Assessment and Treatment of Hypoxemia and Shunting

Hypoxemia…

…cardiac output, oxygen consumption, hemoglobin content, alveolar ventilation or lung disease can each change, sometimes simultaneously and in opposite directions, so as to complexly alter the PaO₂.

Peter D. Wagner ²⁴³

OVERVIEW

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.

ASSESSMENT OF HYPOXEMIA

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.

Box 9-1 Mechanisms of Hypoxemia

EFFECTS OF CARDIAC OUTPUT ON PaO₂

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 PaO_2. 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).

Figure 9-2 Arterial blood is a mixture of oxygenated and shunted blood.

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., PO₂, 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 (PO₂ equilibrates with the PAO₂). In contrast, less than 5% of the arterial mixture is comprised of PO₂ 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., PO₂). Actually, the oxygen content of mixed venous blood (CO₂) more accurately reflects the amount of oxygen present in this blood and, therefore, how much it affects the arterial PO₂. Nevertheless, PO₂ 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 PO₂ 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 PO₂. Thus, when cardiac output falls, shunted blood entering the arterial circulation will have a lower PO₂ 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.

Figure 9-3 Effects of decreased cardiac output on PaO₂ in humans with normal physiologic shunting.

Increased Shunting with Normal Cardiac Output

In the individual with an abnormally high pulmonary shunt, the PO₂ of the shunted blood has a more substantial impact on PaO₂as shown in Figure 9-4. The low PaO₂ that accompanies increased physiologic shunting is a result of the large percentage of venous blood entering the arterial circulation. Note that, in this case, the cardiac output and PO₂ are still normal. Increased shunting is the most common mechanism responsible for the development of hypoxemia.

Figure 9-4 Effect of substantial physiologic shunting on PaO₂.

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 PO₂ from 40 to 30 mm Hg with a constant 30% shunt decreases PaO₂ from 55 mm Hg to approximately 45 mm Hg.²⁴⁴

Figure 9-5 Effects of decreased cardiac output on PaO₂ in the patient with increased physiologic shunting.

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 PO₂, 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.

Figure 9-6 Effects of increased cardiac output on PaO₂ in the patient with increased physiologic shunting.

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 PO₂

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.

On Call Case 9-1 ABGs and Critical Thinking

You are the only person available to care for this patient. You must assess the patient/situation and act accordingly.

Shortly before 11:00 am, acute chest pain, shortness of breath, frequent arrhythmias, and hypotension develop in a 52-year-old woman with severe pneumonia. Interpret the blood gases and patient condition at 11:00 am.

ARTERIAL BLOOD GASES 10:00 am

SaO₂	93%
pH	7.37
PaCO₂	37 mm Hg
PaO₂	72 mm Hg
[HCO₃]	25 mEq/L
FIO₂	0.50

ARTERIAL BLOOD GASES 11:00 am

SaO₂	84%
pH	7.28
PaCO₂	29 mm Hg
PaO₂	49 mm Hg
[HCO₃]	13 mEq/L
FIO₂	0.50

ASSESSMENT

Abnormalities: List abnormal data and other noteworthy information. Classify ABG.

Explanation: List possible diseases, pathology, or other situations that may have led to this patient’s condition.

Evaluation: Suggest additional data that would be useful in helping understand the situation or in making a diagnosis.

INTERVENTION

Importance: Prioritize concern(s) of treatment in order of urgency and/or seriousness as you see the overall situation.

ASSESSMENT OF PHYSIOLOGIC SHUNTING

Introduction

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.

Box 9-2 Indices to Evaluate the Physiologic Shunt

1. Classic shunt calculation

2. Modified shunt equations

3. P(A−a)O₂

4. PaO₂/PAO₂

5. PaO₂/FIO₂

Indices of Physiologic Shunting

Classic Shunt Equation

The classic shunt equation for calculation of physiologic shunting (sp/T) was described in Chapter 6 (Equation 6-3). It is noteworthy that the classic shunt equation corrects for any nonpulmonary (e.g., PO₂) 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.