Transcript ABG
Arterial
Blood Gas interpretation is an easy
skill to master. It simply requires an
understanding of pH, the respiratory
component (pCO2), a metabolic component
(HCO3 and/or Base Excess), what they
represent, and what the normal ranges are.
In chemistry class we learned that pH describes the
concentration of hydrogen ions, and that a pH of 7.0
is perfectly neutral
The acceptable pH range of our blood is 7.35 – 7.45,
which is slightly alkaline
The body needs to maintain the pH of its chemical
broth within fairly narrow limits for proper body
functioning
The body’s own regulatory mechanisms usually
maintain this balance, but certain disease processes,
illnesses, and treatments can cause imbalances that
may become life threatening unless appropriate
interventions are implemented
A pH that is less than 7.0 or greater than 7.7 is not
compatible with life
The body has several buffer systems that work to
maintain the pH within acceptable limits
Of these, the bicarbonate-carbonic acid buffer
system is the most important, and is controlled by
the lungs and kidneys
Normal (aerobic) metabolism produces two forms of
acid
respiratory acid (carbonic acid)
metabolic acids
In order to maintain proper pH balance, the body
attempts to maintain a ratio of 20:1 (bicarbonate to
carbonic acid.) A wide variety of pulmonary and
metabolic problems can create an imbalance, so it is
necessary to look carefully at the respiratory and
metabolic components of ABG interpretation
Carbon dioxide is an end product of metabolism,
and when dissolved in blood becomes carbonic
acid
Carbonic acid is termed a volatile acid because
it dissociates into water and a gas, CO2 which is
exhaled by the lungs
The pCO2 or PaCO2 represents the partial
pressure of carbon dioxide dissolved in arterial
blood, and provides an important measure of the
adequacy of a patient’s ventilation
The lungs normally maintain an acceptable
balance of CO2 in the bloodstream
The normal range for this respiratory component
of ABG’s, the pCO2, is 35 – 45 mmHg, and is
maintained by ventilation
PO2
is the partial pressure of oxygen and
determines the amount of oxygen available
to bind with hemoglobin.
The pH affects the combining power of
oxygen in hemoglobin and with a low pH,
there is less O2 to bind to hemoglobin.
PO2 is decreased in emphysema, pneumonia,
pulmonary edema.
C02 retainers
When the patient is moving a normal volume of
air in and out of the lungs, the pCO2 will stay
within the normal range
Hypoventilation will prevent sufficient removal
of CO2 from the bloodstream, causing a
respiratory acidosis
Some causes of respiratory acidosis include
obstructive lung disease, restrictive lung disease
and hypoventilation as a result of oversedation,
anesthesia or improper ventilator settings (e.g.,
tidal volume too low.) Respiratory acidosis could
also result from a drug overdose and
neuromuscular diseases such as Guillain-Barre
syndrome or myasthenia gravis
Hyperventilation,
on the other hand, causes
CO2 to be “blown off” or removed, causing a
respiratory alkalosis
The pCO2 falls below 35, and the acid-load
decreases, causing an alkalosis
Some possible causes of respiratory alkalosis
include pain, panic attacks, anxiety,
pulmonary embolism, pregnancy, and a tidal
volume that is too high for a ventilator
patient
Notice
that a high value in pCO2 actually
represents an acidosis (retention of CO2),
whereas a high value in pH represents an
alkalosis
Do not try to memorize, but rather to
understand the concept of what the
components represent
A high level of pCO2 simply means there is
retention of CO2 or hypoventilation
CO2 is acidotic in the blood, and too much
causes respiratory acidosis.
HCO3 represents the metabolic component of ABG
interpretation, with a normal range of 22-26 mEq/L
Bicarbonate (HCO3) is a weak base that is regulated
by the kidneys
When there is a loss of acid in the body, or an excess
of base, the HCO3 will be greater than 26, resulting
in metabolic alkalosis
Some causes of metabolic alkalosis include loss of
stomach acid and potassium from vomiting or gastric
suction, and ingestion of large amounts of
bicarbonate. Prolonged therapy with potassiumwasting diuretics, steroid therapy, Cushing's disease,
and aldosteronism can also deplete potassium,
chloride, and hydrogen levels, resulting in metabolic
alkalosis
When there is an excess of metabolic acid, or not
enough base, the HCO3 will be less than 22, causing
metabolic acidosis
Conditions that increase acid-load include diabetic
ketoacidosis or prolonged fasting, lactic acidosis, and
renal failure. Actual loss of bicarbonate ions through
severe diarrhea leads to metabolic acidosis. During
cardiac arrest, or when low cardiac output states (as
in external cardiac compression) are present,
anaerobic metabolism occurs and there is an increase
in the production of lactic acid. Metabolism of lactic
acid is normally effected through the Krebs cycle,
and oxygen is the essential element for this
metabolic process. In the absence of adequate tissue
oxygenation, lactic acid cannot be metabolized; its
quantity increases and the result is metabolic
acidosis.
pH 7.35 – 7.45
pCO2 35-45mmHg
HCO3- 22-26mEq/L
pO2 75 – 100mmHg
How do we treat these problems?
Treat your patient, not the lab values.
Mrs. Puffer is a 35-year-old single mother, just getting off the night shift.
She reports to the ED in the early morning with shortness of breath. She
has cyanosis of the lips. She has had a productive cough for 2 weeks. Her
temperature is 38.5, blood pressure 110/76, heart rate 108, respirations
32, rapid and shallow. Breath sounds are diminished in both bases, with
coarse rhonchi in the upper lobes. Chest X-ray indicates bilateral
pneumonia.
ABG results are:
Problems:
pH= 7.44
PaCO2= 28
HCO3= 24
PaO2= 54
PaCO2 is low
pH is on the high side of normal, therefore compensated respiratory alkalosis.
Also, PaO2 is low, probably due to mucous displacing air in the alveoli affected
by the pneumonia
Solutions:
The alkalosis need not be treated directly. Mrs. Puffer is hyperventilating to
increase oxygenation, which is incidentally blowing off CO2. Improve PaO2 and a
normal respiratory rate should normalize the pH. (get her to deep breath and
cough – assist in her comfort, apply O2 if needed)
Mr. Worried is a 52-year-old widow. He is retired and living alone. He enters the ED
complaining of shortness of breath and tingling in fingers. His breathing is shallow
and rapid. He denies diabetes; blood sugar is normal. There are no EKG changes. He
has no significant respiratory or cardiac history. He takes several antianxiety
medications. He says he has had anxiety attacks before. While being worked up for
chest pain an ABG is done:
ABG results are:
pH= 7.48
PaCO2= 28
HCO3= 22
PaO2= 85
Problem:
pH is high,
PaCO2 is low
respiratory alkalosis
Solution:
If he is hyperventilating from an anxiety attack, the simplest solution is to have him
breathe into a paper bag. He will rebreathe some exhaled CO2.This will increase PaCO2
and trigger his normal respiratory drive to take over breathing control.
* Please note this will not work on a person with chronic CO2 retention, such as a
COPD patient. These people develop a hypoxic drive, and do not respond to CO2
changes.
Carbon
dioxide levels are chronically
elevated (like in the patient with COPD)
The respiratory center becomes less sensitive
to CO2 as a stimulant of the respiratory drive
Therefore the PaO2 provides the primary
stimulus for respirations
Administering excess supplemental oxygen
can potentially suppress the respiratory
center
However, it is unclear whether such a
hypoxic drive exists in the first place
pH:
7.46
PaCO2: 43 mmHg
[HCO3-]: 27 mEq/L
PaO2: 80 mmHg
Met
alk
pH:
7.34
PaCO2: 43 mmHg
[HCO3-]: 20 mEq/L
PaO2: 80 mmHg
met
acid
pH:
7.38
PaCO2: 40 mmHg
[HCO3-]: 25 mEq/L
PaO2: 80 mmHg
Everything
is fine
pH:
7.28
PaCO2: 48 mmHg
[HCO3-]: 22 mEq/L
PaO2: 86 mmHg
Resp
acid
pH:
7.50
PaCO2: 38 mmHg
[HCO3-]: 18 mEq/L
PaO2: 86 mmHg
Met
alk
pH:
7.46
PaCO2: 50 mmHg
[HCO3-]: 26 mEq/L
PaO2: 86 mmHg
Resp
alk
pH:
7.32
PaCO2: 49 mmHg
[HCO3-]: 30 mEq/L
PaO2: 90 mmHg
Met
acidosis with respiratory compensation
(respiratory system is compensating by
adding some alkalitity)
pH:
7.52
PaCO2: 50 mmHg
[HCO3-]: 28 mEq/L
PaO2: 90 mmHg
Met
alk with respiratory compensation
(adding some acid)
pH:
7.33
PaCO2: 50 mmHg
[HCO3-]: 28 mEq/L
PaO2: 92 mmHg
Resp
acidosis with metabolic compensation