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Respiratory failure

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Introduction to respiratory failure

For medical students, ICU nurses and junior ICU trainees

Click here to download the accompanying Powerpoint tutorial with English narration

Charles Gomersall, Gavin Joynt, Sarah Ramsay


  • acute respiratory failure occurs when the pulmonary system is no longer able to meet the metabolic demands of the body
  • hypoxaemic respiratory failure: arterial partial pressure of oxygen (PaO2) less than or equal to 6.7 kPa when breathing room air
  • hypercapnic respiratory failure: arterial partial pressure of carbon dioxide (PaCO2) more than or equal to 6.7 kPa

Basic respiratory physiology

The major function of the lung is to get oxygen into the body and carbon dioxide out.

Gas exchange requires a pressure gradient between alveolar air and blood, a short distance for diffusion of gases and intervening tissues which are permeable to oxygen and carbon dioxide

Getting oxygen in

  • the alveolar partial pressure of oxygen (PAO2) is dependent on the total alveolar pressure and the partial pressures of the other gases in the alveolus
    • the sum of the partial pressures of all the gases is equal to the total alveolar pressure
    • partial pressure of each gas in a mixture of gases is directly related to the proportions in which they are present

    • therefore partial pressure of oxygen can be increased by:
      • increasing alveolar pressure or
      • increasing the proportion of oxygen in the mixture
    • increasing the inspired oxygen concentration increases the proportion of oxygen in alveolar gas while reducing the proportion of nitrogen
    • the alveolar partial pressure of water vapour remains largely constant and therefore does not contribute to changes in PAO2. The proportion of carbon dioxide in alveolar gas does, however, change and therefore factors which affect PACO2 also affect PAO2
    • as carbon dioxide passes into the alveolus and oxygen passes into the blood the PACO2 rises and the PAO2 falls. Ventilation is required replenish the alveolar gas with fresh gas.
    • thus the factors that result in changes in PAO2 are:
      • PACO2
      • alveolar pressure
      • inspired oxygen concentration
      • ventilation

Getting carbon dioxide out

  • CO2 elimination is largely dependent on alveolar ventilation (CO2 crosses the alveolar membrane very readily and so diffusion abnormalities and shunting (see below) have little effect on CO2 elimination).
  • Alveolar ventilation = Respiratory rate x (tidal volume-dead space)
  • Anatomical dead space is constant but physiological dead space depends on the relationship between ventilation and perfusion.
  • Therefore changes in PACO2 are dependent on:
    • respiratory rate
    • tidal volume
    • ventilation-perfusion matching

Pathophysiological mechanisms

The most common cause for hypoxaemic respiratory failure in ICU patients is perfusion of non-ventilated alveoli (shunting).


  • form of ventilation-perfusion mismatch in which alveoli which are not ventilated (eg due to collapse or pus or oedema fluid) but are still perfused. As a result blood traversing these alveoli is not oxygenated. The animation shows an alveolus with normal ventilation and perfusion and an alveolus in which shunting is occurring.

  • this form of respiratory failure is relatively resistant to oxygen therapy. Increasing the inspired oxygen concentration has little effect because it can not reach alveoli where shunting is occurring and blood leaving normal alveoli is already 100% saturated
  • commonest cause of hypoxaemic respiratory failure in critically ill patients
  • hypoxic pulmonary vasoconstriction reduces the blood flow to non-ventilated alveoli and reduces the severity of the hypoxaemia
  • causes of shunting:
    • intracardiac
      • any cause of a right to left shunt eg Fallot's tetralogy, Eisenmenger's syndrome
    • pulmonary
      • pneumonia
      • pulmonary oedema
      • atelectasis
      • collapse
      • pulmonary haemorrhage
      • pulmonary contusion

Ventilation without perfusion

  • this is the opposite extreme of ventilation-perfusion mismatch
  • gas passes in and out of the alveoli but no gas exchange occurs because the alveoli are not perfused. and the ventilation is ineffective. In this respect these alveoli are behaving like other parts of the lung that are ventilated but do not take part in gas exchange (eg the major airways) and these alveoli therefore make up what is called physiological dead space
  • unless the patient is able to compensate for it the reduction in effective ventilation results in an increase in PaCO2.
  • causes include:
    • low cardiac output
    • high intra-alveolar pressure leading to compression or stretching of alveolar capillary (mechanically ventilated patients)

Diffusion abnormality

  • less common
  • may be due to an abnormality of the alveolar membrane or a reduction in the number of alveoli resulting in a reduction in alveolar surface area
  • causes include:
    • Acute Respiratory Distress Syndrome
    • fibrotic lung disease

Alveolar hypoventilation

  • as carbon dioxide passes into the alveolus and oxygen passes into the blood the pressure gradients between alveolar gas and blood are gradually reduced. Ventilation is required to restore the pressure gradients
  • hypoventilation is marked by a rise in PaCO2 and a fall in PaO2

  • Causes of hypoventilation
    • Brainstem
      • brainstem injury due to trauma, haemorrhage, infarction, hypoxia, infection etc
      • metabolic encephalopathy
      • depressant drugs
    • Spinal cord
      • trauma, tumour, transverse myelitis
    • Nerve root injury
    • Nerve
      • trauma
      • neuropathy eg Guillain Barre
      • motor neuron disease
    • Neuromuscular junction
      • myasthenia gravis
      • neuromuscular blockers
    • Respiratory muscles
      • fatigue
      • disuse atrophy
      • myopathy
      • malnutrition
    • Respiratory system
      • airway obstruction (upper or lower)
      • decreased lung, pleural or chest wall compliance

Respiratory monitoring


The signs of respiratory failure are signs of respiratory compensation, increased sympathetic tone, end-organ hypoxia, haemoglobin desaturation

Signs of respiratory compensation

  • tachypnoea
    • tachypnoea is a very good indicator of a severely ill patient
  • use of accessory muscles
  • nasal flaring
  • intercostal, suprasternal or supraclavicular recession

Increased sympathetic tone

  • tachycardia
  • hypertension
  • sweating

End-organ hypoxia

  • altered mental status
  • bradycardia and hypotension (late signs)

Haemoglobin desaturation

  • cyanosis

Pulse oximetry

  • estimates arterial saturation not PaO2 using absorption of two different wavelengths of infrared light
  • the relationship between saturation and PaO2 is described by the oxyhaemoglobin dissociation curve

  • a pulse oximetry saturation (SpO2) ~90% is a critical threshold. Below this level a small fall in PaO2 produces a sharp fall in SpO2
  • sources of error
    • poor peripheral perfusion. This will often lead to a discrepancy between the heart rate displayed by the pulse oximeter and the heart rate measured by other means (eg ECG). Look for any discrepancy when assessing the SpO2
    • dark skin (oximeter over-reads slightly)
    • false nails or nail varnish
    • lipaemia
      • hyperlipidaemia
      • lipid infusion for TPN
      • propofol infusion
    • bright ambient light
    • poorly adherent probe
    • excessive motion
    • carboxyhaemoglobin (SpO2 > SaO2)

Arterial blood gases

This topic will be covered on a separate web page



©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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