Altitude Mountain Sickness Research Articles

Does a change in end-tidal carbon dioxide level predict high altitude mountain sickness?

BackgroundIt is postulated that lack of hypoxic ventilatory response is a predictor for AMS. End-tidal carbon dioxide (ETCO2) is an accurate, noninvasive surrogate measure of ventilation. ObjectivesWe sought to determine if changes in baseline ETCO2 predicts the development of AMS. MethodsThis prospective cohort study took place in three separate high-altitude hiking treks. Subjects included a convenience sample of hikers. Predictor variable was change in ETCO2 levels and outcome variable was AMS. Measurements of ETCO2 levels were obtained at the base and repeated daily at various elevations and the summit of each hike. Concurrently, hikers were scored for AMS by a trained investigator. We utilized correlation coefficients and developed a linear regression model for analysis. Results21 subjects in 3 separate hikes participated: 10 ascended to 19,341 ft over 7 days, 6 ascended to 8900 ft in 1 day, and 4 ascended to 11,006 ft in 1 day. Mean age was 40 years, 67% were males, mean daily elevation gain was 2150 ft, and 5 hikers developed AMS. The correlation coefficients for ETCO2 and development of AMS were −0.46 (95%CI -0.33 to −0.57), and −0.77 (95%CI -0.71 to −0.83) for ETCO2 and altitude. ETCO2 predicted the development of symptoms better than the elevation with AUCs of 0.90 (95%CI 0.81–0.99) versus 0.64 (95%CI 0.45–0.83). An ETCO2 measurement of ≤22 mmHg was 100% sensitive and 60% specific for predicting AMS. ConclusionsETCO2 was strongly correlated with altitude and moderately correlated with AMS and it was a better predictor than altitude.

Dynamic cerebral blood flow changes with FOXOs stimulation are involved in neuronal damage associated with high-altitude cerebral edema in mice

Acute hypobaric hypoxia (AHH) exposure causes altitude mountain sickness (AMS) and life-threatening high altitude cerebral edema (HACE). Despite decades of research, the role of cerebral blood flow (CBF) changes in the pathophysiology of severe AMS remains unclear. The current study evaluated spatiotemporal responses of CBF associated with HACE in mice during the early stages of ascent to high altitudes. First, mice were exposed to AHH to test their tolerance to increasing altitudes (3000–8000 m). Because of its significant influence on both locomotor activity and rotarod behavior tests in mice, further observations were initiated at an altitude of 6000 m to investigate the specific pathophysiology of AMS. Compared with controls, laser speckle contrast imaging (LSCI) revealed a significant decrease in CBF during the early stage (0.5–24 h) at an altitude of 6000 m that was accompanied by a significant increase in brain water content (BWC). Moreover, observations of brain lipid oxidative damage and oxidative stress during the early stage of AHH exposure revealed DNA and cellular damage in cortical and hippocampal regions. Transcriptome profiling of the hippocampus revealed upregulation of forkhead box transcription factors. Similarly, western blot assays revealed upregulation of FOXO1a, FOXO3a, caspase-3 and Bax, and downregulation of Bcl-2, indicating a temporal influence of AHH on mitochondrial function and neuronal apoptosis. Thus, we found that the pathophysiology of HACE occurred with dynamic CBF changes, which triggered oxidative stress and neuronal damage in the mouse brain after AHH exposure. Our findings provide potential strategies for treatment of AHH in the future.

Relationship of altitude mountain sickness and smoking: a Catalan traveller’s cohort study

ObjectivesThe aim of this study is to analyse the relationship between smoking and altitude mountain sickness in a cohort of travellers to 2500 metres above sea level (masl) or higher.SettingTravel...

Genetic Variations in Renin-Angiotensin-Aldosterone System (RAAS) Genes Could Contribute to High Altitude Pulmonary Edema: Review

Background: At High Altitude (HA) (elevation >2500m), inevitable hypobaric hypoxia leads to development of symptoms associated with low oxygen pressure in many non acclimatized sojourners which includes severe forms of altitude mountain sickness (AMS) such as high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). These syndromes are reportedly less common in high altitude native population than in lowlanders which can be attributed to genetic adaptations that have taken place over generations. Methods: Numerous genetic studies have been associated with hypoxic adaptation and susceptibility to high altitude conditions. An increased pulmonary arterial pressure (PAP) and fluid loss has been observed in all forms of AMS with varied intensity. Since renin-angiotensin-aldosterone system (RAAS) has a critical function of maintaining homeostasis in closed circulatory system, the polymorphisms occurring in the genes of RAAS pathway could likely be contributing towards acclimatization/mal-adaptation to high altitude maladies. In view of above, this review has been compiled to associate the genetic variations in RAAS with adaptation/acclimatization to high altitude conditions. Results: Studies conducted so far relate allele frequencies of polymorphic loci in genes encoding components of RAAS pathway such as angiotensinogen (AGT), angiotensin converting enzyme (ACE), angiotensin receptors (AT1) and aldosterone synthase (CYP11B2) and associate them with hypertension, regulation of blood pressure and maintenance of osmotic balance in the body. Conclusions: In this review, various studies have been put together comprehensively indicating the involvement of genetic variants of RAAS genes in resistance or sensitivity of an individual towards development of HAPE.

Altitude mountain sickness among tourist populations: a review and pathophysiology supporting management with hyperbaric oxygen

In the mountain climbing community, conventional prevention of altitude mountain sickness (AMS) relies primarily on a formal acclimatization period. AMS symptoms during mountaineering climbs are managed with medication, oxygen and minor recompression (1524–2438 m altitude) using a portable chamber, such as the Gamow Bag. This is not always an acceptable therapy alternative in a predominantly elderly tourist population. The primary problem with reduced pressure at high altitude is hypoxaemia, which causes increased sympathetic activity, induces pulmonary venous constriction, while increasing pulmonary blood flow and regional perfusion. Rapid assents to altitude contribute to an increased incidence of decompression sickness (DCS). The treatment of choice for DCS is hyperbaric oxygenation, thus, treatment of high-altitude induced hypoxaemia using hyperbaric oxygenation (HBO2) is logical. Life Support Technologies group and the Center for Investigation of Altitude Medicine (CIMA, in Cusco, Peru) propose a comprehensive and multidisciplinary approach to AMS management. This approach encompasses traditional and advanced medical interventions including the use of a clinical HBO2 chamber capable of recompression to three times greater than sea level pressure (3 atmosphere absolute (ATA)). The system uses a series of AMS hyperbaric treatment profiles that LST has previously developed to the US military and NASA, and that take greater advantage of vasoconstrictive effects of oxygen under true hyperbaric conditions of 1.25 ATA. These profiles virtually eliminate AMS rebound after the initial treatment often seen in conventional AMS treatment, where the patient is either treated at altitude, or does not recompress back to sea level or greater pressure (1.25 ATA), but returns directly to the same altitude where AMS symptoms first manifested.

EEG, ECG and oxygen concentration changes from sea level to a simulated altitude of 4000m and back to sea level

In order to describe how high altitude affects the body during a one night stay at 4000m experiments were performed in a hypobaric chamber and compared to a study on Dachstein (mountain in Austria, 2700m). Ten subjects had to perform a reaction time task at different altitudes. The EEG and ECG were recorded simultaneously. Additionally, the oxygen saturation of the blood was measured at different altitudes and the subjects filled out a Lake Louise questionnaire that describes the degree of altitude mountain sickness (AMS). After elevation from 134m to 4000m in the hypobaric chamber heart-rate increased from 68.9bpm to 81.6bpm, RMSSD (root mean square of squared differences of adjacent heart beat intervals) decreased from 54.3ms to 33.3ms, the LF/HF ratio increased from 2.5 to 3.9 and oxygen saturation decreased to 82.7% after 11h at 4000m altitude. The Lake Louise Score (LSS) reached 3.4 after one night at 4000m. EEG beta activity between 14Hz and 18Hz was attenuated at 4000m and also after return to 134m. The results indicate that the subjects were not able to adapt to 4000m within 12h in the hypobaric chamber. Even after 1h after the return to 134m all parameters are still affected from the night at 4000m altitude. ECG and EEG changes are in line with results obtained at 2700m height at Dachstein.

Hyperperfusion encephalopathies: hypertensive encephalopathy and related conditions.

Hypertensive encephalopathy (HTE) is a syndrome typified by headache, seizures, and neurologic signs associated with increased systemic blood pressures; edema in the subcortical white matter is seen on imaging studies and is usually reversible, although infarction or hemorrhage may supervene. Based on previous work, we theorize that HTE is associated with increased perfusion to the brain. Syndromes related to HTE may also be encountered in clinical situations in which perfusion to the brain is acutely increased without systemic hypertension (i.e., after treatment of high-grade carotid stenoses or large intracranial arteriovenous malformations, or in high altitude mountain sickness). We therefore refer to these conditions more generally as hyperperfusion encephalopathies (HPE). The clinical and radiographic data of 110 patients (average age, 50.1 years) who presented at the Brigham and Women's Hospital with clinical and radiographic signs of HPE were reviewed; 104 had systemic hypertension and 6 had postcarotid endarterectomy hyperperfusion syndrome. Edema involved the subcortical white matter and occasionally the cortex in all patients. In patients with systemic hypertension, the edema was usually bilateral and located predominantly in the occipital lobes; other brain regions included the parietal lobes, posterior frontal lobes, cerebellum, and splenium of the corpus callosum. The six patients with postcarotid endarterectomy hyperperfusion syndrome had edema in the hemisphere ipsilateral to the operated side involving the anterior and middle cerebral artery territories. The edema in HPE was associated with: increased low attenuation on CT; decreased T(1) and increased T(2) signal on MR imaging; increased cerebral perfusion on single emission computed tomography (SPECT) and perfusion MR imaging;did not show restricted diffusion on MR imaging. The syndrome resolved completely in most cases after the administration of antihypertensive agents, although rarely small infarcts and hemorrhages occurred. Three patients with thrombocytopenia developed large fatal intracranial hemorrhages. The symptoms of HPE are usually nonspecific, but the radiographic findings are consistent. Treatment should be instituted rapidly and patients should be followed until the condition resolves either clinically or radiographically; hemorrhagic complications, although rare, can be serious.

The Effect of Homeopathic Coca on High Altitude Mountain Sickness: Mt. Everest Base Camp

Homeopathic coca was tested among high altitude trekkers en route to the Mt. Everest base camp to determine its effect on mountain sickness symptoms. Study participants ( n = 24) took homeopathic coca while ascending from 8,000 ft. to 17,600 ft. Measurements included: heart rate, oxygen saturation, and a question naire detailing the occurrence and severity of symptoms. Questionnaire items regarding nausea, headaches, difficulty breathing while asleep all demonstrated statistical significance in the experimental group. Oxygen saturation in the exper imental group was significantly higher. In this placebo-controlled, single-blinded, non-randomized study, homeopathic coca significantly reduced the effects of altitude on trekkers in the experimental group when compared with placebo.