- 1 Introduction to Arterial Blood Gas Interpretation
- 2 Normal Values in ABG Interpretation
- 3 The oxygen dissociation curve
- 4 Bicarbonate Buffering System
- 5 Basic ABG interpretation
- 6 Respiratory acidosis
- 7 Respiratory alkalosis
- 8 Metabolic Alkalosis
- 9 Metabolic Acidosis
- 10 Examples
- 11 Related Articles
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
PaO2 is a measure of oxygenation
The oxygen dissociation curve
- 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
- Renal disease
- 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
- Look at the pH – is it acidosis, alkalosis, or normal?
- If its acidotic, then the patient is acidotic
- If acidotic, calculate the anion gap to help differentiate the cause
- If its alkalotic, the patient is alkalotic
- 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.
- If its acidotic, then the patient is acidotic
- Look at the CO2 – is it normal or abnormal? Is this change in keeping with the pH? (See table below)
- Look at the HCO3- – is it normal or abnormal? Is the change in keeping with the pH?
- Note the changes in bicarb and base excess take at least a couple of days to occur after the initial causatory event.
- 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||↔ pH||Normal Acid Base Status|
|↔ CO2||↓ pH||Metabolic Acidosis|
|↔ CO2||↑ pH||Metabolic Alkalosis|
|↑ CO2||↔ pH||Respiratory Acidosis with full metabolic compensation|
|↑ CO2||↓ pH||Respiratory Acidosis|
|↑ CO2||↑ pH||Metabolic Alkalosis with partial respiratory compensation|
|↓ CO2||↔ pH||Respiratory Alkalosis with full metabolic compensation|
|↓ CO2||↓ pH||Metabolic Acidosis with partial respiratory compensation|
|↓CO2||↑ pH||Metabolic Alkalosis with partial respiratory compensation|
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:
- Depressed respiratory drive (e.g. low GCS)
- Hypoventilation of any other cause
Signs of CO2 retention
- 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
This is due to hyperventilation.
- As PaCO2 lowers, so pH rises
- Any cause of hyperventilation:
Is caused by:
- Loss of hydrogen ions
- Diarrhoea (sometimes vomiting too)
- Excess Bicarbonate
- Ingestion of alkaline substances
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
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 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
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.
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:
- A – Addison’s Disease
- B – Bicarbonate loss
- Renal Failure
- C – Chloride Excess – e.g. from lots of normal saline
- D – Drugs (acetazolamide)
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; LTKR, KARMEL and CAT MUDPILES. Pick your favourite!
Causes – Simple – “LTKR”
- Renal Failure
Causes – Exhaustive list – “CAT MUDPILES”
- Cyanide , carbon monoxide
- Alcoholic ketoacidosis
- Toluline (methybenzine – used as an inhaled narcotic)
- Methanol, metformin
- Diabetic Ketoacidosis
- Iron, isoniazid
- Ethanol, ethylene glycol
Causes – “KARMEL”
- Aspirin (and paracetamol, and other toxins)
- Renal Failure
- Ehylene Glycol
Summary of Blood Gas Differentials
- PaO2 6.6 – very low
- PaCO2 6.5 – high
- pH 7.14
- HCO3 23
- PaO2 7.8 (low)
- PaCO2 8.0 (high)
- pH 7.35 (normal)
- HCO3 31 (high)
- FlO2 .21 (21% oxygen – room air)
- PaO2 8.0 low
- PaCO2 5.0 (normal)
- pH 7.51 High
- HCO3 30
- PaO2 9.5 (low)
- PaCO2 2.8 (low)
- pH 7.40 (normal)
- HCO3 12 -very low
- O2 sats 95%
We are not able to calculate the anion gap in this instance.