Wasted Ventilation


  • Clearance of carbon dioxide is determined by the alveolar ventilation and the physiologic dead space.

Residents frequently ask me: "why is this patient's PaCO2 (partial pressure of Carbon Dioxide in the blood) so high when he has a minute ventilation of 30 liters per minute?"

This is a common trap to fall into: confusing alveolar ventilation (which is difficult to measure) with minute ventilation (which is always measured). The difference between the two is determined by the anatomical dead space.

Two patients have a minute ventilation of 10 liters/minute:

  • Patient A is taking 50 breaths of 200ml tidal volume.

  • Patient B is taking 20 breaths of 500ml tidal volume.

Using misplaced logic one would think that each would have the same PaCO2. In fact patient B has a significant respiratory acidosis, and patient A has a normal blood gas.

Anatomical dead space is approximately 150ml in an adult male. It is important to calculate out the dead-space (Vd/Vt) to tidal volume ratio for each patient: patient A has a Vd/Vt of less than 30% (normal is 30%). Patient B has a Vd/Vt of 75%.
What does this mean?
In the case of patient B, 75% of his respiratory effort is being wasted, leading to severe muscular fatigue and acidosis.

It is also important to realize that patients may have large amounts of  alveolar dead space: a patient can be receiving tidal volumes of 500ml and still have a dead space ratio of 75%: how?
Alveolar dead space is caused by increased volume of zone 1 (zone 1 is where alveolar pressure exceeds the perfusion pressure to the lung unit: alveoli are ventilated but not perfused):

  1. Hypoperfusion - low pulmonary blood volume-pressure leads to underperfusion of non dependent lung segments.

  2. Overdistension of compliant lung units: often caused by excessive PEEP.

Dead space is calculated by measuring the ratio of end tidal CO2 (etCO2) to arterial CO2 (PaCO2), using the equation:

Vd/Vt = PaCO2 - PetCO2/PaCO2

It is important that you are aware of physiologic dead space (anatomical dead space plus alveolar dead space) in the modern setting of low tidal volume ventilation for acute lung injury (click here). Using tidal volumes of 4 - 5ml/kg in patients with significant atelectasis leads to considerable wasted ventilation: as a result a much higher respiratory rate than normal is required (25 to 30, frequently more) to control PaCO2. This frequently leads to problems with auto-PEEP (click here). We know that permissive hypercapnia (click here) is associated with few complications, so most physicians elect to allow the PaCO2to climb rather than compromising oxygenation.


Copyright Patrick Neligan 2002