Print Friendly

Below are a selection of scenarios involving ABG interpretation for you to work through and apply your skills.  If you need a refresher on ABG interpretation then make sure to check out our guide here.  If you feel we’re missing a particular ABG scenario then let us know, or if you’re feeling super keen, create a scenario and we’ll add it to the piece 🙂  

Scenario 1

You are asked to review a 63 year old female who was admitted with shortness of breath. On your arrival the patient appears drowsy and is on 4L of oxygen via nasal cannulae.  You perform an ABG and receive the following results…

  • PaO2: 20 (11-13 kPa)
  • pH: 7.29 (7.35 – 7.45)
  • PaCO2: 9.1 (4.7-6.0 kPa)
  • HCO3: 26 (22-26 mEg/L)
  • Base excess: +1 (-2 to +2)
What does the ABG show?

Oxygenation (PaO2)

Firstly you should recognise that the PaO2 is low, particularly given the patient is receiving supplemental oxygen of 4L via nasal cannulae (36 % oxygen). You’d expect a healthy adult to have a PaO2 of around 26kPa rather than the 17kPa in this patient (FiO2 – 10kPa).

pH

You should then note that the pH reveals an acidosis and look at the CO2 to see if it is contributing to the acidosis (↑CO2).

PaCO2

In this case the PaCO2 is raised significantly and this is likely the cause of the acidosis.

HCO3-

The HCO3 is normal, so the metabolic system is not contributing to the acidosis and also isn’t compensating for the respiratory acidosis, suggesting that this is an acute derangement.

Base excess 

The base excess is within normal limits as there has been no significant change in the amount of HCO3. If this respiratory acidosis was chronic we would expect that the kidneys would have generated more HCO3 to compensate, which would have resulted in an increased BE.

Summary

Respiratory acidosis

Which type of respiratory failure is demonstrated?

The respiratory acidosis has been caused by type 2 respiratory failure (a failure of ventilation) leading to increased levels of CO2 (hypercapnia). This is most likely secondary to the use of a higher than needed concentration of oxygen, as patients with chronic lung conditions (e.g. COPD) can become reliant on their hypoxic drive to maintain an adequate ventilation rate. If they then are treated with high concentrations of oxygen they are no longer hypoxic and therefore their ventilation rate decreases significantly resulting in hypercapnia.

What symptoms or signs are associated with hypercapnia (↑CO2)?
  • Confusion
  • Reduced consciousness level 
  • Asterixis 
  • Bounding pulse

What is the differential diagnosis for this type of respiratory failure?

Type 2 respiratory failure occurs as a result of ventilatory failure. The potential causes of this include those listed below.

Potential causes of type 2 respiratory failure include:

  • Increased airways resistance – COPD / asthma
  • Reduced breathing effort – drug effects (e.g. opiates) / brain stem lesion / extreme obesity
  • A decrease in the area of the lung available for gas exchange –  chronic bronchitis
  • Neuromuscular problems – Guillain-Barré syndrome / Motor neuron disease
  • Deformity –  Ankylosing spondylitis / Flail chest

Scenario 2

A 17 year old patient presents to A&E complaining of a tight feeling in their chest, shortness of breath, 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 whilst they’re breathing room air and the results are shown below…

  • PaO2: 14 (11-13 kPa)
  • pH: 7.49 (7.35 – 7.45)
  • PaCO2: 3.2 (4.7-6.0 kPa)
  • HCO3: 22 (22-26 mEg/L)
  • BE: +2 (-2 to +2)
What does the ABG show?

Oxygenation (PaO2)

A PaO2 of 14 on air is at the upper limit of normal, so the patient is not hypoxic.

pH

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 the alkalosis (e.g. ↓ CO2).

PaCO2

The CO2 is low, which would be in keeping with an alkalosis, so we now know the respiratory system is contributing to the alkalosis and is likely 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-

HCO3- is normal, ruling out a mixed respiratory and metabolic alkalosis, leaving us with an isolated respiratory alkalosis.

Base excess 

Base excess is normal, suggesting there has been no addition of bicarbonate to cause the alkalosis, ruling out the metabolic system as the cause.

Compensation

The bicarbonate is on the low end of normal, but this does not represent compensation. Compensation would involve a much more significant reduction in HCO3.

Summary

Respiratory alkalosis 

Respiratory alkalosis occurs as a result of increased ventilation which can be caused by any of the following:

  • Anxiety – often referred to as a panic attack
  • Pain – causing increased respiratory rate
  • Hypoxia – often seen in ascent to altitude 
  • Pulmonary embolism
  • Pneumothorax
  • Iatrogenic (excessive mechanical ventilation)

The history of a healthy young person hyperventilating with peripheral and peri-oral tingling would be fairly typical of a panic attack (anxiety).

How does hyperventilation lead to perioral and peripheral paresthesia?

As blood plasma becomes more alkalotic, the concentration of freely ionized calcium, the biologically active component of blood calcium, decreases (hypocalcaemia).

Because a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total serum calcium leading to hypocalcaemia.

This hypocalcaemia related to alkalosis is responsible for the paraesthesia often seen with hyperventilation.

Scenario 3

An 48 year old male has been admitted with a 24hr history of abdominal distention and profuse vomiting. A CT scan reveals a large mass causing bowel obstruction. As part of the patient’s assessment the surgical registrar requested that you check his blood gas (on air), with the results shown below…

  • PaO2: 12.7 (11-13 kPa)
  • pH: 7.50 (7.35 – 7.45)
  • PaCO2: 5.5 (4.7-6.0 kPa)
  • HCO3-: 29 (22-26 mEg/L)
  • BE: +3 (-2 to +2)
What does the ABG show?

Oxygenation (PaO2)

A PaO2 of 12.7 on air is normal, so the patient is not hypoxic.

pH

A pH of 7.50 is higher than normal and therefore the patient is alkalotic. The next step is to figure out whether the respiratory system is contributing the the alkalosis (e.g. ↓ CO2).

PaCO2

The CO2 is normal, which is not in keeping with an alkalosis, so we now know the respiratory system is not the cause of this derangement. The next step is to look at the HCO3- and see if it explains the alkalosis.

HCO3

HCO3 is high, which is in keeping with a metabolic alkalosis.

Base excess 

Base excess is increased, in keeping with an excess of HCO3.

Compensation

The respiratory system can attempt to compensate for a metabolic alkalosis by increasing PaCO2 (decreasing ventilation), but in the short term the respiratory system will likely maintain PaCO2 within the normal range.  If the metabolic alkalosis persists however you would expect the PaCO2 to rise and compensate for the metabolic alkalosis, as the respiratory centre becomes progressively desensitized to the increasing levels of PaCO2.

Summary

Metabolic alkalosis

Based upon the history provided, what might have led to this derangement?

Explanation

As a result of this patient’s profuse vomiting, they have lost significant amounts of HCL (e.g. stomach acid). This results in a net loss of H+ ions, meaning less H+ to bind to HCO3 and therefore more free HCO3 in the system. In addition, as a result of vomiting the patient is volume depleted, which results in release of aldosterone and other mineralocorticoids which in turn increase HCO3 reabsorption by the kidneys, further increasing the amount of free HCO3 in the serum.

Scenario 4

You’re asked to review a 59 year old female who has been admitted the acute medical ward of your hospital. The nurse tells you that she appears short of breath despite currently receiving 3 litres of oxygen via nasal cannulae. You take an arterial blood gas with the patient on oxygen and the results are shown below…

  • PaO2: 9.1 (11-13 kPa)
  • pH: 7.30 (7.35 – 7.45)
  • PaCO2: 8.4 (4.7-6.0 kPa)
  • HCO3-: 29 (22-26 mEg/L)
  • BE: +4 (-2 to +2)
What does the ABG show?

Oxygenation (PaO2)

A PaO2 of 9.1 is low, confirming that the patient is hypoxic. It is important to recognise that this PaO2 is much lower than you would expect for a patient on 3L of oxygen.  An oxygen flow rate of 3L via nasal cannulae would be expected to deliver an inspired concentration (FiO2) of around 32%, therefore you would expect that the PaO2 would be approximately 10 kPa less than this (e.g. 22 kPa).  A PaO2 of 9.1 kPa is therefore grossly abnormal and indicates significant hypoxia.

pH

A pH of 7.30 is lower than normal and therefore the patient is acidotic. The next step is to figure out whether the respiratory system is contributing the the acidosis (e.g. ↑ CO2).

PaCO2

The CO2 is raised significantly, which is in keeping with an acidosis (and also type 2 respiratory failure), so we now know the respiratory system is likely the cause of this derangement (or at least a contributor). The next step is to look at the HCO3- and see if it is contributing to the acidosis.

HCO3-

HCO3- is high, which is not in keeping with an acidosis, so the metabolic system is not contributing to the acidosis.  In fact the raised HCO3 is compensating for the low pH.

Base excess 

Base excess is increased, in keeping with an excess of HCO3.

Compensation

There is evidence of metabolic compensation, as the HCO3 is raised significantly.

Summary

Respiratory acidosis with metabolic compensation

Does this blood gas suggest an acute or chronic derangement in CO2? How have you come to this conclusion?

Explanation

This patient has COPD and has a chronically elevated level of CO2. As a result the metabolic system has had time to compensate via the generation and retention of HCO3 to oppose further decreases in pH. This explains why the pH is only slightly acidotic, despite a significantly raised PaCO2. If this derangement in CO2 was acute, there would not have been time for a compensatory response from the metabolic system.

Scenario 5

An 89 year old patient presents with fever, rigors, hypotension and reduced urine output. They appear confused and are unable to provide any meaningful history. The care home that the patient came from has provided some basic documentation. You look through the information available and note that the district nurse changed this patient’s catheter 24 hours ago.  The medical registrar commences antibiotics, aggressive fluid resuscitation and asks you to perform an arterial blood gas, the results of which are shown below. The patient was not on oxygen at the time of the ABG.

  • PaO2: 12.4 (11-13 kPa)
  • pH: 7.29 (7.35 – 7.45)
  • PaCO2: 5.5 (4.7-6.0 kPa)
  • HCO3-: 15 (22-26 mEg/L)
  • BE: – 4 (-2 to +2)
What does the ABG show?

Oxygenation (PaO2)

A PaO2 of 12.4 is normal, ruling out hypoxia as a cause for the patient’s confusion.

pH

A pH of 7.29 is abnormally low and therefore the patient is severely acidotic. The next step is to figure out whether the respiratory system is contributing the the acidosis (e.g. ↑ CO2).

PaCO2

The CO2 is normal and therefore the respiratory system doesn’t appear to be contributing to the acidosis. The next step is to look at the HCO3- and see if it is contributing to the acidosis.

HCO3

HCO3 is low, which is in keeping with an acidosis, so the metabolic system is the cause of this patient’s acidosis.

Base excess 

Base excess is low, in keeping with a metabolic acidosis.

Compensation

There is no evidence of respiratory compensation for this metabolic acidosis (e.g. ↓CO2).

Summary

Metabolic acidosis

What is the likely diagnosis, given the patient's history?

Sepsis – likely urinary given the history of recent catheter change

How has this illness led to the ABG derangement?

Explanation

This patient has presented profoundly septic, with fever, hypotension and evidence of reduced end organ perfusion (reduced urine output).  Reduced end organ perfusion causes tissue hypoxia resulting in cells undergoing anaerobic respiration to generate energy. Anaerobic respiration produces lactic acid as a byproduct, which has resulted in the addition of acid to the patient’s serum causing a lactic acidosis.

Scenario 6

A 22 year old female is brought into A&E by ambulance with a 5 day history of vomiting and lethargy. When you begin to talk with the patient you note that she appears disorientated and looks clinically dry. At present you are unable to gain any further details, but the patient looks very unwell from the end of the bed. You gain IV access, send off a routine panel of bloods and commence some fluids.  You ask the nurse to check the patient’s observations and she notes an increased respiratory rate, low blood pressure and tachycardia. You perform an ABG on advice of your registrar.  The results of the ABG are shown below (patient not on oxygen).

  • PaO2: 13 (11-13 kPa)
  • pH: 7.3 (7.35 – 7.45)
  • PaCO2: 4.1 (4.7-6.0 kPa)
  • HCO3-: 13 (22-26 mEg/L)
  • BE: – 4 (-2 to +2)
What does the ABG show?

Oxygenation (PaO2)

A PaO2 of 13 is normal, ruling out hypoxia as a cause for the patient’s confusion.

pH

A pH of 7.3 is abnormally low and therefore the patient is acidotic. The next step is to figure out whether the respiratory system is contributing the the acidosis (e.g. ↑ CO2).

PaCO2

The CO2 is actually low and therefore the respiratory system doesn’t appear to be contributing to the acidosis. The next step is to look at the HCO3 and see if it is contributing to the acidosis.

HCO3

HCO3 is low, which is in keeping with an acidosis, so the metabolic system is the cause of this patient’s acidosis.

Base excess 

Base excess is low, in keeping with a metabolic acidosis.

Compensation

There is evidence of respiratory compensation for this metabolic acidosis (e.g. ↓CO2).

Summary

Metabolic acidosis with respiratory compensation

What other bedside investigations might be useful in narrowing the differential diagnosis?

Capillary blood glucose – 32 mmol/L

Urine dipstick – Glucose +++ Ketones +++

How has this illness led to the ABG derangement?

Explanation

Diabetic ketoacidosis arises because of a lack of insulin in the body. The lack of insulin and corresponding elevation of glucagon leads to increased release of glucose by the liver, but an inability for cells to utilise the glucose.  High serum glucose levels result in increased urinary excretion of glucose, taking water and solutes along with it in a process known as osmotic diuresis. This leads to polyuria, dehydration and polydipsia.  The absence of insulin also leads to the release of free fatty acids from adipose tissue (lipolysis) as the body needs to generate energy from a source other than glucose. These fatty acids are converted into ketone bodies to be used as an energy source.  The ketone bodies cause the blood to become more acidic (metabolic acidosis).   The body attempts to compensate for the metabolic acidosis by hyperventilating to blow off CO2 and thereby increase pH.  This hyperventilation, in its extreme form, may be observed as Kussmaul respiration.

Comments and suggestions