Circulation, Vol 72, 957-962, Copyright © 1985 by American Heart Association
JW Fasules, JW Wiggins and RR Wolfe
Cardiac catheterization was performed on seven children after recovery from
high-altitude pulmonary edema. All were life-long residents at elevations
above 10,000 feet. Three of the seven had developed pulmonary edema without
antecedent travel to low altitude but had an upper respiratory infection.
Response of pulmonary arterial pressure to 16% inspired oxygen in all seven
was compared with that in six well children who resided at a similar
altitude and had no history of high- altitude pulmonary edema. With hypoxia
the susceptible patients had a greater mean pulmonary arterial pressure
(56.3 +/- 23.8) than the nonsusceptible children (18.8 +/- 3.9, p less than
.05). Comparison with historical hemodynamic responses in children at high
altitudes showed a similar greater mean pulmonary arterial pressure in the
susceptible children. Thus, in children from high altitudes, increased
pulmonary vasoreactivity to hypoxia may play a role in the pathogenesis of
high-altitude pulmonary edema. The development of pulmonary edema in
high-altitude residents with upper respiratory infections and no antecedent
low-altitude journey is consistent with the presence of other factors such
as inflammation, which may play a role in the pathogenesis of the edema.
The finding of right ventricular hypertrophy on an electrocardiogram in
children from high altitudes may be predictive of their susceptibility to
high-altitude pulmonary edema.
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Increased lung vasoreactivity in children from Leadville, Colorado, after recovery from high-altitude pulmonary edema
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