Pulmonary hypertension is associated with diverse cardiac, pulmonary, and systemic diseases in neonates, infants, and older children and contributes to significant morbidity and mortality. However, current approaches to caring for pediatric patients with pulmonary hypertension have been limited by the lack of consensus guidelines from experts in the field. In a joint effort from the American Heart Association and American Thoracic Society, a panel of experienced clinicians and clinician-scientists was assembled to review the current literature and to make recommendations on the diagnosis, evaluation, and treatment of pediatric pulmonary hypertension. This publication presents the results of extensive literature reviews, discussions, and formal scoring of recommendations for the care of children with pulmonary hypertension.

Pediatric Pulmonary Hypertension: Guidelines From the American Heart Association and American Thoracic Society

It has been known for more than 60 years, and suspected for over 100, that alveolar hypoxia causes pulmonary vasoconstriction by means of mechanisms local to the lung. For the last 20 years, it has been clear that the essential sensor, transduction, and effector mechanisms responsible for hypoxic pulmonary vasoconstriction (HPV) reside in the pulmonary arterial smooth muscle cell. The main focus of this review is the cellular and molecular work performed to clarify these intrinsic mechanisms and to determine how they are facilitated and inhibited by the extrinsic influences of other cells. Because the interaction of intrinsic and extrinsic mechanisms is likely to shape expression of HPV in vivo, we relate results obtained in cells to HPV in more intact preparations, such as intact and isolated lungs and isolated pulmonary vessels. Finally, we evaluate evidence regarding the contribution of HPV to the physiological and pathophysiological processes involved in the transition from fetal to neonatal life, pulmonary gas exchange, high-altitude pulmonary edema, and pulmonary hypertension. Although understanding of HPV has advanced significantly, major areas of ignorance and uncertainty await resolution.

Hypoxic pulmonary vasoconstriction.

A 45-year-old healthy man wishes to climb Mount Kilimanjaro (5895 m) in a 5-day period, starting at 1800 m. The results of a recent exercise stress test were normal; he runs 10 km 4 or 5 times per week and finished a marathon in less than 4 hours last year. He wants to know how he can prevent becoming ill at high altitude and whether training or sleeping under normobaric hypoxic conditions in the weeks before the ascent would be helpful. What would you advise?

https://amga.com/wp-content/uploads/2013/09/Bartsch-Swenson-HAI-NEJM-2013.pdf

Acute High-Altitude Illnesses

Cellular hypoxia is the common final pathway of brain injury that occurs not just after asphyxia, but also when cerebral perfusion is impaired directly (eg, embolic stroke) or indirectly (eg, raised intracranial pressure after head injury). We Review recent advances in the understanding of neurological clinical syndromes that occur on exposure to high altitudes, including high altitude headache (HAH), acute mountain sickness (AMS), and high altitude cerebral oedema (HACE), and the genetics, molecular mechanisms, and physiology that underpin them. We also present the vasogenic and cytotoxic bases for HACE and explore venous hypertension as a possible contributory factor. Although the factors that control susceptibility to HACE are poorly understood, the effects of exposure to altitude (and thus hypobaric hypoxia) might provide a reproducible model for the study of cerebral cellular hypoxia in healthy individuals. The effects of hypobaric hypoxia might also provide new insights into the understanding of hypoxia in the clinical setting.

https://www.thelancet.com/pdfs/journals/laneur/PIIS1474-4422(09)70014-6.pdf

The cerebral effects of ascent to high altitudes

Pediatric Pulmonary Hypertension

BACKGROUND High-altitude pulmonary edema (HAPE) is caused by exaggerated hypoxic pulmonary vasoconstriction associated with decreased bioavailability of nitric oxide in the lungs and by impaired reabsorption of alveolar fluid. OBJECTIVE To investigate whether dexamethasone or tadalafil reduces the incidence of HAPE and acute mountain sickness (AMS) in adults with a history of HAPE. DESIGN Randomized, double-blind, placebo-controlled study performed in summer 2003. SETTING Ascent from 490 m within 24 hours and stay for 2 nights at 4559 m. PATIENTS 29 adults with previous HAPE. INTERVENTION Prophylactic tadalafil (10 mg), dexamethasone (8 mg), or placebo twice daily during ascent and stay at 4559 m. MEASUREMENTS Chest radiography was used to diagnose HAPE. A Lake Louise score greater than 4 defined AMS. Systolic pulmonary artery pressure was measured by using Doppler echocardiography, and nasal potentials were measured as a surrogate marker of alveolar sodium transport. RESULTS Two participants who received tadalafil developed severe AMS on arrival at 4559 m and withdrew from the study; they did not have HAPE at that time. High-altitude pulmonary edema developed in 7 of 9 participants receiving placebo and 1 of the remaining 8 participants receiving tadalafil but in none of the 10 participants receiving dexamethasone (P = 0.007 for tadalafil vs. placebo; P < 0.001 for dexamethasone vs. placebo). Eight of 9 participants receiving placebo, 7 of 10 receiving tadalafil, and 3 of 10 receiving dexamethasone had AMS (P = 1.0 for tadalafil vs. placebo; P = 0.020 for dexamethasone vs. placebo). At high altitude, systolic pulmonary artery pressure increased less in participants receiving dexamethasone (16 mm Hg [95% CI, 9 to 23 mm Hg]) and tadalafil (13 mm Hg [CI, 6 to 20 mm Hg]) than in those receiving placebo (28 mm Hg [CI, 20 to 36 mm Hg]) (P = 0.005 for tadalafil vs. placebo; P = 0.012 for dexamethasone vs. placebo). No statistically significant difference between groups was found in change in nasal potentials and expression of leukocyte sodium transport protein messenger RNA. LIMITATIONS The study involved a small sample of adults with a history of HAPE. CONCLUSIONS Both dexamethasone and tadalafil decrease systolic pulmonary artery pressure and may reduce the incidence of HAPE in adults with a history of HAPE. Dexamethasone prophylaxis may also reduce the incidence of AMS in these adults. ClinicalTrials.gov identifier: NCT00274430.

Both tadalafil and dexamethasone may reduce the incidence of high-altitude pulmonary edema: a randomized trial.

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...

Both Tadalafil and Dexamethasone May Reduce the Incidence of High-Altitude Pulmonary Edema

Peth, Simon, Christoph Karle, Christoph Dehnert, Peter Bartsch, and Heimo Mairbaurl. K+ Channel activation with minoxidil stimulates nasal-epithelial ion transport and blunts exaggerated hypoxic pulmonary hypertension. High Alt. Med. & Biol. 7:54–63, 2006.—Increased pulmonary capillary pressure and inhibition of alveolar Na+ transport putatively contribute to the formation of pulmonary edema in alveolar hypoxia such as at high altitude. Since both events might be linked to the inhibition of K+ channels, we studied whether in vivo application of minoxidil, a stimulator of ATP-gated K channels (K+ ATP channel activator) prevents both effects. In a double- blind, placebo-controlled crossover study on 17 volunteers with no known susceptibility to high altitude pulmonary edema, we tested whether a single dose of minoxidil (5 mg) prevents pulmonary hypertension and inhibition of nasal-epithelial Na+ transport in normobaric hypoxia (12% O2, 2 h). In hypoxia, arterial SO2 was decreased to about 80%, and systolic ...

K+ channel activation with minoxidil stimulates nasal-epithelial ion transport and blunts exaggerated hypoxic pulmonary hypertension.

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Both tadalafil and dexamethasone may reduce the incidence of high-altitude pulmonary edema: a randomized trial.

Both Tadalafil and Dexamethasone May Reduce the Incidence of High-Altitude Pulmonary Edema

K+ channel activation with minoxidil stimulates nasal-epithelial ion transport and blunts exaggerated hypoxic pulmonary hypertension.