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    Yes, as I recall deciding when to initiate ventilation was the one exception my bro mentioned where ABGs are actually useful. interesting to hear they may have some use in sepsis and pancreatitis, I may have to look into that. I'm a little sceptical about the use of it as a prognostic marker though. If someone has a low O2 they are likely to be tachypnoeic and have low sats - is that 'second-line' information not sufficient prognostically? Is the ABG still truly necessary?

    And yeah I've just started paeds and CBGs seem sufficient for everything here. Bizarre how different cultures can be between departments
    • TSR Support Team

    TSR Support Team
    (Original post by Ghotay)
    . If someone has a low O2 they are likely to be tachypnoeic and have low sats - is that 'second-line' information not sufficient prognostically?
    If they are already on O2 then their pO2 will be low of course - as above. I think the official scoring systems still mandate an ABG, but probably mainly because a poor sats trace can be unreliable. I'd certainly argue that a clear sats trace recording low is sufficient to give them that 'point(s)'.

    The use is when someone is lying there a bit under the weather but fine as far as you know with sats of like 95. You then do the ABG and find the pO2 is 8 - this shows significant V/Q mismatch indicative of a significant underlying inflammation. This use as a prognostic marker is why they are used in the septic and pancreatitis scores.

    I've heard people complain about doing ABGs in pancreatitis patients who look well, but who say that its fair enough in pancreatitis patients who are needing oxygen. The reality is the opposite - pO2 identifies people as sick who you didn't know were sick yet.

    Other gems regarding ABG vs VBG: a VBG can be useful to rule out hypercapnia, e.g. when a patient is tiring or you're wondering about retention. So it can guide oxygen prescribing in COPD, for example.

    Another interesting tidbit: If you're using them in DKA patients, be cautious of interpreting the K+ in extreme hyperglycaemia as it becomes less representative of lab serum potassium.

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