Kodali is in fact a prolific FOAM author and his website capnography. Back in those days, the college was somewhat undersubscribed with trainees, making them a valuable resource worth investing in; as such the examiner's comments are even furnished with a page reference to the aforementioned graph, something unthinkable in the modern era of disposable multitudes.
Thus, it is possible to track down the aforementioned excellent graph and reproduce it here with no permission whatsoever this version comes from the 3rd edition of the textbook, p. Without going into an excess of detail again , it will suffice to say that:. So, basically, it's all to do with dead space. Alveolar dead space in particular is what affects the end-tidal CO 2 measurement, which is taken at the end of expiration. By that stage, anatomical dead space has completely emptied, and is no longer contributing to the total expired CO 2 value.
One might correctly say that the anatomical dead space contributes to expired capno graphy , but not to end-tidal capno metry, as it affects the shape of the early capnography curve. The college felt strongly enough about this distinction to complain that "many incorrectly attributed anatomical dead space as a contributor to the PaCO 2 -ETCO 2 gradient" in their answer to Question 3 from the second paper of Interestingly, though dead space is the major reason for the PaCO 2 -EtCO 2 gap, according to the examiners "discussion of the various types of dead space did not score marks".
From the above, it follows that there is some normal value for the PaCO 2 -EtCO 2 gap, which would correlate to the volume of alveolar dead space normally, a very small volume in healthy adults. Most textbooks give a range of mmHg, usually without a reference. For some more detailed empirical data, Satoh et al measured this gap in a series of patients, all anaesthetised and supine, and of different ages. The authors found values of 2. The difference increases slightly with age, which the authors attributed to age-related decrease in FRC and increase in alveolar dead space.
The difference was not massive: in the original image below Satoh et al, , Figure 1 groups A to G are decades of age, starting with age As one can see, there was barely mmHg difference between the groups, and all groups up to the age of 76 had individuals with a 0mmHg gap i. There are multiple possible reasons for an increase in the normally small difference between.
These generally fall into three major categories. Either something happened to the lung's perfusion, or something happened to the ventilation of the perfused alveoli, or there is some problem with the way the measurement is being performed. Satoh, Kenichi, et al. How does it differ from arterial CO2 tension and the mixed expired CO2 tension? What factors influence its value? The size of this difference is a simple index of the amount of alveolar dead space.
Alveolar dead space is the part of the inspired gas which passes through the anatomical dead space to mix with gas at the alveolar level, but does not participate in gas exchange. Basically it is the difference between physiological dead space and anatomical dead space. Ventilation and perfusion. Alveolar dead space Alveolar dead space is the part of the inspired gas which passes through the anatomical dead space to mix with gas at the alveolar level, but does not participate in gas exchange.
Examiner's comment Require an explanation of alveolar dead space Factors relating to measurement: - sampling site - calibration - accuracy of measurement - leaks, occulsion delayed alveolar emptying with slow rise of expired CO2, leading to failure to obtain a true plateau Common error: incorrect use of Bohr equation, with substitution of end tidal for mixed expiratory partial pressure of carbon dioxide.
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