scholarly journals Susceptibility to high-altitude pulmonary edema is associated with a more uniform distribution of regional specific ventilation

2017 ◽  
Vol 122 (4) ◽  
pp. 844-852 ◽  
Author(s):  
Michael D. Patz ◽  
Rui C. Sá ◽  
Chantal Darquenne ◽  
Ann R. Elliott ◽  
Amran K. Asadi ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Relative Dispersion ◽  
Pulmonary Vasoconstriction ◽  
High Altitude Pulmonary Edema ◽  
Ventilation Heterogeneity ◽  
Multiple Breath Washout ◽  
History Of ◽  
Magnetic Resonance Imaging Mri

High-altitude pulmonary edema (HAPE) is a potentially fatal condition affecting high-altitude sojourners. The biggest predictor of HAPE development is a history of prior HAPE. Magnetic resonance imaging (MRI) shows that HAPE-susceptible (with a history of HAPE), but not HAPE-resistant (with a history of repeated ascents without illness) individuals develop greater heterogeneity of regional pulmonary perfusion breathing hypoxic gas (O2 = 12.5%), consistent with uneven hypoxic pulmonary vasoconstriction (HPV). Why HPV is uneven in HAPE-susceptible individuals is unknown but may arise from regionally heterogeneous ventilation resulting in an uneven stimulus to HPV. We tested the hypothesis that ventilation is more heterogeneous in HAPE-susceptible subjects ( n = 6) compared with HAPE-resistant controls ( n = 7). MRI specific ventilation imaging (SVI) was used to measure regional specific ventilation and the relative dispersion (SD/mean) of SVI used to quantify baseline heterogeneity. Ventilation heterogeneity from conductive and respiratory airways was measured in normoxia and hypoxia (O2 = 12.5%) using multiple-breath washout and heterogeneity quantified from the indexes Scond and Sacin, respectively. Contrary to our hypothesis, HAPE-susceptible subjects had significantly lower relative dispersion of specific ventilation than the HAPE-resistant controls [susceptible = 1.33 ± 0.67 (SD), resistant = 2.36 ± 0.98, P = 0.05], and Sacin tended to be more uniform (susceptible = 0.085 ± 0.009, resistant = 0.113 ± 0.030, P = 0.07). Scond was not significantly different between groups (susceptible = 0.019 ± 0.007, resistant = 0.020 ± 0.004, P = 0.67). Sacin and Scond did not change significantly in hypoxia ( P = 0.56 and 0.19, respectively). In conclusion, ventilation heterogeneity does not change with short-term hypoxia irrespective of HAPE susceptibility, and lesser rather than greater ventilation heterogeneity is observed in HAPE-susceptible subjects. This suggests that the basis for uneven HPV in HAPE involves vascular phenomena. NEW & NOTEWORTHY 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-susceptible subjects compared with HAPE-resistant subjects. Contrary to our hypothesis, ventilation heterogeneity was less in HAPE-susceptible subjects and unaffected by hypoxia, suggesting a vascular basis for uneven HPV.

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.

Exaggerated Hypoxic Pulmonary Vasoconstriction Without Susceptibility to High Altitude Pulmonary Edema

2015 ◽  
Vol 16 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Christoph Dehnert ◽  
Derliz Mereles ◽  
Sebastian Greiner ◽  
Dagmar Albers ◽  
Fabian Scheurlen ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Vasoconstriction ◽  
High Altitude Pulmonary Edema

scholarly journals Hypoxia-Induced Inflammatory Chemokines in Subjects with a History of High-Altitude Pulmonary Edema

2015 ◽  
Vol 31 (1) ◽  
pp. 81-86 ◽  
Author(s):  
K. P. Mishra ◽  
Navita Sharma ◽  
Poonam Soree ◽  
R. K. Gupta ◽  
Lilly Ganju ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
High Altitude Pulmonary Edema ◽  
Inflammatory Chemokines ◽  
History Of

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.

Blunted hypoxic ventilatory drive in subjects susceptible to high-altitude pulmonary edema

1989 ◽  
Vol 66 (3) ◽  
pp. 1152-1157 ◽  
Author(s):  
Y. Matsuzawa ◽  
K. Fujimoto ◽  
T. Kobayashi ◽  
N. R. Namushi ◽  
K. Harada ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Pulmonary Function Test ◽  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
High Altitude Pulmonary Edema ◽  
Function Test ◽  
History Of ◽  
Low Altitude

It has been proposed that subjects susceptible to high-altitude pulmonary edema (HAPE) show exaggerated hypoxemia with relative hypoventilation during the early period of high-altitude exposure. Some previous studies suggest the relationship between the blunted hypoxic ventilatory response (HVR) and HAPE. To examine whether all the HAPE-susceptible subjects consistently show blunted HVR at low altitude, we evaluated the conventional pulmonary function test, hypoxic ventilatory response (HVR), and hypercapnic ventilatory response (HCVR) in ten lowlanders who had a previous history of HAPE and compared these results with those of eight control lowlanders who had no history of HAPE. HVR was measured by the progressive isocapnic hypoxic method and was evaluated by the slope relating minute ventilation to arterial O2 saturation (delta VE/delta SaO2). HCVR was measured by the rebreathing method of Read. All measurements were done at Matsumoto, Japan (610 m). All the HAPE-susceptible subjects showed normal values in the pulmonary function test. In HCVR, HAPE-susceptible subjects showed relatively lower S value, but there was no significant difference between the two groups (1.74 +/- 1.16 vs. 2.19 +/- 0.4, P = NS). On the other hand, HAPE-susceptible subjects showed significantly lower HVR than control subjects (-0.42 +/- 0.23 vs. -0.87 +/- 0.29, P less than 0.01). These results suggest that HAPE-susceptible subjects more frequently show low HVR at low altitude. However, values for HVR were within the normal range in 2 of 10 HAPE-susceptible subjects. It would seem therefore that low HVR alone need not be a critical factor for HAPE. This could be one of several contributing factors.

scholarly journals Excessive Gas Exchange Impairment during Exercise in A Subject with A History of Bronchopulmonary Dysplasia And High Altitude Pulmonary Edema

2007 ◽  
Vol 8 (1) ◽  
pp. 62-67 ◽  
Author(s):  
Andrew T. Lovering ◽  
Lee M. Romer ◽  
Hans C. Haverkamp ◽  
John S. Hokanson ◽  
Marlowe W. Eldridge
Keyword(s):  
Gas Exchange ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Bronchopulmonary Dysplasia ◽  
High Altitude Pulmonary Edema ◽  
History Of
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