Interpreting Arterial Blood Gases by Michael
Greenlee.
Hi, my name is Michael Greenlee.
I am the Clinical Nurse Educator in the Cardiac
ICU at Boston Children's Hospital.
Today I'm going to be discussing arterial
blood gas analysis, and also known as acid-base
imbalance.
As part of this discussion, I'm going to be
discussing the four conditions-- metabolic
alkalosis, metabolic acidosis, respiratory
acidosis, and respiratory alkalosis.
And at the end of the discussion, we're going
to have four case studies with questions to
each case study for you to answer.
Arterial blood gas analysis is an essential
part of diagnosing and managing a patient's
oxygenation status and acid-base balance.
When the nurse is able to correctly interpret
the results of the blood gas, she will be
able to diagnose and anticipate a course of
treatment.
Understanding the implications of acid-base
balance is very important.
Changes in acid-base balance have important
physiological effects.
Significant changes in blood pH will interfere
with cellular functioning and if uncorrected
will lead to death.
The objective of this discussion is to understand
the components of the arterial blood gas and
the normal ranges for those components.
We will discuss the four conditions that identify
the physiological acid-base state, including
their common causes, signs and symptoms, basic
compensatory responses, and the medical and
nursing interventions we would anticipate
for those conditions.
To obtain a blood gas, the clinician will
assess the option, which will yield information
that is most reliable.
Blood from arterial circulation versus venous
circulation will have different normal ranges
and need to be interpreted with that in mind.
Directly obtaining a blood gas from an arterial
or venous puncture may result in the variable
results, depending on the patient's response
to painful stimulus.
A patient holding his breath or hyperventilating
response will affect results.
And those results will not be representative
of a true baseline.
These are the components of the arterial blood
gas which will be discussed.
For our interpretive purposes, the discussion
will not include PO2 and oxygen saturation
as part of the case study exercises at the
end of this presentation.
Blood Gas Components.
The pH is the measurement of the acidity or
alkalinity of the blood.
It is inversely proportional to the amount
of hydrogen ions in the blood.
The more hydrogen ions are present, the lower
the pH will be.
Likewise, the fewer hydrogen ions present
in the blood, the higher the pH will be.
The normal pH of blood is 7.35 to 7.45.
The body depends on the blood pH to remain
within this normal range in order for normal
metabolism to occur.
When the arterial blood pH falls below 7.35,
the blood is said to be acidic.
Conversely, when the pH and arterial blood
is greater than 7.45, it is said to be alkaline.
When the blood is very acidic or alkaline,
normal physiological functions are adversely
affected-- force of cardiac contractions deteriorate,
vascular response to catecholamines are diminished,
the metabolism of some medications are incomplete,
thus making the patient less responsive to
them.
When diagnosing the patient's acid-base balance
state, the pH is the first component of the
blood gas sampling that is analyzed by a clinician.
Have you ever wondered how human blood might
compare to other fluids in terms of its acid
and base state?
This diagram demonstrates how our blood measures
up to alkaline fluids, such as common household
cleaners and how it measures up to acidic
fluids, such as vinegar and soda pop.
After assessing the pH, the next step to diagnosing
the patient's acid-base condition is analyzing
the carbon dioxide level.
Carbon dioxide, or the pCO2, is the respiratory
component in acid-base balance.
Carbon dioxide is transported on hemoglobin
and dissolves in plasma.
When a CO2 level changes, the pH changes to
the same degree-- but in the opposite direction.
Elevated carbon dioxide in the blood will
lead to acidosis.
Conversely, decreased levels of carbon dioxide
in the blood will lead to alkalosis.
When carbon dioxide combines with water in
our blood, the byproduct is carbonic acid.
Increase of levels of carbonic acid will decrease
the pH, which will lead to an acidic condition.
Changes in arterial blood pH and carbon dioxide
will have important physiological effects
on pulmonary and cerebral circulation.
There are conditions where a cerebral and
pulmonary blood flow may need to be manipulated
by a clinician.
For example, a patient with a head injury
at risk for herniation due to increased intracranial
pressure, may need to have a pH that is normal
to slightly elevated and a PCO2 that is normal
to slightly lower to constrict cerebral vessels.
The constriction of the cerebral vessels will
create greater space in the intracranium and
reduce intracranial pressure.
An example in which a clinician may need to
manipulate pulmonary circulation would be
for a patient with pulmonary hypertension,
a condition that disables blood flow through
pulmonary circulation to the left heart due
to vasoconstriction of the intrapulmonary
vasculature.
A patient who is predisposed to having a pulmonary
hypertensive crisis may be ventilated to slightly
lower PCO2 and higher pH to discourage pulmonary
vasoconstriction.
After assessing the PCO2, the next step to
diagnosing the patient's acid-base condition
is analyzing the bicarbonate level, or tCO2.
The normal level of bicarbonate in our venous
arterial blood is 22 to 26.
Bicarbonate is a physiological buffer that
is maintained, mainly by our kidneys, to attain
a normal pH.
Bicarbonate values outside the normal range
are usually influenced by metabolic conditions
or in response to changes in acid-base status.
It is easy to be confused by tCO2 in reference
to bicarbonate, since CO2 mostly occurs in
the form of HCO3-, bicarbonate in the bloodstream.
Bicarbonate is represented by the total calculated
value of CO2 in the blood.
In an effort to maintain the pH of the blood
within its normal range, the kidneys excrete
or retain bicarbonate.
As a result, when pH decreases, the kidneys
will compensate by retaining bicarbonate.
And as the pH rises, the kidneys will excrete
bicarbonate through the urine.
Although the kidneys provide an excellent
means of regulating the acid-base balance,
the system may take from hours to days to
correct the imbalance.
Although a core portion of blood gas teaching
curricula is focused on interpretation of
acid-base imbalances, the arterial blood gas
can also be used to evaluate blood oxygenation.
The component of the arterial blood gas used
to evaluate this is the PaO2 The normal blood
PaO2 value is 80 to 100 millimeters of mercury.
Some physiological causes for hypoxia include
hypovolemia, anatomic right-to-left shunt
in patients with intracardiac shunting, and
diffusion limitation.
Diffusion limitation occurs when the pathway
of oxygen and carbon dioxide diffusion is
compromised.
Normal pulmonary diffusion occurs when the
oxygen can readily move from the alveolus,
across the capillary endothelium, and into
the red blood cell while concurrent diffusion
of carbon dioxide out of the red blood cell
to the alveolus occurs.
There are many conditions that produce barriers
between the alveoli and capillaries that limit
that exchange.
For example, infants who go on to cardiopulmonary
bypass for cardiac surgery have a significant
total body inflammatory response.
The lungs are significantly affected by the
inflammatory response due to capillary leaking
of lung water into the alveolus.
The water between the capillaries in the alveolus
not only inhibit expansion of alveolus, but
also act as barriers between the surface of
the alveolus and capillary bed.
Therefore, carbon dioxide is retained and
oxygen saturation of the red blood cell is
diminished.
Other examples of conditions that block the
pathway between the alveolus and red blood
cell include pneumothoraces, pleural effusions,
obstructive pulmonary disease, atelectasis,
and pneumonia.
So let us review the normal ranges for each
component of the blood gas.
Take note of the differences in values between
blood that is obtained from an arterial circuit
versus a venous circuit.
In general, the arterial blood will yield
a difference of .05 greater than the venous
blood.
The arterial blood will yield a pCO2 that
is 10 millimeters of mercury less than the
venous blood.
The lower-oxygen content in venous blood is
dependent upon the rate of oxygen consumption
delivery in absorption as it circulates through
the body and back to the lungs to be resaturated.
Bicarbonate levels in arterial and venous
blood will yield the same result.
Understanding these normal ranges will allow
the clinician to diagnose one of the four
acid-base balance conditions.
Physiologic Acid-Base Imbalances.
The four abnormal conditions diagnosed as
physiologic acid-base imbalances are respiratory
alkalosis and acidosis, and metabolic acidosis
and alkalosis.
The first condition we will discuss is respiratory
acidosis.
Respiratory acidosis is condition that results
from an excess of carbon dioxide due to impaired
elimination by the lungs, producing a decreased
pH.
So for respiratory acidosis, the pH will be
low, less than 7.35.
And the CO2 will be elevated, greater than
45, with a normal to low-normal bicarbonate
level.
Listed are some of the most common conditions
that cause respiratory acidosis.
CNS depression associated with the disruption
and centrally mediated respiratory control
centers in the brain caused by head injury,
narcotics, sedatives, or anesthesia will cause
hypoventilation, or shallow breathing.
Pharmacologic agents such as neuromuscular
blockades, upper spinal cord injury, and neuromuscular
disease will disrupt the muscles needed to
produce diaphragmatic rise and fall.
Pulmonary issues that produce a limitation
of diffusion of carbon dioxide out of the
blood cell to be excelled will cause respiratory
acidosis.
A pulmonary embolism event is another condition.
Lower airway obstructions, such as bronchial
obstruction from asthma, or upper airway obstruction,
such as obstructed endotracheal tube, choking,
or stridor, chest wall injury or deformity,
and finally, pain.
That is a bit more abstract.
However, consider a teenager after a sternotomy
for heart surgery.
Post-operatively, he or she may breathe shallowly,
hypoventilate, refuse to cough or ambulate
because it is painful to engage in those very
important activities.
The compensatory response to respiratory acidosis
is immediate if the patient is able to control
her own ventilation.
Mediated by central respiratory centers in
the brain, our lungs will increase the depth
in which we breathe or the rate in which we
breathe to eliminate CO2.
However, when central respiratory centers
in the brain are suppressed, we as clinicians
act as the brain, per se, by adjusting mechanical
ventilation rate and pressures to eliminate
CO2.
Patients with less acute or chronic CO2 retention
will begin to show signs of bicarbonate buffering
in order to normalize blood pH.
Cellular buffering will occur first, but is
not significant enough to influence pH.
Over three to five days, however, the kidneys
will begin to excrete carbonic acid and increase
bicarbonate reabsorption.
That process will yield enough bicarbonate
to significantly influence blood pH over time.
The most classic and common example of chronic
and fully compensated carbon dioxide retention
is the adult with chronic obstructive pulmonary
disease, or former premature babies with bronchopulmonary
dysplasia.
These patients will have a normal blood pH,
CO2 levels in the 50s to 80s with a bicarbonate
level in the 30s to 50s.
The signs and symptoms of respiratory acidosis
include the following: From a pulmonary standpoint,
a person will experience shortness of breath,
respiratory distress, or shallow respirations.
Neurological signs include headache, lethargy,
confusion, restlessness, blurred vision, tremors,
delirium, or even coma.
Cardiovascular effects include tachycardia,
cardiac arrhythmias, hypertension, or pulmonary
hypertension.
You may note the signs and symptoms for each
of the following abnormal acid-base conditions
are similar.
As mentioned in the introduction to this presentation,
our body's normal and basic functions in cellular
metabolism is very sensitive to acid-base
imbalance.
If blood pH is abnormal in one direction or
the other, the normal body system processes
will begin to fail.
And that failure will manifest into these
abnormal signs and symptoms.
Medical and nursing intervention will be targeted
to increase carbon dioxide elimination.
Patients on mechanical ventilation support
will need to have either or both increased
frequency or ventilated breaths, and added
inhale or exhale pressures to each ventilated
breath.
Pharmacologic interventions include using
drugs that will help eradicate diffusion limitation
within the lungs, increased passage of air
to the lungs, or in the case of the patient
who is apprehensive to take in deep breaths
due to pain, pain medication will help.
Surgical interventions, such as chest tube
placement for a pneumothorax, hemothorax,
or pleural effusion might be necessary.
Participating in or having the patient participate
in activities to strengthen respiratory muscle
function, expand alveolus, and clear secretions
are important.
Advanced life support courses teach the mnemonic
D-O-P-E, or DOPE.
This is a clever mnemonic to help a clinician
quickly troubleshoot a condition in which
ventilation is not adequate in a patient on
mechanical ventilation support.
Is the tube displaced?
Is it too high, or is it too far, or positioned
in the carina or in the right mainstem bronchus?
Is there an obstruction due to secretions
or mucus plug?
Is there a tension pneumothorax?
Is the equipment used to ventilate the patient
functioning appropriately?
The next condition is respiratory alkalosis,
which is functionally the opposite of respiratory
acidosis.
There is an increase in pH due to excessive
CO2 loss from an increased respiratory rate.
Conditions that cause respiratory alkalosis
include psychological responses, central nervous
system impediments, increased metabolic demands,
exposure to elevation, pain, or excessive
mechanical ventilation.
These are some of the neurological, cardiovascular,
and miscellaneous signs and symptoms associated
with respiratory alkalosis.
The compensatory response to respiratory alkalosis
is, for the most part, centrally mediated
by our brain stem, which will cause us to
decrease the depth and rate in which we breathe
in response it elevated CO2.
As with respiratory acidosis, the renal response
is much slower.
For a patient who is mechanically ventilated,
we would decrease the pressure in an effort
to decrease tidal volume, and/or we would
decrease the set rate, or consider extubation.
For a patient with acute anxiety, we may give
anti-anxiety medications such as midazolam
or diazepam.
Otherwise, our aim would be to treat the underlying
cause.
People who have anxiety attacks feel as though
they are going to faint or are lightheaded
because they are unable to control their breathing.
So they breathe into a paper bag, and rebreathe
the CO2 within the paper bag to bring its
levels back to normal.
Now we discuss the two metabolic conditions.
The first condition is metabolic acidosis.
Metabolic acidosis is defined by a primary
deficit in bicarbonate ion concentration,
or primary gain of strong acid.
As a result, the pH drops, and the bicarbonate
level is low as well.
Calculating the anion gap can help the practitioner
differentiate the type of metabolic acidosis
that is present.
Metabolic acidosis can be categorized as having
a normal anion gap or a high anion gap.
Listed are some of the conditions that generally
lead to metabolic acidosis.
Increasing anion gap metabolic acidosis occurs
due to the primary gain of a strong acid,
whereas normal anion gap acidosis occurs when
there is a primary loss or deficit of bicarbonate.
The signs and symptoms of metabolic acidosis
become more life threatening when the severity
of acidosis becomes greater.
The most classic type of metabolic acidosis
occurs during a myocardial ischemic attack.
The final condition we will discuss is metabolic
alkalosis.
In metabolic alkalosis, there is a primary
gain of bicarbonate or loss of acid or hydrogen
ions resulting in an elevated pH.
Listed are the most common conditions that
cause metabolic alkalosis.
The loss of hydrogen ions occur through two
mechanisms.
Loss of acid through vomiting, or gain of
bicarbonate common with diuretic use.
Patients who require aggressive diuretic therapy
tend to become hypokalemic or hyponatremic
when we get into a continuous cycle of alternating
supplemental potassium or sodium with diuretics.
The medical and nursing interventions include
treating the underlying cause, using drugs
that will increase the acidity of the blood,
using drugs that will limit acid loss, altering
diuretic therapy, or providing anti-emetics.
Diagnosis.
So when diagnosing the blood gas, the first
part of the diagnosing of a blood gas is looking
at the pH.
Is it normal?
Is it as acidotic?
Or is it alkalotic?
The next component of diagnosing the arterial
blood gas is looking at the pCO2.
Is it higher than 45, which means it's acidotic?
Or is it lower than 35, making it alkalotic?
Finally, it is time to diagnose the metabolic
portion of the arterial blood gas-- the tCO2.
Is it high, causing alkalosis?
Or is it low, causing acidosis?
Case Studies.
So now we'll head into our case studies.
This is case study number 1.
A four-month-old boy with Down Syndrome returned
from the operating room after repair of a
complete AV canal.
He has been in the ICU for three hours since.
Below is some data.
From a cardiovascular standpoint, his heart
rate is 180.
His blood pressure is 52 over 28.
His central venous pressure is 4.
The patient is cool and mottled.
The capillary refill time is 4 seconds.
Bleeding has been moderate since arrival from
the OR, approximately 2 milliliters per kilogram
per hour.
The hematocrit on arrival was 35.
Dopamine is at 3 micrograms per kilogram per
minute.
The urine output has declined.
From a respiratory standpoint, the patient
is on pressure control ventilation.
The PIP, or the Peak Inspiratory Pressure,
is 25.
The PEEP, or positive end-expiratory pressure,
is 4.
The rate is 16.
And the FiO2 to is set at 40%.
Breath sounds are slightly course.
But overall the patient has good aeration.
The O2 sat is 100%.
And the end-tidal CO2 is 30.
The patient is well sedated on a morphine
drip.
The pupils are pinpoint.
The fontanels are soft.
And there's no spontaneous respirations noted.
From the GI prospective, patient has a nasogastric
tube to low wall suction and has no bowel
sounds.
And the arterial blood gas reads as following:
The pH is 7.21.
The PCO2 is 38.
The TCO2 is 14.
The PO2 is 85.
And the oxygen saturations are 100%.
What is your interpretation of this arterial
blood gas?
Is it a metabolic acidosis?
Metabolic alkalosis?
Respiratory acidosis?
Or respiratory alkalosis?
And number two, based on the case study, list
at least three interventions you might anticipate
in response to the arterial blood gas.
The answer to case study number 1 would be
metabolic acidosis.
The possible treatments would be one, the
low cardiac central venous pressure, low blood
pressure, and tachycardia may be indicative
of hypovolemia.
Fluid replacement would be appropriate.
If the hematocrit is low due to ongoing bleeding,
red blood cells would be the best fluid replacement
option.
Number two, a sodium bicarbonate replacement
of 1 to 2 milliequivalents per kilogram would
address the bicarbonate deficiency.
And three, increase in the dopamine may improve
contractility of the heart, thus improving
cardiac output.
Case study number 2.
A four-month-old girl arrived to this ICU
after a Tetralogy of Fallot repair.
She just arrived from the operating room.
Below are the following statistics.
From a cardiovascular standpoint, her heart
rate is 140.
Her blood pressure is 65 over 35.
Her central venous pressure is 9.
The patient is cool.
The capillary refill time is 3 seconds.
The patient has minimal bleeding.
She's on an epinephrine drip, 0.025 micrograms
per kilogram per minute and a milrinone drip
at 0.25 micrograms per kilogram per minute.
From a respiratory standpoint, she's on pressure
control ventilation.
The PIP is set at 25 and the PEEP at 5.
The rate is 16.
The patient has measured tidal volumes of
13 millimeters per kilogram.
The oxygen saturation is 100% on 0.40 FiO2.
And the breath sounds are clear.
The patient received 20 micrograms of fentanyl
and a muscle relaxant from the anesthesiologist
upon arrival to the ICU.
The pupils are pinpoint.
You're ordered to begin a low dose fentanyl
drip.
From a gastrointestinal standpoint, the patient
has a nasogastric tube to low wall suction.
The abdomen is slightly distended, but soft.
So the arterial blood gas reads as following.
The pH is 7.54.
The PCO2 is 30.
The TCO2 is 22.
The PO2 is 101.
And the oxygen saturation is 100%.
So what is your interpretation of this arterial
blood gas?
Metabolic acidosis?
Metabolic alkalosis?
Respiratory acidosis?
Or respiratory alkalosis?
And two, based on the case study, name at
least three interventions you might anticipate
in response to the arterial blood gas.
The answer to case study number 2 is respiratory
alkalosis.
These are the possible treatments: One, decrease
the ventilator rate to help retain carbon
dioxide.
Or two, decrease the peak inspiratory pressure,
which will reduce the tidal volume to help
retain carbon dioxide.
Or three, consider making a plan to wake the
patient up and wean towards extubation.
Now it's time for case study number 3.
A 10-year-old male with cardiomyopathy suffered
a ventricular fibrillation arrest en route
to the cardiac ICU from the emergency room.
The ICU team provided cardiopulmonary support
for 22 minutes before a perfusing rhythm with
a palpable pulse returned.
He was immediately intubated.
An arterial line and central venous line were
placed.
A blood gas was sent to the lab shortly after.
The patient had the following assessment.
From a cardiovascular standpoint, the heart
rate was 122 with a first degree AV block.
The blood pressure is 125 over 56.
The central venous pressure is 14.
The patient is cool to touch.
The pulses are palpable, but faint distally.
His urine output is adequate.
He's on a dopamine drip with 5 micrograms
per kilogram per minute, and epinephrine at
0.1 micrograms per kilogram per minute.
From a respiratory standpoint, the patient
is on volume control ventilation at a rate
of 14 with a set tidal volume of 8 millimeters
per kilogram.
The O2 sat is 94% on 0.60 FiO2.
Breath sounds have fine crackles, diminished
on the left.
The patient has an audible air leak.
From a neurological standpoint, the patient
is unresponsive to noxious stimulation.
The pupils are equal and reactive to light
stimulation.
The team has decided to initiate hypothermia
for a post-cardiac arrest neurological protection.
The arterial blood gas reads the following:
The pH is 7.27.
The PCO2 is 56.
The TCO2 is 26.
The PO2 is 76.
And the O2 saturation is 95%.
So what is your interpretation of this arterial
blood gas?
Metabolic acidosis?
Metabolic alkalosis?
Respiratory acidosis?
Or respiratory alkalosis?
Based on the case study, name at least three
interventions you might anticipate in response
to this arterial blood gas.
The answer to case study number 3 would be
respiratory acidosis.
And the possible treatments would be, one,
increase the ventilator rate to help eliminate
carbon dioxide.
Or two, increase the set tidal volume to help
eliminate carbon dioxide.
Or three, consider diuretics or afterload
reduction if the patient has pulmonary edema
due to congestive heart failure because of
cardiomyopathy.
Now for the final case study, case study number
4.
A three-week-old female who was born at 35
weeks gestation is preparing to extubate after
recovering from a PDA ligation and pyloric
stenosis repair.
She had a prolonged intubation due to pulmonary
edema, but has responded well to diuretic
therapy.
Her assessment is as follows.
From a cardiovascular standpoint, her heart
rate is 155.
Her blood pressure is 59 over 36.
She is warm and well profused.
From a pulmonary standpoint, she's on straight
pressure support ventilation.
She has an oxygen saturation that is 95% on
0.3 FiO2.
The morning chest x-ray was clear.
Her breath sounds are clear.
Respiratory effort, shallow at times.
From a neurological standpoint, she opens
her eyes.
She looks around.
She'll respond appropriately to stimulation.
She usually sleeps for about 2 and 1/2 to
3 hours between bolus nasogastric feeds.
From a gastrointestinal standpoint, she's
been NPO for the past six hours for possible
extubation.
Intravenous fluids are running.
And glucose levels have been stable.
The team asked to have an arterial blood gas
sent to see how her gas exchange was on straight
pressure support ventilation.
She has an arterial blood gas pH of 7.54.
Her PCO2 is 45.
And her TCO2 is 34.
What is your interpretation of this arterial
blood gas?
Is it a metabolic acidosis?
Metabolic alkalosis?
Respiratory acidosis?
Or respiratory alkalosis?
And number two, based on the case study, list
at least three interventions you might anticipate
in response to the arterial blood gas.
The answer to case study number 4 is metabolic
alkalosis.
The possible treatments would be, one, consider
reducing diuretic therapy.
Two, consider checking the whole blood potassium
and replace it if it is low.
Three, consider ammonium chloride or Diamox.
So thank you for joining me and learning about
arterial blood gas analysis.
Have a great day.
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