What is meant by the term ‘respiratory failure’?

Respiratory failure occurs when the respiratory system fails in one or both of its main functions; namely, the oxygenation of blood and the elimination of CO₂. Respiratory failure is categorised as ‘type 1’ or ‘type 2’ on the basis of blood gas analysis:

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  Type 1 respiratory failure is defined as a P_aO₂ < 8.0 kPa with a normal or low P_aCO₂.

  
  
• 
  

  Type 2 respiratory failure is defined as a P_aO₂ < 8.0 kPa with a raised P_aCO₂ > 6.0 kPa.

What is the difference between oxygenation and ventilation?

The respiratory system can be considered as two parts: a gas-exchange system and a ‘bellows’.

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  The gas-exchange system is made up of:

  
  
  
  
  1. 
     

     – Alveolar–capillary units;

     
     
  2. 
     

     – Pulmonary circulation.

  The gas-exchange system is responsible for oxygenation; deficiency leads to hypoxaemia and type 1 respiratory failure.
  
  
  
• 
  

  The bellows system is made up of:

  
  
  
  
  1. 
     

     – Chest wall and pleura;

     
     
  2. 
     

     – Respiratory muscles;

     
     
  3. 
     

     – Airways;

     
     
  4. 
     

     – Nerves;

     
     
  5. 
     

     – Respiratory centre.

  The bellows system is responsible for ventilation: moving air from the atmosphere to the alveoli on inspiration and from the alveoli to the atmosphere on expiration.
  

Importantly, V̇_A facilitates the diffusion of CO₂ from the pulmonary capillaries to the alveoli: V̇_A (and not V̇_E) is inversely proportional to P_aCO₂ (see Chapter 11). Failure of alveolar ventilation leads to increased P_aCO₂; that is, type 2 respiratory failure.

Which pathophysiological processes cause type 2 respiratory failure?

Normally, ventilation is controlled by a negative-feedback mechanism:

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  A rise in P_aCO₂ stimulates the respiratory centre in the medulla oblongata via the peripheral and central chemoreceptors (see Chapter 22).

  
  
• 
  

  The respiratory centre sends excitatory impulses to the respiratory muscles to increase the rate and depth of inspiration. V̇_E and V̇_A both increase.

  
  
• 
  

  Owing to the inverse relationship between P_aCO₂ and V̇_A, P_aCO₂ decreases.

In health, this system is very sensitive: P_aCO₂ is kept within tight limits. If P_aCO₂ rises above 6 kPa, V̇_A must be inadequate and one of the components of ventilation must be malfunctioning:

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  Failure of the respiratory centre to respond appropriately. This may be due to:

  
  
  
  
  1. 
     

     – Respiratory centre depression by opioids or general anaesthesia;

     
     
  2. 
     

     – Reflex desensitisation of the respiratory centre to high P_aCO₂ in order to prevent respiratory muscle fatigue.

  
  
  
  
• 
  

  A problem with chest wall movement. This could be:

  
  
  
  
  1. 
     

     – Mechanical; for example, flail chest;

     
     
  2. 
     

     – Neuropathic; for example, Guillain–Barré syndrome;

     
     
  3. 
     

     – Muscular; for example, myopathies.

  
  
  
  
• 
  

  Respiratory muscle fatigue. Fatigue occurs when the respiratory muscles cannot synthesise sufficient ATP to meet the demands of muscle contraction despite an intact respiratory drive and chest wall.