Objective: The study was undertaken to determine whether normobaric hypoxia causes elevated brain volume and intracranial pressure in individuals with symptoms consistent with acute mountain sickness (AMS). Methods: Thirteen males age = (26 (sd 6)) years were exposed to normobaric hypoxia (12% O-2) and normoxia (21% O-2). After 2 and 10 hours, AMS symptoms were assessed alongside ventricular and venous vessel volumes, cerebral blood flow, regional brain volumes, and intracranial pressure, using high-resolution magnetic resonance imaging. Results: In normoxia, neither lateral ventricular volume (R-2 = 0.07, p = 0.40) nor predominance of unilateral transverse venous sinus drainage (R-2 = 0.07, p = 0.45) was related to AMS symptoms. Furthermore, despite an increase in cerebral blood flow after 2 hours of hypoxia (hypoxia vs normoxia: Delta 148ml/min(-1), 95% confidence interval [CI] = 58 to 238), by 10 hours, when AMS symptoms had developed, cerebral blood flow was normal (Delta-51ml/min(-1), 95% CI = -141 to 39). Conversely, at 10 hours brain volume was increased (Delta 59ml, 95% CI = 8 to 110), predominantly due to an increase in gray matter volume (Delta 73ml, 95% CI = 25 to 120). Therefore, cerebral spinal fluid volume was decreased (Delta-40ml, 95% CI=-67 to -14). The intracranial pressure response to hypoxia varied between individuals, and as hypothesized, the most AMS-symptomatic participants had the largest increases in intracranial pressure (AMS present, Delta 7mmHg, 95% CI=-2.5 to 17.3; AMS not present, Delta-1mmHg, 95% CI=-3.3 to 0.5). Consequently, there was a significant relationship between the change in intracranial pressure and AMS symptom severity (R(2=)0.71, p=0.002). Interpretation: The data provide the strongest evidence to date to support the hypothesis that the "random" nature of AMS symptomology is explained by a variable intracranial pressure response to hypoxia.
Long flights are associated with passenger discomfort. This study, conducted in an altitude chamber equipped to resemble a commercial-aircraft cabin, examined symptoms and oxygen saturation during a 20-hour simulated flight. The frequency of reported discomfort increased with increasing altitude; there was also a drop in arterial oxygen saturation of 4.4 percentage points at a simulated altitude of 8000 ft. There was less discomfort at simulated altitudes of 6000 ft or less. This study examined symptoms and oxygen saturation during a 20-hour simulated flight. The frequency of reported discomfort increased with increasing altitude. There was less discomfort at simulated altitudes of 6000 ft or less. A commonly encountered but generally unrecognized exposure to moderate altitude (6500 to 8000 ft [1981 to 2438 m]) occurs during commercial flight. Although the cabins of commercial aircraft are pressurized to protect occupants from the very low barometric pressures at flight altitudes, sea-level pressure (760 mm Hg) is not maintained. Instead, aircraft are designed to maintain cabin pressure at a level no lower than 565 mm Hg (equivalent to an altitude of 8000 ft) when the airplane is at its maximum operating altitude. 1 Higher levels of pressurization decrease the energy available for other aircraft systems, reduce the operational lifetime of . . .
Acute mountain sickness (AMS) is a common problem among visitors at high altitude, and may progress to life-threatening pulmonary and cerebral oedema in a minority of cases. International consensus defines AMS as a constellation of subjective, non-specific symptoms. Specifically, headache, sleep disturbance, fatigue and dizziness are given equal diagnostic weighting. Different pathophysiological mechanisms are now thought to underlie headache and sleep disturbance during acute exposure to high altitude. Hence, these symptoms may not belong together as a single syndrome. Using a novel visual analogue scale (VAS), we sought to undertake a systematic exploration of the symptomatology of AMS using an unbiased, data-driven approach originally designed for analysis of gene expression. Symptom scores were collected from 292 subjects during 1110 subject-days at altitudes between 3650 m and 5200 m on Apex expeditions to Bolivia and Kilimanjaro. Three distinct patterns of symptoms were consistently identified. Although fatigue is a ubiquitous finding, sleep disturbance and headache are each commonly reported without the other. The commonest pattern of symptoms was sleep disturbance and fatigue, with little or no headache. In subjects reporting severe headache, 40% did not report sleep disturbance. Sleep disturbance correlates poorly with other symptoms of AMS (Mean Spearman correlation 0.25). These results challenge the accepted paradigm that AMS is a single disease process and describe at least two distinct syndromes following acute ascent to high altitude. This approach to analysing symptom patterns has potential utility in other clinical syndromes.
Objective: To determine whether 2 days of staging at 2500–3500 m, combined with either high or low physical activity, reduces acute mountain sickness (AMS) during subsequent ascent to 4300 m. Methods: Three independent groups of unacclimatized men and women were staged for 2 days at either 2500 m ( n = 18), 3000 m ( n = 16), or 3500 m ( n = 15) before ascending and living for 2 days at 4300 m and compared with a control group that directly ascended to 4300 m ( n = 12). All individuals departed to the staging altitudes or 4300 m after spending one night at 2000 m during which they breathed supplemental oxygen to simulate sea level conditions. Half in each group participated in ∼3 hours of daily physical activity while half were sedentary. Women accounted for ∼25% of each group. AMS incidence was assessed using the Environmental Symptoms Questionnaire. AMS was classified as mild (≥0.7 and <1.5), moderate (≥1.5 and <2.6), and severe (≥2.6). Results: While staging, the incidence of AMS was lower ( p < 0.001) in the 2500 m (0%), 3000 m (13%), and 3500 m (40%) staged groups than the direct ascent control group (83%). After ascent to 4300 m, the incidence of AMS was lower in the 3000 m (43%) and 3500 m (40%) groups than the 2500 m group (67%) and direct ascent control (83%). Neither activity level nor sex influenced the incidence of AMS during further ascent to 4300 m. Conclusions: Two days of staging at either 3000 or 3500 m, with or without physical activity, reduced AMS during subsequent ascent to 4300 m but staging at 3000 m may be recommended because of less incidence of AMS.
High‐altitude exposure is characterized by the appearance of periodic breathing during sleep. Only limited evidence is available, however, on the presence of gender‐related differences in this breathing pattern. In 37 healthy subjects, 23 male and 14 female, we performed nocturnal cardio‐respiratory monitoring in the following conditions: (1) sea level; (2) first/second night at an altitude of 3400 m; (3) first/second night at an altitude of 5400 m and after a 10 day sojourn at 5400 m. At sea level, a normal breathing pattern was observed in all subjects throughout the night. At 3400 m the apnea–hypopnea index was 40.3 ± 33.0 in males (central apneas 77.6%, central hypopneas 22.4%) and 2.4 ± 2.8 in females (central apneas 58.2%, central hypopneas 41.8%; P < 0.01). During the first recording at 5400 m, the apnea–hypopnea index was 87.5 ± 35.7 in males (central apneas 60.0%, central hypopneas 40.0%) and 41.1 ± 44.0 in females (central apneas 73.2%, central hypopneas 26.8%; P < 0.01), again with a higher frequency of central events in males as seen at lower altitude. Similar results were observed after 10 days. With increasing altitude, there was also a progressive reduction in respiratory cycle length during central apneas in males (26.9 ± 3.4 s at 3400 m and 22.6 ± 3.7 s at 5400 m). Females, who displayed a significant number of central apneas only at the highest reached altitude, were characterized by longer cycle length than males at similar altitude (30.1 ± 5.8 s at 5400 m). In conclusion, at high altitude, nocturnal periodic breathing affects males more than females. Females started to present a significant number of central sleep apneas only at the highest reached altitude. After 10 days at 5400 m gender differences in the apnea–hypopnea index similar to those observed after acute exposure were still observed, accompanied by differences in respiratory cycle length.
Abstract Introduction Decision making is impaired in hypoxic environments, which may have serious or even lethal consequences for mountaineers. An acclimatisation period prior to high altitude exposures may help to overcome adverse effects of hypoxia. Thus, we investigated possible effects of short-term pre-acclimatisation on decision making in hypoxia. Methods In a randomized controlled study design, 52 healthy participants were allocated to a hypoxia group (HG: short-term pre-acclimatisation by the use of intermittent hypoxia 7 × 1 h at Fi O2 = 12.6%, equivalent to 4500 m) or a control group (CG: sham pre-acclimatisation 7 × 1 h at Fi O2 = 20.9%, equivalent to 600 m). The number of risky decisions was assessed using the Game of Dice Task at four time points during a 12-hours stay in hypoxia (Fi O2 = 12.6%). Results 42 (HG: 27, CG: 25) participants completed the study. The number of risky decisions was significantly ( p = 0.048 as determined by 4 × 2 ANCOVA) reduced in the hypoxia group compared to the control group, partial η2 = 0.11, when the age-effect on decision making was controlled. Self-reported positive affective valence prior to decision making was negatively related to the number of risky decisions, r < − 0.38. Conclusion Short-term pre-acclimatisation might influence decision making in hypoxia in a positive way and might be considered as a risk-reducing preparation method prior to exposures to hypoxic environments. Positive affective states seem to have a medium-sized protective effect against risky decision making.
Negi, PC, R. Marwaha, S. Asotra, A. Kandoria, N. Ganju, R. Sharma, R.V. Kumar, and R. Bhardwaj. Prevalence of high altitude pulmonary hypertension among the natives of Spiti Valley—A high altitude region in Himachal Pradesh, India. High Alt Med Biol 15:504–510, 2014.—The study aimed to determine the prevalence of high altitude pulmonary hypertension (HAPH) and its predisposing factors among natives of Spiti Valley. A cross-sectional survey study was done on the permanent natives of Spiti Valley residing at an altitude of 3000 m to 4200 m. Demographic characteristics, health behavior, anthropometrics, and blood pressure were recorded. Investigations included recording of 12 lead electrocardiogram (ECG), SaO 2 with pulse oximeter, spirometry and echocardiography study, and measurement of Hb levels using the cynmethhemoglobin method. HAPH was diagnosed using criteria; tricuspid regurgitation (TR) gradient of ≥46 mmHg. ECG evidence of RV overload on 12 lead ECG was documented based on presence of 2 out of 3 criteria; R>S in V1, right axis deviation or RV strain, T wave inversion in V1 and V2. Data of 1087 subjects were analyzed who were free of cardiorespiratory diseases to determine the prevalence of HAPH and its predisposing factors. HAPH was recorded in 3.23% (95% C.I. of 0.9–8.1%) and ECG evidence of right ventricular (RV) overload was 1.5% in the study population. Prevalence of HAPH was not different in men and women 2.63% vs. 3.54% p <0.2. Age (Z statistics of 3.4 p <0.0006), hypoxemia (Z statistics of 2.9 p <0.002), and erythrocythemia (Z statistics of 4.7 p <0.003) were independently associated with HAPH. Altitude of residence was not found to be significantly associated with HAPH, although there was a trend of increasing prevalence with increasing altitude. It can be concluded that HAPH is prevalent in 3.23% of natives of Spiti Valley. Increasing age, erythrocythemia and hypoxemia are independent predisposing factors.
Muratali Uulu, Kubatbek, Meerim Cholponbaeva, Melis Duishobaev, Aidana Toktosunova, Abdirashit Maripov, Akylbek Sydykov, and Akpay Sarybaev. A case of subacute infantile mountain sickness in a Kyrgyz child. High Alt Med Biol . 19:208–210, 2018.—Subacute infantile mountain sickness (SIMS) is a syndrome of severe pulmonary hypertension and right heart failure that develops in infants born in the lowlands and subsequently brought to live at high altitudes. Earlier postmortem studies have demonstrated significant remodeling of small pulmonary arteries as well as right ventricular hypertrophy and dilatation. In this report, we present a case of SIMS in a Kyrgyz child born to a native highlander mother evaluated by conventional echocardiography and tissue Doppler imaging. An echocardiogram showed severe pulmonary hypertension, a markedly dilated right ventricle with flattening of interventricular septum, and right ventricular dysfunction. To our knowledge, this is the first report of noninvasive imaging of pulmonary circulation and right ventricle in an infant with SIMS and confirmed the diagnosis using echocardiography.