New strip

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.

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.
Click to expand...

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

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).
 
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.
 
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).

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.
Click to expand...


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

12-2-082012ld.jpg


so id say thats closer to 200 than 150. 190 sounds good to me.
 
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
 
going out on a limb here ...... could this be vtach
 
wlamoreemtb said:
going out on a limb here ...... could this be vtach
Click to expand...

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.
 
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?
 
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
 
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.
Click to expand...

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.
 
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
*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?
Click to expand...

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. :rolleyes:
 
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;):rolleyes:.

MM
 
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