Error message

Deprecated function: The each() function is deprecated. This message will be suppressed on further calls in book_prev() (line 775 of /home/pathwa23/public_html/modules/book/book.module).

High Altitude

  • At altitudes above 18,000ft the total air pressure declines to about half that observed at sea level. While the fractional percentage of oxygen in the atmosphere is roughly the same (i.e. 21%) at high altitudes, the two-fold reduction in total air pressure yields a two-fold reduction in the gas partial pressure of atmospheric oxygen. Consequently, while the partial pressure of inspired oxygen at sea level is typically 150 mm Hg, the inspired oxygen tension at high altitudes is roughly half, that is, about 70 mm Hg. As described below, this reduction in inspired oxygen tension results in a significant decrease in the partial pressure of arterial oxygen to the point of being classified as hypoxemia. After discussing the pathogenesis of reduced arterial oxygen tensions, we discuss how hypoxemia due to high altitudes can be distinguished from other causes of hypoxemia, and then discuss the consequences of chronic habitation at high elevations.
  • The pathogenesis of hypoxemia due to habitation at high altitudes is relatively simple. As discussed in alveolar oxygen, the partial pressure of alveolar oxygen is heavily dependent on the partial pressure of oxygen in the inspired air. Because the inspired oxygen tension (PIO2) is low at high elevations, this provides a much lower starting point for the possible partial pressure of alveolar oxygen. Put another way, the maximum possible alveolar oxygen tension would be that of inspired air; thus, when the partial pressure of inspired air is 70 mm Hg, no physiological mechanism can yield an alveolar oxygen tension above 70 mm Hg. Because the alveolar oxygen tension determines the arterial partial pressure of oxygen, an individual residing at high altitudes will inevitably display arterial oxygen tensions below 70 mm Hg which is already considered below the normal threshold.
  • Overview
    • In reality, diagnosis of hypoxemia due to habitation at high elevation should be obvious given the social history of the patient; however, for the sake of completeness we will discuss how hypoxemia due to high elevations affect a patient's A-a Gradient and how arterial oxygen responds to oxygen therapy.
  • A-a Gradient
    • As described in oxygen pulmonary gas exchange, lower alveolar partial pressures of oxygen will reduce the oxygen diffusion gradient between the alveolar space and the blood in the pulmonary capillaries. This will result in a slowing in the rate of oxygen diffusion from the alveolar space to the pulmonary capillaries; however, in the absence of other overt pathology, the partial pressures of oxygen in these two compartments should equalize by the end of the pulmonary capillaries. Consequently, in a healthy individual at high elevations, the A-a Gradient will be normal.
  • Response to Oxygen Therapy
    • Because the source of hypoxemia at high altitudes is a reduced partial pressure of inspired oxygen, increasing this partial pressure through oxygen therapy should obviously correct the hypoxemia
  • Overview
    • As discussed below, the body responds in a number of ways to chronic habitation at high altitudes. In general, these responses attempt to increase the levels of alveolar oxygen, increase the oxygen carrying capacity of the blood, and increase the unloading of oxygen in the peripheral tissues. However, in some cases the body's attempt to maintain sufficient arterial oxygen levels can lead to derangement of other physiological variables as discussed below.
  • Hyperventilation
    • As detailed in the sections of control of respiration, reductions in arterial oxygen tension are immediately sensed by the peripheral chemoreceptors which then stimulate the brainstem respiratory centers to increase respiratory drive. The response coordinated by the brainstem is one of hyperventilation which in turn increases the alveolar ventilation rate and thus boosts as much as possible the levels of alveolar oxygen. While alveolar oxygen levels are enhanced by this hyperventilatory response, the significant increases in alveolar ventilation results in the body eliminating carbon dioxide far above normal rates. This yields reductions in the alveolar carbon dioxide partial pressure, and thus hypocapnia and consequent respiratory alkalosis.
  • Changes to Oxygen Transport
    • Long-term hypoxemia results in the accumulation of 2,3-Diphosphoglycerate which shifts right-ward the Oxygen-Hemoglobin Dissociation curve discussed in oxygen transport. This shift reduces the affinity of hemoglobin for oxygen and thus facilitates unloading of oxygen in the peripheral tissues.
  • Changes to Oxygen Content
    • In addition, long-term hypoxemia results in an increase in renal production of erythropoietin which enhances erythropoiesis. Enhanced production of erythrocytes ultimately yields a physiological polycythemia that increases the concentration of hemoglobin within the blood and thus boosts the total amount of oxygen per milliliter that the blood can transport.
  • Global Pulmonary Vasoconstriction
    • As discussed in pulmonary blood flow regulation, pulmonary arterioles undergo vasoconstriction in response to low alveolar oxygen tensions. It is thought that this response is designed to direct blood flow away from poorly ventilated areas. However, at high altitudes, low alveolar oxygen tensions are encountered globally within the lungs resulting in a significant increase in the pulmonary vascular resistance. Over tie, this can yield significant secondary pulmonary hypertension and thus compensatory right concentric ventricular hypertrophy.