How to Read the PCO₂//pH Nomogram

The thick red bar moving from left to right across the Pco₂//pH nomogram represents the normal Pco₂ blood buffer line. This red bar is used to identify the pH and changes that occur immediately in response to an acute increase or decrease in Pco₂. The purple bar is used to identify the pH and changes that occur in response to acute metabolic acidosis and metabolic alkalosis conditions. The colored areas that surround the red and purple bars are used to identify (1) partial and complete renal compensation, (2) partial and complete respiratory compensation, and (3) combined metabolic and respiratory acid-base disturbances (see Figure 4-1).

For example, when the pH, Pco₂, and values all intersect in the light purple area—shown in the upper left hand corner of the Pco₂//pH nomogram—partial renal compensation has occurred in response to a chronically high Pco₂ level. When the increases enough to move the pH into the light-blue normal bar, complete renal compensation is confirmed. When the pH, Pco₂, and values all intersect in the in the green area—shown in the lower right hand corner of the Pco₂//pH nomogram—partial renal compensation has occurred in response to a chronically low Pco₂ level. When the decreases enough to move the pH into the light-blue normal bar, complete renal compensation is confirmed.

When the pH, Pco₂, and values all intersect in the in the orange area—shown immediately below the red bar on the left side of the Pco₂//pH nomogram—a combined respiratory and metabolic acidosis is confirmed. When the pH, Pco₂, and values all intersect in the in the blue area—shown immediately above the red bar on the right side of the Pco₂//pH nomogram—a combined respiratory and metabolic alkalosis is confirmed.

Finally, when the pH, Pco₂, and values all intersect in the yellow area—shown in the lower left corner of the Pco₂//pH nomogram—respiratory compensation has occurred in response to metabolic acidosis. When the pH, Pco₂, and values all intersect in the pink area—shown in the upper right corner of the Pco₂//pH nomogram—respiratory compensation has occurred in response to metabolic alkalosis.

Although it is beyond the scope of this textbook to fully explain how each of the acid-base disturbances listed in Box 4-1 can be identified on the Pco₂//pH nomogram, a basic understanding of the following two most commonly encountered Pco₂//pH relationships is important: (1) an acute Pco₂ increase and its effects on the pH and values, and (2) an acute Pco₂ decrease and its effects on the pH and values.*

How Acute PCO₂ Increases Affect the pH and Values

As mentioned previously, the red normal Pco₂ blood buffer bar shown on the Pco₂//pH nomogram is used to identify the pH and values that will result immediately in response to a sudden increase in Pco₂. For example, if the patient’s Paco₂ were to suddenly increase to, say, 60 mm Hg, the pH would immediately fall to about 7.28 and the level would increase to about 26 mEq/L. Furthermore, the Pco₂//pH nomogram shows that these ABG values represent acute ventilatory failure (acute respiratory acidosis). This is because (1) all of the ABG values (i.e., Pco₂, , and pH) intersect within the red normal Pco₂ blood buffer bar, and (2) the pH and readings are precisely what is expected for an acute increase in the Pco₂ of 60 mm Hg (Figure 4-2).

How Acute PCO₂ Decreases Affect the pH and Values

On the other hand, the red normal Pco₂ blood buffer bar shown on the Pco₂//pH nomogram is also used to identify the pH and values that will result immediately in response to a sudden decrease in Pco₂. For example, if the patient’s Paco₂ were suddenly to decrease to, say, 25 mm Hg, the pH would immediately increase to about 7.55 and the level would decrease to about 21 mEq/L. In addition, the Pco₂//pH nomogram shows that these ABG values represent acute alveolar hyperventilation (acute respiratory alkalosis). This is because (1) all of the ABG values (i.e., Pco₂, , and pH) intersect within the red normal Pco₂ blood buffer bar, and (2) the pH and readings are precisely what is expected for an acute increase in the Pco₂ of 25 mm Hg (Figure 4-3).

A Quick Clinical Calculation for the Effect of Acute PaCO₂ Changes on pH and

In addition to using the graphic Pco₂//pH nomogram (see Figure 4-1), the following simple calculations can also be used to estimate the expected pH and value changes that will immediately occur in response to a sudden increase or decrease in Paco₂.

Acute decreases in PaCO₂ (e.g., acute hyperventilation)

Using the normal ABG values as a baseline (i.e., pH 7.40, Paco₂ 40 mm Hg, and 24 mEq/L), for every 5 mm Hg the Paco₂ decreases, the pH will increase about 0.06 unit (from 7.4), and the will decrease about 1 mEq/L. Or, by way of another example, for every 10 mm Hg the Paco₂ decreases, the pH will increase about 0.12 units (from 7.4), and the will decrease about 2 mEq/L. Thus, if a patient’s Paco₂ suddenly decreases to, say, 30 mm Hg, the expected pH change would be around 7.52 and the would be about 22 mEq/L.

Again, it should be noted that if the patient’s Pao₂ is also very low, lactic acid may also be present. In such cases, the patient’s pH and values would both be lower than expected for a particular Paco₂ level.

Using these calculations, Table 4-2 provides a general rule of thumb for the expected pH and changes that occur in response to an acute increase or decrease in the Pco₂ level.

Table 4-2

General Rule of Thumb for the Paco₂//pH Relationship

pH (Approximate)	Paco2 (Approximate)	mEq/L (Approximate)
7.55	25	21
7.50	30	22
7.45	35	23
7.40	40	24
7.35	50	25
7.30	60	26
7.25	70	27

Acute Ventilatory Changes Superimposed on Chronic Ventilatory Failure

Because acute ventilatory changes (i.e., hyperventilation or hypoventilation) are frequently seen in patients who have chronic ventilatory failure (compensated respiratory acidosis), the respiratory care practitioner must be familiar with and be on the alert for (1) acute alveolar hyperventilation superimposed on chronic ventilatory failure, and (2) acute ventilatory failure superimposed on chronic ventilatory failure.

Acute Alveolar Hyperventilation Superimposed on Chronic Ventilatory Failure (Acute Hyperventilation on Compensated Respiratory Acidosis)
ABG Changes	Example
pH: increased	7.53
Paco2: increased	51 mm Hg
: increased	37 mEq/L
Pao2: decreased	46 mm Hg

Like any other person (healthy or unhealthy), the patient with chronic ventilatory failure can also acquire an acute shunt-producing disease (e.g., pneumonia). Some of these patients have the mechanical reserve to increase their alveolar ventilation significantly in an attempt to maintain their baseline Pao₂. However, in regard to the patient’s baseline Paco₂ level, the increased alveolar ventilation is often excessive.

When excessive alveolar ventilation occurs, the patient’s Paco₂ rapidly decreases. This action causes the patient’s Paco₂ to decrease from its normally high baseline level. As the Paco₂ decreases, the arterial pH increases. As this condition intensifies, the patient’s baseline ABG values can quickly change from chronic ventilatory failure to acute alveolar hyperventilation superimposed on chronic ventilatory failure (Table 4-3).

Table 4-3

Examples of Acute Changes in Chronic Ventilatory Failure

Acute Ventilatory Failure on Chronic Ventilatory Failure	Chronic Ventilatory Failure (Baseline Values)	Acute Alveolar Hyperventilation on Chronic Ventilatory Failure
7.21	pH 7.39	7.53
110	Paco2 76	51
43	41	37
34	Pao2 61	46

If the clinician does not know the past history of the patient with acute alveolar hyperventilation superimposed on chronic ventilatory failure, he or she might initially interpret the ABG values as signifying partially compensated metabolic alkalosis with severe hypoxemia (see Box 4-1). However, the clinical situation that offsets this interpretation is the presence of marked hypoxemia. A low oxygen level is not normally seen in patients with pure metabolic alkalosis. Thus, whenever the ABG values appear to reflect partially compensated metabolic alkalosis but the condition is accompanied by significant hypoxemia, the respiratory care practitioner should be alert to the possibility of acute alveolar hyperventilation superimposed on chronic ventilatory failure.

Acute Ventilatory Failure Superimposed on Chronic Ventilatory Failure (Acute Hypoventilation on Compensated Respiratory Acidosis)
ABG Changes	Example
pH: decreased	7.21
Paco2: increased	110 mm Hg
: increased	43 mEq/L
Pao2: decreased	34 mm Hg

Often patients with chronic ventilatory failure do not have the mechanical reserve to meet the hypoxemic challenge of a respiratory disorder. When these patients attempt to maintain their baseline Pao₂, by increasing alveolar ventilation, they consume more oxygen than is gained. When this happens, the patient begins to breathe less. This action causes the Paco₂ to increase and eventually to rise above the patient’s normally high Paco₂ baseline level. This action causes the patient’s arterial pH level to fall, or become acidic. In short, the patient’s baseline ABG values shift from chronic ventilatory failure to acute ventilatory failure superimposed on chronic ventilatory failure (see Table 4-3).

Lactic Acidosis (Metabolic Acidosis)
ABG Changes	Example
pH: decreased	7.21
Paco2: Normal or decreased	35 mm Hg
: decreased	19 mEq/L
Pao2: decreased	34 mm Hg

Because acute hypoxemia is commonly associated with all of the respiratory disorders presented in this textbook, acute metabolic acidosis (caused by lactic acid) often further compromises the patient’s ABG status. This is because oxygenation is inadequate to meet tissue metabolism, so alternate biochemical reactions that do not use oxygen are activated. This is called anaerobic metabolism (non–oxygen-using). Lactic acid is the end-product of this process. When acidic ions move into the blood, the pH decreases. Thus, whenever 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.

As shown in Box 4-1, metabolic acid-base disturbances are subdivided into the following two categories: metabolic acidosis and metabolic alkalosis. An overview of the metabolic acid-base disturbances are presented in the following section.

Metabolic Acidosis

The presence of other acids not related to an increased Paco₂ level or renal compensation can be identified by using the isobars of the nomogram shown in Figure 4-1. The presence of other acids is verified when the calculated reading and pH level are both lower than expected for a particular Paco₂ level in terms of the absolute relationship. For example, according to the normal blood buffer line, an reading of 15 mEq/L and a pH of 7.20 would both be less than expected in a patient who has a Pco₂ of 40 mm Hg. This condition is referred to as metabolic acidosis.

Anion Gap

The anion gap is used to assess if a patient’s metabolic acidosis is caused by either (1) the accumulation of fixed acids (lactic acids, keto acids, or salicylate intoxication) or (2) an excessive loss of .

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 () ions. The normal plasma concentrations of these cations and anions are the following:

The anion gap is the calculated difference between the Na⁺ ions and the sum of the and Cl⁻ ions:

< ?xml:namespace prefix = "mml" />Aniongap=Na+−(Cl−+HCO3−)=140−(105+24)=140−129=11mEq/L

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. An elevated anion gap is frequently caused by the accumulation of fixed acids (e.g., lactic acids, keto acids, or salicylate intoxication) in the blood. Fixed acids produce H⁺ ions that chemically react with—and are buffered by—the plasma . This action causes (1) the level to fall, and (2) the anion gap to rise.

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 reverse the accumulation of the ketone acids.

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

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

Metabolic Alkalosis
ABG Changes	Example
pH: increased	7.56
Paco2: normal	44 mm Hg
: increased	27 mEq/L
Pao2: normal	94 mm Hg

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 nomogram illustrated in Figure 4-1. The presence of metabolic alkalosis is verified when the calculated and pH readings are both higher than expected for a particular Paco₂ level in terms of the absolute relationship. For example, according to the normal blood buffer line, an reading 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 Figure 4-1). This condition is known as metabolic alkalosis.

Clinically, metabolic alkalosis is seen more often than metabolic acidosis. Box 4-4 provides common causes of the metabolic abnormalities.