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The purpose of this
course will be to remove the mystery behind the interpretation of the
arterial blood gases (ABG); raise awareness and understanding of the
various aspects of the ABG, and provide a comfort level with care of the
patient by increasing the knowledge base.
After completion of this course, the
learner will:
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Demonstrate the ability to
distinguish between acidosis
and alkalosis |
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Interpret ABG results |
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Discuss the causes of
respiratory acidosis and
alkalosis |
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Discuss the causes of
metabolic acidosis and
alkalosis |
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Identify the role of the ABG
in a trauma assessment |
Understanding the significance of
the findings for the arterial blood
gases (ABG) is the first step in
interpretation of them. Without this
understanding, the nurse cannot be
expected to realize the implication
of the results.
A study conducted in Illinois at
Freeport Health Network Memorial
Hospital and Swedish American
Hospital demonstrated that a
computer based module aided nurses
to learn ABG interpretation
(Schneiderman, Corbridge, & Zerwic,
2009). Many adult students
demonstrate various methods of
learning to better enhance their
knowledge base. Finding the best
education method for the individual
is the first step to success in
clinical competence.
Whatever the underlying cause for
the acid-base disturbance, one must
gain knowledge for interpretation of
the ABG to establish the best course
of treatment. Therefore, the
healthcare provider will determine
the limitations of therapy based on
the results of the ABG (Kellum,
2007).
When interpreting the ABG results,
one must first know the five major
components of the ABG to be
addressed: oxygen saturation (SaO2),
partial pressure of oxygen (PaO2),
acidity or alkalinity (pH), partial
pressure of carbon dioxide (PaCO2),
and bicarbonate ions concentration
(HCO3)
(Pruitt & Jacobs, 2004).
Let us begin by looking at the pH of
the blood. The acid-base balance of
the blood is maintained by two areas
of the body: the respirations and
the kidneys. The lower pH represents
acidosis and the higher pH
represents alkalosis. The normal
range is 7.35-7.45 mm Hg.
The PaO2
evaluates the oxygen in plasma and
has a normal range of 80-95 mm Hg.
This does not measure the amount of
oxygen attached to the hemoglobin.
SaO2
measures the amount of oxygen
attached to the hemoglobin. The
normal range is 95-99% and should be
above 90%.
PaCO2
evaluates the ventilation component.
The normal range is 35-45. However,
the value is inversely related to
ventilation. For example, decreased
ventilation has a higher value and
increased ventilation has a lower
value. Therefore, hyperventilation
causes alkalosis because the patient
is blowing off carbon dioxide and
hypoventilation causes acidosis
because the patient is retaining
carbon dioxide. The body adjusts for
these conditions by changing the
respiratory rate (Pruitt & Jacobs,
2004).
HCO3
is regulated by the kidneys and
evaluates the metabolic component.
The normal range is 22-26 mEq/L.
Below 22 is considered to be
acidosis and above 26 is alkalosis.
The body can adjust to the
abnormalities in the HCO3
levels but not as quickly as it can
to the abnormal PaCO2
levels. Several days could be
required to make the necessary
adjustments to bring the HCO3
levels to a normal range (Pruitt &
Jacobs, 2004).
|
Test |
Normal Value |
 |
 |
|
pH |
7.35-7.45 |
|
HCO3 |
22-26 |
|
PaCO2 |
35-45 |
|
PaO2 |
80-95 mm Hg |
|
SaO2 |
95-99% |
Four conditions are evaluated based
on the ABGs: respiratory acidosis,
respiratory alkalosis, metabolic
acidosis, and metabolic alkalosis.
As we explore these conditions, the
potential causes, the ABG values,
and the compensatory mechanisms, we
will gain a better understanding of
what is happening within the body.
Respiratory acidosis is an attempt
by the body to compensate for
excessive PaCO2.
The body excretes the extra hydrogen
in the urine and exchanges it for
bicarbonate ions. When this happens
HCO3
rises to restore the body to a
normal pH. Until the pH returns to
normal, the PaCO2
may stay elevated.
Any situation that can cause the
patient to develop a depressed
respiratory status can cause this
medical condition. Examples of these
situations could be hypoventilation,
asphyxia, central nervous system
depression, chronic obstructive
pulmonary disease, infection, and
drug induced respiratory depression.
The ABG values one would see with
respiratory acidosis would be: pH <
7.35; PaCO2
> 45 mmHg; and HCO3
> 26 mEq/L if compensating.
|
Respiratory Acidosis Compensation |
|
|
Acidosis |
Alkalosis |
|
pH |
7.35 |
7.45 |
|
PaCO2 |
45 |
35 |
|
HCO3 |
22→
→ → → |
26
(increases) |
Respiratory alkalosis is a
compensatory mechanism of the body
aimed to increase excretion of HCO3
and retention of the hydrogen ions.
Respiratory alkalosis lowers the HCO3
and restores pH to normal.
Conditions that cause the
respiratory system to be over
stimulated can be extenuating
factors in respiratory alkalosis
such as hyperventilation.
The ABG values one would see with
respiratory alkalosis would be: pH >
7.45; PaCO2
< 35 mm Hg; and HCO3
< 22 mEq/L if compensating.
|
Respiratory Alkalosis Compensation |
|
|
Acidosis |
Alkalosis |
|
pH |
7.35 → → → → |
7.45 (increases) |
|
PaCO2 |
45
→ → → → → |
35
(decreases) |
|
HCO3 |
22
← ← ← ← ← |
26
(decreases) |
When a patient is demonstrating
metabolic acidosis his or her body
is pulling the HCO3
into the cells as a buffer and
therefore, depletes the plasma
level. The body begins compensating
by increasing the ventilation and
thus renal retention of the HCO3
takes place.
When patients present with the
following conditions, one must
consider the patient could be a
candidate for metabolic acidosis:
HCO3
loss from diarrhea; shock; drug
intoxication; salicylate poisoning;
renal failure; diabetic
ketoacidosis; and circulatory
failure producing lactic acid.
ABG values one would see with
metabolic acidosis would be: pH <
7.35; HCO3
< 22; and PaCO2
< 35 mm Hg if compensating.
|
Metabolic Acidosis Compensations |
|
|
Acidosis |
Alkalosis |
|
pH |
7.35 ← ← ← |
7.45 (decreases) |
|
PaCO2 |
45
→ → → → |
35
(decreases) |
|
HCO3 |
22
← ← ← ← |
26
(decreases) |
One generally considers the ABG to
be a test for respiratory
conditions; however, a study of ABGs
in Brazil to test patients for
metabolic acidosis in relation to
sepsis and shock was conducted. The
study revealed a group whom were not
able to clear their inorganic ions
had a higher morbidity rate, whereas
those who were able to correct their
acidosis survived (Noritomi et al.,
2009).
The severely septic patient who
developed acute renal failure upon
arrival to the intensive care unit
(ICU) had a battery of testing to
include the ABG. Results of the ABG
revealed: a pH of 7.32, PaCO2
45, and HCO3
21. Understanding that without
treatment metabolic acidosis will
only become progressively worse, and
steps will be needed to bring the
patient into a compensatory mode to
recovery.
With metabolic alkalosis one will
see an increased level of HCO3.
This could be caused by several
factors such as too much bicarbonate
during a code, excess hydrogen loss
during vomiting or suctioning,
potassium loss from diuretics or
steroids, or excessive alkali
ingestion. The kidneys will increase
the HCO3
excretion trying to conserve the
hydrogen and the respiratory system
will compensate by decreasing the
ventilations and conserving the CO2
and raising the PaCO2.
ABG values one would see with
metabolic alkalosis would be: pH >
7.45; HCO3
> 26 mEq/L and PaCO2
> 45 Hg if compensating.
|
Metabolic Alkalosis Compensation |
|
|
Acidosis |
Alkalosis |
|
pH |
7.35 → → → |
7.45 (increases) |
|
PaCO2 |
45
← ← ← ← |
35
(increases) |
|
HCO3 |
22
→ → → → |
26
(increases) |
An easy way to remember what is
going on in the body with acid and
alkaline and compensation is to
think of it like this: acid is
regulated by the respiratory system,
alkaline is regulated by metabolic
and if compensated everything shifts
in the opposite direction.
|
|
Low |
High |
Normal |
|
pH |
Acidosis |
Alkalosis |
|
|
PaCO2 |
Alkalosis |
Acidosis |
|
|
HCO3 |
Acidosis |
Alkalosis |
Uncompensated |
A look at a glance with the four
disorders demonstrates what happens
with the pH, what the initiating
event causing the disorder, and the
compensatory effect will be shown in
the following table. It is important
to remember that compensating
effects are seen in chronic
conditions.
|
Disorder |
pH |
Initiating Event |
Compensating Effect |
|
Respiratory Acidosis |
↓ |
↑
PaCO2 |
↑
HCO3 |
|
Respiratory Alkalosis |
↑ |
↓
PaCO2 |
↓
HCO3 |
|
Metabolic Acidosis |
↓ |
↓
HCO3 |
↓
PaCO2 |
|
Metabolic Alkalosis |
↑ |
↑
HCO3 |
↑
PaCO2 |
Studies have shown that along with
other indicators such as the Glasgow
Coma Scale (GCS) the ABG results can
serve as a strong indicator of a
patient’s mortality during the
hospital course. A study conducted
by Kaplan and Kellum of trauma
patients revealed the trauma
survivors had lactic acidosis
(Kaplan & Kellum, 2008).
Addressing the GCS of each trauma
patient arriving in the ED is an
important step in the assessment
process. Using the information
included in the following Glasgow
Coma Scale, the nurse can assess eye
opening, motor response, and verbal
response.
|
Eyes Open |
Spontaneous |
4 |
|
To
verbal command |
3 |
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To
pain |
2 |
|
No
response |
1 |
 |
|
Best Motor Response to verbal command |
Obeys |
6 |
|
Best Motor Response to painful stimulus |
Localizes pain |
5 |
|
Flexion-withdrawal |
4 |
|
Flexion-abnormal |
3 |
|
Extension |
2 |
|
No
response |
1 |
 |
|
Best Verbal Response |
Oriented and converse |
5 |
|
|
Disoriented and converses |
4 |
|
|
Inappropriate words |
3 |
|
|
Incomprehensible sounds |
2 |
|
|
No
response |
1 |
Patients arriving in the Emergency
Department (ED) post trauma receive
a head to toe trauma assessment
including the GCS. A GCS of < 8
indicates a severe head injury and
generally has a poor outcome. The
low GCS coupled with a strong ion
gap according to Kaplan and Kellum
(2008) is “a strong predictor of
hospital mortality”. Therefore,
vascular injury must be assessed
along with other areas of assessment
and fluid resuscitation initiated to
prevent further decline.
However, a patient can arrive with a
GCS of 15 indicating he or she has
spontaneous eye opening, obey verbal
commands and he or she is oriented
and conversing. This patient can be
suffering from respiratory distress
caused by a traumatic injury to the
lungs, therefore leaving the GCS to
be a poor indicator of patient
condition.
Take for example the 50 year old
female who arrives via ambulance who
was the driver of a vehicle that ran
head on into the median underpass on
the interstate. She was wearing a
seat belt and collapsed the steering
wheel before the airbag deployed.
When she arrived in the ED she had a
GCS of 15 and was anxious. At
initial inspection she had bruising
to her chest from the seat belt, no
visible head injury noted; her vital
signs were within normal limits.
Shortly after arriving in the ED she
began complaining of needing to have
a bowel movement and difficulty
breathing. Her oxygen saturation
dropped to 88% on room air. An ABG
was obtained with the following
results: pH 7.32, PaCO2 47, and HCO3
28. Vital signs have now made a
slight change from being within
normal limits to: blood pressure
120/70, HR 88, and respiratory rate
30. Understanding the patient’s
blood gas reveals a respiratory
acidosis; preparations begin to
treat the cause when the results of
the x-ray reveal a left side
pneumothorax.
Regardless of the condition of the
patient, an important aspect of the
ABG is to take a systematic approach
to interpretation of the ABG and
determining between the differential
diagnoses. Know the patient history
and begin treatment as soon as
feasible to ensure the best possible
outcomes. Placing the patient at the
top of the pyramid is the absolute
most significant step in the
process.
Barone, J. E., & Madlinger, R. V.
(2006). Should an Allen Test be
performed before radial artery
cannulation? The Journal of Trauma:
Injury, Infection, and Critical
Care, 61(2), 468-470.
Kaplan, L. J., & Kellum, J. A.
(2008). Comparison of acid base
models for prediction of hospital
mortality following trauma. Shock,
00(00), 1-6.
Kellum, J. A. (2007). Disorders of
acid-base balance. Critical Care
Medicine, 35(11), 2630-2636.
Noritomi, D. T., Francisco, G. S.,
Kellum, J. A., Cappi, S. B.,
Biselli, P. J., Alexandre, B. L., et
al. (2009). Metabolic acidosis in
patients with severe sepsis and
septic shock: A longitudinal
quantitative study. Critical Care
Medicine, 37(10), 1-7.
Pruitt, W. C., & Jacobs, M. (2004).
Interpreting arterial blood gases:
Easy as ABC. Nursing, 34(8), 50-53.
Schneiderman, J., Corbridge, S., &
Zerwic, J. J. (2009). Demonstrating
the effectiveness of an online,
computer-based learning module for
arterial blood gas analysis.
Clinical Nurse Specialist, 23(3),
151-155. |