scholarly journals Susceptibility to high-altitude pulmonary edema is associated with increased pulmonary arterial stiffness during exercise

2020 ◽  
Vol 128 (3) ◽  
pp. 514-522
Author(s):  
A. Mulchrone ◽  
H. Moulton ◽  
M. W. Eldridge ◽  
N. C. Chesler
Keyword(s):  
Arterial Stiffness ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Published Data ◽  
Control Subjects ◽  
High Altitude Pulmonary Edema ◽  
Artery Stiffness ◽  
Response To Exercise ◽  
Distal Artery

High-altitude pulmonary edema (HAPE), a reversible form of capillary leak, is a common consequence of rapid ascension to high altitude and a major cause of death related to high-altitude exposure. Individuals with a prior history of HAPE are more susceptible to future episodes, but the underlying risk factors remain uncertain. Previous studies have shown that HAPE-susceptible subjects have an exaggerated pulmonary vasoreactivity to acute hypoxia, but incomplete data are available regarding their vascular response to exercise. To examine this, seven HAPE-susceptible subjects and nine control subjects (HAPE-resistant) were studied at rest and during incremental exercise at sea level and at 3,810 m altitude. Studies were conducted in both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91 Torr) conditions at each location. Here, we report an expanded analysis of previously published data, including a distensible vessel model that showed that HAPE-susceptible subjects had significantly reduced small distal artery distensibility at sea level compared with HAPE-resistant control subjects [0.011 ± 0.001 vs. 0.021 ± 0.002 mmHg−1; P < 0.001). Moreover, HAPE-susceptible subjects demonstrated constant distensibility over all conditions, suggesting that distal arteries are maximally distended at rest. Consistent with having increased distal artery stiffness, HAPE-susceptible subjects had greater increases in pulmonary artery pulse pressure with exercise, which suggests increased proximal artery stiffness. In summary, HAPE-susceptible subjects have exercise-induced increases in proximal artery stiffness and baseline increases in distal artery stiffness, suggesting increased pulsatile load on the right ventricle. NEW & NOTEWORTHY In comparison to subjects who appear resistant to high-altitude pulmonary edema, those previously symptomatic show greater increases in large and small artery stiffness in response to exercise. These differences in arterial stiffness may be a risk factor for the development of high-altitude pulmonary edema or evidence that consequences of high-altitude pulmonary edema are long-lasting after return to sea level.

Exercise-induced VA/Q inequality in subjects with prior high-altitude pulmonary edema

1996 ◽  
Vol 81 (2) ◽  
pp. 922-932 ◽  
Author(s):  
A. Podolsky ◽  
M. W. Eldridge ◽  
R. S. Richardson ◽  
D. R. Knight ◽  
E. C. Johnson ◽  
...  
Keyword(s):  
Standard Deviation ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Control Group ◽  
Pulmonary Capillary ◽  
High Altitude Pulmonary Edema ◽  
History Of ◽  
Capillary Pressures ◽  
Exercise Induced

Ventilation-perfusion (VA/Q) mismatch has been shown to increase during exercise, especially in hypoxia. A possible explanation is subclinical interstitial edema due to high pulmonary capillary pressures. We hypothesized that this may be pathogenetically similar to high-altitude pulmonary edema (HAPE) so that HAPE-susceptible people with higher vascular pressures would develop more exercise-induced VA/Q mismatch. To examine this, seven healthy people with a history of HAPE and nine with similar altitude exposure but no HAPE history (control) were studied at rest and during exercise at 35, 65, and 85% of maximum 1) at sea level and then 2) after 2 days at altitude (3,810 m) breathing both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91 Torr) gas at both locations. We measured cardiac output and respiratory and inert gas exchange. In both groups, VA/Q mismatch (assessed by log standard deviation of the perfusion distribution) increased with exercise. At sea level, log standard deviation of the perfusion distribution was slightly higher in the HAPE-susceptible group than in the control group during heavy exercise. At altitude, these differences disappeared. Because a history of HAPE was associated with greater exercise-induced VA/Q mismatch and higher pulmonary capillary pressures, our findings are consistent with the hypothesis that exercise-induced mismatch is due to a temporary extravascular fluid accumulation.

scholarly journals Acute Lung Edema as a Presentation of Severe Acute Reentry High-Altitude Illness in a Pediatric Patient

2020 ◽  
Vol 2020 ◽  
pp. 1-3
Author(s):  
Alfredo Merino-Luna ◽  
Julio Vizcarra-Anaya
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Pediatric Patient ◽  
Lung Edema ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Illness ◽  
The City ◽  
Determining Factor

Acute high-altitude pulmonary edema (HAPE) is a pathology involving multifactorial triggers that are associated with ascents to altitudes over 2,500 meters above sea level (m). Here, we report two pediatric cases of reentry HAPE, from the city of Huaraz, Peru, located at 3,052 m. The characteristics of both cases were similar, wherein acclimatization to sea level and a subsequent return to the city of origin occurred, and we speculate that it was caused by activation of predisposing factors to HAPE. The diagnosis and management associated with pulmonary hypertension became a determining factor for therapy.

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

1996 ◽  
Vol 81 (2) ◽  
pp. 911-921 ◽  
Author(s):  
M. W. Eldridge ◽  
A. Podolsky ◽  
R. S. Richardson ◽  
D. H. Johnson ◽  
D. R. Knight ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Arterial Occlusion ◽  
Prior History ◽  
Vascular Response ◽  
Pressure Reactivity ◽  
Pulmonary Hemodynamic ◽  
High Altitude Pulmonary Edema ◽  
Pulmonary Arterial ◽  
Response To Exercise

Individuals with a prior history of (susceptible to high altitude pulmonary edema (HAPE-S) have high resting pulmonary arterial pressures, but little data are available on their vascular response to exercise. We studied the pulmonary vascular response to exercise in seven HAPE-S and nine control subjects at sea level and at 3,810 m altitude. At each location, both normoxic (inspired PO2 = 148 Torr) and hypoxic (inspired PO2 = 91 Torr) studies were conducted. Pulmonary hemodynamic measurements included pulmonary arterial and pulmonary arterial occlusion pressures. A multiple regression analysis demonstrated that the pulmonary arterial pressure reactivity to exercise was significantly greater in the HAPE-S group. This reactivity was not influenced by altitude or oxygenation, implying that the response was intrinsic to the pulmonary circulation. Pulmonary arterial occlusion pressure reactivity to exercise was also greater in the HAPE-S group, increasing with altitude but independent of oxygenation. These findings suggest an augmented flow-dependent pulmonary vasoconstriction and/or a reduced vascular cross-sectional area in HAPE-S subjects.

Hemodynamic responses to acute hypoxia, hypobaria, and exercise in subjects susceptible to high-altitude pulmonary edema

1989 ◽  
Vol 67 (5) ◽  
pp. 1982-1989 ◽  
Author(s):  
A. Kawashima ◽  
K. Kubo ◽  
T. Kobayashi ◽  
M. Sekiguchi
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Acute Hypoxia ◽  
Arterial Oxygen Tension ◽  
Resistance Index ◽  
Arterial Oxygen ◽  
Hemodynamic Responses ◽  
Control Subjects ◽  
High Altitude Pulmonary Edema ◽  
History Of

To verify the presence of the constitutional abnormality implicated in the pathogenesis of high-altitude pulmonary edema (HAPE), we evaluated the hemodynamic responses to hypoxia, hypobaria, and exercise in HAPE-susceptible subjects (HAPE-S). HAPE-S were five males with a history of HAPE. Five healthy volunteers who had repeated experiences of mountain climbing without any history of altitude-related problems served as controls. HAPE-S showed much greater increase in pulmonary vascular resistance index (PVRI) than the control subjects, resulting in a much higher level of pulmonary arterial pressure (Ppa), under both acute hypoxia of 15% O2 (Ppa = 29.0 +/- 2.8 vs. 17.8 +/- 0.3 Torr, P less than 0.05) and acute hypobaria of 515 Torr (32.3 +/- 2.8 vs. 19.1 +/- 0.8 Torr, P less than 0.05). Also, PVRI in HAPE-S exhibited a tendency to increase even during light exercise with supine bicycle ergometer (50 W), whereas PVRI in the control subjects significantly decreased, so that HAPE-S showed a greater increase in Ppa (delta Ppa = 16.0 +/- 1.5 vs. 4.9 +/- 1.1 Torr, P less than 0.001) and a greater decrease in arterial oxygen tension (17.8 +/- 4.7 vs. 5.6 +/- 1.7 Torr, P less than 0.05). We thus conclude that HAPE-S have a constitutional abnormality, which can be evaluated at low altitude, in the pulmonary circulatory responses to possible causative factors of HAPE such as hypoxia, hypobaria, and exercise.

scholarly journals Risk factors underlying high-altitude pulmonary edema in the Ecuadorian Andes

2021 ◽  
Author(s):  
Karen Sánchez ◽  
Wilfre Machado ◽  
Anita Villafuerte ◽  
Santiago Ballaz
Keyword(s):  
Blood Pressure ◽  
Logistic Regression ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Acute Mountain Sickness ◽  
Vital Signs ◽  
Blood Analysis ◽  
High Altitude Pulmonary Edema ◽  
Simple Logistic

Abstract Background Ascent to high altitude (> 2500 m) exposes people to hypobaric atmospheric pressure and blood hypoxemia. It provokes a syndrome whose symptoms vary from the mild acute mountain sickness (AMS) to the life-threatening, high-altitude pulmonary edema (HAPE). This study analyzed the risk for developing high-altitude sickness in a group of HAPE patients (n = 59), which was contrasted against a group of AMS patients (n = 240) as the NO HAPE group, after sojourning above 4,000 m height. The objective of this retrospective was to analyse the factors contributing to the HAPE prevalence among travellers and dwellers of the Ecuadorian Andes. Methods AMS and HAPE groups were compared through demographic (ethnicity, sex, and age), environmental (permanent residence altitude and recent stay at sea-level), health status (vital signs), and blood analysis variables. The Cramer´s V, simple logistic regression(SLR), and multiple logistic regression(MLR) analyses revealed patterns of significant associations. Results Analyses revealed that high-altitude indigenous residents were HAPE-prone, while mestizos living at sea level only had AMS. Blood pressure played a role in HAPE risk. Women were more tolerant to HAPE than men. Among indigenes, HAPE prevalence significantly rose after sojourning at sea level, a phenomenon called “reentry HAPE”. Conclusions In Andean indigenes, HAPE could be produced by a poor adaptation to high altitude, a high haemoglobin, and a blunted reactivity of blood pressure to environmentally-induced hypoxia. All the above gives support to the complex gene-environment interactions in the progress of HAPE, which may give some clues about of the etiopathogenesis of non-cardiogenic edema.

scholarly journals Exercise Responses to Metabolic Function on High Altitude Pulmonary Edema Susceptible Individuals

2018 ◽  
Vol 3 (3) ◽  
pp. 224
Author(s):  
Kaushik Halder ◽  
RK Gupta ◽  
Anjana Pathak ◽  
Montu Saha
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Past History ◽  
Minute Ventilation ◽  
Metabolic Responses ◽  
Prior History ◽  
High Altitude Pulmonary Edema ◽  
History Of ◽  
Exercise Induced

<p>The study was aimed to evaluate and compare resting and exercise induced metabolic responses between acclimatized high altitude pulmonary edema (HAPE) susceptible (HAPE-s) and HAPE resistance (HAPE-r) volunteers at sea level. A group of 14 Indian soldiers volunteered for this study, divided into two groups, (i) HAPE-s, with past history of HAPE [n<sub>1</sub> = 7; age = 33.3 ± 4.5 (M ± SD)] and (ii) HAPE-r, with prior history of repeated exposure to high altitude and without suffering HAPE [n<sub>2</sub> = 7; age = 31.9 ± 4.2 (M ± SD)]. Respiratory frequency (f<sub>R</sub>), tidal volume (<sub>T</sub>), minute ventilation (<sub>E</sub>), oxygen consumption (O<sub>2</sub>), carbon dioxide output (CO<sub>2</sub>), heart rate (HR) and respiratory quotient (RQ) were recorded on all the volunteers during resting and exercise conditions. Ventilatory equivalent for oxygen (EqO<sub>2</sub>) and oxygen pulse (O<sub>2</sub>P) were calculated. Significant differences were observed between HAPE-s and HAPE-r volunteers in f<sub>Rrest </sub>(25.3% higher), O<sub>2</sub>P<sub>rest </sub>(23.7% lower), <sub>Emax</sub> (50.9% lower) (all P&lt;0.05), f<sub>Rmax </sub>(55.7% lower), O<sub>2max </sub>(55.5% lower), O<sub>2</sub>P<sub>max </sub>(34.2% lower) (all P&lt;0.01) and CO<sub>2max</sub> (42.1% lower, P&lt;0.001). Rest of the parameters did not show any significant differences between the study groups. The study revealed that resting and exercise induced metabolic responses of HAPE-r volunteers was better as compared to acclimatized HAPE-s volunteers at sea level.</p>

THE HEART AND PULMONARY CIRCULATION IN CHILDREN AT HIGH ALTITUDES

PEDIATRICS ◽  
1964 ◽  
Vol 34 (4) ◽  
pp. 568-582
Author(s):  
Dante Peñaloza ◽  
Javier Arias-Stella ◽  
Francisco Sime ◽  
Sixto Recavarren ◽  
Emilio Marticorena
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Ventricular Hypertrophy ◽  
Ductus Arteriosus ◽  
Healthy Children ◽  
High Altitudes ◽  
High Altitude Pulmonary Edema

Physiologic and anatomic changes have been demonstrated in healthy children born and living at high altitudes. Electrocardiographic and vectorcardiographic studies indicate that after birth the right ventricular preponderance remains throughout infancy and childhood. Anatomic observations have confirmed the presence of right ventricular hypertrophy in healthy children of high altitudes. Cardiac catheterizations reveals mild pulmonary hypertension associated with increased pulmonary vascular resistance, the degree of pulmonary hypertension being higher under 5 years of age. The increased pulmonary resistance is principally related to structural changes of the pulmonary vasculature, while arteriolar vasoconstriction and polycythemia are secondary factors. Pulmonary hypertension and right ventricular hypertrophy are not associated with any kind of symptoms in high-altitude children, and we must understand these changes as related in some way to the mechanisms of natural acclimatization. Patent ductus arteriosus is more frequent at high altitudes than at sea level, and the incidence augments gradually as altitude above sea level increases, the relationship following a curve of parabolic type. It is probable that at high altitude hypoxia and pulmonary hypertension, which remain as chronic conditions after birth, are factors related to the patency of ductus arteriosus. High altitude pulmonary edema may occur in healthy children returning to altitude after being at sea level for a few days or weeks. Rapid improvement of the clinical condition is obtained after continuous oxygen administration; however, death may occur if early treatment is not given. Cardiac catheterization reveals a normal pulmonary wedge pressure and a degree of pulmonary hypertension two or three times greater than that corresponding to healthy children of high altitude. The mechanism of high altitude pulmonary edema is discussed.

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