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.