11/13/24, 7\:31 PM Guide | ABG interpretation

ABG interpretation

Table of contents
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0\:00 10\:28

Introduction

Arterial blood gas (ABG) interpretation is something that can be di
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 re
your patient, allowing you to recognise and treat pathology more rapidly.

Reference ranges

pH\: 7.35 - 7.45
PaCO \: 4.7 - 6.0 kPa || 35.2 - 45 mmHg
2
PaO \: 11 - 13 kPa || 82.5 - 97.5 mmHg
2
HCO -\: 22 - 26 mEq/L
3
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' PaO 2 2
in a patient on high
A 'normal' PaCO 2
in a hypoxic asthmatic patient\: a sign they are tiring and need ITU intervention.
well
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A 'very low' PaO 2 2
in a patient who looks completely well, is not short of breath and has normal O a venous sample.
saturations\: this is likely

Oxygenation (PaO2)

Your
PaO 2
should be >10 kPa (75mmHg) when oxygenating on room air in a healthy patient.
If the patient is receiving oxygen therapy their PaO 2
FiO 2 2
(so a patient on 40% oxygen would be expected to have a PaO should be approximately 10kPa less than the % inspired concentration
of approximately 30kPa /225mmHg).

Oxygen delivery devices and

A common question is "What percentage of oxygen does this device deliver at a given
. Below is a quick reference
guide, providing some approximate values for the various oxygen delivery devices and
practice.
2
Nasal cannulae
As with all oxygen delivery devices, there is a signi
and how well the oxygen delivery device is
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
patient's respiratory rate and their tidal volume. Simple face masks can deliver a maximum FiO 2
of approximately 40%-60% at a

³
Reservoir mask (also known as a non-rebreather mask)
Reservoir masks deliver oxygen at concentrations between 60% and 90% when used at a
³ The
concentration is not accurate and will depend on the
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 the oxygen
suggested
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 PaO 2
is \<10 kPa (75mmHg) on air, a patient is considered hypoxaemic.
If PaO 2
is \<8 kPa (60mmHg) 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 2
\<8 kPa / 60mmHg) with normocapnia (PaCO \<6.0 kPa / 45mmHg).
Type 2 respiratory failure involves hypoxaemia (PaO 2 2
\<8 kPa / 60mmHg) with hypercapnia (PaCO >6.0 kPa / 45mmHg).
Type 1 respiratory failure
Type 1 respiratory failure involves hypoxaemia (PaO 2 2
\<8 kPa /60mmHg) with normocapnia (PaCO \<6.0 kPa / 45mmHg).
It occurs as a result of ventilation/perfusion (V/Q) mismatch; the volume of air
with the 2 2 2
falls and PaCO rises. The rise in PaCO rapidly
triggers an increase in a patient's overall alveolar ventilation, which corrects the PaCO 2 2
but not the PaO due to the di
shape of the CO 2 2 2 2
and O dissociation curves. The end result is hypoxaemia (PaO \< 8 kPa /60mmHg) with normocapnia (PaCO
\< 6.0 kPa / 45mmHg).
¹
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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 2
is \<8 kPa / 60mmHg) with hypercapnia (PaCO >6.0 kPa / 45mmHg). It
occurs as a result of alveolar hypoventilation, which prevents the patient from being able to adequately oxygenate and
eliminate CO from their blood.
2
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 signi
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 CO (respiratory) or HCO - (metabolic). These work as bu
2 3
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 , you already know the pH and the PaO . So for example, you may know your patient’s pH
2 2
is abnormal but you don’t yet know the underlying cause. It could be caused by the respiratory system (abnormal level of CO )
2
or it could be metabolically driven (abnormal level of HCO -).
3
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 CO HCO -
2 3
Respiratory acidosis ↓ ↑ Normal
Respiratory alkalosis ↑ ↓ Normal
Respiratory acidosis with metabolic compensation ↓ / ↔ ↑ ↑
Respiratory alkalosis with metabolic compensation ↑ / ↔ ↓ ↓

Underlying biochemistry

CO binds with H O and forms carbonic acid (H CO ) which will decrease pH. When a patient is retaining CO 2 2 2 3 2
the blood will,
therefore, become more acidic from the increased concentration of carbonic acid. When a patient is ‘blowing o2
there is
less of it in the system and, as a result, the patient's 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 bu
of the pH imbalance is from the respiratory system, the body can adjust the HCO - to counterbalance the pH abnormality
3
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 o2
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 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 2
doesn’t make sense as the cause of the pH abnormality (e.g. normal or ↓ CO 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 CO 2
Piecing this information together with the HCO - we can complete the picture\:
3
HCO - is a base, which helps mop up acids (H+ ions).
3
So when HCO - is raised the pH is increased as there are less free H+ ions (alkalosis).
3
When HCO - is low the pH is decreased as there are more free H+ ions (acidosis).
3
level.
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Carbonic acid equation
So we need to ask ourselves\:
1. Is the HCO - normal or abnormal?
3
2. If abnormal, does this abnormality ↓HCO - and acidosis)?
3
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 CO ).
2
pH HCO - CO
3 2
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 HCO - and CO 3 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 HCO - in the blood, which may be
3
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 HCO - in the blood, suggesting either
3
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 CO ) can be metabolically compensated by increasing or decreasing the levels of
2
HCO - in an attempt to move the pH closer to the normal range.
3
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Metabolic acidosis/alkalosis (changes in HCO -) can be compensated by the respiratory system retaining or blowing o
3 2
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 o2 2
(↑ pH) or retain more CO (↓ 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 - production (to decrease pH) or increase HCO - production (to increase pH). As a result, if you see evidence
3 3
of metabolic compensation for a respiratory disorder (e.g. increased HCO -/base excess in a patient with COPD and CO
3 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 and HCO - will be moving in opposite directions (e.g. ↑ CO 2 3 2 3
↓ HCO - 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

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
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 CO 2
exhaled. As a result, PaCO 2
is reduced and pH increases causing alkalosis.
than normal being
A respiratory alkalosis would have the following characteristics on an ABG\:
↑ pH
↓ CO
2
Causes of respiratory alkalosis include\: ³
Anxiety (i.e. panic attack)
Pain\: causing an increased respiratory rate.
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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 HCO - loss.
3
A metabolic acidosis would have the following characteristics on an ABG\:
↓ pH
↓ HCO
3-
↓ BE
Anion gap
Blood plasma is an aqueous solution containing a variety of chemical species, some of which have a net electrical charge as a
result of the dissociation of salts and acids in the aqueous medium. Species that have a net positive charge are called cations
+ +
(e.g. Na , K )and those with a net negative charge are called anions (chloride & HCO -
3
).
The anion gap is an arti-
3
) from the
+
total number of cations (Na ). There are lots of other anions and cations, however, those shown in brackets have the most
+
signi
the anion gap.
+ -
-
Anion gap formula\: Na - (Cl + HCO )
3
The anion gap (AG) is a derived variable primarily used for the evaluation of metabolic acidosis to determine the presence of
unmeasured anions (e.g. albumin is the main unmeasured anion). The normal anion gap varies with di
typically between 4 to 12 mmol/L.
Causes of a high anion gap metabolic acidosis (typically relate to increased production/ingestion or reduced excretion of H
+
by the kidneys)\:
Diabetic ketoacidosis
Lactic acidosis
Toxins (e.g. aspirin, methanol and ethylene glycol)
Renal failure
Causes of a normal anion gap metabolic acidosis (typically due to loss of bicarbonate which is subsequently replaced by
chloride in the plasma, resulting in a stable overall anion concentration)\:
Gastrointestinal loss of HCO -
3
Renal tubular disease
(e.g. diarrhoea, ileostomy, proximal colostomy)
Addison's disease

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
↑ HCO
3-
↑ 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)
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Mixed respiratory and metabolic acidosis

A mixed respiratory and metabolic acidosis would have the following characteristics on an ABG\:
↓ pH
↑CO
2
↓HCO -
3
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
↓ CO
2
↑ HCO -
3
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

performed on the patient (who is not currently receiving any oxygen therapy).
An ABG is performed and reveals the following\:
PaO \: 14 (11 - 13 kPa) || 105 mmHg (82.5 - 97.5 mmHg)
2
pH\: 7.49 (7.35 - 7.45)
PaCO \: 3.6 (4.7 - 6.0 kPa) || 27 mmHg (35.2 - 45 mmHg)
2
HCO -\: 24 (22 - 26 mEq/L)
3
Oxygenation (PaO )
2
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 ↓ CO ).
2
PaCO
2
The CO 2
the alkalosis, if not the entire cause of it.
is low, which would be in keeping with an alkalosis, so we now know the respiratory system is de
The next step is to look at the HCO - and see if it is also contributing to the alkalosis.
3
HCO -
3
HCO - is normal, ruling out a mixed respiratory and metabolic alkalosis, leaving us with an isolated respiratory alkalosis.
3
Compensation
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There is no evidence of metabolic compensation of the respiratory alkalosis (which would involve a lowered HCO -) suggesting
3
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
on no regular medication.
A 16-year-old female presents to hospital with drowsiness and dehydration. They have no previous past medical history and are
An ABG is performed on room air reveals the following\:
PaO \: 14 (11 - 13 kPa) ||105 mmHg (82.5 - 97.5 mmHg)
2
pH\: 7.33 (7.35 - 7.45)
PaCO \: 3.0 (4.7 - 6.0 kPa) || 22.5 mmHg (35.2 - 45 mmHg)
2
HCO -\: 17 (22 - 26 mEq/L)
3
Oxygenation (PaO )
2
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 ↑ CO ).
2
PaCO
2
The CO 2
was the case).
is low, which rules out the respiratory system as the cause of the acidosis (as we would expect it to be raised if this
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 - to con
3
HCO -
3
HCO - is low, which is in keeping with a metabolic acidosis.
3
Compensation
We now know that the patient has a metabolic acidosis and therefore we can look back at the CO 2
system is attempting to compensate for the metabolic derangement.
to see if the respiratory
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 CO 2
levels.
Interpretation
Metabolic acidosis with respiratory compensation.
Source\: geekymedics.com
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