Transport of O2

Discussion in 'Step I' started by aspiringmd1015, 09.18.14.

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  1. aspiringmd1015

    aspiringmd1015 2+ Year Member

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    need to clear the concept, so from my understanding, the alveolar oxygen diffuses and dissolves in the pulmonary capillaries creating the pa02, then it loads onto the hemoglobin, and the hb takes this o2 to the tissues, from what i read, it says that the o2 which is already dissolved in the plasma (pao2) then diffuses through the tissues, and this pao2 was what was keeping all 4 o2 bound to the hb. Now that the pao2 has dissolved into the tissue, and the pa02 has decreased from previous 100mmhg to 40, now the o2 unloads from the hb to replace this pao2 back to 100. Is this correct? im having a bit of difficulty in understanding that, the initial alveolar oxygen which diffused and dissolved, making a pa02 of 100, thats the same exact dissolved o2 which is being transferred to the tissues?
     
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  3. SBR249

    SBR249 7+ Year Member

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    That's almost correct except for the PaO2 probably doesn't fluctuate that drastically as your scenario posits. What probably happens is:

    1) In the lungs, the increasing PaO2 from diffusion of O2 into the capillary causes the Hb to change into the R form which increases its O2 affinity. This means that it becomes much more energetically favorable for O2 to bind to Hb than to stay dissolved in blood. So that slight increase in PaO2 sets off a reaction whereby all O2 entering the blood almost immediately binds onto Hb and the PaO2 only increases very slow. As the Hb O2 binding sites fill up, an equilibrium plateau is reached whereby more and more O2 stays dissolved in the blood and PaO2 rises more quickly until the equilibrium value is reached.

    2) The reverse happens in the tissues, PaO2 rapidly decreases until it reaches a critical level where Hb reverts to the T form with decreased O2 affinity. Thereafter the PaO2 decreases very slowly as O2 rapidly unloads from the Hb and diffuses through the blood and into the tissues. Once the majority of O2 that will come off the Hb is unloaded, then PaO2 quickly reaches a nadir equilibrium point.

    It's somewhat difficult to visualize but all of this comes from the concept of equilibrium in general chemistry and also by looking at the oxygen dissociation curve of Hb.

    One key point is that during O2 loading and unloading from Hb, the PaO2 probably changes very little as can be seen from the O2 dissociation curve where the steepest part of the curve happens over a narrow PaO2 range.
     
    Last edited: 09.19.14
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  4. aspiringmd1015

    aspiringmd1015 2+ Year Member

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    theres some gray area in my concept though, the pao2 which is in the capillary, is this the same dissolved 02 as the pao2 downstream at the tissue level? as in the portion of dissolved oxygen in the capillaries is contributing to the same o2 which is transferred to the tissues? or the only pao2 in the capillaries feeding the tissues comes from unloading of o2 from hb?
     
  5. SBR249

    SBR249 7+ Year Member

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    Not sure what you mean. PaO2 refers only to the partial pressure of dissolved oxygen in arterial blood, there's no such thing as a PaO2 in interstitial tissue. If you are talking about interstitial PO2 that's a different thing though for purposes of the step the interstitial PO2 immediately adjacent to a capillary should be very close to capillary PaO2 in value. Also, as the capillary network is the most peripheral level of circulation, it is usually considered to be the same thing as "tissue level", so I'm unsure of how (or why?) you are making a distinction between the two.

    As for your question, O2 unloading from the Hb happens in RBCs, to get into the tissues, the O2 must pass through the RBC membrane, through the blood, through the capillary walls, and into the tissue. During that transit through the blood, it becomes dissolved and contributes to the PaO2.

    Think about it as people leaving a large auditorium through a small front lobby to go outside. (Outside=tissue, small lobby=PaO2, large auditorium=Hb, and people=O2) Initially, before the process started, the auditorium was full and the extra people that wouldn't fit had to stand in the lobby. Then when everyone is trying to leave, the people in the lobby leaves first and the people in the auditorium take their place. But since this is a continuous process, the lobby never becomes full again and instead, a continuous flow is established whereby the rate of people entering the lobby from the auditorium equals the rate of people leaving the lobby to go outside. During this period, the auditorium empties at the fastest rate and the number of people in the small lobby at any instant is constant and will remain so as long as there is enough people still left in the auditorium to sustain the flowrate of exiting people. Note, You can also say that anyone who has exited the building and is now outside must have passed through the small lobby. However, there is a distinction in that everyone outside must have passed through the lobby and so they were all in the lobby at some point in time, however only a small number of people were only in the lobby the entire time.
     
  6. aspiringmd1015

    aspiringmd1015 2+ Year Member

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    i see, can you also explain perfusion limiation? im reading it from brs, its very vague.
     
  7. SBR249

    SBR249 7+ Year Member

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    In a normal lung, the gas exchange is perfusion limited because the exchange process across the alveolar membrane and capillary wall is very efficient. Generally, RBCs would only need to go 1/3 of the way through the capillary before the gas exchange has completed and they are fully oxygenated. That means the other 2/3 of the way RBCs travel on their way out of the pulmonary capillaries and into the pulmonary veins is basically not useful. Under these circumstances, the only way to get more oxygen into blood is to basically get more RBCs to follow through the capillaries, in other words, the amount of gas exchange that occurs depends on and is limited by perfusion.

    If there was a defect in the gas exchange (for instance pulmonary fibrosis), then the RBCs may travel the length of the capillary network and not have enough time to fully complete gas exchange because the diffusion rate is just too slow. In that case, the key to getting more oxygen into blood is not to have more RBCs travel past the alveoli but to have better diffusion. Thus, the gas exchange is said to be diffusion limited.

    A good analogy is to think of it as a bunch of people going through a cafeteria line single file. Under normal circumstances food is handed out so efficiently and quickly that everyone's tray is basically full when they get 1/3 of the way down the line. The only way then, to increase the amount of food being handed out, is to have more people go through the line. That's the case for perfusion limited gas exchange. But let's say if a few food handlers are out sick and the cafeteria line is understaffed, the rate at which food is handed out is now a lot slower so people may go through the entire line and come out with half empty trays. In that case, the only way to increase the amount of food being handed out is to increase the rate of food distribution not to send more people into the line. That's the case for diffusion limited gas exchange.
     
    Last edited: 09.20.14
  8. aspiringmd1015

    aspiringmd1015 2+ Year Member

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    srb249, you are a gift from god. strong core concepts. good stuff.
     
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  9. aspiringmd1015

    aspiringmd1015 2+ Year Member

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    also, in a pulmonary shunt(atelactasis), this is a perfusion limited situation, but if you increase the amount of rbc/blood to flow through the capillaries, if the alveoli are collapsed, how will increasing the amount of rbcs benefit, if the alveoli is collapsed in the first place? shouldnt atelactasis be a diffusion limited situation?
     
  10. SBR249

    SBR249 7+ Year Member

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    Which source says atelectasis is a perfusion-limited situation? I've never heard that before and in fact have read sources that claim the opposite.
     
  11. aspiringmd1015

    aspiringmd1015 2+ Year Member

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    kaplans saying it, its saying in atelactasis you get a shunt, and bc of this its perfusion limited. lol da fuq?
     
  12. SBR249

    SBR249 7+ Year Member

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    well I got nothing.
     
  13. DeeJay2728

    DeeJay2728 5+ Year Member

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    Maybe bc in the lungs hypoxia causes vasoconstriction. Patchy atelatasis can cause shunting of blood to better ventilated areas.
     
  14. aspiringmd1015

    aspiringmd1015 2+ Year Member

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    doesnt pulmonary shunt imply that it bypasses the lung completely and goes directly in the the left side of the heart without getting oxygenated?
     
  15. DeeJay2728

    DeeJay2728 5+ Year Member

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    The only time you'll have a shunt that physically bypasses the lung completely is during fetal development.

    But, for example, with a pulmonary embolus... The lung is still being perfused, which is why the patient can present with various s/s (depending on the severity) sob, chest pn, wheezing... or they can even be asymptomatic (unless it's a massive saddle embolus and it knocks out the entire side). But with an embolus, or any situation that causes a decrease of blood flow to a particular portion of the lung, the blood that normally would've perfused that area and did it's gas exchange thing in that area, would be "shunted" to the left heart without getting oxygenated.

    Remember that the lung tissue acts differently with hypoxia. Usually tissues that are oxygen deprived would try everything they can to vasodilate, increase blood flow to hopefully bring in more oxygen. The lung vasoconstricts in areas that are oxygen deprived... The lung would rather send blood to the healthy areas that better able to exchange (respire).
    Which is also why a pulmonary embolus (or any type of shunt) would cause an increase in dead space. If the embolus knocked out a lobe on the right side, for example, that lobe would still be ventilated, but not perfused, so why should the lung send blood to that lobe (respiration would not be efficient in that area), so it vasoconstricts and shunts blood elsewhere.

    Sorry, I hope my rambling made sense... too much coffee.
     
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  16. DeeJay2728

    DeeJay2728 5+ Year Member

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    I think you're getting confused with the arterial PO2 and PaO2. Remember, PaO2 (oxygen tension, dissolved O2, is determined by atmospheric pressure, it follows Henry's Law) and contributes very little to the Oxygen content of around 20ml. The major carrier of O2 is Hb. Hb molecules are the "boats" that carry O2 to the tissues and pick up CO2 that will be expired in the lungs (Bohr and Haldane)
    As the saturated Hb comes out of the lungs and gets into capillaries of tissues that are doing their metabolic thing, the pH decreases (end products of tissue metabolism) and a slightly acidic environment is one of the triggers that causes Hb to unload its O2, and pick up CO2 (waste, also adding to the acidity). Which is why a decrease in pH causes the O2 diss curve to shift to the right (favoring O2 unloading). The reverse happens in the lungs.
    So, changes in O2 levels are mainly concerned with Hb's ability to pick up and drop off which hopefully balances the oxygen demands (metabolism) of the tissue it's servicing.
     
  17. DeeJay2728

    DeeJay2728 5+ Year Member

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    Absolutely right!! That's the way the lungs think. Why should they send more blood (RBC's, Hb) to an area that have collapsed alveoli, so the lungs vasoconstrict, inducing a shunt, and send (shunt) blood over to areas that are able to exchange (The Lungs create a Perfusion limitation).
    And, the collapsed alveoli are just collapsed, they didn't get any thicker or fibrotic. There's nothing wrong with their ability to diffuse. But what would they be diffusing? Collapsed alveoli are usually unable fill up with a sufficient amount of O2, and they can't sufficiently push out CO2. It's more of a mechanical problem, not a diffusion problem.
     
  18. aspiringmd1015

    aspiringmd1015 2+ Year Member

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    yet another question lol sorry guys! in diffusion impairment(ie IPF) increasing the fi02 by giving 100% oxygen will increase/normalize the pa02, but the A-a gradient will still be abnormally elevated bc the PA02 will elevate even higher with increasing the fi02, and with the diffusion problem still existing the pa02 even at normal levels is still creating an abnormally large gradient, yes?
     
  19. SBR249

    SBR249 7+ Year Member

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    Yes, that's right, since the AaO2 is a reflection of the diffusion capacity and since increase FIO2 doesn't fundamentally address the problem of the increased diffusion barrier, you'd still have an abnormal AaO2. However, the only thing you really care about is the PaO2 because that's a measure of the amount of oxygen that gets to the peripheral tissues so as long as you can get that to normal, then you are addressing the symptoms.
     
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  20. aspiringmd1015

    aspiringmd1015 2+ Year Member

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    whenever you develop pulmonary hypertension from copd or fibrosis, you get hypoxemia bc of poor oxygenation, causing organ wide vasoconstriction in an effort to send blood to other areas with the hope of getting oxygenated, but how does this vasoconstriciton of these arterioles cause pressure in the Pulmonary Artery to increase? as the arterioles are branching off of the Pulmonary artery? I do understand that once this pressure does develop, it increases afterload for the RV and causes hypertrophy
     
  21. DeeJay2728

    DeeJay2728 5+ Year Member

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    Pulmonary artery/veins are all considered part of the Pulmonary vasculature.
    There's an increase in resistance (vasoconstriction) distal to the pulmonary artery. It's the same reason you get Right sided hypertrophy... just imagine the Pulmonary artery is also on the right side, so it will also be affected (just like the ventricle it's coming out of). There's a back up, which is why Right sided problems end up with edema of the legs. Left side, Lungs. It's all one circuit... If you know where the block is, you'll know what to expect.
     
    Last edited: 09.25.14
  22. DeeJay2728

    DeeJay2728 5+ Year Member

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    Anything that increases the afterload of the right side (beyond the Pulmonary valve) will give you an increased pressure in the Pulmonary artery, even left sided problems. That's why the mcc of right sided heart failure, is left sided failure.
    Just make sure you pay attention to where the problem is. Anything before the obx, press is increased... anything after, the press is decreased.
     
  23. aspiringmd1015

    aspiringmd1015 2+ Year Member

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    okay cool thanks, after reading over my questions lol ive realized im asking pretty simple questions, but in any case thanks for taking the time out to answer them.
     
  24. DeeJay2728

    DeeJay2728 5+ Year Member

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    Never feel that way, we're ALL overwhelmed!! I'm sure you'll be helping me with some of my "simple questions" in the near future.
     
  25. aspiringmd1015

    aspiringmd1015 2+ Year Member

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    pathoma mentions that elastic recoil in the smaller airways prevents them from collapsing during expiration. But, when i was reading physio elastic recoil is a collapsing force that allows air to flow out?
     
  26. SBR249

    SBR249 7+ Year Member

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    It's both, think of it like a spring. If you compress it, it will resist that. If you stretch it, it will resist that as well.
     

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