# Too Much Oxygen? hmmmm



## HeadNurseRN

I was in a nursing home once and this nurse was talking to another nurse about this lady who was hooked up to a oxygen concentrator via nasal cannula. This lady was alittle loopy but since she was old I figured her brain was fried. Long story short the nurse went on to say she was alittle crazy because theres so much oxygen going to her brain she was losing it. I looked at myself and always thought 02, Oxygen was like chicken noodle soup was when your sick. How can you get enough 02 into you? I know some what about people being oxygen dependency but still. When I became a nurse even I don't know everything. Once you know everything in this field hang up your scrubs and stethoscope.


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## MrBrown

Not sure about the specific context in which you refer however there is such a thing as hyperoxemia ie too much oxygen.

Hence why this crazy concept of shoving 15 litres of oxygen down everybodies throat is a bad thing.


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## jjesusfreak01

MrBrown said:


> Not sure about the specific context in which you refer however there is such a thing as hyperoxemia ie too much oxygen.
> 
> Hence why this crazy concept of shoving 15 litres of oxygen down everybodies throat is a bad thing.



New Wake County rule, effective immediately:

Pts in respiratory distress (even STEMIs) are titrated to between 94 and 99 percent. If they sat above 94% on room air, they need no supplemental O2. We no longer aim for 100%, because then you don't know what their true sat is.


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## Jon

I've been getting some dirty looks lately from BLS providers for withholding O2 from a patient when they have an adequate O2 sat.


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## JPINFV

Naw... at SpO2 of 100, you know their true sat. What you don't know is how much oxygen is actually required to reach that. Once at 100% with 15 L/m you don't know if 4, 6, 10, 12, or any other level below 15 is necessary to maintain an appropriate saturation.


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## JJR512

MrBrown said:


> Not sure about the specific context in which you refer however there is such a thing as hyperoxemia ie too much oxygen.
> 
> Hence why this crazy concept of shoving 15 litres of oxygen down everybodies throat is a bad thing.



Depending on which dictionary one uses, _hyperoxemia_ can mean either an excessive amount of oxygen *or* acidity in the blood.

http://dictionary.reference.com/browse/hyperoxemia
http://medical-dictionary.thefreedictionary.com/hyperoxemia

An excessive amount of oxygen in blood (and tissues and organs) is better known as _hyperoxia_. Just like hypoxia but with the hyp- replaced with hyper-.

http://dictionary.reference.com/browse/hyperoxia
http://medical-dictionary.thefreedictionary.com/hyperoxia

What's more important (and relevant) is the condition known as _oxygen toxicity_.

http://en.wikipedia.org/wiki/Oxygen_toxicity

Here is an older related thread here: [thread=2703]http://www.emtlife.com/showthread.php?t=2703[/thread]


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## Shishkabob

To be fair, even with a 100% O2 sat, you can still hold more oxygen.



I was once called to a surgery facility for a patient with, and I quote, "Elevated O2 sats".

I asked dispatch to clarify that they were elevated, and the dispatcher repeated it.


I said "Roger, show us responding to a patient breathing normally."


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## MMiz

jjesusfreak01 said:


> New Wake County rule, effective immediately:
> 
> Pts in respiratory distress (even STEMIs) are titrated to between 94 and 99 percent. If they sat above 94% on room air, they need no supplemental O2. We no longer aim for 100%, because then you don't know what their true sat is.


What happens when the O2 sat reading is incorrect?  I'd sure hate to be the guy that withheld oxygen from a patient in need.


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## jrm818

You can hold more oxygen, but really it is not that much.  The oxygen content of the blood is: 1.34 x Hb x (SaO2/100)] + 0.003 x PO2

Thus someone with a PO2 of 200mmHG may only have 0.33mlO2/100ml more than someone with a PO2 of 100mmHG.  


Don't underestimate the patient with excessive O2 sat's.  The cosmic wormhole opened by having 110% of your hemoglobin oxygenated can be quite problematic.


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## Shishkabob

Meh, depends.


Say you're about to perform RSI.  Washing out the nitrogen reserves and getting every little bit of O2 in there, from the alveoli to hemoglobin saturation to plasma saturation is wanted.  More O2 = more time for apnea without fear.


(Apnea and 'without fear' in the same sentence?!)


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## jrm818

> What happens when the O2 sat reading is incorrect? I'd sure hate to be the guy that withheld oxygen from a patient in need.



That possible baddness has to be balanced against the demonstrated baddness that occurs when you over-oxygenate patients with COPD, or ACS, and there soon may be convincing evidence of baddness in cardiac arrest and maybe some other settings.

So it comes down to weighing the chance of an error with the chance of error with too much oxygen.  I acutally don't know if there is any good literature on the reliability of pulse oximiters.  Anyone know?


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## jrm818

I'll agree with "depends."  The one time oversaturaiton prior to RSI is different than a constant oversaturation in ACS or COPD.  Different goals, different time courses, etc.


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## JPINFV

Linuss said:


> To be fair, even with a 100% O2 sat, you can still hold more oxygen.



True, but at what cost?


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## JPINFV

Linuss said:


> Meh, depends.
> 
> 
> Say you're about to perform RSI.  Washing out the nitrogen reserves and getting every little bit of O2 in there, from the alveoli to hemoglobin saturation to plasma saturation is wanted.  More O2 = more time for apnea without fear.
> 
> 
> (Apnea and 'without fear' in the same sentence?!)



http://connect.jems.com/forum/topics/using-a-nasal-cannula-at-15

Pertinent to this comment.


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## JPINFV

MMiz said:


> What happens when the O2 sat reading is incorrect?  I'd sure hate to be the guy that withheld oxygen from a patient in need.



What happened to correlating the SpO2 to the patient's presentation?

What happened to correlating the pulse reading on the pulse ox with a manually measured pulse?

In monitors that display the wave form, what happened to looking at the wave form to ensure that the wave form is appropriate (not topping out of bottoming off)? 

Why not give naloxone to every patient with ALOC just in case?

Why not give D50 (or D10) to every patient in case the glucometer is broken?

What if the filter on the 12 lead is accidentally filtering out a STEMI? 

I'd hate to be the guy who deprived the hypoglycemic patient IV dextrose, but I need something more, nay, anything other than paranoia to distrust a glucometer. 

I'd hate to be the guy who delays a STEMI activation because the 12 lead was broken, but I need something more than paranoia, nay, anything other than paranoia to distrust the EKG. 

Is there any evidence that a properly applied pulse oximeter with a good wave form and/or a pulse reading that matches a manually measured pulse or a cardiac monitor should not be trusted just in case?


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## MMiz

JPINFV,

I found the pulse oximeters I used in the field were horribly unreliable.  jj's post:



> Pts in respiratory distress (even STEMIs) are titrated to between 94 and  99 percent. If they sat above 94% on room air, they need no  supplemental O2.



Seems like a pretty crazy protocol.  I'd think that skin perfusion, patient appearance, and complaint would provide some leeway.


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## JPINFV

Just curious, unreliable based on attempting to correlate to patient presentation? ABG? Hospital pulse ox reading at ED?


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## Journey

MMiz said:


> JV,
> 
> I found the pulse oximeters I used in the field were horribly unreliable.  jj's post:
> 
> Seems like a pretty crazy protocol.  I'd think that skin perfusion, patient appearance, and complaint would provide some leeway.



Valid point.

Some forget about the basic factors of what shifts the oxyhemoglobin curve. They assume that all people with an SpO2 of 96% will have the same PaO2. Some also forget get about tissue oxygenation and why we have Svo2 and StO2 monitors.

It is also quite possible for a dying/dead patient to have a high SpO2 value. This is the case when peripheral oxygen consumption is quite low,
resulting in an increased mixed venous saturation. If extraction is very low and the patient is still receiving  oxygen therapy, it is easily possible for the patient to have a high SpO2 value.

The pulse oximeter provides a very useful number but unless you have an understanding of how it is derived and the factors that influence it including many of the complex medical or cardiac situations, it is just a number to write down in the vital signs section of your report.  It may not be the inaccuracy of the pulse oximeter as much as it is the inability of the user to determine how that number relates to the patient.


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## Anjel

Treat your patient not the machine. 

I dont care if the pulse ox tells me its 1000 percent. If my patient is having a hard time breathing or showing cyanosis anywhere. They shall be getting o2 from me. 

Side note: Besides being cold, poor circulation, and co2 poisoning. Does Shock cause an inaccurate reading? Or does that go along with poor circulation.


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## JPINFV

Journey said:


> It is also quite possible for a dying/dead patient to have a high SpO2 value. This is the case when peripheral oxygen consumption is quite low,
> resulting in an increased mixed venous saturation. If extraction is very low and the patient is still receiving  oxygen therapy, it is easily possible for the patient to have a high SpO2 value.



...and, giving the topic of this thread and oxygen administration, you can make an argument that the near dead who have a good O2 saturation with no dyspnea need supplemental oxygen? The indication for supplemental oxygen is not "sick patient." A patient can be sick, even terminally, and not need supplemental oxygen.


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## JPINFV

Anjel1030 said:


> Treat your patient not the machine.
> 
> I dont care if the pulse ox tells me its 1000 percent. If my patient is having a hard time breathing or showing cyanosis anywhere. They shall be getting o2 from me.
> 
> Side note: Besides being cold, poor circulation, and co2 poisoning. Does Shock cause an inaccurate reading? Or does that go along with poor circulation.



I agree, to a point. An O2 saturation is simply a measurement of the percent of hemoglobin bound and the question needs to be asked, when evaluating the number, is "Why?" If the patient is at 95% because the patient is compensating, then yes, oxygen is indicated. If the patient is at 95% and breathing normally, then oxygen really isn't indicated. If the patient is breathing normally and hypoxic, then unless there's a reason to doubt the pulse ox, oxygen is indicated. 

The problem is that a O2 saturation is not just a number to write down. The breathing status is not just some check boxes to mark. Just because a pulse ox is 100% and the patient is breathing 40 breaths per minute does not mean that the saturation is not 100%. This isn't about treating the patient vs treating the assessment tool. It's about using an assessment tool to add a piece to the puzzle. Understanding what that piece is, where it belongs, and what it tells you is infinitely more important than any discussion about treating the patient vs treating the tool. In fact, if you understand what it's telling you, you won't need a cliche to use it properly. 

Shock is poor circulation on a systemic level.


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## jrm818

Anjel1030 said:


> Treat your patient not the machine.
> 
> I dont care if the pulse ox tells me its 1000 percent. If my patient is having a hard time breathing or showing cyanosis anywhere. They shall be getting o2 from me.



Based on what?  Do you/Does anyone have any evidence of harm from witholding supplemental O2 in a patient with a high O2 saturation?  Because there is good evidence of harm from administration of supplemental O2 even in some settings of SOB (COPD exacerbation specifically).


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## Journey

JPINFV said:


> ...and, giving the topic of this thread and oxygen administration, you can make an argument that the near dead who have a good O2 saturation with no dyspnea need supplemental oxygen? The indication for supplemental oxygen is not "sick patient." A patient can be sick, even terminally, and not need supplemental oxygen.



You are going to take that pulse ox number as your indication for O2?

Terminal patients may also have other medications on board which blunt the symptoms of hypoxia which is what hospice specializes in. Their goal is to make the patient's dying body forget about how its tissues are experiencing hypoxia regardless of what number your pulse oximeter states.  In the terminal patient it may not be an issue of "not needing oxygen" but rather reaching a point where you must realize the tissues can no longer utilize the oxygen and other options through pharmacology work better to make the patient comfortable. 

You also have to define "sick" patient in terms of actual disease processes before you can determine the appropriate oxygenation.  A patient with a seasonal cold might look sick but I wouldn't classify them the same as someone who looks sick from sepsis. You must learn some of the basic priniciples of the disease processes and a little pathophysiology.


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## Journey

jrm818 said:


> Based on what?  Do you/Does anyone have any evidence of harm from witholding supplemental O2 in a patient with a high O2 saturation?



Yes which is why we have SvO2 monitoring in the ICUs and StO2 monitoring in the EDs especially for trauma.



jrm818 said:


> Because there is good evidence of harm from administration of supplemental O2 even in some settings of SOB (COPD exacerbation specifically).



COPD? Hopefully you are not referring to the "hypoxic drive".


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## 325Medic

Journey said:


> Yes which is why we have SvO2 monitoring in the ICUs and StO2 monitoring in the EDs especially for trauma.
> 
> 
> 
> COPD? Hopefully you are not referring to the "hypoxic drive".



Too much o2 can react with oxygen free radicles causes your cells / mitrochronidria to essentially destroy causing cell death and death of cellular resp. It goes much further that this though. Thats why during codes and STEMI and stroke for that matter, they say tritate to a sat of 94-99. It has to do with the oxygentation curve.

325.


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## JPINFV

Journey said:


> You are going to take that pulse ox number as your indication for O2?


As a factor among many. It's certainly more practical and scientific than having the indication for a NRB mask be "ambulance."



> Terminal patients may also have other medications on board which blunt the symptoms of hypoxia which is what hospice specializes in. Their goal is to make the patient's dying body forget about how its tissues are experiencing hypoxia regardless of what number your pulse oximeter states.  In the terminal patient it may not be an issue of "not needing oxygen" but rather reaching a point where you must realize the tissues can no longer utilize the oxygen and other options through pharmacology work better to make the patient comfortable.


Hospice patients are also cared for by a team of health care providers who's specialized in hospice care and have more tools at their disposal to determine how much, if any, supplemental oxygen is necessary. I find it hard to believe that either all hospice patients are always a supplemental, or that these teams are hopelessly incompetent until an EMT comes along and says, "Well, I've got an ambulance and an ambulance is an indication for a NRB at 15 L/min, therefore this patient gets oxygen."




> You also have to define "sick" patient in terms of actual disease processes before you can determine the appropriate oxygenation.  A patient with a seasonal cold might look sick but I wouldn't classify them the same as someone who looks sick from sepsis. You must learn some of the basic priniciples of the disease processes and a little pathophysiology.



I believe you're misunderstanding the concepts of "indication" and "contraindication." 

So, are you suggesting that all patients need a NRB mask at 15 L/min regardless of presentation and assessment tools is a valid thought process and that EMS is incapable of determining how much, if any, supplemental oxygen is needed?


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## Journey

JPINFV said:


> As a factor among many. It's certainly more practical and scientific than having the indication for *a NRB mask *be "ambulance."
> 
> 
> *Hospice patients are also cared for by a team of health care providers who's specialized in hospice care and have more tools at their disposal to determine how much, if any, supplemental oxygen is necessary.* I find it hard to believe that either all hospice patients are always a supplemental, or that these teams are hopelessly incompetent until an EMT comes along and says, "Well, I've got an ambulance and an ambulance is an indication for a* NRB at 15 L/min*, therefore this patient gets oxygen."
> 
> 
> I believe you're misunderstanding the concepts of "indication" and "contraindication."
> 
> So, are you suggesting that all patients need a *NRB mask at 15 L/min *regardless of presentation and assessment tools is a valid thought process and that EMS is incapable of determining how much, if any, supplemental oxygen is needed?



There are more ways to deliver oxygen than just a 15 L NRB mask. You can given as little as a half a liter in some cases by a nasal cannula or a special mask. EMT training is very limited and probably time does not allow you to be taught all the various methods of oxygen delivery.

If a patient goes into Comfort Care in the hospital, we no longer do pulse ox checks. It will be determined that the O2 and medication relieving pain and the symptoms of dysnpnea will be titrated to patient comfort. In many situations, we will no longer chase the patient with O2 but will rely on the medication to make them comfortable.  Unfortunately some EMTs are required to do pulse ox checks or oxygen is the only medication they have for comfort during transport which is why the patient may also be placed on a NRB mask. Some EMTs do have a difficult time understanding how we can allow a patient with an SpO2 of 70 to be just on a 2 L NC regardless of being in a comfortable state when they are called to transport a patient home or to a hospital facility and will call hospital staff incompetent. 

There are some medical situations where O2 at 100% is indicated. This is also why we utilize other tools such as SvO2, StO2 and lab values and not just a pulse oximeter.  Initially there are very few contraindications to delivering oxygen to a patient. However, you should be educated to understand the body's response to O2 for V/Q mismatch and pulmonary vasoconstriction and respond with the appropriate treatment which in some cases could be more oxgen. For long term consequences, it will depend on the length of time the patient is on the O2 and method of delivery. Yes, an ambulance can do damage by misunderstanding and misusing PEEP or not being prepared for an asthmatic to repond with a drop in SpO2 initially when albuterol is given along with O2 or when CO2 does rise. But, this is more on the training and education of the provider rather than all oxygen is bad.

On an ambulance especially at the EMT-B level you will not have access to all of this data nor will you be able to pharmacologically make someone comfortable  who is dyspneic so you may have to go with what you have which is oxygen.


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## Journey

325Medic said:


> Too much o2 can react with oxygen free radicles causes your cells / mitrochronidria to essentially destroy causing cell death and death of cellular resp. It goes much further that this though. Thats why during codes and STEMI and stroke for that matter, they say tritate to a sat of 94-99. It has to do with the oxygentation curve.
> 
> 325.



How long do you plan on keep the patient inside an ambulance? Do you there can be some cerebral situations where O2 by mask at 100% is indicated? Do you withhold oxygen to a patient that needs it now to prevent immediate damage to organs for something that might start to happen 24 - 72 hours later?

Are you working adult codes on 21% or have a way to accurately titrate O2 to a specific concentration in an ambulance that is not a Specialty unit?

What Oxygen Curve are you referring to?  The Oxyhemoglobin Dissociation curve should how you can have a pulse ox of 94% but very different PaO2 values for each patient depending of the factors that shift the curve.


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## usafmedic45

> I was in a nursing home once and this nurse was talking to another nurse about this lady who was hooked up to a oxygen concentrator via nasal cannula. This lady was alittle loopy but since she was old I figured her brain was fried. Long story short the nurse went on to say she was alittle crazy because theres so much oxygen going to her brain she was losing it.



Under normal atmospheric pressure, that's not going to happen.  I mean no offense here, but in my experience both as an EMS provider and a respiratory therapist, the amount most non-ICU nurses _know_ about oxygen therapy would barely fill a shot glass.  What they _understand_ about it would usually fill an insulin syringe.




> I looked at myself and always thought 02, Oxygen was like chicken noodle soup was when your sick.



Nope.  Unless there is specifically a problem with oxygenation, there's no evidence to support push more O2 at them.  In fact, there's some evidence that it's harmful.  And, no, it has nothing to do with the "hypoxic drive". 



> How can you get enough 02 into you?



Hyperbaric chamber or diving while breathing pure O2.



> I know some what about people being oxygen dependency but still.



How so?



> When I became a nurse even I don't know everything. Once you know everything in this field hang up your scrubs and stethoscope.



That's a good attitude.  It seems you need to know a bit more about O2 therapy.  I'm happy to help you with that. 



> Do you there can be some cerebral situations where O2 by mask at 100% is indicated? Do you withhold oxygen to a patient that needs it now to prevent immediate damage to organs for something that might start to happen 24 - 72 hours later?



Care to show some evidence to back up the "you need 100% O2 for adequate oxygenation" claim?  It's a common mistake to believe that "high flow O2" is needed to "guarantee" a good outcome. 



> Because there is good evidence of harm from administration of supplemental O2 even in some settings of SOB (COPD exacerbation specifically).



You want to expound on that?  Like someone said, let's not further spin the yarn of 'hypoxic drive'.


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## jrm818

Journey said:


> COPD? Hopefully you are not referring to the "hypoxic drive".





			
				usafmedic45 said:
			
		

> You want to expound on that? Like someone said, let's not further spin the yarn of 'hypoxic drive'.


.

I should have clarified.  I was questioning whether even "SOB" is adequate as an indication for O2 without exception.  I would expect (rightly so?) to be burned as a heretic if I was talking about the hypoxic drive.  I really meant O2 induced hypercarbia and acidosis (and eventually...post EMS care... direct lung injury, as has been mentioned).  The only EMS study that I am aware of that examined this issue found that there was a pretty significant effect on mortality:

http://emtlife.com/showthread.php?t=20513
http://www.bmj.com/content/341/bmj.c5462.abstract


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## Journey

usafmedic45 said:


> Care to show some evidence to back up the "you need 100% O2 for adequate oxygenation" claim?  It's a common mistake to believe that "high flow O2" is needed to "guarantee" a good outcome.



It is also a common mistake to believe a 15 L NRB mask is "high flow O2".

You must understand a few terms like hyperoxyia which is determined by an ABG (Arterial Blood Gas) not SpO2 and  A-a Gradient which is the the difference between oxygen going into the alveoli and that which is in the artery.  You can have an SpO2 of 100% and even with being on 100% oxygen, your PaO2 might just fall into the range on the Oxyhemoglobin Dissociation curve. 

The oxyhemoglobin dissociation curve relates oxygen saturation (SO2) and partial pressure of oxygen in the blood (PO2), and is determined by what is called hemoglobin's affinity for oxygen,that is, how readily hemoglobin acquires and releases oxygen molecules from its surrounding tissue. 

Hyperoxia is defined by many studies as being over 300 mmHg. If patients have multiple disease processes going on, 300 mmHg might be difficult to achieve even on 100% oxygen or just a 15 L NRB mask.

For some neuro and sepsis patients we will run the PaO2 closer to 90 - 100 mmHg  rather than the lower 70 - 90 mmHg or 60 - 80 mgHg for some lung diseases. Some neuro patients will have cerebral vasospasms which require a close attention to FiO2 and fluids.  For other medical patients we will monitor SvO2 or StO2 which involves tissue oxygenation. 

Does this mean all patients need a 15 L NRB mask? No.  But as an EMT do you really know all the disease processes or have enough diagnostic data to make a blanket statement?


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## Journey

jrm818 said:


> .
> 
> I should have clarified.  I was questioning whether even "SOB" is adequate as an indication for O2 without exception.  I would expect (rightly so?) to be burned as a heretic if I was talking about the hypoxic drive.  I really meant O2 induced hypercarbia and acidosis (and eventually...post EMS care... direct lung injury, as has been mentioned).  The only EMS study that I am aware of that examined this issue found that there was a pretty significant effect on mortality:
> 
> http://emtlife.com/showthread.php?t=20513
> http://www.bmj.com/content/341/bmj.c5462.abstract



How carefully did you read that study?



> Hyperoxia was defined as PaO2 of 300 mm Hg or greater; hypoxia, PaO2 of less than 60 mm Hg (or ratio of PaO2 to fraction of inspired oxygen <300); and *normoxia*, not classified as hyperoxia or hypoxia.



Normoxia could be anywhere from 60 to 299 mmHg which could be obtained easily with a NRB mask but more than likely these patients were on a ventilator.




> A preplanned secondary analysis also was performed that was identical to the univariable analysis but used a higher PaO2 cutoff to define *hyperoxia (400 mm Hg rather than 300 mm Hg*).





> There were 2410 patients who did not have arterial blood gas values obtained within the first 24 hours in the ICU and were thus excluded from the study. The remaining 6326 patients were from 120 hospitals. The median number of cardiac arrest cases per hospital was 41 (IQR, 17-72). Baseline characteristics for all groups appear in Table 1 and Table 2. Patients were predominantly white and *from community, nonacademic hospitals*. Sixty-six percent (n = 4146) of patients were living independently prior to hospital admission and 43% (n = 2747) were admitted to the ICU from an emergency department. The most common *comorbid condition was severe cardiovascular disease *(eg, New York Heart Association class IV; n = 732 patients). Of the 6326 patients, *1156 were in the hyperoxia group *(18%), 3999 were in the hypoxia group (63%), and 1171 were in the normoxia group (19%).



Essentially what this study shows is that some hospitals need to refine their ICU management protocols which other hospitals have been doing for 50 years. There may also be other factors such as transport which will require the patient to go back to 100% and then there might be a difficult time walking the patient back down to a lower level.  I didn't see much mentioned about post ROSC hypothermia. Little hospitals will also not have Intensivists to manage all the multisystem issues and drips nor with they have accessible dialysis such as CVVH in their ICUs.  Mortality might not have been any different if the patient had been weaned to normoxia if these other factors still existed. This is why we have flight, specialty and CCT teams very prevalent in the U.S. in some regions. Or, you have protocols to take the patient to the most appropriate facility and not one that can not effectively correct the underlying condition.


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## jrm818

I read my study carefully, but your study and my study are not the same.

Yours is: Association Between Arterial Hyperoxia Following Resuscitation From Cardiac Arrest and In-Hospital Mortality in JAMA 

http://jama.ama-assn.org/content/303/21/2165.short

I was talking about: Austin et. al Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial 

http://www.bmj.com/content/341/bmj.c5462.abstract

I don't understand how we got from COPD to post ROSC mortality.


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## Journey

jrm818 said:


> I read my study carefully, but your study and my study are not the same.
> 
> Yours is: Association Between Arterial Hyperoxia Following Resuscitation From Cardiac Arrest and In-Hospital Mortality in JAMA
> 
> http://jama.ama-assn.org/content/303/21/2165.short





jrm818 said:


> I don't understand how we got from COPD to post ROSC mortality.



That article came from one of your links.

It is also relavent since the management of oxygenation is now being researched for adults after ROSC.  The debate has already been occurring in neonates to where recommendations have been mentioned in NRP but will probably not affect EMS.



jrm818 said:


> I was talking about: Austin et. al Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial
> 
> http://www.bmj.com/content/341/bmj.c5462.abstract.



This just confirms what we know about the explanations that have replaced the "hypoxic drive" theory. In the U.S. we have researched this and we now anticipate such a response which is why BiPAP is now used frequently in the ED as an early intervention. Sometimes CPAP will surfice which is found in EMS. 

Read up on pulmonary vasoconstriction and V/Q mismatching.


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## JPINFV

Journey said:


> There are more ways to deliver oxygen than just a 15 L NRB mask. You can given as little as a half a liter in some cases by a nasal cannula or a special mask. EMT training is very limited and probably time does not allow you to be taught all the various methods of oxygen delivery.


I won't argue against that. However when we're discussing treatment by EMS we're limited to the treatment options and assessment tools available. The patient can benefit by a "special mask" all the patient wants, but if the ambulance doesn't carry it, using it isn't an option. I'm also all for continuing pre-established treatments, but I think that altering a treatment plan needs to have more than "the patient is on an ambulance."



> If a patient goes into Comfort Care in the hospital, we no longer do pulse ox checks. It will be determined that the O2 and medication relieving pain and the symptoms of dysnpnea will be titrated to patient comfort. In many situations, we will no longer chase the patient with O2 but will rely on the medication to make them comfortable.


As I said earlier, the pulse ox is but one part of an assessment and is better than just blindly applying it to everyone. 



> Unfortunately some EMTs are required to do pulse ox checks or oxygen is the only medication they have for comfort during transport which is why the patient may also be placed on a NRB mask. Some EMTs do have a difficult time understanding how we can allow a patient with an SpO2 of 70 to be just on a 2 L NC regardless of being in a comfortable state when they are called to transport a patient home or to a hospital facility and will call hospital staff incompetent.



Ok... and "some" hospital staff members and "some" physicians are idiots. You can put "some" in front of any group of people and be right 99% of the time. That doesn't change the fact that a pulse ox has a place in a full assessment of patients and, in conjunction with that assessment, is a part of determining who needs supplemental oxygen started or increased -by- EMS.



> There are some medical situations where O2 at 100% is indicated. This is also why we utilize other tools such as SvO2, StO2 and lab values and not just a pulse oximeter.  Initially there are very few contraindications to delivering oxygen to a patient. However, you should be educated to understand the body's response to O2 for V/Q mismatch and pulmonary vasoconstriction and respond with the appropriate treatment which in some cases could be more oxgen. For long term consequences, it will depend on the length of time the patient is on the O2 and method of delivery. Yes, an ambulance can do damage by misunderstanding and misusing PEEP or not being prepared for an asthmatic to repond with a drop in SpO2 initially when albuterol is given along with O2 or when CO2 does rise. But, this is more on the training and education of the provider rather than all oxygen is bad.



No one is arguing that all oxygen is bad. People are arguing that misapplied oxygen is bad. Yes, there are conditions that require an FiO2 of 1. However (ignoring the fact that short of CPAP or intubation, an EMS crew won't reach an FiO2 of 1) EMS unfortunately teaches more often than not that the condition requiring that is the presence of an ambulance, which is totally false on it's face. 



> On an ambulance especially at the EMT-B level you will not have access to all of this data nor will you be able to pharmacologically make someone comfortable  who is dyspneic so you may have to go with what you have which is oxygen.



No one is arguing that dyspneic patients shouldn't receive oxygen. People are arguing the eupneic patients with an appropriate saturation doesn't need supplemental oxygen.


----------



## Journey

JPINFV said:


> Ok... and "some" hospital staff members and "some" physicians are idiots. You can put "some" in front of any group of people and be right 99% of the time. That doesn't change the fact that a pulse ox has a place in a full assessment of patients and, in conjunction with that assessment, is a part of determining who needs supplemental oxygen started or increased -by- EMS.



Never said it wasn't but like EMT, it can be just an introductory value with much more to follow through the various diagnostic data that can be done with a few other relatively simple test.  Even with just using the pulse ox you should have a greater understanding of how there are disease processes and other factors that affect the number.




JPINFV said:


> No one is arguing that all oxygen is bad. People are arguing that misapplied oxygen is bad. Yes, there are conditions that require an FiO2 of 1. However (ignoring the fact that short of CPAP or intubation, an EMS crew won't reach an FiO2 of 1) EMS unfortunately teaches more often than not that the condition requiring that is the presence of an ambulance, which is totally false on it's face.


Advance to Paramedic and you might able to titrate the oxygen. It seems your argument is that as an EMT-B you can only apply a 15 L mask which is either not quite 1.0 for an FiO2 or that it is too much. 



JPINFV said:


> No one is arguing that dyspneic patients shouldn't receive oxygen. People are arguing the eupneic patients with an appropriate saturation doesn't need supplemental oxygen.



Again, a patient does not always have to "look sick" to be sick. Or, the complaint might be something else which is a distractor like sickle cell and pain.  Some also get distracted by the diagnosis of "COPD" and forget there are other systems that can fail. You may have to treat more than one system of the body. Unfortunately many EMS protocols are written for one "diagnosis" at a time. 

There is really a vast world of disease processes and not every patient will fit neatly into one protocol.


----------



## JPINFV

Journey said:


> Advance to Paramedic and you might able to titrate the oxygen. It seems your argument is that as an EMT-B you can only apply a 15 L mask which is either not quite 1.0 for an FiO2 or that it is too much.



No thanks. How about I finish up medical school and advance to physician. Do not pass go. Do not collect $200. How would you take it if I said that maybe you should advance to physician to understand how an assessment and clinical decision making works? 

How many services have the ability to run additional testing in the field? Answer: Not many. As such care is provided with an understanding of what tools are available, what interventions are available, and the limitations within. Since EMS doesn't have access to a medical laboratory for such things as ABGs, the only alternative is to throw the kitchen sink at every patient. In which case, why even run the basic POC tests? 




> Again, a patient does not always have to "look sick" to be sick. Or, the complaint might be something else which is a distractor like sickle cell and pain.  Some also get distracted by the diagnosis of "COPD" and forget there are other systems that can fail. You may have to treat more than one system of the body. Unfortunately many EMS protocols are written for one "diagnosis" at a time.



If you're only willing to discuss the application of oxygen in as it relates to the bottom 10% of providers who are going to get irreversibly stuck on a part of medical history, this may not be the board for you. Whether a treatment is appropriate or inappropriate is independent on the ability of any single provider to grasp that concept. 




> There is really a vast world of disease processes and not every patient will fit neatly into one protocol.


I think you're showing a fundamental lack of understanding of the difference between a "protocol" and an "assessment."


----------



## Journey

JPINFV said:


> If you're only willing to discuss the application of oxygen in as it relates to the *bottom 10% of providers *who are going to get irreversibly stuck on a part of medical history, this may not be the board for you. *Whether a treatment is appropriate or inappropriate is independent on the ability of any single provider to grasp that concept.*



Since Paramedics make up less then half or closer to 10% of the providers in many states what are you saying? I initially was speaking more toward an advanced provider but then when you kept referring to a NRB mask, I figured I should take it down a notch to an EMT-B level even though I did continue using terming like Oxyhemoglobin Dissociation Curve, SvO2, A-a gradient and StO2. I do apologize for not explaining those terms more indepth for you. 

If you can not identify what your are treating, how do you know if it is appropriate or inappropriate?  It seems you are still asking for a blanket protocol and that is or should not be the  case.  Providers of patient care should be trained and educated to provide more than just recipe medicine. 




JPINFV said:


> I think you're showing a fundamental lack of understanding of the difference between a "protocol" and an "assessment."



What are your protocols and how do you do an assessment? Aren't vitals signs part of your assessment to initiate a protocol?  Aren't also the one who makes a big deal out of the fact EMTs diagnose? Don't they also do an assessment to do a protocol?


----------



## JPINFV

Something tells me the last two on this list are related.


----------



## Akulahawk

And to get back to what was part of the question originally... yes, it's possible to get too much Oxygen, but you won't see O2 toxicity under normal atmospheric conditions. Even at an FiO 1, the pO2 level in the body is just too low. You'll see other things pop up, but not toxicity.


----------



## usafmedic45

Journey said:


> It is also a common mistake to believe a 15 L NRB mask is "high flow O2".
> 
> You must understand a few terms like hyperoxyia which is determined by an ABG (Arterial Blood Gas) not SpO2 and  A-a Gradient which is the the difference between oxygen going into the alveoli and that which is in the artery.  You can have an SpO2 of 100% and even with being on 100% oxygen, your PaO2 might just fall into the range on the Oxyhemoglobin Dissociation curve.
> 
> The oxyhemoglobin dissociation curve relates oxygen saturation (SO2) and partial pressure of oxygen in the blood (PO2), and is determined by what is called hemoglobin's affinity for oxygen,that is, how readily hemoglobin acquires and releases oxygen molecules from its surrounding tissue.
> 
> Hyperoxia is defined by many studies as being over 300 mmHg. If patients have multiple disease processes going on, 300 mmHg might be difficult to achieve even on 100% oxygen or just a 15 L NRB mask.
> 
> For some neuro and sepsis patients we will run the PaO2 closer to 90 - 100 mmHg  rather than the lower 70 - 90 mmHg or 60 - 80 mgHg for some lung diseases. Some neuro patients will have cerebral vasospasms which require a close attention to FiO2 and fluids.  For other medical patients we will monitor SvO2 or StO2 which involves tissue oxygenation.
> 
> Does this mean all patients need a 15 L NRB mask? No.  But as an EMT do you really know all the disease processes or have enough diagnostic data to make a blanket statement?



Remember, you're talking to a practicing RT and former pulmonary physiology instructor.



> This is why we have flight, specialty and CCT teams very prevalent in the U.S. in some regions



It goes WAY beyond that. 



> O2 induced hypercarbia and acidosis



The study you cited has some issues judging by the abstract.  As you correct a COPD exacerbation, you often get a decrease (transient) in pH due to a correction of the V/q mismatch inherent in COPD which becomes more pronounced when you start seeing loss of dynamic coupling, the hyperinflation in a lot of cases, etc.  The things you're pointing to are the exact origins of the old myth of the "hypoxic drive".


----------



## Journey

usafmedic45 said:


> Remember, you're talking to a practicing RT and former pulmonary physiology instructor.



You might also be an RT who hasn't worked in an acute hospital or in an ICU since your clinical days.  Do you have a Master's degree in Physiology or RT? Or did you just teach basic pulmonary physiology in a tech school?  Signatures don't really mean much here and the first posts I read of yours did not present with alot of RT knowledge. Maybe you were dumbing it down and if you were, I apologize.  Some here say they are almost a doctor but still post like EMT-Bs without any additional education.


----------



## usafmedic45

No worries.   I did post at a rather basic level, but only because I didn't want to absolutely beat the OP over the head with it since I don't know how much they have in terms of an understanding.  Better to give the basics and make sure they are clear and let them show the limits of their knowledge and expand from there.  No offense taken.


I have taught the basic and advanced pulmonary physiology courses for RTs and I also present at conferences and do continuing education on the subject (especially pertaining to high altitude physiology).  Working on my bachelors at the moment, but my goal is actually a doctoral degree in epidemiology with a focus on injury patterns and injury prevention.


----------



## MEDIC802

yes the pulse ox has a place in your assessment but what about treating the pt and not the equipment? It's very rare that pt's that I have come in contact with over the years need o2 via nrb mask @ 15 lpm, a NC @ 2 lpm will be fine with most pt contacts made, unless they are on home oxygen with 1000yards of tubing tangled around furniture ect then there is a problem.


----------



## jrm818

usafmedic45 said:


> \
> 
> The study you cited has some issues judging by the abstract.
> 
> Never judge a book by its cover   Really, the study deserves a full read.  Regardless of putative physiologic mechanisms, a large mortality difference was found in favor of titrated oxygen.
> 
> As you correct a COPD exacerbation, you often get a decrease (transient) in pH due to a correction of the V/q mismatch inherent in COPD which becomes more pronounced when you start seeing loss of dynamic coupling, the hyperinflation in a lot of cases, etc.  The things you're pointing to are the exact origins of the old myth of the "hypoxic drive".



I'm a bit unclear as to how your description of the physiology is a "problem" for the study.  Is the idea that the acidosis is normal and benign?

And maybe a learning point for me: I never heard the "hypoxic drive" described anything like this.  I'd always heard/read it described as an adaptation of the cerebral chemoreceptors to chronic hypercarbia and acidosis, thus blunting the normal breathing stimulus due to accumulating CO2, and leaving only the "hypoxic" component of the respiratory drive.  The explination was that O2 administration supposedly abolished this last remaining impetus to breathe.  Perhaps there was another version?


----------



## usafmedic45

> I'm a bit unclear as to how your description of the physiology is a "problem" for the study. Is the idea that the acidosis is normal and benign?



No, it's that you often see a slight change in pH when you're actually improving the patients condition.   To say that O2 is _the_ cause for the spike in mortality or the increase in CO2 is something that I can't see being a valid point without more evidence.



> I never heard the "hypoxic drive" described anything like this. I'd always heard/read it described as an adaptation of the cerebral chemoreceptors to chronic hypercarbia and acidosis, thus blunting the normal breathing stimulus due to accumulating CO2, and leaving only the "hypoxic" component of the respiratory drive. The explination was that O2 administration supposedly abolished this last remaining impetus to breathe. Perhaps there was another version?



Some of the original "evidence" for the hypoxic drive (which does exist, but it's clinically insignificant in all but a very small minority of patients) in COPD was that giving O2 to these patients caused a rise in CO2 levels which was attributed incorrectly that the O2 was "suppressing" the minute ventilation.  The rise is actually due mostly to the Haldane effect and the reversal of hypoxic pulmonary vasoconstriction.  Even in severe end-stage COPD, it's quite unusual to see a decline in minute ventilation of more than 10%.


----------



## jrm818

usafmedic45 said:


> No, it's that you often see a slight change in pH when you're actually improving the patients condition.   To say that O2 is _the_ cause for the spike in mortality or the increase in CO2 is something that I can't see being a valid point without more evidence.



If you haven't read the full text yet, it really is worth a read.  I'd argue that this trial provides some rather convincing evidence that the mortality (and probably the hypercarbia) were actually _caused _by oxygen administration variations.  This was a well randomized controlled trial with pretty well matched groups.  I've obviously had a bit of a debate over the merits of the study beore (that thread I linked to) but I'd be interested in any more specific thoughts.



usafmedic45 said:


> Some of the original "evidence" for the hypoxic drive (which does exist, but it's clinically insignificant in all but a very small minority of patients) in COPD was that giving O2 to these patients caused a rise in CO2 levels which was attributed incorrectly that the O2 was "suppressing" the minute ventilation.  The rise is actually due mostly to the Haldane effect and the reversal of hypoxic pulmonary vasoconstriction.  Even in severe end-stage COPD, it's quite unusual to see a decline in minute ventilation of more than 10%.



I'm with you now: I was aware of the no change in minute volume evidence, so in my mind I sort of discarded the notion that development of hypercarbia is related to the theory.


----------



## usafmedic45

Most likely the spike in PCO2 associated with the O2 administration is due to the reduction in hypoxic induced pulmonary vasoconstriction, rather than a worsening of the patient condition.  You start perfusing areas that previously were not perfused but were still ventilated, you're going to see your PaCO2 go up. 

I just don't see a causative relationship between the O2 and the rise in mortality.  There's correlation, yes, but I don't see it as causative.  At very least, there needs to be a larger study done to pin it down and reproduce the results.


----------



## jrm818

usafmedic45 said:


> Most likely the spike in PCO2 associated with the O2 administration is due to the reduction in hypoxic induced pulmonary vasoconstriction, rather than a worsening of the patient condition.  You start perfusing areas that previously were not perfused but were still ventilated, you're going to see your PaCO2 go up.
> 
> I just don't see a causative relationship between the O2 and the rise in mortality.  There's correlation, yes, but I don't see it as causative.  At very least, there needs to be a larger study done to pin it down and reproduce the results.



I think your explanation is probably accurate, especially if you add in the influence of the haldane effect, as you note.  However, and perhaps I'm wrong, but I was under the impression that the hypoxic vasoconstriction is rather adaptive in this setting, and its artificial removal may worsen V/Q mismatching and cause pathological CO2 accumulatino because more blood is now perfusing lung areas which are still crummy at removing CO2 even though they are now seeing lots of oxygen.


What is the hang up on the causation thing?  RCT's are the type of study that is designed to establish causality: because only one intervention is changed, and the groups are randomized and well matched, the only outcome differences in the groups should be because of the changed intervention.  Why is that not an acceptable answer here? 

Is it just the numbers (obviously more would be better, but this is really not a small study, and a pre-study power analysis was performed indicating that these are adequate numbers, and statistical significance was easily reached for the mortality claim).  Is it that there is no other confirmatory evidence (I think there is some).  Do you just doubt the biologic plausibility of the whole idea of O2 induced mortality?

I certianly agree that I'd like to see these results replicated in other populations.  Still, I think this study does a lot of work towards demonstrating causation.


----------



## Chap

*oxygen use*

In my EMT class we were taught..."everyone gets oxygen....15ml/min rebreather"  (assuming no facial trauma, etc...)


apparently that isn't the way anymore.  I wish I had known that...


----------



## usalsfyre

Chap said:


> In my EMT class we were taught..."everyone gets oxygen....15ml/min rebreather"  (assuming no facial trauma, etc...)
> 
> 
> apparently that isn't the way anymore.  I wish I had known that...



The kicker is, it NEVER was this way. EMT-Basic is just too dumbed-down to go into how to select appropriate oxygen therapy, so they went with "treat the worst case and most easily correctable condition".


----------



## jjesusfreak01

usalsfyre said:


> The kicker is, it NEVER was this way. EMT-Basic is just too dumbed-down to go into how to select appropriate oxygen therapy, so they went with "treat the worst case and most easily correctable condition".



I had a pt today satting between 94% and 96%, didn't put them on supplemental O2, and it didn't bother me one bit. This was an IFT trip and I was the primary provider. I am an EMT-B. If I have access to a pulseox, and the patient doesn't appear to be in any respiratory distress, I am perfectly capable of titrating supplemental O2 to the patient.


----------



## Shishkabob

jjesusfreak01 said:


> I had a pt today satting between 94% and 96%, didn't put them on supplemental O2, and it didn't bother me one bit. This was an IFT trip and I was the primary provider. I am an EMT-B. If I have access to a pulseox, and the patient doesn't appear to be in any respiratory distress, I am perfectly capable of titrating supplemental O2 to the patient.



My old EMT challenged my decision on that one time:  No signs of respiratory distress, good pulse ox, good CO2, etc etc etc, every assessment was negative for SOB aside from the family stating she looked short of breath.   I kept her on the 2lpm NC... my partner said "Are you sure?  I think we should do a non-rebreather at 15"



No, I'm not sure, I make arbitrary decisions of patient care all the time, my years of education be damned.


----------



## Neo

Journey said:


> How long do you plan on keep the patient inside an ambulance? Do you there can be some cerebral situations where O2 by mask at 100% is indicated? Do you withhold oxygen to a patient that needs it now to prevent immediate damage to organs for something that might start to happen 24 - 72 hours later?
> 
> Are you working adult codes on 21% or have a way to accurately titrate O2 to a specific concentration in an ambulance that is not a Specialty unit?
> 
> What Oxygen Curve are you referring to?  The Oxyhemoglobin Dissociation curve should how you can have a pulse ox of 94% but very different PaO2 values for each patient depending of the factors that shift the curve.



I think your not talking about the same thing here, of course som patient need it he has to get the right amount of O2. puls ox is unstable to use becouse it reacts on skinn temp. o.s.v we do research on free radicals now, and i think we will see a big change in how we administerd O2 to ROSCH and ESTEMI patient and more. If you wonder how fast the reaction is you can see for your self in this formula.  The formation of hydrogen peroxide (H2O2) in the body continuously. The body get rid of most of this through enzymes called peroxidase, which converts H2O2 to two water molecules (the remaining hydro genes come from a molecule that hetet NADPH).

Something H2O2 "escapes" the enzyme and if it comes in contact with divalent iron (which is part of the body) will be formed OH radicals (OH • printed):

H2O2 + Fe2 + -> • OH + OH-+ Fe3 +

• OH is very reactive and will react with other substances, such as unsaturated fatty acids, which are very much in the membrane that surrounds all cells in the body. Let RH be an unsaturated fatty acid, and we get a three-step reaction:

Initiation: RH + OH • -> R • + H2O

Propagenering: R • + O2 -> R-O-O •

and R-O-O • + RH -> R-O-O-H + R •

Termination: Interaction between the radicals and the production of non-initiating and non-propagenerende species.

Propageneringstrinnet can happen a number of times before it stops. The reason for this is that it is both consumed and produced a radical, and radicals are unstable since they contain an unpaired electron.

In propageneringsprosessen is the first step rapidly, and the second step rate determining.


----------



## JJR512

Love is like oxygen. You get too much, you get too high.
Not enough and you're going to die.


----------



## 18G

Pennsylvania protocols just released also state to titrate oxygen to SpO2 >94%. Oxygen use has always been a major pet peeve of mine especially when used to treat MI / ACS. 

This is an evidence based recommendation. High flow oxygen has been shown to cause coronary vasoconstriction thus decreasing coronary blood flow, decreased CO, and worsening of the ischemia.


----------



## lightsandsirens5

18G said:


> Pennsylvania protocols just released also state to titrate oxygen to SpO2 >94%. Oxygen use has always been a major pet peeve of mine especially when used to treat MI / ACS.
> 
> This is an evidence based recommendation. High flow oxygen has been shown to cause coronary vasoconstriction thus decreasing coronary blood flow, decreased CO, and worsening of the ischemia.



It's about freaking time someone changed that one! Maybe more states will follow. I hope to God they do!


----------



## jjesusfreak01

Neo said:


> I think your not talking about the same thing here, of course som patient need it he has to get the right amount of O2. puls ox is unstable to use becouse it reacts on skinn temp. o.s.v we do research on free radicals now, and i think we will see a big change in how we administerd O2 to ROSCH and ESTEMI patient and more. If you wonder how fast the reaction is you can see for your self in this formula.  The formation of hydrogen peroxide (H2O2) in the body continuously. The body get rid of most of this through enzymes called peroxidase, which converts H2O2 to two water molecules (the remaining hydro genes come from a molecule that hetet NADPH).



Titrating O2 to 95% saturation does not result in any larger amount of O2 in the body than the patient would get when breathing normally in a non-emergent situation. Also, why are you posting the radical formation reaction? I had hoped to never see that again after the MCAT.


----------



## JPINFV

Neo said:


> o.s.v we do research on free radicals now, and i think we will see a big change in how we administerd O2 to ROSCH and ESTEMI patient and more.


Just curious, what are the literal translation for ROSCH and ESTEMI? I'm going to go out on a limb and think that they are synonymous with "return of spontaneous circulation" (ROSC) and "ST-elevated MI" (STEMI). I am, however, having problem placing the additional letter. 




> If you wonder how fast the reaction is you can see for your self in this formula.  The formation of hydrogen peroxide (H2O2) in the body continuously. The body get rid of most of this through enzymes called peroxidase, which converts H2O2 to two water molecules (the remaining hydro genes come from a molecule that hetet NADPH).



...don't forget about catalase. The reason hydrogen perioxide bubbles when put onto exposed cuts is not because it's killing bacteria, but because oxidase positive cells (both some types of bacteria and human cells) are breaking it down.


----------



## DitchDoctorGabe

True but dare I say common sense judgment is needed. I don't see a huge issue for a short term transport and the pt. receives high flow oxygen. Granted we are aiming at keeping sats 94% or above and the long term issues is that you have to deal with free oxygen radicals. Plus in the neonates you do run the risk of causing retinopathy of prematurity.


----------



## usafmedic45

> Plus in the neonates you do run the risk of causing retinopathy of prematurity.




Go do some research on the actual epidemiology of RoP and report back.


----------



## ihalterman

jjesusfreak01 said:


> New Wake County rule, effective immediately:
> 
> Pts in respiratory distress (even STEMIs) are titrated to between 94 and 99 percent. If they sat above 94% on room air, they need no supplemental O2. We no longer aim for 100%, because then you don't know what their true sat is.



Our new standard is no O2 for SPo2 >94% unless they complain of SOB.  O2 is a vasoconstrictor, that's a bad thing in an MI.


----------



## Gecko24

MMiz said:


> JPINFV,
> 
> I found the pulse oximeters I used in the field were horribly unreliable.  jj's post:
> 
> 
> 
> Seems like a pretty crazy protocol.  I'd think that skin perfusion, patient appearance, and complaint would provide some leeway.




WHAT, your gonna treat the patient not a monitor?  That is just crazy thinking.


----------



## JPINFV

Gecko24 said:


> WHAT, your gonna treat the patient not a monitor?  That is just crazy thinking.



Yep... let's get rid of all tools while we're at it, starting with cardiac monitors. After all, an atypical MI presentation is probably just a machine error, right?


----------



## Gecko24

JPINFV said:


> Yep... let's get rid of all tools while we're at it, starting with cardiac monitors. After all, an atypical MI presentation is probably just a machine error, right?



I guess we should keep them, if you can not walk into a room and see an ashen grey patient grabbing their chest short of breath and dripping in sweat.  And you hold your judgment of what is going on until you actually hook up your monitor.  Well yeah I guess you need that 12 lead.  I guess if you get a perfect 12 lead and the patient still looks crappy you are not worried?  Treat the patient not the monitor, or you know what the word assume means right?
Tools are only what the word means a tool to help you in your clinical judgment, still falls back on your training.

Now wanna refute that?


----------



## Gecko24

Sorry, I did not mean to jump your ***.  but until you learn the difference between compensated and uncompensated distress and know the values of oxy-hemoglobin curves then you will not understand the effects of resp distress on a patient. Your point is valid on non typical acute cardiac patient, but a perfectly normal EKG does not rule out anything.


----------



## JPINFV

Gecko24 said:


> ...if you can not walk into a room and see an ashen grey patient grabbing their chest short of breath and dripping in sweat.


So... all of your MIs present like this?



> And you hold your judgment of what is going on until you actually hook up your monitor.  Well yeah I guess you need that 12 lead.  I guess if you get a perfect 12 lead and the patient still looks crappy you are not worried?  Treat the patient not the monitor, or you know what the word assume means right?


You should start using your clinical judgment to determine potential causes as soon as you see the patient. You don't shut down just because you got a specific reading or specific exam finding, regardless of what they are, or what tools, be it your eyes or your monitor, says. 



> Tools are only what the word means a tool to help you in your clinical judgment, still falls back on your training.
> 
> Now wanna refute that?


I'm not the one trying to argue that we shouldn't use tools. I've maintained throughout this entire thread that tools should be incorporated into an assessment, not ignored just because a presentation doesn't match it completely. A monitor or pulse ox or blood glucose monitor are a tool, just like our senses. No one part of the assessment should be used to the mutual exclusion of all else, be it a tool or a sense. After all, would you ignore a STEMI because the 65 y/o diabetic female is complaining of abdominal pain and not chest pain?


----------



## JPINFV

Gecko24 said:


> but a perfectly normal EKG does not rule out anything.


It rules a lot of things out. Show me a 3rd degree AV block with a normal EKG. However, I think you're thinking something along the lines of STEMI vs NSTEMI, in which case show me where I said a normal 12 lead ruled out NSTEMI.


----------



## Gecko24

JPINFV said:


> It rules a lot of things out. Show me a 3rd degree AV block with a normal EKG. However, I think you're thinking something along the lines of STEMI vs NSTEMI, in which case show me where I said a normal 12 lead ruled out NSTEMI.



Actually lets just agree to disagree okay.  Because by definition a STEMI is an ST elevated MI.  But a normal 12 lead does not rule out an MI, but it does rule out a STEMI.   There are more than one MI's and the treatment rules dictate various approaches, such as sub endocardial just to name one.  Treatment of choice for a STEMI is PCI.  Others have different treatment algorithms, but then I digress from the original topic.  I will still fall back on the rule, if you need tools as the for-mentioned pulse ox then use it.  I just hope that when you see a patient that is gasping for breath and Cyanosis your fist move is to grab the pulse ox.


----------



## Gecko24

JPINFV said:


> You should start using your clinical judgment to determine potential causes as soon as you see the patient. You don't shut down just because you got a specific reading or specific exam finding, regardless of what they are, or what tools, be it your eyes or your monitor, says.




Um, just for the record.  Isn't that what I said in the first place?  And you took issue at it, LOL


----------



## Gecko24

JPINFV said:


> Yep... let's get rid of all tools while we're at it, starting with cardiac monitors. After all, an atypical MI presentation is probably just a machine error, right?



As so stated?


----------



## Gecko24

Gecko24 said:


> ----> that part--->
> Tools are only what the word means a tool to help you in your clinical judgment, still falls back on your training.
> 
> Now wanna refute that?



like that part?


----------



## JPINFV

Gecko24 said:


> But a normal 12 lead does not rule out an MI, but it does rule out a STEMI.   There are more than one MI's and the treatment rules dictate various approaches, such as sub endocardial just to name one.



Hmm, learn something new... oh, wait.


> in which case show me where I said a normal 12 lead ruled out _*N*_STEMI.



Actually, looks like I covered non-STEMIs there... 



> I will still fall back on the rule, if you need tools as the for-mentioned pulse ox then use it.  I just hope that when you see a patient that is gasping for breath and Cyanosis your fist move is to grab the pulse ox.


Do you want to know how I know you haven't read this thread?


----------



## JPINFV

Gecko24 said:


> Um, just for the record.  Isn't that what I said in the first place?  And you took issue at it, LOL



I take issue with the cliche "treat the patient not the monitor" because you should be treating the patient and the monitor and asking, "why?" if the two aren't correlating as you would expect they are.


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## Gecko24

JPINFV said:


> I take issue with the cliche "treat the patient not the monitor" because you should be treating the patient and the monitor and asking, "why?" if the two aren't correlating as you would expect they are.



It is good your take issue with it, so honestly as a clinician what would you believe?

Your own clinical judgment or that machine?  that is all I stated, and yet you got all pissy?

Tell me?


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## Gecko24

And you should never have taken issue with treat the patient not the monitor, it is a rule taught in every med school, nursing school, and paramedic class ever held.  Or it should have been, if your instructor was worth anything.


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## Gecko24

It all started with Oxyhemoglobin Dissociation Curve theories and my judgment on those.  I apologize, I am sorry.  But I just wanted to convey that a absolute good PSO2 does not correspond to tissue profusion.  The topic got twisted to MI's which was way off topic. But I am good with that too.


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## ffemt8978




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## Gecko24

We would have a great discussion over a few beers, of coarse I would win.  But that is just how I role.


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## JPINFV

Gecko24 said:


> It is good your take issue with it, so honestly as a clinician what would you believe?
> 
> Your own clinical judgment or that machine?  that is all I stated, and yet you got all pissy?
> 
> Tell me?



A tool does not provide clinical judgment. Clinical judgement is the integration of all available information, be that sensory input (what do we hear (including the history), feel, smell, see) or assessment tools. It's just as foolhardy to assume that a tool is wrong for no reason than it's not reading what I'm expecting it to as to ignore signs and symptoms because it's not what I'm expecting. What if what I think is happening is wrong, hence what the information from a history and physical (including appropriate diagnostic tools) not correlating with what I'm expecting? 

As I mentioned earlier in this thread, I need something more than paranoia or wishful thinking to assume that a tool is wrong just because it's not matching perfectly. Yes, the physical exam findings could be misinterpreted. So when things aren't matching as expected, you have to consider that the exam findings were wrong (Did the patient misunderstand or make a mistake during the history? Did I really find ___ on my exam?), the tool is wrong (trouble shoot the tool), or the working and differential diagnoses needs to be reconsidered. Is a differential Dx now more likely than the working Dx? Does something else need to be added? 

If a tool is going to be ignored if it's readings don't match what it is expected to be, why even use the tool?


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## JPINFV

Gecko24 said:


> And you should never have taken issue with treat the patient not the monitor, it is a rule taught in every med school, nursing school, and paramedic class ever held.  Or it should have been, if your instructor was worth anything.



I'm sorry, my school focuses on clinical decision making, not cliches.


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## Gecko24

But I would buy


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## Gecko24

Sigh Okay, I guess you need to get more X's  on your sig and finish school.  The we could talk.


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## Gecko24

I tried?


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## JPINFV

Gecko24 said:


> Sigh Okay, I guess you need to get more X's  on your sig and finish school.  The we could talk.



What you have a problem with the concept that sometimes you need to (grimaces at quoting Ayn Rand), "Check your premises?"


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## Gecko24

Good night forum


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## usalsfyre

I've mentioned this before, but "treat the patient not the monitor" is one of my pet peeves. Yes, monitors have to be clinically correlated, and if they don't as JPINFV noted it needs to be investigated further. As he also noted, if we are supposed to have an inate bias against them, why do we lug the damn things around?

"Treat the patient not the monitor" is simply one more cliche aimed at propping up weak paramedics who didn't have enough clinical education to learn how to integrate diagnostics into their decision making process. It belongs in the same crap pile as "Lidocaine numbs the heart" and "Intubation is the gold standard".


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## MrBrown

usafmedic45 said:


> Go do some research on the actual epidemiology of RoP and report back.



Yes, please do good sir, here .... *blind Brown pulls Brown's eyes out and hands them over, use these.



Gecko24 said:


> And you should never have taken issue with treat the patient not the monitor, it is a rule taught in every med school, nursing school, and paramedic class ever held.  Or it should have been, if your instructor was worth anything.



Meaning what exactly? If Nana with symptoms is having a massive bloody tombstone MI on 12 lead then thats OK?


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## DitchDoctorGabe

usafmedic45 said:


> Go do some research on the actual epidemiology of RoP and report back.



I do not transport neonates that fit in a box, as far as what you asked me to do I have read up in it. I may be reading your post and another persons post wrong but I figured since you are a respiratory therapist you share some insight on this. From what I've read oxygen can contribute to the development of RoP. Any additional input on this?


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## MrBrown

DitchDoctorGabe said:


> I do not transport neonates that fit in a box, as far as what you asked me to do I have read up in it. I may be reading your post and another persons post wrong but I figured since you are a respiratory therapist you share some insight on this. From what I've read oxygen can contribute to the development of RoP. Any additional input on this?



ROP develops because of hyperoxic constriction of the arterioles and capillaries in the retinal tissue causing ischaemic growth of necrotic scar tissue.  Very premature newborns usually require aggressive management because of underveloped respiratory systems - in partic Type II cells in the alveoli (surfactant) which in the past has included cramming a ton of 100% oxygen down their gob.

We now no longer rely on soley on PaO2/ABG as was common in years gone by thanks to the advent of such gadgets as SPO2 and are able to titrate oxygen therapy much better

Blind Brown
26 weeks - 900g
10/86


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