Pulmonary extravascular fluid accumulation in recreational climbers: a prospective study

Cremona, George; Asnaghi, Roberto; Baderna, Paolo; Brunetto, Alessandro; Brutsaert, Tom D.; Cavallaro, Carmelo; Clark, Timothy M; Cogo, Annalisa; Donis, Roberto; Lanfranchi, Paola; Luks, Andrew M.; Novello, Nadia; Panzetta, Stefano; Perini, Liliana; Putnam, Marci; Spagnolatti, L; Wagner, Harrieth; Wagner, Peter D.

doi:10.1016/s0140-6736(02)07496-2

Cited by 179 publications

(134 citation statements)

References 22 publications

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“…However, there is a large overlap of individual values [7] and statistically significant differences can only be obtained in studies of large groups. These blood gas changes might be due to a mild interstitial oedema not visible on chest radiographs [8], but suggested by a slight decrease of vital capacity and increase of closing volume [9,10]; however, these are inconsistent findings [11]. Furthermore, a lower ventilatory drive in hypoxia might contribute to more severe hypoxaemia in AMS, at least in some individuals [12,13].…”

Section: Ams and Hacementioning

confidence: 99%

Acute high-altitude sickness

2017

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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.

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Section: Ams and Hacementioning

confidence: 99%

Acute high-altitude sickness

2017

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“…pulmonary edema; hypobaric hypoxia ALTHOUGH ONLY A MINORITY OF those who go to high altitude develop the potentially fatal condition of highaltitude pulmonary edema (HAPE), there is increasing evidence that the majority of people ascending to altitude may develop subclinical pulmonary edema (9). Forced vital capacity (FVC) falls on ascent to high altitude and is thought to be primarily due to subclinical pulmonary edema (32).…”

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confidence: 99%

Serial changes in nasal potential difference and lung electrical impedance tomography at high altitude

Mason¹,

Petersen

Mélot

et al. 2003

Journal of Applied Physiology

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Mason, Nicholas P., Merete Petersen, Christian Mé lot, Bakyt Imanow, Olga Matveykine, Marie-Therese Gautier, Akpay Sarybaev, Almaz Aldashev, Mirsaid M. Mirrakhimov, Brian H. Brown, Andrew D. Leathard, and Robert Naeije. Serial changes in nasal potential difference and lung electrical impedance tomography at high altitude. J Appl Physiol 94: 2043-2050, 2003. First published December 6, 2002 10.1152 10. /japplphysiol.00777.2002 work suggests that treatment with inhaled ␤2-agonists reduces the incidence of high-altitude pulmonary edema in susceptible subjects by increasing respiratory epithelial sodium transport. We estimated respiratory epithelial ion transport by transepithelial nasal potential difference (NPD) measurements in 20 normal male subjects before, during, and after a stay at 3,800 m. NPD hyperpolarized on ascent to 3,800 m (P Ͻ 0.05), but the change in potential difference with superperfusion of amiloride or isoprenaline was unaffected. Vital capacity (VC) fell on ascent to 3,800 m (P Ͻ 0.05), as did the normalized change in electrical impedance (NCI) measured over the right lung parenchyma (P Ͻ 0.05) suggestive of an increase in extravascular lung water. EchoDoppler-estimated pulmonary artery pressure increases were insufficient to cause clinical pulmonary edema. There was a positive correlation between VC and NCI (R 2 ϭ 0.633) and between NPD and both VC and NCI (R 2 ϭ 0.267 and 0.418). These changes suggest that altered respiratory epithelial ion transport might play a role in the development of subclinical pulmonary edema at high altitude in normal subjects. pulmonary edema; hypobaric hypoxia ALTHOUGH ONLY A MINORITY OF those who go to high altitude develop the potentially fatal condition of highaltitude pulmonary edema (HAPE), there is increasing evidence that the majority of people ascending to altitude may develop subclinical pulmonary edema (9). Forced vital capacity (FVC) falls on ascent to high altitude and is thought to be primarily due to subclinical pulmonary edema (32). The control of pulmonary extravascular lung water (EVLW) has traditionally been attributed to the interplay of Starling forces, with the pulmonary capillary pressure attributed the major regulatory role. It is now realized that sodium transport across the respiratory epithelium plays an important role in the removal of alveolar water (34) and that an intact epithelial barrier is necessary for the resolution of alveolar edema (35). Hypoxia reduces epithelial sodium transport in cultured rat alveolar epithelial monolayers (29) and decreases the expression of alveolar epithelial ion transport proteins (8). In addition, treatment of HAPE-susceptible individuals with inhaled ␤ 2 -agonists, which are known to increase transepithelial sodium transport, decreases pulmonary edema without any effect on pulmonary hemodynamics (44).Measurement of alveolar ion transport in vivo in human subjects is not feasible; however, measurement of the potential difference (PD) generated by ion transport in the nasal mucosa can be used as a marker...

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“…Its existence was first suggested by Cremona 29 , et al who found that 77 per cent of climbers on Monte Rosa (4559m) had evidence of increased closing volumes, suggestive of pulmonary extravascular fluid accumulation. It is unclear, if this condition is predictive for clinical HAPE.…”

Section: Sub -Clinical Hapementioning

confidence: 94%

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

Gurtoo

2018

Def. Life. Sc. Jl.

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, it was sometimes in the mid-nineteenth century that, Bert first showed the association between hypobaria triggered lowering of PiO 2 and high altitude illness 2 . This relationship is best captured by the gas-law equation:PV = nRT where P = pressure, V = volume, n = number of gas molecules, R = universal gas constant, and T = absolute temperature. Since, the partial pressure of a gas, P = Fi x B, at sea level given a B of 760 mmHg (P B ), the partial pressure of inspired O 2 becomes = 20.9 x 760 =159 mm Hg. This fall is most dramatic at 5,486 meters, which is the upper level of functional acclimatisation where a PB of = 395 mm Hg yields a Pi O 2 of 82 mmHg (20.9 x 395), which is nearly half that at sea level. Even at 3000 m, the height of Leh, the barometric pressure (P B ) and inspired PO 2 (PiO 2 ) are only 70 per cent of the sea level values. On the summit of Mt. Everest, at 8848 m, the PiO 2 is less than 30 per cent of its sea level value. These values signify the stress and challenge to the physiology at high altitude. The ADApTATIONTaken suddenly to the top of Mt. Everest (8848 m), a person would lose consciousness in less than 3 min 3 . Taken slowly the same person remains alive and functional. In fact the lowest recorded P A O 2 in a healthy individual at 8400 m on Everest by the Caudwell Xtreme Everest expedition was 19 mmHg (2.55 KPa). The stark contrast between the two scenarios is accounted for by the adaptive process called acclimatisation that tends to increase the oxygen delivery (DO 2 ) to the tissues. The ClAssIC MODelThe classic model holds that this increase in DO 2 is affected by an optimisation between: (i) Pulmonary (ii) haematological and, (iii) cardiovascular processes. Pulmonary process optimisation is the first response to hypobaric hypoxia: hyperventilation is triggered by a combination of stimulation of peripheral chemoreceptor and inhibition of the central chemoreceptors that leads to an increased respiratory rate and depth. This hypoxic ventilator response (HVR) triggers in within a few hours of exposure to hypobaric hypoxia. This HVR tends to restore the falling oxygen gradient across the physiology and Medicine at high Altitude: The exposure and the stress Anil GurtooLady Hardinge Medical College, ABsTRACT Increase in altitude causes decrease in atmospheric barometric pressure that results in decrease of inspired partial pressure of oxygen, a source for stress and pose a challenge to climbers/trekkers or persons posted on high altitude areas. This review discusses about the high altitude sickness, their incidence rates, pathophysiology and the classic model of acclimatisation, which explains about how oxygen requirement in extreme environment is achieved by complex interplay among pulmonary, hematological and cardiovascular processes. The acute high altitude illness (AHAI) is basically composed of two syndromes: cerebral and pulmonary that can afflict un-acclimatised climbers/trekkers. The cerebral syndrome includes acute mountain sickness (AMS) and high altitude cerebral oedem...

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Pulmonary extravascular fluid accumulation in recreational climbers: a prospective study

Cited by 179 publications

References 22 publications

Acute high-altitude sickness

Acute high-altitude sickness

Serial changes in nasal potential difference and lung electrical impedance tomography at high altitude

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

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