Chest Pain and Oxygen

Street Doc

Street Doc

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Pt with legitimate Chest Pain, stable vitals, SPO2 99%, and little or no EKG ectopy. Now, do they get a nonrebreather or nasal cannula? I always use a NRB but lately I have been getting questioned by some RN's.
My reason is this... When someone is having a possible CVA they get a NRB even with a good SPO2 in an attempt to get the most possible O2 past the blockage or bleed. Can someone tell me what the difference in treatment is between a CVA and a MI in respect to oxygen getting through to damaged tissue.
 
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Actually, according to the Mosby Paramedic text, a stable CP patient, and a non-hypoxic CVA patient both receive nasal cannula.
 
By the book, everybody getes 100% O2 by NRB. If anybody has an SaO2 of 99%, chillin' on room air, I give them an NC just to look cool. The NRB is sometimes a little dramatic and can make the patient uncomfortable (I mean...not that prongs up their nose doesn't). The moment their sats go below 95% (of course, with a good waveform), they get 15L so I can stop worrying about it.

The amount of oxygen you're giving them has nothing to do with how much the tissue is getting, assuming their sats are good (>95%). If there's a blockage, heck, you could give IV oxygen (please don't try this, it's called an embolism, and it doesn't end well) and it wouldn't get to the tissue that needs it.
 
I have a rule of thumb - if they are satting above 90, the get the NC - below that - NRB.....
 
Street Doc said:
Pt with legitimate Chest Pain, stable vitals, SPO2 99%, and little or no EKG ectopy. Now, do they get a nonrebreather or nasal cannula? I always use a NRB but lately I have been getting questioned by some RN's.
My reason is this... When someone is having a possible CVA they get a NRB even with a good SPO2 in an attempt to get the most possible O2 past the blockage or bleed. Can someone tell me what the difference in treatment is between a CVA and a MI in respect to oxygen getting through to damaged tissue.
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Also, you're not going to get O2 past the blockage to damaged tissue. Only those MD's or DO's who are trained in the intervention of these processes can do that.

What we are to do as prehospital emergency care providers is to maintain adquate oxygenation (SpO2 = 95-99%) and adequate ventilation (PaCO2 = 35-45 torr). Sometimes that is easier said than done. Which is where knowledge, training, and skill as a patient advocate comes into play.
 
daedalus said:
Actually, according to the Mosby Paramedic text, a stable CP patient, and a non-hypoxic CVA patient both receive nasal cannula.
Click to expand...

Key words in bold.

Street Doc said:
Pt with legitimate Chest Pain, stable vitals, SPO2 99%, and little or no EKG ectopy. Now, do they get a nonrebreather or nasal cannula? I always use a NRB but lately I have been getting questioned by some RN's.
My reason is this... When someone is having a possible CVA they get a NRB even with a good SPO2 in an attempt to get the most possible O2 past the blockage or bleed. Can someone tell me what the difference in treatment is between a CVA and a MI in respect to oxygen getting through to damaged tissue.
Click to expand...

Key words in bold.

Were you just looking for ectopy? What about ischemia on a 12-lead? Structural problems associated with the thoracic region?

What are the underlying problems? What are the associated problems? Length of time for more definitive treatment?

What are the oxygen demands of the patient? Would the demand be met better if cardiac output and perfusing pressures are appropriately managed?

While the SpO2 "number" is okay for some assessments, it tells nothing of tissue oxygenation or O2 delivery. However, other parts of the assessment will provide you with clues to that. Increased MV can compensate, at least for a short while, for some issues concerning the energy cycle.

The idea is to identify, correct and wean the O2 quickly with recommendations of 2 to 6 hours of initiation. All factors must be considered as well as your ability as a Paramedic to manage symptoms and maintain an SpO2 greater than 90% by maintaining cardic output and mean arterial pressures or perfusing pressures. Applying O2 is just one part of the equation. If the patient is very symptomatic with an SpO2 of 95%, that number may be skewed by other issues and clinical judgement will have to overrule recipes.


http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15765131

Conclusions
Oxygen, beyond its indispensable role in cardiac energy metabolism, plays a central role in other biological processes that can be determinants of cardiac function, including the generation of ROS and the determination of cardiac gene expression patterns. Although their role in the pathogenesis of clinical heart failure remains unclear, ROS have been implicated in most processes thought to have a significant effect on cardiac function, including hypertrophy, ion flux and calcium handling, EC coupling, extracellular matrix configuration, vasomotor function, metabolism, gene expression, and downstream signaling of several growth factors and cytokines. Clinical trials based on antioxidant therapies have been, however, generally disappointing. Whether this is a function of the particular antioxidants used is unclear, and planned trials with XO inhibitors and other alternative agents should help answer this question. The role of hypoxia-induced alterations in gene expression in the genesis of heart failure also remains unclear, although experimental data suggest that these changes in gene expression can be either adaptive or maladaptive, depending on context. Given the central role of oxygen in cardiovascular biology, further investigational focus on oxygen-related processes in the genesis of heart failure is warranted.
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Several studies later throughout the past 100 years have still reached no definitive conclusion. Thus, we still abide by getting a patient off the oxygen clock or reducing O2 therapy when conditions allow.
 
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Yeah, her references are better than mine. ;)
 
Per protocol below 95% gets NC, below 90% gets NRM. Per common sense look at patient and provide O2 that keeps them close to pink and away from blue.
 
Yeah 95% means you are getting 95% to the finger. Other tissues/organs could be getting less perfusion for whatever reason, CVA, blood clot etc.
 
Thanks, I trust you guys and gals. I just always remembered back in basic class that all CPs and CVAs get NRB's and figured why should that change just because im a paramedic now. Also thought the RN's didnt like the NRB's because I work in the getto and some health care professionals do as little as possible for some of there patients :sad: (not everyone but even one of em is too many, and its not only hospital staff).
 
rhan101277 said:
Yeah 95% means you are getting 95% to the finger. Other tissues/organs could be getting less perfusion for whatever reason, CVA, blood clot etc.
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95% is 95%. The problem with blocked perfusion is that while 95% of the RBCs passing the blockage is oxygenated, you're looking at a lot less RBCs passing the blockage. The difference between dissolved O2 between room air and a non-rebreather is the difference between extremely little and very little.
 
Street Doc said:
Thanks, I trust you guys and gals. I just always remembered back in basic class that all CPs and CVAs get NRB's and figured why should that change just because im a paramedic now. Also thought the RN's didnt like the NRB's because I work in the getto and some health care professionals do as little as possible for some of there patients :sad: (not everyone but even one of em is too many, and its not only hospital staff).
Click to expand...

It shouldn't matter where you work. Those that stereotype themselves by location do not do any of the medical professions a favor. We'll ask EMT(P)s why a NRBM was used when they bring a patient to our ED in case there were more symptoms that you saw initially that warranted it. If the only answer one can come up with is "its in the protocols", then oh well... We figure you just followed the recipe or your medical director doesn't trust you to think for yourself. If someone has kept up with their education or at least read a few journals lately, they can come back with an intelligent answer to even pursue a conversation, time permitting, about different theories of various therapies.

Right now there are not many right or wrong answers to most O2 therapy used emergently provided you know why you are doing it and for the amount you have chosen. There are few absolutes for O2 or no O2 initially and those can be debated depending on the protocol they are associated with and the guide may not always be SpO2. However, long term use of O2 at high concentrations is fairly well documented for its effects on the body but that may not be an issue for most EMS situations.

One must also recognize the limitations of the field and sometimes hospital staff forget you do not have immediate access to a lab analyzer for an A-a gradient, lactate level or SvO2. ED staff and the ICU staff may also have differing opinions as will the Cardiologist and the Pulmonologist or Critical Care physicians.
 
Sasha said:
Maybe he means nasal cannula? Either way the response was kind of odd.
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Maybe telling us he is from North Carolina?:wacko:

Vent thanks for some good responses and reference material.
 
what about blow by O2 via NRB... helps deliver that extra 1%, pumps out more O2 in LPM, and probably is more effective in reducing pain or n/v that the pt may be experiencing?
 
According to the book I have each patient no matter what gets NRB 15lpm.

Dustin
MFR, NREMT-B Student
 
Ahh, one of the many divergences from cook book and reality.
 
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