College Answer

Points required to pass this question included the normal difference between end-tidal and
arterial partial pressure of C02 and the reasons for this. The patient factors that increase the
difference include increases in alveolar dead space and a slow rise of expired C02. Mention of
pathology e.g. pulmonary embolism and cardiac arrest gained extra marks. Equipment
factors needed to be included e.g. leaks, occlusion of sampling line. Candidates who failed
did not discuss alveolar dead space and very few adequately explained how it increased the
end tidal to arterial partial pressure difference.
There is an excellent graph of expired C02 in “Physiology for the Anaesthetist” by Power
and Kam which helps understand alveolar dead space.
.
Syllabus S2g B1g2
Reference: Power and Kam 1st edition p 84-88

Discussion

This question is virtually identical to Question 3 from the second paper of 2018 and Question 21 from the first paper of 2017. Interestingly, though the examiners here mention that "candidates who failed
did not discuss alveolar dead space", one must walk some sort of fine line here, because in 2018 "discussion of the various types of dead space did not score marks". 

• Normal PaCO₂-EtCO₂ difference = 2-5 mmHg  (Satoh et al, 2015)
• This is due to alveolar dead space, which is small in healthy adults
  • If there was no alveolar dead space, end-tidal CO₂ would be identical to alveolar CO₂
  • Alveoli which are ventilated but not perfused (i.e. alveolar dead space) contain a gas mixture which is identical to inspired gas
  • Thus, the addition of their content to expired gas dilutes the expired CO₂ concentration and decreases the end-tidal CO₂ value
  • Alveolar dead space does not contribute to the end-tidal CO₂ concentration because at the end of expiration all of the anatomical dead space volume has already emptied
• Factors which increase the PaCO₂-EtCO₂ difference include:
  • Changes in pulmonary perfusion
    • Regional decreases in pulmonary perfusion
      • Pulmonary embolism
      • Fat embolism
      • Air embolism
    • Globally reduced pulmonary perfusion:
      • Pulmonary hypertension
      • Cardiac failure (RHF)
      • Cardiac arrest
      • Extreme hypovolaemia (eg. haemorrhagic shock)
      • Very high PEEP or positive inspiratory pressure
  • Changes in ventilation
    • Increased V/Q mismatch or increased alveolar dead space
      • High PEEP or positive airway pressure
    • High FiO2 (causing shunt into poorly ventilated alveoli)
    • Oesophageal intubation
    • Very large shunt fraction (>30%)
  • Measurement error
    • The presence of helium can cause the EtCO2 measurement to be incorrectly elevated in some capnometers (i.e. those which use a reporting algorithm that assumes that the only gases present in the sample are those that the device is capable of measuring)
    • The presence of nitrous oxide can confuse some capnograph devices, and the N₂O may be misinterpreted as CO₂
    • The use of an inline HME filter can reduce the end-tidal CO₂ concentration.
    • The timing of the measurement may be wrong: the measurement is only valid if it is truly end-tidal, and so any scenario where the measurement is taken before the end of expiration would produce a falsely depressed value.