O2 Usage in the field

[traumateam1]

Point.

I'm BLS too... HOWEVER, around here, BLS is trained to follow "if A, do B" protocols... so they give high flow O2 to every patient.

If the patient isn't going to really need the additional O2, and are just in need of a LITTLE O2... no sense covering their face with a big mask, and raising their anxiety and stress, as well as making it harder to understand them.

Same here.. I mean, I understand if the patient is satting well on R/A and not working hard than NC would work. It's weird tho.. cuz in class, the teacher said O2 O2 O2 for MI's.

 

[mycrofft]

There ought to be a new categorization of EMT's based on setting:

Ten minute EMT's, 1 hour EMT's, twelve hour EMT's...so much depends upon how long you have the pt and the benefit/risk ratio of on scene versus in-transit/in hospital treatment. Heck, working on pts at altitude or in-flight is a whole new ball of wax versus say the Salton Sea or Chicago at ground level. Much more finesse of oxygen therapy is needed for a neonate or a long-distance haul for somone with a fresh MI, and less for the guy who choked on a bolus of ribeye at Logan's a block from the hospital.

Blanket protocols are for people the administrators are afraid of and call "technicians". Keep on learning.

 

[JPINFV]

I understand that you are saying, but what do you expect for the EMT-Basic? They spend a class or so on each topic and then move on. The EMT-Basic is like a survey course compared to the EMT-Paramedic.

Is it too much to expect from basics what should be expected from all providers? Namely the ability to logically pick and choose treatments including, but not limited to, dose and route, as well as explain both why that treatment is needed and how that treatment works?

 

[CAOX3]

Good Morning everyone. I have a question about using O2 in the field. I recently got my cert and am back to riding in the back of the unit instead of being up front driving. In my EMT class, they stressed O2, O2, O2! Stubbed your toe? 15lpm by NRB. Chest pains? 15lpm by NRB. They said EVERYONE should be put on 15lpm of O2 by NRB. We actually would have failed the state test if we forgot to put O2 on every patient we touched. We didn't get the option to use a NC *unless* the patient wouldn't tollerate a NRB.

My question...is this normal? The past year and a half I have been riding, I have never seen O2 be put on a patient who stubbed his toe or who cut their arm. To me, just getting in to the swing of things, it seems excessive!

Am I missing something?

Yes, anatomy and physiology. Dont frett, so is the majority of everyone else that you work with. You can take these two classes at your community college. It will be beneficial to you and your patients.

 

[johnnyreb132]

Since y'all are on the topic of oxygen for Basics, is it alright to go ahead and put a NRB on a patient with COPD if their breathing is not the CC or related?

 

[VentMedic]

Since y'all are on the topic of oxygen for Basics, is it alright to go ahead and put a NRB on a patient with COPD if their breathing is not the CC or related?

Do they have a problem with cardiac output, perfusion, V/Q mismatch, decreased carrying capacity or something other than oxygen bound to their Hb?

If none of the above is confirmed, why do you want to put O2 on the patient?

 

[MSDeltaFlt]

Since y'all are on the topic of oxygen for Basics, is it alright to go ahead and put a NRB on a patient with COPD if their breathing is not the CC or related?

Just because a pt is diagnosed with COPD does not necessarily mean they will automatically have a "known hypoxic drive" along with any "known CO2 retention". That being said, why would you want to if they are not complaining about CP/SOB?

 

[johnnyreb132]

Do they have a problem with cardiac output, perfusion, V/Q mismatch, decreased carrying capacity or something other than oxygen bound to their Hb?

If none of the above is confirmed, why do you want to put O2 on the patient?

I was told that, no matter what, if the patient appears to have difficulty breathing and/or abnormal sounds in the lungs, then they get NRB at 15 lpm, despite of the COPD. However, I'm afraid of the off of chance messing up their respirations with the patient's hypoxic drive.

This too brought to you by the Commonwealth curriculum.

 

[VentMedic]

Since y'all are on the topic of oxygen for Basics, is it alright to go ahead and put a NRB on a patient with COPD if their breathing is not the CC or related?

I was told that, no matter what, if the patient appears to have difficulty breathing and/or abnormal sounds in the lungs, then they get NRB at 15 lpm, despite of the COPD. However, I'm afraid of the off of chance messing up their respirations with the patient's hypoxic drive.

Difficulty breathing or not?

If the person is having difficulty breathing, you do whatever you can within the limited scope of the EMT-B to alleviate it. If the person is hypoxic, it is senseless to worry about knocking out the "hypoxic drive". If the patient ceases to breathe in the very short time you are with them, it is probably not due to the "hypoxic drive" but rather respiratory failure and exhaution. Use can then use your BVM. The person would probably have required intubation regardless of the 100% hypoxic drive theory.

CO2 retention only occurs in about 5% of all COPD patients.

Here's a good thread for you to review.

http://www.emtlife.com/showthread.php?t=4225&highlight=hypoxic+drive

 

[JPINFV]

I was told that, no matter what, if the patient appears to have difficulty breathing and/or abnormal sounds in the lungs, then they get NRB at 15 lpm, despite of the COPD.

To be honest, "abnormal lung sounds" is a little too broad for a NRB. Difficulty breathing, shortness of breath, etc, then yea, go with oxygen at a rate and device appropriate for your assessment.

This too brought to you by the Commonwealth curriculum.

Meh, kick all of the commonwealths out of the country. It's the "United States," not "United Commonwealths!"

 

[CAOX3]

Abnormal sounds in the lungs? Those sounds have names and meanings or do they not teach that anymore.

 

[Ridryder911]

Abnormal sounds in the lungs? Those sounds have names and meanings or do they not teach that anymore.

Actually, it is not normally taught or required in the basic EMT curriculum. I agree that many are and should be, but currently not in the scope of the EMT.

R/r 911

 

[ResTech]

johnnyreb132.... dont be afraid to administer oxygen to a COPD patient. A hypoxic patient is a hypoxic patient... If they need oxygen, they need oxygen so give it to them without hesitating. AS others have already said, its highly unlikely your going to make them go into respiratory arrest in the short amount of time you are caring for them. And if they do, breathe for them.

In terms of respiratory drive and need for oxygenation, the only difference between a COPD patient and a non-COPD patient, is their biochemical trigger of respiration. Regardless of what the patients underlying condition is, the cells still require a sufficient level of oxygen to function... which is why we NEVER withhold oxygen.

What they won't teach you in your EMT program and expands on your question:

NORMAL, NON-COPD PATIENT
A non-COPD patient (you and I) breathe based on the level of CO2 or more specifically the hydrogen level sensed within the cerebral spinal fluid. When our bodies sense a rising CO2 level, our receptors sense this rise and our breathing center kicks in to make us breathe faster or just to breathe period to keep the CO2 level normal and maintain homeostasis.

COPD PATIENT
A COPD patient has chronically elevated levels of CO2 (or more specifically hydrogen) and as a result, the receptors become desensitized to these high levels of CO2 which forces the body to disregard this increase since this newly aquired high CO2 level is now the bodies norm. Since the receptors are desensitized and ignore the CO2 level, a new drive (or biochemical trigger) needs to come into play... which becomes the patients oxygen level (or PaO2).

So now, when the oxygen level gets low (hypoxic), the body triggers respiration. And if the body senses too much oxygen, the body basicly says... "hold up, too much oxygen, lets slow down breathing"... this is the hypoxic drive. Sometimes when the body gets flooded by a NRB, the body shuts down breathing all together to try to maintain what it thinks should be normal.

Treat your patient based on your ASSESSMENT of them... if they have COPD and are Asymptomatic, then why give O2 by NRB? That's the question you need to ask yourselve. Remember, the majority of COPD patients are always short of breath with a decreased SpO2 (89-92% is normal for some COPDers). Ask the patient about any changes from their baseline like, "any increase in SOB"?, increased w/ exertion?, increased cough with nasty (perulant) sputum changes? fever or increased maliase (weakness)? more frequent use of their nebulizer/inhalers? have they self-increased their home O2?... just a few questions to keep in mind to establish deviation in baseline COPD status and to see if they are having an exacerbation of their COPD from perhaps a bacterial infection. A large percentage of the time, COPD exacerbations result from infection... so look there too for cause.

For some reason this concept confuses me sometimes but it is important to understand to grasp the answer of your question.

 

[CAOX3]

Actually, it is not normally taught or required in the basic EMT curriculum. I agree that many are and should be, but currently not in the scope of the EMT.

R/r 911

Oh, my fault I was assuming that people that may have to give an albuterol treatment may actually know the difference between a wheeze and rales or asthma and CHF.

Sorry my bad.

 

[VentMedic]

In terms of respiratory drive and need for oxygenation, the only difference between a COPD patient and a non-COPD patient, is their biochemical trigger of respiration. Regardless of what the patients underlying condition is, the cells still require a sufficient level of oxygen to function... which is why we NEVER withhold oxygen.

What they won't teach you in your EMT program and expands on your question:

NORMAL, NON-COPD PATIENT
A non-COPD patient (you and I) breathe based on the level of CO2 or more specifically the hydrogen level sensed within the cerebral spinal fluid. When our bodies sense a rising CO2 level, our receptors sense this rise and our breathing center kicks in to make us breathe faster or just to breathe period to keep the CO2 level normal and maintain homeostasis.

COPD PATIENT
A COPD patient has chronically elevated levels of CO2 (or more specifically hydrogen) and as a result, the receptors become desensitized to these high levels of CO2 which forces the body to disregard this increase since this newly aquired high CO2 level is now the bodies norm. Since the receptors are desensitized and ignore the CO2 level, a new drive (or biochemical trigger) needs to come into play... which becomes the patients oxygen level (or PaO2).

So now, when the oxygen level gets low (hypoxic), the body triggers respiration. And if the body senses too much oxygen, the body basicly says... "hold up, too much oxygen, lets slow down breathing"... this is the hypoxic drive. Sometimes when the body gets flooded by a NRB, the body shuts down breathing all together to try to maintain what it thinks should be normal.

This is part of the "hypoxic drive myth". And again, only 5% of all COPD patients are CO2 retainers. If does not explain the rise in PaCO2 accurately.

Refer to the link I posted earlier from a past discussion on this forum.

And this site:
http://www.learnmoresavelives.com/b...c-drive-mediated-sudden-hyperoxic-death-oh-my

So again: Hypoxia kills. Hypercarbia happens. Sick COPD patients die first and foremost of hypoxia, and while, as we will discuss, sudden increases in hypercarbia may contribute to sudden cardiac arrest, they are not the result of oxygen induced apnea. Instead, by believing that the only way these people will die is if they go apneic from the oxygen, we completely miss that the respiratory failure is what kills them and forget that assisted mechanical ventilation and not just oxygen is the treatment of choice for respiratory failure.

Now, the short answer to the question is that the fact that people act based on the myth of the “hypoxic drive oxygen induced apnea” is actually far more lethal than the oxygen. Patients with COPD (or chronic asthma) have a whole body oxygen deficit at baseline and are essentially in compensated respiratory distress. Now worsen their pulmonary function and they go into decompensating and ultimately decompensated respiratory failure and die of hypoxia.

However, it is important to understand that the rise in PaCO2 is mostly from normal physiologic response to restoration of alveolar oxygen levels, increased deadspace, changes in pulmonary capillary blood flow, and decreased CO2 elimination; only a small amount in a minority of individuals can be blamed on decreased minute volume. This sudden increase in CO2 can be harmful (possibly even fatal) but remember, we have ways of helping people get rid of CO2; those methods are known as assisted or mechanical ventilation. But before we starting blaming ourselves for not expecting this sudden non-apneic increase in CO2, remember that these patients started out in respiratory failure and while high flow oxygen may improve their oxygenation status, respiratory failure is much bigger than just oxygen levels and that little bit of oxygen you’ve added doesn’t fix the respiratory failure

The Death of the Hypoxic Drive Theory

http://home.pacbell.net/whitnack/The_Death_of_the_Hypoxic_Drive_Theory.htm

Hypoxic Drive in COPD: Is the fear of Oxygen based on Fact or Myth?
Mark Siobal (UCSF)
http://www.idasrc.org/Hypoxic_Drive.ppt

 

[daedalus]

Except the heart can cause wheezing as well, and the assesment of that condition is beyond the scope of EMT training. Giving albuterol comes with a lot more responsability and the need for advanced assesment.

 

[ResTech]

its highly unlikely your going to make them go into respiratory arrest in the short amount of time you are caring for them. And if they do, breathe for them.

I'm not necessarily saying I subscribe totally to the "hypoxic drive theory", but from what we were taught in class and what is printed in the Paramedic textbook, this is still a modern concept and a physiological possibility.

 

[ResTech]

Albuterol has a great safety profile and rarely causes side effects that are worse then what the albuterol is being given for (hypoxia).

 

[VentMedic]

I'm not necessarily saying I subscribe totally to the "hypoxic drive theory", but from what we were taught in class and that is printed in the Paramedic textbook, this is still a modern concept and a physiological possibility.

EMS is always slow to change. If you look in the nursing textbooks for the last 10 years, you will see the explanation the links are providing.

In the Pulmonary Lab I put known CO2 retainers on 100% Oxygen for 20 - 30 minutes to perform shunt studies. The 100% O2 is not delivered by a NRBM, which is not high flow and does not guarantee 100% O2, but by a Douglas Bag or closed circuit demand system. I do a baseline ABG at room air and then repeat another ABG at the end of the test on 100%. Even for those who do show they are CO2 retainers on their ABG, their PaCO2 levels don't raise with the test and I have yet to have one quit breathing during the test in 20 years.

 

[ResTech]

I don't think its fair to say "EMS is slow to change"... its higher level healthcare providers that have embraced this concept and practiced it and taught it to EMS.