Arterial Blood-Gas Analysis Interpretation

and Application for the Nonchemist

Steven J. Barker, PhD, MD
Department of Anesthesiology
University of Arizona College of Medicine
Tucson, Arizona

quick responses. The purpose of this chapter is to develop

Learning Objectives:
such an algorithm and apply it to specific clinical
As a result of completing this activity, the participant
examples, wherein we shall interpret both oxygenation
will be able to
and acid-base status, and then prescribe appropriate
 Describe the mechanisms and effects of acid-base
treatment.1–7
disorders, and the patient’s abilities to correct or
compensate
 Fully interpret arterial blood gas (ABG) analysis It is useful to have a simple algorithm or
results, including their use for quantifying both
respiratory and metabolic acid-base disturbances ‘‘checklist’’ to ensure consistent, correct, and
 Treat both acute and chronic acid-base disorders
 Describe the risks, benefits, and alternatives to
quick responses.
pharmacologic therapy

Author Disclosure Information: CASE EXAMPLE

Dr. Barker has disclosed that he has an equity
You are presented with an 80-year-old, 60 kg man who has
position and stock options in Masimo, Inc. and
been found unconscious, lying on the floor of his home.
receives other material support from this company.
The general surgeons suspect peritonitis. He is brought to
the operating room for emergency laparotomy. His vital
signs are blood pressure 90/60, heart rate 120, respiratory
he interpretation and use of ABG data is a task that

T anesthesiologists must often perform under difficult

circumstances. The time is 3:00 AM; we are fatigued
and distracted by multiple other simultaneous tasks; we
need to take action on these ABG results now. In this
setting, which bears similarities to piloting an aircraft on
instruments in bad weather, it is useful to have a simple
algorithm or ‘‘checklist’’ to ensure consistent, correct, and
Supplemental digital content is available for this article. Direct URL citations
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rate 26, oxygen saturation 96%. A preoperative ABG ob-
tained from the patient while he is spontaneously breath-
ing ambient air reveals: pH ¼ 7.20, arterial carbon dioxide
tension (PaCO2) ¼ 25, arterial oxygen tension (PaO2) ¼ 75,
HCO3 ¼ 8. Should you give sodium bicarbonate? How
much? What else do you change?
OXYGENATION
The first step in evaluating the PaO2 is to calculate the
alveolar oxygen tension (PAO2), using the alveolar gas
equation:
PA O2 ¼ FI O2 ðPB  PH2O Þ  ð1 / RQÞPa CO2 ð1Þ

1
2 Barker
where FIO2 ¼ inspired oxygen fraction, PB ¼ barometric
pressure, PH2O ¼ water pressure, and RQ ¼ respiratory
quotient.
For a normothermic (371C) patient, breathing room
air at sea level:
PA O2 ¼ 0:21ð760  47Þ  ð1:25Þ 40
¼ 99:7 mmHg
The alveolar PO2 at sea level is roughly 100 mmHg.
Next, calculate the ratio of PaO2/PAO2. Do not bother with
the alveolar-arterial difference, sometimes erroneously re-
ferred to as the ‘‘gradient.’’ The normal value of this dif-
ference is a function of the FIO2, whereas the normal or
healthy value of the ratio is roughly 0.85 at any FIO2.
Thus, a ‘‘healthy’’ PaO2 during normocapnia at sea level is
approximately 0.85 PAO2 ¼ 85 mmHg.
Now, just for fun, let’s go to the top of Mount Everest,
elevation 29,035 ft, barometric pressure 247 mmHg. Here
is how some humans have actually made it to the summit
without supplemental oxygen:
PA O2 ¼ FI O2 ðPB  PH2O Þ  ð1 / RQÞPa CO2
¼ 0:21ð247  47Þ  ð1:25Þ7:5
¼ 32:6 mmHg
Yes, your PaCO2 on top of Everest is 7.5 mmHg. Talk
about hyperventilation!
Furthermore, your predicted PaO2, using the PaO2/PAO2
ratio of 85%, will be 0.85  32.6 ¼ 27.7 mmHg. In la-
boratory simulations of Everest conditions, this is almost
exactly the resulting PaO2 value. If you are wondering why
the PaCO2 is so low, try repeating this calculation for
normocapnia.
The treatment of hypoxemia is beyond the scope of this
chapter, but in general the tools available in the operating
room fall into 3 categories.
1. Ventilator adjustment: FIO2, positive end-expiratory
pressure, ventilatory mode (reverse inspiratory/expira-
tory pressure, high-frequency ventilation, etc.).
2. Drugs: Diuretics, bronchodilators, PDE-5 inhibitors
(tadalafil [Cialis] is now used for high altitude
pulmonary edema).
3. Procedures: Chest tube, bronchoscopy, etc.
ACID-BASE BALANCE
At a concentration of 0.00004 mEq/L, the hydrogen ion is
one of the least plentiful electrolytes in the extracellular
fluid (ECF). Nevertheless, because of its small size and
positive charge, H þ must be regulated within narrow
limits, or we die. The H þ concentration, denoted [H þ ],
varies between 0.1 Eq/L (gastric) and 0.000000008 Eq/L
(duodenal) within the body (see Supplemental Digital
Content 1, http://links.lww.com/ASA/A82). We commonly
use a logarithmic scale to measure it: pH ¼ log[H þ ]. The
rather wide concentration range above is thus converted to
a pH range between 1.0 and 8.1. An H þ concentration in
the ECF that is either too high (low pH: acidemia) or
too low (high pH: alkalemia) will cause potentially
fatal cardiovascular disturbances, including decreased
myocardial contractility, vasomotor instability, cardiac
arrhythmias, and abnormal enzyme function. The body uses
several defenses against pH changes, but to understand these
we must first review some basics of acid-base chemistry.
Acids, Bases, Buffers
Simply put, an acid is a chemical compound that can give
up a free H þ ion in aqueous solution; a base is a compound
that can accept a free H þ ion. This equilibrium is
represented as:
HA $ H þ þ A  ð2Þ
where HA is an acid, and A is called the ‘‘conjugate base.’’ A
‘‘strong acid’’ is one that shifts this equilibrium to the right,
producing large amounts of H þ . A weak acid shifts the bal-
ance to the left, producing less free H þ . Similar definitions
apply for strong and weak bases. If an acid is strong, then its
conjugate base is by definition weak, and vice versa. There
will be more about this concept later in the chapter.
Simply put, an acid is a chemical compound
that can give up a free H þ ion in aqueous
solution; a base is a compound that can
accept a free H þ ion.
The strength of the acid HA can be quantified by the
ratio of concentrations of the two sides of equation 2:
 
K ¼ H þ ½A   / ½HA ð3Þ
In this and the following equations, square brackets
denote concentrations. K is called the ‘‘dissociation con-
stant’’ and equation 3 is referred to as the ‘‘law of mass
action.’’ A large value of K implies a strong acid and weak
conjugate base. Taking the logarithms of both sides
of equation 3 and rearranging, we find:
log K ¼ log½H þ  þ logð½A   / ½HAÞ
 log½H þ  ¼  log K þ logð½A   / ½HAÞ ð4Þ
pH ¼ pK þ logð½A   / ½HAÞ
In this last step, we have inserted the definitions
pH ¼ log [H þ ] and pK ¼ log K, yielding the familiar
Henderson-Hasselbalch equation. This equation is simply
a logarithmic form of the law of mass action, or definition
of the dissociation constant.
The most important acid-base equilibrium in the body is
that of carbon dioxide and water:
H2 O þ CO2 $ H2 CO3 $ H þ þ HCO
3 ð5Þ
Arterial Blood-Gas Analysis Interpretation
The pK of this reaction is 6.1, making carbonic a rather
weak acid. Henderson-Hasselbalch (equation 4) for this
reaction becomes:
  from the urine, effectively ‘‘pump’’ bicarbonate from the
pH ¼ pK þ log HCO 3 / ½H2 C 3 
  ð6Þ
pH ¼ 6:1 þ log HCO 3 / ð0:03 Pa CO2 Þ
We do not routinely measure blood carbonic acid
(H2CO3) concentration, therefore in the last step we have
substituted the empirical formula: (H2CO3) ¼ 0.03
PaCO2. Equation 6 states a simple and important fact
about acid-base physiology: the pH is determined by the
ratio of the bicarbonate concentration to the PaCO2. We
shall see that this is a key feature of the body’s defenses
against pH changes. Inserting normal blood values
into equation 6:
 a plot of the plasma pH versus bicarbonate, shown
pH ¼ 6:1 þ log 24 / ð0:03  40Þ ¼ 7:4
It is always reassuring when a new formula gives the
correct answer in a known situation.
Body Acids, Buffers, and Defenses
Acids are formed in two ways in the human body. Re-
spiratory acid is formed by the combination of carbon di-
oxide (product of aerobic metabolism) and water, as
shown in equation 5. All other acids are called ‘‘metabolic
acid.’’ The latter include lactic acid produced by anaerobic
metabolism, and sulfuric, hydrochloric, and phosphoric
acids. We have already noted that carbonic or respiratory
acid is a weak acid. In fact, in the normal ECF equilibrium
(equation 5), it takes 800,000 molecules of CO2 to pro-
duce 800 molecules of H2CO3, which in turn produce
one free H þ ion (see Supplemental Digital Content 2,
http://links.lww.com/ASA/A83). This brings us to the
body’s first line of defense against acid ‘‘invasion’’: a system
of ‘‘buffers.’’ A buffer is something that effectively ex-
changes a strong acid for a weaker one, as in the following.
H þ þ Cl  þ NaHCO3 $ H2 CO3 þ NaCl ð7Þ
As this reaction moves to the right, the sodium bicarbo-
nate ‘‘trades’’ the very strong hydrochloric acid for the very
weak H2CO3. A buffer solution thus consists of a weak acid
(H2CO3) and a salt of the conjugate base (NaHCO3), and it
uses this combination to trade strong acid for weak acid,
thereby reducing the amount of free H þ released. Bi-
carbonate, the example we have just considered, is the most
important buffer in the body. Other buffers include pro-
teins, phosphate, and ammonia. Proteins are significant for
two reasons: (1) they are very plentiful in the intracellular
milieu (75% of total body buffering power), and (2) they
can buffer both metabolic and respiratory acid, as shown
below for the protein hemoglobin.
HCl þ KHb $ HHb þ KCl ð8aÞ
H2 CO3 þ KHb $ HHb þ KHCO3 ð8bÞ
Of course, hemoglobin has yet another trick up its sleeve
because it can also bind carbon dioxide. There are two
other front-line defenses against pH changes: respiratory
3
and renal control. The lungs, driven by medullary chemo-
receptors, regulate the PaCO2 level. The kidneys, by ac-
tively excreting H þ into the urine and reclaiming Na þ
urine back into the blood. The kidneys excrete a normal
daily metabolic acid load of 50 mM at a urine pH of 6.0,
and healthy kidneys can handle as much as 10 times that
amount by reducing the urine pH to 4.5. Looking again at
equation 6, the lungs control the denominator and the kid-
neys control the numerator of the ratio that determines pH.
Evaluation of Acid-base Balance
Given the above background on acids, bases, buffers, and
the body’s pH controls, we are now ready to evaluate and
treat the acid-base balance. The first step in this process is
in Figure 1.
Choosing a location on this graph fixes the values of pH
and HCO 3 , and equation 6 (Henderson-Hasselbalch) then
determines the corresponding value of PaCO2. The curves
labeled 20, 30, 40, etc. are lines of constant PaCO2, called
‘‘isobars.’’ They are solutions of the Henderson-Hassel-
balch equation. The normal acid-base status of pH ¼ 7.4,
HCO 3 ¼ 24, PaCO2 ¼ 40 corresponds to the center of the
graph. Note the straight line passing through the center
with a slight negative slope, labeled ‘‘10sl.’’ This ‘‘buffer
line’’ is the path followed by a purely respiratory
disturbance—either hypercapnia or hypocapnia with no
metabolic disturbance at all. The slope of the buffer line
represents the body’s chemical buffering power, and its
units are called ‘‘Slykes,’’ named after the chemist Van
Slyke. The normal slope is actually nearer to 12, but a
value of 10 is easier for the calculations that follow and is
close enough for our purposes.
The two stippled regions along the buffer line, labeled
‘‘acute,’’ are the areas in which an acute, uncompensated
respiratory disturbance will lie. Take for example an acute
respiratory acidosis—the stippled area to the left of the
center of the graph. Referring again to equation 6, we see
that the body’s compensation for this acute hypercapnia will
be to increase the HCO 3 level (the kidneys’ job) to bring the
ratio back toward normal, thus correcting the pH. This
‘‘metabolic compensation’’ may take several days to com-
plete, and it will move us from the ‘‘acute’’ stippled area
upward along the appropriate isobar into the ‘‘chronic’’
stippled area in the upper-left quadrant. Thus, a quick ex-
amination of the pH-bicarbonate diagram not only tells us
that our patient has a respiratory acidosis, but also evaluates
the metabolic compensation. The same reasoning applies to
both acute and compensated respiratory alkalosis, shown in
the lower right quadrant of the diagram.
A pure metabolic acidosis, without compensation,
would follow the PaCO2 isobar down into the lower left
quadrant of Figure 1. Metabolic acidosis manifests as a
decrease in HCO 3 , so the body’s compensatory response is
to decrease the denominator of the ratio in equation 6, that
is, to lower the PaCO2. This compensatory hyperventilation
4 Barker
FIGURE 1. The pH-bicarbonate diagram.
takes us into the stippled area in the lower left quadrant
of Figure 1. Similarly, the respiratory compensation for
metabolic alkalosis is hypoventilation, as indicated by the
stippled area of the upper right quadrant. Because hypo-
ventilation will eventually cause hypoxemia, this compen-
sation is less effective, as indicated by the slopes of the two
stippled areas.
Instead of referring to the stippled areas of Figure 1, we
can also use empirical ‘‘rules of thumb’’ to predict com-
pensation. Remember that the body’s response to pH im-
balance is to restore the ratio of HCO 3 /PaCO2 toward its
normal value of 24/40 ¼ 0.6, because this ratio controls the
pH (equation 6). The following rules are based on clinical
data, and are only approximate predictors.
1. Metabolic compensation for a primary respiratory
disturbance.
Respiratory acidosis: For every 10 mmHg rise in
PaCO2 above 40:
Acute: HCO 3 increases by 1 mEq/L.
Chronic (compensated): HCO 3 increases by
4 mEq/L.
Respiratory alkalosis: For every 10 mmHg fall in
PaCO2 below 40:
Acute: HCO 3 decreases by 2 mEq/L.
Chronic (compensated): HCO 3 decreases by
3 mEq/L.
2. Respiratory compensation for a primary metabolic
disturbance.
Metabolic acidosis with maximum compensation:
PaCO2 ¼ 1.5[HCO 3 ] þ 8.
Metabolic alkalosis with maximum compensation:
PaCO2 ¼ 0.7[HCO 3 ] þ 20.
One additional tool is required to quantify the metabolic
disturbance: ‘‘base excess’’ or BE. The definition of BE is as
follows. ‘‘Titrate the pH to 7.40 by varying only PaCO2. BE
is the difference between the resulting HCO 3 at the end of
this titration and the normal value of 24 mEq/L.’’ It is easier
to understand this definition by using an example on the
pH-bicarbonate diagram, Figure 1. We are given the fol-
lowing ABG results: pH ¼ 7.1, PaCO2 ¼ 32, HCO 3 ¼ 10.
To find BE, we titrate back to a pH of 7.4 by varying only
PaCO2. This titration follows a line parallel to our ‘‘buffer
line.’’ Because the slope of this line is 10 Slykes, and the
pH changes by 0.3 units (from 7.1 to 7.4), the bicarbonate
will decrease by 3 mEq/L (0.3 times 10), reaching a new
value of 7 (10 minus 3) at the head of the arrow. The BE is
thus 724, or 17. A negative BE is also called a ‘‘base
deficit,’’ therefore our blood gas shows a base deficit of 17.
You can now calculate BE in your head if you know the pH
and the bicarbonate. Should we treat this base deficit, and if
so, how? This is our next topic.
There are many possible causes of metabolic acidosis, but
in the operating room it is most often the result of inadequate
oxygen delivery to various organs and tissues. It is the direct
result of anaerobic metabolism, and therefore manifests as a
lactic acidosis. The ‘‘anion gap,’’ defined as [Na þ ] þ [K þ ]
 [Cl]  [HCO 3 ], is above the normal range of 8 to 12.
Similar to most physiological disorders, the ideal prescrip-
tion is to ‘‘treat the underlying cause.’’ If the cause of the
lactic acidosis is tissue hypoperfusion resulting from hypo-
volemic shock, correcting the patient’s volume status may be
all that is needed to restore perfusion and rapidly correct the
acidemia. In contrast, a very low pH (7.1 would fall in that
category) will depress cardiac function significantly, and the
heart may not be able to generate sufficient cardiac output to
restore organ perfusion while the pH remains so low. This is
a judgment call that we must make on a case-by-case basis. If
we decide that the pH must be at least partially corrected
before the heart can do its job, here is how we treat it.
Treatment of Acid-base Disorders
The first step in treating a metabolic acidosis is to
determine the ‘‘bicarbonate deficit.’’ That is, how much
bicarbonate would be required to restore the ECF to its
normal value of 24 mEq/L? The bicarbonate deficit is
simply the base deficit times the weight in kg, times the
ECF fraction. The ECF comprises the following fraction of
body weight:
ECF fraction ¼ 0:5 ðpremature neonateÞ
0:4 ðterm neonateÞ
0:3 ð2-year-oldÞ
0:25 ðolder childÞ
0:2 ðadultÞ
Arterial Blood-Gas Analysis Interpretation
Thus, if the patient above with a BE of 14 is a 70 kg adult,
the bicarbonate deficit will be 14  70  0.2, or 196 mEq.
Treatment of metabolic acidosis with sodium bicarbo-
nate (NaHCO3) is not a risk-free therapy. First, ‘‘bicarb’’
does not make metabolic acid disappear; it effectively
converts it to respiratory acid (see equation 7). The
additional CO2 created by this exchange must be removed
by increased ventilation. Furthermore, full strength sodium
bicarbonate is a hyperosmolar solution (six times plasma
osmolarity) and can thereby cause brain hemorrhage, par-
ticularly in children. Overtreatment can cause alkalemia,
which is just as dangerous as acidemia (see Supplemental
Digital Content 3, http://links.lww.com/ASA/A84). It is also
unnecessary to administer bicarbonate as a bolus; slower ad-
ministration reduces the peak increase in PaCO2. Therefore,
the common recommendation is to give about half the
amount of total bicarbonate deficit, increase ventilation to
compensate for the additional CO2, and reevaluate in roughly
30 minutes. There are two approved alternatives to sodium
bicarbonate: THAM (tris-hydroxymethyl aminomethane)
and Carbicarb, which is an equimolar mixture of sodium
bicarbonate and sodium carbonate (Na2CO3). Both can
buffer metabolic acid with little or no increase in CO2, but
neither has been shown to have any outcomes advantage
over conventional treatment.
Evaluation/Treatment Algorithm
We conclude by encapsulating the above approach to acid-
base evaluation into a simple four-step algorithm, which
we shall apply to our original case example.
Four-step evaluation of acid-base status (see Supple-
mental Digital Content 4, http://links.lww.com/ASA/A85):
1. Evaluate the pH: if pH 4 7.45, patient has alkalemia; if
pH o 7.35, patient has acidemia.
2. Evaluate the PaCO2: if PaCO2 4 45, patient has respiratory
acidosis; if PaCO2 o 35, patient has respiratory alkalosis.
3. Find the BE, using the 10 Slyke approximation: if BE
4 þ 2, patient has metabolic alkalosis; if BE o 2,
patient has metabolic acidosis.
4. Evaluate compensation: determine predicted maximum
compensation by nonprimary variable, using empirical
rules or referring to stippled areas of Figure 1.
Finally, let us use this algorithm to evaluate and treat our
original patient, a 60 kg man with a blood-gas analysis
showing 7.20/25/75/8 (pH/PaCO2/PaO2/HCO
3 ).
1. The patient is acidemic (pH ¼ 7.20).
2. The patient has respiratory alkalosis (PaCO2 ¼ 25).
3. Calculate BE (see Figure 1): titration to pH ¼ 7.4
requires pH to change by 7.4 to 7.2 ¼ 0.2; HCO
3
therefore decreases by 0.2  10 ¼ 2; new HCO 3 ¼
82 ¼ 6; BE ¼ 624 ¼ 18.
4. Evaluate compensation: Maximum predicted respiratory
compensation for this metabolic acidosis is PaCO2 ¼
1.5[HCO 3 ] þ 8¼(1.58)þ8 ¼ 20 mmHg. The patient’s
5
actual PaCO2 is 25 mmHg. Given his physical status, this
patient is nearly at maximum compensation.
Treatment: The amount of bicarbonate required to fully
correct the patient’s BE of 18 is:
NaHCO3 ¼ 60 kg  0:2  18 mEq / L ¼ 216 mEq
A reasonable therapy is to give half this amount, or two
ampoules (55 mEq per ampoule), increase mechanical
ventilation, and obtain another ABG measurement in 15 to
30 minutes.
The simplest interpretation of PaO2 comes
from calculating the ratio of PaO2/PAO2 (using
the alveolar gas equation) and comparing the
result with the normal value of 0.85.
CONCLUSIONS
Interpretation of ABG data is straightforward if we follow a
prescribed algorithm such as the one presented in this lecture.
The simplest interpretation of PaO2 comes from calculating
the ratio of PaO2/PAO2 (using the alveolar gas equation) and
comparing the result with the normal value of 0.85. To
evaluate the acid-base status, simply follow the four-step al-
gorithm, which separates respiratory from metabolic dis-
turbance and evaluates compensation. The pH-bicarbonate
diagram (Figure 1) is an excellent tool for keeping all of these
factors in perspective, and understanding the results of
treatment. Finally, if the patient has a severe metabolic
acidosis that may require treatment, calculate the bicarbo-
nate deficit as shown above. I do not recommend an arbitrary
BE threshold for treatment with sodium bicarbonate; that
decision should take into account all aspects of the patient’s
clinical status. However, once the decision to treat has been
made, it is usually wise to give about half of the bicarbonate
deficit as the initial dose, increase or monitor ventilation, and
then reevaluate acid-base status a short time later. Of course,
there are exceptions to every rule—that is why you spent all
those years in training. However, these guidelines should
serve you well as a starting point, and they are simple enough
that even I can follow them at 3:00 AM.
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