Arterial Blood Gas – ABG – Interpretation
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Introduction to Arterial Blood Gas Interpretation

Arterial Blood Gas interpretation can be a daunting and difficult skill for any medical student or junior doctor. Try to look at as many real life examples as you can, and don’t be afraid to get it wrong!

The use of Venous Blood Gasses is becoming more widespread, especially in the emergency department. Almost all of the same rules apply for VBG interpretation as for ABG interpretation with a couple of caveats:

  • pO2 and pCO2 are unreliable in VBG interpretation. It may be possible to track a pCO2 trend, but take this with a pinch of salt.

Normal Values in ABG Interpretation

4.7-6.0 kPa   /   35-45 mmHg
9.3-13.3 kPa   /   80-100 mmHg
22-28 mmol/L
SaO2(Oxygen saturation)
PA – pressure in the alveoli
Pa – pressure in the artery
To convert kPa to mmHg, multiply by 7.5PaCO2 gives an indication of ventilation – how was is the patient breathing, how is their gas exchange
PaO2 is a measure of oxygenation

The oxygen dissociation curve


Oxygen Dissociation Curve for ABG interpretation
Oxygen Dissociation Curve for ABG interpretation
Note how:
  • The saturation declines rapidly at some points, and barely moves at other points. The curve starts its fast decline at about 90%, thus in the emergency situation, keeping oxygen saturations above 90% is important to avoid hypoxic injury (particularly hypoxic brain injury)
  • Various factors, including pH and temperature can shift the curve to the right or the left

Bicarbonate Buffering System

The bicarbonate buffering system is the method by which the body controls pH and is crucial to understand arterial and venous blood gas results.

CO2  +  H2O   ↔   H2CO3   ↔    H+ + HCO3

The equation demonstrates an equilibrium, between carbon dioxide, and hydrogen ions + bicarbonate. In normal physiology at a normal metabolic rate, this equilibrium exists to keep the pH between 7.35 and 7.45

  • Remember the pH is a logarithmic scale and as such, increases exponentially. The concentration of hydrogen ions at pH 7.1 is double that at pH 7.4.

When a pathological abnormality occurs, this can cause various shifts in the equilibrium. We interpret these shifts to try to assess what the pathological abnormality is.

  • If the concentration of Hydrogen ions increases, the pH will decrease, causing an acidosis. This causes the equation to shift to the left, and more CO2 is produced, of which some (or all) can be blown off by the lungs. This is the mechanism of respiratory compensation.
  • If CO2 is not able to blown off effectively, then the concentration of CO2 increases, as thus then so will the concentration of hydrogen ions, and the pH will not be able to be resolved to normal. This is partial respiratory compensation. 
  • Most causes of acid-base disturbance are due to an acidosis. The causes of these are discussed in more detail below.
  • There can also be metabolic compensation whereby the concentration of HCO3 is altered to try to keep the equilibrium in cases of respiratory dysfunction.
  • In a respiratory alkalosis, CO2 is blown off too quickly, thus the curve shifts to the left, to replace the CO2, and the concentration of hydrogen ions is lowered
  • In a metabolic alkalosis there is a disturbance due a loss of H+ or an excess of HCO3, causing the curve to shift.

Basic ABG interpretation

ABG interpretation is best done as part of an overall case review of a patient. Chronic as well as acute factors in the history can influence the result, particularly:
  • Renal disease
  • Diabetes
  • Drugs; diuretics, aspirin(+are they on oxygen?)
    • The Rule of 19 is a way of assessing whether or not the patient was on oxygen at the time of the sample. Add the PO2 and PCO2 – if the sum of these is >19 then likely to be on inspired oxygen. If the level is lower than this, they are likely to be breathing room air.
  • Symptoms and onset (lung disease?)

Basic ABG Interpretation Rules

  1. Look at the pH – is it acidosis, alkalosis, or normal?
    1. If its acidotic, then the patient is acidotic
      1. If acidotic, calculate the anion gap to help differentiate the cause
    2. If its alkalotic, the patient is alkalotic
    3. ​If its it normal, there may be no acid-base dysfunction, or the patient could have a compensated acidosis or alkalosis. The CO2 and HCO3 values are required for further interpretation.
  2. Look at the CO2 – is it normal or abnormal?  Is this change in keeping with the pH? (See table below)
  3. Look at the HCO3- – is it normal or abnormal? Is the change in keeping with the pH?
    1. Note the changes in bicarb and base excess take at least a couple of days to occur after the initial causatory event.
  4. If the changes aren’t in keeping with the levels, then it is likely to be some sort of compensation! More on how to tell this later on.

Arterial Blood Gas Interpretation Table

↔ CO2↔ pHNormal Acid Base Status
↔ CO2↓ pHMetabolic Acidosis
↔ CO2↑ pHMetabolic Alkalosis
↑ CO2↔ pHRespiratory Acidosis with full metabolic compensation
↑ CO2↓ pHRespiratory Acidosis
↑ CO2↑ pHMetabolic Alkalosis with partial respiratory compensation
↓ CO2↔ pHRespiratory Alkalosis with full metabolic compensation
↓ CO2↓ pHMetabolic Acidosis with partial respiratory compensation
↓CO2↑ pHMetabolic Alkalosis with partial respiratory compensation


Respiratory acidosis

Respiratory acidosis is very straightforward. It is always due to a retention of CO2(Type II Respiratory failure) of which there are only a handful of causes:

  • COPD
  • Depressed respiratory drive (e.g. low GCS)
  • Hypoventilation of any other cause

Signs of COretention

  • Confusion – as a result of peripheral vasodilation
  • Asterixis (renal failure, type 2 resp failure, liver failure)
  • Warm extremeties
  • Bounding pulse
  • Morning headache – CO2 particularly high at these times.

Acute or Chronic?

  • Most well patients with COPD will have a high CO2, but normal pH, because they have metabolically compensated for their high CO2.
  • Patients with an acute cause, will likely have a acidotic pH, because the metabolic system has not had time to compensate
  • COPD patients with an acute exacerbation, or another acute illness an also have an acute CO2 retention on top of their chronic retention.
  • Compensation starts at about 6 hours and is complete (i.e. at the limits of physiology) by 4 days.
  • Assessing the HCO3 in conjunction with the CO2 can help differentiate if the CO2 retention is acute or chronic. This is known as the  1 for 10 rule.

1 for 10 rule

  • ACUTE: For every rise of 10 of the PaCO2 above 40 mmHg, the bicarbonate will rise by 1
  • CHRONIC: For every rise of 10 of the PaCO2 above 40mmHg, the bicarbonate will rise by 4

Respiratory alkalosis

This is due to hyperventilation. 

  • As PaCO2 lowers, so pH rises
  • Any cause of hyperventilation:

Metabolic Alkalosis

Is caused by:

  • Loss of hydrogen ions
  • Excess Bicarbonate

Hydrogen Ion loss

Most commonly cause by diarrhoea. In diarrhoea, there is a loss of K+ into the GI tract. This causes K+ to leave cells, and enter the bloodstream in an attempt to keep K+ levels normal. In order to maintain the electrical charge of the cell, H+ is then taken up by the cell.

May also be caused by burns

Excess Bicarbonate

Normal kidneys are very effective at excreting bicarbonate. Diuretics prevent the re-absorption of sodium from the renal tubule, and thus they promote sodium loss. The normal mechanism for recovering this sodium, involves an exchange with bicarbonate, and thus the ability of the renal tubule to excret bicarbonate is reduced.

May also be cause by too much bicarbonate (sometimes iatrogenic) or ingestion of other alkaline substances.

Metabolic Acidosis

Metabolic acidosis is the most common and the most complex of the acid base disturbances. There are a wide variety of causes, which can be differentiated with the help of the anion gap.

The Anion Gap

This is used to help diagnose acid base disorders. It is usually used in suspected cases of metabolic acidosis. It can either be normal, or raised. Low anion gap does not usually occur.
Anions are negatively charged ions. The two most common ones in the human body are chloride and bicarbonate.
Anions are hard to measure accurately. The anion gap is the difference between the number of measured anions, and the number of unmeasured anions.
Negatively charged proteins make up most of the unmeasured anions in a normal individual, and the main one is albumin.
And thus in a normal individual, there is an anion gap of 4-16, made up mostly of albumin.Some causes of metabolic acidosis, do not produce a large number of unmeasured anions, and the anion gap doesn’t increase. This is normal anion gap metabolic acidosis – NAGMA
Some causes of metabolic acidosis produce a large number of both measured (e.g. HCO3  ) anions, and unmeasured anions. This is High anion gap metabolic acidosis – HAGMA.
In HAGMA, the HCO3  will bind to H+ (which is also produced in excess) and be turned into CO2 which is blown off by the lungs. So although you have produced more HCO3 , the amount of HCO3  is low on an ABG sample because of all the excess H+ binding to it. So the proportion of unmeasurd anions compared to measured anions INCREASES and so in metabolic acidosis the anions gap increases.
To calculate the anion gap, you work out the difference between plasma cations and measureable plasma anions. 
Anion gap = [Na+] – [Cl] – [HCO3]
Some calculations also include potassium, however this would results in a different reference range, and the above formula is generally the accepted version.
Anion Gap = [Na+] + [K+] – [Cl] – [HCO3]
Sometimes it is also necessary to correct for a low albumin level in individuals with liver disease:
Corrected Anion Gap = [AG] + (0.25 x (40 – albumin))
The anion gap is discussed in more detail in a separate article.

Normal Anion Gap Metabolic Acidosis (NAGMA)

This is also sometimes called Hyperchloraemic metabolic acidosis, as the cause is sometimes an increase in chloride ions.
The causes can be remembered with the mnemonic ABCD:

High Anion Gap Metabolic Acidosis (HAGMA)

HAGMA is due to an increase in unmeasured ions (but not albumin). There are several mnemonics to remember the causes, and I have included three below; LTKRKARMEL and CAT MUDPILES. Pick your favourite!

Causes – Simple – “LTKR”

  • Lactate
  • Toxins
  • Ketones
  • Renal Failure


Causes – Exhaustive list – “CAT MUDPILES”

  • Cyanide , carbon monoxide
  • Alcoholic ketoacidosis
  • Toluline (methybenzine – used as an inhaled narcotic)
  • Methanol, metformin
  • Uraemia
  • Diabetic Ketoacidosis
  • Paracetamol
  • Iron, isoniazid
  • Lactate
  • Ethanol, ethylene glycol
  • Salicylate


Causes – “KARMEL”

  • Ketones
  • Aspirin (and paracetamol, and other toxins)
  • Renal Failure
  • Methanol
  • Ehylene Glycol
  • Lactate

Summary of Blood Gas Differentials

Causes of Metabolic Acidosis and ABG interpretation
Causes of Metabolic Acidosis in ABG interpretation


Example 1

Patient breathing room air
  • PaO2     6.6 – very low
  • PaCO2   6.5 – high
  • pH 7.14
  • HCO3     23
This is a primary respiratory acidosis without compensation – because pH is low (acidosis) and CO2 is high (respiratory) and HCO3 is normal – so there is not metabolic compensation.
This is type 2 respiratory failure.
The acidosis is acute because it is not compensated – the bicarbonate is normal.

Example 2

  • PaO2                     7.8 (low)
  • PaCO2                  8.0 (high)
  • pH                          7.35 (normal)
  • HCO3                    31 (high)
High CO2 indicates a respiratory acidosis – but the increased bicarbonate and the normal pH indicated t is fully compensated.
This is likely to be chronic respiratory failure

Example 3

  • FlO2                  .21 (21% oxygen – room air)
  • PaO2                8.0 low
  • PaCO2             5.0 (normal)
  • pH                     7.51 High
  • HCO3               30
pH is high. This is an alkalosis
CO2 is normal – therefore not likely to be hyperventilation
This is a metabolic alkalosis – with a possible other cause of the hypoxia.
In this particularly example the alkalosis was due to diuretics. The patient’s actual presenting complaint was carbon monoxide inhalation, which explains his hypoxia.

Example 4

Patient is on 3L oxygen
2L – 24%
4L – 28%
  • PaO2                9.5 (low)
  • PaCO2             2.8 (low)
  • pH                     7.40 (normal)
  • HCO3               12 -very low
  • O2 sats            95%
The pH is normal, but the PaCO2 is very low. This indicates a fully compensated metabolic acidosis, as indicated by the low bicarbonate.
We are not able to calculate the anion gap in this instance.

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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