ABG Interpretation

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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: -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 PaO2 well above the normal range with this level of oxygen
therapy
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 O 2 saturations – likely a venous sample

Oxygenation (PaO2)
Your first question when looking at the ABG should be “Is this patient hypoxic?”
(because this will kill them long before anything else does).

PaO2 should be >10 kPa on 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).

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
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As with all oxygen delivery devices, there is a significant amount of variability due to
issues with appropriate fitting of the device and the patient’s breathing rate and depth.
Below are some rough 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

Oxygen delivery is highly variable depending upon oxygen flow rate, the quality of the
mask fit, the patient’s respiratory rate and their tidal volume. These 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-rebreathable mask)

This type of mask delivers 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 and the
patient’s breathing pattern. These masks are most suitable for trauma and emergency
use where carbon dioxide retention is unlikely.

Venturi masks

A Venturi mask will give an accurate concentration of oxygen to the patient regardless of
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 COPD).³

Hypoxaemia
If the PaO2 is <10 kPa on air – the patient is hypoxaemic.

If the PaO2 is <8 kPa on air – the patient is severely hypoxaemic and in respiratory
failure. When this is the case we next look at the PaCO2 to determine if this is type 1 or
type 2 respiratory failure.

Type 1 vs type 2 respiratory failure

Type 1 respiratory failure involves hypoxaemia (PaO2 <8 kPa) with normocapnia
(PaCO 2 <6.0 kPa).
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 2

Type 2 respiratory failure involves hypoxaemia (PaO2 <8 kPa) with hypercapnia (PaCO 2
>6.0 kPa).

Type 1 respiratory failure

Type 1 respiratory failure involves hypoxaemia (PaO2 <8 kPa) with normocapnia
(PaCO 2 <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.

Examples of VQ mismatch include:

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

bronchoconstriction
Reduced perfusion with normal ventilation – e.g. pulmonary embolism

As a result of the VQ mismatch, PaO2 falls and PaCO2 rises. The rise in PaCO2 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 (PaCO 2 < 6.0 kPa).¹

Type 2 respiratory failure

Type 2 respiratory failure involveshypoxaemia (PaO2 is <8 kPa) with hypercapnia (PaCO 2
>6.0 kPa).

It occurs as a result of alveolar hypoventilation, which prevents the patient from being
able to adequately oxygenate and eliminate enough CO2 from their blood.

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?

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

We need to think about 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.

If the ABG demonstrates alkalosis or acidosis you need to then begin considering what
is driving this abnormality by moving through the next steps below.

PaCO2
At this point, prior to reading the CO2, you know the pH and the PaO2. 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 CO2 quickly helps rule in or out the respiratory system as the
cause for the derangement in pH.

pH CO2 HCO3–

Respiratory acidosis ↓ ↑ Normal

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 is acidic and decreases the
pH. When a patient is retaining CO2 the blood will, therefore, become more acidic from
the increase in carbonic acid. When a patient is ‘blowing off’ the CO2 there is less of it in
the system than normal and the blood will become less acidotic and more alkalotic.

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 Carbonic acid equation

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

So we need to ask ourselves:

1. Is the CO2 normal or abnormal?

2. If abnormal, does this abnormality fit with the current pH (so 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 CO 2 doesn’t make sense as the cause of the pH (e.g. normal or
↓ CO2 and ↓ pH), it would suggest that the cause for the abnormality in pH is metabolic.

HCO3–
We now know the pH and whether the problem is metabolic or respiratory in nature
from the CO2 level. Piecing this information together with the HCO 3– we can complete
the picture.

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:

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1. Is the HCO3– normal or abnormal?

2. If abnormal, does this abnormality fit with the current pH (↓HCO 3– 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 seen from the CO 2)

pH HCO3– 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 both HCO3– and CO2 are included. It is very
important to look at them 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
Compensation has been touched on already in the above sections, to clarify we have
made it simple below.

Respiratory acidosis/alkalosis (changes in CO2) 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.

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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 HCO3– 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 CO2 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 (i.e.
respiratory & metabolic acidosis / respiratory & metabolic alkalosis).

In these circumstances, the CO2 and HCO3– will be moving in opposite directions (e.g. ↑
CO 2 ↓ HCO 3– in mixed respiratory and metabolic acidosis).

Treatment is directed towards correction of 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
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
↑ CO 2

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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
↓ CO 2

Causes of respiratory alkalosis include³:

Anxiety – often referred to as a panic attack

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

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

1. Increased acid production or acid ingestion

2. Decreased acid excretion / GI or renal HCO3– − loss

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

↓ pH
↓ HCO3-
↓ 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 4 to 12 mmol/L.
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Anion Gap = Na+ – (Cl- + HCO 3--)

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 HCO 3–−:

GI loss of HCO3— 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 – vomiting/diarrhoea

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

Mixed respiratory and metabolic acidosis

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

↓ pH
↑CO2
↓HCO3–

Potential causes include:

Cardiac arrest
Multi-organ failure
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Mixed respiratory and metabolic alkalosis
A mixed respiratory and metabolic alkalosis would have the following
characteristics on an ABG:

↑ pH
↓ CO 2
↑ HCO3–

Potential causes include:

Liver cirrhosis with diuretic use

Hyperemesis gravidarum
Excessive ventilation in COPD

ABG worked examples

Below are two worked examples to check out. Once you’ve done these you can
head over to our ABG quiz for some more scenarios to put your newfound ABG
interpretation skills to the test!

Worked example 1
Patient’s condition

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.

The ABG result shows 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) A PaO2 of 14 on 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). PaCO2 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 HCO3– and see if it is
also contributing to the alkalosis. HCO3– 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
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would involve a lowered HCO3-) suggesting that this derangement is relatively acute (as
metabolic compensation takes a few days to develop). Answer Respiratory alkalosis with
no metabolic compensation. The underlying cause of respiratory alkalosis, in this case, is
a panic attack, with the hyperventilation, peripheral and peri-oral tingling being classical
presenting features.

Worked example 2
Patient’s condition

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.

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) A PaO2 of 14 on 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. ↑ CO 2). PaCO2 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 HCO3– to confirm this. HCO3– HCO3– is
low 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 CO 2 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 CO2 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. Answer
Metabolic acidosis with respiratory compensation. The underlying cause of the metabolic
acidosis, in this case, is diabetic ketoacidosis.

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