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Altitude Sickness
Published in Charles Theisler, Adjuvant Medical Care, 2023
Altitude sickness is the negative effect of low blood oxygen at higher altitudes. Mild altitude sickness is called acute mountain sickness (AMS) and is quite similar to a hangover in that it causes headache, nausea, and fatigue. Acute (sudden) altitude sicknesses can occur as low as 8,000 feet (2,500 meters) above sea level.
Disorders of Consciousness
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Suffocation: Aspiration of blood or vomitus.Compression of the trachea by hemorrhage or a surgical pack.Obstruction of the trachea by a foreign body.Drowning.Status asthmaticus.Strangulation.Altitude sickness.
Obstruction of the Respiratory Orifices, Larynx, Trachea and Bronchia
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
This type of asphyxiation is very rarely observed. Fatalities only occur at high altitudes, for example while mountaineering, in cable cars, hot air balloons or aeroplanes. The decreasing partial O2 pressure is responsible for altitude sickness. This involves hypoxic pulmonary vasoconstriction, whereby the lungs’ ability to absorb O2 is diminished. Moreover, a pulmonary oedema develops due to hypertension. The body's respiratory control does not counteract the mechanism as it responds primarily to the CO2 content of the blood, which, however, does not increase due to decreasing air pressure.
Phospholipid metabolites of the gut microbiota promote hypoxia-induced intestinal injury via CD1d-dependent γδ T cells
Published in Gut Microbes, 2022
Yuyu Li, Yuchong Wang, Fan Shi, Xujun Zhang, Yongting Zhang, Kefan Bi, Xuequn Chen, Lanjuan Li, Hongyan Diao
Altitude sickness is a common high-altitude clinical syndrome after exposure to low-pressure and low-oxygen environments and is especially common when individuals who typically reside in plains areas quickly enter plateau areas over 2500 meters above sea level.2 Shortness of breath and central nervous system symptoms such as headache and dizziness are the main symptoms of acute altitude sickness, which can lead to life-threatening high altitude pulmonary edema and high altitude cerebral edema if left untreated.1 However, affected individuals can also experience gastrointestinal symptoms such as nausea, vomiting and diarrhea after entering plateau areas, which may further worsen dyspnea, dizziness and headache. Although increasing evidence indicates that intestinal mucosal injury is the main cause of gastrointestinal dysfunction, the pathogenesis of gastrointestinal reactions related to high altitude is still unclear.
A New High Affinity Hemoglobin Variant: Hb San Francisco-KP (HBB: c.104T>C)
Published in Hemoglobin, 2021
Jahan Tavakoli, Gwendolyn Ho, Juraj Kavecansky, Ashok P. Pai
Subsequently, the patient was evaluated in our hematology sub-specialty center in November 2018. At this evaluation, the patient reported a recent vacation to Colorado where he experienced what was initially diagnosed as ‘altitude sickness’ with symptoms of headache, fatigue, insomnia and irritability. A complete blood count demonstrated a PCV value of 0.50 L/L and the patient experienced resolution of all symptoms after one judicious phlebotomy session was performed, with no adverse effect reported on exercise capacity. This led to a further evaluation of the etiology of his polycythemia. The initial p50 testing noted a lower value of 20.0 mmHg (reference range 24.0–30.0 mmHg) consistent with a left-shifted oxygen dissociation curve, suggesting an increased oxygen affinity Hb (Figure 1). Hemoglobin electrophoresis did not show any abnormalities and the RBC indices were all within normal ranges, making a concomitant α-thalassemia (α-thal) clinically unlikely. Hemoglobin separation by high performance liquid chromatography (HPLC) (Bio-Rad Laboratories, Hercules, CA, USA) was done as well as isoelectric focusing and capillary electrophoresis. These showed normal proportions of Hb A, Hb A2 and Hb F, without an abnormal separation band. However, isopropanol stability testing was abnormal, thus suggesting the presence of an unstable Hb variant.
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
A wide range of Western drugs is available for the prevention and treatment of altitude sickness. One representative drug is acetazolamide, which exhibits certain antioxidant effects. Hung et al. conducted a study where acetazolamide was administered prophylactically to individuals with a history of acute altitude sickness. Upon reentering high altitude areas, acetazolamide increased parasympathetic activity, thereby expediting the acclimatization process to high altitude, accompanied by changes in HRV (118). Naghan et al. discovered that acetazolamide improved the prognosis of patients with central apnea resulting from opioid abuse, leading to decreased LF and LF/HF of HRV (119). Nevertheless, the precise mechanism and further clinical trials regarding the effects of acetazolamide on HRV need to be investigated. Certain drugs used for cardiovascular diseases also exhibit anti-high altitude sickness effects, and their correlation with HRV has been well established. Studies have demonstrated that metoprolol (a beta-blocker) and trimetazidine (an anti-anginal agent) positively affect HRV in cardiovascular conditions such as essential hypertension, acute myocardial infarction, and coronary artery disease (120–127,133). Nifedipine (a calcium channel blocker) inhibits calcium influx and dilates arterial blood vessels. Nifedipine shows potential anti-high altitude sickness effects and can influence HRV in cardiovascular conditions such as hypertension (128–131). Furthermore, several studies have indicated that the combination of anti-high altitude sickness drugs yields greater improvements in HRV. For instance, the combination of metoprolol with nifedipine, felodipine, beloprim, or trimetazidine has demonstrated more significant enhancements in HRV (110,132,134–137).