Hyper and hypo ventilation with PaCO2 levels - Page 2

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  1. Guide
    Mar 19, '12 by
    Quote from osteward
    okay soooo.....

    low paco2 levels stimulate you to hypoventilate which compensates and ends up increasing co2 levels

    right, so you are retaining enough co2. this allows for production of carbonic acid. this is why you can end up with respiratory acidosis.

    high paco2 levels stimulate you to hyperventilate which compensates and ends up decreasing co2 levels

    right, so you are blowing off the co2. this decreases the production of carbonic acid. this is why you can end up with respiratory alkalosis.

    ??? right?
    the drive to breathe is to get rid of co2. how ever much the body needs to retain or get rid of will determine the rate of ventilation to maintain balance.

    i think that is the simplest way of thinking about it.

    this is not taking into many many other factors that come into play, but strictly addresses the problem in your text.
  2. Mar 19, '12 by
    There exists a very important point that most people do not consider. Carbon dioxide by its self does not really effect breathing. Our primary stimulus to breath is not based on CO2 levels. In fact, pH change is our primary stimulus to breath. Central chemoreceptors in the brain monitor CSF pH and send this information to breathing centres in the brain.An example to illustrate this point is a DKA patient. They typically have very low CO2's, yet hyperventilate. A concerning dichotomy if we think CO2 is the primary stimulus to breath; however, it makes perfect sense from a pH context. Another example would include a COPD patient who has chronically elevated CO2 levels. We can look to a scarecrow explanation such as the hypoxic drive, or realise that chronic CO2 retention results in renal compensation and a relatively normal pH in spite of an elevated CO2. Again, it's all about the pH.
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  3. Guide
    Mar 19, '12 by
    Quote from GilaRRT
    There exists a very important point that most people do not consider. Carbon dioxide by its self does not really effect breathing. Our primary stimulus to breath is not based on CO2 levels. In fact, pH change is our primary stimulus to breath. Central chemoreceptors in the brain monitor CSF pH and send this information to breathing centres in the brain.An example to illustrate this point is a DKA patient. They typically have very low CO2's, yet hyperventilate. A concerning dichotomy if we think CO2 is the primary stimulus to breath; however, it makes perfect sense from a pH context. Another example would include a COPD patient who has chronically elevated CO2 levels. We can look to a scarecrow explanation such as the hypoxic drive, or realise that chronic CO2 retention results in renal compensation and a relatively normal pH in spite of an elevated CO2. Again, it's all about the pH.
    So, what you're saying is that to simplify it correctly would be to get down to the pH, which I did not do.

    This is very interesting to me.
    GilaRRT likes this.
  4. Mar 19, '12 by
    we would like it if high co2 levels always prompted a respiratory compensation mechanism, more/deeper breathing, but alas, co2 levels are symptoms, not conditions. someone with drug od does not deep breathe even if his co2s are high, because his cns is suppressed. someone with a high spinal cord injury does not deep breathe because he can't. someone with copd can deep breathe just fine, but his co2 is elevated, too. why is that?

    in a healthy person, co2 production varies a lot over the course of the day. you know how you have to breathe more deeply when you run up the stairs carrying something heavy? that's because you have produced a lot more co2 in your muscles, because they are working so hard. sitting peacefully in your chair you won't hyperventilate, because you are not producing a lot of co2.

    most people think that the first job of the lungs is to provide oxygen, but that's wrong; it's really acid/base management via co2 management. lung disease shows up first as low arterial oxygenation, because the ability to pull oxygen out of the alveolar air goes away before the lung's ability to excrete co2 into the alveoli.

    now, let's look at your question.
    hyperventilation occurs when the paco2 is less than 35 mmhg and hypoventilation occurs when the paco2 is greater than 45 mmhg. that doesn't make sense to me.
    is this a mistake or am i missing something?

    as an editor i would have reworded that, because it is confusing. i can see why you might think it was backwards, because you're thinking ahead-- hyperventilation is the respiratory compensation for high co2s, but the high co2 occurs because of hypoventilation.

    so i would have said, "low paco2 indicates the presence of hyperventilation. high paco2 indicates the presence of hypoventilation."

    just so you learn something new today :d, this is why. ventilation is a mechanical word, indicating moving air in and out of the lungs. you remember that diffusion occurs across a membrane from an area of high concentration or pressure to an area of low concentration or pressure. this little bit of chemistry explains why you cannot increase your blood oxygen by breathing faster and deeper (assuming room air, here), but you can decrease your blood co2 levels substantially by doing that.

    there's an equation to say why that is, but leaving that off, take my word for it that the pressure of oxygen in room air at sea level is about 80-100torr, roughly 4-5x the concentration of oxygen in the inspired air (air is about 21% oxygen).

    also, because of this equation, arterial oxygen in normal lungs is always 4-5x the inspired oxygen level. so if you are breathing 50% o2, your arterial oxygen should be 200-250 torr. if it isn't, that indicates a problem with alveolar oxygen transport. there's a term for that: the alveolar-arterial (a-a) gradient, the difference between what it ought to be and what it is. the bigger the gradient, the worse the lungs are.

    this is what accounts for a normal pao2, because the oxygen diffuses across the alveolar capillary membrane into the blood on the other side. that blood has just come from the venous side (venous oxygen is lower, of course), so the (room air) oxygen at 80-100torr crosses into the blood by diffusion readily. therefore, it's not possible to have an arterial oxygen any higher than the oxygen pressure in the inspired air. no matter how fast you breathe, you can't make the inspired air have any more oxygen in it.

    co2 is a different matter. for practical intent, there is just about no co2 in inspired air, so any co2 in the blood next to the alveolus will give up its co2 readily. that puts a little co2 in the respiratory tree, but rapid deep breathing washes it out rapidly...making it even easier for the capillary bed to give up more co2 (area of higher pressure to an area of lower pressure, remember?). so, you can hyperventilate and drive your paco2 right on down to very low levels. this is why you get tingly fingers and feet when you hyperventilate, and why they give you a paper bag to rebreathe your own air until its contents more closely resemble normal paco2. cool, huh?

    of course, all this is predicated on having normal lungs. and if everyone had normal lungs, we wouldn't have to learn all this stuff. people with copd do not have normal lungs-- they have lost a lot of those alveolar units so they have a much smaller area of alveolar wall to use for the work of gas exchange.

    remember, oxygen-diffusing capability goes away first, so copd folks tend to have low pao2 even though they breathe fast. but they also have high paco2, because they have lost so much diffusion ability that they can't even clear their co2. these people can huff and puff as much as they can, and they do, but they don't drop their co2 levels even with what looks like hyperventilation.

    hope that helps. write a letter to the publisher and make a suggestion for the next edition!
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  5. Mar 19, '12 by
    and of course, this is all part of the greater scheme of things, to keep the internal mileu at a good ph level. as gill points out, someone with diabetic ketoacidosis will hyperventilate to drive the co2 to very low levels, because (for purposes of this discussion) it helps to think of co2 acting as an acid.

    getting rid of it decreases the body's acid level (after all, that ketoacidosis is going on) in an attempt to compensate-- respiratory compensation for a metabolic acidosis. same thing is seen with someone who eats a lot of asa-- salicylic acid.

    the respiratory drive sensor is an acid/base sensor; high co2 (higher acid, lower ph) makes it demand more ventilation (unless blocked for one reason or another, as above); low co2 (lower acid, higher ph) tends to make it want to breathe less (unless it's trying to compensate for a metabolic acidosis).
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  6. Mar 19, '12 by
    Yes, pH change is going to be the primary stimulus.
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  7. Guide
    Mar 19, '12 by
    This is why I come to AN.
    Probably one of the most entertaining ways to learn...
    Now... is the OP clear on on this... lol... because this discussion really got down to the nitty gritty.
    wooh likes this.
  8. Mar 19, '12 by
    I have seen quite a few ABGs on folks with DKA. pH was pretting darn low. This prompts them to hyperventilate, which drops their CO2 levels. The renal bicarb buffering takes days to have any effect.....

    Bottomline is this, heavy, rapid breathing, you are blowing off CO2. (heading towards respiratory alkalosis)

    Shallow or slow breathing, you are retaining CO2. (heading towards respiratory acidosis)

    All the gobblty goop is fascinating but has nada to do with being an RN. I see many students failing tests because they get too deep in the patho weeds when they should be focusing on nursing interventions and collaborative care and patient safety.....
  9. Mar 19, '12 by
    Quote from mindlor

    All the gobblty goop is fascinating but has nada to do with being an RN. I see many students failing tests because they get too deep in the patho weeds when they should be focusing on nursing interventions and collaborative care and patient safety.....

    Good gawd. Yes it does.

    It's called excersing the brain to critically think in the medical context.

    This includes the study of physiology and pathophys, which last I heard, is a requirement.

    Great thread.
    FlyingScot likes this.
  10. Mar 19, '12 by
    Rns need to critically think in a nursing context. Not a medical context.

    I promise that no one will ever see a question on the NCLEX that approaches the complexity of some of these explanations...

    Nurses are too busy trying to be doctors. They would be well served to instead work on becoming better nurses.

    This is just my opinion and you are certainly entitled to yours. I will just say that of 400 points this semester I have missed 4......2 points per quuestion means I have missed two....so maybe I am on to something? I dunno.......