Adapted From
UNDERSTANDING BLOOD GAS
INTERPRETATION
Good Samaritan Hospital, NICU
Brown B. RN, MSN, Eilerman, B RN, MSN, CNP
PRE TEST (TRUE OR FALSE)
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10.
Acid-base balance is a complex mechanism in which the body
strives to achieve and maintain a homogenous internal
environment?
Regulation of the body Ph and hydrogen concentration is the goal
of the buffer system.
Acid-bicarbonate system is a weak, and slow buffer that occurs in
the extracellular fluid.
When the body is acidotic, the oxygen carrying capacity is reduced?
Permissive Hypercapnia is a strategy that allows increasing level
of PCO2 and pH level of more than 7.20?
Oxygen Saturation (O2 Sat) provides information regarding ph,
blood oxygen level, carbon dioxide, or serum bicarbonate.
A normal Ph indicates an absence of acid-base disturbance?
Excessive retention of Carbonic acid (CO2 combined
with water) and carbon dioxide will result to Respiratory Acidosis.
Metabolic Alkalosis is when there is an excessive acid and alkali
loss?
Abnormal Ph, and an alteration in either PCO2 or HCO3 reflects
Non-compensation.
An arterial or capillary blood gas is a clinical assessment tool for
determining an infant’s pulmonary and metabolic status. The pulmonary
component of the blood gas yields information on ventilation and
oxygenation. The metabolic component reflects potential for changes in
Understanding Blood Gas Interpretation
enzyme function and nerve and muscle activity. Blood gases are the basis
for diagnosis and management of infants with cardiorespiratory disease,
metabolic disorders, and overall management in premature infants. By
integrating acidbase physiology, blood gas interpretation skills, and clinical
history, the neonatal intensive care unit staff can accurately assess an
infant’s current condition and help take the appropriate steps to correct the
imbalance and, therefore, improve outcomes.
Acid-base balance refers to the complex mechanisms through which the
body 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 that can donate hydrogen ions (H+) to alkaline solutions to
neutralize the effect of bases. A base is an alkaline substance that can
combine with acids to accept hydrogen ions neutralizing the effect of the
base. 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
The chemical buffer systems include the carbonic acid-bicarbonate system,
protein buffer system, and the phosphate buffer system. The carbonic acidbicarbonate 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 carbonic acid. This buffer system explains neonatal acidosis
because of the immature kidneys of a preterm infant. These premature
kidneys cannot hold on to bicarbonate, losing it into the urine. Therefore,
there is less bicarbonate to bind with the excess hydrogen, and the blood
becomes acidic. By use of the carbonic anhydrase equation below, one can
see how this process moves in both directions.
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Understanding Blood Gas Interpretation
The protein buffer system is the most powerful and plentiful buffering
system using proteins of cells and plasma. The cell membrane is composed
almost entirely of proteins and lipids. As the extracellular pH changes, the
body adapts by diffusing hydrogen and bicarbonate in and out of the cell
membranes by way of these proteins. This is a slow process, up to several
hours and intracellular electrolytes such as sodium and potassium may be
displaced as the hydrogen or bicarbonate enters the cell. Clinically, this may
account for a degree of hypernatremia or hyperkalemia.
Hemoglobin is part of the protein buffering system. When the body is
acidotic, hemoglobin will act as a buffer. Therefore, the oxygen carrying
capacity may be reduced. In addition, one of the implications of this
buffering system is the displacement of intracellular electrolytes such as
sodium and potassium when H+ enters the cell.
The main components in the phosphate buffer system are monohydrogen
phosphate (HPO4_) and dihydrogen phosphate (H2PO4_). When a strong
acid is added to these two phosphates, only a weak acid is formed, and when
a strong base is added also, only a weak base is formed. Phosphate acts
predominantly as an intracellular and urinary buffer. Because phosphate is
eliminated in the urine, this system is particularly important in buffering
fluids in the kidney tubules.
Respiratory regulation is primarily responsible for the elimination of
volatile acids (carbon dioxide). The respiratory center (lungs) controls the
pH by varying the amount of CO2, which is excreted by exhalation. This is
referred to in the blood gas as the PCO2. The chemoreceptors in the brain
will sense within minutes that the PCO2 is increasing and then will send
messages to the respiratory center to accelerate the rate and depth of
breathing. This way, the lungs can respond to a change in H+ concentration
within minutes.
The metabolic reaction between bicarbonate (HCO3_) and H+ produces
carbonic acid, which will then dissociate into water and CO2 (as described
earlier; see carbonic anhydrase equation above). To prevent CO2 from
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Understanding Blood Gas Interpretation
accumulating 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 anhydrase. This reaction moves to the right when Pco2
levels are high and moves to the left when Pco2 levels are low.
The renal system (kidneys) controls the pH by varying the rate of excretion
of HCO3_, the base that neutralizes carbonic acid. The kidneys are the
slowest physiologic regulators. They take hours to commence their work and
may take up to several days to take effect, but they do have the most
sustained response.
The kidneys provide the most important route for the excretion and
buffering of metabolic acids and are also responsible for maintaining the
plasma levels of HCO3, the most important buffer ofH+. The kidneys control
pHbalance by excreting either acidic urine or basic urine. The overall
mechanism by which the kidneys control the excretion of H+ and the
retention of bicarbonate occurs by four main mechanisms: excretion of H+,
reabsorption of bicarbonate, production of bicarbonate, and formation of
ammonia.
PERMISSIVE HYPERCAPNIA
Although 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 resulting baro-/volutrauma on the lungs can highly
contribute to the development of bronchopulmonary dysplasia. The major
determinant of lung injury is tidal volume or the volume of air instilled into
the lungs by a ventilator. This parameter is also the primary one that
affects Pco2 levels. The higher the tidal volume is, the more the lungs are
stretched and the more baro-/ volutrauma occurs. Permissive hypercapnia is
a strategy that attempts to minimize this by allowing relatively high levels
of Pco2, provided the pH does not fall below a minimal value (typically
7.20). This is accomplished by providing a low inspiratory volume and
pressure and decreasing the extent of lung tissue stretch. The current trend
is to wean the ventilator settings to achieve a Pco2 of 50–60 millimeters of
mercury. Even higher Pco2 levels are tolerated in nonventilated, older
infants with bronchopulmonary dysplasia (Pco2 65–70 millimeters of
mercury). The concept that higher Pco2 levels are bsafeQ and bwell
toleratedQ is based on limited data and needs to be studied further,
although strong trends indicate the possibility of important benefits without
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Understanding Blood Gas Interpretation
increased adverse affects. The specific ideal, safe range for Pco2 levels in the
neonatal population is still under debate.
OXYGENATION
Acid base balance also effects
tissue oxygenation. The Oxygen
Hemoglobin Dissociation Curve is
a measure of the affinity that
hemoglobin has for oxygen.
Oxygen is carried in the blood by
being dissolved in the plasma and
attached to hemoglobin in the red
blood cells. The concentration of
oxygen in the arterial plasma is
expressed as Pao2, whereas the
concentration
of
oxygen
on
hemoglobin is expressed as
percent saturation (SaO2) on the
pulse oximetry monitor. When
there is no oxygen on the
hemoglobin, it is 0% saturated;
when the hemoglobin is carrying
as much oxygen as possible, it is 100% saturated. The desired level of
oxyhemoglobin saturation in a normal healthy term infant is 90%–94%
saturation.
The oxyhemoglobin saturation (% sat or O2 sat) is the most valuable test for
detecting hypoxemia. It is not a sensitive measure for high blood oxygen
levels and provides no information regarding pH, carbon dioxide, or serum
bicarbonate levels. When Pao2 reaches approximately 60 millimeters of
mercury, the hemoglobin is almost completely saturated with oxygen,
making the SaO2 nearly 100%. Therefore, if the SaO2 is more than
approximately 94%, the Pao2 could be either acceptable (50–80 millimeters
of mercury) or undesirably high (N80 millimeters of mercury). Cyanosis is
generally noted only at a Pao2 of less than 40 millimeters of mercury in
neonates.
When an infant has received surfactant, for example, the oxygen saturation
increases, and it is important to wean the Fio2 to maintain a saturation
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Understanding Blood Gas Interpretation
between 90% and 94% to prevent hyperoxygenation and the exposure to
oxygen toxicity. When there is an increased affinity for oxygen, less oxygen
is released at the tissue level. When there is a decreased affinity for oxygen,
then more oxygen is released to the tissues. Factors that can shift the curve
to the right include temperature, pH, and hemoglobin structure. The factors
that shift the curve to the left include hypothermia, alkalemia, hypocapnia,
and fetal hemoglobin. These factors increase the affinity of hemoglobin for
oxygen (Fig 1). 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. 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.
ACID BASE IMBALANCES
Respiratory 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 Pco2 and a normal HCO3_ (Table 1). Respiratory acidosis is due to a
decrease in alveolar ventilation. The treatment consists of determining the
cause and ensuring effective ventilation.
Metabolic acidosis occurs when a disorder adds acid to the body or causes
alkali to be lost faster than the buffer system, lungs, or kidneys can regulate
the load. This condition reflects a low pH, normal Pco2, and a low HCO3_.
The causes of metabolic acidosis consist of the overproduction of acids due to
abnormal metabolism (inborn errors or anaerobic metabolism), the
decreased excretion of acids due to impaired renal function, and the
excessive loss of bicarbonate through the gastrointestinal tract (severe
diarrhea). To determine treatment, determine the cause, consider a hypoxic
event, and determine whether the condition is a metabolic vs mixed
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Understanding Blood Gas Interpretation
acidosis. Treatment will then include ensuring effective ventilation and the
administration of volume and/or buffers such as sodium bicarbonate.
Respiratory alkalosis occurs when CO2 is excreted by the lungs in excess of
its production rate by the body. The level of carbonic acid falls producing an
excess amount of HCO3_ in relation to the acid content. This condition
reflects a high pH, low Pco2, and a normal HCO3_. The cause of respiratory
alkalosis is an increase in alveolar ventilation (may be associated with
central nervous system disorders and birth asphyxia). The treatment
consists of determining the cause and then decreasing minute ventilation.
Metabolic alkalosis occurs whenever acid is excessively lost or alkali is
excessively retained. The acid-base ratio of the body is altered. This
condition reflects a high pH, normal Pco2, and a high HCO3_. The cause of
metabolic alkalosis may be excessive administration of sodium bicarbonate;
loss of acid-containing gastric secretions through vomiting, gastric suction,
or gastric fistula; diuretic therapy resulting in loss of H+ into the urine,
hyperadrenoccorticism, or potassium loss; movement of H+ intracellularly
with potassium deficiency, which may also result from diuretic therapy; and
rarely, H+ loss into the stool. Metabolic alkalosis is often associated with
chronic respiratory disease. The treatment of metabolic alkalosis consists of
determining and treating the cause. Examples may include increasing the
blood volume or replacing potassium or chloride losses. Table 2 summarizes
the blood gas alterations seen in various states.
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Understanding Blood Gas Interpretation
INTERPRETATION OF BLOOD GASES
When interpreting arterial blood gases, a systematic approach should be
used. The following case study will help illustrate this six-step process to
interpret blood gases.
Step One: Evaluate pH
The first step is to evaluate the pH and determine the direction of the acidbase imbalance. A normal pH falls between 7.35–7.45. A pH higher than
.45 equals alkalosis and a pH less than 7.35 equals acidosis. A normal pH
does not necessarily indicate the absence of an acid base disturbance. If
there is more than one acid-base imbalance in process, the pH identifies the
process in control.
Step Two: Evaluate the Respiratory Component
The second step is to evaluate the ventilation. A Pco2 greater than 45
millimeters of mercury is related to ventilatory failure and respiratory
acidosis. A Pco2 less than 35 millimeters of mercury is related to alveolar
hyperventilation and respiratory alkalosis.
Step Three: Evaluate the Metabolic Component
The third step is to evaluate the metabolic process. A bicarbonate level
below 22 milliequivalents per liter and/or a base deficit below _2 reflects a
metabolic acidosis. A bicarbonate level higher than 26 milliequivalents per
liter 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 represents the number of milliequivalents per liter
above or below the normal value. This value calculates the quantity of acid
or alkali required to return the plasma to a normal pH under standard
conditions.
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Understanding Blood Gas Interpretation
Step Four: Compensated, Uncompensated, or Partially Compensated
The fourth step in evaluating blood gases is to determine the primary and
compensating disorder. Many times, two acid-base imbalances occur
together. One is the primary imbalance, and the other is the body
attempting to return the pH to normal. The pH is what determines the
process in control. The body will not compensate to a pH above or below 7.4.
It is important to remember that three stages of compensation can exist.
First, look at the pH and assess whether it is normal, high, or low. With
complete compensation, the pH is normal, although the original cause of the
acid-base problem may be present. Both the Pco2 and HCO3_ are abnormal.
When compensation is complete, to identify the primary disorder, consider a
pH between 7.35 and 7.40 indicative of primary acidosis and a pH between
7.41 and 7.45 indicative of primary alkalosis. During partial compensation,
the pH is trying to approach normal, but is still abnormal, and the Pco2 and
HCO3_ are both abnormal. Noncompensation reflects an abnormal pH and
an alteration of only Pco2 or HCO3_.
Step Five: Oxygenation
The fifth step is to evaluate the oxygenation. This can only be accurately
determined through an arterial blood gas sample. Assess whether the
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Understanding Blood Gas Interpretation
patient is hypoxemic and whether the hypoxemia is mild, moderate, or
severe. Mild hypoxemia may be considered with a Pao2 40-50 millimeters of
mercury; moderate hypoxemia, 30-40 millimeters of mercury; and severe
hypoxemia, below 30 millimeters of mercury.
Step Six: Interpret
The final step is to interpret the blood gas. Analyze the primary disorder,
the oxygenation status, and the degree of compensation. For example, when
analyzing a blood gas with a pH of 7.25, Pco2 of 65, HCO3 of 30, and Po2 of
35, the pH would indicate acidosis. Next, the Pco2 of 65 would indicate the
respiratory component is elevated, indicating respiratory acidosis. The
HCO3 of 30 would indicate that the metabolic component has changed in
the alkalotic direction, indicating compensation. However, the pH is still
outside the reference range, indicating only partial compensation.
Therefore, this blood gas would be bpartially compensated respiratory
acidosis with moderate hypoxemia.Q Table 2 shows changes in blood gas
components in various states.
CASE STUDY
Baby 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 settings are the following: peak inspiratory pressure, 19; positive
end-expiratory pressure, 5; pressure support, 6; rate, 30; and Fio2, 40%. His
current weight is 510 grams, serum glucose is 180, and serum sodium is 51.
This blood gas was drawn from an umbilical artery catheter.
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Understanding Blood Gas Interpretation
pH 7.17
Pco2 45 millimeters of mercury
HCO3, 17 milliequivalents per liter base deficit, _10
Pao2, 55 millimeters of mercury
Evaluate the state of his acid-base balance by going through the six-step
process. Refer to Table 3 for normal values.
Step One
Evaluate pH: A pH of 7.17 is low, which equals acidosis.
Step Two
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 compensated? There is no
compensation because the Pco2 is within reference range. In order for
compensation to take place, the Pco2 would decrease in an attempt to
correct for the severe lack of base.
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Understanding Blood Gas Interpretation
Step Five
Oxygenation: The oxygenation is within the reference range for an arterial
blood gas.
Step Six
Interpret. This gas would be considered an uncompensated metabolic
acidosis with no hypoxemia. In this case, this is likely to be related to
hyperglycemia (blood glucose level of 180 mg/dL) and dehydration as
evidenced by the elevated sodium level (151 mEq/L). Treatment would focus
on correction of the hyperglycemia and either a fluid bolus of normal saline
or an increase in intravenous maintenance fluid volume. No respiratory
changes would be required because the Pco2 is within normal limits.
SUMMARY
With an understanding the acid base balance of the neonate, tissue
oxygenation can be optimized along with the long-term outcome. It is
important to interpret the blood gas correctly so that the need for and effect
of treatment can be fully appreciated.
REFERENCES
1. In: Lynam L, ed. Acid-base basics. Neonatal Network: the Journal of
Neonatal Nursing. 1990;9(1):67 - 68.
2. Coleman NJ, Houston L. Demystifying acid-base regulation.
Retrieved December 19, 2003 from NetNurse Notes, MaNaInk Education
Website: http://www.manaink.com/nurse/acidbase.html; 2002.
3. Porth CM. Pathophysiology. concepts of altered health states
(4th ed). Philadelphia (PA), J.B. Lippincott Company; 1994.
4. Askin DF. Interpretation of neonatal blood gases, Part I: Physiology and
acid–base homeostasis. Neonatal Netw. 1997;16(5):17 - 21.
5. Varughese M, Patole S, Shama A, Whitehall J. Permissive hypercapnia
in neonates: the case of the good, the bad, and the ugly. Pediatr
Pulmonol. 2002;33(1):56 - 64.
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Understanding Blood Gas Interpretation
6. Thome UH, Carlo WA. Permissive hypercapnia. Semin Neonatol.
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), Elsevier;
2005:523- 539.
8. In: Fanaroff AA, Martin RJ, eds. Neonatal-perinatal medicine. (6th ed).
St. Louis (MO): Mosby Year Book; 1997.
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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