O2 in ACS

Though we disagree on points i like this kinda of conversation. Opens up new ideas and allows me to learn new things. As for the "miracle drug", that was a joke pointing to the last few years where everybody got it. I appreciate you bantering with me. If you have any other points to share feel free to PM me, id love to see some more of your opinions.
-Chris
 
shockinainteasy75 said:
C. When it comes to NTG, i said nothing about clot busting, it vasodialates, and even if the clot moves, we now have the chance of it moving to a more branched vessel, decreasing the area of injury/ischemia.
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Your primary benefit from NTG is probably on the demand-side, through preload reduction. The effect of increased collateral flow is probably minimal. There's little to no evidence supporting a benefit of NTG in MI, despite several theoretical mechanisms.

F. No, hyper oxyenation is not a "proven", nor "disproven" fact. Certain agencies support and others refute. That is completely up to the providers and the service area. This can go on and on involving the dispute of pulse oximeters, remembering that pulse ox's determine the % of hemoglobin saturated with something, may not always be oxygen. And even in the studies that support the ill effects of hyperoxygenation, they are quick to point out that the potential positive effects of supplemental oxygen at low concentrations out weigh the potential ill effects of this therapy.
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What is a proven fact though, is that the myocardium at rest extracts ~ 80% of transported oxygen. It's supply-dependent. When demand goes up, coronary blood flow has to go up.

Not only does increasing the pO2 with high FiO2 have a marginal effect on oxygen transport, high pO2 may cause further coronary constriction and worsen coronary perfusion.

While pulse oximeters may detect carboxyhemoglobin as oxyhemoglobin, giving a false high reading, methemoglobin tends towards a lower reading under most circumstances. Giving oxygen just because the patient may have been exposed to CO, without having other information supporting this, seems foolish.
 
A few snippets from one review article:

* "In patients with MI, hyperoxia reduces cardiac output
and stroke volume and increases the mean arterial pressure and
systemic vascular resistance.25–31 If the baseline arterial oxygen
saturations are >90%, high concentration oxygen does not
increase oxygen transport, as the reductions in cardiac output
are in excess of the increase in oxygen content.26 The adverse
haemodynamic responses are greatest in patients with MI not
complicated by heart failure or cardiogenic shock."

* "The magnitude of the reduction in coronary blood flow with
hyperoxia may be substantial in patients with coronary artery
disease. This has been illustrated by two studies19 20 which used
the measurement of intracoronary Doppler flow in subjects
with stable coronary artery disease. Breathing 100% oxygen by
face mask for 10–15 min decreased coronary blood flow by 20–
30% in association with a 23–40% increase in coronary
resistance"

* "These effects are
likely to be secondary to an effect on coronary endothelial
function, with the accelerated oxidative degradation of coronary
endothelium-derived nitric oxide by reactive oxygen species"

* "Another potential mechanism is that hyperoxia resulting
from high concentration oxygen therapy may exacerbate
reperfusion injury to the heart owing to the increased
production of oxygen-free radicals"


Wijesinghe M, Perrin K, Ranchord A, Simmonds M, Weatherall M, Beasley R. Routine use of oxygen in the treatment of myocardial infarction: a systematic review. Heart (2009) 95:198-202 doi.10.1136/hrt.2008.148742
 
systemet said:
* "The magnitude of the reduction in coronary blood flow with
hyperoxia may be substantial in patients with coronary artery
disease. This has been illustrated by two studies19 20 which used
the measurement of intracoronary Doppler flow in subjects
with stable coronary artery disease. Breathing 100% oxygen by
face mask for 10–15 min decreased coronary blood flow by 20–
30% in association with a 23–40% increase in coronary
resistance"
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Intravascular ultrasound (IVUS) is so much fun, however not so much for the patient. Though I am not sure how they determined flow. It measures radius/diameter and you can visualize the plaque. I guess from that you can equate flow...
 
Linuss said:
If you're stumped, you can stare intently at the screen as if trying to read something. Need more time? Print off a 12 and stare even more intently at that, then say something that sounds like a rhythm.
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laughing from this brought me to tears
 
Linuss said:
If you're stumped, you can stare intently at the screen as if trying to read something. Need more time? Print off a 12 and stare even more intently at that, then say something that sounds like a rhythm.
Click to expand...

In my EMT-I class, we can ask for 12-leads in scenarios, however if we then ask what we see, the instructor replies, "looks like a 12-lead".
 
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