Physiology in Medicine: A physiologic approach to prevention and treatment of acute high-altitude illnesses

2015 ◽  
Vol 118 (5) ◽  
pp. 509-519 ◽  
Author(s):  
Andrew M. Luks
Keyword(s):  
High Altitude ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Travel Medicine ◽  
Barometric Pressure ◽  
Time Frame ◽  
Low Oxygen ◽  
Organ Systems ◽  
Prevention And Treatment ◽  
Physiologic Responses

With the growing interest in adventure travel and the increasing ease and affordability of air, rail, and road-based transportation, increasing numbers of individuals are traveling to high altitude. The decline in barometric pressure and ambient oxygen tensions in this environment trigger a series of physiologic responses across organ systems and over a varying time frame that help the individual acclimatize to the low oxygen conditions but occasionally lead to maladaptive responses and one or several forms of acute altitude illness. The goal of this Physiology in Medicine article is to provide information that providers can use when counseling patients who present to primary care or travel medicine clinics seeking advice about how to prevent these problems. After discussing the primary physiologic responses to acute hypoxia from the organ to the molecular level in normal individuals, the review describes the main forms of acute altitude illness—acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema—and the basic approaches to their prevention and treatment of these problems, with an emphasis throughout on the physiologic basis for the development of these illnesses and their management.

Effect of beta-adrenoceptor blockade on renin-aldosterone and alpha-ANF during exercise at altitude

1989 ◽  
Vol 67 (1) ◽  
pp. 141-146 ◽  
Author(s):  
P. Bouissou ◽  
J. P. Richalet ◽  
F. X. Galen ◽  
M. Lartigue ◽  
P. Larmignat ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Barometric Pressure ◽  
Suppressive Effect ◽  
Beta Blockade ◽  
Plasma Norepinephrine ◽  
Plasma Aldosterone Concentration ◽  
Ergometer Exercise

The renin-aldosterone system may be depressed in subjects exercising at high altitude, thereby preventing excessive angiotensin I (ANG I) and aldosterone levels, which could favor the onset of acute mountain sickness. The role of beta-adrenoceptors in hormonal responses to hypoxia was investigated in 12 subjects treated with a nonselective beta-blocker, pindolol. The subjects performed a standardized maximal bicycle ergometer exercise with (P) and without (C) acute pindolol treatment (15 mg/day) at sea level, as well as during a 5-day period at high altitude (4,350 m, barometric pressure 450 mmHg). During sea-level exercise, pindolol caused a reduction in plasma renin activity (PRA, 2.83 +/- 0.35 vs. 5.13 +/- 0.7 ng ANG I.ml-1.h-1, P less than 0.01), an increase in plasma alpha-atrial natriuretic factor (alpha-ANF) level (23.1 +/- 2.9 (P) vs. 10.4 +/- 1.5 (C) pmol/1, P less than 0.01), and no change in plasma aldosterone concentration [0.50 +/- 0.04 (P) vs. 0.53 +/- 0.03 (C) nmol/1]. Compared with sea-level values, PRA (3.45 +/- 0.7 ng ANG I.ml-1.h-1) and PA (0.39 +/- 0.03 nmol/1) were significantly lower (P less than 0.05) during exercise at high altitude. alpha-ANF was not affected by hypoxia. When beta-blockade was achieved at high altitude, exercise-induced elevation in PRA was completely abolished, but no additional decline in PA occurred. Plasma norepinephrine and epinephrine concentrations tended to be lower during maximal exercise at altitude; however, these differences were not statistically significant. Our results provide further evidence that hypoxia has a suppressive effect on the renin-aldosterone system. However, beta-adrenergic mechanisms do not appear to be responsible for inhibition of renin secretion at high altitude.

scholarly journals Cardiac responses to hypoxia and reoxygenation in Drosophila

2015 ◽  
Vol 309 (11) ◽  
pp. R1347-R1357 ◽  
Author(s):  
Rachel Zarndt ◽  
Sarah Piloto ◽  
Frank L. Powell ◽  
Gabriel G. Haddad ◽  
Rolf Bodmer ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Genetic Model ◽  
Heart Function ◽  
Acute Hypoxia ◽  
Hypoxia Inducible Factor ◽  
High Energy ◽  
Hypoxic Exposure ◽  
Low Oxygen ◽  
Cardiac Responses ◽  
Organ Systems

An adequate supply of oxygen is important for the survival of all tissues, but it is especially critical for tissues with high-energy demands, such as the heart. Insufficient tissue oxygenation occurs under a variety of conditions, including high altitude, embryonic and fetal development, inflammation, and thrombotic diseases, often affecting multiple organ systems. Responses and adaptations of the heart to hypoxia are of particular relevance in human cardiovascular and pulmonary diseases, in which the effects of hypoxic exposure can range in severity from transient to long-lasting. This study uses the genetic model system Drosophila to investigate cardiac responses to acute (30 min), sustained (18 h), and chronic (3 wk) hypoxia with reoxygenation. Whereas hearts from wild-type flies recovered quickly after acute hypoxia, exposure to sustained or chronic hypoxia significantly compromised heart function upon reoxygenation. Hearts from flies with mutations in sima, the Drosophila homolog of the hypoxia-inducible factor alpha subunit (HIF-α), exhibited exaggerated reductions in cardiac output in response to hypoxia. Heart function in hypoxia-selected flies, selected over many generations for survival in a low-oxygen environment, revealed reduced cardiac output in terms of decreased heart rate and fractional shortening compared with their normoxia controls. Hypoxia-selected flies also had smaller hearts, myofibrillar disorganization, and increased extracellular collagen deposition, consistent with the observed reductions in contractility. This study indicates that longer-duration hypoxic insults exert deleterious effects on heart function that are mediated, in part, by sima and advances Drosophila models for the genetic analysis of cardiac-specific responses to hypoxia and reoxygenation.

scholarly journals Acute high-altitude sickness

2017 ◽  
Vol 26 (143) ◽  
pp. 160096 ◽  
Author(s):  
Andrew M. Luks ◽  
Erik R. Swenson ◽  
Peter Bärtsch
Keyword(s):  
High Altitude ◽  
Pulmonary Oedema ◽  
Cerebral Oedema ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Mountain Sickness ◽  
Resonance Imaging ◽  
Altitude Sickness ◽  
Pulmonary Vasoconstriction ◽  
Prevention And Treatment ◽  
Mountain Sickness

At any point 1–5 days following ascent to altitudes ≥2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.

Intracranial Pressure at High Altitude and Acute Mountain Sickness

1995 ◽  
Vol 89 (2) ◽  
pp. 201-204 ◽  
Author(s):  
A. D. Wright ◽  
C. H. E. Imray ◽  
M. S. C. Morrissey ◽  
R. J. Marchbanks ◽  
A. R. Bradwell
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Raised Intracranial Pressure ◽  
Rapid Ascent ◽  
Mountain Sickness ◽  
Pressure Changes ◽  
Serial Measurements

1. Raised intracranial pressure has been noted in severe forms of acute mountain sickness and high-altitude cerebral oedema, but the role of intracranial pressure in the pathogenesis of mild to moderate acute mountain sickness is unknown. 2. Serial measurements of intracranial pressure were made indirectly by assessing changes in tympanic membrane displacement in 24 healthy subjects on rapid ascent to 5200 m. 3. Acute hypoxia at 3440 m was associated with a rise in intracranial pressure, but no difference was found in pressure changes at 4120 or 5200 m in subjects with or without symptoms of acute mountain sickness. 4. Raised intracranial pressure, though temporarily associated with acute hypoxia, is not a feature of acute mountain sickness with mild or moderate symptoms.

scholarly journals Respiratory and circulatory control at high altitudes.

1982 ◽  
Vol 100 (1) ◽  
pp. 147-157
Author(s):  
J B West
Keyword(s):  
Oxygen Consumption ◽  
High Altitude ◽  
Acute Hypoxia ◽  
Maximal Oxygen Consumption ◽  
Barometric Pressure ◽  
Mount Everest ◽  
Exercise Ventilation ◽  
Circulatory Control ◽  
Work Level ◽  
Oxygen Requirements

Hyperventilation is one of the most important features of acclimatization to high altitude. Resting ventilation at extreme altitudes increases up to fourfold and exercise ventilation for a given work level increases to the same extent. Hypoxic stimulation of the peripheral chemoreceptors is the chief mechanism for the hyperventilation but there is also evidence that central sensitization of the respiratory centres occurs. Permanent residents of high altitude have a blunted hypoxic ventilatory response compared to acclimatized lowlanders. Cardiac output increases in responses to acute hypoxia but returns to normal in acclimatized lowlanders. Oxygen uptake at extreme altitudes is markedly limited by the diffusion properties of the blood gas barrier. As a consequence the maximal oxygen consumption of a climber near the summit of Mount Everest is near his basal oxygen requirements. Maximal oxygen consumption is so sensitive to barometric pressure that it may be that day-to-day variations will affect the chances of a climber reaching the summit without supplementary oxygen.

scholarly journals Physiology and Medicine at High Altitude: The Exposure and the Stress

2018 ◽  
Vol 3 (3) ◽  
pp. 203 ◽  
Author(s):  
Anil Gurtoo
Keyword(s):  
High Altitude ◽  
Acute Mountain Sickness ◽  
Hemoglobin Concentration ◽  
Barometric Pressure ◽  
Extreme Environment ◽  
Incidence Rates ◽  
Oxygen Requirement ◽  
Classic Model ◽  
Mountain Sickness ◽  
High Altitude Illness

<p>Increase in altitude causes decrease in atmospheric barometric pressure that results in decrease of inspired<br />partial pressure of oxygen, a source for stress and pose a challenge to climbers/trekkers or persons posted on<br />high altitude areas. This review discusses about the high altitude sickness, their incidence rates, pathophysiology<br />and the classic model of acclimatisation, which explains about how oxygen requirement in extreme environment<br />is achieved by complex interplay among pulmonary, hematological and cardiovascular processes. The acute<br />high altitude illness (AHAI) is basically composed of two syndromes: cerebral and pulmonary that can afflict<br />un-acclimatised climbers/trekkers. The cerebral syndrome includes acute mountain sickness (AMS) and high<br />altitude cerebral oedema (HACO) and pulmonary syndrome typically refers to high altitude pulmonary oedema<br />(HAPO). The core physiological purpose, according to the classic model is centered upon the optimisation of<br />increased delivery of oxygen to the cells through a coherent response involving increased ventilation, cardiac<br />output and hemoglobin concentration with aim to increase the oxygen flux across the oxygen cascade, which<br />will help in preventing the development of majority of high altitude illness.</p>

scholarly journals View From Above: Bibliometric and Citation Analysis of Global High Altitude Medicine Research

2020 ◽  
Vol 8 (3) ◽  
pp. 107-115
Author(s):  
Chee Hwui Liew ◽  
Gerard Thomas Flaherty
Keyword(s):  
High Altitude ◽  
Bibliometric Analysis ◽  
Acute Mountain Sickness ◽  
Travel Medicine ◽  
Research Activity ◽  
Medicine Research ◽  
Medicine Journal ◽  
The Usa ◽  
High Altitude Illness ◽  
The Uk

Introduction: High altitude destinations are popular among international travelers. Travel medicine practitioners should be familiar with altitude physiology and high altitude illness recognition, prophylaxis, and management. We performed the first bibliometric analysis of high altitude medicine research. Methods: All articles published in a specialist high altitude medicine journal through April 2020 were mapped against the 34 domains in a theoretical body of knowledge. Citation counts of articles, as well as authors publishing the most articles, were obtained from Scopus. Collaboration analysis was performed using established methods. Results: Mapping of 1150 articles published from 2000 to 2020 identified the leading domains represented by high altitude medicine articles. The top five domains were altitude acclimatization and deterioration (19.4%, n=510); cardiovascular physiology (6.8%, n=180); work at altitude (6.6%, n = 174); acute mountain sickness (6.4%, n=169); respiratory and acid-base physiology (5.9%, n=155). Published articles attracted a total of 13,324 citations, with a mean of 11.6 citations per article. The average number of citations per author was 22.3. The USA was the most productive country with 432 publications (37.6%), followed by the UK (9.5%, n=109) and Switzerland (5.6%, n=64). The collaboration index for multi-authored publications increased from 3.8 in 2002 to 5.4 in 2019. Conclusion: We have performed the first comprehensive bibliometric analysis in high altitude medicine. Efforts to increase the research activity in neglected topics and to promote greater collaboration between high altitude medicine and related fields of study such as travel medicine may be worthwhile.

scholarly journals Acute high-altitude illness: updated principles ofpathophysiology, prevention, and treatment

2020 ◽  
Vol 71 (11-12) ◽  
pp. 267-274
Author(s):  
MM Berger ◽  
LM Schiefer ◽  
G Treff ◽  
M Sareban ◽  
ER Swenson ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Cerebral Edema ◽  
Acute Mountain Sickness ◽  
High Altitude Pulmonary Edema ◽  
Prevention And Treatment ◽  
High Altitude Cerebral Edema ◽  
Mountain Sickness ◽  
High Altitude Illness ◽  
Cardinal Symptom

The interest in trekking and mountaineering is increasing, and growing numbers of individuals are travelling to high altitude. Following ascent to high altitude, individuals are at risk of developing one of the three forms of acute high-altitude illness: acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). The cardinal symptom of AMS is headache that occurs with an increase in altitude. Additional symptoms are anorexia, nausea, vomiting, dizziness, and fatigue. HACE is characterized by truncal ataxia and decreased consciousness that generally but not always are preceded by worsening AMS. The typical features of HAPE are a loss of stamina, dyspnea, and dry cough on exertion, followed by dyspnea at rest, rales, cyanosis, cough, and pink, frothy sputum. These diseases can develop at any time from several hours to 5 days following ascent to altitudes above 2,500-3,000 m. Whereas AMS is usually self-limited, HACE and HAPE represent life-threatening emergencies that require timely intervention. For each disease, we review the clinical features, epidemiology and the current understanding of their pathophysiology. We then review the primary pharmacological and non-pharmacological approaches to the management of each form of acute altitude illness and provide practical recommendations for both prevention and treatment. The essential principles for advising travellers prior to high-altitude exposure are summarized. Key Words: Acute Mountain Sickness, High Altitude Cerebral Edema, High Altitude Pulmonary Edema, Hypoxia

Denis Jourdanet (1815–1892) and the early recognition of the role of hypoxia at high altitude

2013 ◽  
Vol 305 (5) ◽  
pp. L333-L340 ◽  
Author(s):  
John B. West ◽  
Jean-Paul Richalet
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Early Recognition ◽  
Critical Role ◽  
Barometric Pressure ◽  
Low Oxygen ◽  
Rapid Pulse ◽  
The One ◽  
Clear Statement

Denis Jourdanet (1815–1892) was a French physician who spent many years in Mexico studying the effects of high altitude. He was a major benefactor of Paul Bert (1833–1886), who is often called the father of high-altitude physiology because his book La pression barométrique was the first clear statement that the harmful effects of high altitude are caused by the low partial pressure of oxygen. However, Bert's writings make it clear that the first recognition of the critical role of hypoxia at high altitude should be credited to Jourdanet. Jourdanet noted that some of his patients at high altitude had features that are typical of anemia at sea level, including rapid pulse, dizziness, and occasional fainting spells. These symptoms were correctly attributed to the low oxygen level in the blood and he coined the terms “anoxyhémie” and “anémie barométrique” to draw a parallel between the effects of high altitude on the one hand and anemia at sea level on the other. He also studied the relations between barometric pressure and altitude, and the characteristics of the native populations in Mexico at different altitudes. Jourdanet believed that patients with various diseases including pulmonary tuberculosis were improved if they went to altitudes above 2,000 m. This led him to recommend “aérothérapie” in which these patients were treated in low-pressure chambers. Little has been written about Jourdanet, and his work deserves to be better known.

scholarly journals Effects of acute hypoxia and hyperthermia on the permeability of the blood-brain barrier in adult rats

2009 ◽  
Vol 107 (4) ◽  
pp. 1348-1356 ◽  
Author(s):  
Sirajedin S. Natah ◽  
Sathya Srinivasan ◽  
Quentin Pittman ◽  
Zonghang Zhao ◽  
Jeff F. Dunn
Keyword(s):  
High Altitude ◽  
Blood Brain Barrier ◽  
Vasogenic Edema ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Brain Barrier ◽  
Adaptation To Hypoxia ◽  
Sodium Fluorescein ◽  
Blood Brain ◽  
Bbb Permeability

Acute mountain sickness (AMS) develops within a few hours after arrival at high altitude and includes headache, anorexia, nausea, vomiting, and malaise. This afflicts 15–25% of the general tourist population at moderate altitudes. High-altitude cerebral edema (HACE) is considered to be the end stage of severe AMS and has been suggested to be a vasogenic edema, raising the possibility that acute hypoxia may increase blood-brain barrier (BBB) permeability. At present, there are no good small-animal models to study this syndrome. We hypothesize 1) that acute hypoxia can damage the BBB and 2) that rat can be used as a model to study hypoxia-induced changes in BBB permeability, especially if hypoxia-induced hypothermia could be minimized with high ambient temperature (HAT). Male Wistar rats were exposed to 1, 2, and 7 days of hypobaric hypoxia (equivalent to 0.5 atm), and changes in the temperature and BBB permeability were studied. The extravasation of endogenous immunoglobulin G, a large molecule, did not increase during room temperature hypoxia but did increase when hypoxia was combined with HAT. Hypoxia caused a significant increase in the leakage of sodium fluorescein (mol wt 376 Da). The expression of endothelial barrier antigen (EBA), a protein associated with the BBB, was reduced to 50% between 24 and 48 h after exposure to hypoxia, and the loss was exacerbated by HAT. The values almost returned to control levels by 7 days, showing adaptation to hypoxia. Hypoxic rats exhibited sodium fluorescein leakage mainly in focal areas in the brain parenchyma. In conclusion, it is possible to have transient BBB damage through exposure to acute hypoxia, and this damage is exacerbated by increasing body temperature to more of a normothermic value.

Sign in / Sign up

Export Citation Format

Share Document