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12 lead and oxygen


Paramagic14

  

23 members have voted

  1. 1. If pt is NOT SOB but c/o CP do you wait to put oxygen on the pt until the 12 lead is finished.

    • yes
      7
    • no
      12
    • varies
      4


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As stated prior the patient is not aware of any preexisting Heart Problems.

In fact the patient after being informed of an Abnormal ECG is in denial from his behavior alone.

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As stated prior the patient is not aware of any preexisting Heart Problems.

In fact the patient after being informed of an Abnormal ECG is in denial from his behavior alone.

We could give him a set of calipers and the strip ;)

I am nearly ready to trial a Nitro, but I am not convinced this is cardiac.

When did this discomfort start?

Does it get worse wioth exertion?

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Nope - O2 first. If it is ischemic chest pain, then as much O2 that we can get (both attached to hemoglobin and dissolved in the plasma) the better.

you dont know, and perhaps the pt has since changed his or her c/c. perhaps you first heard after pt is fallen out. what is downside to 02 vs upside? unless you are a diver medic!

always, always 02.

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- What is our tend, is the patient getting better physiologically or worse? VS, perfusion status, cap refill, distal temperature, SPO2, GCS etc?

- How long have we been on scene? Serial ECG?

- How long has he been having this pain, is it getting better/worse/same, what started it/makes it better/worse?

- What is the pain on a scale of 1-10?

- Is there any pedal edema or JVD?

If this guy is quite physiologically stable then I might try one spray of .4mg GTN SL but I want to be taking another strip as I'm doing it.

I am leaning towards that this might be something other than cardiac but I'm not convinced.

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To end the scenario expounded upon:

Yes Kiwi there was in the Patients History of trauma an assault and severe beating 3 months prior (and associated amnesia from grade 3 concussion)

One really had to dig with this patients PMHX, the pt was transported to rural hospital without treatment of any sort, no abnormal labs and patient referred to Cardiologist with EHCO,(45 to 55% EF) then MIBI negative findings (ruling out need for angiography) stress testing with a "Persantine Challenge" and Holter Monitoring (no runs of Ventricular Tachycardia)

It was hypothesized by very a knowledgeable Cardiologist that this LBBB most likely occurred during this Traumatic event, as the 12 lead ECGs were pulled from this patients past ICU records from an admission in 1994 to find NSR ONLY.

Point being always rule out History of Trauma when evaluating Chest Pain END MY Senario.

ps If the patient had "allowed" I would have used O2, before 12 Lead I will treat any possible ischemia before I obtain a 12 lead especially in this scenario where lead 3 is immediately available.

SPO2 @ 6000 ft asl are just starting on the drop Altitude vs PaO2 therefore an SP02 ~ acceptable at 91%

But yet to hear anyone pro or con with the use on Nitrous Oxide for the CP ? it is after all .50 FiO2.

cheers

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Something to keep in mind about LBBB. The GUSTO investigators (and subsequent studies of Sgarbossa's criteria) used elevated cardiac biomarkers as evidence of AMI. In other words, they combined STEMI and NSTEMI. That's why I think it's a mistake to suggest that Sgarbossa's criteria is an insenstive marker of acute STEMI if we accept that the ECG finding we call STEMI is a surrogate for an acute occlusive thrombus in an epicardial coronary artery.

The criterion that has caused the most controversy is discordant ST-elevation > 5 mm. Even according to the original algorithm, this is only a score of 2 (probability of AMI 50%). That's because with LBBB the ST-T wave abnormality is proportional to the depth of the S-wave. A QRS complex that is 50 mm deep in lead V2 can have 5 mm of ST-elevation and the ST-elevation is only 10% the depth of the QRS complex, which is fine. A better approach is to say ST-elevation > 0.25 the QRS complex indicates acute STEMI (which was proposed by Smith et al. from Hennepin County Medical Center).

The ECG provided shows a perfectly "normal" looking LBBB that does not satisfy any of Sgarbossa's criteria for AMI in the presence of LBBB. I would obtain serial ECGs and look for ST-T changes that suggest dynamic supply vs. demand characteristics. Absent that, there is no reason to transport this patient for primary PCI or give thrombolytic therapy.

Tom

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Something to keep in mind about LBBB. The GUSTO investigators (and subsequent studies of Sgarbossa's criteria) used elevated cardiac biomarkers as evidence of AMI. In other words, they combined STEMI and NSTEMI. That's why I think it's a mistake to suggest that Sgarbossa's criteria is an insenstive marker of acute STEMI if we accept that the ECG finding we call STEMI is a surrogate for an acute occlusive thrombus in an epicardial coronary artery.

The criterion that has caused the most controversy is discordant ST-elevation > 5 mm. Even according to the original algorithm, this is only a score of 2 (probability of AMI 50%). That's because with LBBB the ST-T wave abnormality is proportional to the depth of the S-wave. A QRS complex that is 50 mm deep in lead V2 can have 5 mm of ST-elevation and the ST-elevation is only 10% the depth of the QRS complex, which is fine. A better approach is to say ST-elevation > 0.25 the QRS complex indicates acute STEMI (which was proposed by Smith et al. from Hennepin County Medical Center).

The ECG provided shows a perfectly "normal" looking LBBB that does not satisfy any of Sgarbossa's criteria for AMI in the presence of LBBB. I would obtain serial ECGs and look for ST-T changes that suggest dynamic supply vs. demand characteristics. Absent that, there is no reason to transport this patient for primary PCI or give thrombolytic therapy.

Tom

How about transport for evaluation when CP is the initial complaint ?

Used elevated cardiac biomarkers as evidence of AMI.

All in favour say EH !

Great Post btw.

ps Are your certain your a Fire Man too ? :shiftyninja:

Edited by tniuqs
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