NRB over NC

Our text book has us giving everyone O2 unless I read it wrong which may have happened.

Yeah, the book is simply outdated.

Thanks for the info I find respiratory therapy fascinating.

That makes one of us. LOL After a point, it's just a job.
 
Even it the pt's O2 is at 100% on room air couldn't giving them O2 help or at least make them think they are getting help? The placebo effect?

The answer to this involves a little math, and a little physiology. It's a little beyond what's covered in an average EMT-B class. It's something that should be covered in medic school.

Oxygen is carried in the circulation in two forms (1) bound to hemoglobin, (2) dissolved in the plasma. We can actually calculate the amount of oxygen carried in arterial blood. This is called the arterial oxygen content or CaO2, and is defined as:

CaO2 = (1.34 * hgb * SaO2) + (0.003 * PaO2)

Where hgb is the hemoglobin concentration in g / dL (normal male about 14-18, female 12-16), SaO2 is the saturation percentage expressed as a decimal (i.e. 100% saturation = 1.00, 98% saturation = 0.98). The PaO2 is a measure of how much oxygen is dissolved in the plasma, as this is a dissolved gas, it's a partial pressure, measured in mmHg. [I've omitted some of the units from this equation, but the end value for CaO2 is expressed in ml 02 per dl arterial blood).

So for the hypothetical situation of an individual who has a 100% oxygen saturation, breathing room air, we can infer that their PaO2 is going to be around 100mmHg. We get this from the oxyhemoglobin dissociation curve, which you can see illustrated here: http://en.wikipedia.org/wiki/Oxygen–haemoglobin_dissociation_curve or better yet, in a good physiology text. It can also be measured with an arterial blood gas.

If we assume this person is a male with a hemoglobin of 16 g/dl, we can fill in the other values, and calculate (1) the amount of oxygen carried on hemoglobin, (2) the amount of oxygen dissolved in the blood, (3) the total arterial oxygen content.

So, first, the hemoglobin bound hemoglobin

= 1.34 * hgb * SaO2 = 1.34 ml /g * 16 g/dl * 1.00 = 21.44 ml

Then the dissolved oxygen in the plasma

= 0.003 * 100 = 0.3 ml.

For a total oxygen content of 21.74 ml, of which 98.6% is hemoglobin bound, and 1.4% is dissolved in the plasma.

So, when we look at this, the first thing we get, is, hey, the vast, vast majority of oxygen is transported as hemoglobin.

Now, of course, our patient is breathing room air, this is diffusing across the alveoli to give us an arterial PaO2 of about 100 mmHg. If we assume we're at sea level, ambient air pressure is about 760 mmHg. 21% of the ambient air gives a partial pressure of about 160 mmHg. This is what we're breathing in This is getting reduced as air in the lungs gets humidified, there's a little bit of shunting -- for a whole lot of reasons this ends up as around 100 mmHg in the arterial blood.

If we give around 100% oxygen, we end up increasing the amount of oxygen in the ambient air from 100 to 760. And we'll end up raising the PaO2, the amount of oxygen dissolved in the plasma. We're not going to raise it anywhere near 760 mmHg, but it's going to increase.

But not by much.

For every 50 mmHg we are able to raise the PaO2, the oxygen content is only going to go up by 0.15 ml. This is an increase of 0.7%.

The point, that I'm finally getting to, is that once the hemoglobin is fully saturated, increasing supplemental oxygen is going to have minimal effects on total arterial oxygen content.

The situations where this may be more relevant, would include

(1) the presence of dysfunctional hemoglobin, e.g. CO-hemoglobin, methemoglobin, where the oxygen saturation is falsely raised.

(2) When the patient is severely anemic, e.g. hemorrhagic shock, when less hemoglobin is present. But even in this case, if the available hemoglobin is fully saturated, additional dissolved oxygen in the plasma is only going to have a small effect.


Please understand, I'm not trying to talk down to you, or be condescending. I will happily explain more, if I can. All the best.
 
Last edited by a moderator:
Even it the pt's O2 is at 100% on room air couldn't giving them O2 help or at least make them think they are getting help? The placebo effect?

Via the placebo effect, possibly. But that is something you have to be VERY careful with.

If the patient has a 100% O2 saturation and doesn't show any signs of hypoxia, what good will giving them oxygen do? Oxygen isn't a wonder drug! (Penicillin has that honor :P)

Remember at sea level, air is only made up of approximately 20-21% O2. If you give the patient more than this (which is what you're doing in most if not all cases of oxygen therapy), that's not something the body is used to.
 
Our text book has us giving everyone O2 unless I read it wrong which may have happened.

You didn't. Sadly :sad:

I've heard that O2 therapy over a period of time (not sure how lung) can have negative affects but I thought short term use (during transport) was not as a big concern. Sounds like I got some research to do. Thanks for the info I find respiratory therapy fascinating.

Take a look at this. It's an excellent site!
http://www.ccmtutorials.com/rs/index.htm
 
Also, regarding the placebo effect:

Yes, giving a patient oxygen and telling them the pain in their compound fracture will improve works. It does. So does telling them:

- wearing a green crystal around their neck will improve nausea
- going to a chiropractor will improve their subjective symptoms of diabetes
- giving them a homeopathetic dilution of ground up pieces of the Berlin wall will improve their constipation
- giving a saline flush will make their chest pain better


But it's not particularly ethical. For what it's worth, I believe a lot of the mystique of the medical profession is deliberately designed to invoke the placebo effect.

There is now some concern that making patients hyperoxemic, i.e. providing oxygen beyond resting conditions, is going to result in the generation of free radicals and worsen existing disease processes. This has been a concern in the management of neonates for years, and is now starting to get some attention in the treatment of adults.

[I am not suggesting that you should withhold oxygen from anyone with clinical signs or symptoms of hypoxia, nor am I suggesting that it would be a good idea to violate your existing protocols and try to explain to your medical director your concerns about reactive oxygen species generation].
 
- wearing a green crystal around their neck will improve nausea
- going to a chiropractor will improve their subjective symptoms of diabetes
- giving them a homeopathetic dilution of ground up pieces of the Berlin wall will improve their constipation
- giving a saline flush will make their chest pain better

[YOUTUBE]http://www.youtube.com/watch?v=HMGIbOGu8q0[/YOUTUBE]
 
- giving them a homeopathetic dilution of ground up pieces of the Berlin wall will improve their constipation

LOL that made my day
 
While i am an EMT and have been taught like everyone else out there that its NRB unless the pt cant tolerate it, If the pt in unconscious and is in need of O2, i will put an NRB on them and if there is no improvement then the pt will be intubated other than, we use cannula to get 100% Spo2.
 
The answer to this involves a little math, and a little physiology. It's a little beyond what's covered in an average EMT-B class. It's something that should be covered in medic school.

Oxygen is carried in the circulation in two forms (1) bound to hemoglobin, (2) dissolved in the plasma. We can actually calculate the amount of oxygen carried in arterial blood. This is called the arterial oxygen content or CaO2, and is defined as:

CaO2 = (1.34 * hgb * SaO2) + (0.003 * PaO2)

Where hgb is the hemoglobin concentration in g / dL (normal male about 14-18, female 12-16), SaO2 is the saturation percentage expressed as a decimal (i.e. 100% saturation = 1.00, 98% saturation = 0.98). The PaO2 is a measure of how much oxygen is dissolved in the plasma, as this is a dissolved gas, it's a partial pressure, measured in mmHg. [I've omitted some of the units from this equation, but the end value for CaO2 is expressed in ml 02 per dl arterial blood).

So for the hypothetical situation of an individual who has a 100% oxygen saturation, breathing room air, we can infer that their PaO2 is going to be around 100mmHg. We get this from the oxyhemoglobin dissociation curve, which you can see illustrated here: http://en.wikipedia.org/wiki/Oxygen–haemoglobin_dissociation_curve or better yet, in a good physiology text. It can also be measured with an arterial blood gas.

If we assume this person is a male with a hemoglobin of 16 g/dl, we can fill in the other values, and calculate (1) the amount of oxygen carried on hemoglobin, (2) the amount of oxygen dissolved in the blood, (3) the total arterial oxygen content.

So, first, the hemoglobin bound hemoglobin

= 1.34 * hgb * SaO2 = 1.34 ml /g * 16 g/dl * 1.00 = 21.44 ml

Then the dissolved oxygen in the plasma

= 0.003 * 100 = 0.3 ml.

For a total oxygen content of 21.74 ml, of which 98.6% is hemoglobin bound, and 1.4% is dissolved in the plasma.

So, when we look at this, the first thing we get, is, hey, the vast, vast majority of oxygen is transported as hemoglobin.

Now, of course, our patient is breathing room air, this is diffusing across the alveoli to give us an arterial PaO2 of about 100 mmHg. If we assume we're at sea level, ambient air pressure is about 760 mmHg. 21% of the ambient air gives a partial pressure of about 160 mmHg. This is what we're breathing in This is getting reduced as air in the lungs gets humidified, there's a little bit of shunting -- for a whole lot of reasons this ends up as around 100 mmHg in the arterial blood.

If we give around 100% oxygen, we end up increasing the amount of oxygen in the ambient air from 100 to 760. And we'll end up raising the PaO2, the amount of oxygen dissolved in the plasma. We're not going to raise it anywhere near 760 mmHg, but it's going to increase.

But not by much.

For every 50 mmHg we are able to raise the PaO2, the oxygen content is only going to go up by 0.15 ml. This is an increase of 0.7%.

The point, that I'm finally getting to, is that once the hemoglobin is fully saturated, increasing supplemental oxygen is going to have minimal effects on total arterial oxygen content.

The situations where this may be more relevant, would include

(1) the presence of dysfunctional hemoglobin, e.g. CO-hemoglobin, methemoglobin, where the oxygen saturation is falsely raised.

(2) When the patient is severely anemic, e.g. hemorrhagic shock, when less hemoglobin is present. But even in this case, if the available hemoglobin is fully saturated, additional dissolved oxygen in the plasma is only going to have a small effect.


Please understand, I'm not trying to talk down to you, or be condescending. I will happily explain more, if I can. All the best.

Thanks for the review of basic blood gas physiology, but you missed the major takeaway point that if the patient doesn't have a need for supplemental oxygen, they don't have a need for supplemental oxygen. It's not an "It might be helpful" sort of equation....there's more evidence that it does harm than offers some unexpected benefit.

EDIT: OOPS. Should have read the rest of the thread before posting. My apologies.

BTW, you bring that sort of thing up to most medics and you get a blank stare so its not covered in a lot of medic courses apparently.


While i am an EMT and have been taught like everyone else out there that its NRB unless the pt cant tolerate it,

Was my class the only one in the mid-1990s teaching something other than NRB or nothing at all? We were taught about NC, NRB, SFM, Venturi masks and trach collars.
 
Last edited by a moderator:
But it's not particularly ethical. For what it's worth, I believe a lot of the mystique of the medical profession is deliberately designed to invoke the placebo effect.

Depends upon whom you ask. I see no real reason to consider it blatantly unethical. We do more or less the same thing with about 90% of albuterol treatments handed out in hospitals every day. People feel better mostly because you're doing something to them, whether or not their underlying pathology is altered by the medication or not.
 
There is nothing bloody magic about oxygen, not everybody needs oxygen, craming 15LPM NRB down every patients gob is not doing to do them any good and in some cases may be harmful.

Supraphysiological amounts of oxygen cause capillary and small arterioles to constrict which in some patients can have a negative effect - for example stroke and head injured patients.
 
Depends upon whom you ask. I see no real reason to consider it blatantly unethical. We do more or less the same thing with about 90% of albuterol treatments handed out in hospitals every day. People feel better mostly because you're doing something to them, whether or not their underlying pathology is altered by the medication or not.

Hmm. I guess it's a question of where do you draw the line? I'd assume that the patients receiving albuterol are at least dyspneic and exhibiting signs of mild respiratory distress? Even if the benefit may be minimal.

For example, I would have issue with someone pushing a bolus of saline and telling the patient they're receiving morphine. Even if this is likely going to reduce their pain.
 
There is sufficient evidence that supraphysiologic administration of oxygen is harmful AND if your standing orders state oxygen is to be titrated to SPO2 or level of illness (which most do) then yes, Brown thinks it is unethical to shove everybody on 15PLM NRB given that it may cause harm in some patients

Perhaps we should expand on that 100 hour wonder course and make this required reading?

http://www.brit-thoracic.org.uk/cli...n/emergency-oxygen-use-in-adult-patients.aspx
 
I'd assume that the patients receiving albuterol are at least dyspneic and exhibiting signs of mild respiratory distress?

Actually most albuterol treatments (in non-ER patients) are given to folks with no immediate respiratory symptoms. It's generally based on history and the lack of knowledge of the docs as to how to prevent an exacerbation of COPD or asthma (read as: albuterol is a piss poor preventive medication when you look at the negative effects it has on patients). The fact that 99.9% of what I spent my time as a "regular" (not in a flight capacity) RT had zero benefit to the patient is a major reason why I finally got fed up with the field and started looking at other options. The other reasons were lack of opportunities to advance, few choices as far as specialization goes (so says the guy who works on an air ambulance....guess I should point out the hypocrisy in that....LOL) and a few other minor piddly things.
 
Last edited by a moderator:
Gosh and here Brown was thinking that we should only give salbutamol to people who needed it :unsure:
 
... Supraphysiological amounts of oxygen cause capillary and small arterioles to constrict which in some patients can have a negative effect - for example stroke and head injured patients.

Especially in patients with ACS who are NOT HYPOXIC (SaO2 > 89%)! Hyperoxia can induce vasoconstriction in coronary blood vessels, which will inhibit oxygenation to the very areas with which you are trying to repurfuse. While the pulse oximetry may convey a nice therapeutic value, the counterproductive effects can be rather insidious.
 
Gosh and here Brown was thinking that we should only give salbutamol to people who needed it

We should only give it to people who need it. The problem is that most hospitals don't follow that common sense approach to it. Personally, once I have my PhD, I hope the US pulls its head out of its ***, approves intravenous albuterol (like most of the rest of the world has) and we let the nurses start giving it like any other medication. There's nothing particularly specially about it being given by nebulization and in fact, even with perfect technique, the patient is lucky to receive half the prescribed dose.
 
I hope the US pulls its head out of its ***, approves intravenous albuterol (like most of the rest of the world has) and we let the nurses start giving it like any other medication.

Intensive Care Paramedics here have IV salbutamol, not where Brown is personally but it is here.
 
I hope the US pulls its head out of its ***, approves intravenous albuterol (like most of the rest of the world has) and we let the nurses start giving it like any other medication.
Point of information: how does this work?

I was told of a paramedic who did this in upstate NY and she was promptly banned from ever riding on an ALS truck ever again, because it was a gross violation of protocols and how the medication was supposed to be administered. Not only that, but albuterol should be administered via the lungs (I am drawing a blank on the proper term) vs IV, because it relives the difficulty breathing and has an immediate concentrated action based on it's method of delivery.
 
Back
Top