When will O2 truly help?

[VentMedic]

Vent,

I would like to think even new EMT-P's, RN's, RRT's would still be doing a complete assessment regardless of the situation.

As this thread has finally come full circle to illustrate that, YES, one has to eventually treat any and all underlying acute conditions, which is exactly what I said in my first posts.....Albeit a little too basic for some of the brain trust in here!

Respectfully,

JW

John, the OP is an EMT-BASIC. If you look around at some of the other forum members, many are still students in EMT-B class. For some this is their first introduction to a few basic and advanced concepts about O2. In EMT-B, oxygen therapy is really not covered very well nor are the disease processes and the oxyhemoglobin dissociation curve.

Many of your posts were very technical as were mine so sometimes some things must be repeated and reinforced for those new to the profession and with only the training that the EMT-B provides so that they may have a solid understanding of the concepts at hand especially if they are reading them for the first time.

So no the subject of oxygen should not be closed since there is so much more for them to learn.

Edited November 23, 2009 by VentMedic

[Brandon Oto]

To reinforce that a little, I'm sympathetic to the cries of "better education" and "better training," but until those changes run through the system, folks like me are left to learn on their own. So while I think it's great to complain that Basics et al. should already know this stuff, I'd much rather that you just explained as much of it as possible. I don't want to get in the way of whatever other discussions you guys want to have, but if you really believe in creating more educated providers, well -- we're reading, and that's why we're asking questions.

[tniuqs]

'chbare'

However, we are still discussing the question about who benefits from oxygen therapy? I think we can say, yes some patients will benefit from supplemental oxygen. However, how much they benefit from the said therapy may be a better concept to discuss. Going back to an anemic patient; There is little doubt that increasing the partial pressure of oxygen will in fact increase the content of arterial oxygen in these patients (assuming no diffusion or oxygen movement problems exist). However, as pointed out earlier the actual impact on content of arterial oxygen is rather small

This is very dependent where the SpO2 or SaO2, some occasions this is a major difference in positive outcomes, sorry to disagree with the above comment and it leads some down a garden path and breaches the vast majority of EMS protocols ... I have yet to directives to titrate O2 to sats of ______ in any EMS protocols.

So hypothetical situation, you find a patient with PMHX of Sickle cell and your suggesting that that O2 is not indicated, question: At what PaO2 will cells start to sickle? (documented in EBM)

Or that even when anemia may or may not be present (clinically) and SpO2 is reading 92 % do you withhold O2 ?

Point being that understanding ODC oxygen dissociation curve (sans shift due H+ or other variables, lets not complicate with 2-3 DPG, or others)[all things being equal] that most EMT-B have very little understanding of what SpO2 and PaO2 fall on the curve?

Or the "suspected" hypovolemic patient and SPo2 is 93% do you not use a NRM at higher flows ?

Or the patient in moderate respiratory distress, does the Krebs cycle not come into play and assist to prevent an increasing metabolic lactic acidosis ?

In addition, we must also appreciate the difference between hypoxemia and hypoxia. There exist very important considerations and implications associated with these two concepts.

I asked this very question of JWade in the inception of this ... perhaps you could enlighten the readers ?

cheers

[chbare]

This is very dependent where the SpO2 or SaO2, some occasions this is a major difference in positive outcomes, sorry to disagree with the above comment and it leads some down a garden path and breaches the vast majority of EMS protocols ... I have yet to directives to titrate O2 to sats of ______ in any EMS protocols.

I did not think we were talking about protocols. I thought this was a discussion about situations where oxygen therapy would be helpful. I clearly stated I think such situations absolutely exist. However, my comment was based around asking how much to specific individuals benefit.

So hypothetical situation, you find a patient with PMHX of Sickle cell and your suggesting that that O2 is not indicated, question: At what PaO2 will cells start to sickle? (documented in EBM) Never once have I suggested oxygen therapy is not indicated for these patients. I am asking how helpful is oxygen therapy for these patients.

Or that even when anemia may or may not be present (clinically) and SpO2 is reading 92 % do you withhold O2 ? Nope, never said I would.

Point being that understanding ODC oxygen dissociation curve (sans shift due H+ or other variables, lets not complicate with 2-3 DPG, or others)[all things being equal] that most EMT-B have very little understanding of what SpO2 and PaO2 fall on the curve? I am not sure I understand your point.

Or the "suspected" hypovolemic patient and SPo2 is 93% do you not use a NRM at higher flows ? Depends. Even at higher flows, NRM's are not generally considered high flow devices. Therefore, we must also consider the patients demand for flow.

Or the patient in moderate respiratory distress, does the Krebs cycle not come into play and assist to prevent an increasing metabolic lactic acidosis ? The Krebs cycle does not utilize oxygen nor does it assist in the prevention of acidosis. While acidosis can result when things do not work however. This may be your point?

Oxygen is utilized during oxidative phosphorylation by cytochrome c oxidase where oxygen acting as an electron acceptor is reduced. While incomplete use of pyruvate through the Krebs cycle will lead to increased lactate, oxidative phosporylation in essence allows the Krebs cycle to function normally. Normal oxidation of pyruvate requires both a working Krebs cycle and electron transport chain. With that, the Cori cycle actually plays a key role in "recycling" lactate. Therefore, moderate respiratory distress may or may not lead to metabolic lactic acidosis. If cellular hypoxia is not present, I would not expect a metabolic lactic acidosis to be present assuming other conditions are not present. Not to say that hypoxia could not develop as a result of sustained respiratory distress however.

I asked this very question of JWade in the inception of this ... perhaps you could enlighten the readers ?

Hypoxia is generally considered a lack of oxygen availability at the cellular level where hypoxemia is a lack of oxygen in the blood. While often related, these are in fact two different concepts.

cheers

Take care,

chbare.

Edited for color coordination.

Edited November 23, 2009 by chbare

[kohlerrf]

I agree, the only 2 situations I can say the administration of specifically oxygen truly helped my pt is;

1)Arriving to the home of a patient on a home room air nebulizer giving themself an albuterol treatment. When I repeat this with 100% O2 off my D tank the pt seem to recover faster. You could say that this is just the effect of the previous medications kicking in, but I don't think so because over the years I have gauged reaction times with initial tratment on Oxygen and initial treatments using room air.

2) The second situation is, believe it or not, Oxygen is my initial drug treatment for un-complicated sinus bradycardia! and it works.

[tniuqs]

Could you Quantify "HELPED" ?

cheers

[kohlerrf]

Could you Quantify "HELPED" ?

cheers

In the case of the home fed asthmatic 100% FiO2 fed nebulizer will help the pt return to their baseline faster and in the case of uncomplicated sinus bradycardia with pure oxygen administration the rate will often times will increase to a sustainable 60 or 70bpm and the B/P will normalize as well. Remember a sign of hypoxia (more prominent in the very young and the very old is bradycardia)

[tniuqs]

In the case of the home fed asthmatic 100% FiO2 fed nebulizer will help the pt return to their baseline faster and in the case of uncomplicated sinus bradycardia with pure oxygen administration the rate will often times will increase to a sustainable 60 or 70bpm and the B/P will normalize as well. Remember a sign of hypoxia (more prominent in the very young and the very old is bradycardia)

Firstly: I am sorry I asked now, point being that one can not quantify "HELPED" one unless using controls as Ventmedics post using Compressed Air vs O2, its ALL anecdotal there is no science in the OP original question, just opinion and conjecture only.

as for the home fed, HUH ?

There is no possible way to deliver an FiO2 with just a SVN or NRM btw

and return to what baseline ?

Do you mean Homeostasis ?

and sinus brady is a sign of Hypoxia.

So then and Peads Brad and the Elderly Brad before becoming tachycardic when they are Hypoxic ? Or am I reading this incorrectly ?

So your saying you treat symptomatic Bradycardia with O2 and this improves Heart Rate?

If I a correct in my reading skills, just where did you get your Paramedic licence out of a box of corn flakes ?

This is very dependent where the SpO2 or SaO2, some occasions this is a major difference in positive outcomes, sorry to disagree with the above comment and it leads some down a garden path and breaches the vast majority of EMS protocols ... I have yet to directives to titrate O2 to sats of ______ in any EMS protocols.

I did not think we were talking about protocols. I thought this was a discussion about situations where oxygen therapy would be helpful. I clearly stated I think such situations absolutely exist. However, my comment was based around asking how much to specific individuals benefit.

Again how can one in the field "Quantify" please note that in Kevkie attachment on the use of thromblytic protocol the target SPO2 ie Keep Sats > 92%. I have yet to see any protocol that does not state use supplementary O2 for any CP or SOB. A better question could be can one PROVE that Oxygen in the field is detrimental, just saying

So hypothetical situation, you find a patient with PMHX of Sickle cell and your suggesting that that O2 is not indicated, question: At what PaO2 will cells start to sickle? (documented in EBM)

The FREE answer to that is in the Sickle Cell Patient they are at a far greater risk of sickling with PaO2 < 50 mmhg or bedside SPO2 < 85% (more or less, and quite dependent on the ODC shift) that may "help" to explain the other queries in regards to the ODC, that little sigmoid shaped graph is far more complex than most would imagine.

Or the "suspected" hypovolemic patient and SPo2 is 93% do you not use a NRM at higher flows ? Depends. Even at higher flows, NRM's are not generally considered high flow devices. Therefore, we must also consider the patients demand for flow.

Preaching to the Choir mate, higher operative word in the above statement (but a good point never the less)The meat of that statement is in any suspected cases of Hypovolemia "higher flows" should be delivered to improve content and capacity of to saturate remaining HGB.

Or the patient in moderate respiratory distress, does the Krebs cycle not come into play and assist to prevent an increasing metabolic lactic acidosis ? The Krebs cycle does not utilize oxygen nor does it assist in the prevention of acidosis. While acidosis can result when things do not work however.This may be your point? Oxygen is utilized during oxidative phosphorylation by cytochrome c oxidase where oxygen acting as an electron acceptor is reduced. While incomplete use of pyruvate through the Krebs cycle will lead to increased lactate, oxidative phosporylation in essence allows the Krebs cycle to function normally. Normal oxidation of pyruvate requires both a working Krebs cycle and electron transport chain. With that, the Cori cycle actually plays a key role in "recycling" lactate. Therefore, moderate respiratory distress may or may not lead to metabolic lactic acidosis. If cellular hypoxia is not present, I would not expect a metabolic lactic acidosis to be present assuming other conditions are not present. Not to say that hypoxia could not develop as a result of sustained respiratory distress however.

So an Oxygen DEBT does not not come into play in a Metabolic Lactic Acidosis ?

Simply stated: The Krebs Cycle (anerobic respiration and production of lactic acid) this is just PART of the SUM "of the PART's" when hypoxia is present.

Hypoxia is generally considered a lack of oxygen availability at the cellular level where hypoxemia is a lack of oxygen in the blood. While often related, these are in fact two different concepts.

Bless you, btw none of my queries were aimed at chbar well other than ODC.

Edited December 8, 2009 by tniuqs

[funkytomtom]

I just finished my intermediate class, and I'm just barely hearing many of these concepts for the first time. Why aren't they addressed?!?!? Now I feel like the idiot. Anyways, its been great reading through all this. Question for chbare, or anyone really; I understand the difference in definitions between hypoxia and hypoxemia, but how is this actually going to play out on a patient?...in the field?

[Brandon Oto]

I just finished my intermediate class, and I'm just barely hearing many of these concepts for the first time. Why aren't they addressed?!?!? Now I feel like the idiot. Anyways, its been great reading through all this. Question for chbare, or anyone really; I understand the difference in definitions between hypoxia and hypoxemia, but how is this actually going to play out on a patient?...in the field?

I suppose the theoretical answer is that if a patient is hypoxic without being hypoxemic, their O2 sat will not reveal their true level of cellular distress.