Carbon Monoxide and Oxygen Transport
Overview |
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- Hemoglobin displays an affinity for carbon monoxide several hundred times greater than it does for oxygen. Consequently, hemoglobin in blood will display equivalent saturation levels at much lower partial pressures of carbon monoxide than that of oxygen. For example, a 50% saturation of hemoglobin may be achieved at partial pressures of carbon monoxide that are several hundred times less than the partial pressures of oxygen that will yield 50% hemoglobin saturation. Thus, the presence of even very low levels of carbon monoxide can result in profound effects on blood oxygen transport. Finally, binding of carbon monoxide to hemoglobin is irreversible and thus affected hemoglobin molecules cannot be successfully recovered simply by correcting carbon monoxide exposure.
Biochemical Sequelae |
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- The presence of carbon monoxide in the blood will result in a profound decline in the capacity of blood to carry oxygen. Thus, although the partial pressure of dissolved oxygen in the blood may be normal, tissues may display severe hypoxia because much of the hemoglobin will be irreversibly bound by carbon monoxide rather than oxygen. Furthermore, because of the cooperative nature of oxygen binding by hemoglobin partial saturation of a hemoglobin molecule with carbon monoxide will increase its remaining affinity for oxygen. Consequently, the Oxygen-Hemoglobin Dissociation Curve discussed in Oxygen Transport will be shifted leftward, reflecting the increased oxygen-affinity of carbon-monoxide-exposed blood. This leftward shift results in less oxygen unloading in peripheral tissues, further exacerbating the hypoxia caused by the lowered oxygen content of carbon monoxide-exposed blood.
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