NRB over NC

[usafmedic45]

Point of information: how does this work?

The same way as if you give it by inhalation or if you give any other sympathomimetic drug (epi, terbutaline, etc). It's absorbed into the bloodstream and you get the desired effect (which is why it takes 10-15 minutes to get full effect from a dose; you wouldn't see that if it were locally acting). You can also give it IM or PO and get the same effects.

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.

Ah, I see your reasoning, but it's badly flawed. There's no substantial evidence that says it's more effective by inhalation. It's not quicker. Works just the same and just as quick if you give it IV. Anecdotally, I'd say it works faster (within five minutes) when given IV based on the handful of cases I've seen. Any patient that gets "instant" relief from albuterol is exhibiting a placebo effect. Also, you're not spraying half the dose into the air this way either when you give it IV.

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.

Because it's not packaged for IV use here in the US, not because it doesn't work if you give it that way. It's a quirk we have here in the US that I don't fully understand but I would imagine it has something to do with keeping my colleagues in respiratory therapy employed since dosing people with albuterol is about 90-95% of the workload for about 90-95% of us.

BTW, apparently the IV formulation is approved here in the US but it just is not very common. It's also able to use off label in that form as a tocolytic according to some anecdotal reports.

 

[Hellsbells]

Hmmm, this wholesale administration of NRB's must be an American idiosyncrasy. EMT education in Canada doesn't involve any sort of stipulation that all pts get oxygen, and should also all get NRB's. This seems completely preposterous to me.

As to the original question, I fail to see what the debate vis-à-vis NC and NRB has to do with diagnosis. If all pts get 02 then there is absolutely no diagnosis at play, no matter how its delivered.

I have heard the notion that "EMT/Paramedics" don't diagnosis. However, I can't remember ever being taught that specifically in school. In order for us to treat pts, we must diagnosis, even to a limited degree. In all reality, once the pt gets to the hospital, the physician will assess the pt and make an independent diagnosis. Its not as if what we determine in the field becomes the last word on the pts chart.

 

[AMF]

Hmmm, this wholesale administration of NRB's must be an American idiosyncrasy. EMT education in Canada doesn't involve any sort of stipulation that all pts get oxygen, and should also all get NRB's. This seems completely preposterous to me.

As to the original question, I fail to see what the debate vis-à-vis NC and NRB has to do with diagnosis. If all pts get 02 then there is absolutely no diagnosis at play, no matter how its delivered.

I have heard the notion that "EMT/Paramedics" don't diagnosis. However, I can't remember ever being taught that specifically in school. In order for us to treat pts, we must diagnosis, even to a limited degree. In all reality, once the pt gets to the hospital, the physician will assess the pt and make an independent diagnosis. Its not as if what we determine in the field becomes the last word on the pts chart.

We do it backwards... the EMT/Ps assess and stabilize, doctors diagnose and treat. the latter sounds more terminal. I'm not sure if you're familiar with the the American populace, but we like to be right.

 

[JPINFV]

the EMT/Ps assess and stabilize, doctors diagnose and treat.

What's the difference between stabilize and treat? Are the interventions taken to stabilize the patient treatments?

What's the point of performing an assessment if you don't use the information gained to develop an idea of what is going on, or in other words, diagnose? If your patient has a blood glucose level of 30, did you not just diagnose hypoglycemia?

 

[Shishkabob]

We do it backwards... the EMT/Ps assess and stabilize, doctors diagnose and treat. the latter sounds more terminal. I'm not sure if you're familiar with the the American populace, but we like to be right.

No, the Paramedics diagnose. If you treat, you've made a diagnosis. It may not be the definitive diagnosis, but it's a diagnosis.



If you start pushing medications and doing things without having an idea as to why, you need to lose your license.

 

[usalsfyre]

We do it backwards... the EMT/Ps assess and stabilize, doctors diagnose and treat. the latter sounds more terminal. I'm not sure if you're familiar with the the American populace, but we like to be right.

Paramedics use history, physical exam and diagnostic test to diagnose and treat disease and injury within their scope of practice. Which is fundamentally the practice of medicine (albeit of limited scope). Honestly we are far closer in job description to a mid-level provider (NP or PA) than anything else, but we are VASTLY undereducated for the role.

Legal niceties or not, that is what we do. Some paramedics may like to say otherwise (usually because they somehow think it will shield them from liability), but it's a word game. The sooner paramedics accept this, the sooner we can move on as a profession.

(all views above are my own)

 

[Too Old To 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,

An anecdote, told third hand is not data, it's a war story. As others pointed out it's not used in the US because it's not approved for IV use in most cases.

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.

In the mid 1990s, no. By the end of the 1990s, a class taught that way would be extremely rare, if not extinct. The use a NRB on all patients BS came about with the 1994 EMT-B curriculum. I won't get into the back story on why that was done, but suffice it to say that there was pressure on the committee putting the new curriculum together to keep it at 110 hours. As a result, almost all of the medicine was taken out of the EMT-B course and it became barely distinguishable from a Boy Scout First Aid course.

As a result, EMS at all levels became a skill set and any hope of it becoming a profession, let alone a trade, were smashed forever.

The NRB is to the EMT as the Albuterol Neb is to the RT. Most patients absolutely don't need it, but they get it anyway because too many doctors subscribe to the Chicken Soup school of medicine.

 

[usafmedic45]

The use a NRB on all patients BS came about with the 1994 EMT-B curriculum.

Which is the one I was trained under when I got into the field initially. Our training program's medical director rejected it as medically unsupportable and made sure we were aware of that fact.

The NRB is to the EMT as the Albuterol Neb is to the RT. Most patients absolutely don't need it, but they get it anyway because too many doctors subscribe to the Chicken Soup school of medicine

It's a good analogy, but I've been much more successful in not putting NRBs on people who need them than I have in trying to talk docs out of non-essential/non-indicated albuterol treatments.

I won't get into the back story on why that was done, but suffice it to say that there was pressure on the committee putting the new curriculum together to keep it at 110 hours

I've never seen a state that actually has a 110 hour course. Ours was 140 or 150 plus clinicals. This is where people need to get their heads out of their asses and realize there's a difference between a guideline and a mandate.

 

[Too Old To Work]

Which is the one I was trained under when I got into the field initially. Our training program's medical director rejected it as medically unsupportable and made sure we were aware of that fact.

He was right, but like everyone else who said that, he wasn't listened to.

It's a good analogy, but I've been much more successful in not putting NRBs on people who need them than I have in trying to talk docs out of non-essential/non-indicated albuterol treatments.

This seems to be a common lament among RTs. I read a couple of respiratory therapy blogs and a lot of posts are put up about stupid Albuterol orders. I ran into this when my mother was in a major teaching hospital. She had zero Hx of COPD or Asthma, but the insisted on giving her Albuterol for dyspnea. I was probably less subtle than I should have been in pointing out that she had a long standing Hx of cardiac disease and CHF and that her anginal equivalent was respiratory distress and pulmonary edema. I got the point across finally, but only because the nurse manager of the unit was the wife of a long time co worker.

I've never seen a state that actually has a 110 hour course. Ours was 140 or 150 plus clinicals. This is where people need to get their heads out of their asses and realize there's a difference between a guideline and a mandate.

Although I'm sure I'll get a lot of hate mail, I will tell you that it was the volunteer services that drove the 110 hour requirement. They were afraid that if they made it too difficult, they'd lose volunteers.

 

[medichopeful]

Although I'm sure I'll get a lot of hate mail, I will tell you that it was the volunteer services that drove the 110 hour requirement. They were afraid that if they made it too difficult, they'd lose volunteers.

Don't take this the wrong way but do you have a source for this? I'm trying to get concrete or professional data on why the hell something with so much responsibility has such a low entry requirement. I'm hoping to get involved in changing this in the future, and I think in order to do that I need as much background as possible!

Again, not calling you out but rather looking for more information.

Thanks!
Eric

 

[Too Old To Work]

Don't take this the wrong way but do you have a source for this? I'm trying to get concrete or professional data on why the hell something with so much responsibility has such a low entry requirement. I'm hoping to get involved in changing this in the future, and I think in order to do that I need as much background as possible!

Again, not calling you out but rather looking for more information.

Thanks!
Eric

Yes, the chair of the committee that developed the curriculum. It was at EMS Today in 1995. There was a lot of dissention in the ranks and part of the explanation for decontenting the curriculum was that the volunteer contingent (more influential then than now) insisted that they would lose members if the course was extended to the proposed 150 (I think) hours.

 

[TacEMT]

This is a good discussion but I had a question regarding "why" to use a NC over a NRM during a cardiac related emergency. I was taught in the very last week of class to use NC on cardiac patients unless they have dyspnea, then use NRM. I can't exactly remeber why, but they said NC would be the appropriate answer for our final and on the National Registry. When I asked, one student suggested that the high flow oxygen of the NRM would make the patient more anxious and worsen the effects and I think someone else explained that it was like hyperventilating and it would cause vasoconstriction which worsen the situation as well. Can someone explain to me the reason why high flow oxygen may not be appropriate for a cardiac patient, or any other emergency? And what is titrate effect and does that somehoe play into all this? Thanks

 

[Lifeguards For Life]

This is a good discussion but I had a question regarding "why" to use a NC over a NRM during a cardiac related emergency. I was taught in the very last week of class to use NC on cardiac patients unless they have dyspnea, then use NRM. I can't exactly remeber why, but they said NC would be the appropriate answer for our final and on the National Registry. When I asked, one student suggested that the high flow oxygen of the NRM would make the patient more anxious and worsen the effects and I think someone else explained that it was like hyperventilating and it would cause vasoconstriction which worsen the situation as well. Can someone explain to me the reason why high flow oxygen may not be appropriate for a cardiac patient, or any other emergency? And what is titrate effect and does that somehoe play into all this? Thanks

Why would you think putting a patient and their ischemic, soon to be infarcted cells on high flow O2(read: toxic levels of free radicals) would be a good thing?

Before answeromg your question in red, consider what is really going on with a cardiac patient? At the most basic level they are suffering from some form of coronary occlusion, constriction, partial blockage, that interferes with the heart getting enough oxygen. Oxygen has no thrombolytic properties. Any blood moving past the "blockage" has plenty of oxygen. This is a perfusion problem, not a ventilation problem. (from your post i assume we are talking an uncomplicated chest pain CC)

Also as others have mentioned supraphysiologic 02 tension has been shown to cause coronary vasoconstriction in animals.

Before considering what makes high flow 02 innapropriate, tell us what makes it appropriate.

In all seriousness, research in this area is in it's infancy, so i wouldn't fret too much.

and furthermore seems to be poorly understood by field practitioners, if they are even aware of it. Any negative implications are most likely just a tad bit on the worse side of negligible,

 

[TacEMT]

What I was taught in class is that, for the most part, all your patients should recieve high flow oxygen with a NRM. However they said when appropriate, which it vague. Also if the person can't tolerate a NRM, you put them on a NC or have them hold the NRM in front of them to give them blow by oxygen. For testing purposes, everyone gets oxygen. As others have mentioned, if they are already at an SpO2 of 100%, then oxygen may not do them any good. However, I would not figure out their SP02 till later on in the asessment until after I have already provided them oxygen.

The cadiac and respiratory systems are two seperate systems. It is a perfusion issue so I can see why oxygen would not help them, but how does it hurt them?

I would think high flow oxygen would be appropriate for some cardiac cases, and yea I do mean chest pains to clarify. If they are suffering from CHF, left side, couldn't that lead to pulmonary edema, which reduces the oxygen exchange? For them, if they are having difficult times breathing, I would give them high flow oxygen.

 

[Lifeguards For Life]

What I was taught in class is that, for the most part, all your patients should recieve high flow oxygen with a NRM. However they said when appropriate, which it vague. Also if the person can't tolerate a NRM, you put them on a NC or have them hold the NRM in front of them to give them blow by oxygen. For testing purposes, everyone gets oxygen. As others have mentioned, if they are already at an SpO2 of 100%, then oxygen may not do them any good. However, I would not figure out their SP02 till later on in the asessment until after I have already provided them oxygen.

The cadiac and respiratory systems are two seperate systems. It is a perfusion issue so I can see why oxygen would not help them, but how does it hurt them?

I would think high flow oxygen would be appropriate for some cardiac cases, and yea I do mean chest pains to clarify. If they are suffering from CHF, left side, couldn't that lead to pulmonary edema, which reduces the oxygen exchange? For them, if they are having difficult times breathing, I would give them high flow oxygen.

If you can see why it is not beneficial, why give it regardless of it's potential to harm a patient? two ways it can harm the patient were given in my last post.

CHF is definitely a possibilitym and can definitely "reduce oxygen exchange".

So imagine your cardiac patient has a clot, which is preventing his left ventricle from getting proper blood flow, and enough oxygen. The left ventricle becomes tired and can't pump effectively. It starts pumping slower, and with less force, it can not keep up with the lungs. So inter atrial pressure increases, along with the pressure in the pulmonary veins and cappiliares. this ultimately causes blood to be forced back through the pulmonary cappilaries, and back into the alveoli.

With the alveoli filling with fluids, how will high flow O2 help them? How will high flow O2 improve their "oxygen exchange"?

I don't believe it is as big a deal as some people would have you believe, nothing to get worked up about, but it is good for you to think about.

 

[TacEMT]

Knowing the exact reason why I believe is way above the EMT-B's level, but it is good to know. I read about the oxygen toxicity and free radicals but this seems like something more for someone on high concentration oxygen for a prolonged period of time. Supposedly, though I could be wrong, that there has never been a case of a person who has stopped breathing when given oxygen because they are on hypoxic drive and getting too much oxygen.

But I am still confused as to how it applies specifically to a cardiac patient. If a patient is suffereing from an angina, the cardiac muscle is not recieving enough oxygen, due to a clot, so wouldn't giving them more oxygen assist with that, unless its a full occlusion? I guess to be more specific, is there some type of chemical or physiological effect that high flow oxygen has on the blood that makes it harmful when given for only a short period of time?

 

[usalsfyre]

How will high flow O2 improve their "oxygen exchange"?/QUOTE]
While I generally agree with what your saying, high concentration O2 will improve oxygen exchange at the alveolar level. Look up partial pressures, Dalton's Law and how gas moves across the alveolar/capillary membrane.

 

[Lifeguards For Life]

I read about the oxygen toxicity and free radicals but this seems like something more for someone on high concentration oxygen for a prolonged period of time.

Yes, I would generally agree with this statement, Which is why I said any ill efffects are likely just a tad worse than negligible, and this whole high flow 02 argument is not as dire as some people would like to tell you.

Even recongizing there is a discrepancy is more than I would expect from most EMT's, it is good to be thinking and questioning.

Supposedly, though I could be wrong, that there has never been a case of a person who has stopped breathing when given oxygen because they are on hypoxic drive and getting too much oxygen.

Good.

The Hypoxic dirve theory is a piece of intellectual beauty to be sure, but it doesn't describe anything that really happens. Just like in science, if it doesn't agree with experiment it's wrong. Even though the theory is beautifully crafted, the theory is wrong and utterly useless.

Talking about theory agreeing with experiment brings us back to the high flow oxygen theory. While this theory is backed by "experiment", and the theory does hold true, it's not neccesarily applicable for EMS. To have any appreciable cellular damage takes time that you usually won't have prehospital. And even if you did have the time, there is a strong possiblity that any injury suffered is completely recoverable.

This theory has been around since the 1950's I believe, yet EMS have still been told to give high flow 02 to everyone, I know I was in EMT school. Yet people haven't been dropping off like flies when giveh high flow O2.

It will be interesting to see where this argument goes in the future. I can see it becoming protocol to not use high flow O2 even for cardiac arrest, during some of our careers.

But I am still confused as to how it applies specifically to a cardiac patient. If a patient is suffereing from an angina, the cardiac muscle is not recieving enough oxygen, due to a clot, so wouldn't giving them more oxygen assist with that, unless its a full occlusion?

Your blood can only carry so much oxygen. In an uncomplicated cardiac patient, the RBC's and plasma already have plenty of oxygen. It's not like you can really super-saturate their blood with oxygen to make up for poor blood flow.

I guess to be more specific, is there some type of chemical or physiological effect that high flow oxygen has on the blood that makes it harmful when given for only a short period of time?

Sure. You already told me about Oxygen free radicals. But the damage you can cause in the short amount of time you will have the patient, is like "the smallest amount of damage you can possibly cause". These radicals are destructive to DNA, proteins, etc. But the amount of free radicals that can accumulate in a short period of time is minimal, and your body is always repairing damages, so it's negligible.

Should we really be giving all our patients high flow o2? well no.
Is it really going to cause any appreciable harm, well probably not.

However, I do think that high flow o2 in a code can infact be much more destrucive than high flow o2 than in your CP or COPD etc. patients.

 

[TacEMT]

How will high flow O2 improve their "oxygen exchange"?/QUOTE]
While I generally agree with what your saying, high concentration O2 will improve oxygen exchange at the alveolar level. Look up partial pressures, Dalton's Law and how gas moves across the alveolar/capillary membrane.

So Dalton's law is about total pressue being partial pressues added together. I'm thinking it might be more toward the decomperssion sickness and barotrauma. If high flox oxygen at 100% is much more then at room air, 21%, then it would have a higher partial pressue right? Would that increase in total pressue, like in the lungs, cause the nitrogen to disolve in blood and when the pressue goes back down, the nitrogen turns back to gas and expands and causes an air embolism that could potentially block blood flow. This would be bad for someone already experiencing some type or perfusion problem due to a cardiac emergency.

 

[usalsfyre]

So Dalton's law is about total pressue being partial pressues added together. I'm thinking it might be more toward the decomperssion sickness and barotrauma. If high flox oxygen at 100% is much more then at room air, 21%, then it would have a higher partial pressue right? Would that increase in total pressue, like in the lungs, cause the nitrogen to disolve in blood and when the pressue goes back down, the nitrogen turns back to gas and expands and causes an air embolism that could potentially block blood flow. This would be bad for someone already experiencing some type or perfusion problem due to a cardiac emergency.

The total pressure doesn't increase, that's determined by atmospheric pressure. What does change is the partial pressures of the component gasses in the mixture. A NRB mask is able to deliver somewhere around 60% O2 to the alveoli (FI02 of 0.6). Meaning, if the mixture of gas is 60% O2/39% nitrogen/1% other crap vs 21/39/1 the pressure that "pushes" O2 across the alveolar membrane via diffusion (remember, gas moves from an area of high pressure to an are of low pressure) will be higher, therefore increasing the ease at which it flows across the membrane and anything elses (blood, boogers or fluid) that may be in the way.