# New strip



## emtbill (Dec 3, 2008)

Hi all,

Long time reader, first time poster.

I had a lot of downtime during my last shift and started looking through the monitor's patient archives and found this strip:

Strip

12 lead

I don't have any patient information so don't ask.

What do you think?


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## FF894 (Dec 3, 2008)

Get to a CCL - hurry.


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## Sasha (Dec 3, 2008)

I'm not good at reading strips or 12leads, but I'm going to venture and guess the first one is SR with a lot of noise.


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## Ridryder911 (Dec 3, 2008)

FF894 said:


> Get to a CCL - hurry.



More like.. "_... Who is your life insurance agent?...._


R/r 911


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## Sasha (Dec 3, 2008)

Like I said, bad at it!


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## marineman (Dec 4, 2008)

Me too sasha, we just started getting into 3 leads last week and haven't touched 12 leads yet. Anyone that's better at this care to tell me what the rhythm is on the 3 lead. 

the only ones we've really looked at so far are different examples in the classroom so I'm having trouble picking out waves vs noise


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## Sasha (Dec 4, 2008)

marineman said:


> Me too sasha, we just started getting into 3 leads last week and haven't touched 12 leads yet. Anyone that's better at this care to tell me what the rhythm is on the 3 lead.
> 
> the only ones we've really looked at so far are different examples in the classroom so I'm having trouble picking out waves vs noise



Sad part is, I've been over 3 and 12 leads and STILL suck!


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## kguy18 (Dec 4, 2008)

Ya not good, tomb stones on the 12 lead....


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## Ridryder911 (Dec 4, 2008)

This is one of those strips that points the need of 12 lead assessment. Yes, one can tell there is definitely potential problems in three lead but accurate interpertation cannot be made off the simple monitoring lead. 

Hence, the reason and need of twelve lead to be able to define the area of problems of ischemia and infarct. 

R/r 911


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## mikie (Dec 4, 2008)

...so what is the rhythm?


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## BLSBoy (Dec 4, 2008)

mikie said:


> ...so what is the rhythm?



Facetious answer;
Almost dead.

Real answer;
Sinus with ST Depression.


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## TomB (Dec 4, 2008)

emtbill said:


> Hi all,
> 
> Long time reader, first time poster.
> 
> ...



Very cool ECG.

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.

Thanks for sharing!

Tom

P.S. What was the computerized interpretation?


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## FF894 (Dec 4, 2008)

BLSBoy said:


> Facetious answer;
> Almost dead.
> 
> Real answer;
> Sinus with ST Depression.



I was thinking Anterior-septal STE with reciprocal changes, no?


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## BLSBoy (Dec 4, 2008)

FF894 said:


> I was thinking Anterior-septal STE with reciprocal changes, no?



I was going for just the strip interp. Looking further at the 12 lead......I see ST Depression OR Elevation in........all leads.


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## FF894 (Dec 4, 2008)

Bascially, you've heard of "the big one" ?  This bad boy is having it....


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## BLSBoy (Dec 4, 2008)

FF894 said:


> Bascially, you've heard of "the big one" ?  This bad boy is having it....



More or less. 

I would love to hear the outcome.


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## tydek07 (Dec 4, 2008)

*Oh my!*

Oh my... wow... that is a OH SH*T rythym... poor guy never had a chance:glare:


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## FF894 (Dec 4, 2008)

Going by 12-Lead I see wide-spread elevation in anterior and septal leads with depression in inferior and lateral leads which would make sense to see reciprocal changes.  He is having an anterior infarct?  I could be wrong though, I'm fairly new at this...


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## TomB (Dec 4, 2008)

emtbill said:


> Hi all,
> 
> Long time reader, first time poster.
> 
> ...




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.


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## boingo (Dec 4, 2008)

BLSBoy said:


> Facetious answer;
> Almost dead.
> 
> Real answer;
> Sinus with ST Depression.



Negative Ghostrider....try again...


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## firemedic31075 (Dec 4, 2008)

Looks like  Atrial Fib with RVR. Also an Anteroseptal infarct along with the reciprocal changes...


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## remote_medic (Dec 4, 2008)

anyone else thinking right bundle branch block?


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## rmellish (Dec 4, 2008)

remote_medic said:


> anyone else thinking right bundle branch block?



I was thinking that AVf and V1 looked something like that....I can't say I have any training in 12 leads though.


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## mdkemt (Dec 4, 2008)

Looks like AFib with anteroseptal MI but I would also do a right sided 12lead because of the ST depression seen in inferior leads.


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## marineman (Dec 5, 2008)

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.


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## emtbill (Dec 5, 2008)

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.
> 
> ...



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

Big help there... 

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.


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## FF894 (Dec 5, 2008)

Negative on the A-fib - it marches out perfectly....  Sinus with anterioseptal infarct with recripocla changes.


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## marineman (Dec 5, 2008)

FF894 said:


> Negative on the A-fib - it marches out perfectly....  Sinus with anterioseptal infarct with recripocla changes.



so if I take out words that I don't understand it's sinus?


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## FF894 (Dec 5, 2008)

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


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## milhouse (Dec 5, 2008)

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.


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## FF894 (Dec 5, 2008)

marineman said:


> so if I take out words that I don't understand it's sinus?



That wasn't directly to you, a few people had said it....


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## FF894 (Dec 5, 2008)

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.


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## remote_medic (Dec 5, 2008)

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





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


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## FF894 (Dec 5, 2008)

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




...Agreed...


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## boingo (Dec 5, 2008)

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?


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## FF894 (Dec 5, 2008)

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?



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

?? no ??


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## rhan101277 (Dec 5, 2008)

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.


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## remote_medic (Dec 5, 2008)

don't think of coronary blood supply as a top/down concept... (I know that is the way textbooks display it)


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## firemedic31075 (Dec 5, 2008)

> Negative on the A-fib - it marches out perfectly.... Sinus with anterioseptal infarct with recripocla changes.



Sometimes when you have A. Fib with RVR it can look regular but only because its so fast.


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## TomB (Dec 5, 2008)

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.



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.


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## rhan101277 (Dec 5, 2008)

TomB said:


> 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.
> 
> ...



Thanks for that great description.  I thought individual muscle bundles were called fascicles, or is that just for skeletal muscle and not cardiac muscle.


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## TomB (Dec 6, 2008)

rhan101277 said:


> Thanks for that great description.  I thought individual muscle bundles were called fascicles, or is that just for skeletal muscle and not cardiac muscle.



They may call bundles of myocytes 'fascicles' but to avoid confusion when discussing ischemia, I wouldn't use the word 'fascicle' unless you're referring to one of the three main branches of the His-Purkinje system (right bundle branch, left anterior fascicle of the left bundle branch, left posterior fascicle of the left bundle branch).


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## wegandy (Dec 6, 2008)

*Looking for zebras*

This conversation reminds me of the old saying, "when you hear hoofbeats, don't look for zebras."  It's interesting and valid to break down the strip and analyze it, but the first thing that jumps out is screaming ST elevation in I and  aVL, and screaming ST depression in II, III, and aVF, so one should think STEMI until proved otherwise.

I have recently had a spate of cases where paramedics sought to rationalize things they saw on monitors as being something else than what they were, all to the patients' extreme disadvantage (read permanent negative patient outcome).  

I hope that in real life we all would have been treating this like an MI until proved otherwise, not attempting to rationalize it as being Atrial Flutter with aberrancy, et cetera.

It's always great to be able to say, "false alarm," but it ain't so great to have to say, "OOPS." when the patient's dead.

Gene
"Champagne for my real friends and real pain for my sham friends." --Tom Waits.


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## TomB (Dec 7, 2008)

wegandy said:


> This conversation reminds me of the old saying, "when you hear hoofbeats, don't look for zebras."  It's interesting and valid to break down the strip and analyze it, but the first thing that jumps out is screaming ST elevation in I and  aVL, and screaming ST depression in II, III, and aVF, so one should think STEMI until proved otherwise.
> 
> I have recently had a spate of cases where paramedics sought to rationalize things they saw on monitors as being something else than what they were, all to the patients' extreme disadvantage (read permanent negative patient outcome).
> 
> ...




At some point, a decision has to be made as to whether or not this patient will receive reperfusion therapy. 

Obviously, the ECG needs to be correlated to the history and clinical presentation.

It's usually the case that the most likely scenario is the correct. However, that kind of thinking could also lead you to give a calcium channel blocker to a patient with WPW.

The reason atrial flutter can be a convincing STE-mimic is because flutter waves, just like QRS complexes, have a vector and amplitude. 

In this case, we can estimate the frontal plane axis of the flutter waves at about -30 degrees (isoelectric in lead II, upright in lead aVL). So if the flutter waves are superimposed on the ST segments, we have ST segment elevation in leads I and aVL, and ST segment depression in leads III and aVF, just like reciprocal changes.

Sometimes, it's a zebra.


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## boingo (Dec 7, 2008)

Not to mention the heart rate is about 200, so MONA doesn't cut it.  Zebra's make hoof beats too!


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## Ridryder911 (Dec 7, 2008)

200?.. I only seen about 80 or so.. I did see a lot of artifact in the initial three lead or what we would call B.S. in the baseline. Twelve lead there is only one P wave per QRS with elevation of the T wave. 

R/r 911


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## boingo (Dec 7, 2008)

I don't know what 12ld you are looking at, but the one posted on the first page is a rate of 200.

The first strip has 19 beats in a 6 second stretch = 190....


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## KEVD18 (Dec 7, 2008)

forgive me if its fallen out of favor, but im still using dubins reccomended method of counting big boxes between r waves. 300, 150, 100, 75, 60, 50 etc.







so id say thats closer to 200 than 150. 190 sounds good to me.


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## wegandy (Dec 7, 2008)

*Zebras*

Sure some of them are zebras.  What I meant to get across, and I probably didn't do it very well, is not to "rule out" a problem based on the "Oh, it's only a zebra" theory.  I'm being influenced by the recently reported case where some medics decided somebody wasn't having an MI and told him to take Pepto-Bismol.  All I meant to say was that when it looks like a STEMI, then it is a STEMI until proved otherwise, and don't make the mistake of failure to take action based on rationalization.  At least take the steps to start the wheels in motion to treat the worst case scenario, then there's time to sort the horses from the zebras.  That's all I meant to say.

Gene


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## TomB (Dec 7, 2008)

Well, in _that_ case.... totally agree!


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## MasterIntubator (Dec 9, 2008)

Looks backwards to me.


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## wlamoreemtb (Mar 3, 2009)

going out on a limb here ...... could this be vtach


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## el Murpharino (Mar 3, 2009)

wlamoreemtb said:


> going out on a limb here ...... could this be vtach



It's not V-tach...


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## emtbill (Mar 3, 2009)

wlamoreemtb said:


> going out on a limb here ...... could this be vtach



It's not VT. The QRS complexes are only about .08 seconds, there's AV association and there's no right axis deviation. There is concordance in the precordial leads though. If you look at the limb leads there's ST elevation in lead I and AVL with reciprocal depression in AVF, II and III, suggesting a lateral infarct. There's also elevation in V1, V2, V3 and V4, suggesting an anteroseptal infarct. My interpretation is sinus tachycardia with possible a first degree AVB with an anteroseptal STEMI.


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## Melbourne MICA (Mar 5, 2009)

*Take a punt*

The rhythm strip is crap. There is so much artifact and the isoelectric line is wandering so much it's hard to tell anything. The 12lead isn't much better.
Still here goes.

*What is the rate? Around 150 - 160/min
*Is the rhythm regular? Yes
*Is there a P wave present - yes (retrograde) 
*Is it normal morphology? No small and peaked. 
*Is the PR interval normal (present)? no  - retrograde p's seem evident in leads III and AVF, V4, V5 possibly V3.
*What is the QRS interval and is it narrow or widened -narrow complex about 1 and bit small squares in limb leads  - widened in leads V1-4
*Are there q waves present not in V leads - hard to tell in limb leads
*Is there ST depression or elevation? Yes in leads III, AVF,V5 and V6
*Other features? RsR present in leads V1 V3 V4

Interpretation? Narrow complex tachycardia with widened QRS with RsR in V leads and some ST depression.

Possibly junctional tachy with BBB and some ischaemia.

What do you think?


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## Melbourne MICA (Mar 5, 2009)

*Determining HR*

http://medresidents.stanford.edu/TeachingMaterials/EKG Basics/EKG Basics - Long.ppt#284,24,What is the heart rate?

http://sprojects.mmi.mcgill.ca/cardiophysio/ekgheartraterhythm.htm

http://gk12.poly.edu/Information/RA...ermine our Heart Rate.ppt#274,2,Instructional Objectives:

http://lanoswww.epfl.ch/personal/schimmin/uni/ecglex/ekg.htm

http://advan.physiology.org/cgi/content/full/29/2/57


I guess before we all figure out this rhythm we need to have a consensus on the HR.

MM


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## Melbourne MICA (Mar 5, 2009)

*Tttttttt*

OOps left out the T wave analysis. Rate is actually around 170/min. At 150/min it would have been worth looking for evidence of flutter. I don't believe this is an infarct though there is ischaemia as you might expect assuming this ECG was from an elderly pt with a tachy arrhythmia of 170/min.

MM


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## TomB (Mar 5, 2009)

emtbill said:


> It's not VT. The QRS complexes are only about .08 seconds, there's AV association and there's no right axis deviation. There is concordance in the precordial leads though. If you look at the limb leads there's ST elevation in lead I and AVL with reciprocal depression in AVF, II and III, suggesting a lateral infarct. There's also elevation in V1, V2, V3 and V4, suggesting an anteroseptal infarct. My interpretation is sinus tachycardia with possible a first degree AVB with an anteroseptal STEMI.



I agree it looks like a narrow QRS, but the other criteria you list do not suggest a non-VT diagnosis. AV dissociation is only present about half the time with VT and is often difficult to appreciate. VT can show a normal axis, right axis deviation, or left axis deviation. Negative concordance favors VT, but an absence of concordance does not rule it out. Just clarifying because wide and fast is VT until proven otherwise! That's one of the most important rules of ECG interpretation.


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## abckidsmom (Mar 5, 2009)

Melbourne MICA said:


> The rhythm strip is crap. There is so much artifact and the isoelectric line is wandering so much it's hard to tell anything. The 12lead isn't much better.
> Still here goes.
> 
> *What is the rate? Around 150 - 160/min
> ...



I was waiting for someone to say that the strip was crap!  This is one I'd have tried to get a cleaner copy of, then gone with the narrow complex tachycardia with BBB and some ischemia.  Might be an elementary label, but it works.  I'm impressed by the ST elevation and depression, but I'm hesitant to call a STEMI alert on it because there's so much other crap on the baseline.  If the stinkin' monitor can't even display a sortof flat 3-lead, it puts the 12 lead into question for me.

I hate a Phillips.  I will not work for an agency that uses them.  Very nice doorstops, they are.  Pretty little wide-screen monitors.


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## Melbourne MICA (Mar 6, 2009)

*Come on you blouses*

Come on you big girls blouses - take a stab adn try and work through this one - its a crap strip but a good one too because it has so many features. I'm not much at my ECG's - I tend to be a pattern reader but I'd like to get better.

To dig my self in a bit more here I'll add this.

There is no concordance in the Vleads. I am aware this idea is no longer recognised as a reliable guide to assist VT diagnosis but there isn't any. V1-V3are different to V4-V6. Whilst the precordials are wide and rapid the limb leads are not unifromly. There is also the rSR pattern in V1-V4 very suggestive of BBB rather than infarct which should have a clean tombstone once established with this much amplitude. The rhythm is clearly fast so its a tachy arrhythmia but thats a bit woosy. Is it SVT with aberancy of VT?

My orginal interpretation was SVT (possibly junctional -narrow - retrograde P's) with BBB (aberency). I've been reading up on criteia for RBBB, LBBB etc and this rhythm certainly has some that fit RBBB.

So come on all you chickens - roll out the detail -don't just say "go to the cath lab" or drive fast or VT. We ECG drop-outs need some help so fire away with the gory details.

MM


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## benkfd (Mar 6, 2009)

Am I seeing R' in V1 -V4?


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## emtbill (Mar 6, 2009)

TomB said:


> I agree it looks like a narrow QRS, but the other criteria you list do not suggest a non-VT diagnosis. AV dissociation is only present about half the time with VT and is often difficult to appreciate. VT can show a normal axis, right axis deviation, or left axis deviation. Negative concordance favors VT, but an absence of concordance does not rule it out. Just clarifying because wide and fast is VT until proven otherwise! That's one of the most important rules of ECG interpretation.



Thanks for the clarification, but I thought VT almost always presents with an extreme right axis deviation? Anyway, good to know. Of course I would always treat wide and fast like VT. I'm very new to advanced 12 lead interpretation like I just tried to do.

What if it was aberrant SVT though and you gave lidocaine? Won't that make the situation worse if you gave lidocaine to a supraventricular dysrhythmia? Personally I would give amiodarone as the AHA recommends since it is also effective on supraventricular rhythms.

What if one incorrectly interprets a rhythm as supraventricular with aberrant conduction and decides to give adenosine when it is in fact of ventricular origin? On first thought I wouldn't think adenosine would make VT any worse since it works on the AV node and in VT the pacemaker is in the ventricles, but evidently I am wrong since it is always a major point to treat wide and fast like VT until proven otherwise.

What about giving adenosine to peds with wide complex tachycardia? In the PALS algorithm they advocate giving a trial of adenosine to apparent VT prior to cardioverion. I suppose aberrantly conducted SVT's are more common in peds than adults?


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## Melbourne MICA (Mar 6, 2009)

emtbill said:


> What if it was aberrant SVT though and you gave lidocaine? Won't that make the situation worse if you gave lidocaine to a supraventricular dysrhythmia? Personally I would give amiodarone as the AHA recommends since it is also effective on supraventricular rhythms.



Ami is the drug of choice now for VT and Adenosine/Ami for SVT. For us here the alternative is Verapamil for SVT and Ami for VT. A bit nasty to give a VT Verapamil - a calcium channel blocker - kills off the pacemaker and asystole results. OOps!!! Lido (we use to use it) might drop BP but won't stop conduction through to the ventricles. Lesser of two potential evils.

Mechanical action is generated via the myocardium/ventricles via calcium -the VT pacemkaer site is the only thing producing output so lose your pacemaker and you get.... nothing.

Effects and side effects - the great balancing act.

MM


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## TomB (Mar 7, 2009)

emtbill said:


> Thanks for the clarification, but I thought VT almost always presents with an extreme right axis deviation? Anyway, good to know. Of course I would always treat wide and fast like VT. I'm very new to advanced 12 lead interpretation like I just tried to do.



VT usually has an other-than-extreme axis. The best way to get a feel of this is to start collecting 12 lead ECGs of arrhythmias, do a Google search, or check out the VT page at the ECGpedia.



emtbill said:


> What if it was aberrant SVT though and you gave lidocaine? Won't that make the situation worse if you gave lidocaine to a supraventricular dysrhythmia? Personally I would give amiodarone as the AHA recommends since it is also effective on supraventricular rhythms.



Lidocaine shouldn't hurt SVT and may even help. On the other hand, as someone else already mentioned, you can kill a patient by giving a CCB to VT. Think twice before giving antiarrhythmics to irregular or polymorphic wide complex tachycardias. Amiodarone could make Torsades or AF with WPW worse.



emtbill said:


> What if one incorrectly interprets a rhythm as supraventricular with aberrant conduction and decides to give adenosine when it is in fact of ventricular origin? On first thought I wouldn't think adenosine would make VT any worse since it works on the AV node and in VT the pacemaker is in the ventricles, but evidently I am wrong since it is always a major point to treat wide and fast like VT until proven otherwise.



Adenosine probably won't hurt a stable regular wide complex tachycardia with a rate < 250, but it's not indicated. It used to be part of the algorithm for wide complex tachycardia of unknown origin, but not anymore.



emtbill said:


> What about giving adenosine to peds with wide complex tachycardia? In the PALS algorithm they advocate giving a trial of adenosine to apparent VT prior to cardioverion. I suppose aberrantly conducted SVT's are more common in peds than adults?



Yes, I noticed that last time I took PALS.


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## eric2068 (Mar 8, 2009)

Two words: Drive Faster. 
It is very crowded with the patient, the tech, and the Grim Reaper.


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## Melbourne MICA (Mar 9, 2009)

*What rhythm is that - conga or quickstep?*

Venty where are you on this one? Theres been a few stabs but a few to many chickens as well. Come on troops we may have to treat a pt like this one day - somebody obviously had to before. For the guys infering this is a nasty looking rhythm please explain in a bit of detail. Some of us EKG fumblers need some pointers. 

(all in good fun troops) I'm sure there are light bulb jokes about cardiologists and their respective multiple interpretations of rhythms like this one. 

MM


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## BLSBoy (Mar 9, 2009)

Melbourne MICA said:


> Venty where are you on this one? Theres been a few stabs but a few to many chickens as well. Come on troops we may have to treat a pt like this one day - somebody obviously had to before. For the guys infering this is a nasty looking rhythm please explain in a bit of detail. Some of us EKG fumblers need some pointers.



Go back to your basics. 
Activate Cath Lab, 2 large bore IVs, monitor vitals, ASA, nitro, Lopressor (if applicable) Morphine or Fentanyl, O2 via most appropiate device, and a healthy diesel bolus. 

Also, if you draw labs, draw em up.


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## Melbourne MICA (Mar 10, 2009)

*The rhythm, the rhythm*



BLSBoy said:


> Go back to your basics.
> Activate Cath Lab, 2 large bore IVs, monitor vitals, ASA, nitro, Lopressor (if applicable) Morphine or Fentanyl, O2 via most appropiate device, and a healthy diesel bolus.
> 
> Also, if you draw labs, draw em up.



I don't disagree with the basics though we don't know anything about the pt. For all we know this might be a paediatric. 

Rather I was getting at analysis of the rhythm and an interpretation with explanation for all - that was the original premise of the post.

MM


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## TomB (Mar 10, 2009)

If you want more evidence this is atrial flutter and not acute injury, take a pair of calipers and set it for whatever you think the QT interval is. Now place the calipers at the beginning of the QRS complex in each lead. Take leads V3 and V4 as examples. Now compare to leads III and V6. What could possibly account for such wild variations in the QT interval? The conclusion is that we're looking at flutter waves superimposed on T waves. The QT interval should be constant across all 12 leads.


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## Fuzzysocks (Mar 14, 2009)

I'm going with the RBBB with ischemia.

If you look at AVF and V5, there's definite flipped T waves.  Depending on where you place the J point, you can rule out elevation in place of RSR' with flipped T's as well as depression in most leads.

Any thoughts?


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## maxwell (Mar 16, 2009)

Hope they gave diesel...


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