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ventilatory failure. Table 5.9 provides an overview summary of acute ventilatory failure superimposed on chronic ventilatory failure and acute alveolar hyperventilation superimposed on chronic ventilatory failure, in relationship to typical baseline ABG values of a patient with chronic ventilatory failure.

TABLE 5.8

Acute Ventilatory Failure Superimposed on Chronic Ventilatory Failure (Acute Hypoventilation on Compensated Respiratory Acidosis)

Arterial Blood Gas Changes

Example

pH: Decreased

7.28

PaCO2: Increased

99 mm Hg

HCO3: Increased

45 mEq/L

PaO2: Decreased

34 mm Hg

TABLE 5.9

Overview Examples of Acute Changes in Chronic Ventilatory Failure

Metabolic Acid-Base Abnormalities

Metabolic acid-base disturbances are subdivided into the following two categories: metabolic acidosis and metabolic alkalosis (see Box 5.1). An overview of the metabolic acid-base disturbances are presented in the following section.

Metabolic Alkalosis

The presence of other bases not related to either a decreased PaCO2 level or renal compensation also can be identified by using the PCO2/HCO3/pH nomogram illustrated in Fig. 5.1. The presence of metabolic alkalosis is verified when the calculated HCO3and pH readings are both higher than expected for a particular PaCO2 level in terms of the absolute PCO2/HCO3/pH relationship. For example, according to the normal blood buffer line, an HCO3reading of 35 mEq/L and a pH level of 7.54 would both be higher than expected in a patient who has a PaCO2 level of 40 mm Hg (see Fig. 5.1). This

extremely common condition is known as metabolic alkalosis. Table 5.10 provides an example of metabolic alkalosis. Box 5.4 provides common causes of metabolic alkalosis.

TABLE 5.10

Metabolic Alkalosis

Arterial Blood Gas Changes

Example

pH: Increased

7.56

PaCO2: Normal

44 mm Hg

HCO3: Increased

36 mEq/L

PaO2: Normal

94 mm Hg

Box 5.4

Common Causes of Metabolic Acid-Base Abnormalities

Metabolic Acidosis

Lactic acidosis (most common)

Ketoacidosis (most commonly associated with diabetes mellitus)

Salicylate intoxication (aspirin overdose)

Renal failure

Chronic diarrhea

Metabolic Alkalosis

Hypokalemia

Hypochloremia

Gastric suctioning

Vomiting

Excessive administration of corticosteroids

Excessive administration of sodium bicarbonate

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Diuretic therapy

Hypovolemia

Metabolic Acidosis

The presence of other acids not related to an increased PaCO2 level also can be identified by using the isobars of the PCO2/HCO3/pH nomogram shown in Fig. 5.1. The presence of other acids is verified when the calculated HCO3reading and pH level are both lower than expected for a particular PaCO2 level in terms of the absolute PCO2/HCO3/pH relationship. For example, according to the normal blood buffer line, an HCO3reading of 15 mEq/L and a pH of 7.20 would both be less than expected in the patient with a PCO2 of 40 mm Hg. This condition is referred to as metabolic acidosis. Table 5.11 provides an example of metabolic acidosis. Note that if the PaO2 is normal, which generally rules out lactic

acidosis, the precise cause of the metabolic acidosis is not readily known. Box 5.4 provides common causes of metabolic acidosis.

TABLE 5.11

Metabolic Acidosis

Arterial Blood Gas Changes

Example

pH: Decreased

7.26

PaCO2: Normal

37 mm Hg

HCO3: Decreased

16 mEq/L

PaO2: Normal (or decreased if lactic acidosis is present)

94 mm Hg (or 37 mm Hg if lactic acidosis is present)

Lactic Acidosis (Metabolic Acidosis).

Because acute tissue hypoxia and acute hypoxemia are commonly associated with any of the respiratory disorders presented in this textbook, acute metabolic acidosis, or lactic acidosis, (caused by lactic acid) often further compromises the patient's ABG status. This is because oxygenation is inadequate to meet tissue metabolism, so alternative biochemical reactions that do not use oxygen are activated. This is called anaerobic metabolism (non–oxygen-using). It is commonly seen in cardiopulmonary exercise testing (CPET) as occurring at the anaerobic threshold, where the VCO2 increases

more rapidly than normal as a function of work done (as measured in the CPET continuously by the VO2). Lactic acid is the

end-product of this process. When acidic ions move into the blood, the pH decreases. Thus whenever moderate to severe acute hypoxemia is present, the possible presence of lactic acid should be suspected. For example, when acute alveolar hyperventilation is caused by a sudden drop in PaO2, the patient's pH may be lower than expected for a particular decrease

in PaCO2 level. Table 5.12 provides an example of lactic acidosis.

TABLE 5.12

Lactic Acidosis (Metabolic Acidosis)

Arterial Blood Gas Changes

Example

pH: Decreased

7.21

PaCO2: Normal or decreased

35 mm Hg

HCO3: Decreased

14 mEq/L

PaO2: Decreased

34 mm Hg

Anion Gap.

The anion gap is used to assess if the patient's metabolic acidosis is caused by the accumulation of fixed acids (lactic acids, ketoacids, or salicylate intoxication) or an excessive loss of HCO3.

The law of electroneutrality states that the total number of plasma positively charged ions (cations) must equal the total number of plasma negatively charged ions (anions) in the body fluids. To calculate the anion gap, the most commonly measured cations are sodium (Na+) ions. The most commonly measured anions are the chloride (Cl) ions and bicarbonate (HCO3) ions. The normal plasma concentrations of these cations and anions are the following:

Na+: 140 mEq/L

Cl: 105 mEq/L

HCO3: 24 mEq/L

The anion gap is the calculated difference between the Na+ ions and the sum of the HCO3and Clions:

The normal range for the anion gap is 9 to 14 mEq/L. When the anion gap is greater than 14 mEq/L, metabolic acidosis is present—that is, an elevated anion gap caused by the accumulation of fixed acids in the blood. Fixed acids produce H+ ions that chemically react with and are buffered by the plasma HCO3. This action causes the HCO3level to fall and the anion

gap to increase.

Clinically, when the patient demonstrates both metabolic acidosis and an increased anion gap, the source of the fixed

acids must be identified for the patient to be appropriately treated. For example, metabolic acidosis caused by lactic acids requires oxygen therapy to reverse the accumulation of the lactic acids. Metabolic acidosis caused by ketone acids requires insulin therapy to help facilitate the movement of glucose into the cells and normalize metabolism.

It is interesting to note that metabolic acidosis caused by an excessive loss of HCO3(e.g., from renal disease or severe diarrhea) does not cause an increase in the anion gap. This is because as the HCO3level decreases, the Cllevel usually increases to maintain electroneutrality. In short, for every HCO3ion lost, a Clanion takes its place (i.e., the law of electroneutrality). This action maintains a normal anion gap. Metabolic acidosis caused by decreased HCO3with an

increased Clis commonly called hyperchloremic metabolic acidosis.

Thus when metabolic acidosis is accompanied by an increased anion gap, the most likely cause of the acidosis is the accumulation of fixed acids. When metabolic acidosis is seen with a normal anion gap, the most likely cause of the acidosis is an excessive loss of HCO3(e.g., caused by renal failure or severe diarrhea).

Errors Associated With Arterial Blood Gas Measurements

Because an ABG error can occur before, during, or after the analysis of the sample, the respiratory therapist must always be on alert for ABG results that do not fit the patient's current clinical condition. Accurate and efficient ABG samplings, along with the correct analysis and interpretation of ABG values, are no simple matters, as anyone who has performed these procedures can testify. Fast and precisely accurate ABG results are often life-critical!

In general, the types of ABG errors can be classified as (1) preanalytic errors, (2) analytic errors, (3) postanalytic errors, and (4) interpretation errors. Preanalytic errors include errors that occur either before or after the sample analysis—for example, improper sample or data handling. Analytic errors include errors that occur during the actual analysis of the ABG sample—for example, blood gas machine malfunctions and poor individual technique. Postanalytic errors include the recording of the ABG results after analysis—for example, incorrect patient name or FIO2 setting. Interpretation errors are

the incorrect classification of any ABG results (see Box 5.1). Table 5.13 provides an overview of common errors of ABG measurements.

TABLE 5.13

Common Errors of Arterial Blood Gas Measurements

Errors

pH

PaCO2

PaO2

Preanalytic Errors Include

 

 

 

Air in syringe or icing plastic syringes

Venous blood sample or contamination

(In fact, sometimes venous blood will pulsate; e.g., in pulmonary hypertension or CHF.)

 

 

 

Anticoagulant type or concentration

↑↓

Metabolic effects (e.g., delay in running the blood sample)

Misidentification of patient

Inappropriately transported sample

Analytic Errors Include

Poor quality assurance (QA) and quality control (QC) programs*

Malfunctioning PO2 and PCO2 electrodes

Out-of-date reagents (cleaning, rinse, and calibration solutions)

Postanalytic Errors Include

Incorrect patient name/location/demographics on report Typographic and transcription errors (e.g., 74 instead of 47 mm Hg) Incorrect FIO2 or ventilator setting on patient chart

Failure to wait at least 20 minutes after an FIO2 or ventilator setting change before sampling

Incorrect sampling time recorded

Failure to notify appropriate personnel of critical results (e.g., impending ventilatory failure and/or acute ventilatory failure)

Slow turnaround time for results to get back to the patient's bedside to be interpreted by the medical staff

Interpretation Errors Include

The incorrect interpretation of any of the acid-base disturbances discussed in this chapter (see Box 5.1) Interpretation errors can result in serious harm and/or death to the patient (e.g., failure to correctly identify

impending ventilatory failure, or acute ventilatory failure, or to identify a mixed acid-base disorders)

*NOTE: Two quick internal checks of blood gas accuracy entail (1) calculating the Henderson-Hasselbalch equation to determine if the measured arterial blood gas (ABG) values correlate and (2) calculating the alveolar-arterial oxygen gradient for the same purpose. The Henderson-Hasselbalch equation ensures that the pH, PCO2,

and HCO3determinations are at least internally consistent. The alveolar-arterial oxygen gradient ensures that the FIO2, PaO2, and PaCO2 calculations are at least

reasonable. For a complete review of these two equations, see Des Jardins, T. (2019). Cardiopulmonary anatomy and physiology: essentials of respiratory care (7th ed.). Clifton Park, NY: Delmar/Cengage Learning.

The “take home message” from this brief section is to be aware of the common sources of ABG errors and be ready to repeat the test if the ABG data do not correlate with the clinical situation. Unexpected or questionable ABG results should always be thoroughly investigated. Failure to do so is unacceptable! Noninvasive “reality checks” on ABG results include observation of the patient's sensorium and vital signs, presence or absence of cyanosis, and the timely readings from pulse oximeters and transcutaneous PO2 and PCO2 electrodes.

Self-Assessment Questions

1.During acute alveolar hyperventilation, which of the following occurs?

1.HCO3decreases.

2.PaCO2 increases.

3.HCO3increases.

4.PaCO2 decreases.

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a.2 only

b.3 only

c.1 and 4 only

d.2, 3, and 4 only

2.When lactic acidosis is present, which of the following will occur? 1. pH will likely be lower than expected for a particular PaCO2.

2.HCO3will likely be higher than expected for a particular PaCO2.

3.pH will likely be higher than expected for a particular PaCO2.

4.HCO3will likely be lower than expected for a particular PaCO2.

a.2 only

b.3 only

c.2 and 3 only

d.1 and 4 only

3.What is the clinical interpretation of the following ABG values (in addition to hypoxemia)? pH: 7.17

PaCO2: 77 mm Hg

HCO3: 27 mEq/L

PaO2: 54 mm Hg

a.Acute alveolar hyperventilation superimposed on chronic ventilatory failure

b.Acute ventilatory failure

c.Acute alveolar hyperventilation

d.Acute ventilatory failure superimposed on chronic ventilatory failure

4.A 74-year-old man with a long history of emphysema and chronic bronchitis enters the emergency department in respiratory distress. His respiratory rate is 34 breaths per minute and labored. His heart rate is 115 beats per minute, and his blood pressure is 170/120. What is the clinical interpretation of the following ABG values (in addition to hypoxemia)?

pH: 7.51

PaCO2: 68 mm Hg HCO3: 52 mEq/L PaO2: 49 mm Hg

a.Acute alveolar hyperventilation superimposed on chronic ventilatory failure

b.Acute ventilatory failure

c.Acute alveolar hyperventilation

d.Acute ventilatory failure superimposed on chronic ventilatory failure

5.Which of the following is classified as metabolic acidosis?

a.pH 7.23; PaCO2 63; HCO326; PaO2 52

b.pH 7.16; PaCO2 38; HCO313; PaO2 86

c.pH 7.56; PaCO2 27; HCO323; PaO2 101

d.pH 7.64; PaCO2 49; HCO351; PaO2 91

6.Which of the following cause metabolic acidosis?

1.Hypokalemia

2.Renal failure

3.Excessive administration of sodium bicarbonate

4.Hypochloremia

a.1 only

b.2 only

c.1 and 4 only

d.2 and 3 only

7.Using the general rule of thumb for the PCO2/HCO3/pH relationship, if the PaCO2 suddenly increased to 90 mm Hg in a patient who normally has a pH of 7.40, a PaCO2 of 40 mm Hg, and an HCO3of 24 mEq/L, the pH will decrease to approximately what level?

a.7.15

b.7.10

c.7.05

d.7.00

8.Which of the following is classified as metabolic alkalosis?

a.pH 7.23; PaCO2 63; HCO326; PaO2 52

b.pH 7.16; PaCO2 38; HCO313; PaO2 86

c.pH 7.56; PaCO2 27; HCO323; PaO2 101

d.pH 7.64; PaCO2 44; HCO346; PaO2 91

9.Lactic acidosis develops from which of the following?

1. Inadequate tissue oxygenation

2.Renal failure

3.An inadequate insulin level

4.Anaerobic metabolism

5.An inadequate glucose level

a.1 only

b.2 only

c.1 and 4 only

d.3 and 5 only

10.Metabolic alkalosis can develop from which of the following?

1.Hyperchloremia

2.Hypokalemia

3.Hypochloremia

4.Hyperkalemia

a.4 only

b.1 and 3 only

c.1 and 4 only

d.2 and 3 only

11.During acute alveolar hypoventilation, the blood:

1.HCO3increases

2.pH decreases

3.PCO2 increases

4.HCO3decreases

a.2 only

b.4 only

c.2 and 3 only

d.1, 2, and 3 only

12.During acute alveolar hyperventilation, the blood:

1.PCO2 increases

2.HCO3increases

3.HCO3decreases

4.pH increases

a.2 only

b.4 only

c.1 and 3 only

d.3 and 4 only

13.In chronic hypoventilation, kidney compensation has likely occurred when the:

1.HCO3is higher than expected for a particular PaCO2

2.pH is lower than expected for a particular PaCO2

3.HCO3is lower than expected for a particular PaCO2

4.pH is higher than expected for a particular PaCO2

a.1 only

b.2 only

c.1 and 4 only

d.3 and 4 only

14.Which of the following represents acute alveolar hyperventilation?

a.pH 7.56; PaCO2 51; HCO344

b.pH 7.45; PaCO2 37; HCO325

c.pH 7.53; PaCO2 46; HCO329

d.pH 7.58; PaCO2 26; HCO321

15.Which of the following represents compensated metabolic alkalosis?

a.pH 7.55; PaCO2 21; HCO319

b.pH 7.52; PaCO2 45; HCO329

c.pH 7.45; PaCO2 26; HCO318

d.pH 7.45; PaCO2 61; HCO341

1For a complete review of the role of the relationship in acid-base balance, see Des Jardins, T. (2019). Cardiopulmonary anatomy and physiology: essentials of respiratory care (7th ed.). Clifton Park, NY: Delmar/Cengage Learning.

2The isobars on the PCO2/HCO3/pH nomogram illustrate the pH changes that develop in the blood as a result of metabolic changes (i.e., HCO3changes) or a combination of metabolic and respiratory (CO2) changes.

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C H A P T E R 6

Assessment of Oxygenation

CHAPTER OUTLINE

Oxygen Transport Review

Oxygen Dissolved in the Blood Plasma

Oxygen Bound to Hemoglobin

Total Oxygen Content of Blood

Case Example

Oxyhemoglobin Dissociation Curve

Oxygenation Indices

Oxygen Tension–Based Indices

Oxygen Saturation–Based and Content-Based Indices

Hypoxemia Versus Hypoxia

Pathophysiologic Conditions Associated With Chronic Hypoxia

True Hypoxia—Can It Be Measured?

Self-Assessment Questions

CHAPTER OBJECTIVES

After reading this chapter, you will be able to:

Describe the two ways in which oxygen is carried in the blood.

Calculate the oxygen tension–based indices equations.

Calculate the oxygen saturation–based and content-based indices equations.

Describe the clinical significance of pulmonary shunting.

List factors that increase and decrease the oxygen content and oxygen-transport calculations.

Discuss mechanisms by which specific respiratory diseases alter oxygen transport studies.

Differentiate between hypoxemia and hypoxia.

Classify the severity of mild, moderate, and severe hypoxemia.

Describe the four types of hypoxia.

List common causes for each type of hypoxia.

Describe the pathophysiologic conditions associated with chronic hypoxia.

Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.

KEY TERMS

Alveolar-Arterial Oxygen Tension Difference (P[A-a]O2)

Anemic Hypoxia

Arterial-Venous Oxygen Content Difference ()

Circulatory Hypoxia

Cor Pulmonale

Erythropoietin

Histotoxic Hypoxia

Hypoxemia

Hypoxia

Hypoxic Hypoxia

Hypoxic Vasoconstriction of the Lungs

Ideal Alveolar Gas Equation to Determine PAO2

Intracellular Oxygen Tension (icO2)

Lactic Acid

Mild Hypoxemia

Mixed Venous Blood

Mixed Venous Oxygen Saturation () Moderate Hypoxemia

Nanostraws

Oxygen Consumption (VO2)

Oxygen Content of Arterial Blood (CaO2)

Oxygen Content of Mixed Venous Blood () Oxygen Content of Pulmonary Capillary Blood (CcO2) Oxygen Extraction Ratio (O2ER)

Oxyhemoglobin Dissociation Curve

Oxyhemoglobin Equilibrium Curve PaO2/FIO2 Ratio

PaO2/PAO2 Ratio Polycythemia

Pulmonary Capillary Blood (CcO2)

Pulmonary Shunt Fraction (QS/QT) Severe Hypoxemia Thermodilution

Total Oxygen Delivery (DO2)

Oxygen transport between the lungs and the metabolizing cells is a function of the blood itself and the cardiovascular system (blood vessels and heart). Oxygen is carried in the blood in two ways: as dissolved oxygen in the blood plasma and oxygen bound to the hemoglobin (Hb). Most oxygen is carried to the tissue cells bound to hemoglobin. The following pages provide the essential knowledge cornerstones needed to effectively and safely assess the patient's oxygenation status.

Oxygen Transport Review

Oxygen Dissolved in the Blood Plasma

A small amount of oxygen that diffuses from the alveoli to the pulmonary capillary blood remains in the dissolved form. The term dissolved means that the gas molecule (in this case oxygen) maintains its exact molecular structure and freely moves throughout the plasma of the blood in its normal gaseous state. Clinically, it is the dissolved oxygen that is measured to assess the patient's partial pressure of oxygen (PO2).

At normal body temperature, about 0.003 mL of oxygen will dissolve in each 100 mL of blood for every 1 mm Hg of PO2.

Therefore in the normal individual with an arterial PaO2 of 100 mm Hg, only about 0.3 mL of oxygen exists in the dissolved

form in every 100 mL of plasma (0.003 × 100 mm Hg = 0.3 mL). Clinically, this is written as 0.3 mL/dL.1 Relative to the total oxygen transport, only a small amount of oxygen is carried to the tissue cells in the form of dissolved oxygen.

Oxygen Bound to Hemoglobin

In the healthy individual, over 98% of the oxygen that diffuses into the pulmonary capillary blood chemically combines with hemoglobin. Clinically, the weight measurement of hemoglobin, in reference to 100 mL of blood, is known as the grams per deciliter (g/dL).2 The normal hemoglobin value for men is 14 to 16 g/dL. The normal hemoglobin value for women is 12 to 15 g/dL. The normal hemoglobin value for infants is 14 to 20 g/dL.

Each gram of hemoglobin is capable of carrying about 1.34 mL of oxygen. Therefore if the hemoglobin level is 12 g/dL and the hemoglobin is fully saturated with oxygen (i.e., carrying all the oxygen that is physically possible), about 16.08 O2

mL/dL will be bound to the hemoglobin:

However, because of normal physiologic shunts (e.g., Thebesian venous drainage and bronchial venous drainage), the actual normal hemoglobin saturation is only about 97% (see chapter 11, Pathophysiologic mechanisms of Hyoxemic Respiratory Failure). Therefore the final amount of arterial oxygen shown in the previous calculation must be adjusted by 97% as follows:

Total Oxygen Content of Blood

To calculate the total amount of oxygen in each 100 mL of blood, the dissolved oxygen and the oxygen bound to the hemoglobin must be added together. The following case example summarizes the mathematics required to determine the total oxygen content of the patient's blood.

Case Example

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A 44-year-old woman with a long history of asthma arrives in the emergency department in severe respiratory distress. Her vital signs are respiratory rate 36 breaths per minute, heart rate 130 bpm, and blood pressure 160/95 mm Hg. Her hemoglobin concentration is 10 g/dL, and her PaO2 is 55 mm Hg (SaO2 85%). On the basis of these data, the patient's total

oxygen content is determined as follows:

1.Dissolved O2

2.Oxygen bound to hemoglobin

3.Total oxygen content

The total oxygen content can be calculated in the patient's arterial blood (CaO2), venous blood (), and pulmonary capillary blood, also known as the oxygen content of capillary blood (CcO2). The mathematics for these calculations is as follows:

1. CaO2: Oxygen content of arterial blood

2. : Oxygen content of venous blood

3. CcO2: Oxygen content of pulmonary capillary blood

3It is assumed that the hemoglobin saturation with oxygen in the pulmonary capillary blood is 100%. 4See Appendix VIII on the Evolve site.

As will be shown later in this chapter, various mathematical manipulations of the CaO2, , and CcO2 values are used

in several different oxygen transport studies that provide important clinical information regarding the patient's ventilatory and cardiac status.

Oxyhemoglobin Dissociation Curve

As shown in Fig. 6.1, the oxyhemoglobin dissociation curve (HbO2 curve), also called the oxyhemoglobin equilibrium

curve, is an S-shaped curve on a nomogram that illustrates the percentage of hemoglobin that is saturated with oxygen

(left side of the graph) related to oxygen at a specific oxygen partial pressure (PO2) (bottom portion of the graph). On the

right side of the graph, the precise oxygen content that is carried by the hemoglobin, for a particular oxygen partial pressure at a normal pH, is provided.

FIGURE 6.1 Oxyhemoglobin dissociation curve at a normal pH.

The steep portion of the oxyhemoglobin dissociation curve falls between 10 and 60 mm Hg, and the upper flat portion falls between 70 and 100 mm Hg. The steep part of the curve demonstrates that oxygen quickly combines with hemoglobin as the PO2 increases or, the converse, quickly breaks away (or dissociates) from the hemoglobin as the PO2 decreases.5 It is also interesting to note that very little additional oxygen combines with hemoglobin between a PO2 of 60 and 100 mm Hg. In fact, a PO2 increase from 60 to 100 mm Hg increases the total saturation of hemoglobin by only 7% (from 90% to 97% saturated) (see Fig. 6.1).

Oxygenation Indices

A number of oxygen transport measurements are available to assess the oxygenation status of the critically ill patient. Results from these studies can provide important information to adjust therapeutic interventions. The oxygen transport studies can be divided into the oxygen tension–based indices and the oxygen saturation–based and content-based indices.6

Oxygen Tension–Based Indices

Arterial Oxygen Tension (PaO2)

The PaO2 has withstood the test of time as a good indicator of the patient's oxygenation status. In general, an appropriate PaO2 on an inspired low oxygen concentration almost always indicates good tissue oxygenation. The PaO2, however, can be misleading in a number of clinical situations. For example, the PaO2 may give a “falsely normal” impression of true tissue

oxygenation when the patient has (1) a low hemoglobin concentration, (2) a decreased cardiac output or reduced blood flow to specific organs (e.g., the heart), (3) peripheral shunting, or (4) been exposed to carbon monoxide. In all of these cases, the PaO2 may be at an appropriate level (normal PaO2) but the actual oxygen content available for tissue metabolism

—the oxygen bound to the hemoglobin—is inadequate.

Alveolar-Arterial Oxygen Tension Difference (P[A-a]O2)

The alveolar-arterial oxygen tension difference (P[A-a]O2) is the oxygen tension difference between the alveoli and arterial blood. The P(A-a)O2 is also known as the alveolar-arterial oxygen tension gradient. The information required for the P(A-a)O2 is obtained from (1) the patient's calculated alveolar oxygen tension (PAO2), which is derived from the ideal alveolar gas equation to determine PAO2 and (2) the patient's PaO2, which is obtained from an arterial blood gas

analysis.

The ideal alveolar gas equation is written as follows:

where PB is the barometric pressure, PAO2 is the partial pressure of oxygen within the alveoli, PH2O is the partial pressure of water vapor in the alveoli (which is 47 mm Hg), FIO2 is the fractional concentration of inspired oxygen, PaCO2

is the partial pressure of arterial carbon dioxide, and RQ is the respiratory quotient. The RQ is the ratio of carbon dioxide production (VCO2) divided by oxygen consumption (VO2). Under normal circumstances, about 250 mL of oxygen per

minute is consumed by the tissue cells and about 200 mL per minute of carbon dioxide is excreted into the lung. Thus the RQ is normally about 0.8 but can range from 0.7 to 1.0. Clinically, a value of 0.8 is generally used for the RQ.

For example, if the patient is receiving an FIO2 of 0.30 on a day when the barometric pressure is 750 mm Hg, and if the patient's PaCO2 is 70 mm Hg and PaO2 is 60 mm Hg, the P(A-a)O2 can be calculated as follows:

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7Blood gases and blood-derived values are customarily rounded up or down to the nearest whole number in clinical practice.

Using the PaO2 obtained from the arterial blood gas, the P(A-a)O2 can now easily be calculated as follows:

The normal P(A-a)O2 on room air at sea level ranges from 7 to 15 mm Hg and should not exceed 30 mm Hg. Although the P(A-a)O2 is very useful in patients breathing a low FIO2, it loses some of its sensitivity in patients breathing a high FIO2. The P(A-a)O2 increases at high oxygen concentrations. Because of this, the P(A-a)O2 has less value in the critically ill patient who is breathing a high oxygen concentration. The normal value for the P(A-a)O2 on 100% oxygen is between 25

and 65 mm Hg. The critical value is greater than 350 mm Hg.

The P(A-a)O2 increases in response to (1) oxygen diffusion disorders (e.g., chronic interstitial lung diseases), (2)

ventilation-perfusion ratio mismatching, (3) right-to-left intracardiac shunting (e.g., a patent ventricular septum), and (4) age. The P(A-a)O2 is normal when alveolar hypoventilation is the cause of the patient’s hypoxemia.

Arterial-Alveolar Pressure Ratio (PaO2/PAO2 Ratio)

The PaO2/PAO2 ratio (also called the a-A ratio or PaO2/PAO2 index) reflects the amount of alveolar oxygen that moves into

the arterial blood, not the calculated difference between alveolar and arterial pressure. The normal range for the young adult is 0.75 to 0.95. The critical value is less than 0.75. With pulmonary shunting, diffusion defects, and ventilationperfusion mismatching, the PaO2/PAO2 ratio decreases in proportion to the amount of lung abnormality. Clinically, the

PaO2/PAO2 ratio is most reliable when (1) the ratio is less than 0.55, (2) the FIO2 is greater than 0.30, and (3) the PaO2 is less than 100 mm Hg. Because of its reliability, the PaO2/PAO2 ratio is useful in following the patient's oxygenation status as the FIO2 changes. In clinical practice, the FIO2 often varies a great deal, and use of the ratio corrects for this problem and

allows comparison of one blood gas with another.

Assuming that the cardiovascular system is otherwise stable, the PaO2/PAO2 ratio is an excellent clinical indicator of pulmonary shunting. It also changes minimally with FIO2 changes and is not affected by PaCO2 changes. It also may be used to predict the FIO2 needed to obtain a desired PaO2 level.

Thus using the data obtained for the case example presented previously in which the PaO2 = 60 mm Hg and PAO2 = 123.4 mm Hg, the patient's PaO2/PAO2 ratio would be calculated as follows:

Arterial Oxygen Tension to Fractional Concentration of Inspired Oxygen Ratio (PaO2/FIO2 Ratio)

The PaO2/FIO2 ratio (also called oxygenation ratio) is useful in determining the extent of lung diffusion defects—for

example, in acute respiratory distress syndrome (ARDS) (see Chapter 28, Acute Respiratory Distress Syndrome) or ventilator-induced lung injury (VILI) associated with mechanical ventilation (see Chapter 11, Respiratory Insufficiency, Respiratory Failure, and Ventilatory Management Protocols). On room air, the normal PaO2/FIO2 ratio range is between 350

and 450.8 A PaO2/FIO2 ratio less than 200 indicates poor lung function. The PaO2/FIO2 ratio also decreases with ventilation-

perfusion mismatching, pulmonary shunting, and diffusion defects.

The PaO2/FIO2 ratio is a relatively easy calculation to use when the PaO2 is less than 100 mm Hg. For example, a PaO2 of 75 mm Hg divided by an FIO2 of 1.0 is 75 (75/1.0 = 75). However, a major limiting factor associated with use of the PaO2/FIO2 ratio is that changes in PaCO2 can cause false readings. For example, if the PaCO2 increases from 40 to 70 mm Hg during a period of hypoventilation, the PaO2 decreases by about the same amount that the PaCO2 increases (e.g., from 85 to 55 mm Hg). Thus if the patient was breathing an FIO2 of 0.4, the PaO2/FIO2 ratio is 55/0.40 = 138. This low

value of 138 suggests that the diffusion of oxygen is more impaired than the actual lung oxygenation status, which in this case is: 85/0.40 = 212. Thus caution should be used when using the PaO2/FIO2 ratio in patients who are hypoventilating

and retaining CO2.

Pulse Oximetric Saturation to Fractional Concentration of Inspired Oxygen Ratio (SpO2/FIO2 Ratio)

The SpO2/FIO2 ratio is commonly used in place of the PaO2/FIO2 ratio to facilitate the early recognition, diagnosis, and

treatment of patients with lung diffusion problems such as acute respiratory distress syndrome (ARDS) and ventilatorinduced lung injuries (VILI) (see VILI in Chapter 11, Respiratory Insufficiency, Respiratory Failure, and Ventilatory Management Protocols, and ARDS in Chapter 28, Acute Respiratory Distress Syndrome). Studies have shown there is a very high correlation between the SpO2/FIO2 ratio and the PaO2/FIO2 ratio—and, importantly, SpO2/FIO2 can be obtained

without having the patient undergo an arterial blood gas stick.

Oxygen Saturation–Based and Content-Based Indices

The oxygen saturation–based and content-based indices can serve as excellent indicators of the individual's cardiac and ventilatory status. These oxygenation indices are derived from the patient's total oxygen content in the arterial blood

(CaO2), mixed venous blood (), and pulmonary capillary blood (CcO2). As explained earlier in this chapter, the CaO2, , and CcO2 are calculated using the following formulas: