1. What are the normal arterial blood gas values in a healthy patient breathing
room air at sea level?
See Table 3-1.
2. What information does arterial blood gas provide about the patient?
Arterial blood gas (ABG) provides an assessment of the following:
n Oxygenation (PaO2). The PaO2 is the amount of oxygen dissolved in the blood and
therefore provides initial information on the efficiency of oxygenation.
n 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.
n Acid-base status (pH, HCO3
, 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 HCO3
and PaCO2 determine pH as follows:
pH ¼ pK þ log½HCO3=ð0:03 PaCO2Þ
To prevent a change in pH, any increase or decrease in the PaCO2 should be accompanied
by a compensatory increase or decrease in the HCO3
. 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.
TABLE 3-1. A R T E R I A L B L O O D G A S V A L U E S A T S E A L E V E L
pH 7.36–7.44
PaCO2 33–44 mm Hg
PaO2 75–105 mm Hg
HCO3 20–26 mmol/L
Base deficit þ3 to 3 mmol/L
SaO2 95%–97%
24
KEY POINTS: MAJOR CAUSES OF AN ANION GAP
METABOLIC ACIDOSIS
Elevated anion gap metabolic acidosis is caused by accumulation of unmeasured anions:
n Lactic acid
n Ketones
n Toxins (ethanol, methanol, salicylates, ethylene glycol, propylene glycol)
n Uremia
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 (AToT). The SID is calculated as follows with the normal
value given:
SID ¼ ð½Na
þ þ ½K
þ þ ½Ca2þ þ ½Mg2þ Þ ð½Cl
þ ½other anions Þ ¼ 40 42 mEq=L
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 HCO3
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?
See Table 3-2.
TABLE 3-2. MA J O R A C I D - B A S E D I S O R D E R S A N D C OMP E N S A T O R Y ME C H A N I SMS *
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.
CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS 25
6. How do you calculate the degree of compensation?
See Table 3-3.
7. What are the common causes of respiratory acid-base disorders?
n Respiratory alkalosis: Sepsis, hypoxemia, anxiety, pain, and central nervous system
lesions
n 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?
n 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.
n The kidneys act to control acid-base balance by eliminating fixed acids and to control
the elimination of electrolytes, bicarbonate, ammonia, and water.
TABLE 3-3. C A L C U L A T I N G T H E D E G R E E O F C OMP E N S A T I O N *
Primary Disorder Rule
Respiratory acidosis (acute) HCO3
increases 0.1 (PaCO2 40)
pH decreases 0.008 (PaCO2 40)
Respiratory acidosis (chronic) HCO3
increases 0.4 (PaCO2 40)
Respiratory alkalosis (acute) HCO3
decreases 0.2 (40 PaCO2)
pH increases 0.008 (40 PaCO2)
Respiratory alkalosis (chronic) HCO3
decreases 0.4 (40 PaCO2)
Metabolic acidosis PaCO2 decreases 1 to 1.5 (24 HCO3
)
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.
26 CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS
n The liver is involved in multiple reactions that result in the production or metabolism
of acids.
n 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 ([Hþ]). pH is a convenient
descriptor for power of hydrogen. Normally the [Hþ] 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 [Hþ]. The pH of a solution is determined by a pH electrode that
measures the [Hþ].
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.
12. List the major consequences of acidemia.
Severe acidemia is defined as blood pH <7.20 and is associated with the following
major effects:
n Impairment of cardiac contractility, cardiac output, and the response to
catecholamines
n Susceptibility to recurrent arrhythmias and lowering the threshold for ventricular
fibrillation
n Arteriolar vasodilation resulting in hypotension
n Vasoconstriction of the pulmonary vasculature, leading to increased pulmonary vascular
resistance
n Hyperventilation (a compensatory response)
n Confusion, obtundation, and coma
n Insulin resistance
n Inhibition of glycolysis and adenosine triphosphate synthesis
n Hyperkalemia as potassium ions are shifted extracellularly
13. List the major consequences of alkalemia.
Severe alkalemia is defined as blood pH >7.60 and is associated with the following
major effects:
n Increased cardiac contractility until pH >7.7, when a decrease is seen
n Refractory ventricular arrhythmias
n Coronary artery spasm/vasoconstriction
n Vasodilation of the pulmonary vasculature, leading to decreased pulmonary vascular
resistance
n Hypoventilation (which can frustrate efforts to wean patients from mechanical ventilation)
n Cerebral vasoconstriction
CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS 27
n Neurologic manifestations such as headache, lethargy, delirium, stupor, tetany, and
seizures
n Hypokalemia, hypocalcemia, hypomagnesemia, and hypophosphatemia
n Stimulation of anaerobic glycolysis and lactate production
14. Is the HCO3 value on the arterial blood gas the same as the CO2 value on the
chemistry panel?
No. The HCO3
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 HCO3
. The ABG HCO3
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 (HCO3
) and carbonic acid (H2CO3). The CO2 is
viewed as an accurate determination of HCO3
because the HCO3
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, HCO3
, 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:
AG ¼ Na
þ ðHCO
3
þ Cl
Þ
A normal value is 12 mEq/L 4 mEq/L. When unmeasured acid anions are present, they are
buffered by HCO3
, thereby decreasing the HCO3
concentration. According to the previous
equation, this decrease in HCO3
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:
Corrected AG ¼ observed AG þ 2:5 ðnormal albumin observed albuminÞ
28 CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS
KEY POINTS: MAJOR CAUSES OF A NONANION
GAP METABOLIC ACIDOSIS
Nonanion gap metabolic acidosis results from loss of Naþ and Kþ or accumulation of Cl . The
result of these processes is a decrease in HCO3
:
n Iatrogenic administration of hyperchloremic solutions (hyperchloremic metabolic acidosis)
n Alkaline gastrointestinal losses
n Renal tubular acidosis
n Ureteric diversion through ileal conduit
n 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.
n 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.
n 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.
n Check the pH to determine acidemia or alkalemia.
n 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.
n 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.
room air at sea level?
See Table 3-1.
2. What information does arterial blood gas provide about the patient?
Arterial blood gas (ABG) provides an assessment of the following:
n Oxygenation (PaO2). The PaO2 is the amount of oxygen dissolved in the blood and
therefore provides initial information on the efficiency of oxygenation.
n 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.
n Acid-base status (pH, HCO3
, 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 HCO3
and PaCO2 determine pH as follows:
pH ¼ pK þ log½HCO3=ð0:03 PaCO2Þ
To prevent a change in pH, any increase or decrease in the PaCO2 should be accompanied
by a compensatory increase or decrease in the HCO3
. 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.
TABLE 3-1. A R T E R I A L B L O O D G A S V A L U E S A T S E A L E V E L
pH 7.36–7.44
PaCO2 33–44 mm Hg
PaO2 75–105 mm Hg
HCO3 20–26 mmol/L
Base deficit þ3 to 3 mmol/L
SaO2 95%–97%
24
KEY POINTS: MAJOR CAUSES OF AN ANION GAP
METABOLIC ACIDOSIS
Elevated anion gap metabolic acidosis is caused by accumulation of unmeasured anions:
n Lactic acid
n Ketones
n Toxins (ethanol, methanol, salicylates, ethylene glycol, propylene glycol)
n Uremia
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 (AToT). The SID is calculated as follows with the normal
value given:
SID ¼ ð½Na
þ þ ½K
þ þ ½Ca2þ þ ½Mg2þ Þ ð½Cl
þ ½other anions Þ ¼ 40 42 mEq=L
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 HCO3
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?
See Table 3-2.
TABLE 3-2. MA J O R A C I D - B A S E D I S O R D E R S A N D C OMP E N S A T O R Y ME C H A N I SMS *
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.
CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS 25
6. How do you calculate the degree of compensation?
See Table 3-3.
7. What are the common causes of respiratory acid-base disorders?
n Respiratory alkalosis: Sepsis, hypoxemia, anxiety, pain, and central nervous system
lesions
n 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?
n 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.
n The kidneys act to control acid-base balance by eliminating fixed acids and to control
the elimination of electrolytes, bicarbonate, ammonia, and water.
TABLE 3-3. C A L C U L A T I N G T H E D E G R E E O F C OMP E N S A T I O N *
Primary Disorder Rule
Respiratory acidosis (acute) HCO3
increases 0.1 (PaCO2 40)
pH decreases 0.008 (PaCO2 40)
Respiratory acidosis (chronic) HCO3
increases 0.4 (PaCO2 40)
Respiratory alkalosis (acute) HCO3
decreases 0.2 (40 PaCO2)
pH increases 0.008 (40 PaCO2)
Respiratory alkalosis (chronic) HCO3
decreases 0.4 (40 PaCO2)
Metabolic acidosis PaCO2 decreases 1 to 1.5 (24 HCO3
)
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.
26 CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS
n The liver is involved in multiple reactions that result in the production or metabolism
of acids.
n 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 ([Hþ]). pH is a convenient
descriptor for power of hydrogen. Normally the [Hþ] 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 [Hþ]. The pH of a solution is determined by a pH electrode that
measures the [Hþ].
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.
12. List the major consequences of acidemia.
Severe acidemia is defined as blood pH <7.20 and is associated with the following
major effects:
n Impairment of cardiac contractility, cardiac output, and the response to
catecholamines
n Susceptibility to recurrent arrhythmias and lowering the threshold for ventricular
fibrillation
n Arteriolar vasodilation resulting in hypotension
n Vasoconstriction of the pulmonary vasculature, leading to increased pulmonary vascular
resistance
n Hyperventilation (a compensatory response)
n Confusion, obtundation, and coma
n Insulin resistance
n Inhibition of glycolysis and adenosine triphosphate synthesis
n Hyperkalemia as potassium ions are shifted extracellularly
13. List the major consequences of alkalemia.
Severe alkalemia is defined as blood pH >7.60 and is associated with the following
major effects:
n Increased cardiac contractility until pH >7.7, when a decrease is seen
n Refractory ventricular arrhythmias
n Coronary artery spasm/vasoconstriction
n Vasodilation of the pulmonary vasculature, leading to decreased pulmonary vascular
resistance
n Hypoventilation (which can frustrate efforts to wean patients from mechanical ventilation)
n Cerebral vasoconstriction
CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS 27
n Neurologic manifestations such as headache, lethargy, delirium, stupor, tetany, and
seizures
n Hypokalemia, hypocalcemia, hypomagnesemia, and hypophosphatemia
n Stimulation of anaerobic glycolysis and lactate production
14. Is the HCO3 value on the arterial blood gas the same as the CO2 value on the
chemistry panel?
No. The HCO3
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 HCO3
. The ABG HCO3
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 (HCO3
) and carbonic acid (H2CO3). The CO2 is
viewed as an accurate determination of HCO3
because the HCO3
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, HCO3
, 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:
AG ¼ Na
þ ðHCO
3
þ Cl
Þ
A normal value is 12 mEq/L 4 mEq/L. When unmeasured acid anions are present, they are
buffered by HCO3
, thereby decreasing the HCO3
concentration. According to the previous
equation, this decrease in HCO3
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:
Corrected AG ¼ observed AG þ 2:5 ðnormal albumin observed albuminÞ
28 CHAPTER 3 BLOOD GAS AND ACID-BASE ANALYSIS
KEY POINTS: MAJOR CAUSES OF A NONANION
GAP METABOLIC ACIDOSIS
Nonanion gap metabolic acidosis results from loss of Naþ and Kþ or accumulation of Cl . The
result of these processes is a decrease in HCO3
:
n Iatrogenic administration of hyperchloremic solutions (hyperchloremic metabolic acidosis)
n Alkaline gastrointestinal losses
n Renal tubular acidosis
n Ureteric diversion through ileal conduit
n 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.
n 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.
n 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.
n Check the pH to determine acidemia or alkalemia.
n 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.
n 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.
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