One might suspect, on first thought, that any respiratory condition that causes hypoxia would also cause hypercapnia. However, hypercapnia usually occurs in association with hypoxia only when the hypoxia is caused by hypoventilation or circulatory deficiency for the following reasons.
Hypoxia caused by too little O2 in the air, too little hemoglobin, or poisoning of the oxidative enzymes has to do only with the availability of O2 or use of O2 by the tissues. Therefore, it is readily understandable that hypercapnia is not a concomitant of these types of hypoxia.
In hypoxia resulting from poor diffusion through the pulmonary membrane or through the tissues, serious hypercapnia usually does not occur at the same time because CO2 diffuses 20 times as rapidly as O2. If hypercapnia does begin to occur, this immediately stimulates pulmonary ventilation, which corrects the hypercapnia but not necessarily the hypoxia.
Conversely, in hypoxia caused by hypoventilation, CO2 transfer between the alveoli and the atmosphere is affected as much as is O2 transfer. Hypercapnia then occurs along with the hypoxia. In circulatory deficiency, diminished flow of blood decreases CO2 removal from the tissues, resulting in tissue hypercapnia in addition to tissue hypoxia. However, the transport capacity of the blood for CO2 is more than three times that for O2, and thus the resulting tissue hypercapnia is much less than the tissue hypoxia.
When the alveolar PCO2 rises above about 60 to 75 mm Hg, an otherwise normal person by then is breathing about as rapidly and deeply as he or she can, and “air hunger,” also called dyspnea, becomes severe.
If the PCO2 rises to 80 to 100 mm Hg, the person becomes lethargic and sometimes even semicomatose. Anesthesia and death can result when the PCO2 rises to 120 to 150 mm Hg. At these higher levels of PCO2, the excess CO2 now begins to depress respiration rather than stimulate it, thus causing a vicious circle: (1) more CO2, (2) further decrease in respiration, (3) then more CO2, and so forth—culminating rapidly in a respiratory death.
DYSPNEA
Dyspnea means mental anguish associated with inability to ventilate enough to satisfy the demand for air. A common synonym is air hunger.
At least three factors often enter into the development of the sensation of dyspnea. They are (1) abnormality of respiratory gases in the body fluids, especially hypercapnia and, to a much less extent, hypoxia; (2) the amount of work that must be performed by the respiratory muscles to provide adequate ventilation; and (3) state of mind.
A person becomes very dyspneic, especially from excess buildup of CO2 in the body fluids. At times, however, the levels of both CO2 and O2 in the body fluids are normal, but to attain this normality of the respiratory gases, the person has to breathe forcefully. In these instances, the forceful activity of the respiratory muscles frequently gives the person a sensation of dyspnea.
Finally, the person’s respiratory functions may be normal and still dyspnea may be experienced because of an abnormal state of mind. This condition is called neurogenic dyspnea or emotional dyspnea. For instance, almost anyone momentarily thinking about the act of breathing may suddenly start taking breaths a little more deeply than ordinarily because of a feeling of mild dyspnea. This feeling is greatly enhanced in people who have a psychological fear of not being able to receive a sufficient quantity of air, such as upon entering small or crowded rooms.
