Arterial blood gas (ABG) interpretation is something many medical students find difficult to grasp (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 results 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.
To see how to perform an arterial blood gas check out our guide here.
If you want to put your ABG interpretation skills to the test, check out our ABG quiz.
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 O2 saturations – likely a venous sample
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
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.
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
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 involveshypoxaemia (PaO2 <8 kPa) with normocapnia (PaCO2 <6.0 kPa).
Type 2 respiratory failure involveshypoxaemia (PaO2 <8 kPa) with hypercapnia (PaCO2 >6.0 kPa).
Type 1 respiratory failure
Type 1 respiratory failure involves hypoxaemia (PaO2 <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.
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 CO2 and O2 dissociation curves. The end result is hypoxaemia (PaO2 < 8 kPa) with normocapnia (PaCO2 < 6.0 kPa).¹
Type 2 respiratory failure
Type 2 respiratory failure involveshypoxaemia (PaO2 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 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)
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 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.
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.
Respiratory acidosis with metabolic compensation
↓ / ↔
Respiratory alkalosis with metabolic compensation
↑ / ↔
CO2 binds with H2O and forms carbonic acid (H2CO3) 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.
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 CO2 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 (e.g. normal or ↓ CO2 and ↓ pH), it would suggest that the cause for the abnormality in pH is metabolic.
We now know the pH and whether the problem is metabolicorrespiratory in nature from the CO2 level. Piecing this information together with the HCO3– 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).
So we need to ask ourselves:
1. Is the HCO3– normal or abnormal?
2. If abnormal, does this abnormality fit with the current pH (↓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 seen from the CO2)
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 has been touched on already in the above sections, to clarify we have made it simple below.
Respiratory acidosis/alkalosis(changes in CO2) can bemetabolically 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 respiratorysystem retaining or blowingoffCO2 in an attempt to move the pH closer to the normal range.
Rate of compensation
Respiratory compensationfor 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 HCO3– 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).
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. ↑ CO2 ↓ HCO3– 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 is caused by inadequate alveolar ventilation leading to CO2 retention.
A respiratory acidosis would have the following characteristics on an ABG:
Causes of respiratory acidosis include:
Respiratory depression (e.g. opiates)
Guillain-Barre – paralysis leads to an inability to adequately ventilate
Respiratory alkalosis is caused by excessive alveolar ventilation (hyperventilation) resulting in more CO2 than normal being exhaled. As a result, PaCO2 is reduced and pH increases causing alkalosis.
A respiratory alkalosis would have the following characteristics on an ABG:
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
Iatrogenic (excessive mechanical ventilation)
Metabolic acidosis can occur as a result of either:
Increased acid production or acid ingestion
Decreased acid excretion / GI or renal HCO3–− loss
A metabolic acidosis would have the following characteristics on an ABG:
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.
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–−:
GI loss of HCO3— diarrhoea, ileostomy, proximal colostomy
Renal tubular acidosis (retaining H+)
Addison’s disease (retaining H+)
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:
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:
Potential causes include:
Mixed respiratory and metabolic alkalosis
A mixed respiratory and metabolic alkalosis would have the following characteristics on an ABG:
Potential causes include:
Liver cirrhosis with diuretic use
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
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.
A PaO2 of 14 on air is at the upper limit of normal, so the patient is not hypoxic.
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).
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– is normal, ruling out a mixed respiratory and metabolic alkalosis, leaving us with an isolated respiratory alkalosis.
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).
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
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.
A PaO2 of 14 on air is at the upper limit of normal, so the patient is not hypoxic.
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).
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– is low in keeping with a metabolic acidosis.
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 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.
Metabolic acidosis with respiratory compensation. The underlying cause of the metabolic acidosis, in this case, is diabetic ketoacidosis.
1. British Thoracic Society . Guideline for emergency oxygen use in adult patients. Thorax 2008; 63(1) [LINK] (accessed 27th June 2016).
2. University of Louisville. Fraction of inspired oxygen. [LINK] (accessed 29th June 2016)