Tuesday, May 28, 2019

I was handed this ECG at triage with no information

I was at triage when this ECG of a 50-something was handed to me.

He speaks no English and I really had no idea what his symptoms were, but someone had pointed to his chest, which is why they recorded an ECG.

What do you think?






























I was pretty alarmed by the ST segments in V4 and V5, and the ST segment of the PVC in V3.

V4 and V5 have QR-waves, in addition to the STE, which suggests:
1. Old MI with persistent STE
2. Old MI with superimposed new STE, or
3. Subacute MI. 

There is also STE in the normally conducted beats of V2 and V3, but that is in the context of a deep QS-wave, which was less alarming.


So I looked for old ECGs, and found these:

Previous
The second beat in each of V4-V6 is a PVC.  The first is normally conducted.
The normally conducted beat in V4 has a QR-wave and STE, but not as much STE as the new ECG.  
The PVC might fool you into thinking that there was previously an absence of Q-wave.


Another Previous
This looks a lot like the new one, but the new one has more STE.
It is helpful to know that a faster heart rate can exaggerate the ST elevation of LV aneurysm.
My suspicion was that this was all old.

We did a bedside echo:

Apical 4-chamber

Large apical aneurysm


Parasternal long axis

Also shows the apical aneurysm



We found that he has a history of LAD occlusion and Left Main stent, and ischemic cardiomyopathy, had a v fib arrest and has an ICD and pacer.

Previous echo had indeed shown an LV aneurysm.

Then the interpreter arrived and confirmed that he does not have chest pain but did have a syncopal event.

We recorded a subsequent ECG:
Looks just like the first



I decided that this is an old MI with persistent ST elevation (LV aneurysm) and we ordered a formal echo that confirmed no new wall motion abnormality.  The patient ruled out for MI.

He was admitted and found to have runs of VT, which explained his syncope.  Although I'm not sure why the ICD did not fire.

What would have happened if we used the rule for differentiating acute STEMI from anterior LV aneurysm?

This is the rule:

If there is one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is acute STEMI, because STEMI has a large upright T-wave.

Problem is, when I did these studies, we only looked at the upright part of the T-wave, but I believe it works for the entire T-wave amplitude, both positive and negative.

For ECG 1, we would have:

V1: 3/15 = 0.20
V2: 5.5/20 = 0.275
V3: 7.5/25 = 0.30
V4 (positive part of T only): 3.5/19.5 = 0.18
V4: (using entire T-wave amplitude) 5.5/19.5 = 0.28

All are less than 0.36, so the rule was accurate in this case.


Learning Points:

1. LV aneurysm is one of the most common causes of inappropriate cath lab activation.
2. It is important to talk to non-English speaking patients through an interpreter
When there are Q-waves:
3. It is important to find old ECGs
4. It is important to look at the heart
5. It is important to look at old records
6. It is important to ascertain that the T-wave amplitude is large, as it is in acute STEMI.  The formula helps you with this.

Finally, the formula may have false negatives in subacute STEMI, because as time goes by, the T-wave amplitude in STEMI diminishes!!



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Comment by KEN GRAUER, MD (5/28/2019):
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Challenging case for many reasons! Dr. Smith provides SUPERB step-by-step narrative as he assessed the initial ECG for the likelihood of an acute cardiac event. His Learning Points embody key “Take-Home” messages that will serve us well when assessing other worrisome tracings, especially when there is limited clinical information at the time the patient presents.
  • I was fascinated by the rhythm in the initial ECG — which I’ve reproduced, together with my proposed Laddergram in Figure-1.
  • Assessment of the cardiac rhythm in this initial tracing is more than an academic exercise — as we need to be able to distinguish between sinus-conducted beats and non-sinus beats in order to optimally assess QRS morphology and ST-T wave changes for potential acute ischemia.
Interesting Features about this Rhythm — When I first looked at this tracing, I was not at all certain of what was going on in this tracing.
  • I saw some P waves in the long lead II rhythm strip — but I was not at all sure if there was an underlying regular atrial rhythm ...
  • The PR interval seemed to be changing in some places — and at least 1 P wave seemed non-conducted ...
  • Looking at the long lead II rhythm strip — there seemed to be at least 4 different QRS morphologies ...
  • Beats that I thought were probably PVCs were not always wide ...
Figure-1: The initial ECG in the ED + my proposed Laddergram (See text).

=====================
My Approach for Assessing this Rhythm: Complicating rhythm assessment for the ECG in Figure-1 is the fact that there is significant baseline artifact in various parts of this tracing. NOTE: Use of Calipers is essential for interpretation of the rhythm in this tracing
  • I began by focusing on the long lead II rhythm strip at the bottom of the tracing. I like to start by looking for a part of the tracing that I am 100% certain about. Perhaps the only thing I was initially certain about in this tracing, was that beats #18 and 19 are sinus-conducted with a prominent (tall and pointed) upright P wave in lead II that manifests a normal PR interval.
  • Surveying the rest of the long lead II rhythm strip — I saw that beats #13 and 16 were also sinus-conducted, each preceded by the same PR interval  that preceded beats #18 and 19.
  • At this point — I was uncertain about additional atrial activity. Use of calipers instantly resolved this uncertainty. Setting my calipers precisely to the one P-P interval that I was certain about (ie, the distance between the P waves preceding beats #18 and #19) — I was able to walk out regular sinus P wave activity throughout almost the entire tracing (RED arrows)! It really helped that the known sinus P waves we saw (ie, preceding beats #13, 16, 18 and 19) were so pointed — since this facilitated recognizing many of the remaining P waves that were partially hidden within the QRS complex or the ST-T wave. The only interruption in this consistent P-P interval occurred for the P wave preceding beat #6 — which I felt given its early occurrence and more rounded shape, was probably a PAC (YELLOW arrow).
  • Allowing for slight variation in QRS morphology that is common in acute patients (who often are moving around in bed), especially when there is as much baseline artifact as we see in Figure-1 — I thought narrow beats #2, 4, 8, 10, 12, 13, 15, 16, 18, 19 and 21 were all sinus-conducted QRS complexes (labeled with a blue “S” in Figure-1).
  • For the remaining beats — I used simultaneously-recorded leads in the 12-lead ECG, as well as the long lead II rhythm strip for assessment of QRS morphology. Starting again with those beats I was fairly certain about — I thought beats #14 and 17 were almost certain to be PVCs — since in simultaneously-recorded lead V3 these QRS complexes were very wide and differently shaped than the sinus-conducted beats in this lead. NOTE: Beats #14 and 17 do not look wide in simultaneously-recorded lead V1 — presumably because much of the QRS complex in lead V1 lies on the baseline (which is why the more leads you look at, the better for assessing QRS width and morphology! ).
  • Since beat #20 in the long lead II rhythm strip looks identical to beats #14 and 17 — beat #20 must also be a PVC (and this beat does look very different from the sinus-conducted beats in simultaneously-recorded leads V5 and V6).
  • Beat #5 looks very wide and different in the long lead II. It is also a PVC.
  • But what about beats #137and 11? These beats do not look very wide in either the long lead II rhythm strip, or in the simultaneously-recorded leads above the long lead II rhythm strip. I believe these beats are also PVCs — because no other answer makes sense to me. Given the caliper-proven regular atrial rhythm — beats #1,3,7,9 and 11 can’t be PACs with aberrant conduction (because this would disturb the underlying regular sinus rhythm). QRS morphology of beats #1,3,7,9 and 11 is not suggestive of an form of aberrant conduction — and the coupling interval of these beats (ie, the distance of the PVC to the preceding sinus-conducted QRS) is virtually the same as the coupling interval for beats #14, 17 and 20 that we felt certain were PVCs.
  • NOTE: This leaves us with having to explain WHY if beats #1,3,7,9 and 11 are PVCs with the same coupling interval as PVCs #14,17 and 20 — Why do these beats have 2 different QRS morphologies? MTheory: It is possible for PVCs to have a similar origin but a different exit site from their circuit within the ventricles — in which case the coupling interval may be the same, but QRS morphology of these PVCs with a similar origin site may differ … That said, I acknowledge that I cannot prove my theory.
  • Beyond-the-Core: Note that the PR interval preceding beats #2, 4, 8, 10, 12 and 15 is longer than the PR interval preceding sinus-conducted beats #13, 16, 18 and 19. The reason for this is concealed conduction” — which is a presumption that the PVCs preceding each of these beats conducts far enough retrograde to delay forward conduction of the next sinus beat (dotted lines in the laddergram, showing transmission from these PVCs into the AV nodal tier).
  • Bottom Line: I’d interpret the rhythm in Figure-1 as showing sinus rhythm with extremely frequent PVCs and a PAC. PVCs are multiform — since their morphology is not always the same. The P wave that occurs at the very end of the QRS complex of beat #5 is not conducted — because it occurs during the absolute refractory period. The P wave that occurs early in the ST segment (just after beat #17) is also not conducted for the same reason. Slight PR interval prolongation is seen following many of the PVCs due to the phenomenon of “concealed conduction” — but there is no evidence of any AV block! Now that we know which beats are sinus-conducted (labeled by an “S”) and which are ventricular (labeled by a “V”) — we can more easily follow Dr. Smith’s rationale for why this is not an acute STEMI. 
Our THANKS to Dr. Smith for presenting this fascinating case!
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FOR MORE:
  • Regarding use of Laddergrams — CLICK HERE .
  • Regarding concealed conduction — CLICK HERE.

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