AMS is generally not related to gender, training, alcohol intake, or cigarette smoking. Smoking may represent some kind of acclimatization to hypoxia and is associated with a slightly decreased risk to develop AMS. However, in addition to all the well-known negative health effects, smoking will also impair long-term altitude acclimatization and
lung function. Persons suffering from hypertension, coronary artery disease, and diabetes do not appear to be more prone to AMS than healthy persons.[11, 35] Richalet and colleagues recently documented in a large sample of mountaineers that a low Daporinad concentration ventilatory response to hypoxia at exercise and marked desaturation at exercise in hypoxia are strong risk factors for high-altitude illness. Similarly, check details pronounced arterial oxygen desaturation during sleep has been suggested to be an important risk factor for the development of AMS. Periodic breathing typically occurs during sleeping at high altitudes and may be advantageous up to about 3,000 to 3,500 m because oxygen saturation is stabilized at a relatively high level. At altitudes up to 5,000 m, periodic breathing even appears to override the negative feedback loop in patients with risk of sleep-disordered breathing leading
to revolving sleep apneas. Between 4,500 and 5,500 m altitudes, periodic breathing is replaced by high-frequency breathing driven directly by hypoxia-sensitive neurons in the brain stem. However, at Leukotriene-A4 hydrolase higher altitudes,
frequent arousals cause total sleep deprivation and mental and physical impairments. Patients with AMS can develop HACE when SaO2 further drops, for example, by further ascent or when additionally HAPE occurs. Therefore, further ascending with AMS or existing HAPE are risk factors for HACE, which is thought to be a progression of AMS representing the final encephalopathic, life-threatening stage of cerebral altitude effects.[7, 11, 37] One risk for the development of HAPE relates to individual susceptibility. A genetic predisposition may lead to an exaggerated pulmonary vascular response to hypoxia and as a consequence to pulmonary hypertension.[3, 12] Pulmonary hypertension is the hallmark in the development of the disease, but also other genetic defects might contribute to the pathogenesis (eg, defect of the transepithelial sodium transport). Additionally, a large patent foramen ovale in the heart may contribute to exaggerated arterial hypoxemia and facilitate HAPE at high altitude. Other individual risk factors include hypothermia as well as anatomical or functional abnormalities (eg, having only one lung) facilitating pulmonary hypertension. Finally, men may be more susceptible to HAPE than women, although the mechanisms are probably multifactorial.