Clinical Chemistry 43: 215-221, 1997;
(Clinical Chemistry. 1997;43:215-221.)
© 1997 American Association for Clinical Chemistry, Inc.
Evaluation of the newborn's blood gas status
Robert T. Brouillettea and
David H. Waxman
The Department of Pediatrics, McGill University/Montreal Children's Hospital, Montreal, QC, Canada.
a Address correspondence to this author at: 2300 Tupper St., C-920, Montreal, QC, Canada H3H 1P3. Fax 514-934-4356; e-mail rbronew{at}newborn.mchis.mcgill.ca
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Abstract
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Blood gas measurements and complementary, noninvasive
monitoring techniques provide the clinician with information essential
to patient assessment, therapeutic decision making, and
prognostication. Blood gas measurements are as important for ill
newborns as for other critically ill patients, but rapidly changing
physiology, difficult access to arterial and mixed venous sampling
sites, and small blood volumes present unique challenges. This paper
discusses considerations for interpretation of blood gases in the
newborn period. Blood gas measurements and noninvasive estimations
provide important information about oxygenation. The general goals of
oxygen therapy in the neonate are to maintain adequate arterial
PaO2 and SaO2, and to
minimize cardiac work and the work of breathing. Pulse oximetry and
transcutaneous oxygen monitoring are extraordinarily useful techniques
of estimating and noninvasively monitoring the neonate's oxygenation,
but each method has limitations. Arterial blood gas determinations of
pCO2 provide the most accurate determinations of the
adequacy of alveolar ventilation, but capillary, transcutaneous, and
end-tidal techniques are also useful. An approach to and examples of
acid-base disorders are presented. Three hemoglobin variants relevant
to the newborn are considered: fetal hemoglobin, carboxyhemoglobin, and
methemoglobin. Blood gases obtained in the immediate perinatal period
can help assess perinatal asphyxia, but particular attention must be
paid to the sampling site, the time of life, and the possible and
proven diagnoses.
Key Words: indexing terms: neonatal respiration • bronchopulmonary dysplasia • hemoglobin • carbon dioxide monitoring • oxygen monitoring • acid-base disorders • perinatal asphyxia
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Introduction
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The perinatal period (labor, parturition, and the days following) is one
of fundamental change in the cardiorespiratory status of the
baby. Nutritional, excretory, and respiratory systems must rapidly
assume new responsibilities as the organism changes from a dependent to
a free-living individual. Respiratory gas exchange, formerly a
placental function, must be established by the lungs within minutes
after birth. The cardiovascular system undergoes changes just as
dramatic, with conversion from two circulations in parallel to two
circulations now in series. Therefore, frequent and serious
difficulties in cardiorespiratory adaptation in the perinatal and
neonatal periods are not surprising.
Blood gas measurements and complementary, noninvasive monitoring
techniques provide the clinician with information essential to patient
assessment, therapeutic decision making, and prognostication. Blood gas
measurements are as important for ill newborn infants as for other
critically ill patients, but unique challenges are provided by rapidly
changing physiology, difficult access to arterial and mixed venous
sampling sites, and small blood volumes. However, one must not negate
the importance of historical and physical findings in the ill newborn.
This information must be integrated with the laboratory data to best
understand and treat the patient.
Normal values for arterial blood gases are very dependent on postnatal
age (Fig. 1
). Values of
PaO2 and
SaO2 may also be
lower in premature infants, caused by reduced lung function, and at
high altitude, caused by reduced inspired oxygen tension. The most
accurate method of measuring
PaO2 and
SaO2
involves placement of an indwelling catheter in either the aorta via an
umbilical artery or in a peripheral artery; however, use of such
catheters must be restricted to critically ill neonates because of
frequent and serious thrombotic and infectious complications
(1)(2). A problem associated with peripheral
arterial catheters is hemodilution. For these catheters to remain
patent, they are usually perfused with heparinized saline solution.
Unless the catheter is cleared of perfusate, diluted samples will have
lower PCO2 and
bicarbonate values (3). Sampling methods should minimize
blood loss and assure an undiluted arterial blood sample
(4). Intermittent sampling of a peripheral artery often
changes PaO2
significantly when the infant responds to pain by crying and can
therefore underestimate or overestimate baseline
PaO2
(5)(6). The site of arterial access must be
considered if the ductus arteriosus, which connects the aorta and
pulmonary artery, is still patent because a right-to-left shunt at this
level will result in lower oxygen values in the descending aorta than
in the blood perfusing the brain and eyes. In patients with chronic
lung disease or mild-to-moderate acute cardiorespiratory problems,
capillary blood gases are often utilized. Capillary values for pH and
PCO2 are usually within 0.05
and 7.5 mmHg (1 kPa) of corresponding arterial values; however,
PO2 underestimates
PaO2 and,
therefore, cannot exclude hyperoxemia (7). Capillary
PO2 values are no longer useful,
having been supplanted by the noninvasive techniques of transcutaneous
(tc) PO2 and pulse oximetry
monitoring that more reliably estimate
PaO2 and
SaO2,
respectively.1
Pulse oximetry or
tcPO2 monitoring should be combined
with capillary blood gases to obtain an accurate and comprehensive
evaluation of oxygenation. Capillary blood gases are not reliable for
seriously ill patients, or for those with shock, hypotension, or
peripheral vasoconstriction. In the first day of life, poor perfusion
to the hands and feet ("acrocyanosis") precludes the use of
capillary blood gases. In these settings, arterial blood gases are
required.
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Figure 1. Normal term infants' arterial blood gases in the first
2 h after birth are shown as means (•, solid lines)
± 1 SD (shaded areas).
Note the magnitude and rapidity of change in the first 30 min after
birth. Mean values for term infants experiencing "slight fetal
distress" are shown as  , dotted lines (Tunell R et al.
In: Stetson JB, Surger PR, eds. Neonatal Intensive Care. St.
Louis: Warren H. Green, 1976, p. 99).
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Precision, measured as the CV for replicate samples, of modern blood
gas analyzers should be within 0.2% for pH, 4% for
PCO2, and 3% for
PO2 (Table 1
). Accuracy, measured as deviation from a known calibrator, for
blood gas analyzers must be verified on a regular basis. Total analytic
error for PaO2 and
PaCO2 approaches
the clinically acceptable error (Table 1
).
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assessment of oxygenation
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Blood gas measurements and noninvasive estimations provide
important information about oxygenation. Oxygen delivery
(DO2) to tissues is the product of
cardiac output (c.o.) and blood oxygen content
(CaO2),
DO2 = c.o. x
CaO2. Ignoring
the negligible oxygen dissolved in plasma, the equation can be expanded
to DO2 = (HR x SV) x
(SaO2 x
1.34 x Hgb), where HR = heart rate, SV = stroke volume,
SaO2 = hemoglobin
saturation, and Hgb = hemoglobin content. Insufficient oxygen
delivery to tissues, hypoxia, can therefore be caused by cardiac
failure (decreased HR and (or) SV leading to decreased c.o.), or by low
hemoglobin (anemia) or low Sao2
(hypoxemia) leading to low
CaO2 (Table 2
). When insufficient oxygen is provided to tissues, hypoxia
leads to metabolic acidosis. Thus, blood gas measurements, specifically
PO2,
SaO2,
pH, and base excess, can help to assess patient oxygenation
but must be combined with other clinical and laboratory assessments to
provide a comprehensive picture.
The general goals of oxygen therapy in the neonate are to maintain
adequate PaO2 and
SaO2, and to
minimize cardiac work and the work of breathing (8). It is
important to realize that "optimal oxygenation" will result in
different
PaO2/SaO2
goals for different types of neonatal patients. Most commonly,
premature infants in respiratory failure should have
PaO2 values
between 6.66 and 10.66 kPa (50–80 mm Hg) (9). These goals
minimize the chances of blindness caused by retinopathy of prematurity
(10) and lower the inspired O2 and airway
pressure requirements that, if higher, might increase the likelihood of
bronchopulmonary dysplasia (BPD) (11). By contrast,
full-term infants with diaphragmatic hernia or persistent pulmonary
hypertension may require
PaO2 values of
10.66–13.33 kPa (80–100 mm Hg) to maintain stability, minimize
pulmonary resistance, and avoid worsening pulmonary hypertension
(12). Infants with BPD or chronic lung disease show
improved growth and less pulmonary hypertension (cor pulmonale) when
SaO2 is kept
>92% during wakefulness, sleep, and feeding (11).
Liberal use of supplemental oxygen may be deleterious by promoting
ductus arteriosus closure in some infants with congenital heart
disease, such as hypoplastic left heart, by lowering pulmonary vascular
resistance in other infants with large left-to-right shunts.
Pulse oximetry and transcutaneous oxygen monitoring are extraordinarily
useful techniques of estimating and noninvasively monitoring the
neonate's oxygenation. In most settings they complement blood gases by
permitting the clinician to noninvasively follow trends in patient
oxygenation. However, neither technique can replace arterial blood gas
monitoring in the critically ill patient because neither provides
comprehensive and exact information on oxygenation, ventilation,
acid–base status, and hemoglobin variants. Pulse oximetry has become
more widely used because it usually reflects
SaO2 accurately,
is easy to use, and very rarely results in complications (Table 3
). Neither pulse oximetry nor transcutaneous oxygen monitoring
is reliable for severe hypotension or peripheral vasoconstriction
(13)(14). A false estimate of
SaO2 can occur if
the pulse oximeter probe is applied incorrectly, resulting in poor
signal or an optical shunt, or if motion of the patient or probe
occurs(14)(15). There has been concern that
pulse oximetry monitoring, if not supplemented with intermittent
arterial blood gas determinations, will not adequately protect the
extremely premature infant from hyperoxia that predisposes to
development of retinopathy of prematurity and blindness
(10). For the smallest premature infants, whose retinas
are still developing, exclusive reliance on noninvasive pulse oximetry
to avoid hyperoxia is not recommended. Instead, keeping pulse oximetry
SaO2 in the
88–92% range and intermittently using arterial blood gases to verify
SaO2 and
PaO2 is preferable
(16)(17).
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Table 3. Advantages and limitations of pulse oximetry and
transcutaneous monitoring for neonatal oxygen
assessment.
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assessment of alveolar ventilation
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Arterial blood gas determinations of
PCO2 provide the most accurate
determinations of the adequacy of alveolar ventilation. The
PaCO2
concentration in a given patient reflects the balance between metabolic
production of CO2 and excretion by ventilation. Thus, a
clinician might respond to an increased
PaCO2 by
decreasing metabolic rate (sedation, paralysis, or reduction of thermal
stress) or by increasing ventilation [increasing ventilator rate or
tidal volume, decreasing added dead space, reducing airway resistance,
or by surfactant administration in premature infants with respiratory
distress syndrome, (RDS) to improve compliance].
The clinician must establish a target or acceptable range for
PaCO2 for a given
patient. Although the normal range of
PaCO2 after the
first hours of life can be considered 4.66–6 kPa (35–45 mm Hg),
desirable CO2 values for a specific situation may be either
higher or lower. For instance, in persistent pulmonary hypertension of
the newborn, pulmonary artery pressures can be lowered by either
respiratory or metabolic alkalosis (18). Modest
respiratory alkalosis can rapidly lower pulmonary vascular resistance
in some such patients. Because marked hypocapnea can decrease cerebral
blood flow and has been associated with neurologic deficits, most
clinicians no longer aim for
PCO2 values <3.33 kPa (<25
mm Hg) (19). Infants with BPD (chronic lung disease) often
tolerate PCO2 values of
6.66–8 kPa (50–60 mm Hg) (20), essentially
"deciding" that normal blood gas status is not worth the markedly
increased work of breathing necessary to achieve it. An approach termed
"permissive hypercapnia" or "gentle ventilation" with lower
ventilator pressures while tolerating slightly increased
PaCO2 resulted in
decreased chronic lung disease for premature infants with
RDS (21).
For most neonates and small infants,
tcPCO2 monitoring is usually
preferred over end-tidal CO2 monitoring
(PETCO2) as
a means of estimating and "trending"
PaCO2, and
therefore alveolar ventilation (22)(23). Small
tidal volumes, rapid respiratory rates, and inhomogeneous alveolar
ventilation/perfusion in neonates with lung disease often preclude
PETCO2
monitoring in the newborn, especially in small prematures. By contrast,
tcPCO2 shows good correlation
with PaCO2 and
provides an excellent trend monitor, accurately reflecting changes in
PaCO2. The
tcPCO2 monitor, unlike the
tcPO2 monitor that must be heated to
43–44 °C, does not cause skin burns. When used at a temperature of
40–42 °C, the tcPCO2
electrode can be left in place for 4 h in neonates and 8 h in
infants and older children (24)(25). Because
tcPCO2 values sometimes are
markedly inaccurate, in vivo calibration against an arterial or
capillary blood gas is often required. Overestimation errors in
hypercarbic patients are particularly frequent.
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assessment of acid–base status
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Blood gases provide essential information on acid–base status
both in critically ill neonates and in chronically or less severely ill
patients. One can approach the analysis of simple acid–base disorders
by answering three questions. First, is the condition one of acidosis
or alkalosis (is the pH less than or greater than 7.4)? Second, is the
primary cause metabolic (is bicarbonate high or low) or respiratory (is
PCO2 high or low)? Third, is
the compensation appropriate? Fig. 2
shows a clinically useful approach to blood gas interpretation
in the newborn and infant (26).
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Figure 2. Approach for the analysis of simple acid–base disorders
(from: Koeppen BM, Stanton BA. Renal Physiology. St. Louis:
Mosby Year Book, 1992, p. 137)
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To properly analyze and describe blood gases, certain terms must be
defined. The suffix "emia" refers to the state of blood, for
example, acidemia is a condition of excess blood acidity as
indicated by pH. The suffix "osis" refers to a pathologic process
in which acid or base is gained or lost from the body
(27). Acidosis may not lead to acidemia, depending on the
patient's ability to compensate. Compensation is a response to the
primary disorder, attempting to bring the pH as close as possible to
neutral. Full compensation is often unachieved, and blood gases that
appear to have fully compensated for the primary problem are most
likely displaying a mixed picture, rather than complete correction.
Table 4
presents some of the most common causes of acid–base disorders
in neonates. Metabolic acidosis is most commonly caused by inadequate
tissue perfusion (shock) caused by hypovolemia, decreased cardiac
output, or sepsis. Hypoxemia caused by lung or heart disease often
contributes to the tissue hypoxia and resulting lactic acidosis seen
with hypoperfusion states. Sepsis in the newborn, as in older
individuals, may cause metabolic acidosis by decreasing perfusion
("cold shock") and by interfering with cellular aerobic metabolism
("warm shock"). To compensate for metabolic acidosis, term neonates
and infants will attempt to lower
PCO2 by hyperventilating;
however, compensation is usually not complete, that is, not to a pH of
7.4. A suggested guideline for the desired
PCO2 is as follows: The last
two digits of the pH should equal the expected
PCO2 (28). If the
actual PCO2 is much higher
than expected, there may also be a respiratory acidosis. Premature
infants are often not able to compensate for a metabolic acidosis by
hyperventilation and respiratory alkalosis. After treating the primary
underlying problem causing the metabolic acidosis, slow infusions of
sodium bicarbonate are often given.
One common problem in the management of infants with BPD is
distinguishing a primary, chronic, respiratory acidosis with metabolic
compensation from a diuretic-induced metabolic alkalosis with
respiratory compensation. In infants with BPD, lung mechanics,
ventilation/perfusion relations, and work of breathing are abnormal.
This results in a chronically high
PCO2—a primary respiratory
acidosis. Renal compensation causes bicarbonate retention, bringing the
pH back towards normal, but compensation is usually not complete, that
is, pH remains <7.40. Diuretics are used to improve lung mechanics, to
decrease lung water, and to improve gas exchange. Thiazide and
especially loop diuretics result in a loss of chloride, potassium, and
sodium, and in retention of bicarbonate. When high doses of diuretics
are used without salt replacement, metabolic alkalosis can result, with
pH values >7.40. Under these circumstances, respiratory drive can be
depressed, worsening the hypoventilation. Lowering the dose of
diuretics, changing from a loop to a thiazide diuretic, replacement of
salt, or use of acetazolamide to lower plasma bicarbonate are
strategies that can be used to minimize this problem.
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hemoglobin variants in the newborn
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Modern blood gas instruments often include options to measure
hemoglobin and its variants such as fetal hemoglobin,
carboxyhemoglobin, and methemoglobin. These capabilities can sometimes
be used to our advantage in neonatal medicine. Fetal hemoglobin has a
left-shifted oxyhemoglobin dissociation curve, with a 50% saturation
point ~2.8 kPa vs 3.47–3.6 kPa (21 mm Hg vs 26–27 mm Hg) for adult
hemoglobin. Fetal hemoglobin is well designed to facilitate oxygen
transport across the placenta. In the neonate, however, fetal
hemoglobin releases less oxygen at any given capillary
PO2. Pulse oximetry estimates of
arterial hemoglobin saturation are as accurate for fetal as for adult
hemoglobin. The PO2 to achieve
"adequate" saturation will be lower for fetal than for adult
hemoglobin. In practice, if pulse oximetry is being used to guide
oxygen therapy, measurement of adult and fetal hemoglobin percentage
adds little to clinical management. It should be realized, however,
that PaO2 values in the
5.5–7 kPa (41–53 mm Hg) range are often high enough to achieve
88–92% SaO2 for
premature infants with predominantly fetal hemoglobin.
In the neonatal setting, carboxyhemoglobin is of interest primarily in
infants of smoking mothers. Carbon monoxide crosses the placenta and
binds strongly to fetal hemoglobin, making it unavailable for oxygen
transport (29). Effects of carbon monoxide include the
functional anemia of carboxyhemoglobin, a left shift of the hemoglobin
dissociation curve making oxygen less available to tissues, and an
inhibition of mitochondrial cytochrome oxidase. Pulse oximeters use
only two light wavelengths, thereby assuming that only deoxyhemoglobin
and oxyhemoglobin are present. A CO-oximeter is required to measure
carboxyhemoglobin.
The recent use of inhaled nitric oxide to treat pulmonary hypertension
in the newborn and in older patients has refocused attention on
methemoglobinemia. Inhaled nitric oxide binds to hemoglobin rapidly in
the pulmonary circulation, resulting in selective relaxation of
pulmonary vascular smooth muscle. The nitric oxide–hemoglobin complex
is converted to methemoglobin, and toxic concentrations of nitric oxide
can result in methemoglobinemia. To date, methemoglobinemia has not
been a serious problem in neonates receiving 5–80 ppm inhaled nitric
oxide. Intermittent CO-oximeter measurements of methemoglobin should be
performed in patients receiving inhaled NO, especially at
concentrations >40 ppm, to keep methemoglobin concentrations <5% of
total hemoglobin (30).
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blood gases in the immediate perinatal period with special
reference to perinatal asphyxia
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Blood gases can provide important information on patient status
even before arterial blood sampling becomes possible after birth (Table 5
). Before the onset of labor, the fetus, compared with the
normal adult, exists in a hypoxemic, normocarbic, nonacidotic
environment. During the stress of normal labor, some tissue hypoxia and
placental insufficiency occur, resulting in a mixed respiratory and
metabolic acidosis. After birth, as pulmonary gas exchange is
established, PCO2, pH, and
PO2 values move toward normal adult
values; the largest changes occur in the first few minutes after birth
(Fig. 1
). Accordingly, the most important factors to consider when
interpreting blood gases are the sampling site, the time of life, and
the possible and proven patient diagnoses.
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Table 5. Comparison of 95% confidence limits* and decision
levels during pregnancy, during labor, and from the clamped
umbilical cord.
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Perinatal asphyxia occurs when there is inadequate placental gas
exchange to meet ongoing fetal tissue needs for oxygen consumption and
carbon dioxide elimination. The combination of lactic acidosis, the
product of anaerobic metabolism, and CO2 accumulation
results in a mixed acidosis. It is important to note that current work
suggests that only 10–20% of cerebral palsy cases is accounted for by
perinatal asphyxia (31). Unfortunately, during labor,
there is no noninvasive, simple method of monitoring fetal well-being
that is both highly sensitive and highly specific. Fetal heart rate
monitoring, either electronic or auscultatory, is reassuring when
normal but has a false-positive rate >99%. Measurement of pH from
capillary blood samples taken from the presenting part can provide
additional information on fetal well-being when there is concern
because of an abnormal fetal heart rate pattern. Values >7.24 are
reassuring, whereas those <7.2 suggest that obstetric management
options should be reevaluated (32).
In summary, although arterial blood gases can provide much useful
information about the physiologic state of the patient, a clear and
systematic approach is required to give meaning to the values. From
procurement to analysis, potential sources of error must be considered
and a complete understanding of what blood gases can and cannot tell
you is needed to best treat the critically ill newborn.
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Acknowledgments
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We thank Pierre Senécal for helpful suggestions and Rosanna
Barrafato for preparation of the manuscript.
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Footnotes
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1 Nonstandard abbreviations: c.o., cardiac output; SV, stroke volume; RDS, respiratory distress syndrome; tc, transcutaneous; and BPD, bronchopulmonary dysplasia. 
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Top
Abstract
Introduction
