FIGURE 20.1 Ventilation–perfusion (V/Q) relationships and associated blood gas abnormalities.

Pathophysiology

Dead space ventilation increases in the following situations:

1. When the alveolar–capillary interface is destroyed; e.g., emphysema

2. When blood flow is reduced; i.e., low cardiac output

3. When alveoli are overdistended; e.g., during positive-pressure ventilation

ARTERIAL BLOOD GASES: An increase in V_D/V_T above 0.3 results in both hypoxemia (decreased arterial PO₂) and hypercapnia (increased arterial PCO₂), which is analogous to what would happen if you held your breath. The hypercapnia usually appears when the V_D/V_T is above 0.5 (5).

Intrapulmonary Shunt

A V/Q ratio below 1.0 (Fig. 20.1, lower panel) occurs when pulmonary capillary blood flow is excessive relative to ventilation. The excess blood flow, known as intrapulmonary shunt, does not participate in pulmonary gas exchange. There are two types of intrapulmonary shunt. True shunt indicates the total absence of gas exchange between capillary blood and alveolar gas (V/Q = 0), and is equivalent to an anatomic shunt between the right and left sides of the heart. Venous admixture represents the capillary flow that does not equilibrate completely with alveolar gas (0<V/Q <1). As the venous admixture increases, the V/Q ratio decreases until it becomes a true shunt (V/Q = 0).

The fraction of the cardiac output that represents intrapulmonary shunt is known as the shunt fraction. In normal subjects, intrapulmonary shunt flow (Qs) represents less than 10% of the total cardiac output (Qt), so the shunt fraction (Qs/Qt) is less than 10% (1,2,4).

Pathophysiology

Intrapulmonary shunt fraction is increased in the following situations:

1. When the small airways are occluded; e.g., asthma

2. When the alveoli are filled with fluid; e.g., pulmonary edema, pneumonia

3. When the alveoli collapse; e.g., atelectasis

4. When capillary flow is excessive; e.g., in nonembolized regions of the lung in pulmonary embolism

ARTERIAL BLOOD GASES: The influence of shunt fraction on arterial O₂ and CO₂ tensions (PaO₂, PaCO₂, respectively) is shown in Figure 20.2. The PaO₂ falls progressively as shunt fraction increases, but the PaCO₂ remains constant until the shunt fraction exceeds 50% (4). The PaCO₂ is often below normal in patients with increased intrapulmonary shunt as a result of hyperventilation triggered by the disease process or by the accompanying hypoxemia.

Inhaled Oxygen

The shunt fraction also determines the influence of inhaled oxygen on the arterial PO₂. This is shown in Figure 20.3 (4). As intrapulmonary shunt increases from 10 to 50%, an increase in fractional concentration of inspired oxygen (FIO₂) produces less of an increment in the arterial PO₂. When the shunt fraction exceeds 50%, the arterial PO₂ is independent of changes in FIO₂, and the condition behaves like a true (anatomic) shunt. This means that, in conditions associated with a high shunt fraction (e.g., acute respiratory distress syndrome), the FIO₂ can often be lowered to non-toxic levels (FIO₂ below 60%) without further compromising arterial oxygenation. This can be a valuable maneuver for preventing pulmonary oxygen toxicity.

FIGURE 20.2 The influence of shunt fraction on arterial PO₂ (PaO₂) and arterial PCO₂ (PaCO₂). From Reference 4.

FIGURE 20.3 The influence of shunt fraction on the relationship between the inspired oxygen (FIO₂) and the arterial PO₂ (PaO₂). From Reference 4.

MEASURES OF GAS EXCHANGE

The calculation of dead space ventilation (V_D/V_T) is based on the difference between the PCO₂ in exhaled gas and end-capillary (arterial) blood. In the normal lung, the capillary blood equilibrates fully with alveolar gas, and the exhaled PCO₂ (PECO₂) is equivalent to the arterial PCO₂ (PaCO₂). As dead space ventilation (V_D/V_T) increases, the PECO₂ de-creases relative to the PaCO₂. The Bohr equation shown below (derived by Christian Bohr, father of Neils Bohr, one of the founders of quantum mechanics) is based on this principle.

(20.1)

Thus, when the PECO₂ decreases relative to the PaCO₂, the calculated V_D/V_T rises. The PECO₂ is measured in a random sample of expired gas (mean ex-haled PCO₂), and is not measured at the end of expiration (end-tidal PCO₂).

Intrapulmonary Shunt Fraction

The intrapulmonary shunt fraction (Qs/Qt) is derived by the relationship between the O₂ content in arterial blood (CaO₂), mixed venous blood (CvO₂), and pulmonary capillary blood (CcO₂).

(20.2)

The problem with this formula is the inability to measure the pulmonary capillary O₂ content (CcO₂) directly. As a result, pure oxygen breathing (to produce 100% oxyhemoglobin saturation in pulmonary capillary blood) is recommended for the shunt calculation. However in this situation, Qs/Qt measures only true shunt.

The A-a PO₂ Gradient

The PO₂ difference between alveolar gas and arterial blood (PAO₂–PaO₂) is an indirect measure of ventilation–perfusion abnormalities (5–7). The PAO₂–PaO₂ (A-a PO₂) gradient is determined with the alveolar gas equation shown below.

(20.3)

This equation defines the relationship between the PO₂ in alveolar gas (PAO₂), the PO₂ in inhaled gas (PIO₂), the PCO₂ in arterial blood (PaCO2), and the respiratory quotient (RQ). The RQ defines the relative rates of exchange of O₂ and CO₂ across the alveolar–capillary interface: i.e., RQ = VCO₂/VO₂. The PIO₂ is determined using the fractional concentration of inspired oxygen (FIO₂), the barometric pressure (P_B), and the partial pressure of water vapor (P_H2O) in humidified gas:

(20.4)

If equations 20.3 and 20.4 are combined (for the alveolar PO₂), the A–a PO₂ gradient can be calculated as follows:

(20.5)

In a healthy subject breathing room air at sea level, FIO₂=0.21, P_B=760 mm Hg, P_H2O=47 mm Hg, PaO₂=90 mm Hg, PaCO₂=40 mm Hg, and RQ=0.8:

(20.6)

This represents an idealized rather than normal A-a PO₂ gradient, because the A-a PO₂ gradient varies with age and with the concentration of inspired oxygen.

Influence of Age

As shown in Table 20.1, the normal A-a PO₂ gradient rises steadily with advancing age (6). Assuming that most adult patients in an ICU are 40 years of age or older, the normal A-a PO₂ gradient in an adult ICU patient can be as high as 25 mm Hg when the patient is breathing room air. However, few ICU patients breathe room air, and the A-a PO₂ gradient is increased further when oxygen is added to inhaled gas (see next).

Table 20.1 Normal Arterial Blood Gases

Influence of Inspired Oxygen

The influence of inspired oxygen on the A-a PO₂ gradient is shown in Figure 20.4 (7). The A-a PO₂ gradient increases from 15 to 60 mm Hg as the FIO₂ increases from 21% (room air) to 100%. According to this relationship, the normal A-a PO₂ gradient increases 5 to 7 mm Hg for every 10% increase in FIO₂. This effect is presumably caused by the loss of regional hypoxic vasoconstriction in the lungs. Hypoxic vasoconstriction in poorly ventilated lung regions diverts blood to more adequately ventilated regions, and this helps to preserve the normal V/Q balance. Loss of regional hypoxic vasoconstriction during supplemental O₂ breathing maintains blood flow in poorly ventilated lung regions, and this increases intrapulmonary shunt fraction and increases the A-a PO₂ gradient.

The FIO₂ is difficult to estimate accurately when supplemental O₂ is delivered via nasal prongs or “open” face masks (see Chapter 22), and this limits the accuracy of the A-a PO₂ gradient in these situations.

Positive-Pressure Ventilation

Positive-pressure mechanical ventilation elevates the pressure in the airways above the ambient barometric pressure. Therefore, when determining the A-a PO₂ gradient in a ventilator-dependent patient, the mean airway pressure should be added to the barometric pressure (8). In the example presented in equation 20.6, a mean airway pressure of 30 cm H₂O would increase the A-a PO₂ gradient from 10 to 16 mm Hg (a 60% increase). Thus, neglecting the contribution of positive airway pressure during mechanical ventilation will underestimate the degree of abnormal gas exchange.

The a/A PO₂ Ratio

Unlike the A-a PO₂ gradient, the a/A PO₂ ratio is relatively unaffected by the FIO₂. This is demonstrated in Figure 20.4. The independence of the a/A PO₂ ratio in relation to the FIO₂ is explained by the equation below.

(20.7)

FIGURE 20.4 The influence of FIO₂ on the alveolar-arterial PO₂ gradient (A-a PO₂) and the arterial-alveolar PO₂ ratio (a/A PO₂) in normal subjects. From Reference 7.

Because the alveolar PO₂ is in both the numerator and denominator of the equation, the influence of FIO₂ on the PAO₂ is eliminated. Thus, the a/A PO₂ ratio is a mathematical manipulation that eliminates the influence of FIO₂ on the A-a PO₂ gradient. The normal a/A PO₂ ratio is 0.74 to 0.77 when breathing room air, and 0.80 to 0.82 when breathing 100% oxygen (7).

The PaO₂/FIO₂ Ratio

The PaO₂/FIO₂ ratio is used as an indirect estimate of shunt fraction. The following correlations have been reported (9).

The major limitation of the PaO₂/FIO₂ ratio is the inability to estimate the FIO₂ accurately when supplemental O₂ is delivered through nasal prongs or “open” face masks (see Chapter 22). (This limitation has also been described for the A-a PO₂ gradient.)

Blood Gas Variability

The arterial PO₂ and PCO₂ can vary spontaneously without a change in the clinical condition of the patient. This is demonstrated in Table 20.2, which shows the spontaneous variation in arterial PO₂ and PCO₂ over a one-hour period in a group of clinically stable trauma victims (10). Note that the arterial PO₂ varied by as much as 36 mm Hg, while the arterial PCO₂ varied by as much as 12 mm Hg. This variability has also been observed in patients in a medical ICU (11). Because of this degree of spontaneous variation, routine monitoring of arterial blood gases can be misleading.

Table 20.2 Spontaneous Blood-Gas Variability

HYPOXEMIA

Hypoxemia can be defined as an arterial PO₂ below what is expected for a patient’s age, as defined in Table 20.1. However, hypoxemia usually doesn’t raise red flags until the arterial PO₂ falls below 60 mm Hg (or the arterial O₂ saturation falls below 90%). The causes of hypoxemia can be separated into 3 categories based on the physiological process involved (12,13). Each group of disorders can be distinguished by the A-a PO₂ gradient and/or the mixed venous PO₂, as shown in Table 20.3.

Table 20.3 Sources of Hypoxemia

Hypoventilation

Alveolar hypoventilation causes both hypoxemia and hypercapnia, similar to breath-holding. There is no V/Q imbalance in the lungs, so the A-a PO₂ gradient is not elevated. The common causes of alveolar hypoventilation are listed in Table 20.4. Most cases of hypoventilation in the ICU are the result of drug-induced respiratory depression or neuromuscular weakness. Obesity-related hypoventilation (Pickwickian syndrome) is also a consideration, as this condition is present in up to one-third of morbidly obese patients (body mass index >35 kg/m²) (14).

Table 20.4 Alveolar Hypoventilation in the ICU

Respiratory Muscle Weakness

Most cases of respiratory muscle weakness in the ICU are the result of an idiopathic polyneuropathy and myopathy that is specific to ICU patients, particularly those with sepsis, prolonged mechanical ventilation, and prolonged neuromuscular paralysis (15). The standard method of evaluating respiratory muscle strength is to measure the maximum inspiratory pressure (PI_max), which is the maximum pressure recorded during a maximum inspiratory effort against a closed valve. The normal PI_max varies with age and gender, but most healthy adults can generate a negative PI_max of at least 80 cm H₂O (16). A PI_max that does not exceed -25 cm H₂O is considered evidence of respiratory muscle failure (17). (See Chapter 45 for more information on neuromuscular weakness syndromes in the ICU.)

V/Q Mismatch

Most cases of hypoxemia are the result of a V/Q mismatch in the lungs. Virtually any lung disease can be included in this category, but the common ones encountered in the ICU are pneumonia, inflammatory lung injury (acute respiratory distress syndrome), obstructive lung disease, hydrostatic pulmonary edema, and pulmonary embolism. The A-a PO₂ gradient is almost always elevated in these conditions, but the elevation can be minimal in patients with severe airways obstruction (which behaves like hypoventilation).

DO₂/VO₂ Imbalance

As explained in Chapter 10, a decrease in systemic O₂ delivery (DO₂) is usually accompanied by an increase in O₂ extraction from capillary blood, and this serves to maintain a constant rate of O₂ uptake (VO₂) into the tissues. The increased O₂ extraction from capillary blood results in a decrease in the PO₂ of venous blood, and this can have an deleterious effect on arterial oxygenation, as explained below.

Mixed Venous PO₂

The O₂ in arterial blood represents the sum of the O₂ in mixed venous (pulmonary artery) blood and the O₂ added from alveolar gas. When gas exchange is normal, the PO₂ in alveolar gas is the major determinant of the arterial PO₂. However, when gas exchange is impaired, the contribution of the alveolar PO₂ declines and the contribution of the mixed venous PO₂ rises (18). The greater the impairment in gas exchange, the greater the contribution of the mixed venous PO₂ to the arterial PO₂. (If there is no gas exchange in the lungs, the mixed venous PO₂ would be the sole determinant of the arterial PO₂.)

The diagram in Figure 20.5 demonstrates the influence of mixed venous PO₂ on the arterial PO₂ when gas exchange is impaired. The curves in the graph represent the transition from mixed venous PO₂ to arterial PO₂ as blood flows through the lungs. The slope of each curve reflects the efficiency of gas exchange in the lungs. Note that the curve representing the V/Q abnormality results in a lower arterial PO₂ because the slope is decreased (indicating impaired oxygen exchange in the lungs). If this curve begins at a lower mixed venous PO₂, as indicated, the curve shifts downward, resulting in a further decrease in arterial PO₂. This illustrates how a decrease in mixed venous PO₂ can aggravate the hypoxemia caused by a V/Q abnormality. It also indicates that, in the presence of a V/Q abnormality, the mixed venous PO₂ is an important consideration in the evaluation of hypoxemia.

The relationship between O₂ delivery (DO₂), O₂ uptake (VO₂), and the mixed venous PO₂ (PvO₂) can be stated as follows:

(20.8)

(k is a proportionality constant.) Thus, any condition that reduces DO₂ (e.g., low cardiac output, anemia) or increases VO₂ (e.g., hypermetabolism) can decrease the PvO₂ and aggravate the hypoxemia caused by abnormal gas exchange in the lungs.

FIGURE 20.5 The influence of a V/Q abnormality on the transition from venous to arterial PO₂, and the added effect of a low mixed venous PO₂ (PvO₂).

Diagnostic Evaluation

The evaluation of hypoxemia can proceed according to the flow diagram in Figure 20.6. This approach uses three measures: A-a PO₂ gradient, mixed venous PO₂, and maximum inspiratory pressure. The PO₂ in superior vena cava blood (central venous PO₂) can be used as the mixed venous PO₂ when there is no indwelling pulmonary artery catheter.

The first step in the approach involves a determination of the A-a PO₂ gradient. After correcting for age and FIO₂, the A-a PO₂ gradient can be interpreted as follows:

1. Normal A-a PO₂ gradient indicates hypoventilation rather than a cardiopulmonary disorder. In this situation, the most likely problems are drug-induced respiratory depression and neuromuscular weakness. The latter condition can be uncovered by measuring the maximum inspiratory pressure (PI_max), which is described earlier.

2. Increased A-a PO₂ gradient indicates a V/Q abnormality (cardiopulmonary disorder) and a possible superimposed DO₂/VO₂ imbalance (e.g., a decrease in cardiac output). The mixed venous (or central venous) PO₂ will help to identify a DO₂/VO₂ imbalance.

a. If the venous PO₂ is 40 mm Hg or higher, the problem is solely a V/Q mismatch in the lungs.

b. If the venous PO₂ is below 40 mm Hg, there is a DO₂/VO₂ imbalance adding to the hypoxemia created by a V/Q mismatch in the lungs. The source of this imbalance is either a decreased DO₂ (from anemia or a low cardiac output) or an increased VO₂ (from hypermetabolism).

FIGURE 20.6 Flow diagram for the evaluation of hypoxemia.

Spurious Hypoxemia

Spurious hypoxemia is a rarely reported phenomenon that is characterized by hypoxemia in an arterial blood sample without corresponding hypoxemia in circulating blood (as measured by pulse oximetry) (19). This phenomenon seems to occur only in patients with hematologic malignancies who have marked leukocytosis (WBC >100,000) or thrombocytosis (platelet count >1,000,000). The reduced PO₂ in the blood sample has been attributed to O₂ consumption by activated leukocytes in the sample, a phenomenon that has been called leukocyte larceny (20). This does not explain why marked thrombocytosis can also produce spurious hypoxemia because platelets are not oxygen-guzzlers like activated leukocytes. Regardless of the mechanism, there is no accepted method of preventing spurious hypoxemia (rapid cooling of blood samples has had inconsistent results), so you should be aware of the phenomenon and the value of pulse oximetry for validating in vitro PO₂ measurements (pulse oximetry is described in the next chapter).

HYPERCAPNIA

Hypercapnia is defined as an arterial PCO₂ (PaCO₂) above 46 mm Hg that does not represent compensation for a metabolic alkalosis (21). The causes of hypercapnia can be identified by considering the determinants of PaCO₂ in the following relationship, where VCO₂ is the rate of CO₂ production in the body, V_A is the rate of alveolar ventilation, and k is a proportionality constant (1).

(20.9)

Alveolar ventilation is the portion of the total ventilation (V_E) that is not dead space ventilation (V_D/V_T); that is, V_A = V_E (1 – V_D/V_T). Therefore, equation 20.9 can be restated as follows:

(20.10)

This equation identifies three major sources of hypercapnia: (a) increased CO₂ production (VCO₂), (b) hypoventilation (1/V_E), and (c) increased dead space ventilation (V_D/V_T).

Hypoventilation

Hypoventilation was discussed briefly in the last section on hypoxemia, and Table 20.4 shows the common causes of hypoventilation. Because hypoxemia is so common in ICU patients, hypercapnia may be the first sign of hypoventilation from neuromuscular weakness or drug-induced respiratory depression. This is also the case in obesity-hypoventilation syndrome, where hypercapnia while awake is often the first evidence of hypoventilation. On the other hand, hypercapnia is a relatively late sign in neuromuscular disorders, and does not appear until the maximum inspiratory pressure or PI_max (described earlier) is below 50% of normal (17).

V/Q Abnormality

As mentioned earlier, hypercapnia is not a feature of increased intrapulmonary shunt until late in the process (which is why hypercapnia is not a feature of pulmonary edema or other infiltrative lung processes until they are far advanced). Hypercapnia is more a feature of increased dead space ventilation (such as occurs in advanced emphysema, where there is destruction of the alveolar-capillary interface), and the PaCO₂ usually begins to rise when dead space ventilation accounts for more than 50% of total ventilation (V_D/V_T >0.5).

Increased CO₂ Production

An increase in CO₂ production is usually related to oxidative metabolism, but non-metabolic CO₂ production is possible when extracellular acids generate hydrogen ions that combine with bicarbonate ions and generate CO₂. Whatever the source, increased CO₂ production is normally accompanied by an increase in minute ventilation, which eliminates the excess CO₂ and maintains a constant arterial PCO₂. Therefore, excess CO₂ production does not normally cause hypercapnia. However, when CO₂ excretion is impaired, an increase in CO₂ production can lead to an increase in PaCO₂. Thus, increased CO₂ production is an important factor in promoting hypercapnia only when the ability to eliminate CO₂ is impaired.

Overfeeding

Overfeeding, or the provision of calories in excess of daily needs, is a recognized cause of hypercapnia in patients with severe lung disease and acute respiratory failure (22). Nutrition-associated hypercapnia occurs predominantly in ventilator-dependent patients, and can delay weaning from mechanical ventilation. Overfeeding with carbohydrates is particularly problematic because the oxidative metabolism of carbohydrates generates more carbon dioxide than the other nutrient substrates (lipids and proteins). This is described in more detail in Chapter 47.

Diagnostic Evaluation

The bedside evaluation of hypercapnia is shown in Figure 20.7. The evaluation of hypercapnia, like hypoxemia, begins with the A-a PO₂ gradient (23). A normal or unchanged A-a PO₂ gradient indicates that the problem is alveolar hypoventilation (the same as described for the evaluation of hypoxemia). An increased A-a PO₂ gradient indicates a V/Q abnormality (an increase in dead space ventilation) that may or may not be accompanied by an increase in CO₂ production.

Measuring CO₂ Production

The rate of CO₂ production (VCO₂) can be measured at the bedside with specialized metabolic carts that are normally used to perform nutritional assessments. These carts are equipped with infrared devices that can measure the CO₂ in expired gas (much like the end-tidal CO₂ monitors described in Chapter 21), and can determine the volume of CO₂ excreted per minute. In steady-state conditions, the rate of CO₂ excretion is equivalent to the VCO₂. The normal VCO₂ is 90 to 130 L/minute/m², which is roughly 80% of the VO₂. As mentioned earlier, an increased VCO₂ is evidence for one of the following conditions: generalized hypermetabolism, overfeeding (excess calories), or metabolic acidoses.

FIGURE 20.7 Flow diagram for the evaluation of hypercapnia.

A FINAL WORD

It is important to remember that the arterial PO₂ is not a useful measure for determining the amount of oxygen in the blood (this requires the hemoglobin concentration in blood and the percent saturation of hemoglobin with oxygen, as shown in Equation 10.6 in Chapter 10). Instead, the PaO₂ (along with the PaCO₂) is used to evaluate gas exchange in the lungs, and can be useful in identifying the source of the problem with gas exchange.

An approach to O₂ and CO₂ balance that is superior in many ways to the measurement of arterial blood gases is described in the next chapter.

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Measures of Gas Exchange

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Hypoxemia

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Hypercapnia

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