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 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

Headache, nausea, vomiting, insomnia and peripheral edema are the most important symptoms of acute mountain sickness (AMS), which occur within 6 to 12 h. after exposure to altitudes of more than 2500 m a. s. l. Usually, these symptoms resolve spontaneously; however, they may progress to life-threatening cerebral edema in some cases. High-altitude pulmonary edema (HAPE) is a noncardiogenic edema, which is often preceded by acute mountain sickness. Frequency and severity of these illnesses depend on the altitude, the rate of ascent and the degree of individual susceptibility. A low hypoxic ventilatory drive, sodium and water retention as well as increased capillary permeability are the most important pathophysiological factors which contribute to hypoxemia and edema formation in AMS. They are also important in the pathophysiology of HAPE. In addition, excessive hypoxic pulmonary artery hypertension is most likely crucial in the pathogenesis of HAPE. Constitutional factors which regulate ventilation and pulmonary artery pressure under hypoxia are considered the most important determinants of susceptibility to AMS and HAPE.
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PMID:[Clinical aspects and pathophysiology of altitude sickness]. 837 71

The central autonomic network (CAN) is an integral component of an internal regulation system through which the brain controls visceromotor, neuroendocrine, pain, and behavioral responses essential for survival. It includes the insular cortex, amygdala, hypothalamus, periaqueductal gray matter, parabrachial complex, nucleus of the tractus solitarius, and ventrolateral medulla. Inputs to the CAN are multiple, including viscerosensory inputs relayed on the nucleus of the tractus solitarius and humoral inputs relayed through the circumventricular organs. The CAN controls preganglionic sympathetic and parasympathetic, neuroendocrine, respiratory, and sphincter motoneurons. The CAN is characterized by reciprocal interconnections, parallel organization, state-dependent activity, and neurochemical complexity. The insular cortex and amygdala mediate high-order autonomic control, and their involvement in seizures or stroke may produce severe cardiac arrhythmias and other autonomic manifestations. The paraventricular and other hypothalamic nuclei contain mixed neuronal populations that control specific subsets of preganglionic sympathetic and parasympathetic neurons. Hypothalamic autonomic disorders commonly produce hypothermia or hyperthermia. Hyperthermia and autonomic hyperactivity occur in patients with head trauma, hydrocephalus, neuroleptic malignant syndrome, and fatal familial insomnia. In the medulla, the nucleus of the tractus solitarius and ventrolateral medulla contain a network of respiratory, cardiovagal, and vasomotor neurons. Medullary autonomic disorders may cause orthostatic hypotension, paroxysmal hypertension, and sleep apnea. Neurologic catastrophes, such as subarachnoid hemorrhage, may produce cardiac arrhythmias, myocardial injury, hypertension, and pulmonary edema. Multiple system atrophy affects preganglionic autonomic, respiratory, and neuroendocrine outputs. The CAN may be critically involved in panic disorders, essential hypertension, obesity, and other medical conditions.
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PMID:The central autonomic network: functional organization, dysfunction, and perspective. 841 66

Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of headache, insomnia, anorexia, nausea, and dizziness, to more serious manifestations, such as vomiting, dyspnea, muscle weakness, oliguria, peripheral edema, and retinal hemorrhage. Although the primary cause of these symptoms is related to the reduced oxygen content and humidity of the ambient air at high altitudes, the physiologic pathway relating hypoxemia to AMS and its sequelae remains unclear. Tips on self-diagnosis and symptom recognition are critical elements to be included in educating patients who are contemplating a trip to high altitudes. Preventive strategies include allowing 2 days of acclimatization before engaging in strenuous exercise at high altitudes, avoiding alcohol, and increasing fluid intake. Conditioning exercise for patients older than 35 years is also recommended before departure. A high-carbohydrate, low-fat, low-salt diet can also aid in preventing the onset of AMS. Acetazolamide (125 mg two or three times daily, or once at bedtime) has also been shown to reduce susceptibility to AMS and the incidence of HAPE and HACE. Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS.
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PMID:A trek to the top: a review of acute mountain sickness. 855 56

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

Ephedra is an amphetamine-like compound with a potent sympathomimetic effect. Ephedrine, its active component, is widely used for weight loss, to enhance athletic performance or as component of some drugs. Its cardiovascular effects include tachycardia, increased inotropy, arterial vasoconstriction and hypertension, and these are the effects for which it is used therapeutically. However, it can also cause adverse effects, such as neuropathy, myopathy, psychosis, addiction, stroke, insomnia, myocarditis, arrhythmias, myocardial infarction or sudden death. We present the case of a patient, with pre-existing psychiatric conditions, who developed congestive heart failure and pulmonary oedema in the context of severe biventricular dysfunction and myocardial necrosis secondary to longstanding ephedrine abuse. Secondary causes of dilated myocardiopathy such as alcohol abuse, autoimmunity, hemochromatosis, thyroid alterations, viral or bacterial myocarditis and coronary heart disease, were ruled out. Five years after total cessation of use of the drug containing ephedrine, the patient is symptom-free, with partial recovery of left ventricular ejection fraction.
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PMID:[Myocardial necrosis and severe biventricular dysfunction in the context of chronic ephedrine abuse]. 2030 Jul 11

High altitude problems like hypoxia, acute mountain sickness, high altitude cerebral edema, pulmonary edema, insomnia, tiredness, lethargy, lack of appetite, body pain, dementia, and depression may occur when a person or a soldier residing in a lower altitude ascends to high-altitude areas. These problems arise due to low atmospheric pressure, severe cold, high intensity of solar radiation, high wind velocity, and very high fluctuation of day and night temperatures in these regions. These problems may escalate rapidly and may sometimes become life-threatening. Shilajit is a herbomineral drug which is pale-brown to blackish-brown, is composed of a gummy exudate that oozes from the rocks of the Himalayas in the summer months. It contains humus, organic plant materials, and fulvic acid as the main carrier molecules. It actively takes part in the transportation of nutrients into deep tissues and helps to overcome tiredness, lethargy, and chronic fatigue. Shilajit improves the ability to handle high altitudinal stresses and stimulates the immune system. Thus, Shilajit can be given as a supplement to people ascending to high-altitude areas so that it can act as a "health rejuvenator" and help to overcome high-altitude related problems.
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PMID:Shilajit: A panacea for high-altitude problems. 2053 96

Altitude physiology began with Paul Bert in 1878. Chronic mountain sickness (CMS) was defined by Carlos Monge in the 1940s in the Peruvian Andes as consisting of excess polycythemia. Hurtado et al performed studies in the Peruvian Andes in the 1950s to 1960s which defined acclimatization in healthy altitude natives, including polycythemia, moderate pulmonary hypertension, and low systemic blood pressure (BP). Electrocardiographic changes of right ventricular hypertrophy (RVH) were noted. Acclimatization of newcomers to altitude involves hyperventilation stimulated by hypoxia and is usually benign. Acute mountain sickness (AMS) in travelers to altitude is characterized by hypoxia-induced anorexia, dyspnea, headache, insomnia, and nausea. The extremes of AMS are high-altitude cerebral edema and high-altitude pulmonary edema. The susceptible high-altitude resident can lose their tolerance to altitude and develop CMS, also referred to as Monge disease. The CMS includes extreme polycythemia, severe RVH, excess pulmonary hypertension, low systemic BP, arterial oxygen desaturation, and hypoventilation.
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PMID:Cardiovascular medicine at high altitude. 2389 41

Upon reaching a height over 2500 m above seal level symptoms of altitude illness can develop over 1 - 5 days. The risk is mainly -determined by the altitude and rate of ascent and the symptoms vary. Most common are symptoms of acute mountain illness (AMS) but more dangerous high altitude cerebral edema (HACE) and high altitude pulmonary edema (HAPE) can also develop. The causes of AMS, HACE and HAPE are lack of oxygen and insufficient acclimatization, but the presenting form is determined by the responses of the body to the lack of oxygen. The most common symptoms of AMS include headache, fatique and nausea, but insomnia and nausea are also common. The most common symptoms of HAPE are breathlessness and lassitude whereas the cardinal sign of HACE is ataxia, but confusion and loss of consciousness can also develop. In this article all three main forms of altitude illness are reviewed. The emphasis is on preventive measures and treatment but new knowledge on pathogenesis is also addressed.
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PMID:[High altitude illness and related diseases - a review]. 3166 13