Assessment and Treatment of Hypoxemia and Shunting

Assessment and Treatment of Hypoxemia and Shunting


The ability of the lungs to transfer oxygen from the atmosphere to the pulmonary capillary blood (i.e., external respiration) is the first critical step in the overall process of oxygenation. The clinical assessment of oxygen transfer in the lungs is a two-part evaluation.

First, the adequacy of oxygen transfer must be evaluated. Assessment of the adequacy of oxygen transfer in the lungs is essentially hypoxemic (i.e., PaO2) evaluation. An adequate PaO2 is one that is sufficiently high so as not to suggest the likelihood of tissue hypoxia.

Second, the efficiency of oxygen transfer through the lungs should be considered. In other words, “Is the PaO2 appropriate for the given FIO2?” Thus, the second part of oxygen transfer evaluation is essentially an assessment of pulmonary shunting.

The first section of this chapter briefly describes the classification and assessment of hypoxemia. Special reference is also made to the effects of cardiac output and mixed venous blood on PaO2. The next portion of this chapter addresses the evaluation and quantification of pulmonary shunting. The various clinical indices that have been used to estimate and quantify pulmonary shunting are surveyed. The use of some of these indices in the differential diagnosis of clinical hypoxemia is also discussed.

This is followed by a description of the clinical signs and symptoms associated with hypoxemia, hypercapnia, and hyperoxemia. Finally, methods for treating hypoxemia are discussed. The value and clinical indications for oxygen therapy, body positioning, mechanical ventilation, and the use of positive end-expiratory pressure (PEEP) are explored.


Hypoxemia is defined in this text as a below- normal PaO2 in the blood. The severity of hypoxemia is an important indicator of the likelihood of hypoxia concomitant with the hypoxemia. Table 2-7 is provided in Chapter 2 for classification of the severity of hypoxemia.

Five mechanisms by which hypoxemia may occur are shown in Figure 9-1. Hypoxemia may be due to a low partial pressure of inhaled oxygen (PIO2) (which is present at high altitude), when exhaled gas is rebreathed continuously in a confined area, or when a gas with less than 21% oxygen is inspired (see Fig. 9-1,B). This mechanism, however, is rarely responsible for hypoxemia in the acute care setting.

In the hospital, there are really only four potential causes of hypoxemia (Box 9-1). These causes include hypoventilation (see Fig. 9-1,C); absolute shunting (see Fig. 9-1,D); relative shunting, commonly referred to as ventilation/perfusion mismatch (see Fig. 9-1,E); and diffusion defects (see Fig. 9-1,F). Almost all hypoxemia (excluding changes in cardiac output) in the hospital setting may be presumed to be due to one or more of these four mechanisms. The differential diagnosis of hypoxemia is discussed in a subsequent section of this chapter.


A decrease in cardiac output is not generally considered to be a primary cause of hypoxemia, and no mention of cardiac output is made in Box 9-1 regarding the causes of hypoxemia. Notwithstanding, it is not correct to presume that the cardiac output has no effect on PaO2. The relative influence of cardiac output on PaO2 in various clinical situations is explored.

Arterial Blood as a Mixture

The clinician must always keep in mind that arterial blood is a mixture of blood from two sources. Oxygenated blood is leaving functional alveolar-capillary units and entering the arteries. Also, some mixed venous blood is always entering the arterial circulation via the normal anatomic shunt (Fig. 9-2).

Note that, in a healthy individual breathing room air, the PaO2 (100 mm Hg) is slightly lower than the average partial pressure of oxygen in the average alveolus (i.e., PAO2 ≅ 105 mm Hg) and significantly higher than the mixed venous partial pressure of oxygen (i.e., PimageO2, which is approximately 40 mm Hg). Arterial PaO2 nearly approximates alveolar PAO2 because roughly 95% of arterial blood originates from normally functioning alveolar- capillary units where the blood end-capillary PO2 (PimageO2 equilibrates with the PAO2). In contrast, less than 5% of the arterial mixture is comprised of PimageO2 contributed from the shunted blood.

Throughout the discussion regarding the effects of cardiac output on PaO2, the amount of oxygen in the shunted blood is shown as a pressure measurement (e.g., PimageO2). Actually, the oxygen content of mixed venous blood (CimageO2) more accurately reflects the amount of oxygen present in this blood and, therefore, how much it affects the arterial PO2. Nevertheless, PimageO2 is used here to illustrate this concept in the most straightforward manner.

Changes in Cardiac Output or Shunting

Decreased Cardiac Output with a Normal Shunt

A decrease in PimageO2 typically accompanies a decrease in cardiac output if oxygen consumption remains constant. Because tissues are exposed to less blood, they must extract more oxygen from available blood, which results in a lower PimageO2. Thus, when cardiac output falls, shunted blood entering the arterial circulation will have a lower PimageO2 than shunted blood when cardiac output is normal (Fig. 9-3). Nevertheless, it is important to note that in otherwise normal lungs, a decrease in cardiac output lowers PaO2 only slightly because shunted blood accounts for only 5% of the total arterial blood mixture. Thus, although PaO2 decreases slightly with a decrease in cardiac output, the effect of a decreased cardiac output on PaO2 in the normal lung is minute.

Decreased Cardiac Output with an Increased Shunt

When substantial shunting is present, any change in cardiac output has a more profound effect on PaO2. This is because changes in cardiac output affect the PO2 of the shunted blood, and the larger the physiologic shunt, the greater is the percentage of shunted blood entering the arterial circulation.

Figure 9-5 shows how a decline in cardiac output affects PaO2 in the patient compromised with preexisting pathologic shunting. Note the lower PaO2 shown in Figure 9-5 compared with Figure 9-4, despite identical shunt fractions of 25%. Note also that a decrease in cardiac output has a greater impact on PaO2 in the individual with increased physiologic shunting (see Fig. 9-5), compared with the individual who has only a normal anatomic shunt (see Fig. 9-3). It has in fact been shown that a decrease in PimageO2 from 40 to 30 mm Hg with a constant 30% shunt decreases PaO2 from 55 mm Hg to approximately 45 mm Hg.244

Increased Cardiac Output with an Increased Shunt

In the presence of a large physiologic shunt and hypoxemia, cardiac output is more likely to increase rather than decrease in the individual with an intact cardiovascular system.245 The increase in cardiac output is due at least partly to stimulation of the peripheral chemoreceptors secondary to the hypoxemia. Cardiac output tends to increase quickly, due primarily to an increased heart rate, and in a dose-response fashion.245 In other words, the more severe the hypoxemia, the greater the increase in cardiac output.

Increasing cardiac output tends to enhance tissue oxygenation both by an increase in the blood reaching the tissues and, to a lesser extent, by increasing PaO2. The increase in cardiac output improves PaO2 by increasing PimageO2, which is shown in Figure 9-6. This result is the opposite effect to that shown in Figure 9-5 where cardiac output is decreased.

Clinical Implications

In clinical practice, the PaO2 is often used as a crude index of pulmonary shunting. When the fractional concentration of inspired oxygen (FIO2) is held constant, an increase in PaO2 is usually attributed to an improvement in lung function and the pulmonary shunt. Conversely, a decline in PaO2 suggests further deterioration in pulmonary gas exchange and worsening of the pulmonary shunt.

The logic of these assumptions is sound, and most often these assumptions prove to be correct. Sometimes, however—particularly in the critically ill patient with substantial pulmonary dysfunction—a change in PaO2 may be primarily due to a nonpulmonary change.246 As has been shown, cardiac output has a notable effect on PaO2 in patients with increased physiologic shunts. Furthermore, the influence of cardiac output on PaO2 is related directly to the size of the shunt.

It is wise to suspect a change in cardiac output when abrupt, unexplained hypoxemia is observed in the critically ill patient with apparently stable pulmonary status. Cardiac output can be measured directly in the patient with a pulmonary artery catheter in place. In the absence of a pulmonary catheter, the patient should be monitored for signs of low cardiac output, such as those described in Chapter 10.

Other Mechanisms of Decreased PimageO2

The clinician should understand that the preceding discussion about how cardiac output affects PaO2 is really an oversimplification. First, as stated previously, the actual PaO2 that results from the mixture of oxygenated and shunted blood depends more on the oxygen content of the two components than on their respective oxygen tensions.

Second, it should be understood that the mixed venous oxygen content or tension does not depend solely on cardiac output. Anemia, increased metabolism, and abnormal distribution of systemic perfusion are only some of the other factors that can significantly affect mixed venous oxygen levels and, consequently, the PaO2. It has been shown, however, that cardiac output is probably a primary factor in many clinical situations.



It is often useful in the clinic to quantitate the efficiency of oxygen transfer in external respiration. Analysis of oxygen-loading efficiency can aid the clinician in the differential diagnosis of lung disease and can provide valuable information about severity or progression of pulmonary disease. In addition, some indices of oxygen loading can be useful in guiding oxygen therapy and related treatment of lung disorders.

The PaO2 alone provides little information regarding the efficiency of oxygen loading into the pulmonary capillary blood. The physiologic shunt, on the other hand, is the percentage of the venous blood that remains unoxygenated after traveling from the right side of the heart to the left side of the heart. It includes blood that is absolutely shunted (i.e., anatomic shunts and true capillary shunts) and alveolar-capillary units in which perfusion exceeds ventilation (i.e., relative shunts). Thus, monitoring physiologic shunting is an excellent way to quantitate the efficiency of oxygen uptake via the lungs. The indices that can be used to measure or to estimate physiologic shunting are shown in Box 9-2.

Indices of Physiologic Shunting

Classic Shunt Equation

The classic shunt equation for calculation of physiologic shunting (imagesp/imageT) was described in Chapter 6 (Equation 6-3). It is noteworthy that the classic shunt equation corrects for any nonpulmonary (e.g., PimageO2) mediated effects on arterial oxygenation, which have been described earlier in this chapter. This is accomplished by directly measuring mixed venous oxygen content and by using this value in the denominator of the equation. In fact, the classic shunt calculation is the only index of oxygen-loading efficiency of those shown in Box 9-2 that takes into account these nonpulmonary factors.

Calculation of (imagesp/imageT) via the classic shunt equation is thus the only accurate way to measure physiologic shunting when cardiac output is unstable. Also, by using this index, the clinician can distinguish between PaO2 disturbances of pulmonary versus cardiovascular origin. The physiologic shunt as calculated via the classic shunt equation is therefore the most sophisticated and accurate measure of the efficiency of the lungs to transfer oxygen. The classic shunt equation and measurement is therefore the gold standard in the measurement of the efficiency of oxygen uptake by the lungs.

Probably the most notable deterrent to routine measurement of the physiologic shunt is the requirement for mixed venous blood samples. Mixed venous blood samples are available only when a pulmonary artery (Swan-Ganz) catheter is in place.

It should also be noted that imagesp/imageT changes somewhat depending on the FIO2 at which it is measured. The pulmonary shunt tends to decrease as FIO2 is increased from 0.21 to 0.40, remains constant from FIO2 0.40 to 0.70, then increases as FIO2 moves above 0.70.253

Nevertheless, imagesp/imageT, which is calculated through the classic shunt equation, is the measurement of choice whenever a pulmonary artery catheter is in place. Similarly, when precise monitoring of pulmonary shunting is indicated, such as in the patient with severe pulmonary shunting (e.g., PaO2 of 60 mm Hg on FIO2 of 0.60), some clinicians recommend pulmonary catheterization to facilitate accurate monitoring of the physiologic shunt.247

Estimated Shunt Equations

When mixed venous blood is unavailable, a modified version of the classic shunt equation is sometimes used to estimate physiologic shunting. Estimated shunt equations assume a given arteriovenous oxygen content difference (C[a−image]O2) in their calculations. In some versions of the equation, the difference is assumed to be the normal 5 vol%.248 249 Because it is common for critically ill patients to have a higher cardiac output or lower oxygen extraction than normal (and therefore a lower arteriovenous difference), in some versions, a difference of 3.5 vol% is deemed more accurate.250 A lower C(a−image)O2 has also been demonstrated in patients with hepatopulmonary syndrome and should be used when calculating estimated shunt in this group.282

An example of an estimated shunt equation using a C(a−image)O2 difference of 3.5 vol% is shown in Equation 9-1. Also note that the equation has been rearranged to accommodate inclusion of the arteriovenous difference.

H2O+CO2H2CO3(800)+(800)(1) Equation 9-1

imagesp/imageT = (CimageO2−CaO2)/(CimageO2−CaO2) + 3.5 Equation 9-1

When mixed venous blood gases are unavailable, the estimated shunt equation is probably the best alternative to the classic shunt formula.248 251 Notwithstanding, however, there are really no true substitutes for actually measuring mixed venous oxygen contents in critically ill patients.252

The P(A−a)O2

Normal Values

The alveolar-arterial oxygen tension gradient, or P(A−a)O2, is a well-known noninvasive bedside index that is used to quantitate the efficiency of oxygen loading. If the blood and alveolar gas were perfectly matched, the efficiency of oxygen loading would be high and little or no difference would exist between the mean alveolar PO2 and the arterial PO2. On the other hand, an increase in P(A−a)O2 suggests an increase in the physiologic shunt.

The mean normal P(A−a)O2 is approximately 10 mm Hg in adults younger than 60 years of age breathing room air.254 Individual variations, however, may be great. The upper limit of normal for adults younger than 60 years of age is approximately 20 mm Hg.254 255

Unfortunately, P(A−a)O2 increases with advancing age and may be as high as 35 mm Hg in the healthy individual older than 60 years of age.254 Furthermore, in some individuals, P(A−a)O2 may also change with body position. In individuals older than 44 years of age, P(A−a)O2 increases with the assumption of the supine position.256 257

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Jul 10, 2016 | Posted by in RESPIRATORY | Comments Off on Assessment and Treatment of Hypoxemia and Shunting
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