The document provides an overview of arterial blood gas analysis and interpretation. It discusses:
- The respiratory and metabolic systems work together to maintain blood pH. The respiratory system prioritizes pH over oxygen levels.
- For minor oxygen fluctuations, ventilation is driven by carbon dioxide to retain pH within normal ranges, even at the expense of oxygen. Only severe hypoxia triggers an increase in ventilation.
- The respiratory system responds quickly to changes, within seconds to minutes, while the metabolic system responds more slowly over hours to days.
- A step-by-step method is provided to interpret ABG results by examining pH, carbon dioxide, bicarbonate/base excess, and oxygen levels.
2. INTRODUCTION
ABGs explain about the activity of two systems; the respiratory
system and the ‘metabolic’ system. If one system is disturbed,
the other tries to restore balance. Both systems are primarily
concerned with keeping blood pH in the normal range. Even for
the respiratory system, pH (rather than oxygen) is the priority.
3. THE RESPIRATORY SYSTEM –
OXYGENATION VS PH
For our next breath we are driven by the PaCO2, which is
intimately linked to pH. The hypoxic centre in the brain stem
that monitors PaO2 actually does not respond to minor
fluctuations in the level of oxygenation. This is because
individuals generally live at a level of oxygenation well above
that which is required to sustain life. This ‘margin of oxygen
4. For example, in a metabolic alkalosis, ventilation would fall (at
the expense of a small reduction in oxygenation) to retain CO2
and, thus, return pH to the normal range.
Only when hypoxia is more severe (approximately PaO2 <8 kPa)
does the hypoxic centre ‘wake up’ and take note. Only then, will
it drive ventilation to prevent harmful levels of hypoxia.
5. RESPIRATORY AND METABOLIC
SYSTEMS – THE SPEED
OF RESPONSE
The respiratory system can respond quickly to a metabolic
derangement, with changes occurring to the blood gases within
seconds to minutes. However, the metabolic system (largely
regulated by the kidneys excreting or retaining acid or
bicarbonate) is much slower and changes can take hours to
days.
6. STEP-BY-STEP METHOD FOR
INTERPRETING ARTERIAL
BLOOD GASES
Look at the pH- ‘acidosis’ or ‘alkalosis’!
If within normal range, note whether it is sitting towards the
‘acidotic’ or ‘alkalotic’ end of that range.
Next look at the PaCO2- Identify whether PaCO2 is contributing
to, or attempting to compensate for, the problem.
After that look at the 'base picture’
Finally, look at the oxygen.
7. BASE PICTURE
Base excess (BE) defined as the amount of acid require to
restore a litre of blood to its normal pH at a PaCO2 of 40
mmHg. It increases in metabolic alkalosis and decreases in
metabolic acidosis.
Base deficit/ Negative base excess indicates an excess of acid.
It refers to the amount of base needed to titrate a serum pH
8. Bicarbonate is the greater part of the base buffer, for
most practical interpretations, BE provides essentially
the same information as bicarbonate.
A range around −3 to +3 is normal. In simple terms, a
high BE excess is the same as a high HCO3.
9. If the pH and PaCO2 led to the conclusion that the problem was primarily metabolic,
then sHCO3 (or BE) will do little more than confirm that; sHCO3 being high in an
alkalosis, low in an acidosis.
In case of respiratory problem, BE can tell us something of the duration of the problem.
If, for example, in a respiratory acidosis, the if sHCO3 within the normal range, the
probable explanation is that there has not yet been time to respond (ie the problem is
an acute respiratory acidosis).
In a respiratory ‘acidosis’ (perhaps with the pH in the lower half of the normal range), a
high sHCO3 would indicate a longer time course (i.e the problem is a chronic
respiratory acidosis).
10. OXYGEN LEVEL
When the only derangement is PaO2, clearly the respiratory
failure is type 1.
When PaO2 is low yet PaCO2 normal, type 1 respiratory failure
is present, and such a result implies lung (or pulmonary
vascular) disease.
11. Type 2 respiratory failure is extremely an issue of ventilation, that is, the
business of pumping air in and out of the lungs. When underventilation
occurs, for what ever reason (e.g muscular weakness or opiate overdose),
the PaCO2 will increase and PaO2 must decrease (even if the lungs are
perfectly healthy).
Type 1 and type 2 respiratory failure can occur simultaneously. Indeed, the
combination is common in severe chronic obstructive pulmonary disease.
12. One needs to measure the alveolar–arterial gradient, that is, the difference between the
alveolar partial pressure of oxygen (PAO2) and the PaO2. The PaO2 is measured in the ABG,
the PAO2 has to be calculated using the alveolar gas equation:
PAO2 = PIO2 − PaCO2 / 0.8
where PIO2 is the partial pressure of oxygen in the inspired air (approximately 21 kPa when
breathing room air, but 24 kPa when using a 24% Venturi mask and so on) and 0.8 is the
‘respiratory quotient’ (ie the ratio between the CO2 produced and the O2 utilized).
The alveolar–arterial gradient (PAO2–PaO2) can then be calculated.
In healthy young adults, the difference should be less than 2 kPa. If the patient is older,
breathing higher concentrations of O2 or over ventilating, then the gap can widen, although
in healthy patients this would not usually be expected to be greater than 4 kPa.
If the alveolar–arterial gradient is higher than it should be, then a type 1 respiratory failure
is present. This implies a problem with V/Q matching (i.e a problem with either the lungs or
the pulmonary vasculature).
13.
14. PROBLEM TO SOLVE
A 32-year-old woman presented
with a 3-hour history of
breathlessness. On examination,
she appeared distressed and
tachypnea. ABGs breathing air:
pH: 7.55
PaC02: 2.6 mm Hg
Standard HC03: 22
Actual HC03: 16.5
Base excess: –2
Pa02: 11.7
INTERPRETATION
pH = ‘alkalosis’
PCO2 contributing → respiratory
alkalosis
sHCO3 normal → acute
respiratory alkalosis
A–a gradient = 6.1 (high) → there
is a problem with the lungs or
pulmonary vasculature.
Therefore, this is not anxiety-
related hyperventilation. The
result is consistent with
pulmonary embolism or acute
severe asthma.
18. ANION GAP
The anion gap is the difference between measured cations (positively
charged ions like Na+ and K+) and measured anions (negatively charged
ions like Cl- and HCO3-).
The most common application of the anion gap is classifying cases of
metabolic acidosis, states of lower than normal blood pH.
The human body is electrically neutral; therefore, in reality, does not have a
true anion gap.
19. Calculation relies on measuring specific cations, Na+ and K+ and specific anions, Cl-
and HCO3-. The equation is as follows:
(Na+ + K+) – (Cl- + HCO3-) = Anion Gap.
The anion gap formula can be manipulated to expose the presence of unmeasured
cations and anions as shown below.
([Na+] + [K+] + [UC]) = ([Cl-] + [HCO3-] + [UA])
Rearrangement shows:
([Na+] +[K+]) – ([Cl-] + [HCO3-]) = [UA] – [UC]
Anion Gap = UA – UC
If there is anion gap, calculate delta gap to determine additional metabolic disorders.
If there is anion gap start analysis for non anion acidosis.
20. When acid is added to blood, H+ increases and HC03- decreases.
The concentration of anion which is associated with acid, also
increases. The change in anion concentration provides a convenient
way to analyse and help to determine the cause of metabolic acidosis
by calculating anion gap.
The value is equal to12±4 mEql/Lt and is usually due to negatively
charged plasma proteins as the charges of other unmeasured cations
and anions tend to balance out.
21.
22. If the anion of the acid added to plasma is Cl-, the anion gap will be
normal (decrease in HCO3- is matched by increase in Cl-.)
HCl+NaHCO3- NaCl+H2CO3 CO2+H2O
The condition will be known as hyperchloremic metabolic acidosis, as
Cl- is added.
Renal loss of HCO3-, is having same affect of adding HCl, as the
kidney has tendency to preserve ECV which will retain NaCl, leading
to net exchange of loss of HCO3- for Cl-.
If the anion of acid is not Cl-, (the anion gap will increase by decrease
HCO3- and Cl-), it may because of unmeasured anions.
