ABG - Interpretation Flashcards
Normal ranges
pH: 7.35 – 7.45
PaCO2: 4.7-6.0 kPa
PaO2: 11-13 kPa
HCO3-: 22-26 mEg/L
Base excess: -2 to +2 mmol/L
Patients 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
Oxygenation (PO2)
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.
Nasal cannulae
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%
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 (PaCO2 <6.0 kPa).
Type 2 respiratory failure involves hypoxaemia (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**).
Type 2 respiratory failure
Type 2 respiratory failure involves hypoxaemia (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)
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 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.
Underlying biochemistry
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:
- Is the CO2 normal or abnormal?
- 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)
- 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.
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 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:
- Is the HCO3– normal or abnormal?
- If abnormal, does this abnormality fit with the current pH (↓HCO3– and acidosis)
- 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)
pH HCO3 CO2
Metabolic acidosis ↓ ↓ Normal
Metabolic alkalosis ↑ ↑ Normal
Met acid with resp comp↓ ↓ ↓
Met alk with respi comp↑ ↑ ↑
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.
