Hypoxemia results from any combination of five distinct mechanisms.

1. Hypoventilation. Hypoventilation from a variety of disorders may result in hypoxemia. Regardless of its specific etiology, hypoxemia resulting from hypoventilation without any other cause for hypoxemia is always associated with an increased P co2, and the P(A-a)o2 is normal. In the case of pure hypoventilation, the additional Co2 displaces the inhaled oxygen and lowers the amount in the alveolus. This lowered amount, however, diffuses normally and mixes normally into the arterial blood.

2. Right-to-left shunt. Right-to-left shunting occurs when blood enters the systemic arteries without traversing ventilated lung. There is always a small degree of right-to-left shunting because of the direct left ventricular return of deoxygenated blood from both the coronary veins and the bronchial arteries. Increased right-to-left shunting occurs in a variety of conditions, including pulmonary consolidation, pulmonary atelectasis, and vascular malformations. Regardless of the specific cause of the right-to-left shunt, there is always an increase in the P(A-a) o2. In addition, right-to-left shunting does not increase Pa co2. In fact, patients with a right-to-left shunt may have an abnormally low Paco2. A hallmark of significant right-to-left shunting is the failure of arterial oxygen levels to increase in response to supplemental oxygen. Although a small improvement is observed with supplemental oxygen, hypoxemia is never fully eliminated because of the continuing mixture of nonoxygenated blood into the systemic circulation.

3. Ventilation-perfusion mismatch. Ideal pulmonary gas exchange depends on a balance of ventilation and perfusion. Any abnormality resulting in a regional alteration of either ventilation or perfusion can adversely affect pulmonary gas exchange, resulting in hypoxemia. A wide variety of etiologies may result in these regional impairments, including pulmonary emboli, pneumonia, asthma, CoPD, and even extrinsic vascular compression. Regardless of its specific etiology, hypoxemia from ventilation-perfusion mismatch is associated with an increased P(A-a)O2 gradient and improves with supplemental oxygen.

4. Diffusion impairment. Pulmonary gas exchange also depends on diffusion across the alveolar-blood barrier. Any condition that influences this diffusion (e.g., adult respiratory distress syndrome, pneumonia, or pulmonary edema) may result in hypoxemia. Regardless of the specific cause of the diffusion impairment, the P(A-a)O2 is increased, and hypoxemia improves with supplemental oxygen.

5. Low inspired oxygen. Decreased ambient oxygen pressure results in hypoxemia. This is most commonly seen at high altitude or in nonobstructive asphyxia. The P(A-a)O2 is normal, and hypoxemia improves with supplemental oxygen. For example, Denver, at 5400 ft above sea level, has an atmospheric pressure of 620 mmHg and an inhaled oxygen partial pressure of only 0.21 * 620 = 130 mmHg, as opposed to 160 mmHg at sea level.

There are three distinct acute compensatory mechanisms for hypoxemia. Initially, minute ventilation increases. Next, pulmonary arterial vasoconstriction decreases perfusion to hypoxic alveoli. While vasoconstriction balances ventilation and perfusion in order to restore arterial oxygenation, it may also cause acute right heart failure and is ineffective with diffuse lung disease. Finally, sympathetic tone increases and improves oxygen delivery by increasing cardiac output, usually with an increased heart rate. Chronic compensatory mechanisms include an increased red blood cell mass and decreased tissue oxygen demands. These compensatory mechanisms appear to be activated at different levels of hypoxemia for different individuals. However, the acute compensatory mechanisms are always activated when PaO2 reaches 60 mmHg, and compensatory mechanisms fail when PaO2 falls below 20 mmHg.

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