.Lab Values.
U NDERSTANDING BLOOD GAS
values and acid-base balance
are fundamental skills of neona-
"LOOD'AS!NALYSISAND
tal nursing. This is because, in the THE&UNDAMENTALSOF
NICU, blood gases are probably
ordered more than any other labo- !CID
"ASE"ALANCE is transported to the lung, where
ratory test. The bedside nurse not
only obtains the specimen, but is Mary Farmand, RNC-NIC, MSN
also crucially involved in interpret-
ing the results because blood gases C OLUMN E DITOR
cannot stand alone; they need to
be evaluated in the context of the Patricia Nash, RN, MSN, NNP-BC
entire clinical picture. This article
provides basic information on the
components of a blood gas, acid-base balance, as well as a
systematic approach to blood gas analysis.
PH LEVEL
Normal cell function is dependent on acid-base balance,
+
which is regulated by the hydrogen ion (H ) concentration
in the blood. Three ways the body has to regulate H+ include
buffer systems, exhalation of carbon dioxide (CO2) via the
lungs, and excretion of H+ by the kidneys. Substances that
donate H+ are called acids, whereas substances that accept
H+ are called bases. Buffers are compounds that either accept
or donate H+.1 The pH scale is the most common method
for measuring H+ concentrations in a solution. Because the
scale is a negative logarithm, small numbers can be expressed.
This is particularly useful when determining the H con- +
centration in plasma because the concentration is so low
(0.000035–0.000045 mEq/liter). pH is a measurement of
+ 2
only free H . Hydrogen ions and pH have an inverse rela-
tionship: as one increases, the other decreases. The pH level
of blood is one of the measurements obtained with a blood
gas. This analysis is performed on samples of blood obtained
from the neonate from arterial, venous, or capillary sources.
A pH within the acceptable range indicates that the neonate
is in acid-base balance. The normal value for plasma pH is
7.35–7.45. A pH below 7.35 indicates acidosis, or an excess
of H+, and a pH above 7.45 indicates alkalosis, or a low H+
1
concentration. Reasons for an imbalance can be determined
by using the additional information about CO2, bicarbonate
(HCO3–), and base excess or deficit levels provided by the
blood gas results.
CARBON DIOXIDE
Carbon dioxide, a waste product of cellular metabolism,
dissolves in the intracellular fluid. As the amount of CO2
increases, it causes a pressure gradient between the intra-
cellular and extracellular fluid. This gradient is what moves
CO2 out of the cell and into the bloodstream via the red
3
blood cells (RBCs). While in the RBCs, the CO2 joins with
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VOL. 28, NO. 2, MARCH/APRIL 2009
water (H2O) to form carbonic
acid (H2CO3). Because of its
ability to combine with H2O to
form H2CO3, CO2 is considered
a “potential acid.”4 Carbonic acid
it reverts back to CO2 and H2O.5
Similarily, a pressure gradient exists
between the CO2 concentration in
the blood and that in the alveoli,
which allows the alveoli to accept
the CO2, making it available for
excretion during exhalation. Thus,
the respiratory system can affect the
acid-base balance within minutes by increasing or decreas-
ing the amount of CO2 exhaled. This change in ventilation
is initiated when chemoreceptors in the medulla and the
carotid and aortic bodies respond to alterations in the levels
of CO2 in the cerebrospinal fluid and plasma.6 An increase
in CO2 causes an increase in H2CO3, which in turn causes a
decrease in pH. Inversely, a decrease in CO2 causes a decrease
in H2CO3 in the body, leading to an increase in pH. By mea-
suring the CO2, one can determine if a respiratory condition
is causing an acid-balance imbalance. The normal value for
CO2 is 35–45 mmHg.
BICARBONATE
Bicarbonate is a compound capable of accepting H+, thus
acting as a buffer or base. Determining the HCO3– level in the
blood also provides insight into the nonrespiratory compo-
nent of acid-base balance. The amount of HCO3– in the body
is controlled by the kidneys through HCO3– reabsorption and
generation. Eighty-five percent of this reabsorption occurs in
the proximal tubules, where the enzyme carbonic anhydrase,
sodium (Na+), and adenosine triphosphate (ATP) are required
for reabsorption to occur (Figure 1). Bicarbonate enters the
lumen of the proximal tubule, where, because of its molecu-
lar size, it is unable to freely cross the tubular cell membrane.
Hydrogen is secreted across the membrane into the tubular
fluid as Na+ crosses from the tubular fluid and enters the cell.
Hydrogen combines with the HCO3– to form H2CO3. Carbonic
anhydrase, located on the luminal membrane, breaks down the
H2CO3 into H2O and CO2. The CO2 then diffuses across the
cell membrane. Once inside the cell, the CO2 combines with
H2O and, with the help of carbonic anhydrase, converts back
into H+ and HCO3–. The HCO3– crosses the basolateral mem-
brane in conjunction with the Na+ and chloride (Cl–) trans-
port. It finally diffuses across the interstitial space and is returned
to systemic plasma. The H+ is then available to cross into the
lumen to again help with the formation of H2CO3.2 The rate of
neonatal HCO3– reabsorption is approximately one-third that
of the adult, limiting the neonate’s ability to alter the pH. This
125
FIGURE 1 ■ Proximal tubular bicarbonate reabsorption.
Renal Tubular
interstitial Tubular cells lumen
fluid
Na + + HCO3 –
Na + Na +
ATP
K+ H+
HCO3 – + H +
H2CO3
H2CO3
Carbonic
anhydrase
H 2O
CO2 +
CO2 CO2 + H2O
From: Guyton, A. C., & Hall, J. E. (2006). Textbook of medical physiology
(11th ed., p. 391). Philadelphia: Saunders. Reprinted by permission.
limitation in HCO3– reabsorption is due to decreased activity of
the transporters responsible for reabsorption: glucocorticoids,
which stimulate the development of HCO3– transport, are defi-
cient in the first few weeks of life.7
Bicarbonate generation occurs in the collecting tubules
and requires phosphate and protein, which are considered
non-HCO3– buffers. Similar to HCO3– reabsorption, H+
moves from the intracellular space to the tubular fluid com-
partment to combine with the HCO3– to form H2CO3. This
acid is then catalyzed by carbonic anhydrase to dissociate into
H+ and HCO3–. Bicarbonate is transported across the mem-
brane in a countertransport with Cl–. The HCO3– returns
to the peritubular fluid and then to the systemic circulation.
The H+ that is secreted into the tubular fluid combines with
a base molecule to be excreted in the urine.2
Neonates are less able than adults to secrete acid.7
Bicarbonate is also generated by the kidney during the metab-
olism of glutamine in the proximal tubule. Each glutamine
molecule is broken down into two molecules of ammonium
(NH4) and an anion. The anion metabolizes into two mol-
ecules of HCO3–, which then cross the basolateral membrane
and enter the blood, decreasing the pH. The H+ also crosses
the membrane, where it joins with ammonia (NH3–) to form
NH4 in the peritubular fluid. Once in the peritubular fluid,
the NH4 is unable to diffuse back and remains in the lumen,
where it is excreted in the urine.2 Although the adult kidney
can increase NH4 production during acidosis, the neonate is
unable to do so. In addition, because of their protein intake
and mineralization of new bone, neonates need to excrete
two to three times the amount of acid as adults.7
The kidneys retain or regenerate HCO3– based on the pH
and CO2 of the plasma.1 When the plasma is more acidic, more
HCO3– is recovered and regenerated by the tubular cells.
Inversely, if the plasma is alkalotic, less HCO3– is retained or
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126
FIGURE 2 ■ Oxygen-hemoglobin dissociation curve.
From: Parry, W., & Zimmer, J. (2006). Acid-base homeostasis and
oxygenation. In G. B. Merenstein & Gardner S. L (Eds.), Handbook
of neonatal intensive care (6th ed., p. 216). Philadelphia: Mosby
Elsevier. Reprinted by permission.
regenerated, and more H+ is excreted. In the neonate, the
normal value for HCO3– is 22–26 mEq/liter. A decrease in
HCO3– causes acidosis, whereas an increase causes alkalosis.
By evaluating the HCO3– level, one can determine if an acid-
base imbalance is metabolic in nature.
BASE EXCESS/DEFICIT
Base excess or deficit is a calculated value that takes into
consideration the amount of HCO3– generation and retention
by the kidneys.8 This calculation provides a clearer measure
of the metabolic component of an acid-base imbalance by
factoring in how a change of PaCO2 will cause a change in
HCO3–.6 Base excess measures the moles of acid needed to
return one liter of blood to a pH of 7.4 and is expressed as a
linear scale.4 Normal values for base excess/deficit are +4 to
– 4 mEq/liter: A positive number indicates alkalosis, whereas
a negative number indicates acidosis.5
OXYGENATION
Although not part of acid-base balance, determining
the level of oxygen is an important part of blood gas analy-
sis because hyperoxia can be just as dangerous as hypoxia.3
Oxygen (O2) enters the lung during inspiration and diffuses
across the alveolar-capillary membrane due to a concentra-
tion gradient.5 Oxygen is then transported to the tissues
either dissolved in the blood (3 percent) and reported as the
partial pressure of oxygen (PaO2) or bound to hemoglobin
(97 percent). Each hemoglobin molecule can bind four mol-
ecules of O2. The amount bound to hemoglobin is reported
as the O2 saturation, which indicates the number of sites filled
divided by the sites available. As the PaO2 increases, the O2
bound to hemoglobin increases. This relationship between
oygen saturation and the partial pressure of oxygen is illus-
trated by the O2-hemoglobin dissociation curve (Figure 2).
MARCH/APRIL 2009, VOL. 28, NO. 2
 This S-shaped curve illustrates that large increases in TABLE 1 ■ Values for Determining Acid-Base Balance in
PaO2 produce smaller and smaller changes in saturation.5 Uncompensated States
The “30-60-90 rule” of the curve explains how, at a PaO2 of pH CO2 HCO3– Base
30, the saturation will be 60 percent, a PaO2 of 60 will have (mmHg) (mEq/liter)
a saturation of 90 percent, and a PaO2 of 90 will increase Normal values 7.35–7.45 35–45 22–26 – 4 – +4
the saturation to only 95 percent. This rule applies to adult ↑ ↓ ↑ ↑
Alkalosis
hemoglobin with a normal pH, PaCO2, and body tempera-
Acidosis ↓ ↑ ↓ ↓
ture.3 The presence of fetal hemoglobin in the neonate affects
the curve by causing a left shift—in other words, there is an Adapted from: Parry, W., & Zimmer, J. (2006). Acid-base homeostasis
and oxygenation. In G. B. Merenstein & Gardner S. L. (Eds.),
increased attraction between O2 and hemoglobin. This means Handbook of neonatal intensive care (6th ed., p. 211). St. Louis:
that O2 is more easily bound to the hemoglobin and is not Mosby Elsevier.
released as readily to the tissues until a lower PaO2 is reached.
This increased attraction may hinder the release of O2 to the
tissues, but it eases the uptake of O2 and the release of CO2 in The following reference ranges were obtained from the
the lungs.5 The increased affinity between fetal hemoglobin Handbook of Neonatal Intensive Care.3 They are intended as
and O2 is very important in fetal life, because the partial pres- a guide. Please refer to your own institution’s guidelines for
sure of O2 is low in utero. Thus, the shift to the left enhances acceptable ranges.
the placental uptake of O2. But this shift to the left can be s Blood gas analysis starts with the pH.
deliterious in the neonate in situations that increase O2 con- Is it in the 7.35–7.45 range?
sumption, such as sepsis. Below 7.35: acidotic
It is important to know the hemoglobin level of the infant Above 7.45: alkalotic
when evaluating the oxygen saturation. An infant with a s Next evaluate the CO2.
hemoglobin of 7 g/dL (4.3 mmol/liter) and an infant with Is it in the 35–45 mmHg range?
a hemoglobin of 14 g/dL (8.7 mmol/liter) may each have Below 35: alkalotic
a 97 percent saturation, but the second patient has twice Above 45: acidotic
as much oxygen in the arterial blood because O2 content s Then evaluate the HCO3–.
is calculated from hemoglobin saturation and hemoglobin s Is it in the 22–26 mEq/liter range?
concentration.4 Below 22: acidotic
Above 26: alkalotic
BLOOD GAS ANALYSIS s Base excess, if available, can provide additional
Blood gas levels provide valuable information, but cannot information.
be evaluated in isolation; current assessments and therapies, Is it in the – 4 to +4 range?
along with past history, need to be taken into consideration Below – 4: acidotic
because they have an impact on the patient’s oxygenation, Above +4: alkalotic
ventilation, and acid-base balance. Congenital heart disease, s Is PaO2 (arterial sample) or PO2 (capillary sample) within
chronic lung disease, and supplemental oxygen therapy can the 60–80 mmHg range? Remember that a capillary
contribute to changes in the infant’s blood gas values.9 For sample is reliable when the PaO2 is less than 60.5
example, a patient with cyanotic heart disease may have an Below 60: hypoxemia
acceptable PaO2 of 35 mmHg, whereas a patient with pul- Above 80: hyperoxemia
monary hypertension may require a PaO2 of 100 torr or s Is saturation within the 92–94 percent range? (This is
greater. Another patient with chronic lung disease may have different from pulse oximetry, where saturations in the
an acceptable PCO2 of 55–60 mmHg or greater, whereas mid- to high-80s are more acceptable for small preterm
an infant without lung disease would have of a PCO2 in the infants.)
normal range. s Is hemoglobin within the 10–16 g/dL range?
Blood gas results can also be altered by the method of sam- (6.2–9.9 mmol/liter)?
pling. The most accurate blood gas measurement is from an The four values in Table 1—pH, CO2, HCO3–, and base—
indwelling arterial line; this is the best determination of the provide the information needed to determine if the patient is in
adequecy of ventilation and oxygenation. Intermittent arterial acid-base balance. The cause of an imbalance can be established
punctures can be done, but are painful and may be associated as either respiratory (CO2) or metabolic (HCO3– or base) by
with crying and desaturation, that can alter the PaO2. Venous identifying which of the values is abnormal. The value will also
sampling and “arterialized” capillary sampling (warming the indicate if the body is able to compensate for an acid-base imbal-
site prior to obtaining the sample) can give only an estima- ance. If the blood gas is compensated for acidosis, the pH will
tion of the adequecy of oxygenation, although they are fairly be normal, the HCO3– will be increased, and the PCO2 will
accurate measurements of pH and PCO2.10 be decreased. If the blood gas is compensated for alkalosis, the

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pH will again be normal, the HCO3– will be decreased, and
the PCO2 will be increased. For example, if the pH is 7.28,
the CO2 is 55 mmHg, and the HCO3– is 25 mEq/liter, then
the acid-base balance is an uncompensated respiratory acidosis
because both the pH and the CO2 levels indicate acidosis and
the HCO3– is normal. If the pH is within normal limits but both
of the other values remain outside the normal limits, the blood
gas is said to be compensated. However, if the pH was 7.33, the
CO2 was 55 mmHg, and the HCO3– was 29 mEq/liter, then
it would be a partially compensated respiratory acidosis because
the body is attempting to adjust the acid-base balance by using
the other (metabolic) system. Even with a compensated blood
gas, it is still possible to determine if the primary problem is aci-
dosis or alkalosis because the pH does not normally compensate
beyond the minimum acceptable level.11 In addition, the meta-
bolic system is able to compensate for the respiratory system
much better than the respiratory system is able to compensate
for the metabolic system.3 In the neonate, compensation is
limited because of immaturity of the respiratory system and the
inability of the kidneys to conserve HCO3–.5
Once you have determined what type of acid-base
imbalance your patient has, the cause for the imbalance
should be determined. In respiratory acidosis, where CO2 is
retained, the most common cause is obstructive lung disease.3
Meconium aspiration, transient tachypnea of the newborn,
respiratory distress syndrome (RDS), and bronchopulmonary
dysplasia are all disorders that cause respiratory acidosis by
interfering with PCO2 elimination. Poor respiratory effort
also can cause CO2 retention. This reduced effort may be
caused by maternal anesthesia before delivery, central apnea,
decreased respiratory drive as a result of sepsis, intracranial
hemorrhage, or metabolic disturbances that affect the respira-
tory center. Diaphragmatic hernia, phrenic nerve paralysis, or
pneumothorax can also increase CO2 retention by decreasing
the tidal volume or respiratory rate.
If CO2 excretion is greater than normal, the patient has
respiratory alkalosis. This is caused by hyperventilation,
which may result from ventilator therapy, early RDS, central
nervous system stimulation, or, in some cases, hypoxemia.3
Metabolic acidosis can result from either adding acid or
losing base. An increase in acid is found during conditions of
hypoxemia, when lactic acid increases in response to anaero-
bic metabolism; with renal failure, which causes an increase
in organic acids or with diabetic ketoacidosis, which increases
ketoacids. Loss of base occurs with renal tubular acidosis,
diarrhea, or as a side effect of drugs such as acetazolamide.
A loss of acid or an addition of base will cause metabolic
alkalosis. Causes can include nasogastric suctioning, severe
vomiting, or medications such as diuretics, digitalis, or cor-
ticosteroids. These medications induce excretion of Na+ and
potassium (K+) from the kidneys, causing depletion. In order
to conserve these ions, H+ are excreted in the urine, thus
increasing the pH.3 Bicarbonate and acetate administration
may also increase base and cause metabolic alkalosis.11
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128
These common causes of acid-base imbalance in the
neonate should be used as a starting point when determining
why an imbalance is occurring. Care should be taken not to
become too focused on one possible cause because the body
continually adapts to changes in homeostasis. Often the cause
of an acid-base imbalance is multifactorial. For this reason,
nurses need to have an understanding of how the body tries to
maintain acid-base balance through the use of buffer systems,
the kidneys, and the lungs.
CONCLUSION
Blood gas measurement is a very common lab determina-
tion obtained in the NICU. Neonatal nurses must be able to
identify blood gas abnormalities and understand the possible
causes of acid-base imbalance to plan their care. Reviewing
blood gas results in a systematic way and understanding the
basics of acid-base balance will help the nurse at the bedside
meet the needs of neonatal patients.
REFERENCES
1. Simpson, H. (2004). Interpretation of arterial blood gasses: A clinical
guide for nurses. British Journal of Nursing, 13, 522–528.
2. Yucha, C. (2004). Renal regulation of acid-base balance. Nephrology
Nursing Journal, 31, 201–206.
3. Parry, W., & Zimmer, J. (2006). Acid-base homeostasis and oxygenation.
In G. B. Merenstein & Gardner S. L. (Eds.), Handbook of neonatal
intensive care (6th ed., pp. 210–222). St. Louis: Mosby Elsevier.
4. Woodrow, P. (2004). Arterial blood gas analysis. Nursing Standard,
18(21), 45–52. Retrieved April 29, 2008, from http://www.nursing-
standard.co.uk/archives/ns/vol18-21/pdfs/v18n21p4552.pdf
5. Askin, D. F. (1997). Interpretation of neonatal blood gases, Part I:
Physiology and acid-base homeostasis. Neonatal Network, 16(5), 17–21.
6. Sirker, A. A., Rhodes, A., Grounds, R. M., & Bennett, E. D. (2002).
Acid-base physiology: The “traditional and the modern” approaches.
Anaesthesia, 57, 348–357.
7. Quigley, R., & Baum, M. (2004). Neonatal acid base balance and
disturbances. Seminars in Perinatology, 28, 97–102.
8. Clancy, J., & McVicar, A. (2007). Intermediate and long-term regulation
of acid-base homeostasis. British Journal of Nursing, 16, 1076–1079.
9. Finger, L. (2008). Arterial blood gas analysis. In J. Verger & R. Lebets
(Eds.), AACN procedural manual for pediatric acute and critical care
(pp. 115–120). St. Louis: Saunders Elsevier.
10. Durand, D. J., & Phillips, B. L. (1996). Blood gases, technical aspects
and interpretations. In J. P. Goldsmith & E. H. Karotkin (Eds.), Assisted
ventilation of the neonate (3rd ed., pp. 257–272). Philadelphia,: WB
Saunders.
11. Askin, D. F. (1997). Interpretation of neonatal blood gases, Part II:
Disorders of acid-base balance. Neonatal Network, 16(6), 23–29.
About the Author
Mary Farmand graduated with an ADN from Santa Monica
College and a BSN from California State University, Long Beach.
She received an MSN from Walden University in 2007. She has exten-
sive experience in neonatal transport, and pediatric nursing. Mary is
currently working as the clinical educator in the neonatal intensive
care unit at SSM Cardinal Glennon Children’s Medical Center in St.
Louis, Missouri.
MARCH/APRIL 2009, VOL. 28, NO. 2