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Case Study with EKG's: Transient Tachycardia


fiznat

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By measuring to different points on the QRS you are proving my point.

There is a subtle irregularity there. Measure again to the same point of the QRS, and you will see it.

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By measuring to different points on the QRS you are proving my point.

There is a subtle irregularity there. Measure again to the same point of the QRS, and you will see it.

Huh? Maybe I'm not getting what you're trying to say here. I am measuring peak of S wave to peak of S wave. I had to stagger the lines so they would be readable. Some of the S waves are deeper than others, but the horizontal (as in, time) point-to-point regularity is pretty consistent.

Someone back me up here...

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Ill back you up here... AZCEP I think your taking the definition of irregular to new heights. When your looking for something to be irregular your looking for longer and shorter r-r, IF any of these are longer its by less than .04 And I ppersonal marched this strip out prior to giving it to Fiznat. and if you look at his underlying A-fib, you will see it is very irregular and it speeds up and gets regular as these wide complexes show up

(edited for spelling)

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I agree, it appears to be an impostor with a possible Dig tox effect. In the initial 12 lead, examine V[sub:5feb72a12d]6[/sub:5feb72a12d] and compare your axis deviation.

R/r 911

An impostor? What do you mean?

I see a left axis deviation and predominately negative complexes (the wide ones) in V6: both suggest a ventricular origin.

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Can i point out that the treatment of asa and ntg fixed the rhythm? Vtach is a sign of transient ischemia. Rapid afib with wide qrs is not. If for some reason you think that this is instead an afib, i suppose you could argue from just the 12 lead. To be honest, i dont see it. Fiznat's S-S anaylisis pretty much proves it. Equal distances between QRSs (in the abscence of ps) x 8 is pretty regular. I think "subtle" variations are either problems with the printer or your eyes. Again, pixels are more certain than your eye, as fiz pointed out.

BUT, even if you were absolutely convinced this was a rapid afib, NTG and ASA would not have done anything but made the patient worse. Alleviating the ischemia led to the cessation of runs of VTach. If you dont agree with the 12-lead, look at everything else going on, particularly the treatment, that lends quite the insight to the etiology of the rhythm. Im not saying there couldnt be ischemia of the atria leading to some conduction disorder that some how leads to wide complex atrial fibrillation, but i would be much more likely to believe Vtach. Earliest signs of cardiac ischemia is? PVCs, ventricular irritability, aka, VTach.

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Back to a more interesting physiological point: I dont think that NTG would have benefited the perfusion during cpr. Nitro (as opposed to other nitrates) primarily vasodilates the venous vasculature, and only minorly the coronary vasculature. Though, touche' to the epi, youre probably right. EVen then, epi doesnt work too well on the venous vasculature, mainly on arterial.

Anyway, Id still say tremendous foresight, and hey, it worked!

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Dig toxicity is a good thought, indeed. But what would happen if you gave this pt Cardizem...even a bolus of it? If it is truly A-Fib with abberancy, slowing the rate down would reveal the a-fib, if I remember correctly. Please, if I missed the mark even just a little bit, please let me know. I'd rather be sure and get it right rather than guessing.

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