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CHAPTER 8 Acid-Base Homeostasis and Oxygenation
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189
Respiratory
acidosis
Respiratory
alkalosis
Metabolic
acidosis
FIGURE 8.1 Acid-base derangements. Large arrow indicates
primary process that produces change in pH. Small arrow indicates
compensatory process.
Metabolic
alkalosis
return pH toward normal. Retention of bicarbon-
ate and corresponding excretion of hydrogen
ions are the compensatory renal mechanisms
that counterbalance respiratory acidosis. Given
sufficient time, this may increase blood bicarbonate
by as much as 3 to 4 mEq/L for each increase of
10 mm Hg in carbon dioxide. Thus, a neonate with
a chronically increased Paco2 and a compensatory
rise in bicarbonate may attain a near-normal pH.
33
Metabolic compensations for deranged respiratory processes can go to remarkable extremes, but
respiratory compensations for deranged metabolic
processes are limited. Hyperventilation cannot lower
the Paco2 much below 10 mm Hg in compensation
for metabolic acidosis. Similarly, hypoventilation is
limited in compensation for metabolic alkalosis by the
onset of hypoxemia.53 Hypoxemia stimulates the respiratory drive, overriding compensatory hypoventilation
and limiting the correction of alkalemia.
33
CORRECTION
Correction of an acid-base disturbance occurs
when the health care provider detects the
pathophysiologic process and directs therapy
at the primary pathologic process, rather than
counterbalancing it with a second pathologic
process.
For example, if respiratory acidosis is present, the clinician assesses the patient to discover
the cause of the carbon dioxide retention and
directs therapy at improving minute ventilation,
the product of respiratory rate and tidal volume,
rather than attempting to increase the retention
of bicarbonate.
Respiratory
parameter
P
CO
2
Metabolic
parameter
HCO
3
Cause
Hypoventilation
Hyperventilation
Add acid or
lose base
Add base or
lose acid
Oxygenation
The remaining components of the blood gas
analysis are the Po2, hemoglobin, and oxygen
saturation.44 Oxygenation is related to but also
distinct from ventilation.10 The two main factors
contributing to oxygenation at the tissue level
are oxygen delivery and oxygen consumption.
Oxygen delivery is the product of the cardiac output and the oxygen-carrying capacity of the blood,
whereas oxygen consumption is determined by
the metabolic needs of the body’s tissues. Tissue
hypoxia may be caused by many different factors that derange the balance between oxygen
delivery and tissue needs. An inability of the
lung to oxygenate the blood would decrease
oxygen delivery because of arterial hypoxemia.
Another cause of tissue hypoxia is interference
with blood flow, as in heart failure. The Pao2
may be normal, but because of heart (pump) failure, oxygenated blood is not delivered in sufficient
quantity. Treatment should be directed toward
improving cardiac output and tissue perfusion (see
Chapter 24). A third cause of tissue hypoxia
is decreased oxygen-carrying capacity of the
blood, as with anemia. In this instance, the
heart and lungs work adequately. Pao2 is normal, but the quantity of hemoglobin available
for oxygen transport is insufficient. Finally,
tissue hypoxia may result from an abnormally
high affinity of hemoglobin for oxygen, which
leads to a decrease in tissue oxygen delivery.
If oxyhemoglobin affinity is increased, oxygen
will not dissociate from hemoglobin unless the
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% Oxygen
Oxygen content
2
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venous, and therefore tissue, Po2 falls to an
unusually low level.
14
Because Pao2 measures only the partial pressure of oxygen in arterial blood (i.e., measures
the amount of dissolved oxygen gas in the
blood), it reflects lung function but not tissue
oxygenation. Despite this, the measurement of
Pao2, together with the measurement of hemoglobin and a clinical assessment of tissue perfusion, is currently used as a surrogate of tissue
oxygenation.
10
Two situations merit special comment. First, in
a preterm infant whose retinal development is
incomplete, high Pao2 is associated with retinopathy of prematurity, especially at a Pao2 of
greater than 100 mm Hg (see Chapter 23). Second,
in patients with cyanotic congenital heart dis-
ease, a right-to-left intracardiac shunt affects
tissue oxygenation. A portion of venous blood
goes directly to the left side of the heart, then into
the systemic circulation, bypassing the lungs. In such
patients, the rise in Pao2 with the administration
of oxygen is limited. Low Pao2 in these patients is
not related to lung disease, although lung disease
may complicate the picture, but results from blood
bypassing gas exchange in the lungs.
Theoretically, in a normal lung with perfectly
matched ventilation and perfusion, the alveolar
(Pao2) and the arterial oxygen tension (Pao2)
should be equal. This is not achieved. A difference
(gradient) exists between the Pao2 and the Pao2.
Minor mismatching of ventilation and perfusion
leads to a functional intrapulmonary shunt. This
creates an alveolar-arterial oxygen gradient (D[a-a]
10,17
O2).
Hg indicates pulmonary disease.
However, a D(a-a)O2 greater than 20 mm
10
OXYHEMOGLOBIN SATURATION
Oxyhemoglobin saturation is the percentage
of hemoglobin that is combined with oxygen.
Oxygen binding with hemoglobin increases as
the partial pressure of oxygen increases, but not
linearly.
10,56
The oxygen dissociation curve is a
measure of the affinity that hemoglobin has for
oxygen (Fig. 8.2).
The “30-60-90 rule” is useful in remembering percent saturation and reconstructing
the adult hemoglobin dissociation curve if
necessary (see Fig. 8.2). At a Pao2 of 30 mm Hg,
the oxygen saturation is 60%; at a Pao2 of 60 mm
Hg, saturation is 90%; and at 90 mm Hg Pao2,
16
saturation
100
90
75
60
50
30 40 60 90 100 700
O
(mm Hg)
Pa
FIGURE 8.2 Oxygen-hemoglobin dissociation curve; the 30-60-90 rule is
demonstrated. Right, The oxygen content for a hemoglobin concentration of 16
and 8 g/dL is given, demonstrating the effect of anemia on venous saturation
and tissue oxygenation.
g/dL
dL22.12
21.1
AV
difference
16.6
8
g/dL
11.12
10.6
AV
difference
6.1
the hemoglobin is 95% saturated. At the normal venous oxygen tension of 40 mm Hg, the
oxygen saturation is 75%. Factors that affect this
affinity include temperature, pH, and hemoglobin
structure. Hypothermia, alkalemia, hypocapnia,
and fetal hemoglobin increase the affinity of
hemoglobin for oxygen (shift the curve to the
left), whereas fever, acidemia, and hypercapnia
decrease the affinity of hemoglobin for oxygen
(shift the curve to the right).
At a given tissue Po2, an increased hemoglobin affinity for oxygen leads to less oxygen
released at the tissue level, whereas a decreased
affinity allows for more oxygen release to the
tissues. Alternately, the Po2 at which the oxy-
gen-binding sites of hemoglobin are 50% saturated
(the P50) is low when the hemoglobin affinity is
great and higher when the hemoglobin affinity
is low.10 The affinity of fetal hemoglobin for
oxygen is higher than adult hemoglobin (see
Figure 7.1). The P50 of fetal hemoglobin is 19 mm
Hg compared with a P50 of 27 mm Hg for adult
hemoglobin. Approximately 70% of hemoglobin
in term infants, and more in preterm infants,
consists of fetal hemoglobin.14 As a result, hemo-
globin in a term infant with a Pao2 of 35 mm Hg
will be 80% saturated, and a “pink” newborn infant
may have a low Pao2.
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191
OXYGEN CONTENT
Oxygen content is calculated from the hemoglobin saturation and hemoglobin concentration. One gram of hemoglobin binds 1.39 mL
of oxygen. The oxygen content in milliliters per
deciliter is the product of the saturation percentage
and the hemoglobin in grams per deciliter plus the
amount of dissolved oxygen. For clinical purposes,
we can neglect the amount of dissolved oxygen in
the plasma because it is only 0.003 mL/dL/mm Hg.
Oxygen content becomes critical in anemia,
which can decrease tissue oxygenation unless
organ blood flow and cardiac output increase to
maintain the delivery of oxygen.
10,55
The blood
of an infant with a hemoglobin of 8 g/dL will have
half the oxygen content compared to that of an
infant with a hemoglobin of 16 g/dL at an equivalent oxygen saturation percentage. In Fig. 8.2, an
infant with 16 g hemoglobin that is 95% saturated
(Pao2 = 90 mm Hg) carries 21.1 mL/dL oxygen,
whereas the infant with 8 g hemoglobin carries
10.6 mL/dL oxygen. Tissues require approximately
4 to 5 mL/dL oxygen to maintain aerobic metabolism. With normal cardiac output, venous blood
contains 4 to 5 mL of oxygen which is less than
the arterial blood. The venous oxygen content in an
infant with 16 g hemoglobin would be between 16
and 17 mL/dL, which corresponds to approximately
75% saturation, or a Pvo2 of 40 mm Hg. However,
unless cardiac output increases, the venous oxygen
content in an infant with 8 g hemoglobin would be
6.1 mL/dL oxygen. The saturation is 55%, which
corresponds to a Po2 of less than 30.
BLOOD FLOW AND SHUNTS
The product of oxygen content and blood flow
returning from the lungs determines the total
amount of oxygen in arterial blood if no intraor extracardiac shunting occurs. Total pulmonary
blood flow can be divided into the amount of blood
in the pulmonary capillaries and the amount that is
shunted through or around the lungs.
A right-to-left shunt occurs when blood
passes from the systemic venous to the systemic
arterial circulation. This can occur because of ana-
tomic defects in the heart (e.g., cyanotic congenital
heart disease), with a persistently patent ductus
arteriosus in the presence of pulmonary arterial
pressures that are higher than systemic arterial
pressures (pulmonary hypertension), or when pulmonary capillary blood perfuses poorly expanded
alveoli (e.g., intrapulmonary shunts). Shunts lower
the final arterial oxygen saturation. The usual
degree of shunting in a newborn is 15% to 20%
of the cardiac output.
Acid-Base and Oxygenation
Disorders
Ventilation is defined as the amount of gas
leaving the lungs per unit of time (e.g., minute
ventilation). Minute ventilation is equal to the
product of the tidal volume and respiratory frequency in breaths per minute. The tidal volume is
composed of (1) gas in the airway and nonperfused
alveoli (physiologic dead space) and (2) gas in the alve-
olar space.
the ratio of CO2 production by the body to the
Paco2. Alveolar ventilation is inversely related
to Paco2. When Paco2 doubles, alveolar ventilation
is approximately one half of the original value. If the
Paco2 triples, alveolar ventilation is approximately
one third of the original value, and so forth.
RESPIRATORY ACIDOSIS
When the lungs become less effective at removing carbon dioxide, Paco2 increases, and respiratory acidemia ensues. The causes of respiratory
acidosis can be separated into pulmonary and
nonpulmonary causes.17 The most common pulmo-
nary cause of respiratory acidosis in term newborns
is obstructive lung disease, such as meconium aspiration48 and transient tachypnea43 of the newborn.
For newborns delivered prior to 34 weeks’ estimated
gestational age, surfactant deficiency and immature
parenchymal lung and neuromuscular development
are the most common reasons for respiratory acidosis. Obstructive lung disease occurs in the recovery
phase of uncomplicated respiratory distress syndrome
(RDS) and in bronchopulmonary dysplasia.47 Also
included in the pulmonary causes of hypoventilation
are conditions that interfere with the expansion of
the lungs, such as diaphragmatic hernia, phrenic nerve
paralysis, a space-occupying mass, or pneumothorax.
These limit the tidal volume.
A nonpulmonary cause of carbon dioxide
retention is poor respiratory effort. A decreased
respiratory drive may be secondary to medications
such as opioids, sepsis, intracranial hemorrhage
(including intraventricular hemorrhage), prematurity, hypothermia, and metabolic disturbances, such
as hypoglycemia.17 Even if the respiratory drive is
10,17
Alveolar ventilation is defined as
17
1
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appropriate, newborns may have an inadequate
neuromuscular ability to ventilate. Ineffective
respiratory mechanics may be related to prematurity, systemic illness with multiorgan dysfunction,
and conditions that decrease muscular tone and
strength such as those found in certain genetic
syndromes (Prader-Willi), maternal conditions
(Graves’ disease), and medication side effects (magnesium sulfate for maternal preeclampsia).
RESPIRATORY ALKALOSIS
In respiratory alkalosis, carbon dioxide clearance
is increased, and thus Paco2 is below normal.20
Respiratory alkalosis occurs as a result of hyperventilation, which may be caused by (1) excessive ventilatory support; (2) central nervous system (CNS)
stimulation that increases the respiratory drive (e.g.,
hyperammonemia from a genetic abnormality of
the urea cycle);11 and (3) hypoxemia, which stimulates respiratory centers through chemoreceptors.
NONRESPIRATORY (METABOLIC)
ACIDOSIS
20
In nonrespiratory (metabolic) acidosis, the metabolic component results from either adding
nonvolatile acid (an acid other than carbonic
acid) or losing base (bicarbonate).
35,48,53
The
underlying mechanisms of metabolic acidosis are (1)
the loss of base in urine or stool, (2) exogenous acid
that is unable to be effectively secreted by the kidneys (high levels of amino acid administration), and
(3) abnormal metabolism that leads to an increase in
nonvolatile acid levels. Nonvolatile acids originate
from lactic acid in circulatory shock and hypoxia,
organic acids in inborn errors of metabolism, and
ketoacids in diabetic acidosis. Loss of bicarbonate
occurs in renal tubular acidosis (inability of the
renal tubules to reabsorb bicarbonate appropriately), with stool loss (diarrhea), or through urinary
excretion.
the mechanism of metabolic acidosis.
50,52,54
Measurement of the anion gap helps identify
15,18,29,54
The anion gap is variably calculated as the serum
sodium concentration minus the serum chloride concentration minus the serum bicarbonate
concentration
33,54
or, alternatively, sodium plus
potassium minus chloride minus bicarbonate.*
The upper limit of the normal anion gap with the
* References 9, 15, 17, 21, 23, 40.
first method is given as 14 mEq/L54 and with the
second method as 15 mEq/L.26 Addition of nonvolatile acids is associated with an increased anion
gap. Loss of base or excess chloride [Cl–] is the
likely mechanism of acidosis with a normal
anion gap.
46,54
The advantage of measuring the
anion gap in understanding the effect of excessive
chloride administration is clear. Given that there
must be a balance between blood cations and anions
to preserve electroneutrality, [Cl–] in excess simply
displaces [HCO
–
], resulting in metabolic acidosis.54
3
In normal anion gap acidosis, low serum potassium
indicates loss of base (e.g., diarrhea), and high serum
potassium points to a renal defect (e.g., renal tubular
acidosis).
33
Albumin is a major component of the anion
gap. Hypoalbuminemia, common in critically ill
neonates and children, may mask the presence of
the anions of lactic and organic or other nonvolatile
15,16,18,26,33
acids.
A “normal” anion gap in combination with low serum albumin indicates that a
nonvolatile acid anion is making up the difference
for “absent” anions that albumin would ordinarily
provide. Correcting the anion gap for hypoalbuminemia is accomplished by adding 2.5 mEq/L to
the anion gap for every g/dL that the concentration
of serum albumin is reduced below the normal
value of approximately 3.5 g/dL.
NONRESPIRATORY (METABOLIC)
ALKALOSIS
15,52
Nonrespiratory (metabolic) alkalosis is caused
by either a loss of acid or an increase of base,
principally bicarbonate.30 Alkalosis occurs when
excessive amounts of bicarbonate, acetate, citrate,
or lactate are given; metabolism of the latter three
anions in the liver generates bicarbonate. Loss of
acid occurs with gastric fluid removal or prolonged vomiting, as can be seen with pyloric
stenosis. Acid loss by renal mechanisms can
occur through the influence of diuretics, digitalis, or corticosteroids.20 Urine electrolytes,
especially chloride, are useful in the differential
diagnosis of metabolic alkaloses. Low urine Cl–
(<20 mEq/L) is associated with chloride (saline)–
responsive metabolic alkalosis from acid loss (e.g.,
vomiting, nasogastric suction), whereas high urine
Cl– is associated with chloride (saline)–unresponsive metabolic alkalosis from renal acid loss (e.g.,
diuretics).
18,33
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193
OXYGENATION
Inadequate cardiac output, anemia, an increased
hemoglobin affinity for oxygen, and hypoxemia (decreased Pao2) may cause tissue hypoxia.
Hypoxemia results from lung disease or cyanotic congenital heart disease. The most common
lung abnormality is mismatched ventilation and
perfusion.10 In newborns, there is always some
degree of ventilation and perfusion mismatch. Two
extreme examples are (1) ventilated and oxygenated
alveoli without perfusion (e.g., pulmonary emboli)
and (2) perfused but nonventilated alveoli (atelectasis). The former is an example of wasted ventilation,
and the latter represents an intrapulmonary shunt.
Either extreme is incompatible with life. Clinically
relevant degrees of ventilation-perfusion mismatch
lie somewhere between those extremes.
Hypoxemia, resulting from ventilation-per-
fusion mismatch, can be overcome with supplemental inspired oxygen. An increased inspired
oxygen concentration will eventually displace
nitrogen from even the most poorly ventilated
alveoli, and alveolar and then arterial oxygen tension will increase. However, when an extrapul-
monary shunt bypasses the lungs, Pao2 does
not increase. This is important because clinicians
can differentiate parenchymal lung disease from
cyanotic congenital heart disease as a cause of
hypoxemia: the latter will not have a significant
increase in Pao2 even with the administration of
100% oxygen.
To perform the hyperoxia test, the clinician
should place the neonate in 100% oxygen for 10
to 15 minutes and obtain a right radial arterial
blood sample. If the Pao2 rises to more than
150 mm Hg, cyanotic congenital heart disease
is very unlikely, and lung disease is the most
common etiology.
Central hypoventilation from narcosis may
cause hypoxemia. As alveolar carbon dioxide
rises, Pao2 falls, and Pao2 decreases. This condition
should be clinically evident and should not be
confused with lung or congenital heart disease.
Other causes of hypoxemia, such as decreased
inspired oxygen tension with increasing altitude
and oxygen diffusion limitation, are uncommon
in the infant.
PREVENTION
Prevention of acid-base and oxygenation disturbances and maintenance of acid-base homeostasis
10
require attention to detail. A clinician must have an
understanding of the physiologic principles of acidbase homeostasis and oxygenation to identify the
underlying mechanism and treat with the appropriate medical intervention(s).
With respiratory disturbances, immediate assessment and prompt therapy, including supplemental inspired oxygen and assisted ventilation,
may help improve oxygenation and the respiratory component of acid-base disturbances (see
Chapter 23). Careful monitoring of fluid and elec-
trolyte intake and output, minimizing blood loss,
and observing for sepsis help the clinician prevent
the development of nonrespiratory acid-base disturbances (see Chapters 4 and 22).
DATA COLLECTION
Monitoring inspired oxygen concentrations and arterial
oxygen tension and supplying appropriate concentrations of additional inspired oxygen will prevent hypoxemia and hyperoxemia (see Chapter 23). Monitoring
may be accomplished intermittently through indwelling arterial catheters or continuously by transcutaneous
oxygen monitors and pulse oxygen saturation devices
(see Chapter 7). Monitoring hemoglobin concentra-
tions and blood loss, with appropriate replacement,
helps ensure adequate blood oxygen content.
Reviewing the patient’s history, performing a
physical examination, and evaluating laboratory data
augment each other in the assessment of disturbances
in acid-base homeostasis and oxygenation (Box 8.2).
History
An adequate obstetric and perinatal history may
warn of potential acid-base and oxygenation disturbances in the newborn:
• Premature delivery predisposes the infant to
infection and respiratory insufficiency.
• Meconium staining may portend infection, lung
disease, and right-to-left shunting with associated
pulmonary hypertension.
• Prolonged rupture of membranes, maternal dia-
betes, or abnormal maternal bleeding may be
associated with either metabolic or respiratory
acid-base disturbances and hypoxemia.
• A neonatal history of vomiting, diarrhea, or
other gastrointestinal disturbances can cause
acid-base disturbances.
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BOX
8.2
EVALUATION OF ACID-BASE
DISTURBANCES AND OXYGENATION
PROBLEMS IN NEONATES
1. History
a. Obstetric and perinatal
b. Neonatal
c. Family
2. Physical examination
a. Vital signs
b. General appearance
c. Respiratory effort
d. Pulmonary examination
e. Cardiac examination
f. Abdominal examination
g. Neurologic examination
3. Laboratory
a. Chest x-ray film
b. Arterial blood gases
c. Urinalysis
d. In selected cases: sepsis evaluation, serum electrolytes, serum
albumin, urine electrolytes, and urine osmolality
• The infant’s general appearance, feeding habits,
and activity level may indicate sepsis or CNS
injury, both of which promote acid-base disturbances and hypoxemia.
• Nosocomial infections and pneumonia may significantly influence acid-base and oxygenation
disturbances.
• A family history of inherited renal problems such as
tubular acidosis may suggest an acid-base disturbance.
• A family history of salt-losing endocrinopathies
may produce an acid-base disturbance.
Physical Examination
SIGNS AND SYMPTOMS
Signs of acid-base disturbance vary widely and
often go undetected. Hypothermia, hypotension,
tachycardia, bradycardia, or poor peripheral perfusion should alert caretakers to the possibility of
metabolic acidosis. An altered respiratory rate
and pattern, grunting respirations, nasal flaring,
and chest wall retractions raise the possibility of
respiratory acidosis or respiratory compensation
for metabolic acidosis. Abnormalities on auscul-
tation of the heart may point to congenital heart
disease and resulting acid-base and oxygenation
abnormalities. Lethargy, seizures, and abnormal
neurologic signs increase concern for acid-base disturbances or hypoxemia.
LABORATORY DATA
Chest Radiograph: A chest x-ray examination may
assist in identifying a respiratory or cardiac cause
for an acid-base disturbance and hypoxemia.
Urinalysis: The routine urinalysis records urine
specific gravity and complements monitoring
of urine output. Urine electrolytes and pH are
helpful in differentiating among the pathophysiologic mechanisms of metabolic derangements.
Arterial Blood Gases: Interpretation of the arterial
blood gases will point to the primary acidbase derangement and may reveal a secondary compensation and define the degree
of hypoxemia.
9,28,37,49
Presently, methods for
monitoring the components of acid-base analysis comprise both invasive and noninvasive
techniques. Intermittent arterial punctures or
indwelling catheters in various vessels (often the
umbilical artery or vein) supply data. However,
we can continuously measure transcutaneous
Po2 or O2 saturation. Monitors can continuously measure expired end-tidal CO2, which
corresponds to the alveolar CO2. (Alveolar and
arterial CO2 are equivalent unless respirations
are excessively rapid.) In addition, skin electrodes
are available that measure Pao2 and Paco2 with
varying success (see Chapter 7).
Although the pathophysiologic condition of the
acid-base disturbance is determined through the
analysis of arterial blood gases, further assessment of
the infant is necessary, as follows:
• Respiratory alkalosis or acidosis can be suspect-
ed on the basis of obstetrical and family history,
physical examination, and chest x-ray or diagnosed by arterial blood gas analysis.
• Metabolic acidosis often accompanies shock and
septicemia. The anion gap and urine electrolytes
may provide additional information to delineate
causes. Blood pressure measurement, a complete
blood cell count, an infectious work-up, serum
and urine electrolytes and pH, serum albumin
and glucose determinations, and assessment of
intake and output of fluids are often needed to
identify the source of metabolic acidosis.
• Oxygenation disturbances may be analyzed from
the preceding laboratory tests and, when indicat-
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195
TABLE
8.2
pH 7.25–7.45 7.18–7.38
Pco2 (mm Hg) 26.8–49.2 32.2–65.8
Po2 (mm Hg) 17.2–40.8 5.6–30.8
HCO
Base deficit (BD) (mmol/L) 0–8
UMBILICAL VENOUS AND ARTERIAL
CORD BLOOD GAS VALUES
VENOUS ARTERIAL
–
(mmol/L) 15.8–24.2 17–27
3
0–8
ed, an echocardiogram to evaluate for structural
heart disease or pulmonary hypertension. If an
echocardiogram is not readily available, performing a hyperoxia test to evaluate for the possibility
of congenital heart disease may be necessary.
Another calculation, the oxygenation index (OI),
is used to assess critically ill neonates receiving
ventilator therapy. The OI is (Fio2 × 100 × mean
airway pressure) divided by Pao2 or, simply
put, work/result. In some centers, an OI of 25
or greater has been considered an indication for
extraordinary ventilatory support, such as inhaled
nitric oxide or extracorporeal membrane oxygenation (ECMO).
CORD BLOOD GAS INTERPRETATION
18
Providers participating in delivery room stabilization, as well as subsequent care of at-risk newborns,
benefit from a thorough understanding of cord gas
interpretation, as well as familiarity with the perinatal conditions that may have an adverse effect
on fetal outcome. Table 8.2 describes normal cord
blood gas values.
38
When reviewing cord gas values, it is import-
ant to note that there is a broader range of
normal values than with postnatal blood gas
values, and the relationship between the venous
and arterial norms is the opposite of that in conventional blood gases.41 With fetal circulation,
the umbilical vein transports oxygenated blood
from the placenta (acting as the fetal lung) to
the fetus. The umbilical arteries transport blood
from the fetus back to the placenta for gas
exchange. The most useful value of cord blood
sampling for the clinician caring for the newborn is the umbilical arterial blood pH because
it is indicative of the fetal metabolic condition
just prior to birth and is most strongly associated
with perinatal mortality and important morbid-
22,37
ities.
UMBILICAL CORD BLOOD GAS
SAMPLING
Controversy exists as to which perinatal circumstances warrant collection and review of umbilical cord
blood gases. The American College of Obstetricians
and Gynecologists’ Committee on Obstetric Practice
updated its opinion statement regarding cord blood
gas analysis in 2012.3 Cord gas collection and
review should occur in circumstances of cesarean delivery for fetal compromise, low 5-minute
Apgar score, severe growth restriction, abnormal
fetal heart rate tracing, maternal thyroid disease,
intrapartum fever, or multiparous gestations.
There are a few points to keep in mind when
collecting and analyzing cord blood. Following
delivery, immediate collection and analysis of
cord blood ensure the greatest sampling accuracy.
However, valid results can be obtained with samples
collected and analyzed within 1 hour at room temperature or analyzed within 6 hours if the samples
are refrigerated.50 The placenta continues to be
metabolically active following delivery, and theoretically, if the blood being sampled is in close
proximity to the placenta, there may be continued gas exchange, yielding cord gas results that
reflect a dynamic state and not necessarily the
prior fetal environment.
5
Over the past decade, delayed cord clamping
has become quite common and is now considered standard practice at the delivery of term and
preterm newborns. Umbilical blood vessel sampling
is possible during delayed cord clamping,4 but does
delayed cord clamping, as compared to immediate
cord clamping, affect the results and interpretation of
arterial or venous cord blood samples? At the time
of birth, dramatic physiologic changes occur as the
fetus moves from a fluid-filled environment, which
relies on the placenta for gas exchange, to an air-filled
environment, whereby the newborn’s cardiorespiratory system fulfills that role. During delayed cord
clamping, gas exchange may occur simultaneously through the placenta and the newborn’s
cardiorespiratory system, which has the potential
to significantly alter sampled cord blood gas
values such as pH, Po2, Pco2, and base deficit. A
recent study51 compared paired samples of arterial and
venous cord blood samples obtained immediately after
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birth with those obtained after delayed cord clamping
in term pregnancies. Statistically significant differ-
ences were noted for pH, Pco2, lactate, and base
excess, but not Po2. The mean differences noted
between immediate cord clamping and delayed
cord clamping were as follows: pH lower by
0.03, Pco2 higher by 3 mm Hg, lactate higher
by 3 mg/dL, bicarbonate lower by 0.3 mmol/L,
and base deficit increased by 0.3 mmol/L. In term
deliveries, a significantly lower pH and higher Pco2
have been found in cord blood samples obtained after
vaginal delivery as compared to operative deliveries.37
The results, although statistically significant, may
not be clinically relevant; however, these differences
should be considered when interpreting cord blood
gas values obtained with delayed cord clamping after
vaginal or operative deliveries.
CORD BLOOD GAS INTERPRETATION
Asphyxia results when there is an interruption
of placental-fetal gas exchange. More specifically, asphyxia is defined as metabolic acidemia following birth measured by a pH of less
than 7.00 and a base deficit of greater than 12
mmol/L.41 General causes of intrapartum asphyxia
are (1) impaired uteroplacental gas exchange (uteroplacental insufficiency), (2) inadequate umbilical
blood flow (cord occlusion), and (3) impaired fetal
cardiac output.
General principles of cord blood gas interpreta-
tion include the following:
1. Umbilical venous blood represents uteroplacental status.
2. Umbilical arterial blood represents fetal and
uteroplacental status.
3. When interpreting an infant’s paired cord gases,
the cord venous gas will always have a higher
pH, a lower Pco2, and a higher Po2 than the
umbilical artery cord gas. If values do not align
with these rules of interpretation, it is likely that
the samples were from the same vessel or misla-
8,40
beled.
Uteroplacental Insufficiency. There are multiple peri-
natal and intrapartum factors that can lead to
uteroplacental insufficiency. Some common clinical conditions include maternal hypotension
or hypertension, maternal hypoxia, maternal
medications, a hyperstimulated uterine contraction pattern, premature placental separation, and
defects in placental development. On many
occasions, uteroplacental insufficiency is mild
in nature and has no lasting effect on neonatal outcome. However, if a critical threshold of
uteroplacental insufficiency is reached, the fetus
becomes hypoxic. The degree and duration of
the hypoxia will determine whether metabolic acidosis will occur.21 When intrapartum
asphyxia is the result of uteroplacental insufficiency, the umbilical venous and arterial
blood gases will both reveal derangements in
acid-base status. However, with fetal hypoxia,
the arterial gas will demonstrate a lower pH,
higher Pco2, and lower Po2 than the venous
cord sample. On many occasions, the cord
gases reveal a paired respiratory acidosis without a metabolic component, which indicates
an acute (less than 30 minutes) event.
Cord Occlusion (see Chapter 2). Identification of true
8
cord prolapse during labor is enough to raise even
the calmest of clinician’s heart rates. However,
there are several less intuitive scenarios leading to
functional cord occlusion that result from stretching or compression of the umbilical vessels. They
include an anatomically short cord; breech presentation; occult cord prolapse; shoulder dystocia;
nuchal cord; body cord; true knot in the cord;
kinking of the cord; cord entanglement between
monoamniotic/monochorionic twins; and following rupture of the membranes, any instance
in which there is compression of the umbilical
cord vessels.
41
The most common cord occlusion scenario is
compression of the umbilical vein and at least
partial patency of the umbilical arteries due to
the differences in the vessel wall structure. The
vein is thin walled and more easily compressed as
compared with the thicker, more muscular arterial wall, which is less prone to compression. Cord
blood gas sampling in this scenario would yield
a near-normal venous gas with an arterial sample
demonstrating metabolic and respiratory acidosis
to various degrees depending on the severity and
duration of the vessel compression. Overall, the
hallmark cord gas findings in cord occlusion are
a widened venoarterial pH, Pco2, and at times,
base deficit differences.
Fetal Circulatory Failure. A myriad of causes can ulti-
mately lead to fetal circulatory failure. Included
CHAPTER 8 Acid-Base Homeostasis and Oxygenation
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197
among these are fetal hemorrhage/anemia, structural heart disease, arrhythmias, cardiomyopathies,
extracardiac malformations, and septic shock.
For example, in progressive fetal anemia, as seen
with Rh isoimmunization, the fetus compensates
for the anemia by increasing cardiac output. As
the anemia worsens, oxygenation becomes
inadequate to meet cellular metabolism, and
heart failure occurs. As cardiac output decreases
and blood flow slows, there is increased oxygen
extraction from the blood and increased production of CO2. This phenomenon will create widened venoarterial pH, Pco2, and Po2 differences.
Cord gases following fetal circulatory failure
have a similar appearance to gases obtained
after cord occlusion.
PATHOLOGIC PREDICTIVE VALUE OF
CORD BLOOD GASES
41
Cord blood gas data and analysis are useful for
immediate management, but pH alone is poorly
predictive of long-term outcomes. Infants who
recover quickly with reassuring neurologic examinations tend to have good long-term outcomes
regardless of cord blood pH.25 Although low cord
blood pH is clearly associated with poor outcome,
association is not cause and effect. The underlying
cause of both acidosis and organ damage is tissue
hypoxia.
25,31
In contrast, an arterial cord pH of
less than 7.00 in combination with abnormal
clinical signs and symptoms is strongly associated with adverse outcomes.57 Low et al. demon-
strated that arterial base deficits of 12 to 16 mmol/L
were associated with moderate or severe newborn
sequelae in 10% of the neonates studied. That number increased to 40% of neonates once the base deficit reached greater than 16 mmol/L.36 Conversely,
mild acidosis is not usually associated with newborn
complications. Although analysis of cord gases can
at times be difficult, paired cord blood gases have a
role in determining underlying etiologies, guiding
further evaluation and appropriate treatment(s).
treated with increased inspired oxygen concentration. Techniques that may be of benefit to treat
respiratory acidosis include continuous positive airway
pressure (CPAP), standard ventilation, high-frequency
ventilation, ECMO, inhaled nitric oxide, and others
(see Chapter 23) . Treatment of respiratory alkalosis
usually consists of reducing minute ventilation.
One of the causes of neonatal central hyperventilation
that requires a high index of suspicion and urgent
evaluation and treatment is hyperammonemia caused
by an inborn error of urea cycle metabolism11 (see
Chapter 27).
Asphyxia often leads to a combined respiratory and metabolic acidosis. Ventilation will
resolve the respiratory acidosis. Improved oxygen delivery and tissue perfusion usually resolve
lactic acidosis without bicarbonate therapy. In
narcosis, temporary ventilator support may be necessary. Narcosis may be reversed with the admin-
istration of naloxone (Narcan) at a dose of 0.1
mg/kg if the possibility of chronic maternal opiate drug abuse has been ruled out. With chron-
ic intrauterine opioid exposure, neonatal Narcan
administration may result in acute withdrawal and
seizures (see Chapter 4).
With any acidosis and alkalosis, determining
the underlying etiology is critical for effective
management. If the cause of metabolic acidosis is
septicemia, intestinal necrosis, or poor cardiac output
severe enough to result in metabolic acidosis, successful treatment of the cause is of far more importance
than buffer therapy for acidosis. Historically, sodium
bicarbonate has been administered for neonatal metabolic acidosis. However, controversy exists on the
true physiologic benefit from sodium bicarbonate
administration.7 Sodium bicarbonate administra-
tion may conversely cause harm, especially with
a bolus administration, because it is a hypertonic
solution that may increase the risk of intraventricular hemorrhage.
13,35,45
It should not be used if
severe lung disease restricts carbon dioxide elimination (see Equation 3).
TREATMENT
In respiratory acidosis, the pathophysiologic mechanism is decreased alveolar ventilation. Treatment
is directed at the underlying cause.15 Hypoxemia
caused by ventilation-perfusion mismatch is
COMPLICATIONS
Unrecognized oxygenation disturbances may
lead to increased mortality or morbidity rates
in survivors. Unrecognized acid-base disorders
are not as important in themselves as they are
198 UNIT TWO Support of the Neonate
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because they serve as indicators of unrecognized serious, perhaps life-threatening pathology such as septicemia or poor cardiac output.
For example, otherwise-normal newborn infants
and trained athletes can be severely acidotic without consequences.
25,27
Everyday, clinical experience in neonatal intensive care confirms that
chronic respiratory acidosis, even with extreme
hypercapnia, can be tolerated for long periods. It
is not always appreciated that acute correction
of chronic acid-base disorders can be more
problematic than the disorder itself. For exam-
ple, sudden correction of respiratory alkalosis
results in potentially damaging acute increases
in cerebral blood flow.23 Sudden correction of
chronic hypercapnia was long ago shown to be
problematic.
17,18,30,40,42
In short, complications
of the correction of the acid-base balance vary
EXAMPLE CASES
Case 1
You are caring for a 7-day-old, former 36-week female infant who has
poor feeding, sleepiness, decreased urine output, and a new oxygen
requirement with Fio2 0.40 on 2-L/min nasal cannula. On exam, she
is only mildly responsive to stimulation; has delayed capillary refill of
3 to 4 seconds throughout, with poorly palpable peripheral pulses,
especially in her lower extremities; and has a respiratory rate in the
80s, with labored breathing and clear breath sounds. Blood pressure
measured with a cuff on her right arm is 65/40, heart rate is regular
in the 160s, and oxygen saturations range in the low 90s in the right
upper extremity. You are concerned about her appearance and order a
chest x-ray, complete blood count (CBC) with differential and platelets,
electrolytes, blood culture, urine culture with Gram stain and microanalysis, C-reactive protein, and arterial blood gas. The first result that
confirms your concerns is the arterial blood gas: pH 7.03, Pco2 30, Po2
55, calculated bicarbonate of 9, base excess of –16. Serum electrolyte
results include the following: sodium of 134, potassium of 5.9, chloride
of 95, and bicarbonate of 10. You calculate an anion gap of 35 (134 +
5.9 – 95 – 10). Your clinical suspicion is that this newborn has coarctation of the aorta that has become critical upon closure of her patent
ductus arteriosus, which is confirmed by echocardiogram. The patient
receives an administration of parenteral prostaglandin, establishment
of arterial and central venous access, and a cardiology consultation.
In patients with metabolic acidosis, it is imperative to identify the
cause of the acidosis, which, in this case was due to decreased oxygen
delivery to tissues below the level of the coarctation, resulting in a
large anion gap metabolic acidosis from lactic acid production due to
anaerobic metabolism.
according to the disturbance and the treatment provided. The treatment of respiratory
acidosis by assisted ventilation can produce
all of the complications of assisted ventilation,
including infection, trauma, oxygen toxicity,
sepsis, air leak, and subglottic stenosis (see
Chapter 23).
Complications of oxygen therapy include
hypoxemia and hyperoxemia. Severe hypox-
emia may cause pulmonary vasoconstriction, a
change from aerobic to anaerobic metabolism
(with eventual metabolic acidosis), bradycardia, hypotonia, and impaired CNS and cardiac
function. Prolonged high inspired oxygen con-
centrations can result in oxygen toxicity, which
may be central to significant morbidities such as
retinopathy of prematurity and bronchopulmonary
dysplasia.
12,28
Case 2
You attended the delivery of a 32-week, 1.6-kg infant after preterm labor with rupture of membranes and clear fluid 1 hour before delivery. The
mother did not receive betamethasone or antibiotics before delivery. He
was delivered vaginally, with Apgar scores of 5 and 7 at 1 and 5 minutes,
respectively. He presented with poor respiratory effort and responded to
drying, stimulation, and positive-pressure ventilation with 30% oxygen after
color and oxygen saturation did not improve with free-flow oxygen. By 5
minutes, he was breathing spontaneously, with an oxygen saturation measured at 85%. He was admitted to the neonatal intensive care unit (NICU)
and placed in a hood with 50% oxygen. On exam, he was grunting, with
marked retractions; had decreased breath sounds with rales; and had a
respiratory rate of 80 with an oxygen saturation of 82%. The rest of the
examination was noncontributory. He was placed on continuous positive
airway pressure (CPAP) of 5 cm H2O and Fio2 0.45, and oxygen saturations
increased to the high 80s. Catheters were placed in the umbilical vein and
artery. A chest x-ray revealed low lung volumes, a fine reticulogranular pattern, and prominent air bronchograms. The arterial blood gas at 2 hours of
life shows a pH of 7.13, a Pco2 of 66, a Po2 of 51, a calculated bicarbonate
of 14, and a base deficit of 5. You suspect the infant has respiratory distress
syndrome based on symptoms beginning at birth, chest x-ray (CXR), and
a blood gas revealing hypoxemia and, predominantly, respiratory acidosis.
Additional supporting factors include prematurity, lack of antenatal steroids,
and exam significant for retractions and poor air exchange. Your management includes surfactant replacement therapy and mechanical ventilation
in addition to antibiotics and a follow-up blood gas. Respiratory acidosis is
a classic finding in respiratory distress syndrome, especially in the preterm
population. Treatment goals are aimed at normalizing both oxygenation and
ventilation and treating for the possibility of infection.
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