As altitude increases, the overall atmospheric pressure decreases. Decreased pressure is the underlying source of altitude illnesses. Whether at sea level or 20,000 feet the surrounding atmosphere has the same percentage of oxygen. As pressure decreases the body has a much more difficult time passing oxygen from the lungs to the red blood cells and thus to the tissues of the body. This lower pressure means lower oxygen levels in the blood and increased carbon dioxide levels. Increased carbon dioxide levels in the blood cause a systemic vasodilatation, or expansion of blood vessels. This increased vascular size stretches the vessel walls causing leakage of the fluid portions of the blood into the interstitial spaces, which leads to cerebral edema or HACE. Unless treated, HACE will continue to progress due to the decreased atmospheric pressure of oxygen. Further ascent will hasten the progression of HACE and could possibly cause death.
While the body has an overall systemic vasodilatation, the lungs initially experience pulmonary vasoconstriction. This constricting of the vessels in the lungs causes increased workload on the right ventricle, the chamber of the heart that receives de-oxygenated blood from the right atrium and pushes it to the lungs to be re-oxygenated. As the right ventricle works harder to force blood to the lungs, its overall output is decreased thus decreasing the overall pulmonary perfusion. Decreased pulmonary perfusion causes decreased cellular respiration—the transfer of oxygen from the alveoli to the red blood cells. The body is now experiencing increased carbon dioxide levels due to the decreased oxygen levels, which now causes pulmonary vasodilatation. Just as in HACE, this expanding of the vascular structure causes leakage into interstitial space resulting in pulmonary edema or HAPE. As the edema or fluid in the lungs increases, the capability to pass oxygen to the red blood cells decreases thus creating a vicious cycle, which can quickly become fatal if left untreated.
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