Oxygen rate for Chest Pain?

[ccmedoc]

was actually thinking about that at work the other day. How long the vasoconstriction takes. This is extremely important, because the patient could be missing out on a good deal of oxygen. I think saying it's largely case by case is sidestepping the issue, though. What factors does the onset of vasoconstrction depend on?

I don't believe it is side-stepping at all. Patients with compromised left ventricular function and high dependance on Hypercapnia have been shown to have a fall in cardiac output and increased PVR in less than 20 min with as little 40% FiO2, this is NC territory. Different disease etiologies could or could not further complicate this. Sounds like a long time, but once the cascade has begun, it is very difficult to stop. Factors such as tissue hypoxia and acidosis tend to complicate the situation due to a number of intrinsic factors. The body tries to protect tissue from hyperoxia due to oxygen being a natural free radical that reacts to form superoxides that, in turn may attack many double bonds in many organ systems. The chemistry can be complicated, but the research and facts about high oxygen concentration and free radicals are out there. If a lower FiO2 would be adequate in the short term, and prevent or minimize long term disability or death, wouldn't it be prudent to start there. As said earlier, if there is no respiratory distress, then why would you think you need high flow??

Effects of supplemental oxygen administration on coronary blood flow in patients undergoing cardiac catheterization

Patrick H. McNulty,1 Nicholas King,1 Sofia Scott,1 Gretchen Hartman,1 Jennifer McCann,1 Mark Kozak,1 Charles E. Chambers,1 Laurence M. Demers,2 and Lawrence I. Sinoway1

Departments of 1Medicine and 2Pathology, Pennsylvania State College of Medicine, Milton S. Hershey Medical Center, Hershey, Pennsylvania

This study showed a significant decrease in cardiac perfusion(coronary blood flow) up to 30% after 5 minutes on 100% oxygen.

[AnthonyM83]

Is hypercapnia another term for relying on their hypoxic drive, such as those with COPD?

If a lower FiO2 would be adequate in the short term, and prevent or minimize long term disability or death, wouldn't it be prudent to start there. As said earlier, if there is no respiratory distress, then why would you think you need high flow

Well, the concern is that they're HEART isn't receiving enough oxygen at certain spots, so they might not be classically short of breath, but certain areas of their heart could be ischemic...and they are presenting...it's the chest pain.

I'm not saying they thus need high flow, b/c we're looking at articles about how they might not, but in response to your question, that's why I would think they might need high flow. I think it's a logical reason.

[ccmedoc]

Well, the concern is that they're HEART isn't receiving enough oxygen at certain spots, so they might not be classically short of breath, but certain areas of their heart could be ischemic...and they are presenting...it's the chest pain.

...in response to your question, that's why I would think they might need high flow. I think it's a logical reason.

Anthony, if their heart is ischemic, then why would we want to administer a treatment that is being proven to increase cardiac ischemia. We seem to be talking in circles. Chest pain, as a symptom, does not indicate the need for high flow oxygen. Without respiratory distress or very low oxygen sats, less than 40% Fio2 should be adequate supplemental oxygen.

Hypercapnia, simply put, is elevated levels of CO2 in the system. COPD sufferers have chronically elevated carbon dioxide levels and rely on these levels to regulate their respiratory rate, depth, etc. "Knocking out the respiratory drive" is not the worry here, as this typically takes a long time..many hours. The concern is the vasoconstriction and subsequent organ damage and failure that ensues (ie. heart, kidney, brain). I thought this was explained pretty clearly by a few people earlier. Not to be nasty, but maybe it is getting tough to sort through the BS that has " always been done this way" and the information that should be applied to practice.

(edited for continuity)

[AnthonyM83]

I get you. My previous post was not an actual argument. It was explaining why people in this thread might think CP patients need high flow. What their logical line of thinking is. Sorry if I didn't make that clear enough.

As a sidenote:

In the article you posted, it says that hypoxia didn't affect the availability of oxygen for myocardial metabolism until around 50%...

If this were true, wouldn't one expect that we shouldn't worry about MI's unless the patient's O2 sat were in the 50s...? This would mean pretty much all concious MI patients even showing SOB should have no heart damage because heart tissue has enough O2...

I might just not know enough about what happens in MIs, but I thought the main concern was ischemia which would lead to tissue death.

[AnthonyM83]

Another thought is, are there any OTHER reasons for substernal CP that might require O2 that wouldn't present with other symptoms?

[ccmedoc]

As a sidenote:

In the article you posted, it says that hypoxia didn't affect the availability of oxygen for myocardial metabolism until around 50%...

Sorry if I appeared snippy :wink: . The part you pick out indicated that normal, or individuals with healthy hearts didn't' have a problem with oxygen availability to coronary circulation with sats as low as 50% at times. It then goes to say that patients with cardiac problems or disease processes that affect cardiac function, showed vulnerability upwards of 85%. Meaning that a compromised individual may show increased cardiac ischemia with a sat of 85%. Already ischemic.This is one reason for the 90% rule in the assessment portion and determining administration. There are many physiologic factors involved in this discussion, and could go on for a VERY long time.. No simple answer. If I ramble I apologize

[AnthonyM83]

Gotcha.

And no worries on rambling. I've quite enjoyed the discussion in this thread.

[Richard B the EMT]

Just on observation of what I remember, and not the textbook, if a patient is having chest pain secondary to pump failure, does not that mean that the blood flow is going to be diminished?

Oxygen, @ 10 LPM via NRB, would assist in the delivery of a bit more oxygenated blood with the diminished blood flow, would it not?

Now, when the rules and regulations under which I operate allow me to cut back on the O2 volume, then I will deliver O2 at a lesser rate. At this time, however, I will continue at high flow, as that is what the NYS DoH wants me to do.

[ccmedoc]

Just on observation of what I remember, and not the textbook, if a patient is having chest pain secondary to pump failure, does not that mean that the blood flow is going to be diminished?

Oxygen, @ 10 LPM via NRB, would assist in the delivery of a bit more oxygenated blood with the diminished blood flow, would it not?

Now, when the rules and regulations under which I operate allow me to cut back on the O2 volume, then I will deliver OE2 at a lesser rate. At this time, however, I will continue at high flow, as that is what the NYS DoH wants me to do.

I cannot respond to this :shock: :roll: ](*,)

[AnthonyM83]

Just on observation of what I remember, and not the textbook, if a patient is having chest pain secondary to pump failure, does not that mean that the blood flow is going to be diminished?

Oxygen, @ 10 LPM via NRB, would assist in the delivery of a bit more oxygenated blood with the diminished blood flow, would it not?

Now, when the rules and regulations under which I operate allow me to cut back on the O2 volume, then I will deliver O2 at a lesser rate. At this time, however, I will continue at high flow, as that is what the NYS DoH wants me to do.

Richard, I think you missed the whole thread...that's what we were discussing.