Topic Progress:

Clinical Case

Based on the information gathered so far, you know your patient’s lung mechanics are as follow:

However, 4h post-admission to ICU, you are called by the bedside as your colleague is concerned…


Given that the FiO2 is already maximally increased, our aim should be to recruit further alveoli for gas exchange by increasing the mean airway pressure (termed ‘MAP’ below). 

Walk through the break-down tree to figure out how!





pressure for
each breath


  1. Increases the mean pressure during the overall respiratory cycle (in some modes, it may not increase the inspiratory pressure)
  2. May improve oxygenation by recruiting collapsed alveoli and decreasing shunt

Increasing inspiratory pressures should only be required when it is is felt that the patient is hypoxic because of hypoventation. This is uncommon if the ventilator has been set appropriately.

More commonly, inspiratory pressures and tidal volumes require manipulation for CO2 clearance rather than hypoxia.

Increases to inspiratory pressures and tidal volumes must be done carefully, as this has the potential to induce barotrauma and lung injury.

  1. Proportionally increases the amount of time at higher pressure
  2. Increases the mean pressure without increasing the peak pressure
  3. Potential issues:
    • Alters the I:E ratio  (shorter expiration) which may result in gas trapping
    • May be uncomfortable for an alert patient

Increasing PEEP seems like a good idea since it will hopefully open and recruit some of the collapsed lung parenchyma seen on the X-Ray and reduce shunt. With more open alveoli, you might even see an improvement in compliance!

Increasing TV (or Pinsp if you were in a PC mode) wouldn’t be ideal. You know that high volumes and high pressures can cause additional damage to an already injured lung and your patient is already at 500mL of TV which corresponds to almost 7mL/kg of ideal body weight. You decide not to touch the TV.

Your only other option is therefore to increase Ti. You decide to try it since the patient is now back on sedation and you don’t expect a recovery over night. But beware- given he is now a little wheezy, we would need to make sure his expiration is complete on the flow curve, and he isnt gas trapping.

Often, increasing problems with hypoxia would prompt a review of the ventilation mode. It might be more appropriate to move to a Pressure Controlled mode, such as PC AC at this point.


Continuing our scenario, lets say in this instance you stick with VC SIMV and you chose to try PEEP at 10cmH2O (from 5cmH2O) and Ti at 2.0s (from 1.7) to start, knowing you might need to adjust the settings again depending on the evolution overnight.

CO2 elimination

You conclude that he has acute respiratory acidosis.

Carbon dioxide removal is dependent on alveolar ventilation.

Alveolar ventilation = respiratory rate x (tidal volume – dead space)

Walk through the break-down tree to figure out how!





dead space

You may recall our discussion of dead space with regard to the ventilator circuit earlier.

  1. Dead space is the volume of gas in each breath that does not take part in gas exchange
  2. Physiologic or total dead space = anatomical dead space + alveolar dead space
    • Anatomical dead space is the gas within the trachea, bronchus, bronchioles and terminal bronchioles
      • In normal adults it is approximately 150mL
    • Alveolar dead space is the amount of gas in alveoli that are not being perfused
      • Occurs in PE, pulmonary haemorrhage and hypotension
  3. Circuit dead space contributes to anatomical dead space in ventilated patients
    • This includes anything beyond the Y connector in the circuit: gas in ETT, catheter mounts, HMEs and closed suction systems
    • This can become significant in paediatric patients or patients with low tidal volumes

Increasing RR seems easy and a logical physiologic response since your patient was breathing faster when he started breathing on his own earlier. However you remember to be prudent since increasing RR will further reduce time for expiration after increasing the Ti (for hypoxia) above.

Increasing TV (or Pinsp if you were in PC-AC) once again is not ideal. You know that high volumes and high pressures can cause additional damage to an already injured lung and your patient is already at 500mL of TV which corresponds to almost 7ml/kg of ideal body weight. You decide to try avoiding an increase in TV.

What about dead space? It is difficult to alter anatomical or alveolar dead space, but you could consider consider shortening the circuit beyond the Y-connector, though this is rarely required.

In summary, you chose to start by simply increasing RR to 18/min (instead of 12/min). This is usually enough to correct the acidosis. You order a gas to be drawn in 30 minutes to evaluate if your ventilator setting adjustment was sufficient.

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