3: Blood Gas and Acid-Base Analysis

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CHAPTER 3 Blood Gas and Acid-Base Analysis

Matthew D. Coleman, MD, Steven T. Morozowich, DO, FASE

1 What are the normal arterial blood gas values in a healthy patient breathing room air at sea level?

TABLE 3-1 Arterial Blood Gas Values at Sea Level

pH	7.36–7.44
PaCO₂	33–44 mm Hg
PaO₂	75–105 mm Hg
HCO₃	20–26 mmol/L
Base deficit	+3 to −3 mmol/L
SaO₂	95%–97%

2 What information does arterial blood gas provide about the patient?

Arterial blood gas (ABG) provides an assessment of the following:

Oxygenation (PaO₂). The PaO₂ is the amount of oxygen dissolved in the blood and therefore provides initial information on the efficiency of oxygenation.

Ventilation (PaCO₂). The adequacy of ventilation is inversely proportional to the PaCO₂ so that, when ventilation increases, PaCO₂ decreases, and when ventilation decreases, PaCO₂ increases.

Acid-base status (pH,

, and base deficit [BD]). A plasma pH of >7.4 indicates alkalemia, and a pH of <7.35 indicates acidemia. Despite a normal pH, an underlying acidosis or alkalosis may still be present.

Oxygenation and ventilation were discussed in Chapter 2 and acid-base status will be the area of focus for this chapter.

3 How is the regulation of acid-base balance traditionally described?

Acid-base balance is traditionally explained using the Henderson-Hasselbalch equation, which states that changes in and PaCO₂ determine pH as follows:

To prevent a change in pH, any increase or decrease in the PaCO₂ should be accompanied by a compensatory increase or decrease in the . The importance of other physiologic nonbicarbonate buffers was later recognized and partly integrated into the BD and the corrected anion gap, both of which aid in interpreting complex acid-base disorders.

KEY POINTS: Major Causes of an Anion Gap Metabolic Acidosis

Elevated anion gap metabolic acidosis is caused by accumulation of unmeasured anions:

Toxins (ethanol, methanol, salicylates, ethylene glycol, propylene glycol)

4 What is the physiochemical approach (Stewart model) for the analysis of acid-base balance?

In 1981 Stewart proposed a conceptually different model for analyzing acid-base disorders. His method used two important principles of solution chemistry: the conservation of mass, and electroneutrality. He described three independent variables that determine the pH in the extracellular fluid. These variables are the strong ion difference (SID), the PaCO₂, and the concentration of weak acids (A_ToT). The SID is calculated as follows with the normal value given:

The concentration of other anions consists of protiens and weak acids. The primary weak acids in the plasma are proteins (primarily albumin), phosphate, and sulfate. In pathologic states other weak acids might include lactate, ketones, or toxins. As anions accumulate, the SID decreases, resulting in an acidosis. If the balance shifts to a predominance of cations, an alkalosis develops. Stewart developed several equations to show that these parameters were independent variables and showed that and pH were dependent on the three independent variables, contrary to the Henderson-Hasselbalch and standard base excess approaches. This model has been most useful in interpreting complex acid-base disorders in patients with mixed acid-base disorders and disorders that were not observable with conventional acid-base analysis such as hypoalbuminemia and hyperchloremic metabolic acidosis.

5 What are the common acid-base disorders and their compensation?

TABLE 3-2 Major Acid-Base Disorders and Compensatory Mechanisms *

Primary Disorder	Primary Disturbance	Primary Compensation
Respiratory acidosis	↑ PaCO₂	↑ HCO₃
Respiratory alkalosis	↓ PaCO₂	↓ HCO₃
Metabolic acidosis	↓ HCO₃	↓ PaCO₂
Metabolic alkalosis	↑ HCO₃	↑ PaCO₂

* Primary compensation for metabolic disorders is achieved rapidly through respiratory control of CO₂, whereas primary compensation for respiratory disorders is achieved more slowly as the kidneys excrete or absorb acid and bicarbonate. Mixed acid-base disorders are common.

6 How do you calculate the degree of compensation?

TABLE 3-3 Calculating the Degree of Compensation *

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Primary Disorder	Rule
Respiratory acidosis (acute)	increases 0.1 × (PaCO₂ − 40) pH decreases 0.008 × (PaCO₂ − 40)
Respiratory acidosis (chronic)	increases 0.4 × (PaCO₂ − 40)
Respiratory alkalosis (acute)	decreases 0.2 × (40 − PaCO₂) pH increases 0.008 × (40 − PaCO₂)
Respiratory alkalosis (chronic)	decreases 0.4 × (40 − PaCO₂)
Metabolic acidosis

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