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Oxygen Transport

  • Oxygen is transported within the blood in a simple dissolved form as well as a chemically-bound form associated with hemoglobin (See: Gases in Liquids). Because hemoglobin-associated oxygen accounts for roughly 97% of the oxygen transported, the dynamic relationship between oxygen and hemoglobin is the primary determinant of oxygen transport. Oxygen transport in the body occurs in two basic steps involving the reversible loading and unloading of hemoglobin with oxygen. Hemoglobin is loaded with oxygen as it passes through the pulmonary capillaries and is then transported to the peripheral tissues where the oxygen is unloaded.
  • The primary factor determining whether oxygen is loaded or unloaded onto hemoglobin is the surrounding partial pressure of oxygen. The quantitative relationship between oxygen partial pressure and the percent of hemoglobin molecules bound to oxygen is provided by the "Oxygen-Hemoglobin Dissociation Curve" described below. Careful analysis of this dissociation curve can provide valuable insights into how oxygen transport is regulated.

Oxygen Transport in Outline
Oxygen is loaded in blood in the pulmonary capillaries where the oxygen tension is 100 mm Hg as a result of alveolar ventilation. Oxygen is unloaded from the blood in the peripheral tissues where the oxygen tension is roughly 40 mm Hg as a result of peripheral tissue oxygen consumption.

Oxygen-Hemoglobin Dissociation Curve
  • Overview
    • The Oxygen-Hemoglobin Dissociation Curve is derived from empirical studies of human blood. The curve can be generated by placing a sample of human blood in an oxygen-free environment and then slowly increasing the partial pressure of oxygen from 0 mm Hg to roughly 150 mm Hg. The percent of hemoglobin within the sample bound to oxygen can be measured using optical techniques, allowing for an assessment of the hemoglobin oxygen-saturation for every value of oxygen partial pressure. The Oxygen-Hemoglobin Dissociation Curve is obtained by plotting the hemoglobin saturation against the oxygen partial pressure.
  • Qualitative Features
    • The key feature of the dissociation curve is its non-linear, sigmoid shape. As observed, the saturation of hemoglobin changes substantially when the partial pressure of oxygen ranges between 20 - 60 mm Hg but tends to plateau at oxygen partial pressures above 80 mm Hg. Consequently, the amount of oxygen released from blood may be very different given the starting and ending partial pressures of oxygen. For example, a drop in oxygen partial pressure from 100 mm Hg to 80 mm Hg will result in little release of hemoglobin-bound oxygen; however, a drop in oxygen partial pressure from 60 mm Hg to 40 mm Hg will result in an enormous release of hemoglobin bound oxygen even though in both cases the oxygen partial pressure was reduced by 40 mm Hg. The sigmoid shape of the oxygen-hemoglobin dissociation curve is the result of hemoglobin's unique biochemistry which allows for oxygen binding in a cooperative fashion. These biochemical features of hemoglobin will be added to this text later under a Hemoglobin Biochemistry page.

Quantitative Features of the Oxygen-Hemoglobin Dissociation Curve
The Oxygen-Hemoglobin dissociation curve is derived by quantifying the saturation of hemoglobin in blood as the partial pressure of oxygen in the blood is slowly raised. As seen, the curve is not linear, reflecting the unique biochemistry of hemoglobin, to which oxygen molecules bind cooperatively.

  • Normal Oxygen Transport
    • The Oxygen-Hemoglobin Dissociation Curve allows for a quantitative appreciation of why oxygen loading and unloading occur at their respective locations. The partial pressure of oxygen is roughly 100 mm Hg within the pulmonary capillaries of a healthy lung; consequently, the hemoglobin oxygen saturation rises to nearly 97%. However, in the peripheral tissues, the partial pressure of oxygen falls to nearly 40 mm Hg due to its metabolic consumption by the body's cells; consequently, the hemoglobin oxygen saturation falls to nearly 60%, resulting in the release of nearly 40% of hemoglobin-bound oxygen.
    • In scenarios of intense exercise when cellular metabolism is greatly increased, the peripheral partial pressure of oxygen may fall to 20 mm Hg, resulting in even more significant quantities of oxygen unloading. In reality, the hemoglobin saturation falls even further in the peripheral tissues than described above due shifts in the oxygen-hemoglobin dissociation curve caused by the environment present in metabolically-active tissues. Once blood returns to the higher oxygen tension environment of the pulmonary capillaries, oxygen is reloaded onto hemoglobin for another cycle of transport.
    • It should be pointed out that the the total amount of oxygen transported depends not only on the changes in hemoglobin saturation but also on the amount of hemoglobin present in blood. If the amount of hemoglobin in the blood is low, as might occur in anemia, even normal changes in its saturation profile between pulmonary and peripheral capillaries may not provide sufficient transport of oxygen.
  • Buffering of Oxygen Transport
    • A special feature of the oxygen-hemoglobin dissociation curve is its tendency to buffer oxygen transport against significant drops in the pulmonary capillary oxygen tension. This is an important feature given that reduced pulmonary capillary oxygen tension is a common consequence of a large variety of pathologies along with breathing at High Altitude. The basis for this buffering is the flattening of the dissociation curve beyond oxygen partial pressures of 80 mm Hg.
    • Because of this plateau, there is little significant difference in hemoglobin saturation even if pulmonary capillary oxygen tension falls from its normal 100 mm Hg to 80 mm Hg. Because hemoglobin saturation remains at nearly 90% at oxygen tensions of 80 mm Hg, a large amount of oxygen will still be unloaded when arterial blood reaches the peripheral tissues. Consequently, hypoxemia is clinically defined as arterial oxygen levels below that of 80 mm Hg, the threshold at which hemoglobin saturation truly begins to decline. This same plateau also explains why delivering high oxygen tension air to a healthy individual does little to improve oxygen transport. Once again, because of the plateau in the curve, higher oxygen tensions than the normal 100 mm Hg only serve to increase the hemoglobin saturation a few percentage points above 97%.

Buffering of Hemoglobin Saturation
The sigmoid shape of the oxygen-hemoglobin saturation curve allows for a natural buffering mechanism against hypoxemia and aids in oxygen delivery to peripheral tissues. As seen, a 10 mm Hg drop in oxygen tension at the right of the curve results in a negligible change in hemoglobin saturation. Consequently, small drops in lung function do not yield major declines in tissue oxygenation. However, the same 10 mm Hg drop in oxygen tension toward the middle of the curve yields a large decline in hemoglobin oxygen saturation. This allows for a large amount of oxygen unloading when blood reaches peripheral cells.

  • Overview
    • The Oxygen-Hemoglobin Dissociation Curve can be modified by a number of environmental factors. It should be noted that these factors do not change the basic sigmoid shape of the curve but rather shift the curve to the left and right. Consequently, these factors will change the hemoglobin saturation of blood for the same partial pressure of oxygen. In general, modulation of the dissociation curve occurs in such a way that oxygen unloading by hemoglobin is enhanced in metabolically active tissues. An easy way to remember these factors and their effect on the dissociation curve is to note that metabolically-active peripheral tissues typically display higher temperatures, higher carbon dioxide tensions, and lower pH.

Modulation of the Oxygen-Hemoglobin Dissociation Curve
A variety of environmental factors can shift the Oxygen-Hemoglobin Dissociation Curve. Effects which are associated with increased peripheral tissue metabolism, such as reduced pH, increased CO2, increased temperature, shift the curve to the right, reducing hemoglobins affinity for oxygen and thus improving oxygen unloading. Chronic hypoxia increases the bloods concentration of 2,3-DPG which also shifts the curve to the right. The presence of HbF and carbon monoxide (CO) shift the curve to the left, increasing the oxygen affinity of hemoglobin.