About EMT intermediate

[MrBrown]

I am no expert on oxygen therapy (we do have a resident expert who I hope will chime in), however the science of o2 therapy is not exact and in fact we still do not know what the best practices are for some situations (oxygen can be harmful)

I think it is safe to say that oxygen therapy should be guided by the clinical condition of your patient and pulse oximetry. A patient with chest pain with no dyspnea and a normal spO2 probably does not need 15 liters.

This big paper from the British Thoracic Societyhttp://www.brit-thoracic.org.uk/Por...Emergency oxygen guideline/THX-63-Suppl_6.pdf (click for the PDF) on pg. 22, 26-27 does list the consequences of hyperoxemia.

The old "too much of anything" whodathunkit is probably a good one here (as with anything really); I know it's not randomized, double-blind prospective or peer reviewed in nature but I thought it'd put it in there.

In 2007 we made a change (I don't know what it was previously) and now basically it goes like this

- not everybody gets oxygen and we only give oxygen if the patient as an abnormal airway, shock, chest pain or SPO2 <95% on air (except COAD)
- 2-4lpm on a NC or 4-6lpm on a simple face mask should be fine for everybody except NRBs or nebulizer masks (8lpm) and BVMs (10lpm)

I mean in reality I think we confuse oxygenation and ventilation or rely too much on pulse oximetery or confuse hypercarbia and hyperoxemia/hyperventilation which are all very different concepts and I wouldn't trust SPO2 totally just like I don't trust somebody who has no other S&S but whos ECG says the printer says has an MI.

In reality however I would also plug that there is a psychologycal benefit of non-medically indicated oxygen at very low rates (say 1-2lpm max on a nasal cannula) for select patients; e.g. the elderly. I've found a litre of oxygen on a cannula can do wonders for nana and the family who all want us to "do something".

 

[VentMedic]

All of you that just posted need to review some basic factors of Oxygen especially about the constriction and dilation of blood vessels. Hypoxia induces vasoconstriction.

The research of harmful effects centered around free radical formation and toxicity. Both conditions take longer than 30 minutes to be of concern. Since there many other factors that you do not know in the field, many medical directors still cover the all the bases with O2 therapy.

Factors you do not know are the lactate level, SvO2, Hb and the content or component values of total saturation. As well, for chest trauma with the suspicion of a pneumo, N2 washout theory is still exercised.

Every patient in the ICU is on a different O2 protocol whether it is neuro, ARDS, COPD, Trauma or Sepsis. We do NOT do blanket orders. No two neuro patients may be the same and the neuro surgeon usually has his/her preferences and that may be different with each patient depending on labs and other diagnostics.

While not every patient needs a NRBM one must assess all factors of the patient to determine the correct therapy. If I have a nursing home patient that was peeing mud and has altered mental status, they will get a NRBM regardless of SpO2 until I saw their lactate level. If that number reveals sepsis, they would be on a high FiO2 until the lactate started trending down and the SvO2 was stable.

4-6lpm on a simple face mask

Your package insert generally says no less than 6 liters and I suggest you follow that recommendation. CO2 retention in the mask WILL dilate cerebral blood vessels or push that CO2 patient over the edge.

For the NRBM, you choose the liter flow by the patient's VT and MV. Setting the liter flow DOES NOT set the FiO2.

Understanding basic equipment is another area that EMT(P)s just don't get enough education on. They get "training". Put prongs in nose and turn flowmeter to 2 and that gives you 28% Oxygen.

They are not taught that the patient's tidal volume with each breath influences how much FiO2 the patient receives. The nonrebreather mask is called a high flow device because it takes a whole lot of oxygen to run it. Few are ever taught the actual definition of high flow device or know which devices are considered high flow.

We could also discuss the Pulse Oximeter. I personally believe no one should use it as a "diagnositc" tool unless they thoroughly understand the oxyhemoglobin dissociation curve.

The ETCO2 monitor should also be used for more than just seeing a pretty wave after intubation. Some do try to treat by the numbers and yet have no clue about V/Q mismatch or deadspace ventilation. They also don't know much more about their wave forms except they see one.

So some have a lot to learn about pathophysiology and some simple human processes before making blanket statements. There is a lot of literature out there and every center and doctor have their own beliefs. It is weeding through the literature to see if it holds up to validity with sample size and METHODOLOGY. This is why I always encourage those who read a review or fluff article in JEMS to pull up the original. Quite often the authors of the original may have a very different view or the meaning is lost when in the effort to translate it into simple terms to those in EMS.

 

[MrBrown]

They are not taught that the patient's tidal volume with each breath influences how much FiO2 the patient receives.

I don't get that ... regardless of size of TV are you not breathing the same mixture of oxygen dissolved in the air? If my TV is say 10ml of air or 100ml of air it's the same air; be it 2.8% or 28%

Mind you I was taught FiO2 is the inspired level of O2 (which I take to be how much you breathe in) not how much disperses across the alveoli and into the plasma (PaO2/ABG) or binds to Hbg (SPO2) ... bloody hell all these O2s! ... breathing is a bit more complex than breathe in, breathe out eh, whodathunkit?

We could also discuss the Pulse Oximeter. I personally believe no one should use it as a "diagnositc" tool unless they thoroughly understand the oxyhemoglobin dissociation curve.

*scurries away go look it up

There is a lot of literature out there and every center and doctor have their own beliefs. It is weeding through the literature to see if it holds up to validity with sample size and METHODOLOGY. This is why I always encourage those who read a review or fluff article in JEMS to pull up the original. Quite often the authors of the original may have a very different view or the meaning is lost when in the effort to translate it into simple terms to those in EMS.

I think JEMS is a useless piece of rubbish not worthy of the title of a "journal" that I personally would not wipe my arse on. We subscribe to it and i read it now and again, but honestly "Journal of EMS" makes it sound like up there with the Lancet, NEJM, JAMA etc; you know a proper scientific publication. While there are some very intelligent MD/DOs, BSs, MPHs and PhDs who write for JEMS most of the articles IMO are trash that should see it renamed "Good old timer trade journal of gurney jockeys to read on the toidee or sit your coffee mug on".

I have spent the last three years picking through scientific and business journals writing university level (up to 5,000 word) research papers and have a university research methods class under my belt so I can read a research paper. Does that make me some sort of super-smart know it all, not at all, I can barely understand the lab value sheets I have been given by physicians to take to the ER but I do know what is flawed research and what is not (might have to look at the PowerPoints from my research methods class again) but still .... emergency medical services involves medicine, medicine is founded in science (not that I agree with it all) so hey lets teach some science and scientific methods here .... WHODATHUNKIT?

 

[ResTech]

Hypoxia induces vasoconstriction.

From a research article.... http://ajpheart.physiology.org/cgi/content/full/292/2/H776

Absent the use of perfluorocarbons, significant hemodilution, or pulmonary compromise, hyperoxia causes little change in the oxygen content of blood. However, hyperoxia normally causes a vasoconstriction, which may itself provide a salutary effect by improving perfusion of some critical vascular beds through venoconstriction (9) and a favorable redistribution of the cardiac output (CO) (10).

I have been taught over the years that oxygen has vasoconstriction properties and that it is the hypoxia that results in vasodilation and increased vascular permeability due to rises in acid production.

I always thought hypoxia only caused vasoconstriction in the pulmonary vessels (ie pulmonary hypoxic vasoconstriction).

Looks like the oxygen free radicals causes a release of thomboxane (what gets inhibited by ASA) and prostaglandins which both cause vasoconstriction....

 

[VentMedic]

From a research article.... http://ajpheart.physiology.org/cgi/content/full/292/2/H776



I have been taught over the years that oxygen has vasoconstriction properties and that it is the hypoxia that results in vasodilation and increased vascular permeability due to rises in acid production.

I always thought hypoxia only caused vasoconstriction in the pulmonary vessels (ie pulmonary hypoxic vasoconstriction).

Looks like the oxygen free radicals causes a release of thomboxane (what gets inhibited by ASA) and prostaglandins which both cause vasoconstriction....

Did you read the whole article and understand what is meant by "hyperoxia" and O2 content?

The FiO2 given does not necessarily mean that is what is present in the blood which is why we measure O2 content, PaO2 and calculate PAO2. The A-a gradient will tell us more about perfusion which is also why we monitor the SvO2.

This article is also written about shock from trauma in rats. It gives not reference to human data.

It is difficult to take on section out of a research article, especially when it is about animals, and expect to correlate it to a broad statement. Once an article like this is published, the ground work is now laid for other scientists to test their theories or challenge this data. That is how research works. This is also how it was found that the MAST and intracardiac epinephrine did not work as well as what was initially thought.

 

[ResTech]

Well here is more supporting data that oxygen causes vasoconstriction... and hypoxia causes vasodilation.

From Wikipedia - Hypoxia (http://en.wikipedia.org/wiki/Hypoxia_(medical))

In most tissues of the body, the response to hypoxia is vasodilation. By widening the blood vessels, the tissue allows greater perfusion.

By contrast, in the lungs, the response to hypoxia is vasoconstriction. This is known as "Hypoxic pulmonary vasoconstriction", or "HPV".

From Cardiovascular Physiology Concepts (http://www.cvphysiology.com/Blood Flow/BF008.htm)

Decreased tissue pO2 resulting from reduced oxygen supply or increased oxygen demand causes vasodilation. Hypoxia-induced vasodilation may be direct (inadequate O2 to sustain smooth muscle contraction) or indirect via the production of vasodilator metabolites. Note, however, that hypoxia induces vasoconstriction in the pulmonary circulation (i.e., hypoxic vasoconstriction), which likely involves the formation of reactive oxygen species, endothelin-1 or products of arachidonic acid metabolism.

Hydrogen ion increases when CO2 increases or during states of increased anaerobic metabolism, which can produce metabolic acidosis. Like CO2, increased H+ (decreased pH) causes vasodilation, particularly in the cerebral circulation.

Lactic acid, a product of anaerobic metabolism, is a vasodilator, although in large part because of its pH effect.

I have never known of hypoxia to cause vasoconstriction except in the pulmonary vessels. If hypoxia caused vasoconstriction, then why is it critical to not allow TBI patients to become hypoxic? The rational is to prevent hypoxia to mitigate increasing intracerebral swelling from the vasodilation that occurs as a result of hypoxia.

I'm still trying to see where your getting this data from to support hypoxia causing systemic vasoconstriction. Could you post some sources?

 

[MrBrown]

I (at least) am saying hyperoxemia causes vasoconstriction because that is what we are taught and what our medical director is saying; I'll see if I can find something more concrete

 

[Shishkabob]

I (at least) am saying hyperoxemia causes vasoconstriction because that is what we are taught and what our medical director is saying; I'll see if I can find something more concrete

We've always been taught ventilate to 30 EtCO2 to cause vasoconstriction.

:wacko:

 

[MrBrown]

We've always been taught ventilate to 30 EtCO2 to cause vasoconstriction.

:wacko:

Foregive me ... but this is one of those Circle of Willis things or what, because that makes no sense! :unsure:

 

[VentMedic]

Foregive me ... but this is one of those Circle of Willis things or what, because that makes no sense! :unsure:

CO2 is a cerebral vasodilator which is why hyperventilation has been indicated for TBI. However, we no longer go past 30 or even 35 as taking the CO2 level below that can cause constriction to where it limits blood flow regardless of what the PaO2 is.

However, it is also good to know that CO2 is a vasoconstrictor as well as a dilator to some degree in the cardiopulmonary system in some patients which is the opposite of cerebral effects.

Hyperventilation and Hyperoxygenation are two very different things. This is why EMS has been questioned for their preintubation method is questioned as they "bag real fast" thinking they are hyperventilating to give more oxygen.

Also one has to look at the whole disease or injury process. You will not know in the field what the oxygenation is at tissue level without an SvO2. For TBIs and sepsis, that is how we adjust the FiO2 and the pressors or fluids in the ICU.

Do you know some of the treatments for pulmonary hypertension for infants or adults? Do you know why 100% O2 is used? And then nitric oxide?

Take NRP?

Ever study some of the CHDs in infants especially the cyanotic heart lesions? Do you know why these infants are sometimes given an FiO2 of 0.16 (16% Oxygen) to keep their SpO2 and SaO2 between 75%-85%?

In your search, look up PVR and SVR. Gain your knowledge through learning hemodynamics.

There is a lot to learn out there and different applications for different patients. One recipe does not fit all patients.

 

[VentMedic]

From Wikipedia - Hypoxia (http://en.wikipedia.org/wiki/Hypoxia_%28medical%29)

Wikipedia?

This could have been written or edited by an EMT who thinks he/she now knows all about the subject after reading a few paragraphs in a couple of research abstracts or JEMS.

But this oxygen discussion has been great as it also shows how much there is to know out than and how this pertains to EMT-Is giving fluids with little to no understanding.

 

[VentMedic]

I don't get that ... regardless of size of TV are you not breathing the same mixture of oxygen dissolved in the air? If my TV is say 10ml of air or 100ml of air it's the same air; be it 2.8% or 28%

Mind you I was taught FiO2 is the inspired level of O2 (which I take to be how much you breathe in) not how much disperses across the alveoli and into the plasma (PaO2/ABG) or binds to Hbg (SPO2) ... bloody hell all these O2s! ... breathing is a bit more complex than breathe in, breathe out eh, whodathunkit?

If you are giving 2 Liters of oxygen by nasal cannula, will it provide the same concentration or FiO2 when the patient is breathing 12 normal breaths and then 20 rapid deep breaths?

Do you know the Venturi principle of air entrainment?

http://books.google.com/books?id=bt...turi principle air entrainment oxygen&f=false

There are several pages here that discuss venturi and FiO2 calculations which are generally based on a 500 cc VT. It also explains what the difference between a high flow and a low flow system is. But, still for EMS testing purposes, a NRBM is a high flow device because it requires a whole lot of O2. For RN and RRT testing purposes, that is an incorrect answer.

I will make one correction about O2 and neonates, high concentrations of O2 will cause vasoconstriction in the retina. Embrology and neonatalogy are sciences that have to be studied extensively and adult world assumptions can not be made.

However, I will repeat again, the effects of CO2 and O2 in the body will be dependent on the body system and whatever chemical or physiological process is occuring in the body as that time. Examples: lactate levels, pH etc. Not all properites have been determined but there are a few that we know such as pulmonary hypertension and CHD. We do know about O2 toxicity and HBO therapy is still being studied for CVAs as well as other disease processes.

 

[MrBrown]

CO2 is a cerebral vasodilator which is why hyperventilation has been indicated for TBI. However, we no longer go past 30 or even 35 as taking the CO2 level below that can cause constriction to where it limits blood flow regardless of what the PaO2 is.

Our clinical procedures state

3.3 TRAUMATIC BRAIN INJURY
• Perform primary survey.
• Gain large bore IV access.
• Intubation is not a priority but if the patient is deeply unconscious with poor airway and/or breathing, intubate them but ...avoid hyperventilation and ventilate to end-tidal CO2 of 35-45 mmHg.

By your logic our procedure is incorrect as we should not be ventilating past 35mmHg EtCO2?

Hyperventilation and Hyperoxygenation are two very different things. This is why EMS has been questioned for their preintubation method is questioned as they "bag real fast" thinking they are hyperventilating to give more oxygen.

I have personally not seen this procedure however my argument is no matter how fast you bag a patient you're still only delivering the same 28% oxygen and if you hyperventilate a patient they may become hypocapenic so it's probably not a good idea but I could be talking out my arse.

Also one has to look at the whole disease or injury process. You will not know in the field what the oxygenation is at tissue level without an SvO2.

Do you look at SvO2 alone or compare SaO2 and SvO2? My thinking would be the difference between the oxygen in the arteries and veins is what's in the tissues but something tells me thats not right

Do you know some of the treatments for pulmonary hypertension for infants or adults? Do you know why 100% O2 is used? And then nitric oxide?


Take NRP?

Ever study some of the CHDs in infants especially the cyanotic heart lesions? Do you know why these infants are sometimes given an FiO2 of 0.16 (16% Oxygen) to keep their SpO2 and SaO2 between 75%-85%?

In your search, look up PVR and SVR. Gain your knowledge through learning hemodynamics.

There is a lot to learn out there and different applications for different patients. One recipe does not fit all patients.

The definition I got of PVR was something about pee! I'd take a gamble at systemic and pulmonary venous resistance however.

Nitric oxide is a pulmonary vasodialator.

Other than that I am having a look at some critical care websites and whatnot; this is rather interesting.

May I sugest http://www.ccmtutorials.com/rs/oxygen/index.htm

Or I could suggest you just put that patient on the the stretcher and take 'em to the hospital! :lol: :lol:

 

[VentMedic]

Our clinical procedures state
3.3 TRAUMATIC BRAIN INJURY
• Perform primary survey.
• Gain large bore IV access.
• Intubation is not a priority but if the patient is deeply unconscious with poor airway and/or breathing, intubate them but ...avoid hyperventilation and ventilate to end-tidal CO2 of 35-45 mmHg.


By your logic our procedure is incorrect as we should not be ventilating past 35mmHg EtCO2?

I stated

Originally Posted by VentMedic
CO2 is a cerebral vasodilator which is why hyperventilation has been indicated for TBI. However, we no longer go past 30 or even 35 as taking the CO2 level below that can cause constriction to where it limits blood flow regardless of what the PaO2 is.

Look at your own protocols. It clearly states 35 - 45. That is a normal range. We usually don't go lower even in some TBI situations. But then, if we do go lower it is not below 30.

I have personally not seen this procedure however my argument is no matter how fast you bag a patient you're still only delivering the same 28% oxygen and if you hyperventilate a patient they may become hypocapenic so it's probably not a good idea but I could be talking out my arse.

Why are you giving only 28% Oxygen? Do you blenderize your O2 in the ambulance?

To hyperventilate is to make the person hypocapenic.

Do you look at SvO2 alone or compare SaO2 and SvO2? My thinking would be the difference between the oxygen in the arteries and veins is what's in the tissues but something tells me thats not right

If your FiO2 is already 100%, you will need fluids and presors to maintain adequate SvO2 as if you are on transport there will be limited things you can do with a transport ventialor. The SaO2 will of course be important but normally we will monitor the SvO2 and not do too many ABGs during transport unless we have ventilation issues. The SpO2 monitor will suffice. In the hospital we will use all numbers for our calculations to determinine hemodynamic status.

The definition I got of PVR was something about pee! I'd take a gamble at systemic and pulmonary venous resistance however.

Are you a Paramedic? I would hope this was at least mentioned in your program since you do give meds like nitro and epinephrine.

Nitric oxide is a pulmonary vasodialator.

Yes and if you assist in transporting specialty teams you may see it frequently now on the ambulances. As well, you will also see it in the homes or outside of them as patient now carry the little tanks of Nitric Oxide with them. So, don't assume that tank is O2. As well, the nebulizers a person (could be a child also) takes at home may be a pulmonary vasodilator and not "albuterol".

Other than that I am having a look at some critical care websites and whatnot; this is rather interesting.

May I sugest http://www.ccmtutorials.com/rs/oxygen/index.htm

That is a very good website as you probably have noticed I have linked to it many times in my posts on this forum.

Or I could suggest you just put that patient on the the stretcher and take 'em to the hospital! :lol: :lol:

I guess when asked to do an IFT transport from one hospital to another you just turn on the L&S and drive real fast.

These are reasons why some CCTs as well as a few flight teams run into serious problems and fail their patient miserably.

 

[eveningsky339]

It is a good thing, Florida does not recognize Intermediates either.

It is basic or medic....period.

The smarter thing to do is recognize only EMT-I's. No Basics needed.

 

[VentMedic]

The smarter thing to do is recognize only EMT-I's. No Basics needed.

After reading some of the posts, I believe for the BLS trucks it should be CNAs/PCTs since they are more familiar with medical patients.

Florida has all ALS services so the Paramedic will remain as the standard for 911.

 

[ResTech]

What posts are you referring to as ignorant?

Hypoxia causes vasodilation... except for pulmonary hypoxic vasoconstriction.

Oxygen causes vasoconstriction.

Information was posted to support that... and not to mention its taught everyday.

Can you please post facts that states hypoxia does not cause vasodilation? And some factual info that states oxygen does not cause vessels to vasoconstrict.

And please stop trying to make people feel stupid, its not working.

 

[VentMedic]

What posts are you referring to as ignorant?

Hypoxia causes vasodilation... except for pulmonary hypoxic vasoconstriction.

Oxygen causes vasoconstriction.

Information was posted to support that... and not to mention its taught everyday.

Can you please post facts that states hypoxia does not cause vasodilation? And some factual info that states oxygen does not cause vessels to vasoconstrict.

And please stop trying to make people feel stupid, its not working.

You take little statements from Wikipedia and try to pass them off as fact. Do you not understand the different body processes? Do you not understand the different effects for different conditions that are present within the body as any given time during a disease process? Do you not understand the difference of oxygenation and hypoxia at tissue level? Do you not understand what SvO2 means? SaO2? O2 Content? Do you not understand what sepsis is? Do you not understand V/Q mismatch? Deadspace ventilation? How about deadspace ventilation as it pertains to pulmonary vasoconstriction?

But of course, what is you favorite line to use? ....just Paramedics?
There is nothing to do but drive the patient to the hospital and knowing all of this book learnin' stuff is of little use.

General blanket statements you have made are not correct. Did you not even read my posts with examples? How about the CCM tutorial link MrBrown posted? If you don't understand the terms I have posted, look them up on a reliable source and not Wiki. You are stuck on a couple of words and can't seem to get past them.

Stop reading Wikipedia and take some college level classes like A&P and pathophysiology but of course that would probably be of llittle use to you with your attitude. I also read your conversation on neuro assessment. Do you really believe the Paramedic should not know anything but their "protocols" or recipes?

You can also stop trying to bring others such as Rid, daedalus, JPNIFV and myself down to match your level of "training". Some in this profession have moved on and want to continue learning. You just want to argue and really could care less about what facts are even when they are spoon fed to you. It is too bad you don't understand what some of us have written or just don't care to.

I suggest you do a little "googling" on a medical search engine where Wikipedia won't keep popping up.

Also, STOP looking for RAT studies. Learn basic physiology first. Then learn how to read research literature. The results of the studies with then be more meaningful to you and you won't take things out of context.

You might try that for IV therapy also since I'm sure you have a whole bunch of blanket statements for that also that you found on Wiki.

 

[ResTech]

YES or NO...

These are the questions....

Hypoxia causes vasodilation... except for pulmonary hypoxic vasoconstriction.

Oxygen causes vasoconstriction.

?????????????????

I posted one thing from Wiki... the other was from actual research.. both concluded the same thing.

Don't try to side step the questions with put downs... just answer the questions... yes or no.

And I did take A&P (which I believe I have mentioned prob like 100 times now) which is why I'm not buying what your saying because it is opposite what I have always been taught on the subject in A&P and other classes over the years... and not to mention recently in Paramedic school.

If science has proven recently that hypoxia does not cause vasodilation and cerebral edema and the research I posted is wrong, than I would be interested to read the new facts on the issue... so post them.

If science has also proven that oxygen has no vasoconstrictive properties then please post the new facts.

Your direct statement was "hypoxia causes vasoconstriction"... and then as always... everyone else was wrong.

 

[VentMedic]

Your direct statement was "hypoxia causes vasoconstriction"... and then as always... everyone else was wrong.

LOL!
Again, you took one sentence from one post but didn't bother to read the rest. Did you see what I was making that reference to? Blanket statements.

Did you not see the comments about SvO2? Lactate? pH? Can you justify what conditions the hypoxia will cause vasodilation? Is it by itself or in conjunction with other factors?

Do you not see the part about 16% O2 and babies? RLF? I gave examples of both vasoconstriction and dilation depending on the circumstance. Do you know what nitric oxide is? Pulmonary hypertension? For babies? For Adults? Even hear of congenital heart disease? Factors of RDS? ARDS?

READ the posts and don't stop at the first word. If you don't understand the terminology, look it up or ask even if you want to PM me as others have done.

You also need to learn the different types of hypoxia.

Sorry but if it is a recipe for O2 therapy, I can not give you one. But, just follow your own EMT protocols and you should be okay.