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Evaluation of Oxygenation, Ventilatory Status, and Acid-Base Balance

REVIEW OF ARTERIAL BLOOD GASES

The analysis of arterial blood gases (ABGs) provides valuable information about a patient’s oxygenation and ventilatory and acid-base status. Table 1 presents the normal values for arterial and mixed venous blood measurements. Blood gas results are often a vital part of the assessment and management of a mechanically ventilated patient, but they should be used with caution. A detailed explanation of the interpretation of oxygenation status and acid-base balance is beyond the scope of this text; the reader is assumed to have a basic understanding of ABG interpretation. Several of the references listed at the end of this chapter provide sources for review of the subject.1-14 Methods for noninvasive evaluation of oxygenation and ventilation are reviewed in Chapter 10 and also are available in other references.15

This review provides tables, figures, and boxes that can be used as resources as the reader progresses through the each tab or section. In addition, various approaches to the interpretation of ABG results in the clinical setting are provided.The American Association for Respiratory Care (AARC) has established a clinical practice guideline (CPG) for blood gas analysis and hemoximetry.16 The CPG provides information about indications, contraindications, hazards and complications, limitations of the procedure, validation of results, assessment of need, assessment of test quality, resources, and infection control in ABG sampling and analysis. AARC also has created a CPG for capillary blood gas sampling for neonatal and pediatric patients.17

An exercise at the end of this review allows readers to test their ability to interpret ABG results.

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Table 1: Normal Arterial and Venous Blood Gas Values*

Parameter Arterial Value Venous Value

Dissolved CO2 (mL/dL) 1.2 1.5

Combined CO2 (mL/dL) 24.0 27.1

Total CO2 (mL/dL) 25.2 28.6

PCO2 (mm Hg) 40 46

pH 7.40 7.37

(mEq/L)24 21

Base excess (mEq/L) ± 2 ±2

PO2 (mm Hg) 90 40

SO2 (%) 97 75

Dissolved O2 (vol%) 0.3 0.12

Combined O2 (vol%) 19.5 14.7

Total O2 (vol%) 19.8 14.82

*Sea level, ambient air conditions, average value for a young adult. Ranges not included.

EVALUATING OXYGENATION Evaluating blood levels of oxygen is essential for the assessment of critically ill patients. A variety of parameters are used to assess oxygen status. Table 2 provides a list of these components and their normal values, including the PaO2, SaO2, and CaO2. Box 1 presents the equations for calculating parameters not directly measured, such as the CaO2.As shown in Table 2, the normal PaO2 is 80 to 100 mm Hg. This value can be affected by other factors, such as age. A normal PaO2 based on age is described by the following equation18:

PaO2 = 104.2 – (0.27 Age)

In the clinical setting, the following equation can be used as a simple estimate of the PaO2:

PaO2 = 105 – Age in years (see Case Study 1)

Altitude affects the PaO2 by altering the inspired oxygen pressure. (NOTE: The FIO2 does not change with altitude. The barometric pressure changes, thus reducing the PIO2 as a person travels from sea level to higher altitudes. Table 4 provides estimated values

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for the PAO2 and PaO2 based on altitude.19,20 For practitioners working at higher elevations, this is valuable information when interpreting a patient’s oxygenation status.)

Box 1: Equations Used to Calculate Oxygenation StatusAlveolar air equation (calculation of alveolar PO2, PAO2):

where PAO2 = alveolar partial pressure of oxygen (mm Hg)FIO2 = inspired oxygen fractionPB = barometric pressure (mm Hg)PH2O = water vapor pressure (at 37C = 47 mm Hg)

R = respiratory quotient ( CO2/ O2; R of 0.8 is commonly used)

With an FIO2 ≤ 0.6 (low value), the effect of R on the PAO2 is small.To estimate the PAO2 for FIO2 values <0.6: PAO2 = FIO2(PB PH2O) (1.25 PaCO2)

Partial pressure of inspired oxygen: PIO2 = FIO2 (PB PH2O)Oxygen content (CaO2): CaO2 = [%Sat Hb 1.34] + (PO2 0.003 mL/dL)

Oxygen consumption ( O2): O2 = Cardiac output (CO) (CaO2 C O2)

Oxygen delivery (DO2): DO2 = CO CaO2

Pulmonary shunt : =

where is the shunted portion of the cardiac output, is total cardiac output, CcO2 is the

content of oxygen of the pulmonary end-capillary, CaO2 is the arterial O2 content, and C O2

is the mixed venous oxygen content. CcO2 is calculated on the assumption that the pulmonary end-capillary PO2 is the same as the PAO2. Mixed venous blood can be obtained from a pulmonary artery catheter.

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Table 2: Measures and Values Used in the Evaluation of Oxygenation Status

Term Abbreviation Average Normal ValuePartial pressure of arterial oxygen PaO2 80-100 mm HgPartial pressure of mixed venous oxygen P O2

40 mm Hg

Alveolar partial pressure of oxygen PAO2 100-673 mm HgFIO2 range: 0.21-1.0

Alveolar-arterial oxygen tension gradient P(A-a)O2 5-10 mm Hg (FIO2 = 0.21)30-60 mm Hg (FIO2 = 1.0)

Ratio of PaO2 to fractional inspired oxygen (PaO2 range = 80-100 mm Hg; FIO2 = 0.21)

PaO2/FIO2 380-475

Ratio of PaO2 to partial pressure of alveolar oxygen (PaO2 range = 80-100 mm Hg; FIO2 = 0.21)

PaO2/PAO2 0.8-1.0

Saturation of arterial oxygen SaO2 97%Saturation of mixed venous oxygen S O2

75%

Oxygen content of arterial blood CaO2 20 vol%Oxygen content of mixed venous blood C O2

15 vol%

Arterial-to-mixed venous oxygen content difference

[C(a − )O2] 3.5- 5 mL/dL

Oxygen delivery DO2 1000 mL/minOxygen consumption O2

250 mL/min

Two terms frequently used to describe low oxygen levels are hypoxia and hypoxemia. Hypoxia refers to lower than normal oxygen pressure in the tissues or alveoli. Hypoxemia describes a low arterial blood oxygen pressure (<80 mm Hg).13 Table 3 lists the criteria used to establish the degree of hypoxia and hypoxemia.

Table 3: Levels of Hypoxemia

Level* PaO2 Value PaO2 Range Saturation (SaO2)

Mild hypoxemia <80 mm Hg 60 to 79 mm Hg 90% to 94%

Moderate hypoxemia <60 mm Hg 40 to 59 mm Hg 75% to 89%

Severe hypoxemia <40 mm Hg <40 mm Hg <75%*Values given are for a young adult and room air. (NOTE: The levels of hypoxemia may be defined differently, depending on the author or institution.)

Types of hypoxia and their causes include the following13: Hypoxemic hypoxia (lower than normal PaO2) (See Table 3.)

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Anemic hypoxia (lower than normal red blood cell count [anemia], abnormal hemoglobin, carboxyhemoglobin)

Circulatory hypoxia (reduced cardiac output, decreased tissue perfusion) Histotoxic hypoxia (cyanide poisoning) Affinity hypoxia (reduced release of O2 from hemoglobin to the tissues [e.g., fetal

hemoglobin])

Causes of hypoxemia include the following: Hypoventilation (increased CO2 resulting from neuromuscular disorders, chronic increased

work of breathing, depression of the respiratory centers) Reduced inspired oxygen (high altitudes, low FIO2) Shunt (atelectasis, pulmonary edema, pneumonia, acute respiratory distress syndrome

[ARDS]) Diffusion defects (pulmonary resection, emphysema, pulmonary fibrosis) Poor distribution of ventilation (obstructed airways, bronchospasm)

Table 4: Calculated Changes in Alveolar and Arterial PO2 with Altitude, with and without Changes in Alveolar Ventilation

Altitude (feet) PB* (mm Hg) PAO2 (mm Hg)

PaO2 (mm Hg) PAO2 (mm Hg)

(PaCO2 variable)

PaO2 (mm Hg)

(PaCO2 = 40 mm Hg)

Sea level 760 101.7 91.7 101.7 (PaCO2 = 40 mm Hg)

91.7

5000 650 78.6 68.6 84.6 (PaCO2 = 35 mm Hg)

74.6

10,000 540 55.5 45.5 67.5 (PaCO2 = 30 mm Hg)

57.5

15,000 430 32.4 22.4 50.4 (PaCO2 = 25 mm Hg)

40.4

20,000 360 17.7 7.7 41.7 (PaCO2 = 20 mm Hg)

31.7

25,000 280 0.9 0 36.9 (PaCO2 = 10 mm Hg)

26.9

Modified from Kacmarek RM, Hess D, Stoller JK: Monitoring in respiratory care, Chicago, 1993, Mosby. PB, Barometric pressure; PAO2, alveolar PO2, calculated from the alveolar air equation; PaO2, arterial PO2, assuming PAO2 PaO2 = 10 mm Hg. *PB is an approximate relative to altitude, because it varies with climatic conditions.

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EVALUATING THE TRANSFER AND UPTAKE OF OXYGEN—P(A-a)O2, PaO2/PAO2, AND PaO2/FIO2

P(A-a)O2

The ability of the lungs to bring in and transfer oxygen to the alveolar capillaries is described by the alveolar-arterial oxygen tension gradient (P[A-a]O2) (see Table 2 and Box 1). The normal P(A-a)O2 is about 5 mm Hg at the age of 20 and increases with age.12 As shown in the equation in Box 1, the PAO2 changes with the FIO2. Because calculating the PAO2 is cumbersome, Table 5 lists PAO2 values for commonly used FIO2 values.

Table 5: Changes in PAO2 with Changes in FIO2*FIO2 PAO2

0.21 1000.35 2000.40 2350.50 3070.60 3880.70 4590.80 5300.90 6021.00 673*Using the equations PAO2 = FIO2(PB PH2O) (1.25 PaCO2) and PAO2 = FIO2(760 47 mm Hg) (1.25 40 mm Hg). With an FIO2 0.6, the factor 1.25 is not used.

Changes in the lung that reduce its ability to transfer oxygen from the alveolus to the pulmonary capillary (e.g., aging, lung disease) cause the PaO2 to drop in relation to the available oxygen (PAO2), just as the P(A-a)O2 is increased under abnormal conditions, such as entilation/perfusion

abnormalities ( ), shunt, and diffusion defects. (See Appendix B in text for a review of these

concepts.)

PaO2/PAO2

Some clinicians use the ratio of arterial-to-alveolar oxygen tension (PaO2/PAO2) to evaluate the transfer of oxygen from the lungs to the pulmonary circulation. The PaO2/PAO2 ratio should remain stable with changes in the FIO2. The ratio basically is a statement of the question, “What fraction of the oxygen is getting to the artery (PaO2) compared with the amount available in the alveolus (PAO2)?” A normal ratio for a PaO2 of 90 mm Hg and a PAO2 of 100 mm Hg (FIO2 = 0.21) is 0.9 (PaO2/PAO2 = 90/100 = 0.9). This value shows that 90% of the O2 available in the alveolus is moving into the capillary. A ratio less than 0.75 indicates a pulmonary problem, such as a shunt, ventilation/perfusion abnormality, or diffusion defect. For example, the ratio of a PaO2 of 50 mm Hg and a PAO2 of 673 mm Hg (100% O2) is 0.07. This suggests that only 7% of the oxygen (100 0.07) is moving from the alveolus into the blood.

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PaO2/FIO2

A simpler clinical parameter is the PaO2/FIO2 ratio, sometimes called the P-to-F ratio. This ratio does not require the calculation of the PAO2 but still describes the amount of oxygen moving into the blood in relation to the amount inspired (FIO2). The PaO2/FIO2 ratio often is used to describe the degree of lung injury. A PaO2/FIO2 ratio of 200 or lower indicates ARDS. A PaO2/FIO2 ratio of 200 to 300 indicates acute lung injury (ALI). (The normal range for the PaO2/FIO2 ratio is 380 to 476 [80 mm Hg/0.21 = 380; 100 mm Hg/0.21 = 476]). A severely low PaO2/FIO2 is any value below 100. Example: 50 mm Hg/1.0 = 50 mm Hg.)

Oxyhemoglobin Dissociation CurveThe oxyhemoglobin dissociation curve (OHDC) describes the relationship of the oxygen tension to the percent saturation of hemoglobin with oxygen. Table 6 shows the relation of specific O2 saturation values to specific PO2 values. Figure 1 shows the OHDC and the ways various factors can affect hemoglobin’s ability to pick up oxygen as the PO2 changes.

Fig. 1 The oxyhemoglobin dissociation curve with normal values and showing the effects of changes in pH (hydrogen ion concentration), PCO2, temperature, 2,3-diphosphoglycerate, and various hemoglobin types on the curve. (Redrawn from Lane EE, Walker JF: Clinical arterial blood gas analysis, St Louis, 1987, Mosby.)

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The following factors cause a right shift in the curve:Hyperthermia (increased temperature)Hypercapnia (increased PCO2)Acidosis (increased hydrogen ion concentration)Increased 2,3-diphosphoglycerate (2,3 DPG)Certain abnormal hemoglobins

Factors that cause a left shift in the curve include the following:Hypothermia (decreased temperature)Hypocarbia (decreased PCO2)Alkalosis (decreased hydrogen ion concentration)Decreased 2,3 DPGCarbon monoxide poisoningFetal hemoglobin

Right shifting of the curve decreases the attraction of hemoglobin and oxygen and promotes unloading of oxygen. Left shifting of the curve increases the attraction of hemoglobin and oxygen and promotes the binding of oxygen.Shifting of the curve to the right or left of normal affects the partial pressure of oxygen required to produce 50% saturation of hemoglobin. In other words, the P50 (PaO2 at 50% saturation) changes as the curve shifts. The P50 at a normal pH is 27 mm Hg. In Figure 1 the P50 is 20 mm Hg when the curve is left shifted and about 32 mm Hg when the curve is right shifted.Although the y, or vertical axis, of the OHDC usually is represented as percent saturation of hemoglobin, it also can be represented as arterial oxygen content (CaO2).

Table 6: Hemoglobin Saturation and Its Approximate PO2 Value at Normal pH

Saturation PO2 (mm Hg)

50% 27 (P50 at normal pH)

75% 40 (mixed venous saturation and P O2)

90% 60

97% 80-100 (normal arterial values)

Oxygen ContentClinicians often place too much importance on PaO2 and SaO2 values without looking at the patient’s hemoglobin level. The CaO2 and the amount of oxygen delivered to the tissues determine the amount of oxygen available for utilization at the tissue level. O2 delivery (DO2) is the product of both cardiac output and arterial oxygen content (see Box 1). Figure 2 shows how the CaO2 decreases as the level of hemoglobin decreases. Patients with severe anemia are at great risk of inadequate oxygen delivery, and patients with a low cardiac output are at similar risk. Even when the CaO2 is adequate, if it is not delivered to the tissues, the tissues will not receive adequate amounts of oxygen

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Figure 2

Fig. 2 The relationship between the CaO2 and PaO2 as a function of blood hemoglobin (Hb) concentrations. Progressive decreases in Hb cause large drops in the CaO2. (From Wilkins RL, Kacmarek B, Stoller JK: Egan’s fundamentals of respiratory care, ed 9, St Louis, 2009, Mosby.)

Pulmonary ShuntA shunt exists when perfusion in the lungs occurs without gas exchange. A pulmonary shunt is the part of the blood that leaves the right side of the heart and passes through the lungs to the left side of the heart without participating in any gas exchange (Box 1 shows the shunt equation). The calculation of shunt provides a value that represents the percentage of cardiac output that is not exposed to ventilated alveoli. Normal anatomical shunt is about 2% to 3% of the cardiac output and is present in all individuals. As the percentage of shunt increases, the PaO2 decreases and hypoxemia results. Shunts exceeding 30% are associated with a high mortality rate. Shunt effects can be caused by such disorders as atelectasis, pulmonary edema, pneumonia, pneumothorax, and complete airway obstruction (see Appendix B of text).

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VENTILATION

EVALUATING VENTILATORY STATUS

CHANGES IN ALVEOLAR VENTILATION ASSOCIATED WITH CHANGES IN PAO2 AND PACO2

Under normal circumstances, alveolar ventilation provides air to the alveoli at a rate of about 4 to 5 L/min (Box 2). At this level, enough gas exchange can occur in the lung to keep ABG values within a normal range. The relationship of alveolar ventilation to alveolar partial pressures of oxygen and carbon dioxide is illustrated by the graph in Figure 3. Note that the PAO2 and PACO2 values are normal with an alveolar ventilation of about 4.5 L/min.

Figure 3

Fig. 3 The effect of changes in alveolar ventilation on the alveolar gases PAO2 and PACO2. (See the text for further

explanation.)

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As alveolar ventilation increases, the alveolar carbon dioxide tension (PACO2) decreases until it plateaus at about 15 to 20 mm Hg. Hyperventilation also increases the alveolar partial pressure of oxygen (PAO2) above normal. The PAO2 plateaus at approximately 120 mm Hg when a person breathes room air. With hypoventilation a reduction in alveolar ventilation occurs, resulting in a rise in the PACO2 and a fall in the PAO2.

Under normal circumstances, the PACO2 is approximately equal to the PaCO2 (40 mm Hg), with the P CO2 slightly higher at 45 mm Hg. When ventilation is inadequate, CO2 rises above its normal value in the alveoli (see Figure 3). As carbon dioxide increases, the carbon dioxide molecules displace oxygen molecules in the alveoli. Thus the PAO2 decreases, and less oxygen is available to diffuse across the alveolar-capillary membrane. Therefore, changes in the PACO2 affect the PaO2. This relationship is illustrated by Figure 3 and is best described by the alveolar air equation (see Box 1). The equation assumes that the PaCO2 is equal to the PACO2. A simplified form of the alveolar air equation is: PAO2 = PIO2 – (PaCO2 1.25), where PIO2 is the partial pressure of inspired oxygen (see Box 1). This is an easy formula to use when quick clinical evaluation of ABGs is needed and a calculator is not readily available. It is more accurate if the patient is receiving a low FIO2 (<0.6).

At sea level (760 mm Hg) and at a normal FIO2 of 0.21 with a water vapor pressure of 47 mm Hg (saturated at 37C), the PIO2 is 149 mm Hg, based on the equation PIO2 = FIO2 (PB 47) = 0.21 (760 – 47), where PB is the barometric pressure. Using the simplified version of the alveolar air equation, PAO2 = PIO2 – (1.25 PaCO2), when the PaCO2 is 40 mm Hg, the alveolar PO2 (PAO2) is 99 mm Hg [149 – (1.25 40)].

As the PaCO2 rises due to hypoventilation, the PAO2 falls. For example, if the PaCO2 is 80 mm Hg, the PAO2 is 149 – (80 1.25), or 49 mm Hg. When this occurs, less oxygen is present in the alveoli. As a result, less oxygen is available to the blood and tissues.

During hyperventilation the PAO2 increases because of the drop in the PaCO2. For example, if the PaCO2 is 20 mm Hg and the PIO2 is 149 mm Hg, the PAO2 is 149 – (1.25 20), or 124 mm Hg. Because more oxygen is now available in the alveoli, more oxygen can be delivered to the arterial blood. (This assumes that the level of shunting and diffusion is normal and that no other

Box 2: Calculation of Alveolar VentilationPer breath: Alveolar ventilation in one breath (VA) equals tidal volume (VT) minus dead space

(VD), which normally is considered to equal anatomical dead space: VA = VT VD.

Per minute: Alveolar ventilation per minute ( ) equals tidal volume minus dead space

multiplied by the respiratory rate: (VT VD) f = , where f is the respiratory rate.

Also: Minute ventilation minus dead space ventilation in 1 minute equals alveolar ventilation

in 1 minute: = , where is the minute ventilation (VT respiratory rate [f])

and is the dead space ventilation per minute (VD f).

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pathological conditions are present that would cause hypoxemia.)In general, as the PaCO2 increases by 1 mm Hg, the PaO2 decreases by 1.25 mm Hg.21 For example, if the PaCO2 increases from 40 to 50 mm Hg, a PaO2 of 100 mm Hg decreases to about 88 mm Hg (Table 7).

Table 7: Effect of PaCO2 on PaO2*

PaCO2 (mm Hg) PAO2 (mm Hg) PaO2 (mm Hg)

40 97 87

64 67 57

80 47 37

*Patient with a normal P(A-a)O2 of 10 mm Hg breathing room air.

ALVEOLAR VENTILATION, PaCO2, AND CO2

A relationship exists among the arterial pressure of carbon dioxide (PaCO2), the amount of

carbon dioxide produced ( CO2), and the alveolar ventilation ( ). Cellular metabolism

produces CO2, and the lungs are the primary organs for removing it. The following formula describes the amount produced and how well CO2 is removed by the lungs to achieve a given PaCO2:<equation>

Using CO2 in milliliters per minute and in liters per minute, this equation can be

rewritten as

where 0.863 is a correction factor for reported in liters per minute, body temperature and

pressure, saturated (BTPS) and the CO2 reported in milliliters per minute, standard

temperature and pressure, dry (STPD).

For example, if the is 4.5 L/min and the CO2 is normal (200 mL/min), the PaCO2 is 38 mm

Hg. If the alveolar ventilation is half of normal (2.25 L/min) and the CO2 is normal, the PaCO2

would be calculated as follows:

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Therefore, when alveolar ventilation is halved, the PaCO2 approximately doubles. Minute ventilation and alveolar ventilation are similar in their effects on the PaCO2, as long as dead space volume remains constant. Table 8 presents additional examples of expected PaCO2 values

as changes in a normal, resting individual.13

Table 8: Expected PaCO2 Based on Minute Ventilation* in Normal Individuals

Minute Ventilation PACO2 (mm Hg) PaCO2 (mm Hg)

4 times normal 20 15-25

2 times normal 30 25-35

Normal 40 35-45

*Note that this is minute ventilation, not alveolar ventilation.

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ACID-BASE BALANCE

CHANGES IN pH, PaCO2, AND SODIUM BICARBONATEAs the arterial partial pressure of CO2 increases, the level of acid in the blood also increases. The pH becomes more acidotic and has a lower numerical value. The advantage of knowing the pH and PaCO2 values is that this information allows evaluation of a patient’s condition and determination of the cause of the instability in these variables. The relationship of the pH, the PaCO2 (mm Hg), and the bicarbonate level (mEq/L) can be described by the Henderson-Hasselbalch equation:

pH = pK + log[( )/(H2CO3)]

The equation can be simplified into the following form13:

where [H+] is the hydrogen ion concentration in nanomoles per liter (nmol/L) and 24 is derived from the dissociation constant for carbonic acid. Table 9 provides values for the hydrogen ion concentration for a given pH. Once the [H+] has been calculated, the pH can be determined from Table 9 For example, if the PaCO2 is 50 mm Hg and the is 24 mEq/L, the pH is calculated as follows:

If the hydrogen ion concentration is 50 nM/L, the pH is close to 7.30.Bicarbonate can also be calculated by rearranging the equation:

If the pH is 7.40 and the PaCO2 is 50 mm Hg, the bicarbonate is 30 mEq/L (see Table 9for the nanomole concentration for [H+] when the pH is 7.40):

Remember that these determinations are estimations of the actual value. They can be useful in clinical situations for a quick determination of a patient’s bicarbonate, pH, and PaCO2

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values when two of the factors are known. Table 10 lists examples of common ABG abnormalities. Figure 4 presents a blood gas flow chart (algorithm) that reviews the mental process required to interpret a set of ABG results.

The following is another common method of applying the Henderson-Hasselbalch equation:

pH = pKa + log[( )/(H2CO3)]

where pK is 6.1, the dissolved CO2 is calculated (PCO2 0.03), and the values are substituted into the equation. For example, using normal values:

= 6.1 + log (20/1)= 6.1 + 1.3

= 7.40 (normal pH)

Table 9: Relationship Between pH and Hydrogen Ion [H+] Concentration

pH Approximate [H+] (nmol/L)

8.0 10

7.8 16

Alkalosis 7.7 20

7.6 26

7.5 32

Normal 7.4 40

7.3 50

Acidosis 7.2 63

7.1 80

7.0 100

6.9 125

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Table 10: Examples of Common Arterial Blood Gas Abnormalities

Conditions pH PaCO2 (mm Hg)

(mEq/L)

PaO2* (mm

Hg)Possible Causes

Normal 7.35-7.45 35-45 24-28 80-100 Normal ventilation without pulmonary pathology

RESPIRATORY

Acute acidosis 7.0-7.34 >45 24-28 80 Hypoventilation, sedation, drug overdose, cardiopulmonary arrest, chest trauma, pneumothorax, central nervous system (CNS) trauma, restrictive pulmonary disease

Chronic acidosis (compensated)

7.35-7.40 >45 30-48 <80 Hypoventilation, chronic obstructive pulmonary disease (COPD), chronic neuromuscular disease, muscle wasting, late CNS injury

Acute alkalosis 7.42-7.70 <35 24-28 >80 Increased alveolar ventilation, hypoxemia (if PaO2 is low), pain, anxiety, mechanical ventilation, encephalitis, cirrhosis of the liver, pulmonary emboli (if PaO2 is low), severe infection, fever, salicylate intoxication

Chronic alkalosis (compensated)

7.41-7.45 <35 12-24 80-100 Long-term mechanical ventilatory support with increased alveolar ventilation

METABOLIC

Acute acidosis 7.0-7.34 35-46 12-22 80-100 Ketoacidosis (alcoholic, starvation, diabetic), uremic acidosis (failure of renal acid excretion), loss of

(diarrhea), renal loss of base

(carbonic anhydrase inhibitors [Diamox], renal tubular acidosis), overproduction of acid (lactic acidosis), conversion of toxins to acids (methanol, ethylene glycol, salicylate)

Compensated 7.35-7.40 <35 12-22 >80 Respiratory compensation for

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acidosis metabolic acidosis as with diabetic acidosis and lactic acidosis

Acute alkalosis 7.42-7.70 35-46 30-48 80-100 ingestion or administration

of bicarbonate, vomiting (acid loss), gastrointestinal (GI) suction (acid loss), diuretic-induced K+ or Cl– loss, steroids, licorice ingestion

Compensated alkalosis

7.41-7.45 >45 30-48 <80 Primary hypokalemic metabolic alkalosis with dehydration/azotemia (rare)

*Assuming no pulmonary pathology other than respiratory hypoventilation and no therapeutic oxygen

CHANGES IN pH CAUSED BY CHANGES IN PaCO2

Table 11 provides another method that can help clinicians evaluate the relationship between the PaCO2 level and the pH.13 This method can be used to determine whether changes in pH are reflections of changes in the PaCO2 or are due to metabolic changes. For example, a PaCO2 of 80 mm Hg is 40 mm Hg above the normal of 40 mm Hg. The pH would decrease by about 0.2 and would be equal to about 7.20 if the change were due to hypoventilation. During hyperventilation, if the PaCO2 is 20 mm Hg, or 20 mm Hg less than normal, then the expected pH would be 7.60. If the actual pH is 7.50, not 7.60, the pH is not entirely due to ventilatory changes. This situation suggests respiratory alkalosis with metabolic acidosis. Again, this relationship is an estimate intended to aid rapid clinical assessment of the patient. (NOTE: Buffers make it more difficult for the blood to become acidotic; therefore, the CO2 must increase more to change the pH compared with how much it must drop to raise the pH.)

Table 11: Relationship Between Changes in PaCO2 and the pH13

Given a starting PaCO2 of 40 mm Hg, every 20 mm Hg increase in PaCO2 decreases pH by 0.10 unit. For example:PaCO2 pH

40 mm Hg 7.40 24 mEq/L60 mm Hg 7.30 26 mEq/L80 mm Hg 7.20 28 mEq/LThis is true in individuals with normal blood buffers. (NOTE: Remember that this is an approximation.)When the PaCO2 decreases 10 mm Hg, the pH increases by 0.10 unit.PaCO2 pH

30 mm Hg 7.50 22 mEq/L20 mm Hg 7.60 20 mEq/L

As the PaCO2 increases, the PaO2 decreases.

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CHANGES IN PLASMA BICARBONATE CAUSED BY CHANGES IN PaCO27,13,22,23

The amount of change in the PaCO2 and the for an acid-base disorder can be calculated.

The following section reviews the determination of these values.

Acute Alveolar HypoventilationDuring hypoventilation, carbon dioxide is not eliminated at a normal rate through the lungs, and CO2 is increased. For each 10 mm Hg increase in the PaCO2, bicarbonate increases about 1 mEq/L. In acute changes, such as acute respiratory acidosis, the following equation can be used:

= 0.10 ΔPaCO2

Where Δ represents change. As an example, the PaCO2 is 40 mm Hg and the is 24

mEq/L. If the PaCO2 increases to 50 mm Hg (ΔPaCO2 = 10), the increases as follows:

= 0.10 ΔPaCO2

= 0.10 10 = 1.0

The increases from 24 to 25 mEq/L.

Acute Alveolar HyperventilationAs the PaCO2 decreases by 10 mm Hg with hyperventilation, bicarbonate decreases about 2 mEq/L.13,22,23 The following equation can be used for acute respiratory alkalosis:

= 0.2 ΔPaCO2

As an example of respiratory alkalosis, the PaCO2 is 40 mm Hg and the is 24 mEq/L

at the start. If the PaCO2 decreases to 20 mm Hg (ΔPaCO2 = 20 mm Hg), the

decreases as follows:

= 0.2 ΔPaCO2

= 0.20 20 = 4.0

The decreases from 24 to 20 mEq/L.

Chronic ChangesIf hypoventilation or hyperventilation continues for 2 to 3 days, normal kidney function helps correct the pH and compensates by retaining or excreting bicarbonate.Because hypoventilation produces a chronic respiratory acidosis, the kidneys’ compensation can be estimated using the following equation:

= 0.35 ΔPaCO2

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In the example for acute respiratory acidosis, the PaCO2 is 50 mm Hg and the is 25 mEq/L. In this example, the ΔPaCO2 is 10 mm Hg; therefore the equation is:

= 0.35 10 = 3.5 mEq/L

The bicarbonate increases from 25 to about 28.5 mEq/L as the kidneys compensate and the pH moves toward normal.

On the other hand, during chronic hyperventilation, compensation by the kidneys results in the excretion of bicarbonate. The following equation can be used to calculate bicarbonate in chronic respiratory alkalosis:

= 0.5 ΔPaCO2

For example, if the PaCO2 is 20 mm Hg (20 mm Hg less than normal) and the is 21 mEq/L, the equation becomes:

= 0.5 20 = 10

As the kidneys compensate, the bicarbonate falls to about 11 mEq/L after a few days.

METABOLIC CHANGES IN BICARBONATE AND pH7,22,23

Another rule of thumb can help describe the relationship between the pH and bicarbonate. When changes in the pH are caused by metabolic rather than respiratory changes, a pH change of 0.15 is approximately equal to a change in base of 10 mEq/L.For example, if the pH rises from 7.40 to 7.55 (an increase of 0.15) as a result of metabolic causes, the base increases by 10 mEq/L (e.g., from a normal of 24 to 34 mEq/L). If the pH drops from 7.40 to 7.25 (a decrease of 0.15), the expected decrease in bicarbonate would be 10 mEq/L, to 14 mEq/L. This is true as long as the change in pH results from purely metabolic causes and the PaCO2 does not change.

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REVIEW Exercises

Case Study 1Evaluate the P(A-a)O2A 40-year-old patient has a P(A-a)O2 of 15 mm Hg. Is this in the normal range for this patient?

Case Study 2Oxygenation StatusA patient has a measured PaO2 of 80 mm Hg and an SaO2 of 97%. The hemoglobin is 10 g %. Does this patient have a normal oxygenation status?

Case Study 3ABG AnalysisA patient has a PaO2 of 50 mm Hg and a PaCO2 of 80 mm Hg. If the PaCO2 were to decrease to a normal of 40 mm Hg, what would you expect the PaO2 to be after the change (assuming the PaO2

changes were due to the PaCO2 changes alone and not to lung pathology)?

Case Study 4Calculate BicarbonateA patient has a PaCO2 of 78 mm Hg and a pH of 7.20. Estimate the patient’s bicarbonate level.

Exercise 5. Interpret the Following Blood Gases 1. pH PaCO2 PaO2

7.39 44 mm Hg 89 mm Hg 25 mEq/L2. pH PaCO2 PaO2

7.12 42 mm Hg 155 mm Hg 13 mEq/L 3. pH PaCO2 PaO2





7.37 66 mm Hg 68 mm Hg 36 mEq/L

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8. pH PaCO2 PaO2









7.21 90 mmHg 45 mm Hg 35 m Eq/L17. pH PaCO2 PaO2










7.43 24 mm Hg 119 mm Hg 15 mEq/L27. pH PaCO2 PaO2 BE* SaO2*

22

7.43 41 mm Hg 94 mm Hg 26 mEq/L + 2 9528. pH PaCO2 PaO2 BE SaO2

7.52 30 mm Hg 45 mm Hg 24 mEq/L + 2 8629. pH PaCO2 PaO2 BE SaO2

7.15 80 mm Hg 80 mm Hg 27 mEq/L 0 9230. pH PaCO2 PaO2 BE SaO2

7.20 55 mm Hg 55 mm Hg 21 mEq/L -8 7931. pH PaCO2 PaO2 BE SaO2

7.60 40 mm Hg 85 mm Hg 39 mEq/L +10 9732. pH PaCO2 PaO2 BE SaO2



7.39 38 mm Hg 65 mm Hg 24 mEq/L 0 92*BE, Base excess; SaO2, oxygen saturation.

Exercise 6. Answer the Following Questions1. List the normal arterial values for the following: pH, total CO2, PaCO2, CaO2, PaO2, SaO2.

2. Give the normal mixed venous values for the following: pH, total CO2,

, , . 3. A 95-year-old patient has a PaO2 of 78 mm Hg on room air. How would you interpret this

result?4. An 18-year-old patient breathing room air is evaluated in the emergency department of a

hospital in Vail, Colorado (elevation = 10,000 feet). The PaCO2 is 30 mm Hg, and the PaO2 is 58 mm Hg. How would you interpret the arterial oxygenation level?

5. What would be a normal value for P(A-a)O2 in a 70-year-old patient?6. A patient has a PaO2/PAO2 of 0.5. How would you interpret this value?7. A PaO2/FIO2 ratio < 200 indicates which of the following?

a. Acute respiratory distress syndromeb. Hypoventilationc. FIO2 >0.6d. Acute lung injury

8. A P50 of 20 indicates that the oxyhemoglobin dissociation curve has done which of the following?a. Shifted leftb. Shifted rightc. Remained in the normal position

9. A patient’s hemoglobin is 8 g, the SaO2 is 97%, and the PaO2 is 100 mm Hg. Given these measurements, which of the following is(are) correct?1. Normal oxygenation2. Reduced CaO2

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3. Anemia4. Low oxygen delivery to the tissuesa. 1 onlyb. 2 and 3 onlyc. 3 and 4 onlyd. 2, 3, and 4 only

10. An excitable patient is admitted to the outpatient clinic after an emotionally traumatic event. ABGs on room air are as follows: PaCO2 = 20 mm Hg, PaO2 = 110 mm Hg, SaO2 = 99%. What would you expect the pH to be if the blood gas changes were due to respiratory changes? How would you interpret these ABG values? What treatment do you think might be appropriate for the patient?

11. A patient in the emergency department is being treated for severe congestive heart failure. ABGs on room air are as follows: PaCO2 = 78 mm Hg, PaO2 = 65 mm Hg, SaO2 = 90%. What would the pH be if these results were due to hypoventilation alone? How would you interpret the acid-base status? What respiratory care might this patient need?

12. An ABG sample has a pH of 7.30 and a PaCO2 of 25 mm Hg. What is the estimated based on these two values?

13. An ABG sample has a pH of 7.39 and a PaCO2 of 61 mm Hg. What is the estimated based on these two values?

14. How much effect would an increase in the PaCO2 from 40 to 50 mm Hg have on a of 25 mEq/L?

15. A patient has a constant CO2 production. The patient’s alveolar ventilation drops from 5 to 2 L/min. If the patient’s PaCO2 was 50 mm Hg at the start, what would you expect the PaCO2

to be after the change in ?

16. A patient hyperventilates from a PaCO2 of 40 to 30 mm Hg. The is 24 mEq/L

initially. What will the be after the change in the PaCO2?17. A stable patient with chronic obstructive pulmonary disease (COPD) routinely has the

following blood gas values: PaCO2 = 52 mm Hg, pH = 7.39, HCO3– = 33 mEq/L. The patient

begins to vomit, and the pH rises to 7.53. In what way might the change in pH affect the HCO3

–?18. A patient has the following ABG values: PaCO2 = 38 mm Hg, pH = 7.30, HCO3

– = 18 mEq/L. The patient’s HCO3

– increases to 28 mEq/L after intravenous administration of HCO3

–. You would expect the pH to change to what value?19. A blood gas slip shows the following values: pH = 7.33, PaCO2 = 68 mm Hg, HCO3

– = 35 mEq/L. How would you interpret these results? (See Figure 4.)

20. If the pH is 7.10 and the PaCO2 is 21 mm Hg, what is the HCO3–? How would you interpret

these results?

24

Fig. 4 Blood gas flow chart showing the process for interpreting a set of blood gas values.

25

References1. Adrogue HE, Adrogue HJ: Acid-base physiology, Respir Care 46:328, 2001.2. Beachey W: Acid-base balance. In Wilkins RL, Stoller JK, Scanlan CL, editors: Egan’s

fundamentals of respiratory care, ed 8, St Louis, 2003, Mosby.3. Davenport HW: The ABCs of acid-base chemistry, ed 5, Chicago, 1969, University of

Chicago Press.4. Des Jardins T: Cardiopulmonary anatomy and physiology: essentials for respiratory care, ed

4, Albany, NY, 2002, Delmar.5. Epstein SK, Singh N: Respiratory acidosis, Respir Care 46:366, 2001.6. Foster GT, Vaziri ND, Sassoon CSH: Respiratory alkalosis, Respir Care 46:384, 2001.7. Huang YCT: Arterial blood gases. In Hess RH, MacIntyre NR, Mishoe SC, et al, editors:

Respiratory care principles and practices, Philadelphia, 2002, WB Saunders.8. Khanna A, Kurtzman NA: Metabolic alkalosis, Respir Care 46:354, 2001.9. Kraut JA, Madias NE: Approach to patients with acid-base disorders, Respir Care 46:392,

2001.10. Malley W: Clinical blood gases: assessment and intervention, Philadelphia, 2005, WB

Saunders.11. Mathews P, Conway L: Arterial blood gases and noninvasive monitoring of oxygen and

carbon dioxide. In Wyka KA, Mathews PJ, Clark WF, editors: Foundations of respiratory care, Albany, NY, 2002, Delmar.

12. Scanlan CL, Wilkins RL: Gas exchange and transport. In Wilkins RL, Stoller JK, Scanlan CL, editors: Egan’s fundamentals of respiratory care, ed 8, St Louis, 2003, Mosby.

13. Shapiro BA, Peruzzi WT, Kozelowski-Templin R: Clinical application of blood gases, ed 5, St Louis, 1994, Mosby.

14. Swenson ER: Metabolic acidosis, Respir Care 46:342, 2001.15. Cairo JM, Pilbeam SP: Mosby’s respiratory care equipment, ed 7, St Louis, 2004, Mosby.16. American Association for Respiratory Care: Clinical practice guideline: blood gas analysis

and hemoximetry: 2001 revision and update, Respir Care 46:498, 2001.17. American Association for Respiratory Care: Clinical practice guideline: capillary blood gas

sampling for neonatal and pediatric patients, Respir Care 39:1180, 1994.18. Sorbini CA, Grassi V, Solinas E, et al: Arterial oxygen tension in relation to age in healthy

subjects, Respiration 25:3, 1968.19. Schoene RB: Adaptation and maladaptation to high altitude. In Pierson DJ, Kacmarek RM,

editors: Foundations of respiratory care, New York, 1992, Churchill Livingstone.20. Kacmarek RM, Hess D, Stoller JK: Monitoring in respiratory care, Chicago, 1993, Mosby.21. Light RW: Conservative treatment of hypercapneic acute respiratory failure, Respir Care

28:561, 1983.22. Otis AB: Quantitative relationships in steady-state gas exchange. In Fenn WO, Rahn H,

section editors: Handbook of physiology, Section 3: Respiration, Washington, DC, 1964, The American Physiological Society.

23. Murray JF: Pathophysiology of acute respiratory failure, Respir Care 28:531, 1983.

Case Study/Exercise Answers

26

Answer: Case Study 1At age 20, the normal P(A-a)O2 is about 5 mm Hg; it increases 4 mm Hg per decade. At age 4,0 this would represent an increase of 8 mm Hg, or a value of 13 mm Hg. The value of 15 mm Hg is reasonably close to normal.

Answer Case Study 2Although the PaO2 and SaO2 are normal, the low hemoglobin will cause a reduction in this patient’s CaO2. Therefore, this patient does not have a normal oxygenation status.

Answer Case Study 3A change in the PaCO2 from 80 to 40 mm Hg is a 40 mm Hg difference; 40 mm Hg × 1.25 = 50 mm Hg. The PaO2 would be expected to increase by about 50 mm Hg to approximately 100 mm Hg.

Answer Case Study 4Use this equation:

Answer Exercise 5:1. Normal2. Uncompensated metabolic acidosis with hyperoxemia3. Uncompensated respiratory acidosis with moderate hypoxemia4. Uncompensated respiratory alkalosis with hyperoxemia5. Compensated respiratory alkalosis with hyperoxemia6. Uncompensated metabolic alkalosis7. Compensated respiratory acidosis with mild hypoxemia8. Partially compensated respiratory acidosis with mild hypoxemia9. Partially compensated respiratory acidosis with mild hypoxemia10. Partially compensated respiratory alkalosis11. Partially compensated respiratory acidosis with severe hypoxemia12. Partially compensated respiratory acidosis with mild hypoxemia13. Partially compensated metabolic acidosis with hyperoxemia14. Partially compensated metabolic alkalosis15. Partially compensated respiratory alkalosis with hyperoxemia16. Partially compensated respiratory acidosis with moderate hypoxemia17. Possible venous sample18. Partially compensated respiratory alkalosis19. Compensated respiratory acidosis with mild hypoxemia20. Uncompensated respiratory acidosis with moderate hypoxemia21. Uncompensated metabolic alkalosis22. Partially compensated metabolic acidosis with mild hypoxemia23. Partially compensated metabolic alkalosis with mild hypoxemia

27

24. Uncompensated respiratory alkalosis with moderate hypoxemia25. Partially compensated respiratory acidosis with mild hypoxemia26. Compensated respiratory alkalosis with hyperoxemia27. Normal ABGs28. Uncompensated respiratory alkalosis with moderate hypoxemia29. Uncompensated respiratory acidosis30. Combined acidosis with moderate hypoxemia31. Uncompensated metabolic alkalosis32. Partially compensated respiratory alkalosis with moderate hypoxemia33. Uncompensated respiratory acidosis with severe hypoxemia34. Normal acid-base balance with mild hypoxemia

Answers Exercise 61. pH = 7.4; total CO2 = 25.2 (mmol/L); PaCO2 = 40 mm Hg; CaO2 = 19.8 vol%; PaO2 = 80 to

100 mm Hg; SaO2 = 97%.

2. pH = 7.37; P CO2 = 46 mm Hg; C O2 = 14.8 vol%; P O2 = 40 mm Hg; S O2 = 75%.3. Remember that PaO2 = 104.2 − (0.27 Age). For a 95-year-old patient, this is a normal

value for PaO2.4. This is a normal PaO2 for this elevation.5. A normal P(A-a)O2 for a 70-year-old person would be about 25 mm Hg. Recall that it is

about 5 mm Hg at age 20 and increases about 4 mm Hg per decade over 20.6. A PaO2/PAO2 of 0.5 is much lower than the normal value of approximately 0.9 to 1. This

suggests that only about 50% of the oxygen available in the alveolus is getting into the arteries.

7. a8. a9. d10. With a decrease in PaCO2 of 20 mm Hg, the pH should increase by 0.2, so that the pH value

would be about 7.6. This is an example of respiratory alkalosis. The patient needs to rebreathe CO2, perhaps by breathing into a bag, and should be calmed down.

11. The increased PaCO2 of 78 mm Hg is about 40 mm Hg above the normal PaCO2. The pH would be about 7.2, a decrease of 0.2 from normal. This is respiratory acidosis; the patient needs increased ventilation to reduce the PaCO2.

12. HCO3– = (24 PaCO2)/(H+); HCO3

– = (24 25)/50; HCO3– = 12 mEq/L

13. HCO3– = (24 PaCO2)/(H+); HCO3

– = (24 61)/40; HCO3– = 36.6 mEq/L

14. An increase in the PaCO2 from 40 to 50 mm Hg (10 mm Hg) increases the HCO3– from 25 to

about 26 mEq/L.

15. Recall that PaCO2 = [0.863 ( CO2)]/ ; the first step is to determine the patient’s V.

Rearranging the equation: CO2 = [ PaCO2]/0.863; CO2 = (5 50)/0.863 = 287

mL/min. With the decrease in , the PaCO2 increases: PaCO2 = (0.863 287)/2 = 124 mm Hg.

16. The PaCO2 drops by 10 mm Hg; the HCO3– will decrease by about 2 to 22 mEq/L.

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17. An increase in pH of 0.15 increases the HCO3– by 10 mEq/L. The expected HCO3

– is about 43 mEq/L.

18. The pH will increase to 7.45.19. Partially compensated respiratory acidosis20. 6.3 mEq/L; partially compensated metabolic acidosis

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