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Genetics and genomics of exposure to high altitude
Published in Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson, Ward, Milledge and West's High Altitude Medicine and Physiology, 2021
Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson
Evidence for a genetic basis for altitude illness can be inferred from patterns of susceptibility including individual patterns, familial patterns, and population patterns. Individual patterns of susceptibility have been recognized for many years although often on an anecdotal rather than scientific basis. For example, Bärtsch et al. (2001) noted that previous history of high altitude disease is one of the best predictors of subsequent illness. In fact, the use of HAPE susceptible and HAPE nonsusceptible individuals has been an important tool in the investigation of this major form of acute altitude illness. Dehnert et al. (2002) studied a group of 76 mountaineers who ascended to the Capanna Margherita at 4559 m altitude. Approximately half of the group had a previous history of HAPE and 66% of these developed the condition on ascent. By contrast, there were no cases of HAPE among those without a previous history. In a study of people who summited on Mount Whitney (4420 m), Wagner et al. (2006) found that a history of AMS was a risk factor for developing the condition. These studies are consistent with individual susceptibility playing a role although they do not distinguish between genetic factors on the one hand or some environmental or development factor on the other. In some cases, physiological measurements can point to risk factors. For example, it has been known for many years that people with excessive pulmonary vascular responses to hypoxia are more likely to develop HAPE (Dehnert et al. 2005; Hultgren et al. 1971). Therefore, genes that may result in pulmonary hypertension are of interest.
The environment and its impact on respiratory health
Published in John W. Dickinson, James H. Hull, Complete Guide to Respiratory Care in Athletes, 2020
Acute altitude illnesses can infrequently occur above 2500 metres elevation, but are much more common above 3000 metres. All three acute altitude illnesses are performance-limiting, but HAPE and HACE are much more serious and can frequently be fatal. For travel to, and events above 2500 metres, event organisers and training camp staff should have access to a clinician with a working knowledge of the diagnosis and management of these conditions. A good resource for this information is the Wilderness Medical Society Consensus Guidelines on the Prevention and Treatment of Altitude Illness. Many groups and travellers choose to bring a pulse oximeter along with them to monitor arterial oxygenation, perhaps with the goal of diagnosing altitude illness. There is much inter-individual variation in arterial oxygenation at altitude, and therefore a single measurement of oxygen saturation is quite variable in its utility for predicting and diagnosing altitude illness. However, the more serious altitude illnesses (HAPE and HACE) are associated with profound desaturation. Thus, oximetry is most useful when monitored longitudinally in order to detect intra-individual trends in oxygenation. If one person has a sudden drop in oxygenation without a significant change in altitude, they merit special attention, and if necessary, treatment.
Death at High Altitude
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
High-altitude pulmonary oedema (HAPE) is a potentially lethal form of altitude sickness typically resulting from rapid ascent to high altitude by unacclimatized visitors to high-altitude regions or from well-acclimatized high-altitude residents returning from low altitudes (re-entry HAPE) [25]. Oedema formation is attributed to (severe) pulmonary hypertension resulting from vasoconstriction due to hypobaric hypoxia [27]. A comprehensible explanation for the characteristically patchy oedema (Figure 30.1) is an uneven hypoxic vasoconstriction leading to a situation where unconstricted vessels fail due to massive pressure exposition [40].
Comprehensive viewpoints on heart rate variability at high altitude
Published in Clinical and Experimental Hypertension, 2023
Jun Hou, Keji Lu, Peiwen Chen, Peng Wang, Jing Li, Jiali Yang, Qing Liu, Qiang Xue, Zhaobing Tang, Haifeng Pei
Autonomic nerves are extensively distributed throughout various tissues and organs, playing a crucial role in regulating the physiological functions of the human body. Dysfunctions of autonomic nerves are associated with the development of numerous diseases when the body experiences hypoxia. High altitude pulmonary edema (HAPE) is a severe non-cardiogenic condition characterized by pulmonary edema, which can be life-threatening and is caused by low atmospheric pressure and hypoxia at high altitudes. When individuals rapidly ascend to high altitudes, their lungs face excessive stress within a short period, which can trigger HAPE (95). Exposure to high altitude hypoxia results in increased sensitivity of the pulmonary vascular system to the sympathetic nervous system and endothelin, while the response to vasodilators diminishes, leading to hypoxic pulmonary vasoconstriction. This constriction increases pulmonary artery pressure, potentially exacerbating HAPE (86,96). Furthermore, acute hypoxia and decreased oxygen saturation can cause ventricular diastolic dysfunction, resulting in HAPE. This condition is characterized by a decrease in HRV, an increase in the LF/HF ratio, and other symptoms (97–99).
Quercetin: a savior of alveolar barrier integrity under hypoxic microenvironment
Published in Tissue Barriers, 2021
Ankit Tripathi, Puja P. Hazari, Anil K. Mishra, Bhuvnesh Kumar, Sarada S.K. Sagi
High altitude pulmonary edema (HAPE) is generally characterized by extravascular fluid accumulation into alveolar spaces of the individuals ascending at an altitude of 2,500 m or above, due to aberrations in the structure & function of the tight junction (TJ) proteins assembly resulting in loss of alveolar barrier function1. HAPE is known to be completely reversed if diagnosed and treated at an early stage1. HAPE typically occurs into two forms- in the first form, it influences non-acclimatized, healthy individuals ascending to HA rapidly; while in the second form or commonly referred to as ‘reentry HAPE, it is sought to affect the acclimatized individuals ascending at HA after a short stay at low altitude regions, depending on the speed, time, and mode of ascent.2 Therefore, studies have substantiated mostly on the time of acclimatization, the pace of ascent, and appropriate planning prior to ascending at HA.2,3 HAPE is a multi-factorial pathological condition arising due to reduced partial pressure of oxygen as a consequence of lower barometric pressure at HA regime.1
Patent Foramen Ovale Closure, A Contemporary Review
Published in Structural Heart, 2018
Raouf Madhkour, Bernhard Meier
Many data suggest an association between high altitude pulmonary edema (HAPE) and the PFO.37,38 In fact, an observational study demonstrated a fourfold frequency of PFO prevalence in HAPE-susceptible subjects compared to the control group (HAPE-resistant subjects). A possible pathophysiological mechanism is that especially a large PFO may contribute to exaggerated arterial hypoxemia at altitude and facilitate HAPE development. 39Sleep apnea syndrome