O2 Usage in the field

I can sure as heck narrow it down, based on history, assessment and presentation.

You should be able to walk in someones house and in 30 seconds be able to determine for the most part by what you see and hear what is going on.

COPDers live a certain way, CHFers live a certain way, diabetics and so on, everyone tailors their living arraignments based on their medical conditions, especially the elderly.

Have you read why lasix is no longer widely used in EMS?

People with no smoking hx with COPD? Know the different types of COPD? Ever hear of Alpha-1 antitrypsin deficiency? CF? Seen young people, 20 and younger in CHF? Left vs Right Heart failure? High vs low output cardiac failure?

Lifestyle can also be very deceiving and making assumptions can lead you down the wrong path. Granted, the treatment at the EMT-B level will probably be the same regardless of what the working diagnosis might be.

BTW, the terms COPDer and CHFer have been around for a long time. However, in respectful medical conversation we still try to identify the patient as a person and not an object by their disease.
 
I might be wrong but I think it's true for laminar flows as well.
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Rho is the density term. This equation should apply for laminar and turbulent flows, you just adjust friction factor f.

This is similar to Poiseuille’s Law which be used to compare the radius and pressure of a respiratory tube to the amount of resistance encountered within the tube.
 
Have you read why lasix is no longer widely used in EMS?

People with no smoking hx with COPD? Know the different types of COPD? Ever hear of Alpha-1 antitrypsin deficiency? CF? Seen young people, 20 and younger in CHF? Left vs Right Heart failure? High vs low output cardiac failure?

Lifestyle can also be very deceiving and making assumptions can lead you down the wrong path. Granted, the treatment at the EMT-B level will probably be the same regardless of what the working diagnosis might be.

BTW, the terms COPDer and CHFer have been around for a long time. However, in respectful medical conversation we still try to identify the patient as a person and not an object by their disease.


Wait the medical field treating people like people? They are treated like diseases and injuries.

Whos MI is this, who/s fx hip is this, I need the belly in ultrasound, get that head bleed to CT scan. Sound all familiar? Anyway.

Understood, however COPD patients that dont smoke and 20 year old failure patients are the exceptions not the rule.

Your right at the BLS level it probably isn't going to change the treatment, however I like to have an idea of what I'm walking in the ER with and yes I know the difference between left and right sided heart failure.

Lifestyle is a very good indicator of medical hx. Sure it can be deceiving but people are also creatures of habit.

The patient, their surroundings and assessment will lead me where I need to go.
 
I've only put a NRB on maybe 10 patients to be honest...

The book emphasizes that O2 for EVERYBODY

Then, I entered the real world :)
 
Understood, however COPD patients that dont smoke and 20 year old failure patients are the exceptions not the rule.

Actually many of the patients seen for COPD have never smoked. They may have been exposed to 2nd hand smoke at their employment or home life. Asthma patients who have had extensive airway remodeling to where they are now chonically obstructed may have never smoiked. As well, many patients who have CF, Alpha-1 antitrypsin deficiency and bronchiectasis have never smoked.

Stereotyping and assuming will skew your ability do a good assessment.


Whos MI is this, who/s fx hip is this, I need the belly in ultrasound, get that head bleed to CT scan. Sound all familiar?

Did you read my post?

However, in respectful medical conversation we still try to identify the patient as a person and not an object by their disease.

I've only put a NRB on maybe 10 patients to be honest...

The book emphasizes that O2 for EVERYBODY

Then, I entered the real world :)

This could also be because as an EMT-B you have not seen seriously ill patients, have not done many calls or did not recognize the need for O2 even if there was one.

Statements like this are broad and really do not tell us anything about whether you think O2 is necessary since you did not back it up with more information.
 
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.

Even on the off chance of "messing up" the hypoxic drive, you can always use a BVM if the pt is unresponsive or talk to the frontal lobe and tell the pt to breathe. It works very well. Say "Mr Whatever, I need you to breathe with me. In through the nose, out through the mouth." It requires you to sit with the pt and actually pay attention to him, rather than doing paperwork during transport, but it does work.

That said, I'd do some reading and studying on your own or take some more classes and further your education. O2 is not needed on every call and a NRB is not the only option for O2 delivery. Have you ever seen a Venturi mask? Those are one of the best O2 devices for a COPD pt with difficulty breathing. You get the high air flow needed and precise control of the amount of O2. Most of my pts that need O2 do well on a nasal cannula. Very few actually require a NRB.
 
Have you ever seen a Venturi mask? Those are one of the best O2 devices for a COPD pt with difficulty breathing. You get the high air flow needed and precise control of the amount of O2. Most of my pts that need O2 do well on a nasal cannula. Very few actually require a NRB.

Venturi masks are nice because they are a true high flow device unlike the NRBM. However, in an acute emergency, one shouldn't be waiting time finding all the little colored adapters or twisting the O2 setting. There are more important issues at hand. Getting the exact percentage of O2 is not nearly as important as meeting the patients respiratory needs and those of the other body systems.
 
Very few of my COPD or Asthma patients require much O2 and the HeliOx is usually in concentrations of 80/20 or 70/30 with the higher number being helium.

You would be surprised by the number of people that are on MAOIs. I rarely will withhold albuterol unless there is a greater chance that the orgin is cardiac. I will then give only if on a monitor and even if it is respiratory related, if in the back of a truck or in the ED, they get a monitor.

Now for the hypoxic drive theory, I've given you some good links so that you can through and see how this concept applies to your patients.

(not addressing YOU vent) It's not just MAOIs. Tricyclics have bad interactions with albuterol, as can digoxin and beta blockers. Your pt should be on the monitor any time you give a drug because you don't know how that pt will react. Each pt is different and may be on different drugs or have different pre-existing conditions. Electrolytes may be off in your pt and you may push them over the edge with your treatment. The point is that you never know. Albuterol may seem harmless, but it does affect the heart too and some pts can't tolerate it.
 
Here is my thoughts:

It is absurd that they teach that way, and that is the way they do it in PA now, too. When I took my EMT, we were taught the proper way, in every aspect. We were shown how to use a cannula, venturi mask, simple face mask and an NBR. I first take vitals, and then do the pulse ox, you have to remember that some pt that has poor profusion (i.e., low bp or other factors) will lead you to false readings or no readings. pt's will get more O2 concentrations on a mask than a NC. 2 LPM is nothing more than "room air". 4 lpm is more the norm and generaly works well in pt's that need it, but don't require any more. I have seen charts on concentration levels, 6 lpm via simple face mask will give more than 6 lpm nasal. Besides, why would you want to blow that much pressure through the nose ? 6 to 10 on a simple mask is also a good choice also depending on the situation.
 
Some things to think about:

CVA/TIA, MI (or other cardiac episode), head injuries, difficulty breathing...

These are what you need to be worried about. In CVA/TIA one major component in most cases is ischemia, and how do we correct ischemia on a BLS level - OXYGEN!, in high concentration. These are patients who require a NRB on 15lpm.

AMI and other cardiac episodes - again, related to ischemia therefore high concentration oxygen.

Head Injuries - If their oxygen saturation drops below 90% their mortality rate if they do have a closed head injury increases 2-3X (same with their systolic BP dropping below 90, but entirely different story).

Difficulty Breathing - Is it CHF, Pulmonary Edema, Pnemounia, Exacerbation of COPD, Asthma, Allergic Reaction. You know individual treatments for these scenarios but most of these require high concentration oxygen. Especially with your asthma pt. who has bilateral expiratory wheezing and is complaining of chest tightness, ALS is not available and BLS doesn't have albuterol or another bronchodilator to solve the problem. On the COPD side of things be careful, yes they need oxygen but if you remember back to class a COPD patient functions based on their hypoxic drive instead of their carbon dioxide retention, therefore - too much oxygen equals the pt. believes they no longer need to breathe. Congrats, their goes their respiratory drive. Again, oxygen is a med so don't take it lightly.

If your service (like most services are) is using pulse oxymetry...

remember what is mild, moderate, and severe hypoxia and treat for the indicated. BUT --- there is always a but... REMEMBER PLEASE do NOT rely on the machine rely on your pt. first and foremost and rely on your assessment to determine how to treat, the machine may not be accurate in both ways. Cold hands and a sat of 70% in a pt. with an RR of 16 unlabored and clear lung sounds that's pink/warm/dry doesn't need to be bagged, but your cyanotic asthma attack that's reading 97% does.

AND FINALLY - NEVER DENY ANY PT. EXPERIENCING DYSPNEA OXYGEN!!!
 
Some things to think about:

CVA/TIA, MI (or other cardiac episode), head injuries, difficulty breathing...

These are what you need to be worried about. In CVA/TIA one major component in most cases is ischemia, and how do we correct ischemia on a BLS level - OXYGEN!, in high concentration. These are patients who require a NRB on 15lpm.
If you re read this thread, you will be surprised to find out that you are very wrong. In fact, the current literature is teaching us to not give 15L O2 to patients with suspected TIA vs CVA unless they are hypoxic. You will find adequate reading material on this on other pages in this thread, as well as on JEMS under Dr. Bledsoe's column. Please also see VentMedic's post regarding said article, it is also in this thread on an earlier page.
 
Some things to think about:

CVA/TIA, MI (or other cardiac episode), head injuries, difficulty breathing...

These are what you need to be worried about. In CVA/TIA one major component in most cases is ischemia, and how do we correct ischemia on a BLS level - OXYGEN!, in high concentration. These are patients who require a NRB on 15lpm.

AMI and other cardiac episodes - again, related to ischemia therefore high concentration oxygen.

It's not as simple as that I'm afraid.

The evidence for giving supplemental oxygen to anyone who is not hypoxic is scant, and there is some suggestion that supplemental oxygen may in fact be harmful to these patients.

CVA/TIA: As previously noted by several others here, high flow O2 is probably actually detrimental to CVA/TIA patients.

AMI/ACS: Again, potentially detrimental. ACS occurs due to mechanical obstruction i.e blood not flowing to the affected area. No amount of supplemental oxygen will change that fact. The amount of O2 dissolved in plasma is negligible at atmospheric pressure and the change that we can induce is even more negligible. Increasing the concentration of O2 will also cause vasoconstriction thereby potentially achieving the direct opposite of what you think you are doing.

In heart failure high concentration O2 decreases cardiac output and stroke volume and increases systemic vascular resistance (exactly what we don't want) Someone with heart failure needs nitrates and CPAP (generalising here for purposes of discussion) and that CPAP is not provided with an FiO2 of 1 for very good reason.

i'm sure VentMedic can correct me or expand upon this, but to state that everyone with CVA/ACS or whatever automatically needs 15l via NRB is not only wrong it is potentially harmful.
 
I think that she (Venty) will also point out that the amount of oxygen you give someone is based on their cardiopulmonary status including work of breathing. While blanket statements like 15 for everybody are wrong, it is also wrong to give everyone 2 LPM NC. Use sound clinical judgement incorporating the latest research. For example, a chest pain patient with severe dyspnea and low sats should probably get the good stuff by mask, while the uncomplicated chest pain will get the cannula. In the hospital, o2 administration will be guided by ABGs and the intelligence of intensivists and RRTs.

I am but a mere mortal compared to the critical care experience of others here but this is my three cents.
 
The old O2 for CVA patients argument.

All I can say is assessment.
 
Unfortunately, it goes back to the old school of .."hey their out there, they have to do something".... Not treating a true hypoxia's situation versus short duration of oxygen at 15 lpm. So a blanket treatment is made for it is better to error for the greater of the community, instead of teaching patho and understanding respiratory physiology and arterial receptors sites.

With the new curriculum, there will be more emphasis upon anatomy but of course it will not be enough as needed. I do hope though that it at least will open the door of changing blanket treatments and develop more discussion and changes for individual treatment and care.

Even such courses as ACLS, ITLS, PHTLS and so on needs to be reviewed and modified. As those courses have became watered down and enforces blanket treatment and non-specific rationales. Such knowledge of oxygen therapy has been wide known for decades but we still continue to push and promote such material.

I do not why it is continues to be so difficult to change the method of our teaching. Why EMS is still so resistant to do things the right way?

R/r 911
 
These are what you need to be worried about. In CVA/TIA one major component in most cases is ischemia, and how do we correct ischemia on a BLS level - OXYGEN!, in high concentration. These are patients who require a NRB on 15lpm.

If they are short of breath, yes. However, if their Spo2 falls it is because of they may be losing their ability to maintain their airway and secretions. Often, by just clearing the airway and repositioning their SpO2 will increase.

AMI and other cardiac episodes - again, related to ischemia therefore high concentration oxygen.
The ischemia is due to a clot. No matter how much O2 you put into that person, it will not dissolve that clot. However, if the cardiac output is failing you need to add meds to increase it without overloading the heart with too many fluids. That will bring the SpO2 up more efficiently than oxygen and increase perfusion.
Head Injuries - If their oxygen saturation drops below 90% their mortality rate if they do have a closed head injury increases 2-3X (same with their systolic BP dropping below 90, but entirely different story).

That depends on whether there is bleeding or ischemia. This is also why we monitior the SjvO2 of TBIs. There are other factors involved which determine our parameters for these patients.
Difficulty Breathing - Is it CHF, Pulmonary Edema, Pnemounia, Exacerbation of COPD, Asthma, Allergic Reaction. You know individual treatments for these scenarios but most of these require high concentration oxygen. Especially with your asthma pt. who has bilateral expiratory wheezing and is complaining of chest tightness, ALS is not available and BLS doesn't have albuterol or another bronchodilator to solve the problem. On the COPD side of things be careful, yes they need oxygen but if you remember back to class a COPD patient functions based on their hypoxic drive instead of their carbon dioxide retention, therefore - too much oxygen equals the pt. believes they no longer need to breathe. Congrats, their goes their respiratory drive. Again, oxygen is a med so don't take it lightly.

All with different etiologies and all require different interventions which are more effective than just O2. With CPAP, you may go from an FiO2 of 1.0 to 0.21 with a CHF patient.

On the COPD side of things be careful, yes they need oxygen but if you remember back to class a COPD patient functions based on their hypoxic drive instead of their carbon dioxide retention, therefore - too much oxygen equals the pt. believes they no longer need to breathe. Congrats, their goes their respiratory drive. Again, oxygen is a med so don't take it lightly.

Please read my many posts on this subject. If the patient is hypoxic, why are you concerned about a hypoxic drive? Also you should be familar with hypoxemia. Just giving a high concentration of oxygen does not necessarily equate to a high PaO2 due to V/Q mismatching.


If your service (like most services are) is using pulse oxymetry...

remember what is mild, moderate, and severe hypoxia and treat for the indicated. BUT --- there is always a but... REMEMBER PLEASE do NOT rely on the machine rely on your pt. first and foremost and rely on your assessment to determine how to treat, the machine may not be accurate in both ways. Cold hands and a sat of 70% in a pt. with an RR of 16 unlabored and clear lung sounds that's pink/warm/dry doesn't need to be bagged, but your cyanotic asthma attack that's reading 97% does.

As well, if you are looking at a patient you assume to have COPD by the cigarette in their mouth, remember they may have a higher level of COHb that is measured by the pulse ox as a total. The SpO2 may be 95% but with 10% COHb, their actual SaO2 might be 85% or less if you as a couple of percentages points for Methemoglobin with nitrate meds.

AND FINALLY - NEVER DENY ANY PT. EXPERIENCING DYSPNEA OXYGEN!!!

Asssessment coupled with a decent understanding is always best.

Essentially, these are all arguments for higher education and a higher level of provider for emergencies or even IFTs that are medical.
 
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I was SO with all Vent was saying until she said "COHb".

^_^
 
15lpm via NC. hehe.

Seriously though, no, you don't need to put 15lpm on every patient. Use your judgment.
 
I spent a week in the hospital.


I know what 6lpm NC is like.



It sucks.... err.. blows.
 
My train of thought was coming from my notes from class. I guess now things have gone otherwise. I'm not a big fan of "Everyone needs O2" either but that's what I was taught. Now with this in front of me it gives me a better view on assessment. Thanks for pointing that out!

Also - here we cannot use BLS CPAP...
 
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