Shunting Explained Clearly (Pulmonary Shunt)

By Adem Lewis / in , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , /

well welcome to another MedCram lecture we’re talking about hypoxemia and today’s topic is shunting we’ve
talked briefly about high-altitude diffusion and hypoventilation the fourth
mechanism that we want to talk about is the shunting mechanism and this is a
little bit different than the previous two and I’d like to sort of diagram what
exactly is a shunt okay so if we look at the pulmonary vascular system we start
out with the pulmonary artery and it’s in blue because it’s deoxygenated and of
course it ends up in the pulmonary vein which is oxygenated and the way to look
at this is two different systems so I’ve drawn this so that it’s pretty
easy to tell that 50% is going in this direction and 50% is going in this
direction this is what we call a 50% shot so that a 50% of the blood goes to
in this case the lungs and 50% is going to a shunt or basically it’s not going
anywhere it’s not going anywhere where there isn’t it’s not going
anywhere where there’s an alveoli or the ability for oxygen to get to it okay so
these are the lungs oxygen can come here oxygen can’t come here because it’s
being shunted away from the lungs and so even though I’ve drawn this with kind of
a blue in red you must understand that there is no o2 coming here whatsoever
and this is exactly what a shunt is is a 50% shot as I mentioned but it doesn’t
have to be 50 you can have less you can have more I’m just making it 50% for
illustrative purposes now before we get started with that kind of a discussion I
want to sort of give you a little bit of a background about the red blood cells
as you know red blood cells carry oxygen and they look like this kind of from the
side because there is no nucleus well inside each red blood cell is the human
globin molecule which is actually made up of for binding parts we’ll talk a
little bit more about this later and this is where oxygen binds to it and you
get something called the hemoglobin oxygen dissociation curve which
basically looks like this okay and basically po2 is on the bottom and
saturation is on the side and what it says is as po2 goes up so does the
saturation but there comes a point where increasing po2 doesn’t increase the
saturation that much more the important thing to take from this is that this
goes to the body after the left ventricle pumps it and the amount of
oxygen that is delivered to the body so the
do too is directly proportional to the saturation of oxygen so that’s going to
be very important is the oxygen saturation
that’s the line share of oxygen that is delivered to the peripheral tissues and
so what I want to do here to avoid confusion is talk a little bit
about the saturation of the blood in the pulmonary artery so pulmonary artery
blood is basically blood that is coming back to the heart
it is not oxygenated it is blood that has already been spent oxygenation wise
in the tissues and the saturation of blood in that area is about 70 percent
so if you were to get a pulse oximeter or some sort of way of measuring the
saturation of oxygen in the venous blood that gets eventually pumped to the
pulmonary artery the answer is 70 percent and in normal
situations this blood goes to the lungs and get Sri oxygenated and it comes back
to the pulmonary vein to the left atrium left ventricle gets pumped out to the
body but in a shunt situation like we have drawn here where in this case 50
percent of the blood is diverted away from it let’s go through and figure out
the arithmetic about what happens so we’ve got 70 percent saturated blood
here and we’ve got 70 percent oxygen saturated blood here well because
there’s lungs here that area becomes oxygenated and let’s just say that it
becomes oxygenated up to the point that it is now 95 percent saturated with
oxygen well in the shunt side of this that 70 percent blood 70 percent
saturated blood doesn’t get to see any alveoli and so it remains at 70 percent
saturated now because this is 50 percent of the blood and this is 50 percent of
the blood when these two combine in the pulmonary vein you simply what you have
here is the arithmetic mean of these two saturation obviously now if
it’s a smaller shunt fraction this 70% is not going to have as much weight but
because I’ve said it’s a 50% shunt meaning 50% of the flow is going to the
lungs and 50% of the flow is not going to the lungs and in fact never sees the
lungs the arithmetic mean of 70 and 95 is the difference between these two is
25 half of 25 is twelve and a half twelve and a half plus seventy is eighty
two point five percent saturation that is definitely a situation where you have
pulmonary hypoxemia okay so hypoxemia is caused by this
shunt fraction so as a result of that even though you’ve got good oxygen here
in the alveoli you see and that’s capital a you see that your lowercase a
is low that means you’re going to have an increased a a gradient what about if
we give one hundred percent oxygen and and this is probably the most important
point to understand and this whole lecture is what happens next
when we add a hundred percent oxygen so we’re going to add we’re going to add a
hundred percent oxygen now what’s going to happen when we add one hundred
percent oxygen that one hundred percent oxygen is going to affect this side of
the equation okay but it’s not going to affect this side of the situation
because this shunt by definition is not seeing any oxygen in the lungs now when
we give 100% oxygen to this side what’s going to happen over here the blood
which is seventy percent saturated instead of it going to ninety five
percent saturated remember here’s our human globin binding curve it’s going to
go up like this and whereas at this po2 the oxygen saturation was 95 now if we
give a hundred percent oxygen that’s essentially 760 millimeters
of oxygen we’re going to be way off the scale over here but we’re only going to
be up to a hundred percent so instead of 95 let’s say that the new saturation for
just the blood coming off this limb is now a hundred percent saturation but
because this area here never got to see the hundred percent oxygen because by
definition it is a shunt we still have 70 percent in this limb and instead of
having an eighty two point five percent saturation the new saturation is going
to be only eighty five percent now this is something that’s different in
response to high-altitude diffusion hypoventilation what we’ll talk about
later is VQ mismatch and this is a very important point is that one hundred
percent oxygen treatment in these type of hypoxemia x’ do not really improve
your hypoxemia and that’s a clue that the mechanism of action here is is a
shunt okay so let’s review shunting the first
thing that we said and this is probably the most important is that it does not respond to 100 percent oxygen that’s the
first time we’ve come across one of those it does have an increased AAA gradient now what are some examples well
if you look at the heart and here is my schematic drawing of a heart we’ve got
the interventricular septum we’ve got the tricuspid valve and the mitral valve
any type of a situation where blood on the right side of the heart goes over to
the left side so like an ASD or like a VSD or even like a patent ductus
arteriosus if it’s going from the left to the right that could do it as well in
this situation you’re going to of right to left shunting now these are
congenital heart anomalies but I can think of another reason why you could
have right to left shunting and that would be in something called a r d s
what is a RDS well in a RDS remember your alveolus looks like this okay and
you’ve got your capillary coming in like this and it gets oxygenated and it comes
out like this but in a RDS a RDS stands for
acute respiratory distress syndrome this is a situation where a lot of basically
Highland containing high-protein fluid leaks out into the alveolus if you would
like you can imagine that there is just basically fluid in the alveolus so in
fact what happens when oxygen tries to get down there there is no oxygen that
can come through and as a result of that this deoxygenated blood goes right
through without seeing any oxygen whatsoever so that’s another way you
could have shunting also pulmonary edema could also do this so that does it for
shunting thanks for joining us Oh

100 thoughts on “Shunting Explained Clearly (Pulmonary Shunt)

  1. Really clear explanation! However just wanted to check, if pulmonary oedema causes pathological shunting, do the following also apply?
    pulmonary embolus, pneumonia, atelectasis, pneumo/haemothorax?

  2. ASD,VSD,PDA = Left to right shunt…….. Tricuspid atresia, Tetralogy of fallot, Transposition = Right to left shunt..

  3. PLEASE HELP. In pneumonia you have alveolar infiltrates correct? In ARDS you have your alveola are filled. Doesn't that mean both situations have deceased ventilation and thus both are shunting.

  4. Hello, thank you for this video! My daughter has had 3 instances of crying/vomiting, then falling unconscious with her eyes open and not breathing. We were told she had a VSD at birth and it hasn't gone away (she's 15 months old). My mom's aunt had a RTL shunt – is it common to pass out/stop breathing with a RTL shunt? What's the reason for this? Thank you for any help!

    (P.S. – we are going to the cardiologist and have an echo scheduled.)

  5. I think it is very important to point out that this is only accurate if you are talking about a R to L shunt. Also you mentioned that a VSD and ASD would be R to L shunts but that is not necessarily correct most of the time (assuming your pulmonary resistance has dropped as it is supposed to) an ASD and VSD and PDA become L to R shunts. Am I correct?

  6. only R to L shunts produce hypoxemia. L to R shunts don't produce hypoxemia. Most L to R shunts will eventually cause R to L shunts because of Eisenmenger Effect (Right sided pressure increases). Of course I don't have time to say all this stuff if you want a 10 minute video. LOL

  7. It's tricky. yes, you are right. but on;y if there is absolutely no ventilation. ARDS causes this most often. PNA can too. but it can also cause V/Q mismatch. If you ever have to guess – always guess V/Q mismatch unless it's obvious that the O2 is not correcting with supplemental o2.

  8. Great video. I'm an RT student doing a project on ARDS and I didn't understand the different ways the term shunting is used…until I watched your video. Thank you!

  9. Excellent video, very clear, simple without oversimplify, and it goes straight to the point in very difficult topic, in addition, beautiful diction; my second language is English and I really appreciate a clean diction, thank you very much

  10. ??? … Isn't ARDS and pulmonary edema examples of wasted ventilation and having nothing to do with shunt ???  I have more questions then answers now …

  11. Great Job!
    This is great, short, concise, all that you need to fully understand the problem!
    I was wondering if you could make a lecture about inotropes in different cardiac pathology…

  12. Your videos are great. They helped me get a A in all my nursing classes. I also have a respiratory degree and I am reviewing. I just have one question about his video. I may be wrong but don't you get a L-R shunt because the pressures on the L side of the heart are greater than the R side of the heart. (through the ASD and VSD) it still results with oxygenated blood on the left side mixing with unoxygenated blood on the right side? Just wondering. Thanks.

  13. Thank you for the video. I do not understand why the Aa gradient is increased. There is nothing in the interstitial space like in diffusion. 

  14. Or you can get a mixed venous blood gas from pulmonary artery catheter to measure O2 Sat and PvO2. Then you get a regular ABG. And now you can get your shunt fraction and C(a-v)O2 difference.

  15. Can i please ask something? At first you were talking about shunting in the pulmonary artery but later when you described the RT to Lt shunt of ARDS, the shunting was happening in the heart. My question is does the pulmonary artery shunting happen in the lungs or somewhere else? also, where does the Rt to Lt shunting of blood due to ARDS happen, in the heart or lungs?

  16. thank you for your videos.
    i have a question; can you please clarify the difference between anatomic dead space and shunting. Please. thank you.

  17. I understood most of this. Thank you very much! But I do have one question though… If hypoxemia due to shunts does not improve well with 100% oxygen therapy, could that be used as a diagnostic tool? To identify the cause of the hypoxemia? Thanks in advance!

  18. Hi Dr.
    This was a great video. But I'm still a little confused. I had a USMLE question that said, Pulmonary Embolism isn't considered shunting, but it's more of a Deadspace problem.

    Why isn't ARDS considered a Deadspace problem, but more of a Shunting problem. Isn't it like of similar? Both situations Ventilation is normal, ….. is it because shunting has normal profusion, while Deadspace have no profusion?

  19. Great video – thanks! One question: why is ARDS/pulmonary oedema considered a shunting problem, and not a diffusion problem? Or is it both?

  20. So by definition a hemothorax is one giant shunt, bipap with high epap would oxygenate better than 100% alone ?

  21. I was told yesterday that I had a shunt, I do not know how to react, or if it was normal the reaction of my doctors, you can tell me the risks.

  22. Hi, can anyone please explain what does R to L shunting in pulmonary embolism mean? Is it R to L cardiac shunting or pulmonary shunting?

  23. Hi! Would appreciate if you could give a reply because I cannot seem to find an answer anywhere else. In shunts like ARDS, does PAO2 not decrease since there is no ventilation? Therefore, doesn't PAO2 and PaO2 both decrease and this lead to no change in the A-a gradient? thank you very much!

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