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>

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 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

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 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.

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

Susceptibility to high-altitude pulmonary edema in Madison and Hilltop rats. I. Ventilation and fluid balance

1995 ◽  
Vol 78 (6) ◽  
pp. 2279-2285
Author(s):  
G. L. Colice ◽  
Y. J. Lee ◽  
J. Chen ◽  
H. K. Du ◽  
G. Ramirez ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Minute Ventilation ◽  
Plasma Renin ◽  
Barometric Pressure ◽  
Simulated Altitude ◽  
Sprague Dawley ◽  
Lung Water ◽  
Fluid Handling ◽  
High Altitude Pulmonary Edema

The pathogenesis of high-altitude pulmonary edema (HAPE) is not well understood. Ventilation and fluid-handling abnormalities at high altitude (HA) may play a role in HAPE. Because ventilatory and cardiopulmonary responses to chronic HA exposure in the Hilltop (H) strain of Sprague-Dawley rat are different from those in the Madison (M) strain, it was hypothesized that these strains would have different susceptibilities to developing HAPE. M and H rats were studied at sea level (SL) and in a hypobaric chamber after 9 and 12 h at a simulated altitude of 24,000 ft (barometric pressure = 295 mmHg) and 1, 12, and 24 h at a simulated altitude of 18,000 ft (barometric pressure = 380 mmHg). Both strains developed HAPE, but the M rat was more susceptible to HAPE, as demonstrated by a higher mortality rate from hemorrhagic pulmonary edema after 9 h at 24,000 ft and an earlier increase in lung water after exposure to 18,000 ft. Minute ventilation was similar in both strains at HA, but arterial PO2 was significantly higher in the M rat. Both strains had a significant decrease in fluid intake and negative sensible water balance at HA. No changes in plasma renin activity, aldosterone concentrations, antidiuretic hormone levels, and atrial natriuretic peptide levels were found at HA. The increased susceptibility of the M rat to HAPE is therefore not explained by ventilation or fluid-handling abnormalities.

scholarly journals Airway responses to methacholine and exercise at high altitude in healthy lowlanders

2010 ◽  
Vol 108 (2) ◽  
pp. 256-265 ◽  
Author(s):  
Riccardo Pellegrino ◽  
Pasquale Pompilio ◽  
Marco Quaranta ◽  
Andrea Aliverti ◽  
Bengt Kayser ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Minute Ventilation ◽  
Lung Mechanics ◽  
Respiratory Resistance ◽  
Interstitial Pulmonary Edema ◽  
Forced Expiratory Flow ◽  
Expiratory Flow ◽  
Airway Responses

Peribronchial edema has been proposed as a mechanism enhancing airway responses to constrictor stimuli. Acute exposure to altitude in nonacclimatized lowlanders leads to subclinical interstitial pulmonary edema that lasts for several days after ascent, as suggested by changes in lung mechanics. We, therefore, investigated whether changes in lung mechanics consistent with fluid accumulation at high altitude within the lungs are associated with changes in airway responses to methacholine or exercise. Fourteen healthy subjects were studied at 4,559 and at 120 m above sea level. At high altitude, both static and dynamic lung compliances and respiratory reactance at 5 Hz significantly decreased, suggestive of interstitial pulmonary edema. Resting minute ventilation significantly increased by ∼30%. Compared with sea level, inhalation of methacholine at high altitude caused a similar reduction of partial forced expiratory flow but less reduction of maximal forced expiratory flow, less increments of pulmonary resistance and respiratory resistance at 5 Hz, and similar effects of deep breath on pulmonary and respiratory resistance. During maximal incremental exercise at high altitude, partial forced expiratory flow gradually increased with the increase in minute ventilation similarly to sea level but both achieved higher values at peak exercise. In conclusion, airway responsiveness to methacholine at high altitude is well preserved despite the occurrence of interstitial pulmonary edema. We suggest that this may be the result of the increase in resting minute ventilation opposing the effects and/or the development of airway smooth muscle force, reduced gas density, and well preserved airway-to-parenchyma interdependence.

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