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  • And really great class by the way. You sum all the important things up in such a short time, it's really good for anyone to study with (for you too, obviously!) I hope you keep making these :D (well...until you're an intern lol!)

  • In COPD patients who are more of the emphysema type (as we know it's never that clear cut but for the sake of explanation..), they usually do not have raised CO2, and if their CO2 starts to get higher in a skinny barrel chest emphysema patient, it's probably because his disease is getting really bad and/or he's exacerbated and is starting to get respiratory fatigue (AKA muscular origin of hypoventilation rather than central)... PS:.. you very probably know all of that but typing it made me study

  • (cont.) For some reason, blue bloaters and Obesity/Hypoventilation syndrome patients, which have certain features in common (and it's thought that these diseases also have somewhat of an overlap with Sleep apnea), just do NOT hyperventilate in response to their Plasma CO2 increase. So the problem is not so much CO2 trapping as NON-compensation in these patients... It's also related to why COPD patients (especially blue bloater types) should not be treated with 100% FiO2 to avoid hypoventilation

  • Hi there substanceP! Just wanted to point out 1 thing: regarding hypoventilation in COPD patients, AKA CO2 retainers and how you explain it. I'm not quite sure you can attribute that to "CO2 trapping", because as you probably know, hyperventilation will compensate for increase in PlasmaCO2 secondary to low Ventilation/Perfusion ratio zones in the lung. In the classic "blue bloater", it's theorized to be of central origin (desensitization to CO2), somewhat overlapping with Obesity/hypoventilation

  • Thanks for the high yield summary :)

  • reid index

  • it's nice to finally see a face behind the great study material! lol.

    geez this sounds really complex!

    good luck

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