Pulmonary hemodynamic response to exercise in subjects with prior high-altitude pulmonary edema

Eldridge, Marlowe W.; Podolsky, Andrea; Richardson, Russell S.; Johnson, Don; Knight, D. R.; Johnson, Eric J.; Hopkins, Susan R.; Michimata, Hideo; Grassi, Bruno; Feiner, John; Kurdak, S. Sadi; Bickler, Philip E.; Wagner, Peter D.; Severinghaus, John W.

doi:10.1152/jappl.1996.81.2.911

Cited by 111 publications

(91 citation statements)

References 18 publications

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“…PASP measurements during hypoxic exposure showed a significantly greater increase in HAPE-susceptible subjects consistent with previous studies in which PASP was obtained either by echocardiography [7,21,22] or by right-heart catheterisation [5,6,9,15]. However, in a previous study with a similar design, there was a large overlap between HAPEsusceptible and nonsusceptible subjects in PASP during hypoxia [8].…”

Section: Pulmonary Vascular Responsesupporting

confidence: 88%

“…The crucial role of high pulmonary artery pressure is confirmed by elevated pulmonary artery pressures in patients with HAPE [2-4], enhanced pulmonary vasoconstrictive response in HAPE-susceptible subjects to acute hypoxia [5][6][7][8] or exercise in normoxia [6,7,9]. It is also confirmed by the fact that interventions decreasing pulmonary artery pressure are effective in the treatment [10, 11] and prevention [4] of HAPE.…”

mentioning

confidence: 99%

“…Most studies report positive associations [8,12,13], although one study found no relationship between HAPE and HVR [14]. Furthermore, some studies have reported associations between susceptibility to HAPE and lower vital capacity [8,9,15,16] or lower functional residual capacity [16].…”

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confidence: 99%

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Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

Dehnert

Grünig²,

Mereles³

et al. 2005

Eur Respir J

106

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Individuals susceptible to high-altitude pulmonary oedema (HAPE) are characterised by an abnormal increase of pulmonary artery systolic pressure (PASP) in hypoxia and during normoxic exercise, reduced hypoxic ventilatory response, and smaller lung volume.In 37 mountaineers with well-documented altitude tolerance, it was investigated whether any combination of these noninvasive measurements, including exercise in hypoxia, could improve the identification of HAPE-susceptible subjects at low altitude.HAPE-susceptible subjects showed a significant higher increase of PASP during hypoxia at rest (48¡10 mmHg) compared with controls (38¡3 mmHg), as well as during normoxic exercise (57¡14 versus 38¡7 mmHg) and hypoxic exercise (69¡13 versus 49¡8 mmHg). PASP could not be assessed in three and eight subjects during normoxic or hypoxic exercise, respectively, due to insufficient Doppler profiles or systemic arterial hypertension. Sensitivity (77-94%) and specificity (76-93%) were not significantly different between the various testing conditions. Additional assessment of hypoxic ventilatory response and lung function parameters did not improve identification of HAPE-susceptible subjects in a multivariate analysis.Due to the greater number of missing values in pulmonary artery systolic pressure measurements during hypoxic exercise, it was concluded that pulmonary artery systolic pressure measurements at rest during hypoxia or exercise in normoxia are most feasible for the identification of high-altitude pulmonary oedema-susceptible subjects.KEYWORDS: Doppler echocardiography, exercise, hypoxia, hypoxic ventilatory response, lung volumes, pulmonary artery pressure H igh-altitude pulmonary oedema (HAPE) is a noncardiogenic pulmonary oedema that occurs at an altitude of 4,559 m in up to 6% of otherwise healthy unselected subjects [1]. Altitude, speed of ascent, pre-acclimatisation and, above all, individual susceptibility are determinants for its occurrence. The combination of fast ascent and susceptibility to HAPE increases the incidence of HAPE at 4,559 m to ,60% [1]. Since HAPE is a life-threatening condition, it would be helpful to identify HAPE-susceptible subjects at low altitude, particularly in those with no previous altitude exposure.It has been widely demonstrated that increased hypoxic pulmonary vasoconstriction leading to abnormally high pulmonary artery pressure is the major contributor in the development of HAPE. The crucial role of high pulmonary artery pressure is confirmed by elevated pulmonary artery pressures in patients with HAPE [2-4], enhanced pulmonary vasoconstrictive response in HAPE-susceptible subjects to acute hypoxia [5][6][7][8] or exercise in normoxia [6,7,9]. It is also confirmed by the fact that interventions decreasing pulmonary artery pressure are effective in the treatment [10, 11] and prevention [4] of HAPE. A previous study suggested that pulmonary artery systolic pressure (PASP) does not exceed 40 mmHg in healthy subjects during acute hypoxic exposure (inspiratory oxygen fractio...

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Section: Pulmonary Vascular Responsesupporting

confidence: 88%

mentioning

confidence: 99%

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Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

Dehnert

Grünig²,

Mereles³

et al. 2005

Eur Respir J

106

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“…The most important is a strong HPV response, as well as higher pressures with even normoxic exercise [64,65]. The exaggerated rise in pulmonary artery pressure in susceptible individuals developing HAPE is accompanied by increased microvascular pressure >20 mmHg, a threshold pressure for formation of alveolar oedema [59,66].…”

Section: Haemodynamicsmentioning

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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“…HAPE typically occurs in young and healthy mountaineers and is precipitated by rapid ascents at altitudes above 2,500-3,000m 45,[48][49][50] . There is an individual susceptibility and it tends to recur 45,48,49,51 . HAPE clinically manifests 2 to 5 days after acute exposure to hypobaric hypoxia, 78% of the cases appear until the 10 th day 38,45 , with the following symptoms: abnormal dyspnea on effort and, later, even at rest, cyanosis, dry cough that evolves to a mucous-sanguinolent cough, and tachycardia 19,38 .…”

Section: Diseases Of Altitudementioning

confidence: 99%

Physical activity at moderate and high altitudes. Cardiovascular and respiratory morbidit

Campos¹,

Costa²

1999

Arq. Bras. Cardiol.

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Pulmonary hemodynamic response to exercise in subjects with prior high-altitude pulmonary edema

Cited by 111 publications

References 18 publications

Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

Acute high-altitude sickness

Physical activity at moderate and high altitudes. Cardiovascular and respiratory morbidit

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