ABG Interpretation

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Paula Zaininger June 12, 2016

Arterial blood gas (ABG) interpretation is something that can be difficult to grasp
initially (we’ve been there). We’ve created this guide, which aims to provide a structured
approach to ABG interpretation whilst also increasing your understanding of each
result’s relevance. The real value of an ABG comes from its ability to provide a near-
immediate reflection of the physiology of your patient, allowing you to recognise and
treat pathology more rapidly.

You may also be interested in our guide to performing an ABG or our ABG quiz.

Normal ranges
pH: 7.35 – 7.45
PaCO2 : 4.7 – 6.0 kPa || 35.2 – 45 mmHg
PaO2 : 11 – 13 kPa || 82.5 – 97.5 mmHg
HCO3–: 22 – 26 mEq/L
Base excess (BE): -2 to +2 mmol/L

Patient’s clinical condition

Before getting stuck into the details of the analysis, it’s important to look at the patient’s
current clinical status, as this provides essential context to the ABG result. Below are a
few examples to demonstrate how important context is when interpreting an ABG:

A ‘normal’ PaO2 in a patient on high flow oxygen: this is abnormal as you

would expect the patient to have a PaO 2 well above the normal range with this
level of oxygen therapy.

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 A ‘normal’ PaCO2 in a hypoxic asthmatic patient: a sign they are tiring and
need ITU intervention.
A ‘very low’ PaO2 in a patient who looks completely well, is not short of
breath and has normal O2 saturations: this is likely a venous sample.

Oxygenation (PaO 2)
Your first question when looking at the ABG should be “Is this patient hypoxic?” as
hypoxia is the most immediate threat to life.

PaO2 should be >10 kPa when oxygenating on room air in a healthy patient.

If the patient is receiving oxygen therapy their PaO2 should be approximately 10kPa
less than the % inspired concentration FiO2 (so a patient on 40% oxygen would
be expected to have a PaO2 of approximately 30kPa).

Oxygen delivery devices and flow rates

A common question is “What percentage of oxygen does this device deliver at a given
flow rate?”. Below is a quick reference guide, providing some approximate values for the
various oxygen delivery devices and flow rates you’ll come across in practice.2

Nasal cannulae

As with all oxygen delivery devices, there is a significant amount of variability

depending on the patient’s breathing rate, depth and how well the oxygen delivery
device is fitted. Below are some guides to various oxygen flow rates and the
approximate percentage of oxygen delivered: 4

1L / min – 24%
2L/ min – 28%
3L/ min – 32%
4L / min – 36%

Simple face mask

The oxygen delivery of simple face masks is highly variable depending upon oxygen flow
rate, the quality of the mask fit, the patient’s respiratory rate and their tidal volume.
Simple face masks can deliver a maximum FiO2 of approximately 40%-60% at a flow
rate of 15L/min. These masks should not be used with flow rates less than 5L/min.³

Reservoir mask (also known as a non-rebreather mask)

Reservoir masks deliver oxygen at concentrations between 60% and 90% when used at
a flow rate of 10–15 l/min.³ The concentration is not accurate and will depend on the
flow of oxygen as well as the patient’s breathing pattern. These masks are most suitable
for trauma and emergency use where carbon dioxide retention is unlikely.
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Venturi masks

A Venturi mask will give an accurate concentration of oxygen to the patient regardless
of the oxygen flow rate (the minimum suggested flow rate is written on each). Venturi
masks are available in the following concentrations: 24%, 28%, 35%, 40% and 60%.
They are suitable for all patients needing a known concentration of oxygen, but 24%
and 28% Venturi masks are particularly suited to those at risk of carbon dioxide
retention (e.g. patients with chronic obstructive pulmonary disease).³

Hypoxaemia
If PaO2 is <10 kPa on air, a patient is considered hypoxaemic.

If PaO2 is <8 kPa on air, a patient is considered severely hypoxaemic and in respiratory
failure.

Type 1 vs type 2 respiratory failure

Type 1 respiratory failure involves hypoxaemia (PaO 2 <8 kPa) with
normocapnia (PaCO2 <6.0 kPa).

Type 2 respiratory failure involves hypoxaemia (PaO 2 <8 kPa) with

hypercapnia (PaCO2 >6.0 kPa).

Type 1 respiratory failure

Type 1 respiratory failure involves hypoxaemia (PaO 2 <8 kPa) with normocapnia
(PaCO2 <6.0 kPa).

It occurs as a result of ventilation/perfusion (V/Q) mismatch; the volume of air

flowing in and out of the lungs is not matched with the flow of blood to the lung tissue.
As a result of the VQ mismatch, PaO2 falls and PaCO 2 rises. The rise in PaCO 2 rapidly
triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2
but not the PaO2 due to the different shape of the CO 2 and O 2 dissociation curves. The
end result is hypoxaemia (PaO2 < 8 kPa) with normocapnia (PaCO2 < 6.0 kPa).¹

Examples of VQ mismatch include:

Reduced ventilation and normal perfusion (e.g. pulmonary oedema,

bronchoconstriction)
Reduced perfusion with normal ventilation (e.g. pulmonary embolism)

Type 2 respiratory failure

Type 2 respiratory failure involves hypoxaemia (PaO 2 is <8 kPa) with hypercapnia
(PaCO2 >6.0 kPa). It occurs as a result of alveolar hypoventilation, which prevents
the patient from being able to adequately oxygenate and eliminate CO2 from their
blood.

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Hypoventilation can occur for a number of reasons including:

Increased resistance as a result of airway obstruction (e.g. COPD).

Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures,
obesity).
Reduced strength of the respiratory muscles (e.g. Guillain-Barré, motor neurone
disease).
Drugs acting on the respiratory centre reducing overall ventilation (e.g. opiates).

pH
Seemingly small abnormalities in pH have very significant and wide-spanning effects on
the physiology of the human body. Therefore, paying close attention to pH
abnormalities is essential.

So we need to ask ourselves, is the pH normal, acidotic or alkalotic?

Acidotic: pH <7.35
Normal: pH 7.35 – 7.45
Alkalotic: pH >7.45

We need to consider the driving force behind the change in pH. Broadly speaking the
causes can be either metabolic or respiratory. The changes in pH are caused by an
imbalance in the CO2 (respiratory) or HCO3– (metabolic). These work as buffers to keep
the pH within a set range and when there is an abnormality in either of these the pH
will be outside of the normal range.

As a result, when an ABG demonstrates alkalosis or acidosis you need to then begin
considering what is driving this abnormality by moving through the next few steps of
this guide.

PaCO2
At this point, prior to assessing the CO 2, you already know the pH and the PaO 2. So for
example, you may know your patient’s pH is abnormal but you don’t yet know the
underlying cause. It could be caused by the respiratory system (abnormal level of CO2)
or it could be metabolically driven (abnormal level of HCO3-).

Looking at the level of CO 2 quickly helps rule in or out the respiratory system as
the cause for the derangement in pH.

pH CO2 HCO 3–

Respiratory acidosis ↓ ↑ Normal

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 Respiratory alkalosis ↑ ↓ Normal

Respiratory acidosis with metabolic compensation ↓/ ↑ ↑

↔

Respiratory alkalosis with metabolic ↑/ ↓ ↓

compensation ↔

Underlying biochemistry
CO2 binds with H2O and forms carbonic acid (H 2CO3) which will decrease pH. When a
patient is retaining CO2 the blood will, therefore, become more acidic from the
increased concentration of carbonic acid. When a patient is ‘blowing off’ CO2 there is
less of it in the system and, as a result, the patient’s blood will become less acidotic and
more alkalotic.

Carbonic acid equation

The idea of ‘compensation’ is that the body can try and adjust other buffers to keep the
pH within the normal range. If the cause of the pH imbalance is from the respiratory
system, the body can adjust the HCO3– to counterbalance the pH abnormality bringing
it closer to the normal range. This works the other way around as well; if the cause of a
pH imbalance is metabolic, the respiratory system can try and compensate by either
retaining or blowing off CO2 to counterbalance the metabolic problem (via increasing or
decreasing alveolar ventilation).

So we need to ask ourselves:

1. Is the CO 2 normal or abnormal?

2. If abnormal, does this abnormality fit with the current pH (e.g. if the CO 2 is high,
it would make sense that the pH was low, suggesting this was more likely a
respiratory acidosis)?
3. If the abnormality in CO2 doesn’t make sense as the cause of the pH abnormality
(e.g. normal or ↓ CO 2 and ↓ pH), it would suggest that the underlying cause for
the pH abnormality is metabolic.

HCO3–
We now know the pH and whether the underlying problem is metabolic or respiratory
in nature from the CO2 level.

Piecing this information together with the HCO 3– we can complete the picture:

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 HCO3– is a base, which helps mop up acids (H+ ions).
So when HCO3– is raised the pH is increased as there are less free H+ ions
(alkalosis).
When HCO3– is low the pH is decreased as there are more free H+ ions (acidosis).

Carbonic acid equation

So we need to ask ourselves:

1. Is the HCO3– normal or abnormal?

2. If abnormal, does this abnormality fit with the current pH (e.g. ↓HCO3– and
acidosis)?
3. If the abnormality doesn’t make sense as the cause for the deranged pH, it
suggests the cause is more likely respiratory (which you should have already
known from your assessment of CO2).

pH HCO 3– CO2

Metabolic acidosis ↓ ↓ Normal

Metabolic alkalosis ↑ ↑ Normal

Metabolic acidosis with respiratory compensation ↓ ↓ ↓

Metabolic alkalosis with respiratory ↑ ↑ ↑

compensation

You may note that in each of these tables HCO3– and CO 2 are both included, as it is
important to look at each in the context of the other.

Base excess (BE)

The base excess is another surrogate marker of metabolic acidosis or alkalosis:

A high base excess (> +2mmol/L) indicates that there is a higher than normal
amount of HCO3– in the blood, which may be due to a primary metabolic
alkalosis or a compensated respiratory acidosis.
A low base excess (< -2mmol/L) indicates that there is a lower than normal
amount of HCO3– in the blood, suggesting either a primary metabolic acidosis or
a compensated respiratory alkalosis.

Compensation
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Compensation has been touched on already in the above sections, to clarify we have
made it simple below:

Respiratory acidosis/alkalosis (changes in CO 2) can be metabolically

compensated by increasing or decreasing the levels of HCO3– in an attempt to
move the pH closer to the normal range.
Metabolic acidosis/alkalosis (changes in HCO3-) can be compensated by the
respiratory system retaining or blowing off CO2 in an attempt to move the pH
closer to the normal range.

Rate of compensation
Respiratory compensation for a metabolic disorder can occur quickly by either
increasing or decreasing alveolar ventilation to blow off more CO2 (↑ pH) or retain
more CO2 (↓ pH).

Metabolic compensation for a respiratory disorder, however, takes at least a few

days to occur as it requires the kidneys to either reduce HCO 3– production (to decrease
pH) or increase HCO 3– production (to increase pH). As a result, if you see evidence of
metabolic compensation for a respiratory disorder (e.g. increased HCO3-/base excess in
a patient with COPD and CO 2 retention) you can assume that the respiratory
derangement has been ongoing for at least a few days, if not more.

It’s important to note that ‘over-compensation’ should never occur and, therefore, if you
see something that resembles this you should consider other pathologies driving the
change (e.g. a mixed acid/base disorder).

Mixed acidosis/alkalosis
It’s worth mentioning that it is possible to have a mixed acidosis or alkalosis (e.g.
respiratory and metabolic acidosis/respiratory and metabolic alkalosis).

In these circumstances, the CO 2 and HCO3– will be moving in opposite directions

(e.g. ↑ CO2 ↓ HCO3– in mixed respiratory and metabolic acidosis).

Treatment is directed towards correcting each primary acid-base disturbance.

You can see some causes of mixed acidosis and alkalosis below.

Causes of acid/base disturbances

So far we have discussed how to determine what the acid-base disturbance is, once we
have this established we need to consider the underlying pathology that is driving
this disturbance.

Respiratory acidosis
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Respiratory acidosis is caused by inadequate alveolar ventilation leading to CO 2
retention.

A respiratory acidosis would have the following characteristics on an ABG:

↓ pH
↑ CO2

Causes of respiratory acidosis include:

Respiratory depression (e.g. opiates)

Guillain-Barre: paralysis leads to an inability to adequately ventilate
Asthma
Chronic obstructive pulmonary disease (COPD)
Iatrogenic (incorrect mechanical ventilation settings)

Respiratory alkalosis
Respiratory alkalosis is caused by excessive alveolar ventilation (hyperventilation)
resulting in more CO2 than normal being exhaled. As a result, PaCO 2 is reduced and pH
increases causing alkalosis.

A respiratory alkalosis would have the following characteristics on an ABG:

↑ pH
↓ CO2

Causes of respiratory alkalosis include: ³

Anxiety (i.e. panic attack)

Pain: causing an increased respiratory rate.
Hypoxia: resulting in increased alveolar ventilation in an attempt to compensate.
Pulmonary embolism
Pneumothorax
Iatrogenic (e.g. excessive mechanical ventilation)

Metabolic acidosis
Metabolic acidosis can occur as a result of either:

Increased acid production or acid ingestion.

Decreased acid excretion or rate of gastrointestinal and renal HCO3–
loss.

A metabolic acidosis would have the following characteristics on an ABG:

↓ pH
↓ HCO3-
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 ↓ BE

Anion gap

The anion gap (AG) is a derived variable primarily used for the evaluation of metabolic
acidosis to determine the presence of unmeasured anions. To work out if the
metabolic acidosis is due to increased acid production or ingestion vs decreased
acid excretion or loss of HCO3– you can calculate the anion gap. The normal anion
gap varies with different assays but is typically between 4 to 12 mmol/L.

Anion gap formula: Anion gap = Na+ – (Cl- + HCO3-)

An increased anion gap indicates increased acid production or ingestion:

Diabetic ketoacidosis (↑ production)

Lactic acidosis (↑ production)

Aspirin overdose (ingestion of acid)

A decreased anion gap indicates decreased acid excretion or loss of HCO3–:

Gastrointestinal loss of HCO 3– (e.g. diarrhoea, ileostomy, proximal colostomy)

Renal tubular acidosis (retaining H+)
Addison’s disease (retaining H+)

Metabolic alkalosis
Metabolic alkalosis occurs as a result of decreased hydrogen ion concentration,
leading to increased bicarbonate, or alternatively a direct result of increased
bicarbonate concentrations.

A metabolic alkalosis would have the following characteristics on an ABG:

↑ pH
↑ HCO3-
↑ BE

Causes of metabolic alkalosis include:

Gastrointestinal loss of H + ions (e.g. vomiting, diarrhoea)

Renal loss of H + ions (e.g. loop and thiazide diuretics, heart failure, nephrotic
syndrome, cirrhosis, Conn’s syndrome)
Iatrogenic (e.g. addition of excess alkali such as milk-alkali syndrome)

Mixed respiratory and metabolic acidosis

A mixed respiratory and metabolic acidosis would have the following
characteristics on an ABG:
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 ↓ pH
↑CO2
↓HCO3–

Causes of mixed respiratory and metabolic acidosis include:

Cardiac arrest
Multi-organ failure

Mixed respiratory and metabolic alkalosis

A mixed respiratory and metabolic alkalosis would have the following
characteristics on an ABG:

↑ pH
↓ CO2
↑ HCO3–

Causes of mixed respiratory and metabolic alkalosis:

Liver cirrhosis in addition to diuretic use

Hyperemesis gravidarum
Excessive ventilation in COPD

ABG worked examples

We’ve included two worked ABG examples below. Once you’ve worked through them,
head over to our ABG quiz for some more scenarios to put your newfound ABG
interpretation skills to the test!

Worked example 1

Vignette

A 17-year-old patient presents to A&E complaining of a tight feeling in their chest,

shortness of breath and some tingling in their fingers and around their mouth. They
have no significant past medical history and are not on any regular medication. An ABG
is performed on the patient (who is not currently receiving any oxygen therapy).

An ABG is performed and reveals the following:

PaO2 : 14 (11 – 13 kPa) || 105 mmHg (82.5 – 97.5 mmHg)

pH: 7.49 (7.35 – 7.45)
PaCO2 : 3.6 (4.7 – 6.0 kPa) || 27 mmHg (35.2 – 45 mmHg)
HCO3–: 24 (22 – 26 mEq/L)

Oxygenation (PaO2)
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A PaO 2 of 14 on room air is at the upper limit of normal, so the patient is not hypoxic.

pH

A pH of 7.49 is higher than normal and therefore the patient is alkalotic.

The next step is to figure out whether the respiratory system is contributing the alkalosis
(e.g. ↓ CO2).

PaCO 2

The CO2 is low, which would be in keeping with an alkalosis, so we now know the
respiratory system is definitely contributing to the alkalosis, if not the entire cause of it.

The next step is to look at the HCO 3– and see if it is also contributing to the alkalosis.

HCO 3–

HCO3– is normal, ruling out a mixed respiratory and metabolic alkalosis, leaving us
with an isolated respiratory alkalosis.

Compensation

There is no evidence of metabolic compensation of the respiratory alkalosis (which

would involve a lowered HCO3-) suggesting that this derangement is relatively acute (as
metabolic compensation takes a few days to develop).

Interpretation

Respiratory alkalosis with no metabolic compensation.

The underlying cause of respiratory alkalosis, in this case, is a panic attack, with
hyperventilation in addition to peripheral and peri-oral tingling being classical
presenting features.

Worked example 2

Vignette

A 16-year-old female presents to hospital with drowsiness and dehydration. They have
no previous past medical history and are on no regular medication.

An ABG is performed on room air reveals the following:

PaO2 : 14 (11 – 13 kPa) ||105 mmHg (82.5 – 97.5 mmHg)

pH: 7.33 (7.35 – 7.45)
PaCO2 : 3.0 (4.7 – 6.0 kPa) || 22.5 mmHg (35.2 – 45 mmHg)
HCO3–: 17 (22 – 26 mEq/L)

Oxygenation (PaO2)
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A PaO 2 of 14 on room air is at the upper limit of normal, so the patient is not hypoxic.

pH

A pH of 7.33 is lower than normal and therefore the patient is acidotic.

The next step is to figure out whether the respiratory system is contributing the
acidosis (i.e. ↑ CO2).

PaCO 2

The CO2 is low, which rules out the respiratory system as the cause of the acidosis (as we
would expect it to be raised if this was the case).

So we now know the respiratory system is NOT contributing to the acidosis and this is,
therefore, a metabolic acidosis.

The next step is to look at the HCO 3– to confirm this.

HCO 3–

HCO3– is low, which is in keeping with a metabolic acidosis.

Compensation

We now know that the patient has a metabolic acidosis and therefore we can look back
at the CO2 to see if the respiratory system is attempting to compensate for the metabolic
derangement.

In this case, there is evidence of respiratory compensation as the CO 2 has been lowered
in an attempt to normalise the pH.

An important point to recognise here is that although the derangement in pH seems

relatively minor this should not lead to the assumption that the metabolic acidosis is
also minor.

The severity of the metabolic acidosis is masked by the respiratory system’s attempt at
compensating via reduced CO2 levels.

Interpretation

Metabolic acidosis with respiratory compensation.

The underlying cause of the metabolic acidosis, in this case, is diabetic ketoacidosis.

Further worked examples

Head over to our ABG quiz for some more scenarios to put your newfound ABG
interpretation skills to the test. Our quiz platform also has over 3000 free MCQs across
a broad range of topics.

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References
1. The British Thoracic Society. Guideline for emergency oxygen use in adult
patients. Thorax 2008; 63(1). Available from: [LINK] (accessed 27th June 2016).
2. The University of Louisville. The fraction of inspired oxygen. Available from:
[LINK] (accessed 29th June 2016).

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