Oxygen Transport Disturbances

The oxygen-carrying capacity of hemoglobin determines how much oxygen is carried in the blood. Other environmental factors and diseases can affect oxygen carrying capacity and delivery.

Carbon dioxide levels, blood pH, and body temperature affect oxygen-carrying capacity. When carbon dioxide is in the blood, it reacts with water to form bicarbonate and hydrogen ions. As the level of carbon dioxide in the blood increases, more hydrogen is produced and the pH decreases. This increase in carbon dioxide and subsequent decrease in pH reduce the affinity of hemoglobin for oxygen. The oxygen dissociates from the hemoglobin molecule, shifting the oxygen dissociation curve. Therefore, more oxygen is needed to reach the same hemoglobin saturation level as when the pH was higher. A similar shift in the curve also results from an increase in body temperature. Increased temperature, such as from increased activity of skeletal muscle, causes the affinity of hemoglobin for oxygen to be reduced.

Diseases like sickle cell anemia and thalassemia decrease the blood’s ability to deliver oxygen to tissues and its oxygen-carrying capacity. In sickle cell anemia, the shape of the red blood cell is crescent-shaped, elongated, and stiffened, reducing its ability to deliver oxygen.

In this form, red blood cells cannot pass through the capillaries. This is painful when it occurs.  Thalassemia is a rare genetic disease. Patients with thalassemia produce a high number of red blood cells, but these cells have lower-than-normal levels of hemoglobin. Therefore, the oxygen-carrying capacity is diminished.

Hypercarbia Related to Carbon Dioxide Transport Disturbances

Hypercarbia is defined by an increase in carbon dioxide in the bloodstream. Carbon dioxide is a metabolic end-product of normal metabolism, with increased production in various clinically relevant disease processes. If a patient is unable to fully compensate due to some type of central nervous system or lung impairment, acidosis results. Though hypercarbia is common in hospital settings, mortality from progressive respiratory acidosis is high if untreated.

First, hypoventilation resulting in inadequate carbon dioxide removal from the body. Hypoventilation can be further subdivided by cause: inadequate respiratory drive from the central nervous system (CNS) depression, respiratory muscle insufficiency, or ventilation-perfusion mismatch—though these are not mutually exclusive.

Second, excess carbon dioxide (CO2) production with inadequate respiratory compensation.  CO2 is an end product of metabolism in humans. It has many biological and physiological effects, beyond just serving as the waste product of metabolism.  In critically ill patients, there can be excess production from numerous causes, including fever, metabolic acidosis, sepsis, thyroid disease, and others. Any of these can overwhelm the body’s ability to compensate. Increased CO2 production is especially dangerous in patients with underlying lung or CNS disorders.

Third, exogenous carbon dioxide exposure. CO2 is often used for insufflation for various surgical procedures. While generally well-tolerated, this can cause hypercarbia and resultant circulatory complications. Patients exposed to CO2 enriched environments, such as an enclosed space with limited circulation, are also at risk for hypercarbia.   

Fourth, chronic hypercarbia in a setting of lung disease. This is often a slow onset failure of ventilation, allowing time for renal compensation. On blood gas analysis, the pH will often be in the normal range, with elevation in CO2 above the normal range and elevated bicarbonate.