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late normal pregnancy . Am J Obstet Gynecol 1981 ; 140 : 730 – 736 .
196 Medawar PB . Some immunological and endocrinological problems
raised by the evolution of viviparity in vertebrates . Symp Soc Exper
Biol 1953 ; 7 : 320 .
197 Norwitz ER , Schust DJ , Fisher SJ . Implantation and the survival of
early pregnancy . N Engl J Med 2001 ; 345 : 1400 – 1408 .
198 Wilder R . Hormones, pregnancy, and autoimmune diseases . Ann NY
Acad Sci 1998 ; 840 : 45 – 50 .
199 Redman CW . HLA - DR antigen on human trophoblast: a review . Am
J Reprod Immunol 1983 ; 3 : 175 – 177 .
53
Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade,
M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd.
5
Maternal – Fetal Blood Gas Physiology

Renee A. Bobrowski
Department of Obstetrics and Gynecology, Saint Alphonsus Regional Medical Center, Boise, ID, USA
Introduction
Abnormalities in acid – base and respiratory homeostasis are
common among patients requiring intensive medical support,
but many clinicians fi nd the physiology cumbersome. As a result
of both their illness and our therapeutic interventions, critically
ill patients frequently require assessment of metabolic and respi-
ratory status. An understanding and clinical application of basic
physiologic principles is therefore essential to the care of these
patients. It is also important that clinicians involved in the care
of critically ill gravidas be familiar with the metabolic and respira-
tory changes of pregnancy as well as their effect on arterial blood
gas interpretation.
The arterial blood gas provides information regarding acid –
base balance, oxygenation, and ventilation. A blood gas should
be considered when a patient has signifi cant respiratory symp-
toms or experiences oxygen desaturation, or as a baseline in the
evaluation of pre - existing cardiopulmonary disease. In this
chapter we focus on fundamental physiology, analytic consider-
ations, effective interpretation of an arterial blood gas, and acid –
base disturbances.
Essential physiology
Acid – base homeostasis
Normal acid – base balance depends on production, buffering, and
excretion of acid. The delicate balance that is crucial for survival
is maintained by buffer systems, the lungs and kidneys. Each day,
approximately 15 000 mEq of volatile acids (e.g. carbonic acid)
are produced by the metabolism of carbohydrates and fats. These
acids are transported to and removed via the lungs as carbon

dioxide (CO
2
) gas. Breakdown of proteins and other substances
results in 1 – 1.5 mEq/kg/day of non - volatile or fi xed acids (pre-
dominantly phosphoric and sulfuric acids), which are removed
by the kidneys.
Buffers are substances that can absorb or donate protons and
thereby resist or reduce changes in H
+
ion concentration. Acids
produced by cellular metabolism move out of cells and into the
extracellular space where buffers absorb the protons. These
protons are then transported to the kidney and excreted in urine.
The intra - and extracellular buffer systems that maintain homeo-
stasis in the human include the carbonic acid – bicarbonate system,
plasma proteins, hemoglobin, and bone.
The carbonic acid – bicarbonate system is the principal extracel-
lular buffer. Its effectiveness is predominantly due to the ability
of the lungs to excrete carbon dioxide. In this system, bicarbon-
ate, carbonic acid and carbon dioxide are related by the
equation:

CO H O CO H CO
Gaseous
phase
Dissolved
Carbonic
acid
22 223
↔+↔ ↔

Carbonicc
anhydrase
Lung Kidney
HHCO
Bicarbonate
+−
+
↓↓
3

Carbon dioxide is produced as an end - product of aerobic
metabolism and physically dissolves in body fl uids. A portion of
dissolved CO
2
reacts with water to form carbonic acid, which
dissociates into bicarbonate and hydrogen ions. The concentra-
tion of carbonic acid is normally very low relative to that of dis-
solved CO
2
and HCO
3
−
. If the H
+
ion concentration increases,
however, the acid load is buffered by bicarbonate, and additional
carbonic acid is formed. The equilibrium of the equation is then
driven to the left, and excess acid can be excreted as carbon
dioxide gas.
The Henderson – Hasselbalch equation expresses the relation-

ship between the reactants of the carbonic acid – bicarbonate
system under conditions of equilibrium:
Chapter 5
54
Acid – base disturbances
Disturbances in acid – base balance are classifi ed according to
whether the underlying process results in an abnormal rise or fall
in arterial pH. The suffi x - osis refers to a pathologic process that
causes a gain or loss of acid or base. Thus, acidosis describes any
condition that leads to a fall in blood pH if the process continues
uncorrected. Conversely, alkalosis characterizes any process that
will cause a rise in pH if unopposed. The terms acidosis and
alkalosis do not require the pH to be abnormal. The suffi x - emia
refers to the state of the blood, and acidemia and alkalemia are
appropriately used when blood pH is abnormally low ( < 7.36) or
high ( > 7.44), respectively [1] .
In addition, alterations in acid – base homeostasis are classifi ed
based upon whether the underlying mechanism is metabolic or
respiratory. If the primary abnormality is a net gain or loss of
CO
2
, this is respiratory acidosis or alkalosis, respectively.
Alternatively, a net gain or loss of bicarbonate results in metabolic
alkalosis or acidosis, respectively. If only one primary process is
present, then the acid – base disturbance is simple, and bicarbon-
ate and PCO
2
always deviate in the same direction. A mixed
disturbance develops when two or more primary processes are
present, and the changes in HCO

3
−
and PCO
2
are in opposite
directions.
The compensatory response attempts to normalize the

HCO PCO
32
−
[]
ratio and maintain pH. Renal and pulmonary
function must be adequate for these responses to be effective and
adequate time must be allowed for the complete response. The
compensatory response for a primary respiratory abnormality is
via the bicarbonate system or acid excretion by the kidney and
requires several days for a complete response. Compensation for
a metabolic aberration is through ventilation changes and occurs
quite rapidly.
Compensatory responses cannot, however, completely return
the pH to normal, with the exception of chronic respiratory alka-
losis. The more severe the primary disorder, the more diffi cult it
is for the pH to return to normal. When the pH is normal but
PCO
2
and HCO
3
−
are abnormal or the expected compensatory

responses do not occur, then a second primary disorder exists.
The four types of acid – base abnormalities and the compensatory
response associated with each are listed in Table 5.1 .
Respiratory and acid – base changes during pregnancy
A variety of physiologic changes occur during pregnancy, affect-
ing maternal respiratory function and gas exchange. As a result,
an arterial blood gas obtained during pregnancy must be inter-
preted with an understanding of these alterations. Since these
changes begin early in gestation and persist into the puerperium,
they must be taken into consideration regardless of the stage of
pregnancy [2] . In addition, the altitude at which a patient lives
will affect arterial blood gas values, and normative data for each
individual population should be established [3] .
Minute ventilation increases by 30 – 50% during pregnancy
[4,5] and alveolar and arterial PCO
2
decrease. Normal maternal
arterial PCO
2
levels range from 26 to 32 mmHg [6 – 8] . Since the

pH pK
HCO
P
metabolic
respiratory
CO
=+
[]
()

=
−
log
3
2
s

As the equation demonstrates, the ratio of [
HCO
3
−
] to PCO
2

determines pH (H
+
ion concentration) and not individual or
absolute concentrations. This ratio is infl uenced to a large extent
by the function of the kidneys ( HCO
3
−
) and lungs (PCO
2
). The
constant s represents the solubility coeffi cient of CO
2
gas in
plasma and relates PCO
2
to the concentration of dissolved CO

2

and HCO
3
−
. The value of s is 0.03 mmol/L/mmHg at 37 ° C. The
dissociation constant (pK) of blood carbonic acid is equivalent
to 6.1 at 37 ° C.
The lungs are the second component of acid – base regulation.
Alveolar ventilation controls PCO
2
independent of bicarbonate
excretion. When the bicarbonate concentration is altered, respira-
tory changes attempt to return the ratio of
HCO PCO
32
−
[]
toward
the normal 20/1. Thus, in the presence of metabolic
acidosis (decreased HCO
3
−
), ventilation increases, PCO
2
is
lowered, and the ratio normalizes. In metabolic alkalosis, the
opposite occurs as PCO
2
rises in response to the primary

increase in HCO
3
−
.
The kidney is the fi nal element of acid – base regulation. The
main functions of the renal system are excretion of fi xed acids
and regulation of plasma bicarbonate levels. Carbonic acid that
has been transported to the kidney dissociates into H
+
and HCO
3
−

in renal tubular cells. Each H
+
ion secreted into the tubular lumen
is exchanged for sodium, and HCO
3
−
is passively reabsorbed into
the blood. Essentially all bicarbonate must be reabsorbed by the
kidney before acid can be excreted, because the loss of one HCO
3
−

is equivalent to the addition of one H
+
ion. Mono - and diphasic
phosphates and ammonia are urinary buffers that combine with
H

+
ions in the renal tubules and are excreted. Under normal
conditions, the amount of H
+
excreted approximates the amount
of non - volatile acids produced.
The buffer systems, the lungs and kidneys interact to maintain
very tight control of the body ’ s acid – base balance. The sequence
of responses to a H
+
ion load and the time required for each may
be summarized:

Extracellular buffering
by HCO
immediate
Respiratory buf
→
()
−
3
ffering
Ps
minutes to hours
Renal excretion
of H s
hour
CO
→
↓

()
↑
+
2
ss to days
In contrast, when P changes
Intracellular b
CO
()
2
:
uuffering
minutes
Renal excretion of H
hours to days
→
()
()
+

Unlike the response to an acid load, no extracellular buffering
occurs with a change in PCO
2
. Since HCO
3
−
is not an effective
buffer against H
2
CO

3
, the only protection against respiratory aci-
dosis or alkalosis is intracellular buffering (i.e. by hemoglobin)
and renal H
+
ion excretion.
Maternal–Fetal Blood Gas Physiology
55
Oxygen delivery and consumption
All tissues require oxygen for the combustion of organic com-
pounds to fuel cellular metabolism. The cardiopulmonary system
serves to deliver a continuous supply of oxygen and other essen-
tial substrates to tissues. Oxygen delivery is dependent on oxy-
genation of blood in the lungs, oxygen - carrying capacity of the
blood and cardiac output. Under normal conditions, oxygen
delivery (DO
2
) exceeds oxygen consumption (VO
2
) by about
75% [17] . The amount of oxygen delivered is determined by the
cardiac output (CO, L/min) times the arterial oxygen content
(CaO
2
mL/O
2
/dL):

DO CO C O dL L
a22

10=× ×
Arterial oxygen content (CaO
2
) is determined by the amount
of oxygen that is bound to hemoglobin (S
a
O
2
) and by the amount
of oxygen that is dissolved in plasma (P
a
O
2
× 0.003):
CO Hb SO PO
aaa222
1 39 0 003=××
()
+×
()

It is clear from this formula that the amount of oxygen dis-
solved in plasma is negligible and, therefore, that arterial oxygen
is dependent largely on hemoglobin concentration and arterial
oxygen saturation. Oxygen delivery can be impaired by condi-
tions that affect either cardiac output (fl ow), arterial oxygen
content, or both (Table 5.3 ). Anemia leads to low arterial oxygen
content because of a lack of hemoglobin binding sites for oxygen
[18] . The patient with hypoxemic respiratory failure will not have
suffi cient oxygen available to saturate the hemoglobin molecule.

Furthermore, it has been demonstrated that desaturated hemo-
globin is altered structurally in such a fashion as to have a dimin-
ished affi nity for oxygen [19] . It must be kept in mind that the
amount of oxygen actually available to tissues also is affected by
the affi nity of the hemoglobin molecule for oxygen. Thus, the
oxyhemoglobin dissociation curve (Figure 5.1 ) and those condi-
tions that infl uence the binding of oxygen either negatively or
positively must be considered when attempts are made to maxi-
mize oxygen delivery [20] . An increase in the plasma pH level or
a decrease in temperature or 2,3 diphosphoglycerate (2,3 - DPG)
will increase hemoglobin affi nity for oxygen, shifting the curve to
the left and resulting in diminished tissue oxygenation. If the
fetus depends upon the maternal respiratory system for carbon
dioxide excretion, the decreased maternal PCO
2
creates a gradient
that allows the fetus to offl oad carbon dioxide. Thus, fetal PCO
2

is approximately 10 mmHg higher than the maternal level when
uteroplacental perfusion is normal.
Maternal alveolar oxygen tension increases as alveolar carbon
dioxide tension decreases, and arterial PO
2
levels rise as high as
106 mmHg during the fi rst trimester [7,9] . Airway closing pres-
sures increase with advancing gestation, causing a slight fall in
arterial PO
2
in the third trimester (101 – 104 mmHg) [7,9,10] . The

arterial PO
2
level, however, is dependent upon the altitude at
which the patient resides. The mean arterial PO
2
for gravidas at
sea level ranges from 95 to 102 mmHg [9,11] , while the average
values reported for those living at 1388 m are 87 mmHg [12] and
61 mmHg at 4200 m [13] . As with carbon dioxide transfer, the
fetus depends upon the oxygen gradient for continued diffusion
across the placenta. Maternal arterial oxygen content, uterine
artery perfusion and maternal hematocrit contribute to fetal oxy-
genation and compromise of any of these factors can cause fetal
hypoxemia and eventually acidemia [14] .
Despite the increased ventilation, maternal arterial pH remains
essentially unchanged during pregnancy [7,15] . A slightly higher
pH value has been noted in women living at a moderate altitude,
with a reported mean of 7.46 at 1388 m above sea level [3] .
Bicarbonate excretion by the kidney is increased during normal
pregnancy to compensate for the lowered PCO
2
, and serum bicar-
bonate levels are normally 18 – 21 mEq/L [2,7,8,16] . Thus, the
metabolic state of pregnancy is a chronic respiratory alkalosis
with a compensatory metabolic acidosis (Table 5.2 ).
Table 5.1 Summary of acid – base disorders: the primary disturbance, compensatory response, and expected degree of compensation.
Primary disturbance Compensatory response Expected degree of compensation
Metabolic acidosis
Decreased
HCO

3
−

Decreased
P
CO
2


P

a
CO
2
= [1.5 × (serum bicarbonate)] + 8

P

a
CO
2
= last two digits of pH
Metabolic alkalosis
Increased
HCO
3
−

Increased
P

CO
2


P

a
CO
2
= [0.7 × (serum bicarbonate)] + 20
Respiratory acidosis Increased
P
CO
2

Increased
HCO
3
−

Acute: pH ∆ = 0.08 × (measured
P

a
CO
2
− 40)/10
Chronic: pH ∆ = 0.03 × (measured
P

a
CO
2
− 40)/10
Respiratory alkalosis Decreased
P
CO
2

Decreased
HCO
3
−

Acute: pH ∆ = 0.08 × (40 − measured
P

a
CO
2
)/10
Chronic: pH ∆ = 0.03 × (40 − measured
P

a
CO
2
)/10
Table 5.2 Arterial blood gas values during pregnancy at sea level.
Normative data should be established for individual populations residing

at high altitude.
Parameter Normal range
pH 7.40 – 7.46

P
CO
2
26 – 32 mmHg

P
O
2
101 – 106 mmHg


HCO
3
−

18 – 21 mEq/L
Chapter 5
56
to some areas, with relative hypoperfusion of other areas, limiting
optimal systemic utilization of oxygen [21] .
The patient with diminished cardiac output secondary to
hypovolemia or pump failure is unable to distribute oxygenated
blood to tissues. Therapy directed at increasing volume with
normal saline, or with blood if the hemoglobin level is less than
10 g/dL, increases oxygen delivery in the hypovolemic patient.
The patient with pump failure may benefi t from inotropic

support and afterload reduction in addition to supplementation
of intravscular volume.
Relationship of oxygen delivery to consumption
Oxygen consumption (VO
2
) is the product of the arteriovenous
oxygen content difference (C
(a – v)
O
2
) and cardiac output. Under
normal conditions, oxygen consumption is a direct function of
the metabolic rate [22] .

VO C O CO dL L
av22
10=××
−
()

The oxygen extraction ratio (OER) is the fraction of delivered
oxygen that is actually consumed:

OER VO DO=
22

The normal OER is about 0.25. A rise in the OER is a compen-
satory mechanism employed when oxygen delivery is inadequate
for the level of metabolic activity. An OER of less than 0.25 sug-
gests fl ow maldistribution, peripheral diffusion defects, or frac-

tional shunting [22] . As the supply of oxygen is reduced, the
fraction extracted from blood increases and oxygen consumption
is maintained. If a severe reduction in oxygen delivery occurs, the
limits of oxygen extraction are reached, tissues are unable to
sustain aerobic energy production, and consumption decreases.
The level of oxygen delivery at which oxygen consumption begins
to decrease has been termed the “ critical DO
2
” [23] . At the critical
DO
2
, tissues begin to use anerobic glycolysis, with resultant
plasma pH level or temperature falls, or if 2,3 - DPG increases,
hemoglobin affi nity for oxygen will decrease and more oxygen
will be available to tissues [20] .
In certain clinical conditions, such as septic shock and adult
respiratory distress syndrome, there is maldistribution of fl ow
relative to oxygen demand, leading to diminished delivery and
loss of vascular autoregulation, producing regional and microcir-
culatory imbalances in blood fl ow [21] . This mismatching of
blood fl ow with metabolic demand causes excessive blood fl ow
10
10
20
30
40
50
60
70
80

90
100
0
20 30 40 50 60 70 80 90 100
P
50
O
2
tension (mmHg)
pH
pH
DPG
Temp
DPG
Temp
Percent oxyhemoglobin
Figure 5.1 The oxygen binding curve for human hemoglobin A under
physiologic conditions (middle curve). The affi nity is shifted by changes in pH,
diphosphoglycerate (DPG) concentration, and temperature, as indicated.
P

50

represents the oxygen tension at half saturation. (Reproduced by permission from
Bunn HF, Forget BG. Hemoglobin: molecular, genetic, and clinical aspects.
Philadelphia: WB Saunders, 1986.)
Table 5.3 Commonly used formulas for assessment of oxygenation.
Formula Normal value
Est. alveolar oxygen tension

P

A
O
2
= 145 −
P

a
CO
2


Pulmonary capillary oxygen content

C

c ′
O
2
= [Hb](1.39) + (
P

A
O
2
)(0.003)

Arterial oxygen content

C

a
O
2
= (1.39 × H b ×
S

a
O
2
) + (
P

a
O
2
× 0.003)
18 – 21 mL/dL
Mixed venous oxygen content

C
O
2
= (1.39 × H b ×
S
O
2
) + (
P

O
2
)(0.003)

Oxygen delivery

D
O
2
=
C

a
O
2
×
Q

T
× 10
640 – 1,200 mLO
2
/min
Oxygen consumption

V
O
2
=
Q

T
(
C

a
O
2
−
C

v
O
2
) = 13.8 (Hb) (Q
T
) (
S

a
O
2
−
S

v
O
2
)/100
180 – 280 mLO

2
/min
Shunt equation

Q

sp
=
C
c ′ O
2
−
C

a
O
2

3 – 8%

Q

t

C
c ′ O
2
−
C
O

2


Estimated shunt


Est. Qsp/Qt =
CC′O
2
– CaO
2

[C
C′O
2
– CaO
2
] + [CaO
2
– CvO
2
]



P

a
CO
2

, partial pressure of arterial carbon dioxide;
P

a
O
2
, partial pressure of arterial oxygen;
P
O
2
, partial pressure of venous oxygen; Hb, hemoglobin;
S

a
O
2
, arterial oxygen
saturation;
S
O
2
, venous oxygen saturation;
Q

T
, cardiac output.
Maternal–Fetal Blood Gas Physiology
57
catheter [29] . An adequate volume of maintenance fl uid or fl ush
solution must be withdrawn from the catheter and discarded

before obtaining the sample for analysis. But the diffi culty is
estimating the appropriate amount to withdraw. Although a 2.5 -
mL discard volume has been suggested, it has also been recom-
mended that each intensive care unit establish its own policy
based upon individual catheter and connection systems [1,30,31] .
Air bubbles in the collection syringe cause time - dependent
changes in the arterial blood gas. Air trapped as froth accelerates
these changes because of the increased surface area [32] . The
degree of change in PO
2
depends upon the initial PO
2
of the
sample. Since an air bubble has a PO
2
of 150 mmHg (room air),
the bubble will cause a falsely elevated PO
2
if the sample PO
2
is
< 150 mmHg. The opposite occurs if the sample has an initial
PO
2
> 150 mmHg. [1,33] . Oxygen saturation is most signifi cantly
affected when the sample PO
2
is < 60 mmHg since saturation
changes rapidly with changes in PO
2

, as predicted by the oxyhe-
moglobin dissociation curve. PCO
2
in the sample decreases
within several minutes of exposure to ambient air [32,34] .
When a blood sample remains at room temperature following
collection, PO
2
and pH may decrease while PCO
2
increases.
Specimens analyzed within 10 – 20 minutes of collection give accu-
rate results even when transported at room temperature [35,36] .
In most clinical settings, however, the time between sampling and
laboratory analysis of the specimen exceeds this limit. Therefore,
the syringe should be placed into an ice bath immediately after
sample collection. The combination of ice and water provides
better cooling of the syringe than ice alone, and a sample may be
stored for up to 1 hour without adversely affecting blood gas
results [34] .
Several additional factors can infl uence blood gas results.
Insuffi cient time between an adjustment in fractional inspired
oxygen or mechanical ventilator settings and blood gas analysis
may not accurately refl ect the change. Equilibration is quite rapid,
however, and has been reported to occur as soon as 10 minutes
after changing ventilator settings of postoperative cardiac patients
[37] . General anesthesia with halothane will falsely elevate PO
2

determination as it mimics oxygen during sample analysis [38 –

41] . Finally, severe leukocytosis causes a false lowering of PO
2
due
to consumption by the cells in the collection syringe [42] . The
effect of the white blood cells may be minimized, but not neces-
sarily eliminated, by cooling the sample immediately after it is
obtained.
The blood gas analyzer
The blood gas analyzer is designed to simultaneously measure the
pH, PO
2
, and PCO
2
of blood. An aliquot of heparinized blood is
injected into a chamber containing one reference and three mea-
suring electrodes. Each measuring electrode is connected to the
reference electrode by a Ag/AgCl wire. The electrodes and injected
sample are kept at a constant 37 ° C by a warm water bath or heat
exchanger. The accuracy of the measurements depends upon
routine calibration of equipment, proper sample collection, and
constant electrode temperature.
lactate production and metabolic acidosis [23] . If this oxygen
deprivation continues, irreversible tissue damage and death
ensue.
Oxygen delivery and consumption in pregnancy
The physiologic anemia of pregnancy results in a reduction in the
hemoglobin concentration and arterial oxygen content. Oxygen
delivery is maintained at or above normal despite this because
cardiac output increases 50%. It is important to remember, there-
fore, that the pregnant woman is more dependent on cardiac

output for maintenance of oxygen delivery than the non - preg-
nant patient [24] . Oxygen consumption increases steadily
throughout pregnancy and is greatest at term, reaching an average
of 331 mL/min at rest and 1167 mL/min with exercise [10] .
During labor, oxygen consumption increases by 40 – 60%, and
cardiac output increases by about 22% [25,26] . Because oxygen
delivery normally far exceeds consumption, the normal pregnant
patient usually is able to maintain adequate delivery of oxygen to
herself and her fetus, even during labor. When a pregnant
patient ’ s oxygen delivery decreases, however, she can very quickly
reach the critical DO
2
, especially during labor, compromising
both herself and her fetus. The obstetrician, therefore, must make
every effort to optimize oxygen delivery before allowing labor to
begin in the compromised patient.
Blood gas analysis
The accuracy of a blood gas determination relies upon many
factors, including blood collection techniques, specimen trans-
port, and laboratory equipment. Up to 16% of specimens may be
improperly handled, diminishing diagnostic utility in a number
of cases [27] . Factors that can infl uence blood gas results include
excessive heparin in the collection syringe, catheter dead space,
air bubbles in the blood sample, time delays to laboratory analysis
as well as other less common causes. This section highlights con-
siderations for obtaining a blood sample and potential sources of
error, and briefl y describes laboratory methods.
Sample collection
The collection syringe typically contains heparin to prevent clot-
ting of the specimen. Excessive heparin in the syringe before

blood collection, however, can signifi cantly decrease the PCO
2

and bicarbonate of the sample. The spurious PCO
2
level results
in a falsely lowered bicarbonate concentration when calculated
using the Henderson – Hasselbalch equation. Although sodium
heparin is an acid, pH is minimally affected because whole blood
is an adequate buffer. Expelling all heparin except that in the dead
space of the syringe and needle will ensure adequate dilution by
obtaining a minimum of 3 mL of blood and reduce or avoid
anticoagulant - related errors [28] .
In the intensive care setting, an arterial catheter is often placed
when frequent blood sampling is anticipated. Dilutional errors
occur when a blood sample is contaminated with fl uids in the
Chapter 5
58
Pulse oximetry is ideal for non - invasive arterial oxygen satura-
tion monitoring near the steep portion of the oxyhemoglobin
dissociation curve, namely at a P
a
O
2
less than or equal to 70 mmHg
[44] . P
a
O
2
levels greater than or equal to 80 mmHg result in very

small changes in oxygen saturation, namely 97 – 99%. Large
changes in the P
a
O
2
from 90 mmHg to 60 mmHg can occur
without signifi cant change in arterial oxygen saturation. This
technique, therefore, is useful as a continuous monitor of the
adequacy of blood oxygenation and not as a method to quantitate
the level of impaired gas exchange [45] .
Poor tissue perfusion, hyperbilirubinemia, and severe anemia
may cause inaccurate oximetry readings [44] . Carbon monoxide
poisoning leads to an overestimation of the P
a
O
2
. When methe-
moglobin levels exceed 5%, the pulse oximeter cannot reliably
predict oxygen saturation. Methylene blue, the treatment for
methemoglobinemia, will also lead to inaccurate oximetry read-
ings. Normal values for maternal pulse oximetry readings (S
p
O
2
)
are dependent upon gestational age, position, and altitude of
residence [46 – 48] .
Mixed venous oxygenation
The mixed venous oxygen tension (P
V

O
2
) and mixed venous
oxygen saturation (S
V
O
2
) are parameters of tissue oxygenation
[22] . P
V
O
2
is 40 mmHg with a saturation of 73%. Saturations less
than 60% are abnormally low. These parameters can be measured
directly by obtaining a blood sample from the distal port of the
pulmonary artery catheter. The S
V
O
2
also can be measured con-
tinuously with a fi beroptic pulmonary artery catheter. Mixed
venous oxygenation is a reliable parameter in the patient with
hypoxemia or low cardiac output, but fi ndings must be inter-
preted with caution. When the S
V
O
2
is low, oxygen delivery can
be assumed to be low. However, normal or high does not guar-
antee that tissues are well oxygenated. In conditions such as septic

shock and adult respiratory distress syndrome, the maldistribu-
tion of systemic fl ow may lead to abnormally high S
V
O
2
in the
face of severe tissue hypoxia [21] . The oxyhemoglobin dissocia-
tion curve must be considered when interpreting the S
V
O
2
as an
indicator of tissue oxygenation [19] . Conditions that result in a
left shift of the curve cause the venous oxygen saturation to be
normal or high, even when the mixed venous oxygen content is
low. The S
V
O
2
is useful for monitoring trends in a particular
patient, because a signifi cant decrease will occur when oxygen
delivery has decreased secondary to hypoxemia or a fall in cardiac
output.
Blood gas interpretation
The processes leading to acid – base disturbances are well described,
and blood gas analysis may facilitate identifi cation of the cause of
a serious illness. Since many critically ill patients have metabolic
and respiratory derangements, correct interpretation of a blood
gas is fundamental to their care. Misinterpretation, however, can
result in treatment delays and inappropriate therapy. Several

Blood pH and PCO
2
are potentiometric determinations, with
the potential difference between each electrode and the reference
electrode quantitated. The pH electrode detects hydrogen ions,
and the electrical potential developed by the electrode varies with
the H
+
ion activity of the sample. The potential difference between
the pH and reference electrode is measured by a voltmeter and
converted to the pH. The PCO
2
electrode is actually a modifi ed
pH electrode. A glass electrode is surrounded with a weak bicar-
bonate solution and enclosed in a silicone membrane. Carbon
dioxide in the sample diffuses through this membrane which is
permeable to CO
2
but not water and H
+
ions. As CO
2
diffuses
through the membrane, the pH of the bicarbonate solution
changes. Thus, the pH measured by the electrode is related to
CO
2
tension.
The measurement of PO
2

is amperometric, as the current gen-
erated between an anode and cathode estimates the partial pres-
sure of oxygen. The PO
2
electrode surrounds a membrane
permeable to oxygen but not other blood constituents. The elec-
trode consists of an anode and a cathode, and constant voltage is
maintained between them. An electrolytic process that occurs
in the presence of oxygen produces current, and the magnitude
of the current is proportional to the partial pressure of oxygen in
the sample. As oxygen tension increases, the electrical current
generated between the anode and cathode increases.
Bicarbonate concentration as reported on a blood gas result is
not directly measured in the blood gas laboratory. Once pH and
PCO
2
are determined, bicarbonate concentration is calculated
using the Henderson – Hasselbalch equation or determined from
a nomogram. In contrast, the total serum CO
2
(tCO
2
) content is
measured by automated methods and reported with routine
serum electrolyte measurements.
Oxygen saturation (SO
2
) is the ratio of oxygenated hemoglobin
to total hemoglobin. It can be plotted graphically once PO
2

is
determined, calculated using an equation that estimates the oxy-
hemoglobin dissociation curve, or determined spectrophoto-
metrically by a co - oximeter. The latter is the most accurate
method since saturation is determined by a direct reading.
Pulse oximetry
The oximetry system determines arterial oxygen saturation by
measuring the absorption of selected wavelengths of light in pul-
satile blood fl ow [43] . Oxyhemoglobin absorbs much less red and
slightly more infrared light than reduced hemoglobin. Oxygen
saturation is therefore the ratio of red to infrared absorption.
Red and infrared light from light - emitting diodes are projected
across a pulsatile tissue bed and analyzed by a photodetector. The
absorption of each wavelength of light varies cyclically with pulse.
The patient ’ s heart rate, therefore, is also determined. When
assessing the accuracy of the arterial saturation measured by the
pulse oximeter, correlation of the oximeter determined heart rate
and the patient ’ s actual pulse rate indicates proper electrode
placement. The oximetry probe is usually placed on a nail bed or
ear lobe. Under ideal circumstances, most oximeters measure
saturation (S
p
O
2
) to within 2% of S
a
O
2
[43] .