Monday, September 24, 2018

Tachycardia and ST Elevation.

This Case was sent from Anonymous.

A middle-aged patient was sent to the ED with tachycardia. He denied any sensation of palpitations, but his heart rate was consistently 150 bpm. The other vitals were normal. He had JVD and swollen legs, but clear lungs and a normal room air oxygen saturation.

He denied all typical and atypical ischemic symptoms. He noted, however, that he had had marked fatigue starting about 5 days ago, but that he was actually feeling much better today.

The initial ECG:

The rhythm appeared to be atrial flutter, but also concerning were the ST segment elevations in I, aVL, V2, and V3, as well as ST depression in the reciprocal inferior leads.

But atrial flutter can alter the baseline such that there is only apparent STE or STD (see example cases below) 

Is this:
1) true STEMI (acute or subacute)?
2) PseudoSTEMI due to the underlying atrial flutter wave?
3) PseudoSTEMI due to old MI (persistent STE after previous anterior MI, also known as LV aneurysm morphology?

The physician's thoughts: This pattern is concerning for anterior wall OMI, specifically a proximal LAD lesion. There are Q waves in V1-V3, suggesting an old anterior MI, but the T waves in V2 and V3 are fairly tall, suggesting some degree of acute ischemia. Also, there are no T wave inversions which would suggest a subacute, evolved, or reperfused MI.

The patient, with an easy smile, again denied any symptoms.

Atrial flutter can mimic the ECG signs of an MI. (For example, see this case, this case, this case, these erroneous computer interpretations, and this case report

K. Wang makes this comment: "A great case. It's important, as you did, to point out, that atrial flutter waves can cause findings suggestive of STEMI. In this tracing, the answer is in the lead aVL. There, the beginning of the ST segment is higher than the top of the flutter wave in front of the QRS, proving that the ST segment is indeed elevated."

To clarify the ECG, the emergency physician administered IV metoprolol to slow the ventricular response. However, the patient became borderline hypotensive after this (although still completely symptom-free). A bedside echo was performed:
There is akinesis of the anterior wall, best seen on the parasternal short axis (PSSA) view.
So there is a myocardial infarction.
But is it old or new?
There is no evidence of aneurysm formation on this echo (the myocardial wall is not thin); therefore, it appears to be acute or subacute.

The cardiac catheterization team was activated. The blood pressure dropped precipitously while in the lab preparing for the angio, and the patient was electrically cardioverted. An occlusion of the proximal LAD was then found and intervened on.

The troponin obtained in the ED was almost 10 ng/mL, suggesting a subacute occlusion.

This was recorded next AM:
There are QS-waves with continued ST Elevation with large upright T-waves in V2 and V3

Smith comment:

Is this the so-called “left ventricular aneurysm” pattern? --LV aneurysm can be distinguished by the size of the T-wave, specifically the T/QRS ratio:

--LV aneurysm has a relatively small T-wave, often with some slight (shallow) inversion.

--Acute MI has a large upright T-wave, but may be inverted if reperfused (shallow in the case of Wellens' pattern A; deep in patthern B, which is a later evolution). However, Wellens' waves are preceded by R-waves, not by QS-waves.

LV aneurysm rule: One should especially suspect LV aneurysm, and use the rule, when there are QS-waves in any of V1-V4. A QS-wave means a single negative deflection, without any R-wave or with only a tiny r-wave.

Here is the rule:

If there is one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is acute MI. If less then 0.36, it is either subacute (over 6 hours) or old.(see references 1, 2). In this case, the T/QRS ratio is largest in V3 at 5/9 = 0.55.

If this were the presenting ECG, you would not want to say that those QS-waves are due to old MI with persistent ST Elevation (LV aneurysm morphology).

But now we are post-reperfusion, so what does the ECG tell us?
That there is persistent ischemia in spite of reperfusion.

This is a bad prognostic sign. The STE and hyperacute T-waves at this point could be either persistent ischemic or re-occlusion. If there had been intervening resolution on the ECG, it would represent re-occlusion. But in this case it was persistently elevated ST segments and hyperacute T-waves. This is typical of "no reflow," which is a result plugging of downstream small vessels by platelet-fibrin aggregates. Read about it here:

Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction (Lancet 1997)

[Alternative explanation for persistently upright T-waves: post-infarction pericarditis (which happens in transmural MI)].

T/QRS ratio to differentiate anterior STEMI from anterior LV aneurysm:

Case by Anonymous, continued

My personal M and M session:
If there is a similar “next time,” I may change my approach.

First, I deferred the echo too long. My initial reasoning was that this was just a rhythm problem, and that checking the Ejection Fraction at a rate of 150 was unreliable, and would be falsely low. Had I done the echo before the metoprolol, I likely would have felt more justified in considering cardioversion first!

Second, in retrospect, cardioversion would have been better than medications, both because his hemodynamics were precarious, and because it would have clarified the ECG interpretation. I delayed cardioversion because the patient looked “too good” for electrical therapy. Furthermore, the patient was likely in atrial flutter for greater than 48 hours, theoretically raising the risk of post-conversion CVA.

But sometimes ST changes will disappear with conversion of atrial flutter to NSR, and urgent angiography can be avoided. Or, in this case, the true ST segment changes will be revealed, and appropriate timing of angiography can be determined.

Smith comment:

I agree. Electrically cardiovert, then re-assess.

Comment by KEN GRAUER, MD (9/24/2018):
Excellent case for discussion. I’ll focus my comments on the 2 ECGs in this case, which for clarity I have put together in Figure-1. I’ll verbalize the thought process in my assessment, which led me to conclusions that mirror those detailed by Dr. Smith.
Figure-1: Comparison of the 2 tracings in this case. TOP — Initial ECG in the ED, obtained from this middle-aged patient with tachycardia. BOTTOM — ECG #2, obtained the following morning after cardioversion and cardiac catheterization (See text).
  • ECG #1 — shows a regular SVT (= SupraVentricular Tachycardiawith a narrow QRS complex, and a ventricular rate of ~150/minute. Sinus P waves are absent.
  • PEARL #1: It is helpful to keep in mind the differential diagnosis of a regular SVT rhythm in which sinus P waves are not clearly evident. For practical purposes, when the ventricular response is this fast, the differential diagnosis consists of 4 entities: iSinus tachycardia (which could still be present, if sinus P waves were hidden within the preceding ST-T wave); iiReentrySVT (such as AVNRT or AVRT); iiiAtrial Flutter with 2:1 AV conduction; and, ivAtrial Tachycardia with 2:1 AV conduction. Awareness of this short differential list greatly facilitates clinical decision-making.
  • The rhythm in ECG #1 is not sinus tachycardia. We know this is — because although there is atrial activity, the P wave in lead II is negative (slanted RED arrows). Unless there is lead misplacement or dextrocardia — a negative P wave in lead II excludes the possibility of a sinus mechanism.
  • PEARL #2: In my experience, AFlutter is by farthe most commonly overlooked arrhythmia. The best way to avoid missing the diagnosis of AFlutter is to, “Think AFlutter until proven otherwise” — whenever you encounter a regular SVT at a rate close to ~150/minute, in which sinus P waves are not evident. If you regularly look for AFlutter in such cases — then you are far less likely to overlook it (See ECG Blog #40).
  • PEARL #3: You can virtually prove that the rhythm in ECG #1 is AFlutter even before slowing the rate by using CALIPERS. Set your calipers to exactly HALF the R-R interval — and see if you can precisely march out 2:1 AV conduction. If so — See in how many leads you are able to do so. We illustrate application of this technique in Figure-1. The non-sinus negative deflection before the QRS in lead II (slanted RED arrow) is perfectly equidistant from a similar-looking negative deflection right after the QRS (slanted PINK line).
  • The best leads to look for flutter waves with typical AFlutter are most often the inferior leads + leads aVR and V1 — and clear evidence of 2:1 AV conduction is seen in all these leads in this example (slanted PURPLE lines). Flutter waves are actually also seen in most of the remaining leads. Some cases of AFlutter only show flutter waves in 1 or 2 leads — but the more leads you clearly see 2:1 conduction in — the more confident of your diagnosis you can be without necessarily needing to slow the rate. NOTE: Reasons ECG #1 is unlikely to be ATach, are that this rhythm is much less common in a non-EP setting than AFlutter — and, that with 2:1 conduction, this would entail an atrial rate ~300/minute, which is clearly above the atrial rate usually seen with ATach.
As emphasized by Dr. Smith — AFlutter can alter the ECG baseline, making it extremely difficult to assess for acute ST-T wave changes. This is especially true when “typical” AFlutter is present, in which there are large amplitude flutter waves in the inferior leads, as well as in other leads. For this reason, I was not initially certain that the tall T waves with apparent ST elevation in the anterior leads of ECG #1 was indicative of an acute event. And, even though there are QS complexes in leads V1,V2 — with no more than tiny initial r waves in V3,V4 of ECG #1— these QRS morphologic changes do not always persist on repeat ECG under more controlled conditions after the rate has slowed.
  • PEARL #4: No matter how you might try to imagine “interference” from flutter waves affecting ST-T wave appearance in the anterior leads of ECG #1 — there is ≥2mm of ST segment elevation in lead aVL (LIGHT GREEN arrows, seen within the GREEN rectanglethat can notbe explained away by flutter waves distorting the ST segment. That’s because we see NOTHING resembling flutter waves occurring at half-the-R-R interval distance away from the ST elevation in lead aVL (DARK GREEN arrows in this lead). In my experience — Lead aVis often a “magical lead” for providing the support needed to convince me that suspected ST elevation in equivocal cases is real.
  • Clinically — the case presented here is perfectly consistent with probable “silent MI” occurring about 5 days earlier (when this patient noted marked “fatigue”) — with persistent tachycardia and the likely large anterior STEMI accounting for gradual progression of right-sided heart failure (JVD, swollen legs noted). I took this as further support of my suspicion of recent acute STEMI.
PEARL #5: The best way to hone your Clinical ECG Interpretation skills — is to follow up on those cases about which you initially had questions on. Comparison of the initial ECG with ECG #2, obtained the next morning — provides us with an excellent opportunity to do this (Figure-1).
  • Note with reestablishment of sinus P waves in ECG #2 — that the double negative deflections in lead II (as well as in other leads) have disappeared.
  • Note in lead aVL similar shape and amount of ST elevation as we suspected from assessment of ECG #1 during AFlutter. Same is true (albeit to a lesser amount) in lead I.
  • Note the presence of “mirror image” reciprocal ST depression in each of the inferior leads in ECG #2. This was present in ECG #1 — though it was much more difficult to be certain this ST depression was real and not just superposition from AFlutter in the initial ECG.
  • Note similar QS complexes and poor R wave progression with persistent anterior ST elevation after conversion to sinus rhythm.
Our THANKS to Dr. Smith for presentation of this highly insightful case!

Friday, September 21, 2018

New Lecture on High Sensitivity Troponin Protocols in the ED

It is my task to educate our residents on chest pain, ECGs, and troponin.  So for years I have been lecturing on the topic of chest pain and troponin.

I put the last one online in 2015, and has had 25,000 views.  It is embedded at the bottom of this post, and is called:

Approach to Potential Ischemic Chest Pain in the Emergency Department

The first 25 minutes are all about the data on worrisome characteristics of chest pain.  Most of the rest would now be slightly out of date.

Below is the new one: 
High Sensitivity Troponin; Considerations for Implementing ED protocols.

There is a huge amount of new data since 2015, and it will keep accumulating.

I have tried to distill a huge literature down to fewer important studies, and I give my bottom line summary, but there is still a huge amount of data.  This is my reading of the literature.  It is not peer-reviewed.  I'm sure there are many who would disagree with my summary slides.  But I present a lot of data so that you can make your own decision.  A file of the outline of the slides can be accessed on my Google Drive via the link.

The purpose of this lecture is to expose you to the broad spectrum of high sensitivity based protocols that your ED might choose from.  You will not be able to use it on your next patient, but use it to institute a protocol that works for your institution.  So just sit back and listen.

One thing I forgot to address in the lecture: Acute Occlusion Myocardial infarction (OMI).  There is no evidence that hs troponin will help in the early diagnosis of acute coronary occlusion vs. non-occlusive MI.  It does help in early diagnosis of MI (of OMI/NOMI), but does not differentiate.

Thanks to Scott Joing for recording this.  Scott is our tech wizard and fine emergency physician, and co-editor of Ma and Mateer's standard EM ultrasound textbook.  He is the creator of

Also thanks to my incredibly bright and knowledgeable troponin research partners, both of whom know much more about troponin than I do.  They are Fred Apple and Yader Sandoval 
(, and also to the Cardiac Biomarkers Research Lab, especially Karen Schulz, at Hennepin and Minneapolis Medical Research Foundation.

High Sensitivity Troponin; Considerations for Implementing ED protocols.

The text of the slides can be seen here in .rtf format:

The text of the slides can be seen here in .rtf format:

This is the previous lecture from 2015.  

The first 25 minutes have a lot of good stuff on chest pain. The high sensitivity info which comes later is somewhat out of date.

Thursday, September 20, 2018

See what happens when hyperacute T-waves are missed

Written by Pendell Meyers, edits by Steve Smith

A man in his 60s with history of hypertension and MI 10 years ago, with PCI, presented to an outside hospital complaining of chest pain that started while mowing the lawn. His chest pain was located in the central chest, non-radiating, and associated with diaphoresis, nausea, and vomiting.

Here is his ECG on arrival:

What do you think?

This ECG is all but diagnostic of subepicardial ischemia of the anterior, lateral, and inferior walls, most likely due to Occlusion MI (OMI), probably of the LAD. This is evidenced by hyperacute T-waves in leads V3-V6. Leads II and aVF also have hyperacute T-waves. The R-wave progression is extremely poor which is also common in large anterolateral Occlusion MI (OMI). There is a very small amount of STE in some of the anterior, lateral, and inferior leads which do NOT meet STEMI criteria.

This ECG is highly suspicious for LAD OMI. If you have any doubts, you should record another one every 5 minutes until you are convinced.

The most likely location for an occlusion producing OMI changes in the anterolateral and inferior leads is the proximal-to-mid LAD. Usually this will be either a type II LAD (which supplies the apex) or a type III LAD (which goes even further and curves around the apex to the inferior aspect of the apex).

Remember that the ECG reports what is happening to the myocytes, then you must use that information to make inferences about what the patient needs. Acute coronary occlusion is the most common and most treatable cause of this pattern, but it is not the only cause. The myocytes do not know why they are dying, they can only report their death and hope you can see it and figure it out. Takotsubo, spasm, low flow with a preexisting stable coronary lesion, etc. are other causes of acute focal myocyte death which produce the same ECG findings.

This patient clearly needs emergent angiography and reperfusion of the LAD lesion that is causing his Occlusion MI until proven otherwise. 

Here is his prior ECG on file from the outside hospital from long ago:

This ECG from years ago shows anterolateral OMI with signs of prolonged/subacute MI (QS waves, poor anterior R wave progression) but also reperfusion including terminal T-wave inversions in V1-V5. One must always be careful when looking for "baseline" ECGs, because the prior ECG on file may have been during another ACS event, as this one clearly was. This ECG was presumably performed during the patient's prior MI, most likely during a period of reperfusion or after PCI of the LAD (this information is not available). 
This ECG can never be a baseline ECG. If subsequent ECGs were available, they would have shown resolution of these reperfusion T-waves over days to weeks. In such a case, the presentation ECG would not represent pseudonormalization (because the ECG would have returned to baseline). However, if this ECG had been recorded within the previous week, then the presentation ECG would indeed be indicative of pseudonormalization (reocclusion during an ACS event causing reperfusion T-wave inversions to re-inflate and turn positive, or "pseudonormal").

The EM physicians at the outside hospital activated the cath lab transfer protocol (unless cardiology cancels the activation, our cath lab is activated, and the patient is transferred immediately from the outside hospital to our cath lab).

The case was reviewed by all parties, and it was stated correctly that the ECG does not meet the STEMI criteria.

Cath lab activation was cancelled but the transfer was accepted for urgent cardiology evaluation.

40 minutes after the first ECG, just before transport, a repeat ECG was obtained:

Continued, active OMI of the anterior, lateral, and inferior walls.

In the ambulance during transport, the patient suddenly suffered VF arrest.

He was defibrillated immediately and had return of normal mental status.

Upon arrival, providers again reviewed the ECGs and found no reason on ECG for emergent catheterization. Given the VF arrest during transport, however, they appropriately all agreed that cath should happen sooner rather than later.

They took him almost immediately for catheterization. They found an acute lesion of the LAD at the site of the prior stents, including 70% proximal LAD lesion and 95% mid-LAD stenosis with TIMI 3 flow at the time of cath. There was also a chronic total occlusion of the RCA. The LAD lesion was acute and required 3 stents to restore flow. Here are the images of the acute LAD lesion:

The mid-LAD is nearly occluded, but with distal flow. 

In this view it appears to be a total occlusion, however the video shows delayed slow flow through the LAD lesion.



Troponin T peaked at 3.86 ng/mL (very high).

Echo the next day showed EF 35% with wall motion abnormalities of the mid-anterolateral, mid-anterior, mid-inferior, mid-inferolateral, mid-inferior, mid-anterior septum, mid-inferior septum, anterior apex, lateral apex, inferior apex, septal apex, and the apical cap. This distribution matches the distribution of OMI findings on ECG (although some of the WMA could be explained by the previous Q-wave infarct in the prior ECG).

Here are his repeat ECGs after intervention:

This shows new Q-waves in V4-V6, with persistent STE and positive T-waves in the anterolateral leads which matches left ventricular aneurysm morphology. These findings are consistent with full thickness infarction. In Dr. Smith's experience one must wait at least 2 weeks to find out if this electrical LVA morphology will resolve, and whether it will be accompanied by anatomic aneurysm.

Similar findings.

Learning Points:

Patients deserve to have their Occlusion MI recognized prior to (or even in the total absence of) STEMI criteria.

Expert ECG interpretation could have prevented this man's cardiac arrest, and almost certainly would have resulted in a much smaller MI and therefore better long term prognosis.

The STEMI vs. NSTEMI paradigm is not the best way to decide who needs emergent reperfusion therapy. The most recent available RCT evidence (the FTT Meta-analysis published in 1994) would suggest that this patient receives mortality harm from emergent reperfusion therapy (thrombolytics), because his ECG does not meet STEMI criteria (see diagrams below representing the mortality effects of thrombolytics from the FTT meta-analysis). This is obviously false, and this demonstrates how the STEMI vs. NSTEMI paradigm has brainwashed us into failing to recognize other ECG findings which predict Occlusion MI. In the FTT meta-analysis there was no expert ECG interpretation, there was simply an undefined trichotomous classification of "ST elevation," "ST depression", or "normal" ECG. Additionally the studies in the FTT meta-analysis were done in an era without cardiac catheterization, and thus they were unable to distinguish between occlusions and non-occlusions among those without ST elevation. For more, see The OMI Manifesto.

 Comment by KEN GRAUER, MD (9/21/2018):
I would suggest the following alternative title for this blog post = “A difficult and unfortunate way to learn” … And, there is a lot to learn in this case:
  • First — The wrong question was asked …  The question apparently asked by decision-makers was, “Is there ECG evidence of an acute STEMI”. Instead, in a patient like this with new-onset chest pain — the question that should have been asked is, “Does this initial ECG suggest an acute process?” — because if it does, then urgent cath to define the anatomy is clearly indicated.
  • Somewhere along the way — the initial ECG was misinterpreted. It’s hard to tell from the information available where this mistake occurred. The EM physicians at the outside hospital appropriately activated the cath lab transfer protocol — but that order was subsequently negated by others ... So while true that strict ECG criteria for acute STEMI were not met — the “correct interpretation” of this initial ECG given the clinical context of new-onset chest pain should have been precisely as described above by Dr. Meyers = hyperacute T waves in multiple leads, in association with slight ST segment elevation + poor R wave progression (actually, loss of r wave from V2-to-V3).
  • The correct interpretation of this initial ECG (which I’ve reproduced in Figure-1) should have included the clinical correlation that the above described abnormal ECG findings in multiple leads are highly suspicious for acute LAD occlusion ( = OMI), with clear indication for immediate cath and coronary reperfusion.
  • When multiple leads all show abnormal findings — then the findings you are seeing are probably real. So despite the fact that strict criteria for acute STEMI are not met in the TOP tracing in Figure-1 — hyperacute T waves (defined as taller, broader and fatter-than-expected with respect to the QRS complex) are seen in leads I, II, aVF, and V3-V6. Among the remaining leads — there is some ST elevation in lead III — and, an inappropriately straight ST segment with overly prominent T wave in V2. In addition, lead aVR shows an unexpectedly deep and broad inverted T wave (doubtlessly reflective of a reciprocal change to the upright hyperacute T waves in multiple leads). This makes for no less than 10 out of 12 leads on this initial ECG that are obviously abnormal. When 10 leads show a consistent theme of ECG abnormalities — then these ECG findings must be taken as real.
Figure-1: The first 2 tracings in this case. TOP — Initial ECG of this 60-year old man with a history of prior MI, who presented with new-onset chest pain. BOTTOM — Prior ECG obtained years earlier on this patient (See text).
 Additional lessons to be learned in this case are suggested by comparison with the prior ECG (BOTTOM tracing in Figure-1).   
  • As per Dr. Meyers — We have no idea as to when in this patient’s history the prior ECG was obtained. We suspect this tracing was obtained during reperfusion of this patient’s previous MI — but the meaning of the distinctly biphasic T waves in V2,V3 — with T inversion in V4,V5 might portend a very different clinical significance depending on whether infarction had just happened, was in the process of resolving, or had happened several years earlier.
  • Regardless of when this prior ECG was obtained — the learning point is that IF there had been any doubt about the acuity of the initial ECG — comparison of the 2 tracings in Figure-1 should confirm that the changes in the initial ECG are definitely acute and strongly suggestive of acute OMI.

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