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 *

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	PaCO₂ decreases 1 to 1.5 × (24 − )
Metabolic alkalosis	PaCO₂ increases 0.25 to 1 × (HCO₃⁻ − 24)

* Compensatory mechanisms never overcorrect for an acid-base disturbance; when ABG analysis reveals apparent overcorrection, the presence of a mixed disorder should be suspected.

Data from Schrier RW: Renal and electrolyte disorders, ed 3, Boston, 1986, Little, Brown.

7 What are the common causes of respiratory acid-base disorders?

Respiratory alkalosis: Sepsis, hypoxemia, anxiety, pain, and central nervous system lesions

Respiratory acidosis: Drugs (residual anesthetics, residual neuromuscular blockade, benzodiazepines, opioids), asthma, emphysema, obesity-hypoventilation syndromes, central nervous system lesions (infection, stroke), and neuromuscular disorders

8 What are the major buffering systems of the body?

Bicarbonate, albumin, intracellular proteins, and phosphate are the major buffering systems. The extracellular bicarbonate system is the fastest to respond to pH change but has less total capacity than the intracelluar systems, which account for 60% to 70% of the chemical buffering of the body. Hydrogen ions are in dynamic equilibrium with all buffering systems of the body. CO₂ molecules also readily cross cell membranes and keep both intracellular and extracellular buffering systems in dynamic equilibrium. In addition, CO₂ has the advantage of excretion through ventilation.

9 What organs play a major role in acid-base balance?

The lungs are the primary organ involved in rapid acid-base regulation. Carbon dioxide produced in the periphery is transported to the lung, where the low carbon dioxide tension promotes conversion of bicarbonate to carbon dioxide, which is then eliminated. The respiratory regulatory system can increase and decrease minute ventilation to compensate for metabolic acid-base disturbances.

The kidneys act to control acid-base balance by eliminating fixed acids and to control the elimination of electrolytes, bicarbonate, ammonia, and water.

The liver is involved in multiple reactions that result in the production or metabolism of acids.

The gastrointestinal tract secretes acidic solutions in the stomach, and absorbs water and other electrolytes in the small and large intestines. This can have a profound effect in acid-base balance.

10 What is meant by pH?

pH is the negative logarithm of the hydrogen ion concentration ([H⁺]). pH is a convenient descriptor for power of hydrogen. Normally the [H⁺] in extacellular fluid is 40 nmol/L, a very small number. By taking the negative log of this value we obtain a pH of 7.4, a much simpler way to describe [H⁺]. The pH of a solution is determined by a pH electrode that measures the [H⁺].

11 Why is pH important?

pH is important because hydrogen ions react highly with cellular proteins, altering their function. Avoiding acidemia and alkalemia by tightly regulating hydrogen ions is essential for normal cellular function. Deviations from normal pH suggest that normal physiologic processes are in disorder and the causes should be determined and treated.

14 Is the HCO₃ value on the arterial blood gas the same as the CO₂ value on the chemistry panel?

No. The is a calculated value, whereas the CO₂ is a measured value. Because the CO₂ is measured, it is thought to be a more accurate determination of . The ABG is calculated using the Henderson-Hasselbalch equation and the measured values of pH and PaCO₂. In contrast, a chemistry panel reports a measured serum carbon dioxide content (CO₂), which is the sum of the measured bicarbonate () and carbonic acid (H₂CO₃). The CO₂ is viewed as an accurate determination of because the concentration in blood is about 20 times greater than the H₂CO₃ concentration; thus H₂CO₃ is only a minor contributor to the total measured CO₂.

15 What is the base deficit? How is it determined?

The BD (or base excess) is the amount of base (or acid) needed to titrate a serum pH back to normal at 37° C while the PaCO₂ is held constant at 40 mm Hg. The BD represents only the metabolic component of an acid-base disorder. The ABG analyzer derives the BD from a nomogram based on the measurements of pH, , and the nonbicarbonate buffer hemoglobin. Although the BD is determined in part by the nonbicarbonate buffer hemoglobin, it is criticized because it is derived from a nomogram and assumes normal values for other important nonbicarbonate buffers such as albumin. Thus in a hypoalbuminemic patient the BD should be used with caution since it may conceal an underlying metabolic acidosis.

16 What is the anion gap?

The anion gap (AG) estimates the presence of unmeasured anions. Excess inorganic and organic anions that are not readily measured by standard assays are termed unmeasured anions. The AG is a tool used to further classify a metabolic acidosis as an AG metabolic acidosis (elevated AG) or a non-AG metabolic acidosis (normal AG). This distinction narrows the differential diagnosis. The AG is the difference between the major serum cations and anions that are routinely measured:

A normal value is 12 mEq/L ± 4 mEq/L. When unmeasured acid anions are present, they are buffered by , thereby decreasing the concentration. According to the previous equation, this decrease in will increase the AG. Keep in mind that hypoalbuminemia has an alkalinizing effect that lowers the AG, which may mask an underlying metabolic acidosis caused by unmeasured anions. This pitfall can be avoided by correcting the AG when evaluating a metabolic acidosis in a hypoalbuminemic patient:

KEY POINTS: Major Causes of a Nonanion Gap Metabolic Acidosis

Nonanion gap metabolic acidosis results from loss of Na⁺ and K⁺ or accumulation of Cl⁻. The result of these processes is a decrease in :

Iatrogenic administration of hyperchloremic solutions (hyperchloremic metabolic acidosis)

Alkaline gastrointestinal losses

Renal tubular acidosis

Ureteric diversion through ileal conduit

Endocrine abnormalities

17 List the common causes of a metabolic alkalosis

Metabolic alkalosis is commonly caused by vomiting, volume contraction (diuretics, dehydration), alkali administration, and endocrine disorders.

18 List the common causes of elevated and nonelevated anion gap metabolic acidosis

Nonelevated AG metabolic acidosis is caused by iatrogenic administration of hyperchloremic solutions (hyperchloremic metabolic acidosis), alkaline gastrointestinal losses, renal tubular acidosis (RTA), or ureteric diversion through ileal conduit. Excess administration of normal saline is a cause of hyperchloremic metabolic acidosis.

Elevated AG metabolic acidosis is caused by accumulation of lactic acid or ketones, poisoning from toxins (e.g., ethanol, methanol, salicylates, ethylene glycol, propylene glycol) or uremia.

19 Describe a stepwise approach to acid-base interpretation

Check the pH to determine acidemia or alkalemia.

If the patient is breathing spontaneously, use the following rules:

If the PCO₂ is increased and the pH is <7.35, the primary disorder is most likely a respiratory acidosis.

If the PCO₂ is decreased and the pH >7.40, the primary disorder is most likely a respiratory alkalosis.

If the primary disorder is respiratory, determine if it is acute or chronic.

If the PCO₂ is increased and the pH is >7.40, the primary disorder is most likely a metabolic alkalosis with respiratory compensation.

If the PCO₂ is decreased and the pH <7.35, the primary disorder is most likely a metabolic acidosis with respiratory compensation.

Metabolic disorders can also be observed by analyzing the base excess or BD.

If there is a metabolic acidosis, calculate the AG and determine if the acidosis is a non-AG or AG acidosis, remembering to correct for hypoalbuminemia.

If the patient is mechanically ventilated or if the acid-base disorder doesn’t seem to make sense, check electrolytes, albumin, and consider calculating the SID. Also consider the clinical context of the acid-base disorder (e.g., iatrogenic fluid administration, massive blood resuscitation, renal failure, liver failure, diarrhea, vomiting, gastric suctioning, toxin ingestion). This may require further testing, including measuring urine electrolytes, serum, and urine osmolality, and identifying ingested toxins.

SUGGESTED READINGS

1. Casaletto J.J. Differential diagnosis of metabolic acidosis. Emerg Med Clin North Am. 2005;23:771-787.

2. Corey H.E. Stewart and beyond: new models of acid-base balance. Kidney Int. 2003;64:777-787.

3. Kraut J.A., Madias N.E. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol. 2007;2:162-174.

4. Morris C.G., Low J. Metabolic acidosis in the critically ill. Part 1. Classification and pathophysiology. Anaesthesia. 2008;63:294-301.

5. Morris C.G., Low J. Metabolic acidosis in the critically ill. Part 2. Cause and treatment. Anaesthesia. 2008;63:396-411.

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