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!!



===================================
Comment by KEN GRAUER, MD (5/28/2019):
===================================
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!
====================
FOR MORE:
  • Regarding use of Laddergrams — CLICK HERE .
  • Regarding concealed conduction — CLICK HERE.

Sunday, May 26, 2019

A man in his sixties with chest pain at midnight with undetectable troponin


Written by Pendell Meyers


A male in his 60s with no known past medical history presented at midnight with chest pain over the past 3 hours. The pain started just after eating, and at first he thought it was "reflux," however he decided to call 911 after a few hours when it did not improve.

Here is his presenting ECG:
What do you think?












Here are the relevant findings:
Slight STE in V1
2.5 mm STE in V2
Slight STD in V4-V6
Definite STD in II, III, and aVF
Hyperacute T-waves in V2, and likely also in aVL

These findings are highly specific for LAD occlusion. We have many cases of this pattern on this blog, involving STE and hyperacute T-waves in V1-V2, with STD in the lateral leads (see below for links). In this case there is also reciprocal STD in inferior leads and hyperacute T-waves in aVL. 


Side note: Sometimes this pattern includes morphology which some have described as "new tall T-wave in V1," or sometimes "T-wave in V1 greater than in V6" which is essentially just a description of a hyperacute T-wave in V1, with the exception that it would be better described as both tall and fat/large/wide/bulky T-waves, not just "tall". Dr. Smith noted "new tall T-wave in V1" in 14% of cases of early repolarization vs. 34% of subtle LAD occlusions in the derivation study of the anterior OMI formula. This initial ECG does not have this pattern, however lookout for this pattern in the serial ECGs.


Our team recognized that this ECG represents LAD occlusion. But it does not technically meet STEMI criteria. We immediately called the interventionalist to explain our concerns. They evaluated the patient and were also concerned, however they felt that immediate cath was not warranted because the STEMI criteria were not met.

We began maximal medical therapy, including nitroglycerin infusion. 

To make matters more difficult, the first troponin of course returned undetectable (our contemporary assay rarely budges until 4-6 hours after onset of OMI).

During this time, we incessantly performed serial ECGs, trying to find one that convinced cardiology. 

Here is the clearest one we could get:

By my measurement, there is at least 1 mm in V1, and at least 2 mm in V2. This meets formal STEMI criteria for a male over age 40. The T-wave in V1 is now relatively hyperacute compared to the first ECG. Lead aVL is definitely hyperacute now that we have a clear tracing of it. ST depression in V4-V6 is more evident.

Despite the fact that we believed this ECG meets STEMI criteria, cardiology colleagues disagreed. This is not uncommon, and not unexpected, as prior evidence (see the end of the post for literature review) shows that we have very poor inter- and even intra-reader reliability for measuring the ST segment.

The cardiologist stayed in the room personally to see if the patients symptoms and ECG findings would be persistent despite medical therapy.

Sure enough, the ECG findings and ischemic pain indeed persisted over the course of 20-25 minutes, and the cardiologists correctly decided to proceed with emergent cath rather than further medical management, as is recommended by multi-national guidelines regardless of the ECG findings or interpretation.

We got one last ECG before the patient went to cath:
Now there is ST depression in V3, almost as if a de Winter's T-wave is developing.


 The time between presentation and cath was just under 2 hours.

100% mid LAD thrombotic occlusion was found and stented with excellent angiographic result.

Here is an ECG the next day confirming downstream reperfusion:
Of note, there is lack of pathologic Q-waves and expected reperfusion findings, suggesting relatively favorable infarct size compared to the at-risk territory.

Echo showed wall motion abnormalities of the anterior, septal, lateral, and apical areas. 

Peak troponin T was 1.87 ng/mL.



Learning Points:

We must be expert at subtle ECG findings of Occlusion MI, because our current paradigm is insufficient.

Serial ECGs can often help to make a difficult decision easier.

Persistent ischemia despite maximal medical management is highly likely to be due to Occlusion MI and is an indication for emergent catheterization regardless of ECG findings.

Contemporary troponin assays are frequently undetectable within the first 4-6 hours of Occlusion MI, when the benefit of emergent reperfusion is maximal.

See these other cases of LAD occlusion with similar subtle patterns of STE and hyperacute T-waves in V1-V2, with STD in V5-V6:

How long would you like to wait for your Occlusion MI to show a STEMI? Sometimes serial ECGs minimizes the delay.











McCabe et al, Journal of the American Heart Association. Physician accuracy in interpreting potential ST-segment elevation myocardial infarction electrocardiograms. Journal of the American Heart Association 2013;2:e000268.
A cross-sectional survey was performed by having emergency medicine physicians, cardiologists, and interventional cardiologists review 36 ECGs from the Activate-SF database of prospective STEMI activations. 12 (33%) of the 36 cases had no culprit lesion (defined as no STEMI), whereas the other 24 (66%) were true positives with total acute occlusion (defined as STEMI). This corresponded well with the actual overall rate of false positive STEMI activations in the entire registry of 36% which was recorded from prospective practice. For each ECG clinicians were asked, “based on the ECG above, is there a blocked coronary artery present causing a STEMI?” 124 physicians interpreted a total of 4392 ECGs. Overall kappa value of interreader agreement was only 0.33, reflecting poor agreement. Overall sensitivity and specificity for true positive STEMI (occlusion) was only 65% (95%CI 63-67%) and 79% (95%CI 77-81%). There was a 6% increase in the odds of successful interpretation with every 5 years of experience since medical school graduation. After adjusting for experience there was no difference in the odds of overall accurate interpretation between specialties. However, interventional cardiologists had the highest group specificity at 89%, while emergency medicine attendings had the highest group sensitivity at 74%. This excellent study is supported by many others showing poor inter-rater reliability (35-37).
Carley et al. What’s the point of ST elevation? Emergency Medicine Journal 2002;19:126-128.
Cross sectional study in which 63 clinicians who commonly prescribe thrombolytics for acute MI were asked to identify and quantify the degree of STE present in 3 sample ECG complexes. They were also asked to mark the ECG where they identified the J-point. Overall, STE was not identified in 23 (12%) cases. For figures 1-3 below, the percentage of doctors who correctly identified the J-point correctly was 29%, 61%, and 13%.

Tandberg et al. Observer variation in measured ST-segment elevation. Annals of Emergency Medicine 1999 Oct;34;448-52.
A blinded, paired-sample survey was administered to 52 subjects including emergency physicians, emergency medicine residents, and senior medical students. They were given a packet of 40 ECGs, blinded to the fact that it actually consisted of a random order of identical pairs of only 20 ECGs from patients with “enzymatically proven myocardial infarction.” They were asked to measure all ECGs, then the difference between the each reader’s two measurement of the same ECG was studied. The average difference in segment height among all groups was 0.28 mm. Overall statistical agreement between paired ST-segment measurements was very good (K=0.85). However, “one fifth of the time, intraobserver measurements of paired ST-segment elevations differed by more than half a millimeter.” When specifically asked whether the ST-segment elevation was greater than or equal to 2.0 mm, readers disagreed with themselves in 14% of cases.


===================================
Comment by KEN GRAUER, MD (5/27/2019):
===================================
Superbly (and very tactfully) written case by Dr. Pendell Meyers, on this previously healthy 60s male who presented with new-onset chest pain. My 2 questions on reviewing this case are:
  • Question #1: What will this Cardiologist do the next time he/she sees a similar case?
  • Question #2: Why will they do what they answered for Question #1 the next time?
For clarity — I’ve put together in Figure-1 the first 2 ECGs shown in this case — since the decision to cath was made before the 3rd tracing was obtained. 
  • NOTE: ECG #2 was not the 2nd tracing done in this case — because multiple ECGs were being frequently done after ECG #1 in an attempt to convince cardiology to take this patient to emergent cath ...
Figure-1: The first 2 tracings obtained from the patient in this case (See text).
Dr. Meyers convincingly restates the case that has been made many times in this blog:
  • The current paradigm for recognizing is insufficient — because too many cardiologists remain “stuck” on requiring millimeter definition of acute STEMI.
  • Reliance on this “millimeter definition” is potentially harmful to the patient — because emergent cath is indicated for persistent symptoms and clear evidence of acute ischemia. Time is muscle.
  • Despite literature documentation of poor inter- and intra-reader reliability among even expert clinicians — the ECG findings in ECG #1 should not be negated.
  • Reliance on contemporary troponin assays is a faulty strategy — because these won’t be elevated until valuable time has passed.
  • On the other hand — Stat Echo during symptoms can provide immediate confirmation that the findings in ECG #1 are real and merit immediate cath!
To this cardiologist’s credit — he/she did stay in the room and personally monitored the patient while medical therapy was being given — and total time from ED presentation until cath was under 2 hours.
  • That said — it should have taken less time to convince cardiology that new-onset chest pain in a previously healthy man in his 60s who presents with ECG #1 should immediately go to cath.
  • ECG #2 — clearly shows progression of ischemic findings, and should definitely have been enough if there was reluctance based on ECG #1.
  • SOUL-Searching — Acute medicine is an incredibly challenging profession. The reality is, that we have to learn from mistakes. None of us are flawless. I learned these sometimes very difficult lessons as an Attending charged with training and supervising residents over my 30-year career in academics. My only hope is that the cardiologist(s) involved in this case spent some time after cath seriously soul-searching what he/she might have done differently in this case — and what he/she will do the next time they encounter a similar situation.
MThoughts on ECG #1:  Dr. Meyers superbly highlighted the KEY findings (above). I’ll add the following thoughts:
  • The ST elevation + hyperacute appearance of the ST-T wave in lead V2 of ECG #1 should be recognized from 5 feet away. Calling the T wave in this lead “disproportionately tall” does not do it justice.
  • We know lead V2 is not an “aberration” — because of the distinctly abnormal shape of the ledge-like (straight) ST segment shape in neighboring lead V3. (Although more subtle — the T wave in V3 is also disproportionately tall-with-wider-than-it-should-be-base given the small r wave in this lead.).
  • Many other leads show ST segment flattening/straightening (V4, V5, V6) — with frank ST depression in leads II, III and aVF.
  • As per Dr. Meyers — there is a subtle-but-real hyperacute appearance to the ST-T wave in lead aVL.
  • Beyond-the-Core: If you look at the PVC in lead aVR — I believe the coved initial part of the ST segment in this lead is distinctly atypical, and reflects acute ST elevation.
Bottom Line re ECG #1: In a previously healthy patient with new-onset chest pain — One can’t discount the acute appearance of the ST-T wave in lead V2. That this is real is amply evidenced by ST flattening and/or depression in multiple other leads.
  • Regarding ECG #2 — The main difference I see between ECG #1 and ECG #2 is that there is now clear ST elevation in lead V1. I understand the tendency to try to convince oneself that “there is only 1 lead that has changed” — but this is a serial change in a patient with ongoing chest pain. Careful lead-to-lead comparison of QRS morphology in the 6 chest leads of both tracings confirms that chest lead electrode positioning has not appreciably changed. Therefore, the clear new ST segment elevation with hyperacute appearance now seen in lead V1 of ECG #2 is real.
  • My only hope is that the cardiologist(s) involved in this case takes another look at these 2 ECGs — and then compares this to the 3rd ECG in this case as a reminder of what happens when you wait just a little bit longer ...
Our THANKS to Dr. Meyers for highlighting events in this case.


Friday, May 24, 2019

LBBB. Is there Occlusion MI (OMI)? Is so, which artery is it?

This was sent to me by Mohammed Shogaa:

Case:

A previously healthy patient presented in acute pulmonary edema, and had this ECG recorded:
Sinus tachycardia
What do you think?













Mohammed was impressed by the concordant ST depression in inferior leads.  This is indeed a good sign of OMI in LBBB, and in this case it is indeed helpful to make the diagnosis.

Inferior ST depression in normal conduction, as I have always written, is RECIPROCAL to ST elevation in lead aVL, and is often more visible than the STE in aVL (see example images at end of post).  Here, there is indeed STE in aVL, but it is less than 1 mm.  Our data would suggest that concordant STE in aVL that is less than 1 mm is not as specific as one might like for OMI, although it is indeed abnormal and should really heighten your suspicion.

When it is accompanied by inferior reciprocal concordant STD, that should make you even more suspicious.

Here the inferior reciprocal STD is indeed more than 1 mm.   So I would call this diagnostic of OMI in LBBB, even though, technically, it does not meet the Smith Modified Sgarbossa criteria.

There is also excessively discordant ST depression (ST/S greater than 30%) in lead V6.  This is very specific for occlusion!

Which artery is it?

Just as in normal conduction, the measurements of ST Elevation in many OMI do not meet the STEMI "criteria," the measurements in LBBB frequently do not meet the Smith Modified Sgarbossa criteria.

Criteria are simply cutoffs with imperfect sensitivity and specificity.

Of leads V1-V4, V2 has the most proportionally discordant STE, with STE at 2.5-3 mm and an S-wave of 13 mm.  If we assume STE is 3 mm, then the ratio is 3/13 = 0.23.  Remember that 25% is 80% sensitive and 99% specific.  But 20% is 84% sensitive and 98% specific.  So really, 20% is a very useful cutpoint.

The cath lab was activated.

A 100% LAD occlusion, proximal to the first diagonal, was found and opened.

Here are the subsequent ECGs:
Much more normal LBBB


Later still:
More normalized



Later still:
The LBBB is resolved and there are (Wellens'-like) inverted reperfusion T-waves in V1-V3.


Learning Point:

Criteria are guidelines only.

This first ECG had 2 different findings that ALMOST met the Smith modified Sgarbossa criteria.  Plus excessively discordant ST depression, which is the 2nd of 2 Smith modified rules (ratio of STD greater than 30% of preceding R-wave).

Both strongly suggested a proximal LAD occlusion.




References

Meyers HP et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study


Smith SW et al. Diagnosis of ST-Elevation Myocardial Infarction in the Presenceof Left Bundle Branch Block With the ST-Elevation to S-WaveRatio in a Modified Sgarbossa Rule.  Full text.


Here are 3 cases of high lateral OMI in which the STD in inferior leads is more apparent than the STE in I and aVL:







===================================
Comment by KEN GRAUER, MD (5/24/2019):
===================================
Objective assessment of acute patients with LBBB has been greatly facilitated by Smith-Modified-Sgarbossa Criteria (SMS Criteria). As discussed in detail by Dr. Smith above — application of these criteria to the case at hand predicted acute OMI for this patient who presented to the ED in acute pulmonary edema.
  • The “beauty” of SMS Criteria — is that they provide a method with user-friendly calculations that clinicians can readily learn to apply.
  • In addition to the use of SMS Criteria — I have always favored a qualitative approach, in which recognition of ST-T wave Shaping that just should not bthere reliably clues me into accurate diagnosis. The more leads on a 12-lead tracing that show abnormal ST-T wave morphology — the more comfortable I am that there is acute pathology. And when there are multiple leads showing ST-T wave changes that “shouldn’t be there” in addition to objective SMS Criteria — I become even more confident in my diagnosis.
  • NOTE — It may take a while to become comfortable with qualitative assessment when there is LBBB. Herein lies the “art” of electrocardiography. In the hope of illustrating this concept — I’ve put together the initial ECG obtained in the ED on this patient ( = ECG #1 in Figure-1) — together with the 3rd ECG in this case, that was obtained some time after reperfusion ( = ECG #3).
Figure-1: The 1st and 3rd tracings obtained from the patient in this case (See text).


The problem in diagnosis that arises — is that LBBB may: i) Mask infarction Q waves; ii) Produce poor R wave progression, if not frank anterior QS complexes; iii) Manifest ST-T wave depression in lateral and also inferior leads as an expected repolarization change from LBBB without ischemia; and/or, iv) Result in at least some degree of anterior ST elevation (and/or anterior T wave peaking).
  • Taking these expected physiologic changes of LBBB into account — I look first for ST-T wave changes that simply do not reflect a physiologic response.
  • In my experience, when there is an acute event in a patient with LBBB — only 1 or a few leads may show ST-T wave Shaping that just should not be there. In such cases, once I identify even 1 or a few leads are definitely abnormal — it often becomes easier to appreciate more subtle morphologic abnormalities in other leads.
  • The more leads showing definitely abnormal ST-T wave morphology — the greater the likelihood of an acute cardiac event. This is especially true when SMS Criteria are also positive.
My Thoughts on ECG #1:  In this case — I thought there were no less than 7 leads showing definitely abnormal findings in the initial ECG ( = ECG #1 in Figure-1).
  • My attention was immediately captured by the shape of the slight-but-definite ST elevation in lead aVL (RED arrow in this lead). The rounded shape of this ST segment with downward coving is not a normally expected response.
  • Each of the inferior leads in ECG #1 show reciprocal ST depression. The most markedly abnormal shape is the abrupt angulation (GREEN arrow) at the point where the end of the QRS complex joins the beginning of the ST segment. The horizontal “ledge-like” ST depression seen in these inferior leads (BLUE arrows) is distinctly abnormal.
  • Similar, clearly abnormal horizontal “ledge-like” ST depression is also noted in lead V5 (BLUE arrow in this lead). This shape of ST depression should not be seen with non-ischemic LBBB.
  • Finally — the acute angulation where the elevated J-point merges with the ST segment especially in lead V1, but also in lead V2 is clearly abnormal in shape (RED arrows in these leads).
  • In contrast — I thought the ST-T wave shape in other leads was far less decisive. The shape of the downsloping ST segments in leads I and V6 is not unlike the shape of lateral ST-T wave depression expected in non-ischemic LBBB. I found the shape of the ST segment in lead V3 the most difficult to assess. This ST segment in lead V3 lacks the angulation highlighted by the RED arrows in leads V1 and V2 — so by itself, I would not have been convinced of abnormality. However, in the context of clear abnormality of the ST segment in neighboring leads V1 and V2 — I suspected abnormal ST elevation extended at least to lead V3. I thought the ST segment in lead V4 was indecisive.
BOTTOM Line: Although there is no mention of chest pain in this case — acute pulmonary edema is clearly a clinical setting that is commonly associated with acute MI. In this clinical context — the presence of LBBB (not known to be new or old) + at least 7 (if not 8) leads with clearly abnormal ST-T wave deviation in the distribution we see in Figure-1 strongly suggests acute LAD occlusion until proven otherwise.
My Thoughts on ECG #3:
  • The best way to improve on recognition of clearly abnormal ST-T wave findings in the setting of LBBB — is to routinely go back and compare the initial ECG of each case you encounter, with follow-up tracings obtained after acute reperfusion. NOTE the dramatic improvement in ST-T wave appearance in ECG #3 — compared to the clearly abnormal ST-T wave findings in each of the 7 highlighted leads in ECG #1 (Figure-1).


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