As
we ascend in altitude, the lower pressure of oxygen in the atmosphere
translates to a lower amount of oxygen being carried in our blood (called
hypoxia). Exposure to hypoxia elicits a number of respiratory, cardiovascular,
blood and kidney responses to adapt to the lower levels of oxygen in the body.
However, the higher we ascend, the more at risk we are to developing
hypoxia-induced acute mountain sickness (AMS). Symptoms can include fatigue,
nausea, vomiting, lack of appetite, headache, dizziness and difficulty
sleeping. It is difficult to predict who will be most susceptible in the
development of these symptoms and there is a lot of variability in terms of the
severity between individuals.
Dr.
Andy Lovering from the University of Oregon is leading a study that will attempt
to address the possibility of predicting the development of AMS prior to
ascent.
A
bit of background: When we are in utero,
we have a few cardiopulmonary adaptations that account for the fact that the
placenta is the gas exchange organ, rather than the lung. So, blood is shunted
away from the lungs through a hole in the atrial wall, called the foramen
ovale. This hole directs blood from the right to left heart bypassing the lungs
altogether. There are also blood vessels in the lungs that bypass the gas
exchange membranes (alveoli), called intrapulmonary shunts (IPS).
Even
in adulthood, we all have IPSs. In the case of high altitude, when most
pulmonary blood vessels constrict in response to hypoxia, these shunts become a
low resistance pathway, directing blood away from the gas exchange membranes
just like in utero. Furthermore,
about 30% of the adult population has an open (patent) foremen ovale (PFO),
which can be another source of shunting of blood away from the lungs. The
consequences of these shunts are that blood is not directed to the gas exchange
part of the lungs, potentially negatively impacting oxygenation, particularly
when exposed to hypoxic stress. To the extent to which this may lower oxygen
saturation at altitude, the presence of these shunts may serve as a predictor
for the development of AMS symptoms.
Using
a technique called “agitated saline contrast echocardiography”, subjects were
prescreened in Kelowna for both PFOs and IPSs. Basically, microbubbles in
saline were injected into subjects’ veins and cardiac ultrasound was used to
track their movement through the heart. Now that we are on the mountain, AMS
scores (a measure of symptoms) and blood oxygen saturation are being tracked as
we ascend up to the Pyramid lab and over the first few days after we arrive.
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