ABG Quiz

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Posted by Paula Zaininger , Dr Lewis Potter and Dr Michael Mackay | Data Interpretation , Laboratory Tests , Quiz , Respiratory
June 27, 2016

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This article provides a collection of different ABG interpretation scenarios for you to work
through.

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If you need a refresher on ABG interpretation then make sure to check out our guide.

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 10L of oxygen via a mask. You perform an
ABG and receive the following results…

PaO2: 7.0 (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)

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Oxygenation (PaO2)

The PaO2 is low, so we know the patient is in respiratory failure, however, we don’t yet know
what type.

pH

You should then note that the pH reveals an acidosis and look at the CO 2 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. In the
context of low PaO2, a raised PaCO2 suggests the patient type 2 respiratory failure.

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 (BE)

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

The respiratory acidosis has been caused by type 2 respiratory failure (a failure of
ventilation) leading to increased levels of CO 2 (hypercapnia).

Confusion
Reduced consciousness level
Asterixis
Bounding pulse

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
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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)

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 to 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:
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 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).

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
A 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)

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 to 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.
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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

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 the 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)

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

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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 to 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

Explanation

This patient has COPD and has a chronically elevated level of CO 2. 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

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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)

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 to 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. ↓CO 2).

Summary

Metabolic acidosis
Sepsis – likely urinary given the history of recent catheter change

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.

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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 the 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)

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 to 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. ↓CO 2).

Summary

Metabolic acidosis with respiratory compensation

Capillary blood glucose – 32 mmol/L
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Urine dipstick – Glucose +++ Ketones +++

Diabetic ketoacidosis (DKA)

Explanation

Diabetic ketoacidosis arises because of a lack of insulin in the body. The lack of insulin and a
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.

Scenario 7
A 56-year-old man was found unconscious at home with a respiratory rate of 6 breaths per
minute and pinprick pupils. An ambulance was called and the paramedics administered
some naloxone. On arrival to A&E his ABG showed the following (not on oxygen at the time
of the ABG):

PaO2: 7.9 (11-13 kPa)

pH: 7.31 (7.35 – 7.45)
PaCO2: 7.1 (4.7-6.0 kPa)
HCO3-: 22 (22-26 mEg/L)
BE: +1 (-2 to +2)

Oxygenation (PaO2)

A PaO2 of 7.9 is low, so we know the patient is in respiratory failure, but we need to know the
CO2 before we can say which type of respiratory failure.

pH

A pH of 7.31 is abnormally low and therefore the patient is acidotic. The next step is to
figure out whether the respiratory system is contributing to the acidosis (e.g. ↑ CO2).

PaCO2

The PaCO2 is high and therefore the respiratory system is contributing to the acidosis.

Given the PaO 2 is low we can say this gentleman has type 2 respiratory failure (low PaO 2 and
raised PaCO2)

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The next step is to look at the HCO 3.

HCO3–

HCO3– is within normal range. Given the relatively fast onset of symptoms, there would not
have been time for metabolic compensation.

Base Excess

Base excess is within normal range. Again, there is no metabolic compensation.

Summary
Respiratory acidosis with type 2 respiratory failure.

The history suggests this man has taken an overdose of opioids given the reduced level of
consciousness, respiratory depression and pinpoint pupils. The respiratory depression has
led to hypoxia, hypercapnia and ultimately a respiratory acidosis.

Scenario 8
A 77-year-old lady was admitted to hospital 10 days ago with a fractured neck of femur. The
orthopaedic team repaired the fracture and she has been an inpatient on the orthopaedic
ward recovering ever since. Her nurse is becoming increasingly worried about her as her
oxygen requirement is increasing (she is now on 3L), her respiratory rate is 35 breaths per
minute and she is complaining of calf pain and feeling very short of breath. You review her
and do an ABG which shows the following:

PaO2: 6 (11-13 kPa)

pH: 7.51 (7.35 – 7.45)
PaCO2: 3.1 (4.7-6.0 kPa)
HCO3-: 21 (22-26 mEg/L)
BE: 0 (-2 to +2)

Oxygenation (PaO2)

3 litres of oxygen is equivalent to 32%, we would therefore expect a PaO2 of approximately

22 kPa for a patient on this level of oxygen. A PaO2 of 6 kPa is therefore very low.

pH

A pH of 7.51 is abnormally high and therefore the patient is alkalotic. The next step is to
figure out whether the respiratory system is contributing to the acidosis (e.g. ↓ CO2).

PaCO2

The PaCO2 is low and therefore the respiratory system is contributing to the alkalosis.

The next step is to look at the HCO 3.

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HCO3–

HCO3– is within the normal range, so the metabolic system is not contributing to the alkalosis
and also isn’t compensating for it.

Base Excess

Base excess is within normal range. Again, there is no metabolic compensation.

Summary
Respiratory alkalosis and type 1 respiratory failure.

From the clinical history, this patient may have a deep vein thrombosis and a secondary
pulmonary embolus. This caused the patient to feel breathless and need an increased
amount of oxygen to maintain saturations. The patient is likely hyperventilating to maintain
her oxygen saturations, but as a result is exhaling excessive amounts of CO2, leading to
alkalosis.

Scenario 9
A 24-year-old medical student has just returned from his elective in Ghana. In the last few
days, he has developed severe diarrhoea and has now presented to A&E. On assessment, he
is very dehydrated and tachypnoeic. An ABG is performed showing the following:

PaO2: 14.6 (11-13 kPa)

pH: 7.32 (7.35 – 7.45)
PaCO2: 4.0 (4.7-6.0 kPa)
HCO3-: 13 (22-26 mEg/L)
BE: -4 (-2 to +2)

Oxygenation (PaO2)

A PaO2 of 14.6 is high, this is likely due to hyperventilation.

pH

A pH of 7.32 is low, suggesting this gentleman is acidotic. We now need to look at the PaCO 2
to assess if this is contributing (e.g. ↑CO2).

PaCO2

The PaCO2 is low and therefore the respiratory system is not contributing to the acidosis. In
fact, with this low CO2 we could expect an alkalosis, so we need to consider if this is an
attempt by the respiratory system to compensate for a metabolic acidosis.

The next step is to look at the HCO 3.

HCO3–
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HCO3– is low, which is in keeping with our suspicion of a metabolic acidosis.

Base Excess

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

Summary
Metabolic acidosis with respiratory compensation.

The patient is losing HCO3– through the gastrointestinal tract as a result of the diarrhoea,
leading to a metabolic acidosis. The respiratory system is attempting to compensate by
‘blowing off’ carbon dioxide to create a respiratory alkalosis in an attempt to neutralise the
acidosis and bring the pH back into normal range.

Scenario 10
A 64-year-old man is admitted to A&E with central crushing chest pain. As the nurses are
getting him attached to the ECG he has a cardiac arrest. Thankfully CPR was started
immediately and after 6 minutes he regained spontaneous circulation and began breathing
again. An ABG (on 15L O2) following this sequence of events showed the following:

PaO2: 9.5 (11-13 kPa)

pH: 7.14 (7.35 – 7.45)
PaCO2: 8.1 (4.7-6.0 kPa)
HCO3-: 15.2 (22-26 mEg/L)
BE: – 9.7 (-2 to +2)

Oxygenation (PaO2)

A PaO2 of 9.5 is very low, particularly in the context of 15L O 2, this suggests the presence of
impaired ventilation, likely secondary to the cardiac arrest.

pH

A pH of 7.14 is low, suggesting this gentleman is acidotic. We now need to look at the PaCO 2
to assess if this is contributing (e.g. ↑CO2).

PaCO2

PaCO2 is high, in keeping with type 2 respiratory failure and also in keeping with a respiratory
acidosis. This is again likely secondary to impaired ventilation.

The next step is to look at the HCO 3.

HCO3

HCO3– is low, suggesting that the metabolic system is also contributing to the acidosis.

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

Summary
Mixed respiratory and metabolic acidosis.

This patient had a cardiac arrest which meant there was a period of impaired ventilation and
end-organ perfusion. These led to hypercapnia causing a respiratory acidosis, in addition to
the accumulation of products of anaerobic respiration (as a result of hypoxia and reduced
end-organ perfusion) causing metabolic acidosis.

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