O2 txt in a COPDer

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nvshelat

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:eek:

Had this qtn on my Step 1 yesterday. Almost laughed when I came across it bc I remember looking it up before the test thinking, well they prolly won't ask it... and of course they did! Anyway, I put that the dude is dependent on O2 receptors - even though I was told this past summer that I'd be strung up if I ever said this to an anesthesiologist - bc thats the answer they want. It's the only one that made sense anyway.
I did a quick search, seems divided on whether you can take a COPDer, give them O2, and walk away. Any new thoughts?

Anyway, I'm glad that that thing is OVER! Who-hoo!!! :hardy::hardy: Hopefully my score will be good enough to join you guys in what seems like a pretty cool profession :thumbup:
:thumbdown: to the Comlex tomorrow. After that, I'm gonna sit on the beach (or in a bar) and forget about life for a while. Laaaa laaa laa dee dee da...

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Old but good:
http://www.ncbi.nlm.nih.gov/pubmed/6778278?dopt=Abstract

Oxygen treatment does inhibit the hypoxic drive but it seems to be only of temporary effect on minute ventilation. Increase in PCO2 with oxygen therapy in COPD patients, then, is said to be primarily a result of the increased dead space ventilation that occurs with oxygen therapy.

The NEJM articles on the matter suggest a targeted oxygen saturation in the 90-92% range, in attempting to avoid the hypercapnia associated with higher FiO2's while yet keeping the patient decently oxygenated.
 
actually pretty routine (i thought) to keep copd'ers sats a little lower so as not to shut down the respiratory drive...hell, thats where they live anyways. is this controversial?

comlex is a joke next to usmle ;-) -- (well, for me anyways) -- so the hard part is over!
good luck!
 
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actually pretty routine (i thought) to keep copd'ers sats a little lower so as not to shut down the respiratory drive...hell, thats where they live anyways. is this controversial?

comlex is a joke next to usmle ;-) -- (well, for me anyways) -- so the hard part is over!
good luck!

The idea that oxygen therapy shuts down respiratory drive is an inaccurate one, but it does seem to be commonly propagated...I know that I've heard it a lot. Higher FiO2 does cause hypercapnia but chiefly because blood flow changes in the lungs cause increased V/Q mismatch and more dead space ventilation.

At 15 minutes the above study found little to no difference in minute ventilation between those COPD patients who received 100% O2 and control. Respiratory drive was not significantly affected by high flow oxygen.
 
On a side note... I was recently learned when putting COPDers on the vent to be aware of mivnute ventilation as this characters live with a respriatory acidosis and compensate with the metabolic alkalosis. Thus MV should be adjusted to find their PaCO2 and not normal PaCO2. Otherwise might see some electorlyte shifts and arrhythmias. Anyone seen this?
 
hmmmm...thanks. never questioned what was told to me MANY MANY times....
come to think of it...i commonly heard this from surgeons, never from an anesthesiologist.
 
On a side note... I was recently learned when putting COPDers on the vent to be aware of mivnute ventilation as this characters live with a respriatory acidosis and compensate with the metabolic alkalosis. Thus MV should be adjusted to find their PaCO2 and not normal PaCO2. Otherwise might see some electorlyte shifts and arrhythmias. Anyone seen this?

I thought that was pretty standard, didn't know it was controversial
 
quick answer-
inhibition of Hypoxic pulmonary vasoconstriction increases V/Q mismatch
 
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