Almost any of the conditions discussed in the past few sections of this chapter can cause serious cellular hypoxia throughout the body. Sometimes O2 therapy is of great value; other times, it is of moderate value; and at still other times, it is of almost no value. Therefore, it is important to understand the different types of hypoxia, and then we can discuss the physiological principles of oxygen therapy. The following is a descriptive classification of the causes of hypoxia:
1. Inadequate oxygenation of the blood in the lungs because of extrinsic reasons
a. Deficiency of O2 in the atmosphere
b. Hypoventilation (neuromuscular disorders)
2. Pulmonary disease
a. Hypoventilation caused by increased airway resistance or decreased pulmonary compliance
b. Abnormal alveolar ventilation-perfusion ratio (including either increased physiological dead space or increased physiological shunt)
c. Diminished respiratory membrane diffusion
3. Venous-to-arterial shunts (“right-to-left” cardiac shunts)
4. Inadequate O2 transport to the tissues by the blood
a. Anemia or abnormal hemoglobin
b. General circulatory deficiency
c. Localized circulatory deficiency (peripheral, cerebral, coronary vessels)
d. Tissue edema
5. Inadequate tissue capability of using O2
a. Poisoning of cellular oxidation enzymes
b. Diminished cellular metabolic capacity for using oxygen because of toxicity, vitamin deficiency, or other factors
This classification of the types of hypoxia is mainly self-evident from the discussions earlier in the chapter. Only one type of hypoxia in the classification needs further elaboration: the hypoxia caused by inadequate capability of the body’s tissue cells to use O2.
Inadequate Tissue Capability to Use Oxygen. The classic cause of inability of the tissues to use O2 is cyanide poisoning, in which the action of the enzyme cytochrome oxidase is blocked by the cyanide to such an extent that the tissues simply cannot use O2, even when plenty is available. Also, deficiencies of some of the tissue cellular oxidative enzymes or of other elements in the tissue oxidative system can lead to this type of hypoxia. A special example occurs in the disease beriberi, in which several important steps in tissue utilization of oxygen and the formation of CO2 are compromised because of vitamin B deficiency.
Effects of Hypoxia on the Body. Hypoxia, if severe enough, can cause death of cells throughout the body, but in less severe degrees it causes principally (1) depressed mental activity, sometimes culminating in coma, and (2) reduced work capacity of the muscles.
OXYGEN THERAPY IN DIFFERENT TYPES OF HYPOXIA
O2 can be administered by (1) placing the patient’s head in a “tent” that contains air fortified with O2, (2) allowing the patient to breathe either pure O2 or high concentrations of O2 from a mask, or (3) administering O2 through an intranasal tube.
Recalling the basic physiological principles of the different types of hypoxia, one can readily decide when O2 therapy will be of value and, if so, how valuable.
In atmospheric hypoxia, O2 therapy can completely correct the depressed O2 level in the inspired gases and, therefore, provide 100 percent effective therapy.
In hypoventilation hypoxia, a person breathing 100 percent O2 can move five times as much O2 into the alveoli with each breath as when breathing normal air.
Therefore, here again O2 therapy can be extremely beneficial. (However, this O2 therapy provides no benefit for the excess blood CO2 also caused by the hypoventilation.)
In hypoxia caused by impaired alveolar membrane diffusion, essentially the same result occurs as in hypo ventilation hypoxia because O2 therapy can increase the PO2 in the lung alveoli from the normal value of about 100 mm Hg to as high as 600 mm Hg. This action raises the O2 pressure gradient for diffusion of oxygen from the alveoli to the blood from the normal value of 60 mm Hg to as high as 560 mm Hg, an increase of more than 800 percent. This highly beneficial effect of O2 therapy in diffusion hypoxia is demonstrated in Figure1, which shows that the pulmonary blood in this patient with pulmonary edema picks up O2 three to four times as rapidly as would occur with no therapy.
Fig1. Absorption of oxygen into the pulmonary capillary blood in pulmonary edema with and without oxygen tent therapy.
In hypoxia caused by anemia, abnormal hemoglobin transport of O2, circulatory deficiency, or physiological shunt, O2 therapy is of much less value because normal O2 is already available in the alveoli. The problem instead is that one or more of the mechanisms for transporting oxygen from the lungs to the tissues are deficient. Even so, a small amount of extra O2, between 7 and 30 percent, can be transported in the dissolved state in the blood when alveolar O2 is increased to maximum even though the amount transported by the hemoglobin is hardly altered. This small amount of extra O2 may be the difference between life and death.
In the different types of hypoxia caused by inadequate tissue use of O2, there is abnormality neither of O2 pickup by the lungs nor of transport to the tissues. Instead, the tissue metabolic enzyme system is simply incapable of using the O2 that is delivered. Therefore, O2 therapy pro vides no measurable benefit.
CYANOSIS
The term cyanosis means blueness of the skin, and its cause is excessive amounts of deoxygenated hemoglobin in the skin blood vessels, especially in the capillaries. This deoxygenated hemoglobin has an intense dark blue purple color that is transmitted through the skin.
In general, definite cyanosis appears whenever the arterial blood contains more than 5 grams of deoxygenated hemoglobin in each 100 milliliters of blood. A person with anemia almost never becomes cyanotic because there is not enough hemoglobin for 5 grams to be deoxygenated in 100 milliliters of arterial blood. Conversely, in a person with excess red blood cells, as occurs in polycythemia vera, the great excess of available hemoglobin that can become deoxygenated leads frequently to cyanosis, even under otherwise normal conditions.
