, and of these 41 a total of 32 (78%) experts completed all three rounds. The final list contained 28 statements in 5 categories (altitude physiology, sleeping at altitude, AMS, HACE, and HAPE). This list represents an expert consensus on the desired minimum knowledge for laypersons planning high-altitude travel. Conclusion: Using the Delphi method, the STrengthening Altitude Knowledge initiative yielded a set of 28 statements representing essential learning objectives for laypersons who plan to travel to high altitudes. This list could be used to develop educational interventions

Capillary supply and fiber morphometry in rat myocardium after intermittent exposure to hypobaric hypoxia.

Panisello, Pere, Joan Ramon Torrella, Teresa Pagés, and Ginés Viscor. Capillary supply and fiber morphometry in rat myocardium after intermittent exposure to hypobaric hypoxia. High Alt. Med. Biol. 8:322-330, 2007. Three groups of male rats were submitted to an intermittent hypobaric hypoxia (IHH) program for 22 days (4 h/day, 5 days/week) in a hypobaric chamber at a simulated altitude of 5000 m. Hearts were removed at the end of the program (H group) and 20 and 40 days later (P20 and P40 groups). A control group (C) was maintained at sea-level pressure. Transverse sections from myocardium were cut and histochemically stained in order to measure fiber morphometry and capillaries. We observed a progressive increase from C to H to P20 animals in capillary (4124 to 4733 to 4816 capillaries/mm2) and fiber densities (2844 to 3125 to 3284 fibers/mm2) associated with significant reductions in fiber area (273, 235, and 227 μm2), perimeter (69, 64, and 62 μm), and diffusion distances (18.2, 16.9, and 16.6 μm). The most significant differences between C and hypoxic groups were found when morphometrical and vascular fiber parameters were combined. The myocardium of the latter had more capillaries per fiber area and per fiber perimeter. These findings indicate that the IHH program elicits an adaptive response of rat myocardium to a more efficient O2 delivery to mitochondria of cardiac muscle cells. Capillarization and fiber morphometric changes showed marked differences over time. In all cases, P20 had higher capillarization parameters and fiber morphometry reductions than H, thus indicating that a delay of about 20 days exists after the hypoxic stimulus ceases to reach complete angiogenesis and fiber morphometry changes. However, P40 animals showed a recovery to basal values of the parameters related to fiber morphometry (area, perimeter, and diffusion distances), but maintained high capillarity values (capillary density, NCF, CCA, CCP)

Volume regulating hormone responses to repeated head-up tilt and lower body negative pressure

Background: We hypothesized the existence of different hormonal response patterns to repeated lower body negative pressure (LBNP) and head-up tilt (HUT) in healthy males. We compared hormonal, cardiovascular and plasma volume changes from rest to stress within- and between-LBNP and HUT applications. Hormones investigated included adrenocorticotropic hormone (ACTH), aldosterone, plasma renin activity (PRA), atrial natriuretic peptide (ANP) and arginine vasopressin (AVP). Materials and methods: Three sequential 30-min bouts of LBNP at -55 mmHg (n = 14) or 70° HUT (n = 9) were preceded by 30-min supine rest, and a 60-min supine rest followed the 3rd stimulus. Results: Plasma renin activity increases above baseline, in relation to aldosterone, were larger with LBNP than with HUT. The 3rd HUT application resulted in a greater increase in aldosterone compared to LBNP. Mean arterial blood pressure was elevated significantly during 1st and 3rd HUT application. ACTH responses were highly correlated with those of aldosterone in both LBNP and HUT (r(2)  = 0·96). AVP responses, in contrast to ANP, to the three consecutive stress situations were not significantly different, both with LBNP and HUT. Conclusions: We speculate that the observed differences in blood pressure and hormonal responses to LBNP and HUT are caused by divergent effects of blood pooling in the splanchnic region, despite similar reductions in splanchnic perfusion. Apparently with repeated central hypovolaemia, especially by the 3rd application of stress, plasma aldosterone levels rise (along with ACTH), conceivably increasing its volume-guarding effect

Ventilation during simulated altitude, normobaric hypoxia and normoxic hypobaria

To investigate the possible effect of hypobaria on ventilation (V̇e) at high altitude, we exposed nine men to three conditions for 10 h in a chamber on separate occasions at least 1 week apart. These three conditions were: altitude (Pb=432, FiO2=0.207), normobaric hypoxia (Pb=614, FiO2=0.142) and normoxic hypobaria (Pb=434, FiO2=0.296). In addition, post-test measurements were made 2 h after returning to ambient conditions at normobaric normoxia (Pb=636, FiO2=0.204). In the first hour of exposure V̇e was increased similarly by altitude and normobaric hypoxia. The was 38% above post-test values and end-tidal CO2 (PetCO2) was lower by 4 mmHg. After 3, 6 and 9 h, the average V̇e in normobaric hypoxia was 26% higher than at altitude (petCO2 was higher than at altitude. Changes in V̇e and PetCO2 in normoxic hypobaria were minimal relative to normobaric normoxia post-test measurements. One possible explanation for the lower V̇e at altitude is that CO2 elimination is relatively less at altitude because of a reduction in inspired gas density compared to normobaric hypoxia; this may reduce the work of breathing or alveolar deadspace. The greater V̇e during the first hour at altitude, relative to subsequent measurements, may be related to the appearance of microbubbles in the pulmonary circulation acting to transiently worsen matching. Results indicate that hypobaria per se effects ventilation under altitude conditions