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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)
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 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. 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 CO2 (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

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:

  • 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.

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 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 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)
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. ↓CO2).

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.


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. ↓CO2).

Summary

Metabolic acidosis with respiratory compensation

Capillary blood glucose – 32 mmol/L

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 PaO2 is low we can say this gentleman has type 2 respiratory failure (low PaO2 and raised PaCO2)

The next step is to look at the HCO3.

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: (-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 HCO3.

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 PaCO2 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 HCO3.

HCO3

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 O2, 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 PaCO2 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 HCO3.

HCO3

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

Base Excess 

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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