Partial Pressure of Oxygen
The normal range of Pao2 is 80 to 100 mm Hg in healthy young persons breathing room air at sea level. Pao2 decreases with age, altitude, and lung disease. Hypoxemia occurs when the lungs fail to adequately oxygenate arterial blood. Pao2 is a reflection of lung function and not hypoxia per se. Hypoxia can occur without hypoxemia and vice versa. Causes of hypoxemia and hypoxia are listed in Table 27-1. The best Pao2 in critically ill mechanically ventilated patients is unknown, but a target Pao2 of 55 to 80 mm Hg (at sea level) is usually acceptable. Pao2 must be balanced against the potentially toxic effects of Fio2 and alveolar distending pressure. For mechanically ventilated patients with severe lung disease, permissive hypoxemia may be a desirable alternative to applying potentially injurious ventilator setting to normalize the Pao2.
Table 27-1Clinical Causes of Hypoxemia and Hypoxia ||Download (.pdf) Table 27-1 Clinical Causes of Hypoxemia and Hypoxia
• Decreased inspired oxygen: altitude
• Shunt: atelectasis, pneumonia, pulmonary edema, ARDS
• Diffusion defect: pulmonary fibrosis, emphysema, pulmonary resection
• Hypoventilation: respiratory center depression, neuromuscular disease
• Poor distribution of ventilation: airway secretions, bronchospasm
• Hypoxemic hypoxia: a lower than normal (hypoxemia)
• Anemic hypoxia: decreased red blood cell count, carboxyhemoglobin, hemoglobinopathy
• Circulatory hypoxia: decreased cardiac output, decreased local perfusion
• Affinity hypoxia: decreased release of oxygen from hemoglobin to the tissues
• Histotoxic hypoxia: cyanide poisoning
The relationship between Pao2 and oxygen saturation of hemoglobin (Sao2) is described by the oxyhemoglobin dissociation curve (Figure 27-1). This is a sigmoid relationship, with hemoglobin having a greater affinity for oxygen at a high Po2 (eg, in the lungs, where the Po2 is high) and a lower affinity for oxygen at a lower Po2 (eg, in the tissues, where Po2 is low). The affinity of hemoglobin for oxygen is also affected by the environment of the hemoglobin molecule, which can shift the curve to the left or to the right. Shifts of the curve to the right decrease the affinity of hemoglobin for oxygen (promote oxygen unloading), and shifts of the curve to the left increase the affinity of hemoglobin for oxygen (promote oxygen binding). Because of the variable relationship between hemoglobin saturation and Po2, saturation cannot be precisely predicted from Po2, and vice versa. To accurately evaluate oxygen saturation, CO-oximetry should be performed. CO-oximetry also allows measurement of total hemoglobin concentration, oxygen saturation, methemoglobin level, and carboxyhemoglobin level.
Oxyhemoglobin dissociation curve and factors that shift the curve.
Oxygen content (Co2) is a combination of dissolved oxygen and that combined with hemoglobin (Hb).
The amount of oxygen dissolved in plasma is small and related to the Po2. The importance of Pao2 is that it determines the Sao2 and thus the amount of oxygen bound to hemoglobin. Note that a decrease in Pao2 and Sao2 may not result in a decrease in Co2 if there is a concomitant increase in [Hb] (polycythemia).
Oxygen delivery is determined by cardiac output and oxygen content:
Note that oxygen delivery to tissues is determined by both Q̇c and Co2. Thus, hypoxia can result from either a decrease in Q̇c or Co2. Moreover, a decrease in oxygen delivery may not occur with a decrease in Co2 if there is a concomitant increase in Q̇c.
Alveolar Po2 (Pao2) is a mathematically derived value using the alveolar gas equation:
where Fio2 is the inspired O2 fraction, Pb is barometric pressure, Ph2o is water vapor pressure (47 mm Hg at 37°C), and R is the respiratory quotient (V̇co2/V̇o2). For calculation of Pao2, R = 0.8 is commonly used. Note that the effect of R on Pao2 depends on the Fio2. For Fio2 0.60 or greater, the effect of R on Pao2 becomes negligible. For a high Fio2 0.60 or greater, the alveolar gas equation thus becomes:
For Fio2 less than 0.60, the alveolar Po2 is estimated by:
There are several oxygen-pressure-based indices. Each of these relates Pao2 to either Pao2 or the Fio2. P(a–a)o2 is calculated by subtracting the Pao2 from the Pao2. An increase in P(a–a)o2 can result from V̇/Q̇ disturbances, shunt, or diffusion limitation. Changes in Paco2 will not affect the P(a–a)o2 because Paco2 is included in the calculation of Pao2. A problem with the use of the P(a–a)o2 is that it changes as Fio2 changes. The normal P(a–a)o2 is 5 to 10 mm Hg breathing room air, but 30 to 60 mm Hg when breathing 100% O2. This variability, when the Fio2 is changed, limits its usefulness as an indicator of pulmonary function with Fio2 changes and invalidates it as a predictor of the change in Pao2 if the Fio2 is changed. The P(a–a)o2 is affected not only by the Fio2 but also by the degree of intrapulmonary shunt and V̇/Q̇ mismatch. In critically ill patients, the P(a–a)o2 does not correlate well with the degree of pulmonary shunt. The P(a–a)o2 is also affected by changes in mixed venous oxygen content.
The Pao2/Pao2 is calculated by dividing the Pao2 by Pao2. Unlike the P(a–a)o2, the Pao2/Pao2 remains relatively stable with Fio2 changes. A Pao2/Pao2 less than 0.75 indicates pulmonary dysfunction due to V̇/Q̇ abnormality, shunt, or diffusion abnormality. The Pao2/Pao2 is most stable when it is less than 0.55, when the Fio2 is greater than 0.30, and when the Pao2 is less than 100 mm Hg. The Pao2/Pao2 is more useful than the P(a–a)o2 for comparing the pulmonary function of patients on different Fio2 and for following a patient's pulmonary function as Fio2 is changed.
The Pao2/Fio2 is easier to calculate than P(a–a)o2 and Pao2/Pao2 because it does not require calculation of Pao2. The Pao2/Fio2 is used in the classification of the acute respiratory distress syndrome (ARDS). A Pao2/Fio2 of 100 mm Hg or less is consistent with severe ARDS, Pao2/Fio2 greater than 100 but less than 200 indicates moderate ARDS, and Pao2/Fio2 greater than 200 but less than or equal to 300 indicates mild ARDS, when patients are receiving 5 cm H2O or greater positive end-expiratory pressure (PEEP).
The oxygenation index (OI) relates Pao2, Fio2, and mean airway pressure (P̄aw):
Although not commonly used in adults, this index is used to classify respiratory failure in infants and children.
Shunting is the portion of the cardiac output that moves from the right side of the heart to the left side of the heart without participating in gas exchange. Shunt is calculated from the oxygen content of pulmonary end-capillary (Cc′o2), arterial (Cao2) and mixed venous (Cv̄o2) blood:
where Q̇S is shunted cardiac output, Q̇T is total cardiac output, Cc′o2 is pulmonary end-capillary oxygen content, Cao2 is arterial oxygen content, and Cv̄o2 is mixed venous oxygen content.
The arterial oxygen content (Cao2) is calculated from arterial blood gas values, and mixed venous oxygen content (Cv̄o2) is calculated from pulmonary artery blood gas values. Cc′o2 is calculated based on the assumption that pulmonary end-capillary Po2 is equal to the alveolar Po2. When Pao2 is greater than 150 mm Hg, it is assumed that the end-capillary blood is 100% saturated with oxygen. When a pulmonary artery catheter is not in place to sample mixed venous blood, shunt can be estimated from the equation:
The 3.5 vol% can replace Cao2 – Cv̄o2 if there is cardiovascular stability and body temperature is normal. The Cc′o2 – Cao2 can be replaced by (Pao2 – Pao2) × 0.003 in settings where it can be assumed that the Sao2 is 100%. When the patient has a high Pao2 (>150 mm Hg), the modified shunt equation can be used:
Oxygen Delivery and Oxygen Consumption
Oxygen delivery (Do2) is the volume of oxygen delivered to the tissues each minute and is calculated as:
Normal Do2 is 1000 mL/min. Of this, the tissues normally extract 250 mL/min (V̇o2), and 750 mL is returned to the lungs. V̇o2 can be calculated using the Fick equation:
Oxygen extraction is the oxygen consumption divided by the oxygen delivery.