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Abstract

Blood gases are the most common and Understanding


one of the most important laboratory
values performed in the neonatal
intensive care unit. Because of
Blood Gas
technological advances including
surfactant and high-frequency
Interpretation
ventilation, the need for immediate
responses to rapidly changing clinical By Beth Brown, RNC, MSN, and
conditions is of utmost importance. An
Bonnie Eilerman, RN, MSN, CNP
arterial or capillary blood gas is a
clinical tool for determining an infant’s
pulmonary and metabolic status. An

A
infant can easily be overventilated, n arterial or capillary blood gas is a clinical assessment tool for
underventilated, or metabolically determining an infant’s pulmonary and metabolic status. The pulmo-
unstable, which can affect their long- nary component of the blood gas yields information on ventilation and
term outcome. Therefore, nurses need to
oxygenation. The metabolic component reflects potential for changes in
enzyme function and nerve and muscle activity. Blood gases are the basis for
have a basic understanding of acid-
diagnosis and management of infants with cardiorespiratory disease, metabolic
base physiology and accurate
disorders, and overall management in premature infants. By integrating acid-
interpretation skills to be a competent base physiology, blood gas interpretation skills, and clinical history, the
and skilled neonatal intensive care unit neonatal intensive care unit staff can accurately assess an infant’s current
nurse. This article presents a brief condition and help take the appropriate steps to correct the imbalance and,
review of blood gas interpretation. therefore, improve outcomes.
n 2006 Elsevier Inc. Acid-base balance refers to the complex mechanisms through which the body
All rights reserved. strives to achieve and maintain a homogenous internal environment. This
environment is reflected in a serum pH of 7.35 to 7.45. An acid is a substance
Keywords: Blood gasses, Infant,
that can donate hydrogen ions (H+) to alkaline solutions to neutralize the effect
Metabolic status of bases. A base is an alkaline substance that can combine with acids to accept
hydrogen ions neutralizing the effect of the base.1 The body has many ways to
achieve this environment, mainly through the use of buffer systems. The goal of
the buffer systems is to regulate the H+ concentration in the body and, therefore,
regulate the pH. This concentration must be kept as steady as possible because
only slight changes in H+ from the normal value can cause significant alterations
in all physiological processes. Delivery of oxygen to the cell, the cellular use of
oxygen, and the hormonal regulation of metabolism are all affected by the pH of
the body. There are three main body systems that help to regulate pH: the
chemical buffer systems, the respiratory center, and renal control.

Buffer Systems

T he chemical buffer systems include the carbonic acid-bicarbonate system,


protein buffer system, and the phosphate buffer system. The carbonic acid-
bicarbonate system is a weak, yet fast buffer that occurs in the extracellular
fluid. Carbon dioxide (CO2) and water are made from the oxidization of
carbohydrates, fats and proteins. These combine to form carbonic acid.
Carbonic acid then splits into hydrogen, an acid, and bicarbonate, a base.
Bicarbonate, which is regenerated and stored in the kidneys, can also bind to
any excessive amount of hydrogen, thereby reversing the equation and forming
From the Good Samaritan Hospital, Neonatal carbonic acid.2 This buffer system explains neonatal acidosis because of the
Intensive Care Unit, Cincinnati, OH. immature kidneys of a preterm infant. These premature kidneys cannot hold on
Address correspondences to Beth Brown, RNC,
MSN, 1174 Kylemore Court, Dayton, OH 45459. to bicarbonate, losing it into the urine. Therefore, there is less bicarbonate to
n 2006 Elsevier Inc. All rights reserved.
1527-3369/06/0602-0130$10.00/0
doi:10.1053/j.nainr.2006.03.005 Newborn and Infant Nursing Reviews, Vol 6, No 2 (June), 2006: pp 57 - 62 57
58 Brown and Eilerman

bind with the excess hydrogen, and the blood becomes carbonic acid. The kidneys are the slowest physiologic
acidic. By use of the carbonic anhydrase equation below, regulators. They take hours to commence their work and
one can see how this process moves in both directions. may take up to several days to take effect, but they do have
H2 O þ CO2 H2 CO3 Hþ þ HCO
the most sustained response.
X X 3
water carbon carbonic hydrogen bicarbonate The kidneys provide the most important route for the
dioxide acid ion excretion and buffering of metabolic acids and are also
The protein buffer system is the most powerful and responsible for maintaining the plasma levels of HCO3, the
plentiful buffering system using proteins of cells and most important buffer of H+. The kidneys control pH balance
plasma. The cell membrane is composed almost entirely of by excreting either acidic urine or basic urine. The overall
proteins and lipids.2 As the extracellular pH changes, the mechanism by which the kidneys control the excretion of H+
body adapts by diffusing hydrogen and bicarbonate in and and the retention of bicarbonate occurs by four main
out of the cell membranes by way of these proteins. This is mechanisms: excretion of H+, reabsorption of bicarbonate,
a slow process, up to several hours and intracellular production of bicarbonate, and formation of ammonia.2
electrolytes such as sodium and potassium may be
displaced as the hydrogen or bicarbonate enter the cell.
Clinically, this may account for a degree of hypernatremia
Permissive Hypercapnia
or hyperkalemia.
Hemoglobin is part of the protein buffering system.
When the body is acidotic, hemoglobin will act as a buffer.
A lthough a normal level of Pco2 is 35–45 millimeters
of mercury, in many situations, levels outside this are
considered bacceptable.Q Mechanical ventilation and the
Therefore, the oxygen carrying capacity may be reduced.2
resulting baro-/volutrauma on the lungs can highly
In addition, one of the implications of this buffering
contribute to the development of bronchopulmonary
system is the displacement of intracellular electrolytes
dysplasia. The major determinant of lung injury is tidal
such as sodium and potassium when H+ enters the cell.
volume or the volume of air instilled into the lungs by a
The main components in the phosphate buffer system
ventilator. This parameter is also the primary one that
are monohydrogen phosphate (HPO4) and dihydrogen
affects Pco2 levels. The higher the tidal volume is, the
phosphate (H2PO4). When a strong acid is added to these
more the lungs are stretched and the more baro-/
two phosphates, only a weak acid is formed, and when a
volutrauma occurs. Permissive hypercapnia is a strategy
strong base is added also, only a weak base is formed.
that attempts to minimize this by allowing relatively high
Phosphate acts predominantly as an intracellular and
levels of Pco2, provided the pH does not fall below a
urinary buffer. Because phosphate is eliminated in the
minimal value (typically 7.20). This is accomplished by
urine, this system is particularly important in buffering
providing a low inspiratory volume and pressure and
fluids in the kidney tubules.3
decreasing the extent of lung tissue stretch. The current
Respiratory regulation is primarily responsible for the
trend is to wean the ventilator settings to achieve a Pco2
elimination of volatile acids (carbon dioxide). The res-
of 50–60 millimeters of mercury. Even higher Pco2 levels
piratory center (lungs) controls the pH by varying the
are tolerated in nonventilated, older infants with broncho-
amount of CO2, which is excreted by exhalation.2 This is
pulmonary dysplasia (Pco2 65–70 millimeters of mercu-
referred to in the blood gas as the Pco2. The chemo-
ry). The concept that higher Pco2 levels are bsafeQ and
receptors in the brain will sense within minutes that the
bwell toleratedQ is based on limited data and needs to be
Pco2 is increasing and then will send messages to the
studied further,5 although strong trends indicate the
respiratory center to accelerate the rate and depth of
possibility of important benefits without increased adverse
breathing. This way, the lungs can respond to a change in
affects.6 The specific ideal, safe range for Pco2 levels in
H+ concentration within minutes.
the neonatal population is still under debate.
The metabolic reaction between bicarbonate (HCO3)
and H+ produces carbonic acid, which will then dissociate
into water and CO2 (as described earlier; see carbonic Oxygenation
anhydrase equation above). To prevent CO2 from accumu-
lating and carbonic acid from forming again, leading to
acidosis, the lungs will excrete the CO2. The carbonic
anhydrase equation is catalyzed by the enzyme carbonic
A cid base balance also effects tissue oxygenation. The
Oxygen Hemoglobin Dissociation Curve is a measure
of the affinity that hemoglobin has for oxygen. Oxygen is
anhydrase. This reaction moves to the right when Pco2 levels carried in the blood by being dissolved in the plasma and
are high and moves to the left when Pco2 levels are low.4 attached to hemoglobin in the red blood cells. The
The renal system (kidneys) controls the pH by varying concentration of oxygen in the arterial plasma is expressed
the rate of excretion of HCO3, the base that neutralizes as Pao2, whereas the concentration of oxygen on hemo-
Understanding Blood Gas Interpretation 59

With a left shift, there is an increased attraction between


oxygen and hemoglobin. Therefore, hemoglobin picks up
oxygen more easily and does not release it until a lower
Pao2 level is reached. This can impede oxygen release to
the tissues, but it facilitates the unloading of carbon dioxide
and the uptake of oxygen in the lungs.4 Fetal hemoglobin
has decreased 2.3 diphosphoglycerate (DPG) and has a
high oxygen affinity causing a shift to the left. Fetal
hemoglobin is the main hemoglobin that transports oxygen
in the developing fetus during the last 7 months of
pregnancy. This special hemoglobin has a higher affinity
for oxygen, so it holds on to oxygen tighter. Once
delivered, infants automatically turn off the production of
hemoglobin F (fetal) and turn on the production of
hemoglobin A (adult). It takes about 2 years for an infant
to completely switch over to adult hemoglobin.
Fig 1. Oxyhemoglobin disassociation curve can be shifted to
the left by hypothermia, alkalosis, hypocarbia, or decreased 23 Acid Base Imbalances
DPG. The curve can be shifted to the right by hyperthermia,
acidosis, hypercarbia, or increased 2–3 DPG levels. This figure is
reprinted from Comprehensive Neonatal Nursing, with permis-
sion from Elsevier Inc.
R espiratory acidosis occurs when carbon dioxide is not
promptly vented by the lungs and the CO2 combines
with water to form carbonic acid. This condition results in
a buildup of CO2. A blood gas may exhibit a low pH, high
globin is expressed as percent saturation (SaO2) on the pulse
Pco2 and a normal HCO3 (Table 1).9 Respiratory acidosis
oximetry monitor. When there is no oxygen on the
is due to a decrease in alveolar ventilation. The treat-
hemoglobin, it is 0% saturated; when the hemoglobin is
ment consists of determining the cause and ensuring
carrying as much oxygen as possible, it is 100% saturated.
effective ventilation.
The desired level of oxyhemoglobin saturation in a normal
Metabolic acidosis occurs when a disorder adds acid to
healthy term infant is 90% –94% saturation.7
the body or causes alkali to be lost faster than the buffer
The oxyhemoglobin saturation (% sat or O2 sat) is the
system, lungs, or kidneys can regulate the load. This condi-
most valuable test for detecting hypoxemia. It is not a
tion reflects a low pH, normal Pco2, and a low HCO3.9 The
sensitive measure for high blood oxygen levels and
causes of metabolic acidosis consist of the overproduction
provides no information regarding pH, carbon dioxide, or
of acids due to abnormal metabolism (inborn errors or
serum bicarbonate levels. When Pao2 reaches approximate-
anaerobic metabolism), the decreased excretion of acids due
ly 60 millimeters of mercury, the hemoglobin is almost
to impaired renal function, and the excessive loss of
completely saturated with oxygen, making the SaO2 nearly
bicarbonate through the gastrointestinal tract (severe
100%.8 Therefore, if the SaO2 is more than approximately
diarrhea). To determine treatment, determine the cause,
94%, the Pao2 could be either acceptable (50 – 80 milli-
consider a hypoxic event, and determine whether the con-
meters of mercury) or undesirably high (N80 millimeters of
dition is a metabolic vs mixed acidosis. Treatment will then
mercury). Cyanosis is generally noted only at a Pao2 of less
include ensuring effective ventilation and the administra-
than 40 millimeters of mercury in neonates.8 When an infant
tion of volume and/or buffers such as sodium bicarbonate.
has received surfactant, for example, the oxygen saturation
Respiratory alkalosis occurs when CO2 is excreted by the
increases, and it is important to wean the Fio2 to maintain a
lungs in excess of its production rate by the body. The level
saturation between 90% and 94% to prevent hyperoxyge-
nation and the exposure to oxygen toxicity.
When there is an increased affinity for oxygen, less Table 1. Summary of Blood Gases
oxygen is released at the tissue level. When there is a
decreased affinity for oxygen, then more oxygen is released pH Pco2 HCO3
to the tissues. Factors that can shift the curve to the right
Respiratory acidosis A7.35 z Normal
include temperature, pH, and hemoglobin structure. The Metabolic acidosis A7.35 Normal A
factors that shift the curve to the left include hypothermia, Respiratory alkalosis z7.45 A Normal
alkalemia, hypocapnia, and fetal hemoglobin. These factors Metabolic alkalosis z7.45 Normal z
increase the affinity of hemoglobin for oxygen (Fig 1).
60 Brown and Eilerman

of carbonic acid falls producing an excess amount of HCO3 Table 2. Classification of Blood Gases
in relation to the acid content. This condition reflects a high
pH, low Pco2, and a normal HCO3.9 The cause of Bass
Disturbance pH Pco2 HCO3 excess/deficit
respiratory alkalosis is an increase in alveolar ventilation
(may be associated with central nervous system disorders Respiratory
and birth asphyxia). The treatment consists of determining acidosis
the cause and then decreasing minute ventilation. Uncompensated b7.35 z Normal Normal
Metabolic alkalosis occurs whenever acid is excessive- Compensated Normal z z Excess N +2
ly lost or alkali is excessively retained. The acid-base ratio Respiratory
of the body is altered. This condition reflects a high pH, alkalosis
normal Pco2, and a high HCO3.9 The cause of metabolic Uncompensated N7.35 A Normal Normal
Compensated Normal A A Deficit N 2
alkalosis may be excessive administration of sodium
Metabolic
bicarbonate; loss of acid-containing gastric secretions
acidosis
through vomiting, gastric suction, or gastric fistula; Uncompensated b7.35 Normal A Deficit N 2
diuretic therapy resulting in loss of H+ into the urine, Compensated Normal A A Deficit N 2
hyperadrenoccorticism, or potassium loss; movement of Metabolic
H+ intracellularly with potassium deficiency, which may alkalosis
also result from diuretic therapy; and rarely, H+ loss into Uncompensated N7.45 Normal z Excess N +2
the stool. Metabolic alkalosis is often associated with Compensated Normal z z Excess N +2
chronic respiratory disease. The treatment of metabolic
alkalosis consists of determining and treating the cause.
Examples may include increasing the blood volume or a base deficit below 2 reflects a metabolic acidosis. A
replacing potassium or chloride losses. Table 2 summa- bicarbonate level higher than 26 milliequivalents per liter
rizes the blood gas alterations seen in various states. and/or a base excess of more than 2 reflects a metabolic
alkalosis. Significant changes in bicarbonate levels are due
to a metabolic process. The base excess/deficit value
Interpretation of Blood Gases represents the number of milliequivalents per liter above or
below the normal value. This value calculates the quantity
W hen interpreting arterial blood gases, a system-
atic approach should be used. The following case
study will help illustrate this six-step process to interpret
of acid or alkali required to return the plasma to a normal
pH under standard conditions.
blood gases.
Step Four: Compensated, Uncompensated, or Partially
Step One: Evaluate pH Compensated
The first step is to evaluate the pH and determine the The fourth step in evaluating blood gases is to
direction of the acid-base imbalance. A normal pH falls determine the primary and compensating disorder. Many
between 7.35–7.45. A pH higher than 7.45 equals alkalosis times, two acid-base imbalances occur together. One is the
and a pH less than 7.35 equals acidosis. A normal pH does primary imbalance, and the other is the body attempting to
not necessarily indicate the absence of an acid base return the pH to normal. The pH is what determines the
disturbance. If there is more than one acid-base imbalance process in control. The body will not compensate to a pH
in process, the pH identifies the process in control. above or below 7.4. It is important to remember that three
stages of compensation can exist. First, look at the pH and
Step Two: Evaluate the Respiratory Component assess whether it is normal, high, or low. With complete
compensation, the pH is normal, although the original
The second step is to evaluate the ventilation. A Pco2
cause of the acid-base problem may be present. Both the
greater than 45 millimeters of mercury is related to
Pco2 and HCO3 are abnormal. When compensation is
ventilatory failure and respiratory acidosis. A Pco2 less
complete, to identify the primary disorder, consider a pH
than 35 millimeters of mercury is related to alveolar
between 7.35 and 7.40 indicative of primary acidosis and a
hyperventilation and respiratory alkalosis.
pH between 7.41 and 7.45 indicative of primary alkalosis.
During partial compensation, the pH is trying to approach
Step Three: Evaluate the Metabolic Component
normal, but is still abnormal, and the Pco2 and HCO3 are
The third step is to evaluate the metabolic process. A both abnormal. Noncompensation reflects an abnormal pH
bicarbonate level below 22 milliequivalents per liter and/or and an alteration of only Pco2 or HCO3.
Understanding Blood Gas Interpretation 61

Step Five: Oxygenation Table 3. Normal Blood Gas Values

The fifth step is to evaluate the oxygenation. This can Source Arterial Capillary
only be accurately determined through an arterial blood pH 7.35 -7.45 7.35 - 7.45
gas sample. Assess whether the patient is hypoxemic Po2 50 - 80 mm Hg 40 - 50 mm Hg
and whether the hypoxemia is mild, moderate, or severe. Pco2 35 - 45 mm Hg 35 - 45 mm Hg
Mild hypoxemia may be considered with a Pao 2 HCO3 22 - 26 mEq/L 22 - 26 mEq/L
40 - 50 millimeters of mercury; moderate hypoxemia, HCO3 (preterm) 20 - 24 mEq/L 20 - 24 mEq/L
30- 40 millimeters of mercury; and severe hypoxemia, Bass excess/deficit 2 + 2 2 + 2
below 30 millimeters of mercury. Anion gap 8 - 12 mEq/L 8 - 12 mEq/L

Step Six: Interpret


rate, 30; and Fio2, 40%. His current weight is 510 grams,
The final step is to interpret the blood gas. Analyze the serum glucose is 180, and serum sodium is 151. This
primary disorder, the oxygenation status, and the degree of blood gas was drawn from an umbilical artery catheter.
compensation. For example, when analyzing a blood gas
with a pH of 7.25, Pco2 of 65, HCO3 of 30, and Po2 of 35, pH 7.17
the pH would indicate acidosis. Next, the Pco2 of 65 Pco2, 45 millimeters of mercury
would indicate the respiratory component is elevated, HCO3, 17 milliequivalents per liter
base deficit, 10
indicating respiratory acidosis. The HCO3 of 30 would
Pao2, 55 millimeters of mercury
indicate that the metabolic component has changed in the
alkalotic direction, indicating compensation. However, the
Evaluate the state of his acid-base balance by going
pH is still outside the reference range, indicating only
through the six-step process. Refer to Table 3 for nor-
partial compensation. Therefore, this blood gas would be
mal values.
bpartially compensated respiratory acidosis with moderate
hypoxemia.Q Table 2 shows changes in blood gas com-
ponents in various states.
Step One

Case Study Evaluate pH: A pH of 7.17 is low, which equals


acidosis.

B aby Brown (Fig 2) is a 24-week-gestation male infant


who is 4 days old. His birth weight was 600 grams,
and he is on a conventional ventilator. The ventilator Step Two
settings are the following: peak inspiratory pressure, 19;
positive end-expiratory pressure, 5; pressure support, 6; Evaluate the respiratory component: A Pco2 of
45 millimeters of mercury is in the reference range.

Step Three

Evaluate the metabolic component: The HCO3 is


17 milliequivalents per liter, and base deficit is 10,
which reflects a metabolic acidosis.

Step Four

Compensated, uncompensated, or partially compensat-


ed? There is no compensation because the Pco2 is within
reference range. In order for compensation to take place,
Fig 2. 24 week gestational age male whose blood gas is: pH the Pco2 would decrease in an attempt to correct for the
7.17 pCO2 45 mm Hg HCO3 17 mEq/L BD-10 paO2 55 mm Hg. severe lack of base.
62 Brown and Eilerman

Step Five with the long-term outcome. It is important to interpret the


blood gas correctly so that the need for and effect of
Oxygenation: The oxygenation is within the reference treatment can be fully appreciated.
range for an arterial blood gas.

Step Six
References

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Interpret. This gas would be considered an uncompen- of Neonatal Nursing. 1990;9(1):67 - 68.
sated metabolic acidosis with no hypoxemia. In this case, 2. Coleman NJ, Houston L. Demystifying acid-base regulation.
this is likely to be related to hyperglycemia (blood Retrieved December 19, 2003 from NetNurse Notes, MaNaInk Education
Website: http://www.manaink.com/nurse/acidbase.html; 2002.
glucose level of 180 mg/dL) and dehydration as 3. Porth CM. Pathophysiology. concepts of altered health states
evidenced by the elevated sodium level (151 mEq/L). (4th ed). Philadelphia (PA), J.B. Lippincott Company; 1994.
Treatment would focus on correction of the hyperglyce- 4. Askin DF. Interpretation of neonatal blood gases, Part I: Physiology
and acid–base homeostasis. Neonatal Netw. 1997;16(5):17 - 21.
mia and either a fluid bolus of normal saline or an 5. Varughese M, Patole S, Shama A, Whitehall J. Permissive
increase in intravenous maintenance fluid volume. No hypercapnia in neonates: the case of the good, the bad, and the ugly.
respiratory changes would be required because the Pco2 Pediatr Pulmonol. 2002;33(1):56 - 64.
6. Thome UH, Carlo WA. Permissive hypercapnia. Semin Neonatol.
is within normal limits. 2002;7(5):409 - 419.
7. Kornhauser MS. Blood gas interpretation, In: Spitzer AR, ed.
Intensive care of the fetus and neonate. (2nd ed). Philadelphia (PA),
Summary Elsevier; 2005:523 - 539.
8. In: Fanaroff AA, Martin RJ, eds. Neonatal-perinatal medicine.
(6th ed). St. Louis (MO): Mosby Year Book; 1997.

W ith an understanding the acid base balance of the


neonate, tissue oxygenation can be optimized along
9. Askin DF. Interpretation of neonatal blood gases, Part II: disorders
of acid base balance. Neonatal Netw. 1997;16(6):23 - 29.

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