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ARTERIAL BLOOD GAS AND

pH ANALYSIS
Clinical Approach and Interpretation

Peter H. Breen, MD, FRCPC

Analysis of arterial blood gas and pH is performed during anesthe-

sia or critical care medicine for three main indications:
Assessment of acid-base balance
Assessment of pulmonary oxygenation of arterial blood
Assessment of alveolar ventilation by measurement of arterial blood
Pco,
Total physiologic and alveolar dead spaces are evaluated by com-
paring the alveolar Pco, (assumed equal to arterial Pco.) with the mixed
expired and mixed alveolar (usually end-tidal) Pco21 respectively.
This article provides a clinical approach and interpretation of arte-
rial blood gas and pH analysis. Arterial blood gas and pH analysis
involves many abbreviations (Appendix).

ARTERIAL BLOOD ACID-BASE BALANCE

Overview

Acid-base balance normally is measured and analyzed from arterial

blood samples. The data, however, are interpreted clinically to apply to
This work was supported by Public Health Service Research Grant HL-42637 from
the National Heart, Lung, and Blood Institute (Bethesda, MD), and by Public Health
Service Research Grant MOl RR00827 from the National Center for Research Resources
(Bethesda, MD).

From the Department of Anesthesiology, College of Medicine, University of California,

Irvine, University of California Irvine Medical Center, Orange, California

ANESTHESIOLOGY CLINICS OF NORTH AMERICA

VOLUME 19 • NUMBER 4 • DECEMBER 2001 885

886 BREEN

the entire volume of extracellular fluid. Acid-base balance depends on

three independent factors:
Respiratory component, in which pulmonary ventilation results in
carbon dioxide elimination and controls the arterial Pco, (Paco.z)
Nonvolatile weak acid buffers (predominantly hemoglobin)
Metabolic component, primarily affected by tissue metabolism and
gastrointestinal system and is regulated by the kidneys
For the student of acid-base balance, most confusion stems from
explanations and interpretations of the metabolic component. The four
major presentations of the metabolic component are standard base ex-
cess, strong ion difference between plasma strong cations and anions,
bicarbonate ion (HC03·), and anion gap ([Na+] +[K]+ - [CI-] -
[HC03-]).
Schlichtig et aP5 provide in-depth derivations, explanations, and
comparisons of the metabolic components of acid-base balance. Readers
interested in a more clinical and physiologically based review of acid-
base disturbances and their analyses are referred to the classic landmark
review by Narins and Emmett." A shorter, more practical, clinically
based approach is offered by Haber," Additional excellent reviews are
recommended for those seeking better understanding of the acid-base
system.* This section summarizes only the practical graphic approach of
acid-base balance presented by Schlichtig et aP5.36 because its simplicity
and utility appeals to clinicians.
The final result of acid-base balance is the regulation of the concen-
tration of hydrogen ions in blood (normal [H+] = 40 nM/L). The [H+]
normally is presented as pH, where pH equals the negative logarithm
(base 10) of [H+]. Accordingly, the normal [H+] of 40 nM/L corresponds
with a pH of 7.40. During acidemia, [H"] increases and pH decreases.
During alkalemia, [H +] decreases and pH increases. The use of logarith-
mic notation of blood acid-base balance is partly because the effective
range of a buffer generates a characteristic S shape when acid or base
concentration is plotted against pH but does not when plotted against
[H+]. The significance of a logarithmic scale for [H+] must be recognized.
Analogous to the Richter scale for earthquake intensity, an integer in-
crease in pH (e.g., 7-8) indicates a ten-fold reduction in [H+]. A doubling
of [H+] (e.g., 40-80 nM/L) decreases the pH by 0.3 (e.g., 7.40-7.10).
Acid-base balance is regulated by the respiratory center (i.e., respira-
tory component) and the kidney (i.e., metabolic component). In this
article, the effects of changing dissolved carbon dioxide in blood (chang-
ing Pco, by changing alveolar ventilation), the metabolic effects on acid-
base balance, and the buffer capacity of blood and extracellular fluid are
examined.

Respiratory Component (Peo 2)

Dissolved carbon dioxide is measured as the partial pressure of
carbon dioxide in arterial blood (Paco.z). The concentration of dissolved
'References 12, 18, 19, 24, 26, 28, and 32.
 ARTERIAL BLOODGAS AND pH ANALYSIS 887

carbon dioxide linearly is related to Peo2 by its solubility ([dissolved

CO 2] = Pco-: solco; whereby solco, = 0.0306 mM/mm Hg). Carbon
dioxide reacts reversibly with water to generate carbonic acid (H 2C03) ,
which immediately dissociates into hydrogen and bicarbonate ions:
CO2 + H 20 H H 2C03 H H+ + HC03 (Equation 1)

The hydration of carbon dioxide is rapid in red blood cells because they
contain the enzyme, carbonic anhydrase. According to the law of mass
action, the dissociation of carbonic acid may be written as:
(Equation 2)
whereby K is the dissociation constant.
It is almost impossible to measure the concentration of undissoci-
ated carbonic acid in solution. The amount of dissolved carbon dioxide
easily is measured, however, and the amount of undissociated carbonic
acid is proportional to the amount of dissolved carbon dioxide. Accord-
ingly, by taking the negative logarithm of both sides of equation 2, by
substituting Peo2 • solco, for H 2C03 and solving for pH, the familiar
Henderson-Hasselbalch equation can be derived:
pH = pK' + log ([HC03 - ]I [Solco, . Peo2]) =
6.1 + log ([HC03 - ]I [0.0306· Peo2]) (Equation 3)

The Henderson-Hasselbalch equation assumes that all dissolved

carbon dioxide exists as carbonic acid, although only 0.33% actually is
hydrated, and thepK' is 6.1. The true pK of carbonic acid is approxi-
mately 3.1.
High Pco, (e.g., alveolar hypoventilation during chronic obstructive
pulmonary disease) causes respiratory acidosis by driving equation 1 to
the right. In the Henderson-Hasselbalch equation (equation 3), increased
Pco, decreases the log expression and decreases pH. Pco, directly is
measured in blood gas and pH analyzer machines with a carbon dioxide
electrode.

Metabolic Component

Changes to the metabolic component result from the addition of

strong acids or bases to the acid-base system, where strong acid or base
means always ionized (i.e, always dissociated from H+ or OH-). As
opposed to lung excretion for carbon dioxide, strong acids or bases
require excretion by the kidney (e.g., inorganic acids [e.g., HCl] or
bases [e.g., NaOH, KOH]) or metabolism (organic acids [e.g., lactate',
acetoacetate', and P-hydroxybutyrate- dehydrogenase]).
Equation 1 reveals that [HC03 -] by itself would be a poor discrimi-
nator of the metabolic component. Equation I, however, does not act in
isolation, nor does any acid-base system in the body. The ratio of Pco,
888 BREEN

to HC03- defines the [H+] in clinical practice, as shown in equation 3.

The last example of high Pco, (pure respiratory acidosis) results in an
increase in both [H +] and [HC03 - ] (Equation 1 is driven to the right),
even though the metabolic component has not changed. In metabolic
alkalosis, the addition of strong base decreases H + and mass action
forces Equation 1 to the right to increase HC03-. Thus, both respiratory
acidosis and metabolic alkalosis increase [HC03-] but have opposite
effects on pH.
The parameter, standard-base excess, measures the purely metabolic
component of acid-base balance of the extracellular fluid. A negative
standard-base excess is obtained during metabolic acidosis, and a posi-
tive standard-base excess is obtained during metabolic alkalosis. The
standard-base excess (mM) estimates the amount of strong acid or base
that would be needed to correct a metabolic disturbance, usually as 0.3
. weight(kg) . standard base excess, whereby 0.3 . weight (kg) estimates
the extracellular fluid space in liters. For example, a 60-kg woman with
a standard base excess of - 8 would require (60 . 0.3 . 8 =) 144 mM of
sodium bicarbonate to correct the acidosis. The administration of sodium
bicarbonate is almost always a temporary maneuver, while simultane-
ously working to correct the primary disorder causing the metabolic
acidosis (typically related to underperfusion of tissues and lactate pro-
duction in the operating room). Full correction is seldom advisable.
Standard-base excess is difficult to calculate by hand, but automati-
cally is computed by most blood gas and pH analyzers from directly
measured Pco, and pH. Alternatively, the standard-base excess can be
read off of a graphic nomogram (i.e., graphic approach).

Buffering Capacity

A buffer is a molecule, usually a protein such as hemoglobin, that

takes up H+ ions when pH decreases and that releases H+ ions when
pH increases, preventing marked changes in [H+]. For example, when a
strong acid is added to blood, the hemoglobin buffer system can buffer
and reduce the change in pH by 90%, compared with the condition
when blood and hemoglobin are absent. The nonvolatile weak acid
buffer system is primarily hemoglobin.
Standard-base excess represents the metabolic component by assum-
ing that the mean buffer strength of the human extracellular fluid equals
that of blood with 5 g/dL hemoglobin. Despite individual variation of
hemoglobin, the effective buffer system changes little.

Graphic Approach To Acid-Base Analysis

Figure 1 depicts acid-base balance in terms of the two independent

variables of acid-base balance, respiratory PAC02 (mm Hg, x axis) and
metabolic standard-base excess (mM, y axis).35.36 Measured Pco, is plot-
ted against calculated standard-base excess. pH isopleths are plotted on
 ARTERIAL BLOOD GAS AND pH ANALYSIS 889

30

20

~
E
...... 10
w
CD
en 0
.~
'0
.0
l'Cl
iii -10
:E

-20

-30
10 20 30 40 50 60 70 80 90
Respiratory Paco2 (mm Hg)

Figure 1. The average or typical human compensations for acid-base imbalances. Arrows
show direction of compensatory changes from uncompensated acid-base imbalances.
Linear pH isopleths permit location of a patient data set on the diagram when only pH and
Pace, are known. Slopes of solid lines are shown in Box 1. SSE = standard-base excess,
M = metabolic acidosis or alkalosis; AR = acute respiratory acidosis or alkalosis; CR =
chronic respiratory acidosis or alkalosis. (From Schlichtig R, Grogono AW, Severing·
haus JW: Human Paco, and standard-base excess compensation for acld-base imbalance.
Crit Care Med 26:1173-1179, 1998; with permission.)

the same graph. If the blood gas and pH analyzer machine does not
calculate standard-base excess, standard-base excess may be found as
the y value of the point that intersects measured PaC02 and measured
pHa. A change in ventilation (respiratory component) moves the inter-
section of Pco, and standard-base excess horizontally. A metabolic
change moves the point vertically.
Compensation occurs when a primary respiratory perturbation or a
primary metabolic perturbation provokes a compensatory change in the
other acid-base component. During acute respiratory acid-base distur-
bances, standard-base excess equals 0 because there has not been time
formetabolic compensation to occur. Chronic respiratory aberrations lie
vertically between no metabolic compensation (standard-base excess =
0) and complete compensation (pH = 7.40). The kidney eventually
increases or decreases standard-base excess but rarely to the point of
complete compensation. Metabolic disturbances lie horizontally between
o to complete respiratory compensation. Respiratory compensation is
generally immediate. Box 1 summarizes relationships governing the
amount of respiratory or metabolic compensation in response to a distur-
bance to the other variable.
A pitfall of this approach (and also for the currently taught HC03 -
 ARTERIAL BLOOD GAS AND pH ANALYSIS 890

Box 1. Acid·Base Balance: Expected Human Metabolic or

Respiratory Compensation
a SBE Metabolic Compensation
Acute respiratory acidosis or alkalosis 0 (no compensation)
Chronic respiratory acidosis or alkalosis 0.4 • ~Pac02
aPaco 2 Respiratory Compensation
Metabolic alkalosis 0.6 • ~SBE
Metabolic acidosis 1.0 • ~SBE
A = change in variable; SSE = standard base excess; PaC02 = arterial blood PCC:!.
Modified from Schlichtig R, Grogono AW. Severinghaus JW: Human Paco2 and standard base
excess compensation for acid-base [Link] Care Med 26:1173-1179,1998; with permis-
sion.

approach to acid-base balance) is the condition of chronic respiratory

acidosis with superimposed metabolic acidosis. For example, chronic
hypoventilation results in decreased pH because of increased Pco., Meta-
bolic compensation increases standard-base excess to correct pH par-
tially. A superimposition of a metabolic lactic acidosis could normalize
standard-base excess; however, the continued increase in Pco, and de-
crease in pH would suggest only acute respiratory acidosis, masking the
serious presence of the acute metabolic (i.e., lactic) acidosis. In this
situation, clinical presentation may help make the diagnosis. More im-
portantly, examination of the anion gap would detect the presence of
unmeasured anion (in this example, lactate) Anion gap29 is based on
electroneutrality and detects the difference between measured and un-
measured ions in plasma:
Anion Gap = Na ' + K+ - Cl" - HC03+ (Equation 4)
Normally, anion gap equals the anion contributed by the weak acid
buffer system (equation 4). An increase in the anion gap helps detect
the presence of significant unmeasured strong ions, such as lactate- and
l3-hydroxybutyrate-. Note that anion gap is useful only to unravel the
cause of a metabolic acidosis, where unmeasured anions may result from
the presence of salicylate poisoning, lactic acidosis, diabetic ketoacidosis,
and others. In contrast, anion gap does not detect the cause of a metabolic
alkalosis", because the ions responsible for the disturbance (usually
decrease in [Cl <j) are already measured.
Further details of acid-base balance are outside the scope of this
article. Please see the section following this article by W. Wilson, which
provides clinical approaches to specific acid-base balance pathology.

ARTERIAL BLOOD PARTIAL PRESSURE OF OXYGEN

(Po2 )
Oxyhemoglobin Dissociation Relationship
The sigmoid relationship of oxygen saturation of blood hemoglobin
(S02) as a function of P02 is a basic concept for anesthesiologists. The
 ARTERIAL BLOOD GAS AND pH ANALYSIS 891

blood oxyhemoglobin dissociation curve readily can be estimated by

drawing a smooth line through several approximate coordinates (Fig. 2):
Pso (S02 = 50%; P02 = 27 mm Hg, the P0 2 at which hemoglobin is 50%
saturated with O2); mixed venous blood point (S02 = 75%, P02 = 40 mm
Hg); elbow of oxyhemoglobin dissociation curve (S02 = 90%, P0 2 = 60
mm Hg); and arterial blood point (502 = 100%, P02 = 100 mm Hg).
When hemoglobin is 100% saturated with oxygen, further increase in
blood oygen content can occur only by increasing P0 2 to increase dis-
solved oxygen (0.003 mL O2 . dL -I [blood] . mm Hg-I [P02]).
There are less appreciated features of the oxyhemoglobin dissocia-
tion relationship. In conditions of normal Hb and high P02 (> 100 mm
Hg), the small decrease in arterial blood oxygen content and decrease in
Pa02 generally are ignored. In this condition of Hb saturation with
oxygen, however, a decrease in Pa02 can be an early, sensitive monitor
of gas exchange aberration (e.g., early basilar atelectasis, pulmonary
edema) before significant reduction of blood oxygen content occurs. In
severe anemia and ventilation with oxygen, dissolved oxygen signifi-
cantly can contribute to total blood oxygen content. For example, if Hb
= 6 g/dL and Pa02 = 700 mm Hg, hemoglobin-bound oxygen is 8.0 g/
dL (8.0 ·1.34 mL 02/g Hb), and dissolved oxygen is 2.1 mL/dL, 21% of
the total blood oxygen content (10.1 mL/dL). Similarly, dissolved oxygen

100

--
0~ 80

.e
c:
0

....:::JlU
60
t Temperature
..l-pH
t Peo2
en 40
.c
:I:
20

0
0 20 40 60 80 100

P02 (mm Hg)

Figure 2. Oxyhemoglobin dissociation curve. Oxygen saturation of blood hemoglobin (S02)
as a function of P02 , estimated by drawing a smooth line through several approximate
coordinates: P so (S02 = 50%; P02 = 27 mm Hg, the P02 at which hemoglobin is 50%
saturated with O2); mixed venous blood point (S02 = 75%; P02 = 40 mm Hg); elbow of
oxyhemoglobin dissociation curve (S02 = 90%; P02 = 60 mm Hg); and arterial blood point
(S02 = 100%; P02 = 100 mm Hg). The oxyhemoglobin dissociation curve shifts to the
right (unloading of O2 in the peripheral tissues) during increased temperature, increased
Pcos, or decreased pH (43).
892 BREEN

content can be significant when normal hemoglobin is deactivated. Dur-

ing carbon monoxide poisoning.t- 8 oxygen-binding sites are inactivated
competitively by carbon monoxide to produce carboxyhemoglobinemia.
During administration of sodium nitrite, normal hemoglobin is oxidized
and converted to methemoglobin," which does not carry oxygen.

Tissue Oxygen Consumption Versus Arterial Blood

Oxygen Delivery

The product of arterial blood oxygen content (<:;a02) and cardiac

output (QT) is oxygen delivery (Q02) to the tissues (Q02 = QT' Cao.) .
In healthy tissues, a decrease in Q02 does not decrease tissue oxygen
consumption (V02.1i) because oxygen extraction proportionately in-
creases." V0 2.1i is regulated by the tissue metabolic needs; however, when
Q02 decreases below a critical threshold (e.g., during hypoxia, anemia,
or decreased QT), V0 2.1i decreases linearly with the decrease in Q02
because further increases in oxygen extraction are not sufficient." During
critical care medicine, pathologic oxygen supply dependency (Vo2 varies
directly with Q02 despite normal or increased Q02) can occur in patients
with adult respiratory distress syndrome or sepsis.v-15. 37 High mortality
rates may result from tissue hypoxia and ensuing multiple organ fail-
ure." During pathologic oxygen supply dependency, regional heteroge-
neity exists," and gut demonstrates one of the first decreases in V0 2
(certainly before skeletal muscle)." Lactate measurements alone do not
prove tissue hypoxia. Sepsis can cause inactivation of pyruvate dehydro-
genase, and can cause lactic acidosis without tissue hypoxia."

Assessment of Arterial Blood Oxygenation

Assessment of the efficiency and adequacy of pulmonary oxygen-

ation of arterial blood can be made by examining the gradient between
alveolar P0 2 and arterial blood P0 2 or by calculating the pulmonary
shunt.

Determination of the Alveolar-Arterial P02 (PA-ao2) Gradient

Alveolar P0 2 (PA02) may be determined by:
PA02 = PI02 . (PB - PH20) - Paco-/R (Equation 5)
whereby PI02 is the fraction of inspired oxygen, PB is the barometric
pressure, PH20 is the water vapor partial pressure, alveolar Pco, (PAeo2)
is estimated from Paco-, and R is the respiratory quotient (ratio of
pulmonary carbon dioxide elimination and oxygen uptake [Veo 2/Vo2]).
A common point of confusion for students of respiratory physiology
is that PH20 is subtracted first from PB. Because there is a large surface
area for constant water evaporation in the respiratory tract, water be-
 ARTERIAL BLOOD GAS AND pH ANALYSIS 893

haves like any volatile liquid (e.g., volatile liquid anesthetics). Accord-
ingly, PH20 depends only on body temperature (47 mm Hg at 37° C) and
is independent of total barometric pressure and the presence of other
gases (e.g., oxygen, carbon dioxide).
The gradient between PA02 and Pao, is a measure of oxygenation
deficiency. Pulmonary shunt (perfused lung regions that receive no
ventilation) and low alveolar ventilation-to-perfusion (VA/Q) lung re-
gions contribute to an increase in the PA-a02 gradient. The PA-a02 gradient
does .not distinguish between shunt (e.g., basilar atelectasis) and low
VA/Q (e.g., chronic obstructive pulmonary disease) pathophysiology
readily. From the previous discussion of the sigmoid shape of the oxyhe-
moglobin dissociation curve (see Fig. 2), it is evident that any given
PA-a02 gradient becomes more significant as Pao; decreases and hemo-
globin begins to desaturate. Accordingly, a more informative measure of
oxygenation deficit may be the determination of pulmonary shunt or
venous admixture.

Determination of Pulmonary Shunt or Venous Admixture

In a simple two-compartment lung model (Fig. 3), consisting of a
perfused, oxygen-ventilated lung compartment and a shunt lung com-
partment that is normally perfused but not ventilated," pulmonary
shunt fraction readily can be derived as:
Qs/QT = (CC'02 - Cao2)/(CC'02 - CV02) (Equation 6)
whereby QT is total cardiac output, CC'02 is the end-capillary oxygen
content, and cvo, is the mixed venous Co 2, CC'02 is the oxygen content
of blood leaving the normal lung unit, calculated from its PA02 (see
equation 5) and represents ideal oxygenation of arterial blood. Intu-
itively, the numerator of the shunt equation quantifies the oxygenation
deficit (idealoxygenation, CC'Olt minus actual oxygenation, Cao-), nor-
malized by QT, which is estimated by the inverse of the denominator
(i.e., 1/[Cc'o2 - CVo2]). The term, 1/(Cc'o2 - Cvo-), closely approxi-
mates the expression, 1/(Caof - Cvo.), which is proportional to QT
during conditions of constant VOlt as given by rearrangement of the Fick
equation:
QT = Vo 2/(Cao2 - CV02) (Equation 7)
Pulmonary shunt fraction (QS/QT) is normally less than 5%. If the
lung .is ventilated with Pro, less than 1, the oxygenation defects of low
VA/Q units are added to those of shunt lung regions and equation 7
becomes an expression for venous admixture. (Q\,A). An attempt to
discriminate between pulmonary shunt units (VA/Q = 0) and venous
admixture units (low VA/Q) can be made by placing the patient on
oxygen ventilation. The difference between the venous admixture frac-
tion and the shunt fraction estimates the amount of low VA/Q units.
This approach, however, is limited because low VA/Q lung units may
collapse and convert themselves to shunt units during oxygen breathing
894 BREEN

QT
Figure 3. Two-compartment lung model of pulmonary shunt. The normal lung compartment
on the left is ventilated and perfused. The shunt lung region on the right is perfused but
not ventilated (zero VA!O ratio). By mass balance for oxygen content, OsiOr = (CC'02-
Cao2)/(Cc'02 - CV02), where as is shunt blood flow, Or is total blood flow (cardiac output),
and Cc'o., Cao2' and CIl0 2 are the end-capillary, arterial, and mixed venous blood O2
contents, respectively. VA, alveolar ventilation; PA02, alveolar Po2. If the ventilation obstruc-
tion on the right is partial instead of complete, the shunt region becomes venous admixture,
i.e. lung region of low (but not zero) VA!O ratio. Contrast this figure, depicting units of low
VA!O ratio that affect mostly oxygenation of arterial blood, with Figure 4, which depicts lung
units of high VA!O that affect mostly CO2 elimination from mixed venous blood.

(i.e., absorption atelectasis). Absorption atelectasis occurs because pul-

monary capillary blood uptake of oxygen exceeds the low ventilatory
ability to replace alveolar oxygen in these low VA/Q lung regions.

ARTERIAL BLOOD PARTIAL PRESSURE OF CARBON

DIOXIDE (Pco2 )

Assessment of Alveolar Ventilation

The use of arterial blood PC02 (PacOz) to assess the adequacy of

alveolar ventilation and to adjust ventilatory parameters is well estab-
Iished,': 2, 27. +I whereby the fraction of alveolar carbon dioxide (FAC02 ) is:
FAcOz = VC02,tJVA + FlC02 (Equation 8)
 ARTERIAL BLOOD GAS AND pH ANALYSIS 895

VC02,1i is the tissue carbon dioxide production, VAis alveolar ventilation,

and FIC02 is the inspired carbon dioxide fraction (normally 0). Note that
PAC02 = FAC02 . dry barometric pressure.
During anesthesia or critical care medicine, the concentrations of
carbon dioxide are monitored by three measurements (in the following
diminishing order of frequency):
Pco, of the last alveolar gas exhaled from the lung that can be sampled
at the airway opening is called the end-tidal Pco, (PETC02). PETC02
often is used to estimate PAC02 (effect of alveolar dead space, VOAUJ
is ignored) and Paco, (diffusion equilibrium is assumed between
the perfused alveolar compartment and arterial blood)'?
Paco, of arterial blood leaving the lung (arterial blood sample) is
the perfusion-weighted average PAC02. Pulmonary shunt slightly
increases Pace; by the addition of mixed venous Pco, (P\iC02),
which does not participate in gas exchange'?
P\iC02 in blood returning from the tissues to the lung can be sampled
from a catheter in the right ventricular outflow tract or the pulmo-
nary arterial tree
The following sections describe the use and importance of PaC02 in
the derivation and interpretation of pulmonary dead space.

Total Physiologic Dead Space

The effective or alveolar ventilation (VA) equals VE (VI· f) minus

the amount of wasted or dead space ventilation (Vn) (i.e., the amount
of ventilation that does not participate in gas exchange). If an entire
exhaled breath is collected in a container, the resulting concentration of
carbon dioxide is called the mixed expired Pco, (PEc02)' By simple mass
balance of carbon dioxide, the total physiologic dead space as a fraction
of VI is:
VOph/VI = (Paco, - PEco2)/Paco2 (Equation 9)
This derivation takes advantage of the relatively linear dissociation
curve for carbon dioxide in blood over the physiologic range (mL carbon
dioxide dissolved per ~OO mL blood as a function of Pco.), allowing the
substitution of carbon dioxide partial pressure for blood carbon dioxide
content. During ventilation with an anesthesia circle circuit, where mixed
expired gas collection is difficult, PEC02 can be measured from a small
bypass mixing chamber (i.e., bymixerji'->' placed on the expiration limb
of the breathing circuit. Normally, VOphy is about one third of VI. The
components of VDph / 1, 41 are instrumental dead space, anatomic dead
space, and alveolar dead space.

Anatomic Dead Space

The anatomic dead space (Voana ) is the volume of the conducting

airways (i.e., pharynx, trachea, bronchial tree) that does not participate
896 BREEN

in gas exchange. The measurement of [Link] generally includes the instru-

mental (mechanical) dead space, the volume of the breathing system
from the connection of the inspiration limb to the mask or endotracheal
tube.

Alveolar Dead Space: Special Relationship of Pace,

and PETC02

Alveolar dead space ([Link]) is the effective alveolar volume that

does not receive pulmonary perfusion": 30, 39 (i.e., West zone 1).1,45 [Link]
markedly can change during anesthesia and affect carbon dioxide elimi-
nation, interpretation of PaC02, and the indices of exhaled carbon dioxide.
In a two-compartment lung model (Fig. 4),3' Z7, 39 ignoring inter-lung
ventilation and applying mass balance for carbon dioxide, the alveolar
dead space fraction is:
[Link]/[Link] = (PaC02 - Pacoz)/PAC02 (Equation 10)
whereby PACOz is estimated by PETCOz3O or by average alveolar expired
Pco, (PAECOz).lO VT. lv is the total alveolar tidal volume. Essentially, Vo. lv,
which lacks perfusion and contains little carbon dioxide, dilutes PAco z

Ventilation

~L pm "
20mm Hg
PACOl
40mmHg

VDai v
Pcol
OmmHg
Paco,
40mmHg

Figure 4. Effect of alveolar dead space (Voa ,, ) . The right lung compartment receives no
perfusion and contains no CO2 (ignoring inter-lung unit ventilation). By mass balance for
CO2, [Link]" = (Paco, - PETC02)! Paco 2 • PAC02 , PETC02' Paco., and PiiCO" alveolar,
end-tidal, arterial, and mixed venous PC02' respectively. For the sample condition shown,
[Link].1v = (40-20)/40 = 50%. (Adapted from Breen PH: Capnography: The Science
Behind the Lines. In A.S.A. Annual Refresher Course Lectures. Park Ridge, IL, American
Society of Anesthesiologists, 1994; 126: 1-7; with permission.)
 ARTERIALBLOOD GAS AND pH ANALYSIS 897

down to the value of PETC02 during exhalation. Alveolar dead space causes
the gradient between PAEC02 (or PETC02) and Paco-.
What are the causes of VD,lv? The following is a summ!1ry of some
causes of VD,lv that can occur during the perianesthesia period:
Pulmonary Embolus
Thrombosis (e.g., venous)
Air (e.g., sitting neurosurgery)
Amniotic fluid (e.g., complicated delivery)
Carbon dioxide (e.g., laparoscopy)
Fat (e.g., orthopedic surgery)
Decreased Pulmonary Arterial Pressure
Decreased cardiac output (e.g., hypovolemia)
Nondependent lung region (e.g., sitting position)
Increased Alveolar Gas Pressure
Positive end-expiratory pressure (PEEP)
Large tidal volume ventilation
Any factor that effectively restricts perfusion to ventilated alveolar
regions may increase VD. h l whether by physical blockage of the pulmo-
nary arterial tree (e.g., thromboembolism), by low pulmonary arterial
pressures (e.g., sitting position, conditions of low QT), or by high alveo-
lar gas pressure (e.g., high ventilatory pressures).
The alveolar dead space fraction relationship and interpretation of
Pace; PETC02f and other indices' of exhaled carbon dioxide can be com-
plex and are addressed in the following sections.

Carbon Dioxide Expirogram Versus Capnogram

The typical capnogram, the plot of tidal Pco, versus time, is dis-
played in Figure [Link] The Pco, of the last alveolar gas to be exhaled
past the airway opening is defined as PETC02• This measurement is
noninvasive, inexpensive, and generally available in the anesthesia suite;
hence, PETC02 often is used to estimate PAC02 and Paco., Inspection of
the plot of exhaled volume versus time (see Fig. SB), however, reveals
that most volume has been exhaled by the early portion of the alveolar
plateau. PETC02f which does not contain volume information, does not
represent the overall average alveolar expired Pco, (PAEC02) .
Accordingly, a more meaningful method to display the exhaled Pco,
waveform may be the carbon dioxide expirogram,": to, 20, 38 the plot of
Pco, versus exhaled volume (Fig. 6A). The carbon dioxide expirogram
normalizes each exhaled Pco, value by the amount of expired volume.
Compare the capnogram (thin line, see Fig. SA) with the carbon dioxide
expirogram (see Fig. 6A) for the same exhalation. The slope of the
alveolar plateau in the capnogram (see Fig. SA) is more horizontal

From Breen PH: Carbon dioxide kinetics during anesthesia: Pathophysiology and
monitoring. Anesthesiology Clinics of North America 16:259-293, 1998.
898 BREEN

A
40

30

20

Exhaled
[Link]
.
PC02
10 ~
PEEP
» Baseline
I ,.~
0

B
600

500

400 /"
.,/
.'
300 .,.",.,."

I
,, ,-
•.-
./
200 1.:,,· -
, ••r

,,r,..-»
100 i ..··-
/'
O-¥~---r----r-----,----r----,-J

o 0.5 1.0 1.5 2.0 2.5

Time (sec)

Figure 5. Capnogram (Pc0 2 versus time, Panel A) and expirogram (exhaled tidal volume
versus time, Panel B) during baseline mechanical ventilation of an anesthetized dog (thin
line) and during ventilation with 7 cm H20-positive end-expiratory pressure (PEEP, thick-
line). PAEC02 , PETC02 , and Paco., average alveolar expired, end-tidal, and arterial Pcoz,
respectively. Phases I, II, and III are the inspiratory baseline, expiratory upstroke, and
alveolar plateaus, respectively. (Adapted from Breen PH, Mazumdar B, Skinner SC: Com-
parison of end-tidal Pcoz and average alveolar expired PC02 during positive end-expiratory
pressure. Anesth Analg 82:368-373, 1996 ; with permission.)
 ARTERIAL BLOOD GAS AND pH ANALYSIS 899

Figure 6. CO2 expirogram (exhaled Pco; versus tidal volume) during baseline and PEEP
(7 em H20 ) ventilation (plotted from data shown in Figure 9). Pace, and PAEC02' arterial
and average alveolar expired Pe02. Phases I, II, and III are the inspiratory baseline,
expiratory upstroke, and alveolar plateaus, respectively. Areas Z and Y represent the
effects of anatomic and alveolar dead spaces, respectively. (Adapted from Breen PH,
Mazumdar B, Skinner SC: Comparison of end-tidal Pco, and average alveolar expired Pco,
during positive end-expiratory pressure. Anesth Analg 82:368-373, 1996; with permission.)
900 BREEN

than the upward sloping plateau in the carbon dioxide expirogram (see
Fig.6A).
Slow respiratory frequency can exaggerate this flat alveolar plateau
in the capnogram. During slow respiratory rate, when exhalation stops
before the end of the expiratory phase, the side-stream capnometer
continues to sample alveolar gas from the breathing tube, and the
mainstream capnometer continues to measure Pco, from the stationary
alveolar gas sample in the airway cuvette. This continued sampling of
exhaled Pco, in the absence of exhaled flow artificially can create a
horizontal tail on the alveolar plateau of the capnograrn.'?
From the carbon dioxide expirogram, the average alveolar expired
Pco, (PAEC02) can be obtained, and is important in the understanding of
alveolar dead space during anesthesia.

Comparison of Average Alveolar Expired Pc02 (PAEC0 2)

with Paco,
To determine PAEC02l 4, 9, 10 exhaled Pco, is plotted versus exhaled
volume (combining upper and lower panels of Figure 5) to generate
the carbon dioxide expirogram (see Fig. 6).to Using a modified Fowler
analysis," line BE can be positioned so that the areas of triangles FGE
and GBC are equal. Segment FE is defined as Voana, and PAEC02 is the
midpoint of line Be. Conceptually, this analysis of the carbon dioxide
expirogram treats an expiration as pure dead space (segment FE) fol-
lowed by pure alveolar gas (segment ED) with a Pco, equal to PAEC02.
Compared with the capnogram (see Fig. 5), PAEC02 occurs later on the
alveolar plateau of the carbon dioxide expirogram (see Fig. 6A), and the
slope of the alveolar plateau is greater.
Figures 5 and 6 also display the effect of adding 7 em H 20 PEEP
during mechanical ventilation of the lungs of an anesthetized dog." In
the capnogram (see Fig. SA), the alveolar plateaus have similar slopes
during baseline mechanical ventilation (thin line) and during ventilation
with PEEP (thick line). In contrast, the carbon dioxide expirogram (see
Fig. 6) displays a marked increase in alveolar plateau slope with PEEP.
The weighting of exhaled PC02 by exhaled volume in the carbon dioxide
expirogram (see Fig. 6) results in a steeper slope of the alveolar plateau
of the carbon dioxide expirogram during PEEP, compared with the
capnogram (see Fig. SA).
The positive slope of the alveolar plateau means that PETC02 is
greater than PAEC02 • This overestimation of PAEC02 by PETC02 is im-
portant in the analysis of the alveolar dead space fraction (Voalv/VTahl
equation 10). In the data shown in Figure 6, when PEEP increased the
slope of the alveolar plateau, VOalv/VTalv falsely was underestimated if
PETC02 was used as an estimate of PAC02. With steep alveolar plateau
slope, PETC02 can be greater than Paco., with resultant calculation of
negative (and undefined) Voalv fraction.'?
The generation of the carbon dioxide expirogam and calculation of
 ARTERIALBLOOD GAS AND pH ANALYSIS 901

PAECO z should be implemented easily during clinical anesthesia. Flow

and Pco, measurements are readily available in the clinical arena. Digital
data acquisition and computer processing generate the carbon dioxide
expirogram." Because trapezoid BCDE and the area under the data
curve (see Fig. 6) equal the carbon dioxide volume exhaled per breath
(VCOZ•b r ) , the on-line digital determination of segment FE (Voon o) and
then PAECOz can proceed by quadratic equation solution or by iterative
techniques.v 10 Clinical studies need to address the benefits for patient
care versus the higher cost of this monitoring technology.

VENOUS BLOOD AND TISSUE COMPARTMENTS

Most attention to blood gas and pH analysis focuses on the arterial

blood compartment. Consideration of the venous blood and tissue com-
partments, however, is often imperative in the overall assessment of
acid-base balance, tissue oxygenation, and carbon dioxide elimination.
Two vignettes are described.

Effect of Low-Stable Cardiac Output on Redistribution

of Body Carbon Dioxide Stores

. The steady-state relationship for FACO z (VCo.z/VA) is not affected by

QT, to the extent that VA remains constant." QT, however, affects the
distribution and total amount of carbon dioxide in the body," At low QT,
retention of carbon dioxide occurs in the peripheral tissue compartment,
resulting in higher Pvco; which restores normal carbon dioxide delivery
to the lung. PACO z and Paco-, however, remain constant because VA and
VCOZ,Ii remain stable.

Significance of Arterial Blood Versus Venous Blood

P0 2 and Pc0 2 During Cardiopulmonary Resuscitation

Reports in the cardiopulmonary resuscitation literature" 22 indicate

that restoration of native cardiac output is signaled best by an increase
in PETCOz• In periods of low QT, the state of body carbon dioxide stores
is measured best in the tissue and venous blood compartments, where
carbon dioxide retention and severe increases in Pvco, occur because of
markedly decreased QT and venous return." Because pulmonary perfu-
sion is low, during the usual hyperventilation in cardiopulmonary resus-
citation, low PETCOz and Paco, often result, with potential for a false
sense of security of adequate QT for critical organ perfusion. Similarly,
high Po; measured in arterial blood does not reflect the markedly low
venous Po, and tissue hypoxia.
902 BREEN

NON-STEADY-STATE CONSIDERATIONS OF BLOOD

GAS AND pH ANALYSIS

Historically, the study of gas kinetics in the body mostly has been
confined to equilibrium states." 27 The perianesthesia period often in-
volves conditions of non-steady state. The study of gas kinetics patho-
physiology during non-steady state requires novel approaches. In this
section, a clinically relevant example of non-steady-state gas kinetics
perturbation is examined, along with the changes in blood gases.

How Does an Abrupt Decrease in Cardiac Output

Decrease Pulmonary Carbon Dioxide Elimination and
Arterial Blood Paco2 ?

To answer this question, vena cava balloons were inflated in an~s­

thetized dogs to decrease QT (measured by thermodilution)." When QT
was decreased from 2.8 to 1.5 L/min in one dog, PETCq2 decreased
within a few breaths from 38 to 28 mm Hg. Over a range of QT decreases
(Fig. 7A), the slope of the percentage decrease in PETCOz versus the
percentage decrease in <;2T was 0.73. A similar relationship held for
pulmonary vco, versus QT. For example, a decrease in QT from 3.0 to
2.4 L/min (20% decrease) resulted in a decrease in Parco, from 40 to
34.2 mm Hg (14.5%). The decrease in PETCOz (percentage) was more than
the accompanying decrease (percentage) in PaC02 (see Fig. 7B). During a
decrease in QT, the decrease in PETCOz (and Vco.) resulted from two
factors." During an abrupt decrease in QT, carbon dioxide transfer to
the lung decreased, whereas VE was maintained, so that the carbon
dioxide level in the central compartment (Paco, or PACOz) decreased.
The decrease in pulmonary perfusion pressure caused VO.h 7 which fur-
ther diluted PACO z (i.e., Paco.) down to the value of PETCOz (see Fig. 4).
In contrast, the traditional equilibrium equation for carbon dioxide
kinetics (PACOz a VCOz/VA, see equation 8) does not even contain a term
referencing QT. Z7 Hence, during steady state, QT does not affect PACO z
(i.e., Pacoj) to the extent that total VA remains constant.v 3 In this study,
however, VA decreased because of the increase in VO.h _ With sustained
decrease in QT, the decrease in VA results in progressive carbon dioxide
accumulation in the lung (increased PACOz and Paco.) and the tissues
(increased P\,c 02 ) . Accordingly, the increase in [Link] initially decreases
PETCOz (equation 10), but the sustained effects of increased dead space
progressively increase Paco, and PETCOz in parallel.F Other investiga-
tors'? show a similar relationship between QT and carbon dioxide elimi-
nation in patients.
In a multicompartmental, numeric analysis model of the lung and
cardiovascular system," similar relationships hold for non-steady-state
oxygen kinetics during an abrupt decrease in QT. Pulmonary Voz de-
creases as QT decreases (decreased pulmonary extraction of oxygen).
Subsequently, pulmonary Voz recovers (increased) because of the de-
 ARTERIAL BLOOD GAS AND pH ANALYSIS 903

60
A •
•
Dog I
Dog 2
•
N
0
u!- 50 • Dog 3
I.l
~ 40 • Dog 4
a.I
• Dog 5
'"
C': 30
a.I
s..
~
a.I 20
• m==0.73±.05
2
~ R ==0.89
10 P<.OOI
~
0

B
40
•
N
0
U
C': 30
~
a.I
'"
C':
a.I
20
s.. m==0.47±.04
~ 2
a.I
10 R ==0.84
~
P<.OOI
~
0
•

o 10 20 30 40 50 60 70 80 90

% Decrease QT

Figure 7. Percent decreases in end-tidal Pco, (PETC02 • panel A) and arterial Pco 2 (Paco 2 •
panel B) during decreases in cardiac output (Or) effected by inflating vena cava balloons
in anesthetized dogs. m, slope of overall regression line; R2. coefficient of determination
(Adapted from Isserles SA. Breen PH: Can changes in end-tidal Pc0 2 measure changes in
cardiac output? Anesth Analg 73:808-814.1991; with permission.)

crease in mixed venous content of oxygen. Pulmonary V0 2 recovers to

baseline faster than pulmonary vco, because tissue oxygen stores are
IOO-fold less than tissue carbon dioxide stores. Arterial blood Pao, in-
creases transiently because QT decreases (global increase in VA/Q). Pao,
decreases because of decreased yA/Q of perfused lung, in tum because
of the appearance of high VA/Q regions during low QT. The high VAl
Q lung units also increase end-tidal P0 2 relative to Paolo

References

1. Breen PH: Capnography: The science behind the lines. 111 American Society of Anesthe-
siologists Annual Refresher Course Lectures. Park Ridge, IL, American Society of
Anesthesiologists 126:1-7, 1994
904 BREEN

2. Breen PH: Carbon dioxide kinetics during anesthesia: Pathophysiology and monitor-
ing. Anesthesiology Clinics of North America 16:259-293, 1998
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thesiology, vol 10. Philadelphia, WB Saunders, 1996, pp 271-292
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Address reprint requests to

Peter H. Breen, MD, FRCPC
Department of Anesthesiology
University of California, Irvine
University of California Irvine Medical Center
Building 53, Room 227
Orange, CA 92868

e-mail: pbreen@[Link]
906 BREEN

APPENDIX
Legend of Abbreviations
II indicates concentration (e.g., [H+» So, oxygen saturation of hemoglobin
Co, blood content of oxygen V flow
Corfu carboxyhemoglobin VA alveolar ventil ation
f respiratory frequency VA/Q ventilation:perfusion ratio
Flo, fraction of inspired oxygen Vo dead space ventilation
Fco, fraction of carbon dioxide ve.. alveolar dead space
(=Peo,/dry PB) ve.; anatomic dead space
HC::OJ bicarbonate anion Vo r hy physiologic dead sp ace
H2COJ carbonic acid VE expired (min) ventilation
PCo, partial pressure of carbon dioxide VT tidal volume
(see Modifiers below) VeO,.b, carbon dioxide volume exhaled
po, partial pressure of oxygen per breath
Qo, delivery of oxygen tissue carbon dioxide production
QT cardiac output tissue oxygen consumption
R respiratory quotient (VC02/V02)

Modifiers: a = arterial; A = alveolar: iii = average alveolar expired; B = barometric; E =

expired; E = mixed expired; ET = end-tidal; I = inspired; V = mixed venous (e.g., PACe" alveolar Pco,)
Dot over Q (QT) and V (V) means per lIlillllte.