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TABLE 22-2 Expected PaO2 in Patients Inhaling Various Concentrations of Oxygen, mmHg

The expected PAo2 when the patient is given oxygen can be estimated by multiplying the actual delivered percentage of oxygen by 6. Thus, a patient getting 60% oxygen would be expected to have a PAo2 of about 60 * 6, or 360 mmHg.

ALTITUDE The Pao2 expected when a patient is breathing room air varies with height above sea level. The greater the altitude, the lower the P o2 in the air and the greater the tendency for the patient to hyperventilate ( T.a.ble.,2.2,:3.).

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TABLE 22-3 Changes in Po2 at Various Altitudes

TABLE 22-3 Changes in Po2 at Various Altitudes

The Pao2 drops about 3 to 4 mmHg for each 1000-foot rise above sea level. Up to an altitude of approximately 10,000 ft, the Sa o2 remains about 90 percent. However, above 10,000 ft, the Sao2 progressively falls about 1 percent for each 1 mmHg drop in P o2 until at 20,000 ft altitude the Pao2 is about 35 mmHg and the Sao2 is only about 65 percent.

When a person breathes air at 30,000 ft, where the barometric pressure is about 226 mmHg, the Pa o2 is only 21 mmHg. At this height above sea level, almost three-fourths of the alveolar air is nitrogen. However, if the person breathes pure oxygen instead of air, most of the space in the alveoli formerly occupied by nitrogen becomes occupied by oxygen. Nevertheless, even if the person is breathing 100% oxygen at 30,000 ft, the Pa o2 is only 139 mmHg (Table.22-4).

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TABLE 22-4 Effects of Acute Exposure to Low Atmospheric Pressure on Alveolar Gas Concentrations and on SaO2

AGE Even in healthy individuals, pulmonary changes that cause a fall in the Pa o2 occur with advancing age. On the average, the Pao2 falls about 3 to 4 mmHg per decade after the patient reaches 20 to 30 years of age. Thus, an otherwise normal 20-year-old patient with a Pa o2 of about 90 to 100 mmHg (breathing room air at sea level) might be expected to have a Pao2 of only about 75 to 80 mmHg at 80 years of age.

Alveolar-Arterial Oxygen Differences

One method of determining the degree to which lung function is impaired is to determine the alveolar-arterial oxygen gradient [P(A - a) o2]. The Pao2 can be determined from arterial blood samples and the PAo2 and be determined from the alveolar air equation previously discussed. One can also estimate the PA o2 in patients with a normal cardiac output breathing room air by subtracting the Pa co2 from 145. This is possible because PAo2 and PAco2 add up to about 145 mmHg when a patient breathes room air at sea level. Since the PAco2 is usually the same as the Paco2, the PAo2 can be estimated from the arterial gas pressure by the following formula:

If the patient has a Paco2 of 40 mmHg,

This equation can be used to determine the P(A - a) o2. The PAo2 is estimated from the above formula, and the Pao2 is determined from arterial blood gas analysis. If the Pao2 were 90 mmHg, the P(A - a)o2 would be 15 mmHg, which is relatively normal. A P(A - a)o2 of 20 to 30 mmHg on room air usually indicates mild pulmonary dysfunction, and a P(A - a)o2 greater than 50 mmHg on room air usually indicates severe pulmonary dysfunction. The causes of an increased A-a gradient include intrapulmonary shunt (relatively less ventilation than perfusion, or a low V/Q ratio), intracardiac shunt, and diffusion abnormalities.

Oxyhemoglobin Saturation

NORMAL RELATIONSHIPS When arterial blood gas study results are obtained, clinicians are often concerned by PaO 2 levels in the 60 to 90-mmHg range. A Pao2 of 60 mmHg correlates to an Sao2 of 90%. Furthermore, if the hemoglobin level is 15.0 g/dL and the tissue removes 5.0 mL of oxygen from each 100 mL of blood, the Po2 of the venous blood falls to about 36 mmHg, which is only 4 mmHg below the normal value. Thus, the tissue P o2 often changes minimally despite a marked fall in Pao2.

On the other hand, if the Pao2 rises far above the upper limit of normal (90 to 100 mmHg), the oxygen saturation of hemoglobin cannot rise above 100%. Therefore, even if the Pao2 rose to 600 mmHg or more, the saturation of hemoglobin would increase only 1 to 2% because, at Pa o2 of 100 mmHg, the Sao2 is only 98 to 99%. This, combined with some evidence (predominantly in animals) that an Fi o2 greater than 50 can be associated with pulmonary toxicity, should guide the clinician to supply only the amount of oxygen required to produce a Pao2 between 70 and 100 mmHg.

Under circumstances of normal body temperature [37°C (98.6°F)] and blood pH 7.40, certain standard relationships exist between the oxyhemoglobin saturation and the plasma Po2 (Taible.ii22..-.5). Thus, the relationship between Sao2 and plasma Po2 is almost linear when the Sao2 is 60 to 90%. However, as the Sao2 rises above 90%, the Po2 begins to rise much faster than the saturation. A simplification to remember for clinical practice is that a Pa o2 of 30, 40, 50, and 60 correspond approximately to an Sao2 of 60, 70, 80, and 90 percent, respectively.

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