Clinical Features of Patients with High-Altitude Pulmonary Edema in Japan

Kobayashi, Toshio; Koyama, Sekiya; Kubo, Keishi; Fukushima, Masao; Kusama, Shozo

doi:10.1378/chest.92.5.814

Cited by 91 publications

(57 citation statements)

References 24 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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“…Hypoxia increases both pre-and postcapillary pulmonary vascular resistances and this can occur in a nonuniform fashion. [26][27][28][29] This results in a generalized increase in pulmonary vascular pressures and, furthermore, can markedly increase pulmonary capillary pressures in areas with unchanged precapillary arteriolar resistances. Furthermore, in dogs, norepinephrine infusion increases postcapillary pulmonary vascular resistance to a greater extent than precapillary resistance.…”

Section: Hypoxia and A Hyperadrenergic Statementioning

confidence: 99%

Pulmonary oedema associated with airway obstruction

et al. 1990

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“…The radiographic characteristics of HAPEhave been described by several authors (2,(8)(9)(10); however, most papers have concentrated on the distribution and characteristics of infiltrates in the lungs. In the present study, we analyzed serial posteroanterior chest roentgenograms of patients with HAPE taken in the standing position on admission and following recovery.…”

Section: Introductionmentioning

confidence: 99%

Radiographic and Hemodynamic Changes during Recovery from High-Altitude Pulmonary Edema.

et al. 1994

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It has been suggested that accentuated pulmonary hypertension is a contributing factor in the development of high-altitude pulmonary edema (HAPE).The purpose of this study was to evaluate the chest radiographic features associated with pulmonary hemodynamic changes in HAPE.We studied 16 patients with HAPEusing posteroanterior chest roentgenograms taken in the standing position both on admission and following recovery. The cardiothoracic ratio (CTR) as well as the area and volume of the main pulmonary artery were measured. During HAPE,we found slight enlargement of the CTR, especially the right ventricle, and prominence of the main pulmonary artery. These abnormalities significantly improvedin the recovery state. The changes in area and volume of the main pulmonary artery were closely correlated with a decrease in CTRduring recovery from HAPE,and correlated with the pulmonary hemodynamic changes observed by right heart catheterization (n=4). Radiographic changes reflect the alterations in pulmonary hemodynamics in patients with HAPE. (Internal Medicine 33: 525-528, 1994)

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Clinical Features of Patients with High-Altitude Pulmonary Edema in Japan

Cited by 91 publications

References 24 publications

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

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

Pulmonary oedema associated with airway obstruction

Radiographic and Hemodynamic Changes during Recovery from High-Altitude Pulmonary Edema.

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