Higher pulmonary artery pressure in children than in adults upon fast ascent to high altitude

Kriemler, Susi; Jansen, C.; Linka, André; Kessel-Schaefer, Arnheid; Zehnder, M.; Schürmann, T.; Kohler, Malcolm; Bloch, Konrad E.; Rocca, H. P. Brunner-La

doi:10.1183/09031936.00166407

Cited by 26 publications

(22 citation statements)

References 24 publications

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“…It is tempting to speculate that in the present study, intact alveolar fluid clearance may have prevented HAPE in children with exaggerated hypoxic pulmonary hypertension. A previous small study (17) suggested that after rapid ascent to this altitude the increase of pulmonary artery pressure was maximal a few h after arrival. Here, we could not confirm this finding, since pulmonary artery pressure was comparable 4 -6, 18 -20, and 40 h after arrival.…”

Section: Discussionmentioning

confidence: 96%

“…Surprisingly, in children and adolescents there is very little information on cardiovascular adjustments to acute high altitude exposure (26). A recent small study (17) suggests that the initial altitude-induced increase of pulmonary artery pressure is more pronounced in children than in their fathers. We speculated that if confirmed this exaggerated increase of pulmonary artery pressure could suggest that the risk of developing HAPE and acute right ventricular pressure overload may be greater in children than in adults.…”

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confidence: 97%

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Pulmonary artery pressure and cardiac function in children and adolescents after rapid ascent to 3,450 m

Allemann

Stüber

Marchi

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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High-altitude destinations are visited by increasing numbers of children and adolescents. High-altitude hypoxia triggers pulmonary hypertension that in turn may have adverse effects on cardiac function and may induce life-threatening high-altitude pulmonary edema (HAPE), but there are limited data in this young population. We, therefore, assessed in 118 nonacclimatized healthy children and adolescents (mean ± SD; age: 11 ± 2 yr) the effects of rapid ascent to high altitude on pulmonary artery pressure and right and left ventricular function by echocardiography. Pulmonary artery pressure was estimated by measuring the systolic right ventricular to right atrial pressure gradient. The echocardiography was performed at low altitude and 40 h after rapid ascent to 3,450 m. Pulmonary artery pressure was more than twofold higher at high than at low altitude (35 ± 11 vs. 16 ± 3 mmHg; P < 0.0001), and there existed a wide variability of pulmonary artery pressure at high altitude with an estimated upper 95% limit of 52 mmHg. Moreover, pulmonary artery pressure and its altitude-induced increase were inversely related to age, resulting in an almost twofold larger increase in the 6- to 9- than in the 14- to 16-yr-old participants (24 ± 12 vs. 13 ± 8 mmHg; P = 0.004). Even in children with the most severe altitude-induced pulmonary hypertension, right ventricular systolic function did not decrease, but increased, and none of the children developed HAPE. HAPE appears to be a rare event in this young population after rapid ascent to this altitude at which major tourist destinations are located.

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 97%

Pulmonary artery pressure and cardiac function in children and adolescents after rapid ascent to 3,450 m

Allemann

Stüber

Marchi

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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“…These novel findings suggest that the hypoxemia experienced by COPD patients going to an altitude as encountered in many tourist destinations or during commercial air travel is causing considerable impairment of the pulmonary and systemic circulation that may possibly contribute to exercise limitation or even predispose to cardiac failure. In the literature, many previous studies observing effects of acute exposure to hypobaric or normobaric hypoxia have described increases in PAP in healthy subjects: Kriemler et al [21] performed an echocardiographic field study on 20 healthy individuals (mean age 44 years) and revealed an increase in mean sPAP from 24 mm Hg at 450 m to 32 mm Hg on the first day at 3,450 m. Similar results from younger study collectives have been reported by several other authors describing sPAP values ranging from 30 ± 6 mm Hg at 3,730 m to 41 ± 3 mm Hg at 5,000 m [22][23][24][25][26][27][28]. Thus, with an estimated sPAP of 28 mm Hg (24; 35) at 490 m, the current COPD patients already started with higher pressures at low altitude when compared to healthy subjects, and furthermore showed a greater increase when ascending to 2,590 m; such values were reported for healthy subjects only at very high altitudes (> 4,500 m) [22][23][24][25][26][27].…”

Section: Discussionmentioning

confidence: 99%

Right and Left Heart Function in Lowlanders with COPD at Altitude: Data from a Randomized Study

et al. 2018

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Background: Changes in pulmonary hemodynamics and cardiac function in patients with chronic obstructive pulmonary disease (COPD) traveling to altitude have not been assessed despite an increasing prevalence of the disease. Objectives: We hypothesized that pulmonary artery pressure (PAP) significantly increases and cardiac function deteriorates during exposure to hypobaric hypoxia as encountered by traveling to moderate altitude or air flight. Methods: A total of 37 patients (17 female; median age [quartiles] 66 years [60; 69] with COPD GOLD grade 2–3 [FEV₁ 57% predicted (49; 71)]) living < 800 m underwent echocardiography in Zurich (490 m) and after 1 night at Davos Jakobshorn (2,590 m) in a randomized order of allocation. Results: The transtricuspid pressure gradient increased from 23 mm Hg (18; 29) to 32 mm Hg (25; 41) (p < 0.0001; Δmedian [95% CI] 7.5 [2.0; 13.0]), the right ventricular fractional area change decreased from 45% (39; 49) to 38% (33; 43) (p = 0.002), while the heart rate and systolic blood pressure increased from 70 bpm (64; 78) to 82 bpm (70; 86) (p < 0.0001) and from 133 mm Hg (123; 141) to 136 mm Hg (126; 148) (p = 0.002), respectively, and left ventricular diastolic dysfunction was more prevalent (24–54%, p = 0.02). Conclusions: This is a first study assessing changes in pulmonary hemodynamics and cardiac function in patients with COPD during a short altitude sojourn. Despite the increase in PAP and indications of change in cardiac function, the exposure was well tolerated. None of the patients had to descend to lower altitude for symptomatic altitude-related disease.

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“…21.1 ). Their relatives have not been studied, but children and their fathers at 3,450 m show similar PA pressure increases [ 26 ], suggesting HPV is, in part, genetically determined as is the hypoxic ventilatory response (HVR) [ 27 ]. The prevalence of heightened pulmonary vascular responsiveness in the general population may be as high as 10 % [ 28 ] and may contribute to the out of proportion pulmonary hypertension that develops later in life in patients with sleep apnea, heart failure, and chronic lung disease.…”

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confidence: 74%

High-Altitude Pulmonary Edema (HAPE)

Schoene

Swenson

2013

High Altitude

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Much of the clinical impact of acute altitude illnesses stems from fl uid accumulation in interstitial spaces and nowhere is this more apparent than in the lungs as the edema escapes into the alveoli to cause life-threatening hypoxemia. This chapter will update our knowledge of HAPE over the past decade about the vasculature, alveolar epithelium, innervation, immune response, and genetics of the lung in hypoxia, as well as prophylactic and therapeutic strategies to reduce the toll of this most common alpine life-threatening illness. 406extend to HPV, would predict greater HAPE susceptibility. Although HAPE can develop in sedentary persons, exercise [ 6 ] and its pulmonary hemodynamic consequences (discussed below) are important precipitating factors.Symptoms, signs, and physiologic changes in lung function typical of pulmonary edema [ 1 -3 , 7 ] evolve in 2-4 days after ascent, often preceded or accompanying AMS (see Chap. 20 ), but can occur later with further ascent. Arterial saturations can fall as low as 40 % and PaO 2 s in the low 20 mmHg range. HAPE in its severest stage with profound hypoxemia can lead to high-altitude cerebral edema [ 8 ]. Repeat occurrences of HAPE do not always involve infi ltrates in the same areas, which suggests that fi xed structural aspects of lung parenchyma or vessels do not account for the timing of edema or its locale [ 9 ]. A special exception is unilateral absence of a pulmonary artery, in which edema always occurs in the contralateral lung receiving the entire cardiac output [ 10 ].It has been suggested that many persons (50-75 %) may have subclinical HAPE that resolves spontaneously despite remaining at altitude [ 11 -13 ]. This incidence equals that of AMS, which itself can cause mild gas exchange impairment [ 14 ] by unknown mechanisms perhaps related to altered autonomic infl uences on the pulmonary circulation and/or airways leading to ventilation-perfusion mismatching. Subclinical HAPE may be considerably overestimated without radiography [ 15 ] because indirect measures of interstitial edema such as spirometry, closing volume, and/or transthoracic impedance can vary for other reasons related to mountaineering including intense exercise and increased cardiac output, cold/dry air-induced bronchoconstriction, and hypocapnia [ 16 ]. With radiographically mild HAPE, only modest abnormalities were detectable [ 15 ] suggesting many lung function parameters are not sensitive enough to detect small changes in interstitial fl uid and may require highresolution tissue density measurements by CT or MR imaging. Reentry HAPE occurs when longterm high-altitude residents return to high altitude following a brief low-altitude sojourn. It has a strong familial basis and affl icts children more than adults [ 17 ], perhaps due to a twofold greater magnitude of HPV in preteen children (age 6-9) compared to teenagers (age 14-16) when tested 40 h after ascent to high altitude [ 18 ]. PathophysiologyFrom its fi rst modern descriptions, pulmonary hypertension and HAPE have been inex...

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Higher pulmonary artery pressure in children than in adults upon fast ascent to high altitude

Cited by 26 publications

References 24 publications

Pulmonary artery pressure and cardiac function in children and adolescents after rapid ascent to 3,450 m

Pulmonary artery pressure and cardiac function in children and adolescents after rapid ascent to 3,450 m

Right and Left Heart Function in Lowlanders with COPD at Altitude: Data from a Randomized Study

High-Altitude Pulmonary Edema (HAPE)

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