Physiologic Studies of Pulmonary Edema at High Altitude

Hultgren, Herbert N.; López, C. Castañón; Lundberg, Einar; Miller, Henry S.

doi:10.1161/01.cir.29.3.393

Cited by 197 publications

(78 citation statements)

References 6 publications

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“…Consistently, pulmonary heamodynamic measurements at rest performed in early HAPE [17] and in all patients admitted to the hospital with HAPE [22][23][24][25][26][27], show that left atrial pressure, as assessed by occluded (or wedged) PAP, right atrial pressure and cardiac output are normal in HAPE. Recently, using the method of arterial occlusion, which is likely to measure pressures in vessels close to 100 mm in diameter [28], it was demonstrated that the pulmonary capillary pressure (Pc) is elevated in HAPE.…”

Section: Effects Of Acute Exposure To High Altitudesupporting

confidence: 56%

High-altitude pulmonary hypertension: a pathophysiological entity to different diseases

Maggiorini¹,

León‐Velarde²

2003

European Respiratory Journal

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High-altitude pulmonary hypertension: a pathophysiological entity to different diseases. M. Maggiorini, F. Léon-Velarde. #ERS Journals Ltd 2003. ABSTRACT: Pulmonary hypertension is a hallmark of high-altitude pulmonary oedema (HAPE) and of congestive right heart failure in subacute mountain sickness (SMS) and chronic mountain sickness (CMS) in the Himalayas and in the end-stage of CMS (Monge9s disease) in the Andes.There are studies to suggest that transmission of excessively elevated pulmonary artery pressure and/or flow to the pulmonary capillaries leading to alveolar haemorrhage is the pathophysiological mechanism of HAPE.In the Himalayas, HAPE was successfully prevented by extending the acclimatisation period from a few days to 5 weeks, however, this did not prevent the occurrence of congestive right heart failure after several weeks of stay at 6,000 m. This leads to the concept that rapid remodelling of the small precapillary arteries prevents HAPE but not the development of right heart failure in SMS and CMS.Unresponsiveness of pulmonary hypertension to oxygen at high altitude and its complete resolution only after weeks of stay at low altitude suggest that structural rather than functional changes are its pathophysiological mechanism. Since pulmonary hypertension at high altitude is the driving force leading to high-altitude pulmonary oedema and "high-altitude right heart failure" in newcomers and residents of high altitude, the authors propose to adjust current terminology accordingly. The physiological response of the pulmonary circulation to hypobaric and normobaric hypoxia is to increase pulmonary arteriolar resistance. The magnitude of hypoxic pulmonary vasoconstriction is highly variable between humans, probably based on genetics and adaptive mechanisms. Sites of hypoxic pulmonary vasoconstriction are small pulmonary arterioles and veins of a diameter of v900 mm, the veins accounting for y20% of the total increase in pulmonary vascular resistance caused by hypoxia [1,2]. The structural changes in small pulmonary arteries and veins appear to reflect this genetically based and adaptive process [3][4][5] in humans and animals. Excessive hypoxic pulmonary vasoconstriction, and thus susceptibility to develop a right heart failure within weeks at high altitude, was first described in Colorado cattle [6]. Indian soldiers stationed at an altitude between 5,800-6,700 m [7] and Han infants in Lhasa [8] develop severe congestive right heart failure within weeks or months after arrival at high altitude. An excessively elevated pulmonary artery pressure (PAP) has not only been reported to cause high altitude cor pulmonale within weeks, months, or years in newcomers, but also in high-altitude residents of the Andes and nonacclimatised climbers prone to high-altitude pulmonary oedema (HAPE) [9]. The results of these studies suggest that an excessive rise in PAP is a common denominator in HAPE [9], the syndrome described by SUI et al. [8] in infants and by ANAND et al. [7] in adults at 6,700 m and termed "subacute...

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Section: Effects Of Acute Exposure To High Altitudesupporting

confidence: 56%

High-altitude pulmonary hypertension: a pathophysiological entity to different diseases

Maggiorini¹,

León‐Velarde²

2003

European Respiratory Journal

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“…The crucial role of high pulmonary artery pressure is confirmed by elevated pulmonary artery pressures in patients with HAPE [2][3][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: 81%

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

Dehnert

Grünig²,

Mereles³

et al. 2005

European Respiratory Journal

105

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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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“…Right heart catheterisation at high altitude revealed mean (range) pulmonary artery pressures of 60 mmHg, but normal pulmonary artery wedge pressures [58][59][60]. These pioneering studies put to rest the idea that HAPE was acute left heart failure at high altitude.…”

Section: Haemodynamicsmentioning

confidence: 99%

“…Bronchoalveolar lavage (BAL) shows a protein-rich exudate and mild alveolar haemorrhage, which initially is noninflammatory, but may progress after several days to a more inflammatory picture, as discussed later [55][56][57]. Echocardiographic and pulmonary artery catheterisation studies at high altitude show marked pulmonary hypertension [58][59][60].…”

Section: Hapementioning

confidence: 99%

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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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Physiologic Studies of Pulmonary Edema at High Altitude

Cited by 197 publications

References 6 publications

High-altitude pulmonary hypertension: a pathophysiological entity to different diseases

High-altitude pulmonary hypertension: a pathophysiological entity to different diseases

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

Acute high-altitude sickness

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