New strip

Looks like Atrial Fib with RVR. Also an Anteroseptal infarct along with the reciprocal changes...
 
anyone else thinking right bundle branch block?
 
Looks like AFib with anteroseptal MI but I would also do a right sided 12lead because of the ST depression seen in inferior leads.
 
When I first looked and saw all the crap between the QRS complexes I thought A-Fib, but that's pretty regular all the way across so I don't think it's A-fib. Still waiting for something definitive.
 
TomB said:
I think this is either ST with acute anterior STEMI or 2:1 atrial flutter masquerading as acute STEMI.

This particular mimic was identified as a problem in Southern California's regional STEMI system.

What was the computerized interpretation?

Sorry if this turns out to be a double post. I'm new to the forum. It let me post to another thread, but my reply for this one didn't show up for some reason.
Click to expand...

Strip says "Extreme Tachycardia with wide complex, no further rhythm analysis attempted".

Big help there... :rolleyes:

Also, pt was an 82 year old male. I'll try to get some more information about the call the next time I go home for duty.
 
Negative on the A-fib - it marches out perfectly.... Sinus with anterioseptal infarct with recripocla changes.
 
Oh yeah, negative on the RBBB. Cannot accuratly asses V1 due to marked ST elevation. I don't interpret that as RSR but rather significant elevation due to reciprocal changes. Could do a 4-R sure, do a posterior while we are at it, 16-lead for extra points :)
 
from what ive seen in the rhythm, I'm gonna call it a ST w/ 2nd degree av block type 1. Because what I'm seeing is that the PR interval seems to be getting wider and you loose drop a P wave (well at least you cant see it probably still there just hidden).

i might be wrong though, can you be ST w/ 2dav block. because looking in my ekg book its only giving the example for bradycardia.
 
Sorry - yes, it is a sinus rhythm. P waves with corresponding QRS at regular pattern. The way to find this out for sure on the real strip is to use another piece of paper and starting at the edge mark off the tip of the R-wave with a pen for 2 or 3 complexes, then slide the piece of paper down the strip. If the next series of complexes line up to the lines, its sinus. If its off, then you've got something else.
 
FF894 said:
Oh yeah, negative on the RBBB. Cannot accuratly asses V1 due to marked ST elevation. I don't interpret that as RSR but rather significant elevation due to reciprocal changes. Could do a 4-R sure, do a posterior while we are at it, 16-lead for extra points :)
Click to expand...



My point is that the RBBB could be showing as ST elevation...depends on what you define as the J point vs the "bunny ears" of each ventricle depolarizing. Just another thought...

My gut tells me big anterior wall MI with inferior reciprocal changes
 
remote_medic said:
My point is that the RBBB could be showing as ST elevation...depends on what you define as the J point vs the "bunny ears" of each ventricle depolarizing. Just another thought...

My gut tells me big anterior wall MI with inferior reciprocal changes
Click to expand...


...Agreed...
 
For those of you who think this is a sinus mechanism, what is the heart rate? :unsure: Is this a regular rhythm? Is it narrow or wide? Are what you think are st elevation seen in contiguous leads, or are they global?
 
boingo said:
For those of you who think this is a sinus mechanism, what is the heart rate? :unsure: Is this a regular rhythm? Is it narrow or wide? Are what you think are st elevation seen in contiguous leads, or are they global?
Click to expand...

160ish
Regular
Narrow
Contiguous in I & aVL, v1-v6

?? no ??
 
This is kind of off topic. What if a fascicle of heart muscle is acting up from a small blockage. The other part of the heart is getting oxygen so shouldn't it just aggravate the portion without oxygen. Maybe it could get as bad as a whole bundle of muscle, but the rest of the heart should beat. Unless you have a blockage near the top of either one of the coronary arteries, shouldn't the rest of the heart muscle work?

I mean I understand if its halfway down, then maybe it would effect the lower inferior portion which would drastically effect pumping ability. Then again I could see that just a simple small portion of cells being aggravated could cause the electrical signal to hose up since those cells aren't going to be working properly.
 
don't think of coronary blood supply as a top/down concept... (I know that is the way textbooks display it)
 
Negative on the A-fib - it marches out perfectly.... Sinus with anterioseptal infarct with recripocla changes.
Click to expand...

Sometimes when you have A. Fib with RVR it can look regular but only because its so fast.
 
rhan101277 said:
This is kind of off topic. What if a fascicle of heart muscle is acting up from a small blockage. The other part of the heart is getting oxygen so shouldn't it just aggravate the portion without oxygen. Maybe it could get as bad as a whole bundle of muscle, but the rest of the heart should beat. Unless you have a blockage near the top of either one of the coronary arteries, shouldn't the rest of the heart muscle work?

I mean I understand if its halfway down, then maybe it would effect the lower inferior portion which would drastically effect pumping ability. Then again I could see that just a simple small portion of cells being aggravated could cause the electrical signal to hose up since those cells aren't going to be working properly.
Click to expand...

I wouldn't use the word fascicle, since it's easily confused with the branches of the His-Purkinje system (unless that's what you were talking about).

Ischemia frequently causes wall motion abnormalities (hypokinesis, akinesis, dyskinesis) that can effect pumping ability.

An occlusion 'higher up' in a coronary artery (proximal occlusion) threatens more of the myocardium, since all the distal branches are affected. So a proximal occlusion of the RCA causes injury to the inferior wall of the left ventricle the same way an occlusion half way down would. It also causes injury to the right atria and right ventricle, because the occlusion is 'higher up'.

Ischemia generally extends from the endocardium to the epicardim (inside out) as the ischemic zone extends over time. By the time it reaches the surface, it's considered a 'transmural' infarct. This can weaken the ventricular wall to the point where it ruptures.

By the 3-6 hour mark, serious and irreversible damage is done to the heart (assuming the absence of robust collateral circulation).

Time is muscle.
 
You must log in or register to reply here.
Back
Top