Explain the potential causes of a difference between the measured end tidal CO2 and
the arterial partial pressure of CO2.
Many candidates didn’t distinguish between the different types of dead space. In general this topic was not well understood.
Among the possible college comments to an SAQ, none can be less productive than "in general this topic was not well understood", as one can easily establish that independently from the observation that the pass rate was 30%. Fortunately, this SAQ is identical to Question 3 from the second paper of 2018 and Question 9 from the first paper of 2009, both of which had some productive comments from the examiners.
- 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
- Anatomical 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.
Satoh, Kenichi, et al. "Evaluation of differences between PaCO2 and ETCO2 by Age as measured during general anesthesia with patients in a supine position." Journal of Anesthesiology 2015 (2015).
Nunn, J. F., and D. W. Hill. "Respiratory dead space and arterial to end-tidal CO2 tension difference in anesthetized man." Journal of Applied Physiology 15.3 (1960): 383-389.
Shankar, Kodali Bhavani, et al. "Arterial to end tidal carbon dioxide tension difference during caesarean section anaesthesia." Anaesthesia 41.7 (1986): 698-702.
Fletcher, R., and B. Jonson. "Deadspace and the single breath test for carbon dioxide during anaesthesia and artificial ventilation: effects of tidal volume and frequency of respiration." British journal of anaesthesia 56.2 (1984): 109-119.
Donnellan, Michael E. "Capnography: Gradient PACO2 and PETCO2." Applied Technologies in Pulmonary Medicine. Karger Publishers, 2011. 126-131.
Kodali, Bhavani Shankar. "Capnography outside the operating rooms." Anesthesiology: The Journal of the American Society of Anesthesiologists 118.1 (2013): 192-201.