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Control of breathing
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
Individuals who rapidly ascend to altitudes above 2440 m are at risk for one of three forms of acute altitude illness, including acute mountain sickness (AMS), high altitude cerebral edema (HACE), and high altitude pulmonary edema (HAPE), which are described in Chapters 20, 21, and 22, respectively. On the surface, it would seem that impaired HVR would predispose to these diseases as individuals with blunted HVR would have lower PaO2 at any given altitude, which would set in motion maladaptive responses and the associated adverse consequences. Strong support for such a link, however, has been lacking.
Death at High Altitude
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
High-altitude cerebral oedema (HACE) has been defined as a condition occurring in persons who have recently arrived at high altitude, usually secondary to AMS or HAPE, and marked by disturbances of consciousness potentially progressing to deep coma, psychiatric changes of varying degree, confusion and ataxia of gait [16]. It is mostly seen as an aggravatio per continuitatem of severe AMS and occurs commonly with HAPE. As in HAPE, reported incidences vary substantially and have been described (conceding obvious differences in study designs, ascent rates and data acquisition) ranging from 0.5 per cent (varying rates of ascent in 5355 visitors to 4555 m in Tibet) [6] to 31 per cent (Vedic pilgrims at 4300 m in Nepal) [7]. HACE most commonly develops over 24–48 hours after initial symptoms of AMS have been detected. Typically, changes in consciousness with drowsiness, progressing lassitude and evident confusion are accompanied by ataxic gait [16]. The initial state of HACE has been compared to the state of mild drunkenness [8]. Patients presenting symptoms of HACE necessitating hospitalization should receive a complete evaluation including a complete history as well as a physical and laboratory examinations including serum electrolytes, blood cell count and renal function. Examination of cerebrospinal fluid may be used to rule out central nervous system (CNS) infections. CNS imaging using magnetic resonance (MR) tomography (e.g. FLAIR, DWI, SWI) may be helpful if available.
Occupational and Environmental Lung Diseases
Published in James M. Rippe, Lifestyle Medicine, 2019
Sunkaru Touray, Emil Tigas, Nicholas A. Smyrnios
High-altitude cerebral edema (HACE) is considered an end-stage form of acute mountain sickness and is characterized by the presence of ataxia and altered mental status in an unacclimatized climber and can occur in the absence of acute mountain sickness or pulmonary edema.
5-Hydroxymethylfurfural (HMF) formation, occurrence and potential health concerns: recent developments
Published in Toxin Reviews, 2021
Ankit Choudhary, Vikas Kumar, Satish Kumar, Ishrat Majid, Poonam Aggarwal, Sheenam Suri
Oxygen is necessary for cell survival. Hypoxic condition (deficiency of oxygen) has various harmful and life-changing effects on human health. Hypoxia may be induced by many factors, including altitude and self-related conditions i.e. degenerative diseases (atherosclerosis, cancer and ischemia) (Pattinson et al.2005, Shapla et al.2018). Several cellular mechanisms are studied and that can alter hypoxic conditions, among which extracellular signal-regulated kinase (ERK) -mediated transactivation of the transcription factor and hypoxia-inducible factors (HIF) are believed to play a major role (Sung et al.2013). The mitochondrial membrane potential is also decreased and affects hypoxic cells in a negative way (Iijima et al.2018). In vitro study of the cell line ECV304 (human umbilical cord vein endothelial cell), Wilhelm et al. (2011) showed that cells pretreated with HMF (200 μg/ml for 1 h) before being exposed to hypoxic conditions (0.3% oxygen for 24 h) exhibited increased activity of mitochondrial membrane potential and reduced the levels of ERK levels. In their further study with a Kunming mice model, the authors showed that pre-exposure to HMF (100 μg/ml, 1 h) significantly decrease the extent of hypoxia-induced permeability of the blood-brain barrier (BBB). Therefore, HMF increases the survival rate under hypobaric hypoxic conditions. Also, it can be a therapeutic agent against high-altitude cerebral edema (HACE), high-altitude pulmonary edema (HAPE) and acute mountain sickness (AMS) (Wilhelm et al.2011, Shapla et al.2018).
Compound Danshen Dripping Pill inhibits high altitude-induced hypoxic damage by suppressing oxidative stress and inflammatory responses
Published in Pharmaceutical Biology, 2021
Yunhui Hu, Jia Sun, Tongxing Wang, Hairong Wang, Chunlai Zhao, Wenjia Wang, Kaijing Yan, Xijun Yan, He Sun
Acute high-altitude hypoxia affects the blood flow and the efficiency of oxygen utilization, causing multi-organ injury and ultimately leading to life-threatening high-altitude cerebral edoema (HACE) or high-altitude pulmonary edoema (HAPE) (Imray et al. 2010). Decreased barometric pressure and subsequent reduction in available oxygen are the primary causal factors in these medical conditions (Clarke 2006). Acetazolamide, dexamethasone and montelukast are widely used to prevent acute altitude sickness. However, they produce a variety of adverse effects, including headache, sensory abnormalities, cardiopalmus osteoporosis and increased risk of infection (Fagenholz et al. 2007; Nieto Estrada et al. 2017). Thus, there is an increasing need for the development of alternative therapies to treat and prevent these conditions.
Physiological and oxidative stress responses to intermittent hypoxia training in Sprague Dawley rats
Published in Experimental Lung Research, 2020
Megha A. Nimje, Himadri Patir, Rajesh Kumar Tirpude, Prasanna K. Reddy, Bhuvnesh Kumar
Acute mountain sickness (AMS) is characterized by headache, nausea, general malaise, and frequently debilitates un-acclimatized individuals.3–5 AMS susceptibility is greatest in un-acclimatized lowlanders rapidly ascending above 2500 m and performing sustained physical work. The lowlander sojourning to high altitude is usually rapid and does not allow sufficient time for progressive acclimatization, increasing the incidence and severity of AMS in people newly exposed to high elevations.4 In one of the studies,6 the incidence and severity of AMS in un-acclimatized soldiers were observed to be 20 to 70% between altitude ascents of 2000 to 3960 m. In a study of the incidence of AMS in conference attendees in the Rocky Mountain foothills (1,920 m to 2,957 m), Nafstadet al3 observed that 25% of participants (n = 3,158) displayed symptoms of AMS. Maggiorini and coworkers4 reported concurring results of AMS in the climbers of Swiss Alps and reported a strong correlation between incidence and altitude: 9% at 2,850 m, 13% at 3050 m, 34% at 3,650 m and 53% at 4,559 m. This pattern is supported by studies that note a similar increase in incidence with rapid ascent and higher altitudes.7–9 AMS is usually self-limited, but may progress into high-altitude cerebral edema (HACE) or high-altitude pulmonary edema (HAPE), both of which are potentially life threatening.