Why is there a difference between end tidal CO2 and PaCO2?

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In this episode we talk about this very common phenomenon in anaesthesia, the difference between ETCO2 and PaCO2.
Essentially this all comes down to patient and equipment factors.
BUT the essential element that makes the largest difference is DEAD SPACE.
we discuss the factors effecting it, and the Bohr equation that measures dead space.
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Опубликовано:

8 июл 2024

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Комментарии : 5

@shadow32j 2 года назад

interesting conversation! :)

@suggar46 2 года назад

I have more trouble trying to understand why some patients have higher eTCO2 than PaCo2. Can you comment on it?

@ABCsofAnaesthesia 2 года назад

great question! this article is probably most comprehensive : www.ncbi.nlm.nih.gov/pmc/articles/PMC5330081/#:~:text=Sir%2C,accurately%20reflect%20the%20PaCO2. The PaCO2 - EtCO2 gradient is largely dependent on the physiological dead space and the slope of the alveolar plateau in phase 3 of the capnograph. An increase in the dead space can result in an increase in the gradient. Negative PaCO2 - EtCO2 values were first observed during anaesthesia more than 50 years ago by Nunn and Hill. Reversal of the gradient can be seen normally in 50% of infants, pregnant, and obese patients. Other causes are mechanical ventilation with large tidal volumes and low frequency, increased cardiac output and CO2 production, low functional residual capacity (FRC) and total lung compliance.[1] Thoracoscopy involves CO2 insufflation in the thorax for better visualisation and access. If there is a preexisting communication between the pleura and the bronchial tree, there can be direct absorption of CO2 and falsely high EtCO2 readings.[2] This can lead to negative PaCO2 - EtCO2 gradient where PaCO2 may be only mildly elevated. There are reported cases of negative arterial to end-tidal gradient in cases of malignant hyperthermia (MH).[1,3] The PCO2 of most alveolar gas is less than PaCO2, but in the terminal part of the expirate, the alveolar PCO2 may increase rapidly towards mixed venous PCO2 and exceeds PaCO2 in the presence of MH because a large amount of CO2 is discharged into the lungs.[3] In our case, the reasons could be multiple, i.e., bronchopleural communication, and low FRC under anaesthesia. In addition, the presence of subcutaneous emphysema suggests extensive CO2 tracking and absorption contributing to the hypercarbia.[4] CO2 desufflation and resumption of two lung ventilation led to the normalisation of EtCO2 without any deleterious effects.