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Peter Bärtsch - One of the best experts on this subject based on the ideXlab platform.
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Genetic Predisposition to High-Altitude Pulmonary Edema.
High altitude medicine & biology, 2020Co-Authors: Christina A. Eichstaedt, Christoph Dehnert, Peter Bärtsch, Heimo Mairbäurl, Jie Song, Nicola Benjamin, Christine Fischer, Kai Schommer, Marc M. Berger, Ekkehard GrunigAbstract:Background: Exaggerated Pulmonary arterial hypertension (PAH) is a hallmark of High-Altitude Pulmonary Edema (HAPE). The objective of this study was therefore to investigate genetic predisposition ...
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High-Altitude Pulmonary Edema.
Comprehensive Physiology, 2012Co-Authors: Erik R Swenson, Peter BärtschAbstract:High-Altitude Pulmonary Edema (HAPE), a not uncommon form of acute altitude illness, can occur within days of ascent above 2500 to 3000 m. Although life-threatening, it is avoidable by slow ascent to permit acclimatization or with drug prophylaxis. The critical pathophysiology is an excessive rise in Pulmonary vascular resistance or hypoxic Pulmonary vasoconstriction (HPV) leading to increased microvascular pressures. The resultant hydrostatic stress causes dynamic changes in the permeability of the alveolar capillary barrier and mechanical injurious damage leading to leakage of large proteins and erythrocytes into the alveolar space in the absence of inflammation. Bronchoalveolar lavage and hemodynamic pressure measurements in humans confirm that elevated capillary pressure induces a high-permeability noninflammatory lung Edema. Reduced nitric oxide availability and increased endothelin in hypoxia are the major determinants of excessive HPV in HAPE-susceptible individuals. Other hypoxia-dependent differences in ventilatory control, sympathetic nervous system activation, endothelial function, and alveolar epithelial active fluid reabsorption likely contribute additionally to HAPE susceptibility. Recent studies strongly suggest nonuniform regional hypoxic arteriolar vasoconstriction as an explanation for how HPV occurring predominantly at the arteriolar level causes leakage. In areas of high blood flow due to lesser HPV, Edema develops due to pressures that exceed the dynamic and structural capacity of the alveolar capillary barrier to maintain normal fluid balance. This article will review the pathophysiology of the vasculature, alveolar epithelium, innervation, immune response, and genetics of the lung at high altitude, as well as therapeutic and prophylactic strategies to reduce the morbidity and mortality of HAPE.
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physiological aspects of high altitude Pulmonary Edema
Journal of Applied Physiology, 2005Co-Authors: Peter Bärtsch, Marco Maggiorini, Heimo Mairbäurl, Erik R SwensonAbstract: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 ede...
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augmented sympathetic activation during short term hypoxia and high altitude exposure in subjects susceptible to high altitude Pulmonary Edema
Circulation, 1999Co-Authors: Herve Duplain, Peter Bärtsch, Laurent Vollenweider, Alain Delabays, Pascal Nicod, Urs ScherrerAbstract:Background—Pulmonary hypertension is a hallmark of High-Altitude Pulmonary Edema and may contribute to its pathogenesis. Cardiovascular adjustments to hypoxia are mediated, at least in part, by the sympathetic nervous system, and sympathetic activation promotes Pulmonary vasoconstriction and alveolar fluid flooding in experimental animals. Methods and Results—We measured sympathetic nerve activity (using intraneural microelectrodes) in 8 mountaineers susceptible to High-Altitude Pulmonary Edema and 7 mountaineers resistant to this condition during short-term hypoxic breathing at low altitude and at rest at a High-Altitude laboratory (4559 m). We also measured systolic Pulmonary artery pressure to examine the relationship between sympathetic activation and Pulmonary vasoconstriction. In subjects prone to Pulmonary Edema, short-term hypoxic breathing at low altitude evoked comparable hypoxemia but a 2- to 3-times-larger increase in the rate of the sympathetic nerve discharge than in subjects resistant to ed...
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High altitude Pulmonary Edema.
Respiration; international review of thoracic diseases, 1997Co-Authors: Peter BärtschAbstract:Altitude, speed and mode of ascent and, above all, individual susceptibility are the most important determinants for the occurrence of High-Altitude Pulmonary Edema (HAPE). This illness usually occurs only 2-5 days after acute exposure to altitudes above 2,500-3,000 m. Chest radiographs and CT scans show a patchy predominantly peripheral distribution of Edema. Wedge pressure is normal at rest, and there is an excessive rise in Pulmonary artery pressure (Ppa) which precedes Edema formation. Bronchoalveolar lavage in patients with advanced HAPE shows evidence of inflammatory response with increased capillary permeability. There are, however, no prospective data indicating whether the inflammatory response is a primary cause of HAPE or a consequence of Edema formation. Excessive rise in Ppa appears to be a crucial pathophysiologic factor for HAPE. Recent observations of high Ppa in HAPE-susceptible sujects who did not develop Pulmonary Edema after rapid ascent to high altitude suggest either that Ppa does not necessarily reflect capillary pressure in these individuals or else that additional factors, such as an inflammatory response and/or a decreased fluid clearance from the lung, are necessary for the development of Pulmonary Edema. The treatment of choice is immediate descent. When this is impossible and supplemental oxygen is not available, treatment with nifedipine is recommended until descent is possible.
Marco Maggiorini - One of the best experts on this subject based on the ideXlab platform.
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exaggerated hypoxic Pulmonary vasoconstriction without susceptibility to high altitude Pulmonary Edema
High Altitude Medicine & Biology, 2015Co-Authors: Christoph Dehnert, Sebastian Greiner, Dagmar Albers, Fabian Scheurlen, Stefanie Zugel, Marco Maggiorini, Derliz Mereles, Peter Vock, Thomas Böhm, Ekkehard GrunigAbstract:Abstract Dehnert, Christoph, Derliz Mereles, Sebastian Greiner, Dagmar Albers, Fabian Scheurlen, Stefanie Zugel, Thomas Bohm, Peter Vock, Marco Maggiorini, Ekkehard Grunig, and Peter Bartsch. Exaggerated hypoxic Pulmonary vasoconstriction without susceptibility to high altitude Pulmonary Edema. High Alt Med Biol 16:11–17, 2015.—Background: Abnormally high Pulmonary artery pressure (PAP) in hypoxia due to exaggerated hypoxic Pulmonary vasoconstriction (HPV) is a key factor for development of High-Altitude Pulmonary Edema (HAPE). It was shown that about 10% of a healthy Caucasian population has an exaggerated HPV that is comparable to the response measured in HAPE-susceptible individuals. Therefore, we hypothesized that those with exaggerated HPV are HAPE-susceptible. Methods and Results: We screened 421 healthy Caucasians naive to high altitude for HPV using Doppler echocardiography for assessment of systolic PAP in normobaric hypoxia (PASPHx; Po2 corresponding to 4500 m). Subjects with exaggerated HPV and...
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Both Tadalafil and Dexamethasone May Reduce the Incidence of High-Altitude Pulmonary Edema
Annals of Internal Medicine, 2006Co-Authors: Marco Maggiorini, Christoph Dehnert, Thomas Böhm, Hans-peter Brunner-la Rocca, Simon Peth, Manuel Fischler, Alain M. Bernheim, Stefanie Kiencke, Konrad E. Bloch, Robert NaeijeAbstract:In this double-blind trial, 29 adults with a history of High-Altitude Pulmonary Edema (HAPE) were randomly assigned to receive prophylactic tadalafil, dexamethasone, or placebo during a 24-hour asc...
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Do changes in lung function predict High-Altitude Pulmonary Edema at an early stage?
Medicine and science in sports and exercise, 2006Co-Authors: Oliver Senn, Marco Maggiorini, Hans-peter Brunner-la Rocca, Manuel Fischler, Christian F. Clarenbach, Rahel Thalmann, Patrick Egger, Konrad E. BlochAbstract:ABSTRACTPurpose:Ascent to high altitude is associated with alterations in lung function. The mechanisms of these changes and whether they reflect early stages of High-Altitude Pulmonary Edema (HAPE) has been debated. Therefore, we investigated the time course of Pulmonary function in relation to hem
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physiological aspects of high altitude Pulmonary Edema
Journal of Applied Physiology, 2005Co-Authors: Peter Bärtsch, Marco Maggiorini, Heimo Mairbäurl, Erik R SwensonAbstract: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 ede...
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Prevention of High-Altitude Pulmonary Edema by Nifedipine
The New England journal of medicine, 1991Co-Authors: Peter Bärtsch, Marco Maggiorini, Peter Vock, Manfred Ritter, Christof Noti, O. OelzAbstract:Abstract Background. Exaggerated Pulmonary-artery pressure due to hypoxic vasoconstriction is considered an important pathogenetic factor in High-Altitude Pulmonary Edema. We previously found that nifedipine lowered Pulmonary-artery pressure and improved exercise performance, gas exchange, and the radiographic manifestations of disease in patients with High-Altitude Pulmonary Edema. We therefore hypothesized that the prophylactic administration of nifedipine would prevent its recurrence. Methods. Twenty-one mountaineers (1 woman and 20 men) with a history of radiographically documented High-Altitude Pulmonary Edema were randomly assigned to receive either 20 mg of a slow-release preparation of nifedipine (n = 10) or placebo (n = 11) every 8 hours while ascending rapidly (within 22 hours) from a low altitude to 4559 m and during the following three days at this altitude. Both the subjects and the investigators were blinded to the assigned treatment. The diagnosis of Pulmonary Edema was based on chest radio...
Erik R Swenson - One of the best experts on this subject based on the ideXlab platform.
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Early hours in the development of High-Altitude Pulmonary Edema: time course and mechanisms.
Journal of applied physiology (Bethesda Md. : 1985), 2020Co-Authors: Erik R SwensonAbstract:Clinically evident High-Altitude Pulmonary Edema (HAPE) is characterized by severe cyanosis, dyspnea, cough, and difficulty with physical exertion. This usually occurs within 1–2 days of ascent oft...
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Susceptibility to High-Altitude Pulmonary Edema is associated with a more uniform distribution of regional specific ventilation
Journal of applied physiology (Bethesda Md. : 1985), 2017Co-Authors: Michael D. Patz, Erik R Swenson, Chantal Darquenne, A. R. Elliott, Amran K. Asadi, Rebecca J. Theilmann, David J. Dubowitz, G. Kim Prisk, Susan R. HopkinsAbstract:Uneven hypoxic Pulmonary vasoconstriction (HPV) is thought to incite High-Altitude Pulmonary Edema (HAPE). We evaluated whether greater heterogeneity of ventilation is also a feature of HAPE-suscep...
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High-Altitude Pulmonary Edema.
Comprehensive Physiology, 2012Co-Authors: Erik R Swenson, Peter BärtschAbstract:High-Altitude Pulmonary Edema (HAPE), a not uncommon form of acute altitude illness, can occur within days of ascent above 2500 to 3000 m. Although life-threatening, it is avoidable by slow ascent to permit acclimatization or with drug prophylaxis. The critical pathophysiology is an excessive rise in Pulmonary vascular resistance or hypoxic Pulmonary vasoconstriction (HPV) leading to increased microvascular pressures. The resultant hydrostatic stress causes dynamic changes in the permeability of the alveolar capillary barrier and mechanical injurious damage leading to leakage of large proteins and erythrocytes into the alveolar space in the absence of inflammation. Bronchoalveolar lavage and hemodynamic pressure measurements in humans confirm that elevated capillary pressure induces a high-permeability noninflammatory lung Edema. Reduced nitric oxide availability and increased endothelin in hypoxia are the major determinants of excessive HPV in HAPE-susceptible individuals. Other hypoxia-dependent differences in ventilatory control, sympathetic nervous system activation, endothelial function, and alveolar epithelial active fluid reabsorption likely contribute additionally to HAPE susceptibility. Recent studies strongly suggest nonuniform regional hypoxic arteriolar vasoconstriction as an explanation for how HPV occurring predominantly at the arteriolar level causes leakage. In areas of high blood flow due to lesser HPV, Edema develops due to pressures that exceed the dynamic and structural capacity of the alveolar capillary barrier to maintain normal fluid balance. This article will review the pathophysiology of the vasculature, alveolar epithelium, innervation, immune response, and genetics of the lung at high altitude, as well as therapeutic and prophylactic strategies to reduce the morbidity and mortality of HAPE.
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physiological aspects of high altitude Pulmonary Edema
Journal of Applied Physiology, 2005Co-Authors: Peter Bärtsch, Marco Maggiorini, Heimo Mairbäurl, Erik R SwensonAbstract: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 ede...
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inhibitors of hypoxic Pulmonary vasoconstriction prevent high altitude Pulmonary Edema in rats
Wilderness & Environmental Medicine, 2004Co-Authors: John T. Berg, S Ramanathan, Erik R SwensonAbstract:Objective Rapid ascent to high altitude causes hypoxic Pulmonary vasoconstriction (HPV) and leads to High-Altitude Pulmonary Edema (HAPE) in susceptible humans. Vasodilating agents lessen HAPE (as evidenced by radiographic and gas exchange measurements), but data establishing their effectiveness on alveolar protein content and hemorrhage are lacking. This study was designed to assess whether preventing HPV reduces the alveolar-capillary barrier leak characteristic of HAPE. Methods Rats were pretreated with saline (control group) or acetazolamide (20 mg/kg) or nickel chloride (60 mg/kg) (experimental groups) to prevent HPV and were exposed to high altitude (0.5atm for 24 hours) in a hypobaric chamber. High-Altitude Pulmonary Edema was then assessed by gravimetric analysis of heart and lung tissue, a visual score of lung hemorrhage, and measurement of protein content in bronchoalveolar lavage fluid. Results Saline-treated rats developed a mild protein leak indicative of early HAPE that was prevented by inhibition of HPV: protein in bronchoalevolar lavage fluid of saline-treated rats, 21.6±3.2 mg/dL (mean±SEM); HPV-inhibited rats, 12.6±0.7 mg/dL; air-exposed rats, 13.4±1.4 mg/ dL ( P P =.032). Finally, right ventricle weight (adjusted for initial body weight) increased in saline-treated rats: saline-treated, 0.64±0.02; HPV-inhibited, 0.56±0.02; air-exposed, 0.59±0.02 ( P Conclusion The results demonstrate that treatment with NiCl 2 or acetazolamide prevents HAPE in rats and are consistent with a role for elevated Pulmonary artery pressure in the pathogenesis of HAPE.
Urs Scherrer - One of the best experts on this subject based on the ideXlab platform.
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augmented sympathetic activation during short term hypoxia and high altitude exposure in subjects susceptible to high altitude Pulmonary Edema
Circulation, 1999Co-Authors: Herve Duplain, Peter Bärtsch, Laurent Vollenweider, Alain Delabays, Pascal Nicod, Urs ScherrerAbstract:Background—Pulmonary hypertension is a hallmark of High-Altitude Pulmonary Edema and may contribute to its pathogenesis. Cardiovascular adjustments to hypoxia are mediated, at least in part, by the sympathetic nervous system, and sympathetic activation promotes Pulmonary vasoconstriction and alveolar fluid flooding in experimental animals. Methods and Results—We measured sympathetic nerve activity (using intraneural microelectrodes) in 8 mountaineers susceptible to High-Altitude Pulmonary Edema and 7 mountaineers resistant to this condition during short-term hypoxic breathing at low altitude and at rest at a High-Altitude laboratory (4559 m). We also measured systolic Pulmonary artery pressure to examine the relationship between sympathetic activation and Pulmonary vasoconstriction. In subjects prone to Pulmonary Edema, short-term hypoxic breathing at low altitude evoked comparable hypoxemia but a 2- to 3-times-larger increase in the rate of the sympathetic nerve discharge than in subjects resistant to ed...
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Inhaled nitric oxide for High-Altitude Pulmonary Edema
The New England journal of medicine, 1996Co-Authors: Urs Scherrer, Laurent Vollenweider, Alain Delabays, Milos Savcic, Urs Eichenberger, Gian-reto Kleger, Antonin Fikrle, Peter E. Ballmer, Pascal Nicod, Peter BärtschAbstract:Background Pulmonary hypertension is a hallmark of High-Altitude Pulmonary Edema and may contribute to its pathogenesis. When administered by inhalation, nitric oxide, an endothelium-derived relaxing factor, attenuates the Pulmonary vasoconstriction produced by short-term hypoxia. Methods We studied the effects of inhaled nitric oxide on Pulmonary-artery pressure and arterial oxygenation in 18 mountaineers prone to High-Altitude Pulmonary Edema and 18 mountaineers resistant to this condition in a High-Altitude laboratory (altitude, 4559 m). We also obtained lung-perfusion scans before and during nitric oxide inhalation to gain further insight into the mechanism of action of nitric oxide. Results In the High-Altitude laboratory, subjects prone to High-Altitude Pulmonary Edema had more pronounced Pulmonary hypertension and hypoxemia than subjects resistant to High-Altitude Pulmonary Edema. Arterial oxygen saturation was inversely related to the severity of Pulmonary hypertension (r = -0.50, P = 0.002). In s...
O. Oelz - One of the best experts on this subject based on the ideXlab platform.
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Prevention of High-Altitude Pulmonary Edema by Nifedipine
The New England journal of medicine, 1991Co-Authors: Peter Bärtsch, Marco Maggiorini, Peter Vock, Manfred Ritter, Christof Noti, O. OelzAbstract:Abstract Background. Exaggerated Pulmonary-artery pressure due to hypoxic vasoconstriction is considered an important pathogenetic factor in High-Altitude Pulmonary Edema. We previously found that nifedipine lowered Pulmonary-artery pressure and improved exercise performance, gas exchange, and the radiographic manifestations of disease in patients with High-Altitude Pulmonary Edema. We therefore hypothesized that the prophylactic administration of nifedipine would prevent its recurrence. Methods. Twenty-one mountaineers (1 woman and 20 men) with a history of radiographically documented High-Altitude Pulmonary Edema were randomly assigned to receive either 20 mg of a slow-release preparation of nifedipine (n = 10) or placebo (n = 11) every 8 hours while ascending rapidly (within 22 hours) from a low altitude to 4559 m and during the following three days at this altitude. Both the subjects and the investigators were blinded to the assigned treatment. The diagnosis of Pulmonary Edema was based on chest radio...
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Blood rheology in acute mountain sickness and High-Altitude Pulmonary Edema.
Journal of applied physiology (Bethesda Md. : 1985), 1991Co-Authors: W. H. Reinhart, U. Waber, O. Oelz, Bengt Kayser, Abhay Kumar Singh, Peter BärtschAbstract:The role of blood rheology in the pathogenesis of acute mountain sickness and High-Altitude Pulmonary Edema was investigated. Twenty-three volunteers, 12 with a history of High-Altitude Pulmonary Edema, were studied at low altitude (490 m) and at 2 h and 18 h after arrival at 4,559 m. Eight subjects remained healthy, seven developed acute mountain sickness, and eight developed High-Altitude Pulmonary Edema. Hematocrit, whole blood viscosity, plasma viscosity, erythrocyte aggregation, and erythrocyte deformability (filtration) were measured. Plasma viscosity and erythrocyte deformability remained unaffected. The hematocrit level was lower 2 h after the arrival at high altitude and higher after 18 h compared with low altitude. The whole blood viscosity changed accordingly. The erythrocyte aggregation was about doubled 18 h after the arrival compared with low-altitude values, which reflects the acute phase reaction. There were, however, no significant differences in any rheological parameters between healthy individuals and subjects with acute mountain sickness or High-Altitude Pulmonary Edema, either before or during the illness. We conclude that rheological abnormalities can be excluded as an initiating event in the development of acute mountain sickness and High-Altitude Pulmonary Edema.