1. #1
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    Question Question For The Medical Guys

    I have a question relating to hypoxic drive. If a regular healthy persons hypoxic drive is triggered by increased levels of CO2, and a person who has COPD is triggered by low levels of O2, is that not saying the same thing?

    Low levels of O2 is equal to high levels of CO2 - one is of greater value than the other. Right?

    The description in my First Responder manual is:

    "In normal people, the breathing reflex is triggered by high levels of carbon dioxide (CO2) in the blood. Patients with emphysema, chronic bronchitis, and chronic asthma may have a condition known as Chronic Obstructive Pulmonary Diseas (COPD). They retain CO2 and thus have chronically high levels of this gas. Their breathing reflex is triggered only when the oxygen level in their blood is low."

    Therefore high levels of CO2 will trigger, which is the same as saying that low levels of O2 will do the same.....????? Volumetrically a COPD patient will have a greater volume of CO2 in their blood than will a regular patient, but when the volume of either gas is below that persons "norm" then the hypoxic is triggered. Right?

    I am not trying to make something relatively simple complicated... just looking at it from another view point. Any and all suggestions/responses are welcome. Thanks in advance.
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    Low levels of O2 is equal to high levels of CO2 - one is of greater value than the other. Right?
    Not exactly; which is why you might have problems when giving a COPD patient pure oxygen, such as by a nonrebreather mask.

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    During my 4yrs we have not run into the problem - yet.

    It just seemed like a problem in semantics here. Kind of the glass is 1/2 full or 1/2 empty idea. Low O2 or high CO2.....

    All comments are welcome.
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    Basically, you can give a COPD patient high flow oxygen.... but you need to be careful if your going to be with them for hours. A COPD patient's drive to breathe is when his O2 level in the blood is low. By giving him O2 over a extended amount of time, you basically negate his will to breathe and he cant stop breathing on you

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    that about sums it up ..........in keeping it simple ....
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    Thats the bad part about tubing them. In many situations, they need a tube (nasal or RSI) but you got to think outside the box. "I can tube them.... but will they be able to wean themselves off the tube or will they be put on a ventilator the rest of their life?

    You gotta make the call but it helps to see the bigger picture. There are alternatives to tubing a patient. I know in the area where I'm at, if the patient doesnt want a tube, we bag them and the hospital has some sort of face mask that basically forces air down their throat.... but it makes them breathe. Tubing them can take away their bodies notion to breathe because all the air is supplied in their lungs

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    Question Two Seven.......................

    Hypoxic Drive............ Hmmmm...... Isn't that what makes your little truck go????
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    On any given call, BCAS response is usually only about 10 minutes behind us, if they haven't in fact chased us up the driveway And the ride to the nearest hospital is about 12 min at code 3, from pretty much anywhere in our district, so "overdosing" a patient with O2 is not really a factor - generally speaking.

    As for 'tubing' them, we carry canulas onboard, but have never used them, in favour of a non-rebreather - but then as I say, we have not (to my knowledge) had a COPD patient yet either.

    I suppose another way to phrase my question is:

    If a COPD pt breathes because he has low O2 levels, and a normal person breathes because he has high CO2, then for the normal person, what would be a typical value for the amount of O2 vs CO2 in his blood. And how does that compare to the COPD pt, gas for gas? What percentage of O2/CO2 is present in each pt? What is considered "normal" levels for each?
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    MalahatTwo7,

    I believe the explanation you seek lies in the physiology of the breathing mechanism. Breathing is controlled in 2 ways:
    1) Central Chemoreceptors (or pneumotaxic center) in the pons (base of brain) and
    2) Peripheral Chemoreceptors in the carotid bodies (in the carotid arteries) and aortic bodies (in the aorta.

    Each control breathing in different ways. The Central Chemoreceptors respond to a decrease in pH by increasing the breathing rate. The decrease in pH is caused by an increase in CO2. The CO2 diffuses across the blood/brain barrier from the blood stream to the Cerebrospinal Fluid. There, the CO2 combines with water to produce hydrogen ions (H+), thus decreasing the pH. The decrease in pH triggers the Central Chemoreceptors to stimulate the nerves that control breathing (by controlling the diaphragm). The Central Chemoreceptors are not very responsive to O2 levels (more specifically the PO2). Therefore, high blood levels of CO2 only controls breathing in an indirect manner. If one were to decrease the pH of the cerebrospinal fluid in a different manner, breathing would increase while the CO2 level in the blood remains “normal”. Also, if one were to increase the pH in the cerebrospinal fluid to a normal level (i.e., 7.2), the breathing rate would decrease, even though the blood CO2 level is high. This actually occurs as the body adjusts to a decrease in pH by sending bicarbonate ions to the cerebrospinal fluid to raise the pH to normal levels. The bicarbonate ion combines with the hydrogen ion to form water and CO2.

    The Peripheral Chemoreceptors on the Carotid arteries and the Aorta are very responsive to O2 levels and not very responsive to CO2 levels (and thus, pH). Low O2 levels stimulate the carotid bodies to send an impulse via the Glossopharyngeal Nerve to the Central Chemoreceptors to stimulate breathing. Low O2 levels also stimulate the aortic bodies to send impulses via the Vagus Nerve to the Central Chemoreceptors which in turn stimulate breathing. The key is that Peripheral Chemoreceptors do not respond to low O2 until the PaO2 is reduced to less than 60 mm Hg.

    In the COPD patient has difficulty in exchanging gases (O2 and CO2) across the alveolar membrane because the membrane is severely damaged. This means that O2 in the blood is low as it is difficult for O2 to diffuse from the alveoli to the blood. CO2 is high because it is difficult for CO2 to diffuse from the blood to the alveoli. The body continues to use O2 and produce CO2.

    As mentioned above, the CO2 is high in the COPD patient but the pH of the cerebrospinal fluid is relatively normal. Therefore, breathing is controlled more by the Peripheral Chemoreceptors and O2 levels than by CO2 levels. So, adding O2 to the COPD patient will cause in increase in CO2 because the increase in O2 will decrease the breathing rate and thus the already impaired diffusion of CO2 from the blood to the alveoli will decrease. In addition. The increase in O2 will also worsen the ventilation-perfusion ratio (V/Q). But that gets complicated.

    I was just about to post this when I saw you added to your original post.

    The normal amount of O2 in the blood is divided between the O2 transported in the dissolved state in water (by the plasma and within the erythrocyte) and that transported by hemoglobin. For a person having a “normal” PO2 of 95 mm Hg. 0.29 ml of O2 is dissolved in 100 ml of water. If the Po2 falls to 40 mm Hg, the O2 drops to 0.12 ml per 100 ml of water. The difference (0.17ml) is what the body actually uses. The 0.12 ml is a residual level in the water. In other words, the body does not use all of the O2 dissolved in the blood. Also, by using Henry’s Law, you can estimate the dissolved O2 content by using:
    Dissolved O2 (ml/dl) = PO2 X 0.003

    Now, hemoglobin carries O2 by binding the O2 molecule to the heme portion of hemoglobin. Each hemoglobin molecule can combine with a maximum of 4 O2 molecules. There are approximately 15 g/dl of hemoglobin in the blood (“normal” conditions). 1.34 ml of O2 will combine with each gram of Hemoglobin. Depending on the size of the individual and consequently the blood volume, you can calculate the amount of O2 in the blood.

    97% of the O2 is transported by hemoglobin and 3% in the dissolved state.

    The amount of CO2 transported by the blood is divided among:
    1) CO2 combined with hemoglobin (carbaminohemoglobin) (12%),
    2) Dissolced in the Plasma and Erythrocyte fluids (8%), and
    3) Combined in the form of the bicarbonate ion (80%).

    Approximately 48 ml/dl of CO2 is carried by the arteries and 52 ml/dl is carried by the veins.

    I’ll leave the math for your enjoyment as I am tired, its late, and I’m going to bed.

    I hope this helps and I hope I didn’t mess it up.

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    Well Fire... I think I can say I was not expecting a full medterm description but oddly it does help. Let me try this in slower language and see if I understood what you were saying:

    Basically in a COPD person, breathing processes could become inhibited over an extended period of time, if that person were to be placed on O2 therapy.

    This is because their breathing is controlled by reduced levels of O2, which by the introduction of oxy becomes inhibited because the higher levels of O2 "suggest" to the body that it has the required amount of gas in the system. Which in turn causes a general shut down of the breathing process..... Right?
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    Originally posted by ThNozzleman

    Not exactly; which is why you might have problems when giving a COPD patient pure oxygen, such as by a nonrebreather mask.
    pretty much kinda right, varies patient to pt (and by protocol)

    Usually, a person would have to have severe COPD to have O2 via NRB shut down their breathing pre hospital.

    If you have a combined scene to hospital time less than 1 hour, typically a protocol will say non rebreather anyway, but you might also get specific instruction for specific patients from the family physician or ER staff.

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    I've been told by several docs that shutting down someone's hypoxic drive won't happen prehospital. It will actually take 24 hours at 15 lpm via NRB to shut someone down. As for intubation never thought about that. I've worked a whole lot more BLS than ALS.

    I've never researched these numbers, this is just what has come up in conversation with ER docs
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    Thanks for the input and comments guys 'n gals. I wrote my First Responder Re-Cert on Saturday, along with the practical exams that come with it. Naturally this question was a part of the test - I am not likely to get the two confused EVER! LOL.

    The information regarding post emergency care, in the hospital etc was very informative, because our books make reference to the danger of potential hypoxic drive shut down, but no real time indicator..... Now we "know the rest of the story".

    It just remains to be seen how well I did on the written exam. I was told by the examiner that I did well on my practical; should know in about 3-6 weeks.
    If you don't do it RIGHT today, when will you have time to do it over? (Hall of Fame basketball player/coach John Wooden)

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