In this article, we will look at more practical aspects of how to read an ABG and treatment following your interpretation. If you’re looking on how to perform an ABG, read this article.
An ABG is vital in any medical emergency call, providing valuable information on a patient’s clinical state quickly. The body tightly controls pH with the carbonic acid equilibrium and organ dysfunction tends to disrupt this. ABGs allow us to identify and assess the severity of this dysfunction.
- Always put the oxygen percentage/device on an ABG
- Aim to document how convinced you were a sample was arterial (was it an easy, self-filling sample over a very prominent artery with the right colour? Did it take multiple attempts with probably mixed sampling?)
- Ensure there are no clots in the sample
- If the machine allows, input the temperature as this will correct values accordingly
- VBGs are better for ruling out an abnormality than ruling in one e.g. PCO2 is higher in a venous sample so a normal value in venous sampling suggests a normal arterial value. You cannot use a VBG to make a diagnosis of Type 2 respiratory failure or assess oxygenation.
Interpreting an ABG
If you need a refresher of ABG interpretation from medical school, take a moment to read this article. The most important thing is that you use the patient’s clinical condition to guide your interpretation.
- Expect a low PaCO2 in acute asthma. A normal level suggests they are tiring and potentially in a life-threatening state.
- Expect a high PaO2 if a patient is receiving supplementary oxygen. A normal PaO2 suggests significant hypoxia (or that the sample could be venous). Often the expected PaO2 is estimated at 10kPa lower than the inspired oxygen percentage
Consider the gas in front of you using the diagram below and these normal values (varies depending on hospital)
- pH: 7.35-7.45
- pO2: 11-14 kPa
- pCO2: 4.5-6.5kPa
- HCO3-: 22-26
- BE: -2 to +2
There may be compensation by the respiratory or metabolic system (whichever is unaffected) to attempt to return the pH to normal. Identifying metabolic compensation in the context of respiratory acidosis provides evidence that the issue is chronic (at least more than 12-24h).
Low PaO2 / Respiratory Failure / Respiratory Acidosis
Ensure you’ve read our article on Hypoxia to identify the cause to aid interpretation & treatment.
This is split into Type 1 (low oxygen or “one” thing wrong) or Type 2 Respiratory Failure (low oxygen & raised PaCO2 or “two” things wrong).
Type 1 Respiratory Failure tends to be due to ventilation-perfusion mismatch. There is an incorrect overlap of the parts of the lung getting aerated and perfused, which means the oxygen content of the blood is low. As we breathe faster in response to rising PaCO2, this tends to be normal. The treatment is directed at dealing with whatever’s causing the mismatch.
Type 2 Respiratory Failure (or Respiratory Acidosis) is due to hypoventilation. You should urgently escalate all causes which include airway obstruction (such as COPD), chest wall causes (e.g. deformities, fractures or obesity), reduced strength (neuromuscular disorders) or more central causes (opiates, tiring from acute asthma).
In T2RF you want to aim for saturations of 88-92%. These patients tend to have chronic respiratory failure and can therefore tolerate these lower saturations. Initial treatment aims to address the underlying cause (reducing work of breathing in COPD with acute treatment or reversal of opioid toxicity).
An ABG identifies whether the patient has acutely deteriorated (low pH) and whether this is chronic (raised bicarbonate). It takes a few days for the patient’s kidneys to raise bicarbonate levels to compensate for a chronically high PaCO2 (or raised pH). Knowing whether a patient has chronic respiratory failure helps point you towards the patient having some sort of more chronic problem from the above list. Acute deterioration (can be in addition to chronic respiratory failure) is usually more worrying and makes it more likely that ventilatory support (such as NIV) is required and hence the need for urgent escalation.
Consider an ABG in any patient who is hypoxic to work out
- Level of hypoxia & whether you can provide adequate oxygenation on a ward or you need higher-level care such as ITU & more acute treatment to correct the VQ mismatch
- Whether there is T1RF or T2RF to target saturations accordingly
- In T2RF, escalate for consideration of ventilatory support such as NIV
This is due to hyperventilation either as the patient is hypoxic (see above), has underlying lung issues triggering hyperventilation or has states causing hyperventilation: pain, salicyclate overdose, pregnancy, sepsis, CNS stimulation from cerebral disease. Anxiety/Panic are only to be considered once other causes are ruled out & it is dangerous to assume this is the cause.
- Assume a respiratory alkalosis is due to anxiety or a panic attack is dangerous. Assume the cause is life-threatening until proven otherwise
In metabolic acidosis, there is an excess of acid or base has been lost. Usually, this is identifiable on history & clinical assessment.
- ABCDE (don’t forget blood glucose & hydrate as needed!)
- Review any stoma output/diarrhoea
- Screen & treat for an overdose
- Review renal function, electrolytes & inflammatory markers
- Urine dip
- Consider endocrine/renal input as appropriate
Understanding Anion Gap
In addition to maintaining acid-base equilibrium, there should be electroneutrality too. We can use this principle to compare the routine ions we measure to see if they are balanced and if not, infer that there must be some other external acid accounting for the imbalance & acidosis.
Anion Gap = (Na + K) – (Cl + HCO3)
We take the anions (chloride and bicarbonate) from the cations (sodium & potassium). The difference is usually made up by albumin and other weak acids. If the gap is raised (more than 16, varies across hospitals), other anions must be accounting for the difference e.g. lactate. This is called a raised anion gap metabolic acidosis & simply put it means acid has been formed or ingested other than the usual ones we account for.
You will know MUDPILES or another acronym for remembering the causes of raised anion gap metabolic acidosis.
- Diabetic Ketoacidosis
- Lactic acidosis
- Ethylene Glycol
Normal anion gap metabolic acidosis is rarer. It can be caused by lab error or low albumin. Causes also include gastrointestinal loss of HCO3 (diarrhoea, stomas), renal tubular acidosis or Addison’s disease.
- Identifying the cause for metabolic acidosis is simply a thorough A to E assessment looking for common causes: intoxication, ketoacidosis and sepsis
- Anion gap can be used to offer support to your clinical assessment or where there is doubt. Normal anion gap is rarer and should prompt discussion with seniors or specialty teams
Often a loss of H+ ions results in alkalosis either from the gastrointestinal tract (vomiting/diarrhoea) or through the kidneys (diuretics, heart failure, nephrotic syndrome, cirrhosis, Conn’s syndrome). In the most frequent causes, the patient is hypovolaemic and therefore responds to 0.9% sodium chloride.
Another cause is corrected respiratory acidosis. Patients quickly develop respiratory acidosis, but retaining bicarbonate (compensatory metabolic alkalosis) takes time. Conversely, if the Type 2 Respiratory Failure is corrected, the metabolic alkalosis persists until the kidney has a chance to remove the excess bicarbonate.
- Metabolic alkalosis tends to be less clinically concerning (but more detailed information is included in the references)
- Often it is in the context of a hypovolaemic hypochloraemic state which responds to 0.9% sodium chloride
Further Reading & References
Written by Dr Keryn Hall FY2 & Dr Akash Doshi CT2
We are sorry that this post was not useful for you!
Let us improve this post!
Tell us how we can improve this post?