Withholding oxygen in MI

[johnmedic]

Hello. Vague question but our MPD mentioned a change in protocols for "chest painers" at a county meeting. This change was to - when dealing with chest pain of cardiac origin - not administer oxygen unless pt's spO2 was low 90's or below, stating that there's a risk of detrimental effects when o2 was administered in MI despite adequate circulating oxygen levels.
Note that medical history isn't a factor for this.

First: I will be asking him for info when I speak to him next. I'm just coming to you guys because I can't wait & I know I'm not the only one who has witnessed oxygen reverse chest pain / correct dysrhythmias despite a relatively high initial spO2.

Q: What detrimental effects? I know it's not indicated but why contraindicated?

Sent from my G2X on tapatalk. Forgive my typos. ; )

 

[Shishkabob]

Take a look at the AHAs 2010 guidelines on supplemental O2.

However, there is insufficient evidence to support its routine use in uncomplicated ACS. If the patient is dyspneic, hypoxemic, or has obvious signs of heart failure, providers should titrate therapy, based on monitoring of oxyhemoglobin saturation, to ≥94% (Class I, LOE C)

Granted, I still give an NC to someone complaining of chest pain that I deem might be cardiac related, but an NC is pretty much all I use. No need for an NRB / 6lpm NC / etc etc.

 

[usafmedic45]

I know I'm not the only one who has witnessed oxygen reverse chest pain / correct dysrhythmias despite a relatively high initial spO2.

I have six words for you:
Anecdotal evidence.
Placebo effect.
Confirmation bias*


*-also called "cherry picking the data"

 

[18G]

There is research from the 1950's and validated using current technology that shows hyperoxia results in decreased coronary perfusion as a result of coronary artery vasoconstriction. Also, a decrease in cardiac output was noted in some of the research.

If you stop and think about it, it makes perfect sense. What is the main problem with an MI? A coronary artery is occluded right? If the patient already has a normal level of oxygenation with say an SpO2 of 97%, than how is increasing that to 99% really going to make any difference? The hemoglobin is saturated and already contains a level of oxygen necessary to meet the body's demands. The problem is the heat muscle distal to the occlusion isn't getting the proper amount due to the blockage.... not because the oxygen isn't available in the body.

It has also been found through the research that providing high-flow O2 or increasing the SpO2 above 94% does not have any effect on the ischemic heart tissue.

Oxygen has no thrombolytic properties and it is a known vasoconstrictor.

 

[usafmedic45]

There is research from the 1950's and validated using current technology that shows hyperoxia results in decreased coronary perfusion as a result of coronary artery vasoconstriction. Also, a decrease in cardiac output was noted in some of the research.

If you stop and think about it, it makes perfect sense. What is the main problem with an MI? A coronary artery is occluded right? If the patient already has a normal level of oxygenation with say an SpO2 of 97%, than how is increasing that to 99% really going to make any difference? The hemoglobin is saturated and already contains a level of oxygen necessary to meet the body's demands. The problem is the heat muscle distal to the occlusion isn't getting the proper amount due to the blockage.... not because the oxygen isn't available in the body.

It has also been found through the research that providing high-flow O2 or increasing the SpO2 above 94% does not have any effect on the ischemic heart tissue.

Oxygen has no thrombolytic properties and it is a known vasoconstrictor.

Well said. This sort of thing is exactly why we need to do a better job of educating folks about the different forms of hypoxia.

 

[18G]

when dealing with chest pain of cardiac origin - not administer oxygen unless pt's spO2 was low 90's or below, stating that there's a risk of detrimental effects when o2 was administered in MI despite adequate circulating oxygen levels.

Nice to see some progressive thinking on this and protocols going away from indiscriminate oxygen use!

 

[Shishkabob]

Though, one could also make an argument that hyper-saturating the plasma COULD be beneficial if a hole is too small for a RBC, but big enough for plasma

 

[johnmedic]

Excellent, thank you all. Yes I obviously realize that it isn't going to fix to the the occlusion, just have been taught that in ACS: more oxygen-bound hemoglobin can't hurt aside from the usual contraindications. This is the first time I'm hearing about the vasoconstrictive properties of oxygen.
Great posts.

Sent from my G2X on tapatalk. Forgive my typos. ; )

 

[usafmedic45]

Though, one could also make an argument that hyper-saturating the plasma COULD be beneficial if a hole is too small for a RBC, but big enough for plasma

Modified Gamow bags anyone?

 

[18G]

more oxygen-bound hemoglobin can't hurt aside from the usual contraindications. This is the first time I'm hearing about the vasoconstrictive properties of oxygen.
Great posts.

This is a huge part of the problem. For way too long it has been taught that oxygen is innocent and can't hurt to have too much. This is wrong which is why changes is protocols are happening.

It's not only MI/ACS that oxygen is being discouraged unless absolutely indicated. Also, CVA, ROSC, and Neonatal Resuscitation. I have also read some information that showed COPD patient's had worse outcomes when their oxygen saturations were maintained higher than their baseline at like around 99-100%.

I'm just curious how your Paramedic program never taught the vasoconstrictive property of oxygen? How do you explain importance of proper ventilation in the head injured patient?

 

[usafmedic45]

I'm just curious how your Paramedic program never taught the vasoconstrictive property of oxygen? How do you explain importance of proper ventilation in the head injured patient?

You realize the issue with ventilation in closed head trauma has less to do with the oxygen and more do to with carbon dioxide tensions, right? Let's not confuse the kid by muddling the two together unnecessarily.

 

[johnmedic]

I can't quote on my phone but regarding the ventilation of a head inured patient, they explained the danger in the excess elimination of co2 to dangerously low levels during *hyper*ventilation. But I never felt that normal respirations would cause a co2 drop significant enough to exacerbate ACS. Naturally I can understand now that hyperoxemia can contribute.

Sent from my G2X on tapatalk. Forgive my typos. ; )

 

[Handsome Robb]

I'm just curious how your Paramedic program never taught the vasoconstrictive property of oxygen? How do you explain importance of proper ventilation in the head injured patient?

I was under the impression the goal was to lower CO2 levels to cause cerebral vasoconstriction in a pt with suspected increased ICP and the O2 is more vasoconstrictive in coronary arteries.

Edit: Usaf beat me to it. Darn.

 

[usafmedic45]

But I never felt that normal respirations would cause a co2 drop significant enough to exacerbate ACS

It's not going to in most cases, at least not based on the research I have seen on the subject of CO2 as a vasoactive agent. 18G just could have worded the discussion a bit better. He (she?) is on the mark for the most part with the comments about oxygen as a vasoconstrictor.

 

[04_edge]

Anyone care to explain how 02 causes vasoconstriction? Im well aware that hypocapnia can lead to it, but have not heard of 02 causing it before. A link would be adequate, im down for a good read.

 

[mycrofft]

Thanks for the high-caliber entries.

Original field tx protocols were written before the technology needed to have a small portable and reliable (sort of) means's of determining these factors.

 

[usafmedic45]

Anyone care to explain how 02 causes vasoconstriction? Im well aware that hypocapnia can lead to it, but have not heard of 02 causing it before. A link would be adequate, im down for a good read.

Pubmed.gov is probably a good place to go looking for the literature. "Oxygen, vasoconstriction" will probably yield more than you ever wanted to know on the subject.

 

[JPINFV]

A physio book would work just as well. Arteriole constriction due to oxygen is a well understood and relatively basic concept. When the oxygen demand of a segment of tissue has been met, there's little need to supply copious amounts of blood to that region, so the arterioles and the branches of capillaries constrict. You simply do not have enough blood volume to supply every single bit of tissue with blood every single millisecond. There's also no need to do so, so you end up, if you take a snap shot, some capillaries and arterioles are dilated while others are constricted.

It should also be noted that the blood supply in the pulmonary circuit works the exact opposite, with areas of high oxygen concentration being preferentially perfused.

 

[Handsome Robb]

http://studentorgs.vanderbilt.edu/vems/Oxygen Therapy in Cardiac Patients.pdf

There's a short blurp on it for ya.

 

[18G]

http://studentorgs.vanderbilt.edu/vems/Oxygen Therapy in Cardiac Patients.pdf

There's a short blurp on it for ya.

Thank you for posting the great article!