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.

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.

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 Genetics of pulmonary hypertension and high-altitude pulmonary edema

2020 ◽  
Vol 128 (5) ◽  
pp. 1432-1438
Author(s):  
Christina A. Eichstaedt ◽  
Nicola Benjamin ◽  
Ekkehard Grünig
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Clinical Feature ◽  
Future Research ◽  
Inherited Disease ◽  
Research Perspectives ◽  
Protein Receptor ◽  
High Altitude Pulmonary Edema

Heritable pulmonary arterial hypertension (PAH) is an autosomal dominantly inherited disease caused by mutations in the bone morphogenetic protein receptor 2 ( BMPR2) gene and/or genes of its signaling pathway in ~85% of patients. A genetic predisposition to high-altitude pulmonary edema (HAPE) has long been suspected because of familial HAPE cases, but very few possibly disease-causing mutations have been identified to date. This minireview provides an overview of genetic analyses investigating common polymorphisms in HAPE-susceptible patients and the directed identification of disease-causing mutations in PAH patients. Increased pulmonary artery pressure is highlighted as an overlapping clinical feature of the two diseases. Moreover, studies showing increased pulmonary artery pressures in HAPE-susceptible patients during exercise or hypoxia as well as in healthy BMPR2 mutation carriers are illustrated. Finally, high-altitude pulmonary hypertension is introduced and future research perspectives outlined.

Physiological aspects of high-altitude pulmonary edema

2005 ◽  
Vol 98 (3) ◽  
pp. 1101-1110 ◽  
Author(s):  
Peter Bärtsch ◽  
Heimo Mairbäurl ◽  
Marco Maggiorini ◽  
Erik R. Swenson
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Right Heart Catheterization ◽  
Lung Edema ◽  
Heart Catheterization ◽  
Edema Formation ◽  
Pulmonary Vasoconstriction ◽  
Large Molecular Weight ◽  
High Altitude Pulmonary Edema

High-altitude pulmonary edema (HAPE) develops in rapidly ascending nonacclimatized healthy individuals at altitudes above 3,000 m. An excessive rise in pulmonary artery pressure (PAP) preceding edema formation is the crucial pathophysiological factor because drugs that lower PAP prevent HAPE. Measurements of nitric oxide (NO) in exhaled air, of nitrites and nitrates in bronchoalveolar lavage (BAL) fluid, and forearm NO-dependent endothelial function all point to a reduced NO availability in hypoxia as a major cause of the excessive hypoxic PAP rise in HAPE-susceptible individuals. Studies using right heart catheterization or BAL in incipient HAPE have demonstrated that edema is caused by an increased microvascular hydrostatic pressure in the presence of normal left atrial pressure, resulting in leakage of large-molecular-weight proteins and erythrocytes across the alveolarcapillary barrier in the absence of any evidence of inflammation. These studies confirm in humans that high capillary pressure induces a high-permeability-type lung edema in the absence of inflammation, a concept first introduced under the term “stress failure.” Recent studies using microspheres in swine and magnetic resonance imaging in humans strongly support the concept and primacy of nonuniform hypoxic arteriolar vasoconstriction to explain how hypoxic pulmonary vasoconstriction occurring predominantly at the arteriolar level can cause leakage. This compelling but as yet unproven mechanism predicts that edema occurs in areas of high blood flow due to lesser vasoconstriction. The combination of high flow at higher pressure results in pressures, which exceed the structural and dynamic capacity of the alveolar capillary barrier to maintain normal alveolar fluid balance.

scholarly journals High altitude pulmonary edema misdiagnosed as pneumonia

2019 ◽  
Vol 91 (3) ◽  
pp. 68-70
Author(s):  
A Sh Sarybaev ◽  
A M Maripov ◽  
K Muratali-Uulu ◽  
M B Cholponbaeva ◽  
N A Kushubakova ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Present Article ◽  
Early Treatment ◽  
Treatment Options ◽  
Signs And Symptoms ◽  
Rare Form ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Illness ◽  
Clinical Conditions

High altitude pulmonary edema (HAPE) is a relatively rare form of high altitude illness. However, without immediate treatment, HAPE is fatal. Furthermore, HAPE is characterized by non-specific signs and symptoms, and many clinical conditions may mimic it. In the present article, we report a case of HAPE misdiagnosed as pneumonia. We also discuss the issues of prevention and early treatment options in this illness.

High-Altitude Pulmonary Edema in Children With Underlying Cardiopulmonary Disorders and Pulmonary Hypertension Living at Altitude

2004 ◽  
Vol 158 (12) ◽  
pp. 1170 ◽  
Author(s):  
Bibhuti B. Das ◽  
Robert R. Wolfe ◽  
Kak-Chen Chan ◽  
Gary L. Larsen ◽  
John T. Reeves ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Edema ◽  
High Altitude ◽  
High Altitude Pulmonary Edema

scholarly journals Comorbid cerebral and pulmonary edema at 7010 m/23000 ft.: an extreme altitude perspective

2014 ◽  
Vol 14 (1) ◽  
pp. 87-90
Author(s):  
Inam Danish Khan
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Clinical Decision Making ◽  
Medical Science ◽  
Clinical Decision ◽  
High Altitude Pulmonary Edema ◽  
Extreme Altitude ◽  
High Altitude Cerebral Edema ◽  
High Altitude Illness ◽  
High Index Of Suspicion

High Altitude Cerebral Edema (HACE) and High Altitude Pulmonary Edema (HAPE) are two dreaded altitude emergencies which can independently lead to complications. Two cases of suspected comorbid HACE and HAPE were managed at 5800 m/19000 ft in Karakoram Himalayas. Altitude acclimatization, purported to prevent high altitude illness, may not be protective. Comorbid HACE and HAPE at extreme altitude may present atypically necessitating high index of suspicion and prompt clinical decision making in challenging situations. One man HAPE bag/PHC is an excellent temporary measure in cases of delayed descent/evacuation. Due attention to extreme altitude emergencies is required in view of increased recreational, scientific and military activities at extreme altitude. DOI: http://dx.doi.org/10.3329/bjms.v14i1.17040 Bangladesh Journal of Medical Science Vol.14(1) 2015 p.87-90

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.

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