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Posted

Most of the posts seem to be regarding lowering O2. I have a question regarding upping it. I recently ran a call where the PT was a 21 M with a hx of Wolff-Parkinson-White Syndrome experiencing 5 on 5 chest pain. Since the call I have looked up Wolff-Parkinson-White Syndrome and understand the basics of it. When the medic got on scene he told me to up the NRB from 15lpm to 25lpm and then had the pt preform a vagul maneuver before the ALS crew initiated transport. Can someone explain the upping of O2? I'm not questioning the medic but I'm curious because isn't there a point where the body won't get more O2? Thanks guys.

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Posted
But why should someone who is satting at 98% get O2? Why should someone satting at 94% get 15Lpm?

Why are we even talking about lpm when it is such a completely irrelevant factor?

Posted
NRB from 15lpm to 25lpm

:shock:

Way to blast the guys face off

Posted

Why are we even talking about lpm when it is such a completely irrelevant factor?

Perhaps because we are not reading the posts prior? The point of the thread is that research "could" be indicating that high flow O2 may be detrimental to patient outcomes. Not specific to individual conditions as in WPW, this is a accessory pathway that is quite rare and the definitive treatment is obligatory surgery for thses pathways.

It is highly unlikely that grunt or cough is going to be successful to convert to nsr .... welding may work. The thing is that welding in the field for this condition is a bit aggessive when the patient is awake and telling you of pain 5/5 and a query is just what level of Paramedic diagnosed this condition or was it PMHX that lead someone to believe that a 20 y/o with narrow complex tachycardia was WPW....looking for salvadore dali's "moustache" are we?

But Bushy does have a good point, the windblown look is really svelt and very trendy........

cheers

Posted
Way to blast the guys face off

I did as the medic told me to. I'm just asking why he would have increased the rate so high. Is this part of an ALS protocol?

tniuqs: If I understand your post correctly, let me clarify. The Pt had been diagnosed by a doctor several years prior with WPW syndrome and told us so.

Posted

I did as the medic told me to. I'm just asking why he would have increased the rate so high. Is this part of an ALS protocol?

Sounds like some lame arse attempt at ghetto CPAP. :?

The good news is that, after you turn it up that high, you won't be able to hear any of the other stupid things this guy tells you to do. :lol:

Posted

I would say stick to the book on this one, more O2 can hardly hurt them, unless they are COPD (am i thinking of the right illness?), and even then it would take quite a while to cause serious damage.

Posted

Sounds like some lame arse attempt at ghetto CPAP. :?

The good news is that, after you turn it up that high, you won't be able to hear any of the other stupid things this guy tells you to do. :lol:

Now calm down, have you ever put a non re-breather on yourself. Try it. Difference between 10, 15 and 25 is just a little more cool air. Doesn't even crease your cheeks at 25 let alone blast his face off. All your doing is wasting oxygen.

Posted

The nerdy/logical part of me would like to point out that even if negligible, there is a difference in amount of oxygen patient receives, between 15lpm and 25lpm.

When you exhale, the CO2, does not all leave the mask through those tiny rings of holes on the side. As more O2 enters the mask from the bag, it replaces the CO2/O2 mixed air in the mask by pushing it out the holes. This takes a bit. If your flow is 25lpm, that CO2 in the mask is displaced much faster. One is closer to 100% O2 than the other.

BTW, what setting do you guys use when bagging a patient? We use 15lpm, but hospital always has us increase it to pretty much wide open when we get to the ER (floating ball is to the very top).

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