2, 3 BPG and RBC

Adventure travel has become more prevalent, and increasing numbers of people are accessing areas at high altitude (often defined as >6,500 ft or 1,950 m) where the defining environmental feature is hypobaric hypoxia. Exposure to low oxygen tension in the atmosphere results in development of a series of important physiological responses that allow individuals to adapt to and tolerate the hypoxic conditions. In some cases, maladaptive responses predispose affected individuals to various forms of acute and chronic high-altitude illness. Acute exposure to ambient environmental altitude results in reduced driving pressure of oxygen into the alveoli, with associated hypoxia, and causes several physiologic changes that affect all individuals traveling to high-altitude regions, regardless of preexisting respiratory disease.

At altitude, low PaO2 levels trigger a hypoxic respiratory response mediated by the carotid bodies. With exertion at altitude, minute ventilation increases as tidal volume and respiratory rate increase. Production of 2,3-bisphosphoglyceric acid (2,3-BPG) by RBCs is increased and shifts the oxyhemoglobin dissociation curve toward the right to balance the initial leftward shift due to respiratory alkalosis. The initial shift of this curve to the left allows for improved alveolar oxygen uptake but also somewhat impairs oxygen delivery to the tissues; the increase in 2,3-BPG helps to balance this response (choice C is correct; choice A is incorrect).

The increase in minute ventilation results in respiratory alkalosis (choice B is incorrect). Hypoxic pulmonary vasoconstriction is another physiologic adaptation to acute hypobaric hypoxia and results in increased pulmonary vascular resistance and pulmonary artery pressures, findings that seem to play a central role in the pathophysiologic characteristics of high-altitude illness (choice D is incorrect).1

Footnotes

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