Any paramedic who has studied the STEMI mimics has heard of the classic benign early repolarization pattern of a "fish-hooked" J-point with upwardly concave (smiley-faced) ST-segment, often best appreciated in lead V4.
But, as the excellent work of Stephen Smith, M.D. demonstrates, not all cases of early repolarization present this way, and it can often be very difficult to differentiate between early repolarization and LAD occlusion.
So, we took a run-of-the-mill "male pattern" early repolarization pattern, removed the computerized interpretation, and posted the ECG to our Facebook fan page.
The variety of interpretations was shocking!
Some of the common interpretations included Wolff-Parkinsons-White syndrome, pericarditis, hyperkalemia, and (less commonly) acute anterior STEMI. Very few mentioned early repolarization.
This just goes to show how important and valuable Stephen Smith's work on this topic really is!
Here's the same ECG with the computerized interpretation.
I have a sneaking suspicion that some of the very same paramedics who rail against computerized interpretive algorithms are unconsciously influenced by the computerized interpretation whether they realize it or not.
That may not be a bad thing.
A baseline reading of "normal ECG" creates a comfort level for this normal variant. Keep in mind, ST-elevation in leads V2 and V3 for a young male is not a normal variant. It's a normal finding! But these T-waves are a little more impressive than we might expect, so I'm calling it a variant.
So what gives away that it's not hyperacute anterior STEMI?
Dr. Smith has an abstruse formula (he probably doesn't think it's abstruse but then again the man's a physicist as well as a physician) that was recently published in the Annals of Emergency Medicine.
(1.196 x STE at 60 ms after the J-point in V3 in mm) + (0.059 x computerized QTc) – (0.326 x R-wave Amplitude in V4 in mm)
A value greater than 23.4 is quite sensitive and specific for LAD occlusion.
Dr. Smith adds these qualifiers:
"It is critical to use it only when the differential is subtle LAD occlusion vs. early repol. If there is LVH, it may not apply. If there are features that make LAD occlusion obvious (inferior or anterior ST depression, convexity, terminal QRS distortion, Q-waves), then the equation MAY NOT apply. These kinds of cases were excluded from the study as obvious anterior STEMI. ST elevation (STE) is measured at 60 milliseconds after the J-point, relative to the PR segment, in millimeters."
What does this mean for the field provider? I'm a firm believer in keeping it simple.
The bottom line (in my opinion) is that we should suspect the possibility of benign early repolarization when:
- R-wave progression is intact (this is big)
- There is a tall R-wave in lead V4
- The QTc is on the low end of normal (in this case < 400 ms)
- There is an absence of reciprocal changes
- ST-elevation is upwardly concave
- U-waves are easily identifiable (additional tip shared by Dr. Smith in private conversation)
- There are no changes on serially obtained ECGs
None of these rules of thumb are 100% but we're trying to make a logical game-time decision and knowledge is power.
Simply knowing that the differential diagnosis is early repolarization vs. LAD occlusion would be an important improvement when faced with an ECG like this (which frankly isn't anywhere near as difficult as some others we've seen).
- Early repolarization is a common and underappreciated STEMI mimic
- It does not always present with "fish-hooked" J-points
- The ST-elevation and T-waves can often be scary with early repolarization
- The key here is knowing that the differential is LAD occlusion vs. early repolarization
I encourage everyone to read the archived early repolarization cases at Dr. Smith's ECG Blog by clicking here.
Here is the conclusion to 51 year old male: Chest Pain. You may wish to review the case.
Here is the ECG again:
There is a regular sinus rhythm at a rate of about 70. The QRS is narrow. The axis is normal, at about 15 degrees.
Let's take a look at the constellation of ST changes:
There is ST elevation in leads I, aVL, V2-V6. There is slight ST depression in III and aVF (and arguably in lead II) with ugly looking T wave inversions. Some of you also noted the suspicious looking Q waves in III and aVF.
Pericarditis and Early Repol were put forth as possibilities. Remember though, that neither of those will have reciprocal changes (excepting myocarditis, which may present as STEMI). Here, we have reciprocal changes inferiorly. If you were inclined to be thinking about STEMI mimics in this case, those changes should put ischemia at the top of the list. In addition, as some of you pointed out, the ST changes do not look like Early Repol, and the amount of ST elevation here is alarming.
The crew in this case, along with the physician, decided this was STEMI. The patient was given Heparin, ASA, anti-emetics, and Morphine. His condition improved enroute, and his BP climbed to 124/75.
Upon arrival at the hospital, he was taken directly to the cath lab. There was a complete blockage of the LAD.
Here is the cath lab image showing the blockage:
Here is the image after revascularization:
I don't know about you, but I always find these images amazing. Fortunately, our patient was discharged from the hospital to cardiac rehab a few days later. He was expected to recover nicely.
Enjoy the holiday!
This is the discussion for Elderly Female: Chest Pain. You may wish to review the case.
Ok, this was not an obvious case, at least, not until the end. As far as the patient goes, I think we all agree about the differentials: ACS vs. possible aortic dissection (due to the pain radiating to her back).
The patient had no history of problems with aneurisms, but no history of CAD either. Pain starting while under exertion, with substernal chest pain, and diaphoresis sure sounds like ACS. You could check for differences in BP in each arm, which the crew did, but this finding in a dissecting aortic aneurism is often absent. But, never bad to keep in mind other possibilities of what's going on. Now, let's review the initial ECG:
The patient had a hard time sitting still due to her discomfort, and the resulting wandering baseline and irregular rhythm present challenges to interpretation. We have a rhythm that is A-Fib. We have slight ST elevation in V1-V3 (possibly slight in V4), and ST depression in V5 and V6. Anterior MI? Maybe, but maybe not.
Several of you astutely noted that the morphology appeared to resemble LVH with secondary reploarizaion abnormalities, the so called "Strain Pattern". One addition challenge here, is that this printout does not appear to let the QRS complexes run into eachother, rather it cuts them off at the level of the overlying or underlying QRS complex. This makes it difficult to measure.
The monitor interpretation did indeed say that voltage criteria for LVH was met. However, as Tom B has mentioned so many times on this site, it is more important to recognize the morphology of Strain Pattern, than actually know the voltage criteria. Here is a snapshot of Strain morphology typical in the lateral precordial leads:
Here are leads V5 and V6 from our patient:
Similar morphology? Looks like it… we would like to see the degree of depression proportional to the height of the R wave, but unfortunatlely the complexes are chopped by the machine, adding another challenge to the interpretation. No history of MI, and the "QS" looking complexes of the right precordials sure add to the look of Strain pattern. For more on LVH and Strain pattern, check out this previous case from ems12lead.com.
What about the ST depression in the inferior leads? Let's take a look:
Could this be attributed to Strain pattern? Strain pattern can manifest itself in the inferior leads, but according to Dr, Smith of Dr. Smith's ECG Blog, "usually you can tell because the voltage will be high in the limb leads, as usually measured in aVL". That was not the case here, so I think the ST depression in the inferior leads looks to be very suspicious.
Another thought proposed about this was the possibility of "Dig Effect". Here is an example of what Dig effect looks like (note the "scooped" appearance of the ST segment):
In our patient, I see flatter, downward sloping ST depression, but the baseline is wandering somewhat and it's not an easy call. It's hard to argue if you had it on your list of differentials though, especially with the history of AF.
So what do we have? A patient who seems to have ACS with an ECG that looks like Strain pattern, but also has concerning ST depression in the inferior leads. In the comments section of this case, I think VinceD summed it up best when he said: "We'd have to watch her like a hawk and worry about worst first with this clinical picture. She doesn't qualify for urgent PCI (at the moment)…" At the moment is the key.
That is precisely the same take the crew had, and they decided to watch her like a hawk and do serial ECG's… Once again, here was the clinching ECG acquired moments from the community hospital:
In less than twenty minutes, you can see the side by side changes here:
We can see the ST elevation increased in V2 and V3 from approximately 1mm to approximately 3mm, and in V4 the increase was from about isolectric to an astounding 5mm! In addition, the ST depression in the inferior leads increased by about 1mm. Indeed, they were born out to be reciprocal changes. Keep in mind it took less than 20 minutes for these changes to be recorded on the 12 leads.
The key to this case was the serial 12 leads done by the crew. While I don't think anyone could find fault with the cath lab not being activated after the first 12 lead, it was too late to send her directly to the cath lab by the time the last one, which revealed the STEMI, was acquired. The cath lab was activated as soon as possible, and ground transportation to it was dispatched immediately. Unfortunately an unavoidable delay still occured. A D2B time of <90 minutes could not be achieved.
Although the STEMI was recognized, this case does not have a happy ending. The bloodwork showed a highly elevated Troponins (exact value unknown), but upon arrival at the cath lab, for reasons unknown, she refused all treatments.
Key Learning Points:
1- Know your morphologies and differentials. It helps you get a better patient history, and helps you figure out what's going on with the ECG.
2- In the words of Dr. Corey Slovis: "One ECG begets another"… DO SERIAL ECG'S! And, espcially if the patient's presentation changes, get another 12 lead. Many STEMI's are missed because serial 12 leads are not done. One ECG is a snapshot in time. Like one set of vitals. But they are also dynamic, and as we've seen in this case and others on this blog, they can change dramatically in very short periods of time.
Thanks for all the comments! I’m not allowed to blog while I’m on duty (the policy has nothing to do with me personally) so if it seems like I’m not responding, I’m probably just at work.
The paramedic who submitted this case has requested the follow-up information from his supervisor, but unfortunately she’s out-of-town for the next 2 weeks.
In the meantime, we can lay out the issues.
Obviously, this is a scary looking ECG because there is significant ST-elevation in the precordial leads.
However, this ECG also meets the voltage criteria for LVH.
Could it be a strain pattern (typical secondary repolarization abnormality)?
It’s difficult to tell with the wandering baseline throughout this ECG, but if you line up the point at which the PR-segment hits the QRS complex in leads V1, V2, and V3 you can see that each of these leads shows approximately 4 mm of ST-elevation.
You will recall that with a “strain pattern” the degree of ST-elevation is proportional to the depth of the S-wave in the opposite direction! So the lead with the deepest S-wave should have the most significant ST-T wave abnormality in the opposite direction.
It’s not easy to tell the exact depth of the S-wave because the complexes are running together, but these measurements are probably fairly close.
There’s no way that a typical strain pattern would show the same amount of ST-elevation in one lead with S-waves that are 22.5 mm deep and another with S-waves that are only 6 mm deep.
Here’s the most disturbing finding, in my opinion.
There appears to be reciprocal behavior between the inferior leads and the high lateral leads.
So, if this is a STEMI mimic (for example, benign early repolarization superimposed on top of left ventricular hypertrophy) it’s a darned good one! I wouldn’t blame any paramedic for calling in a STEMI Alert for this patient.
So what should the hospital do when they are in receipt of a patient like this? I asked Stephen Smith MD from Dr. Smith’s ECG Blog and here’s what he said.
“If I were the ED physician, I would aggressively treat the blood pressure with NTG (up to 250 mcg/min or even higher) until the BP came way down. I would do a bedside cardiac ultrasound and look for anterior wall motion. If pain did not go away, and echo did not definitely show good wall motion, I would activate the cath lab.”
It’s always nice to get Dr. Smith’s perspective! I’ve learned a lot from his blog over the past 2 years. If you’re not familiar with his website you should take the time to check it out! His case studies are top notch!
Hopefully we’ll have the outcome in about 2 weeks.
Thank you for all of the excellent comments on this case! I was delighted to see such a high level dialog when I checked my blog this morning.
Normally I would to answer each of you individually, but since there are 22 comments (so far) I thought I would try a different strategy and post the answer, along with tips for the correct interpretation of this ECG (at least in the context of “STEMI / not a STEMI” while you are out in the field).
This was not a STEMI.
It was most likely left ventricular hypertrophy with a strain pattern and mild hyperkalemia.
First, let’s look at the 12-lead ECG and make the case for LVH.
You’ll recall from my previous posts on the topic that I’ve said it’s more important to recognize the so-called “strain pattern” than the voltage criteria.
The reason is simple.
If the “strain pattern” isn’t causing a problem (mimicking an acute anterior STEMI) then you’re waisting your time calculating the QRS voltage.
This ECG has the general appearance of “T-wave discordance”. In other words, the T-waves are deflected opposite the main deflection of the QRS complex, which is highly suggestive of a secondary ST-T wave abnormality.
In this case, the most likey cause is left ventricular hypertrophy.
I say “generally appearance of T-wave discordance” because it’s not true in every lead. That’s why I mentioned in a previous post that there are “some caveats”.
When I’m looking for appropriate T-wave discordance, I mentally remove isoelectric or equiphasic leads, particularly in the transition zone (the point at which a QRS goes from mostly negative to mostly positive in the precordial leads).
Let’s circle the leads I would mentally remove from this 12-lead ECG to decide whether or not “T-wave discordance” is present.
With those leads removed, are the T-wave deflected opposite the QRS complexes?
Could that be a coincidence?
The high lateral leads in particular are showing a very typical looking strain pattern.
This can be a problem because it could easily be mistaken for “lateral ischemia” or reciprocal changes secondary to acute STEMI!
Does this ECG meet the voltage criteria for LVH?
Not exactly, but I believe we can make the case using the Romhilt-Estes point scoring system. This ECG would get at least a 4 (probable LVH), and it’s right on the borderline for left atrial enlargement and delayed intrinsicoid deflection in leads V5 and V6 which would give it a score of 5 or 6.
But I don’t think that’s important.
The next question we want to ask is, is the degree of the secondary ST-T wave abnormality proportional to the amplitude of the QRS complex in the opposite direction?
The answer is yes.
Remember, we’re looking at the ST-segments and the T-waves together.
At first glance it looks like there might be more ST-elevation in lead V1 than lead V2. However, I believe this is an optical illusion created by the biphasic P-waves in lead V1, as well as the more defined (less diffuse) J-points in lead V1.
Let’s blow this up a little bit.
When we use the TP-segments as a baseline, we can see that it’s debatable as to whether or not lead V1 shows more ST-elevation, but it’s obvious that lead V2 shows a more pronounced ST-T wave abnormality.
The T-waves seem a little bit narrower than we might have expected with LVH, perhaps with a slightly later take-off. Also, the QTc is well within “normal” at 419 ms.
I don’t have the exact lab value, but the feedback I received on this case was that the patient had a potassium level that was “on the high end of mild hyperkalemia” (so I’m guessing between a 6 and 7).
Consider the following graphic that compares the T-waves of hyperkalemia to the T-waves of acute anterior STEMI.
There isn’t much documentation out there as to what hyperkalemia is supposed to look like in the presence of a secondary ST-T wave abnormality, but you’ll notice that with hyperkalemia, the T-waves are narrow and have a late take-off, while with acute anterior STEMI, the T-waves are more “broad-based”.
This was a very difficult case. So what can we learn from it?
In my mind, it’s very simple (and it needs to be simple for field use — complicated equations involving calipers are not simple).
T-wave discordance strongly suggests the possibility of a secondary ST-T wave abnormality. That being the case, I would wait for changes on serially obtained ECGs before calling a STEMI Alert.
Remember, in some studies LVH is the most common cause of ST-elevation in chest pain patients, so we need a solid strategy to deal with this STE-mimic!
I hope we can continue our useful discussion about this ECG! I look forward to reading more of your comments.
A 41 year old male is pulled over during morning rush-hour by sheriff’s deputies.
He states that he is on his way to the hospital because he is having chest pain. EMS is called to the scene.
The patient is awake, alert, and oriented to person, place, time, and event.
His skin is pink, warm, and moist.
He appears acutely ill and anxious.
He states that he has a history of high blood pressure and renal insufficiency. He takes several medications, but he can only recall that one of them is a beta blocker.
Onset: 1 hour ago while sleeping.
Provoke: Nothing makes the pain better or worse.
Quality: Patient describes the pain as a poorly localized “fullness” or “pressure”.
Radiate: The patient cannot tell whether or not the pain radiates.
Severity: The patient reluctantly gives the pain a 7/10.
Time: The patient states he has had the pain on several occasions over the past few months but did not seek medical treatment.
Vital signs are assessed.
SpO2: 99 on RA
The cardiac monitor is attached.
A 12-lead ECG is captured.
What is your analysis of this ECG?
Does anything about it concern you?
Is this a STEMI?
Why or why not?
Note: This 12-lead ECG was captured in the back of an ambulance with the motor and generator running, but it shows excellent data quality.
This is an awesome PowerPoint presentation from one of my favorite ECG textbooks, 12-Lead ECG – The Art of Interpretation.
You owe it to yourself to purchase this book (and no, they don’t pay me to say that).
Make sure you use “full screen” so you can see all of the features of this important presentation. Pay special attention to slides 33-47!
Slide 45 shows a strain pattern from left ventricular hypertrophy (LVH).
Slide 47 shows a split screen with a strain pattern from right ventricular hypertrophy (RVH) on the left and acute infero-posterior STEMI on the right.
This is the book that taught me how to recognize strain patterns! So pay attention because this is one of the most important STEMI mimics!
I know I promised to go over the voltage criteria for left ventricular hypertrophy (LVH) but I lied!
Personally? I think it’s a distraction. As far as STEMI recognition goes, it misses the point entirely!
The ECG will either show a so-called “strain pattern” (or repolarization abnormality) or it will not! If it does, there’s a chance it will mimic an acute anterior STEMI.
Just because the voltage criteria for LVH is satisfied on a particular ECG does not mean that a secondary ST-T wave abnormality will be present! Even if it is, it will not necessarily mimic acute anterior STEMI.
What I’m trying to say (again) is this:
It’s far more important to recognize a strain pattern than it is to calculate the voltage criteria for left ventricular hypertrophy on a 12-lead ECG!
Having said that, I do know most of the voltage criteria for left ventricular hypertrophy, so I’m not trying to discourage you from learning. I just want to put it in context!
Let’s look at a couple of examples courtesy of my friend Tom Bernesser who is a paramedic in North Carolina. Both of these ECGs are actual “false positives” from North Carolina’s RACE program.
That means they presented with signs and symptoms consistent with ACS, acute STEMI was identified on the prehospital 12-lead ECG (including the computerized interpretive statement), the paramedic and the ED physician agreed the patient satisfied the reperfusion criteria, the patient was fast-tracked to the cardiac cath lab, and no culprit artery was found.
This is an atypical “strain pattern” with many typical features.
I suspect the possibility that leads V1 and V2 might have been accidentally transposed but that doesn’t really matter. For the purposes of STEMI recognition, the typical features outweigh the atypical features.
In the first place, you should immediately notice the “widened QRS-T angle” that is the hallmark of a secondary repolarization abnormality. You will notice the same finding for LBBB and paced rhythm!
Importantly, the degree of the secondary ST-T abnormality is, generally speaking (there are some caveats), proportional to the size (or amplitude) of the QRS complex in the opposite direction!
If you take nothing else away from this post, please learn this “trick”.
It’s really no different from the concept I demonstrated in the post called Wolff-Parkinson-White (WPW) – STEMI Mimic.
Herein lies a problem with prehospital 12-lead ECGs!
With left ventricular hypertrophy (LVH) the QRS complexes are often “cut off” at the top or bottom or they run together with other QRS complexes which can create the illusion that the QRS complexes are smaller, so you have to train your eye!
Take a look at this ECG and find the most severe ST-T wave abnormality.
That’s easy! Lead I clearly shows the most pronounced ST-T wave abnormality. The ST-segment is depressed, downwardly concave, and shows a deep inverted T-wave.
Does the amplitude of the R-wave in the opposite direction explain it? No way! It’s even smaller than the QRS complex in lead II, and the ST-T wave abnormality in lead II isn’t nearly as severe!
What is the second-worse ST-T wave abnormality? Lead V3! Does the depth of the S-wave in the opposite direction explain it? Not really.
But wait! Are we certain we’re getting an accurate “read” on the amplitude of the R-wave in lead I and the depth of the S-wave in lead V3?
I’m not so sure!
I suspect the possibility that the computer is “cropping” the QRS complexes to fit them on the ECG paper. See the little horizontal line that marks the “top” and “bottom” of these QRS complexes?
I’ve seen it many times before!
So ask yourself this question:
Generally speaking, does there seem to be a relationship between the QRS-complex and the degree of ST-elevation or depression in the opposite direction?
If the answer is “Yes!” then don’t call the STEMI Alert. Instead, perform serial ECGs and look for changing ST-segments and T-waves! ST-segments and T-waves shouldn’t “evolve” or change over time if it’s a simple secondary ST-T wave abnormality!
Using the new “trick” you have learned, what do you think of this ECG?
More discussion to follow.
Left Ventricular Hypertrophy May Result In Profound ST Elevation – Dr. Smith’s ECG Blog
If you’ve been following the Prehospital 12-Lead ECG blog for a while, you know that I’m advocate of using Sgarbossa’s criteria to help identify acute STEMI in the presence of left bundle branch block (LBBB) or paced rhythm.
According the Sgarbossa’s original criteria, 5 mm of discordant ST-segment elevation is required to identify AMI in the presence of LBBB.
Why 5 mm when normally we require only 1 or 2 mm of ST-elevation?
Because in the setting of left bundle branch block or paced rhythm, it’s normal for the ST-segment and T-wave to be defected opposite the main deflection of the QRS complex!
That’s why it’s necessary to consider the depth of the QRS complex when examining the amount of discordant ST-segment elevation. The deeper the S-wave, the greater the secondary ST-T wave abnormality in the opposite direction!
In the original article I wrote on the topic, I showed this example 12-lead ECG to show why the 5 mm criterion is problematic.
As you can see, this 12-lead ECG shows sinus rhythm with left bundle branch block and > 5 mm of discordant (opposite the QRS complex) ST-elevation in leads V1, V2, and V3 (the right precordial leads). The T-wave are huge!
The problem is, this patient was not experiencing acute myocardial infarction. The ST-segments are elevated > 5 mm because the S-waves are extremely deep (off the bottom of the ECG paper for leads V2 and V3).
Had we used the modified criterion of discordant ST-elevation that is = or > to 0.2 the QRS complex (ST/QRS ratio) we would have seen that in lead V1 the S-wave is 50 mm deep. Thus, we would require at least 12.5 mm of ST-segment elevation to consider this finding positive for acute STEMI.
(Credit to Dr. Smith’s ECG Blog)
There’s another way the modified criterion can help you!
Consider this 12-lead ECG that shows a ventricular paced rhythm. It’s been in my collection for many years, and I regret that I no longer recall where it came from.
This ECG does not meet Sgarbossa’s criteria for diagnosing AMI in the presence of LBBB. With the exception of lead V6, the paced QRS complexes show appropriate T-wave discordance, and none of the ST-segments are elevated to 5 mm or more.
But wait! The ST-segments are elevated far greater than 0.25 the depth of the QRS complex in leads II, III, and aVF! This patient is experiencing acute inferior STEMI!
The intrinsic QRS complex in the right precordial leads also shows an > R/S ratio in lead V1 and V2 and ST-segment depression suggesting posterior extension, which clinches the diagnosis.
So remember, when using Sgarbossa’s criteria, huge QRS complexes can cause false positive and tiny QRS complexes can cause false negatives, unless you use the modified rule that considers ST-segment elevation as a percentage of the QRS complex!
Found on the Lifenet Receiving Station (LBBB with concordant ST-depression in leads V3 and V4)
62 year old male CC: Chest pain (LBBB with ST-elevation > 0.2 the QRS complex)
58 year old female CC: Chest pain – Conclusion (meets all 3 of Sgarbossa’s criteria)
STEMI best seen in PVC (Dr. Smith’s ECG Blog)
A really interesting 12-Lead ECG was posted to the Cardiology & Electrocardiography (ECG, EKG) Experts group on Facebook the other day.
If you’re not familiar, this is one of the groups / fan pages on Facebook I help moderate with Jason Winter who also started the Cardiology & Electrocardiography Experts blog.
What’s so interesting about this ECG is that it shows a relatively infrequent STEMI mimic. In addition, it helps demonstrate a point I’ve been pondering about several of the STEMI mimics in general.
Let’s take a look.
The patient was a 29 year old male with no complaints. The ECG was captured during a routine workup according to the contributor Chris de Beer (thanks again for the interesting ECG, Chris).
The ECG shows a WPW pattern as evidenced by a short PR interval and delta waves. The delta waves create a pseudo-infarct pattern (Q-waves) in the septal leads.
You might recall from my previous post about left ventricular hypertrophy (LVH) that I think recognizing the so-called “strain pattern” is actually more important than knowing the “voltage criteria” for LVH.
I’m sure some of you are waiting for “Part II” of the left ventricular hypertrophy series, but I’m still waiting for inspiration!
What does this ECG have in common with a strain pattern from left ventricular hypertrophy (LVH)? What does it have in common with left bundle branch block (LBBB)? What does it have in common with ventricular rhythms? Including paced rhythms?
The answer is, it has a widened QRS-T angle! To put it another way, the T-waves and ST-segments are deflected opposite the main deflection of the QRS complex, and (this point is the most critical) the degree of the ST-T abnormality is proportional to the size of the QRS complex.
Think of this as a supplement to Sgarbossa’s criteria and the “rule of appropriate T-wave (and ST-segment) discordance”.
Here’s a graphic to help illustrate the point.
When you see a pattern like this, regardless of cause, it should set off alarm bells that you are dealing with a STE-mimic and not acute STEMI!
Note that the S-wave in lead V3 is cut off by the bottom of the ECG paper. This is a common problem with prehospital 12-lead ECGs! We must presume that the S-wave would be the deepest in lead V3 if we were able to view the entire QRS complex.
That doesn’t mean the patient isn’t experiencing acute myocardial infarction (although this patient is asymptomatic so let’s pretend he was over the age of 30 and complaining of chest discomfort).
It just means you should wait before pulling the trigger on the cardiac cath lab.
Look for changes on serially obtained ECGs instead!
Here’s an interesting PowerPoint presentation that corresponds to a previous post.
I found slide 14 to be particularly interesting.
This is a topic that doesn’t get enough attention. Often the quarterly STEMI meetings go over the success stories but not the failures. It’s often said that if you don’t have any false positives you aren’t trying hard enough.
I don’t disagree, but they should be reported, and the ECGs should be analyzed for teaching points. Hindsight is 20/20 and I understand that, but very few 12-lead ECGs are more interesting than those that caused a false positive cardiac cath lab activation.
Find them, scan them, and post them! I can’t think of a better educational tool than an archive of STE-mimics that actually led to a patient being emergenty cathed!
Speaking of false positive cardiac cath lab activations, read these comments by Sameer Mehta, MD, FACC, MBA in the Cath Lab Digest.
He says in part:
I cautioned against complacency towards proceeding with emergent cath/percutaneous coronary intervention (PCI), citing precisely the high false alarms that have been mentioned in this outstanding study reported by Dr. David Larson. By the American College of Cardiology (ACC)/American Heart Association (AHA) criteria for primary stenting, the rates for these ‘false alarms’ should be less than 15%. By this standard, the 14% of the false alarms cited by Dr. Larson at the Minneapolis Heart Institute Foundation at Abbott Northwestern Hospital is quite acceptable. Yet the authors have creditably deemed these rates as unacceptably high. The reader must also be made aware that the Minneapolis experience, with its Spoke and Wheel, pharmaco-invasive model of triage for primary PCI is one of the most advanced programs in the world, and one that has established superb guidelines and pathways for very effective triage for STEMI patients. I emphasize the excellent caliber of the work at Minneapolis Heart Institute since their high false alarm rates may actually be some of the lowest in the nation, and that the problems of these false alarms may be much higher at other institutions, in particular, at low-volume STEMI institutions…
There are several ways for individual institutions to get their arms around this burgeoning problem. It is obvious that the emergency department (ED) physicians are under great stress to diagnose STEMI – they have to be very accurate and very fast. It is a new responsibility that has been assigned to them quite rapidly…
[S]everal contributing authors as well as I have strongly emphasized the need to monitor the false alarm rates. We have declared these rates to be the best parameters of measuring the efficacy of a STEMI program…
[A]dministrations and medical staff must mandate high caliber for ED physicians that would participate in STEMI programs. Rigorous training in EKG interpretation is the cornerstone of this new role and continuous quality improvement (CQI) processes must be rigid in this assurance. To be perfectly candid, if any institution cannot provide such quality ED physicians, it has no business in declaring its ability to perform 24/7 STEMI interventions. In a situation where the high accuracy of the ED physician cannot be ensured, the institution must seriously consider to reverting to the time-tested method of the cardiologist evaluating the presenting EKG.
In STEMI Interventions: Managing the Chaos (transcript in .pdf) found at theheart.org, Tim Henry, MD gives a different perspective:
[E]ven the issue of false-positives is of some debate. For instance, Dr. Dave Larson who works with me had a very nice paper in JAMA a year ago that looked at this. We found that 14% of our patients don’t have a clear culprit artery, but of those patients, there are about 40% who have positive enzymes. So there are other things that cause acute STEMI that are not necessarily related in need PCI. For instance, you can have spasm, you can have thrombus that resolves, and you can have stress cardiomyopathy. There are a variety of things that can do it. So if your patient has true ST-elevation and positive enzymes it’s hard to call that a false positive. So, I just think that what you do is a true false-positive rate, using it with ED and paramedic activating the cath lab is really between 6% to 8%, which we certainly think is acceptable.
It’s an interesting debate, and one I think we’re going to be hearing more about as D2B times below 90 minutes become commonplace in the wake of the D2B Alliance and AHA Mission: Lifeline.
One of the most confusing ST-elevation mimics for paramedics is the “strain pattern” (or repolarization abnormality) occasionally found with left ventricular hypertrophy.
This is important because left ventricular hypertrophy is one of the most common causes of ST segment elevation in chest pain patients.
Many 12 lead ECG classes teach paramedics to recognize the voltage criteria for LVH (or at least one of the voltage criteria) but I don’t think most 12 lead ECG classes do an adequate job explaining exactly what a “strain pattern” looks like.
As a result, once the student identifies the voltage criteria for LVH, the interpretation stops. Similarly, once the student identifies the presence of “wide” QRS complexes, the interpretation often stops.
It’s as if we’re teaching students that it’s impossible to identify STEMI in the presence of baseline abnormalities.
It’s more difficult, but it’s certainly not impossible. The whole point is to know what a “normal” abnormality looks like. This is not an oxymoron! It’s the key to advanced 12 lead ECG interpretation.
In many cases, an ECG can meet the voltage criteria for LVH but show only minimal distortion of the ST segments and T waves. In other cases, the ECG will show the characteristic ST segment depression and T wave inversion in the lateral leads, but not the exaggerated ST segment elevation and T wave prominence in the right precordial leads.
Let’s look at some examples. Let us assume that we are dealing with a patient complaining of chest discomfort.
This is exactly the kind of ECG that gives paramedics a lot of trouble. It demonstrates a strain pattern (or repolarization abnormality) with left ventricular hypertrophy. The good news is that it’s a very typical looking strain pattern!
Since this 12 lead ECG is not in the standard U.S. format, I used “cut” and “paste” to structure it into a pattern more typical of prehospital 12 lead ECGs in the U.S.
In the first place, you will notice that the rhythm is sinus at about 75 beats per minute (using the large block method).
The frontal plane axis is probably around 30 degrees (40 degrees if you correct by 10 degrees due to the fact that lead III is slightly positive). This is important because a common misconception is that left axis deviation will be present with left ventricular hypertrophy. By no means is this always the case!
The QRS width is less than 120 ms, so we know that we’re not dealing with a bundle branch block.
What about the ST segment elevation and huge T waves in the right precordial leads! Surely this patient is experiencing acute anterior STEMI!
Negative, ghostrider! (For my international friends, this is a reference to the movie Top Gun).
Let’s look at the relationship between the QRS complex and the T waves in this ECG. The general pattern is one of discordance. In other words, When the QRS complex is positive (especially in the lateral leads I, aVL, V5 and V6) the T wave is negative. This is sometimes referred to as a widened QRS/T angle.
In addition, the ST segments are downwardly concave and the T waves are asymmetrical.
These are the cardinal findings with strain patterns (or repolarization abnormalities) secondary to left ventricular hypertrophy.
This ECG also shows ST segment elevation in the right precordial leads (V1, V2 and V3). You will note that the ST segments are upwardly concave and the severity of the ST segment elevation and T wave height is proportional to the depth of the S wave.
This is extremely important! With left ventricular hypertrophy, the deeper the QRS complex, the higher the ST segment and more pronounced the T wave abnormality.
This is also true of the ST segment depression and T wave inversion typically found in the lateral leads. The higher the R wave, the deeper the ST segment depression and more pronounced the inverted T wave.
Consider the following graphics to illustrate the point.
The most pronounced ST/T wave abnormality is found in lead V2. It’s difficult to tell because the QRS complexes run into one another, but the S wave is extremely deep in lead V2, possibly as deep as 35 mm (blue arrows). With LVH, you should expect the lead with the deepest S wave to show the most ST segment elevation and/or T wave height!
The red curve shows the upward concavity of the ST segment, which is another common finding with LVH. I have seen upwardly convex ST segments with LVH, but it’s rare, and it always makes me suspicious of acute anterior STEMI!
I’ve outlined the shape of the T wave with orange lines. You can see that the T waves are asymmetrical, another finding consistent with a “strain pattern” or depolarization abnormality with LVH.
In the left precordial leads, the most most pronounced ST/T wave abnormality is found in lead V5. Again, it’s difficult to discern because the QRS complexes run into one another (as they often do with LVH) but the height of the R wave may be as high as 30 or even 40 mm (blue arrows).
The red curve shows the downwardly concave ST segment depression (exactly opposite the right precordial leads).
I have outlined the T wave inversion with orange lines to show the asymmetry. Again, a common finding with “strain patterns” or depolarization abnormalities with LVH.
In Part II, we’ll review the voltage criteria for left ventricular hypertrophy.
ECG Challenges from AACN Advanced Critical Care (links to article about STEMI mimics)
Mimics of acute STEMI (left ventricular aneurysm)
In it, he observes:
When we take a class in STEMI recognition, the ECGs, once you know how to read them, are all pretty clear cut. You can flash the 12-leads on the screen and a well-taught class will call out in unision “Inferior, Anterior, Anterior, Inferior, Lateral,” etc. You get tricky and you throw in the ST imposters, but they catch on. “Left Bundle, Right Bundle, LVH, Inferior, Anterior, Left Bundle,” etc.
The problem is when you get back on the street not all 12-leads are so cut and dried…
I couldn’t have said it better myself.
Unfortunately, a lot of paramedics feel so good about themselves after taking a basic 12 lead ECG STEMI recognition class that they buy into the mindset that paramedics can interpret an ECG as good as a physician.
In 99% of cases, it simply isn’t true. Not because paramedics can’t be taught to read an ECG as good as a physician, but because paramedics aren’t taught to read an ECG as good as a physician.
Peter goes on to discuss a recent article published in the American Journal of Cardiology that essentially shows that interpretation of ST segment elevation on the 12 lead ECG can be difficult, even for cardiologists.
This finding is not surprising. I have written about the problem of ST segment elevation in a previous post.
Peter goes on to quote the study’s “bottom line”:
This study’s findings reflect the diagnostic limitations encountered by cardiologists when the ECG is used as the sole diagnostic tool for STEMI. If experienced readers, using the current criteria and guidelines, cannot accurately and consistently distinguish between STEMI and NISTE, less-experienced readers cannot be expected to do so.
And then adds
So take heart, paramedics, we aren’t expected to be seers. Just do the best you can to identify what you can. Cast a wide net when you do your 12-leads. Do serial 12-leads. One that is not obvious can soon grow into a not subtle one. Call the obvious ones, and bring attention to the possible ones. Evaluate based on patient presentation and ECG.
I am mostly in agreement, especially with regard to performing serial 12 lead ECGs. However, while we may not be expected to “be seers” in all situations, we can “be seers” in most situations.
With the proper training.
Tomas Garcia MD, author of “12 Lead ECG – The Art of Interpretation” once told me the most common reason cardiologists fail their board exams is ECG interpretation.
ECG interpretation can be difficult. Admitting that is the first step to developing real expertise. It’s sort of the same as tracheal intubation in this regard. Just because you can intubate a patient with typical anatomy doesn’t mean you can handle a difficult airway.
Just because you can identify a homerun STEMI after an 8-hour introduction to 12 lead ECG class doesn’t mean you’re going to pick up on ventricular aneurysm.
There are always going to be false positive cardiac cath lab activations. If it never happens, you’re not being aggressive enough. If it happens too often, you’re being too aggressive.
Can you be taught to identify the mimics of acute STEMI?
Can you be taught to identify acute STEMI in the presence of baseline abnormalities that mimic acute STEMI?
It’s difficult but it’s not impossible.
*** Update 02/16/09 ***
Peter had posted this ECG from the study and reported that only 5 out of 15 experienced ECG interpreters called it correctly.
In the comments he reports:
5 out of 15 experts correctly said this was a STEMI.
“A 57-year-old man with chest pain. There were QS waves in V1–V2. There was mild STE in V1–V2. There was terminal T-wave inversion V2–V6. There was T-wave inversion in I and aVL. Peak troponin I 26.84 ng/ml. Peak CKMB 29.6 ng/ml. Coronary angiography showed proximal left main stenosis 40%, proximal left anterior descending artery stenosis 95%, left circumflex artery 60%. The patient underwent PPCI of his proximal left anterior descending artery. STEMI was diagnosed by 5/15 readers (33%).”
I had guessed the ECG showed left ventricular aneurysm.
Consider this ECG from Brady WJ, ST Segment and T Wave Abnormalities Not Caused by Acute Coronary Syndromes. Emerg Med Clin N Am 24 (2006) 91-111.
As I noted in the comments, ventricular aneurysm is a difficult mimic because it’s not really a mimic at all. It’s an “old” MI with persistent ECG abnormalities.
It would be interesting to know if an acute thrombosis was found during intervention, of if this was one of those patients for whom chronic atherosclerosis finally became so occlusive that it caused cardiac injury.
My guess is that the ECG didn’t look a whole lot different after stenting.
By the way, Stephen Smith from Dr. Smith’s ECG Blog has as a decision rule to help you distinguish between acute anterior STEMI and left ventricular aneurysm (of course he does)!
Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. Am J of Emerg Med 2005 May; 23(3):279-287
ECG Challenges from AACN Advanced Critical Care (links to article about STEMI mimics)
41 year old male CC: Chest pain (looks like BER, proves to be acute STEMI)
23 year old male CC: Chest pain (benign early repolarization)
In this excellent article from the March 2007 Journal of the Emergency Medical Services, Tim Phalen discusses the importance of performing serial 12 lead ECGs.
Here are some of the highlights.
“Acute myocardial infarctions (AMIs) aren’t like broken bones and, therefore, ECGs aren’t static like X-rays. If an EMS crew were treating a hip fracture and could somehow perform the X-ray on scene, what would it show? A broken hip, of course. And if the X-ray wasn’t performed until the patient arrived at the emergency department (ED), would the broken hip still be visible?
When dealing with a fracture, whether the X-ray is obtained immediately, in 10 minutes or in 10 hours, the interpretation and diagnosis usually won’t change. But what’s true for X-rays isn’t necessarily true for ECGs. In fact, an ECG can significantly change in a very sort period of time — as can the corresponding interpretation.”
“[I]t can be difficult to determine if the presence of LBBB on the ECG of a suspected AMI patient is preexisting or is a new onset. If the LBBB is infarct-induced, it has a high mortality rate — up to 60%. Therefore, the patients who may need reperfusion the most are the least likely to receive it. However, dynamic changes on serial ECGs shed light on the situation. A hallmark of infarct is change over time. If a patient has had an LBBB for the past 15 years, it’s not likely to change much during the next 15 minutes. But when changes occur in a short period of time, suspect AMI.”
Those are some excellent points.
It’s also helpful to understand the expected appearance of baseline abnormalities. For example, the rule of “appropriate T-wave discordance” states that with bundle branch blocks and paced rhythms, the T-wave should be deflected opposite the terminal deflection of the QRS complex. So LBBB is an abnormal finding, but discordant T-waves (and ST-segments) within the context of LBBB are a normal finding (to a point).
On the other hand, while baseline abnormalities like LBBB or paced rhythm may cause a discordant shift of the ST-segment and T-wave, the ST-segment should not be moving! A moving ST-segment suggests dynamic changes in supply v. demand characteristics.
In other words, ischemia.
The criterion seems quite simple.
In the absence of contraindications, reperfusion therapy should be administered to patients with symptom onset within the prior 12 hours and ST elevation greater than 0.1 mV (1 mm) in at least 2 contiguous precordial leads or at least 2 adjacent limb leads, or new or presumably new LBBB on the presenting ECG.
However, as I noted in the electrocardiogram section of the myocardial infarction article in the English Wikipedia (I used to edit the Wikipedia quite often, but I probably won’t anymore since I have a blog):
This criterion is problematic [...] acute myocardial infarction is not the most common cause of ST segment elevation in chest pain patients. Over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead. The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm.
Brady et al. said it best in Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians (Acad Emerg Med 2001; 8(4):349-360):
“ST segment elevation is perhaps the “most demanding” of the electrocardiographic features seen in the chest pain patient; it is “demanding” in that its presence must be explained and, if the etiology involves AMI, urgent therapeutic decisions must be made. Unfortunately, STE is a not uncommon finding on the ECG of the chest pain patient; its cause infrequently involves AMI.”
Think about that. Its cause infrequently involves AMI.
How infrequently? In Cause of ST segment abnormality in ED chest pain patients (Am J Emerg Med 2001 Jan;19(1):25-8) Brady et al. performed a retrospective ECG review of adult chest pain patients in a university hospital emergency department (ED) over a 3-month period.
ST segment elevation was determined if the ST segment was elevated >1 mm in the limb leads or >2 mm in the precordial leads (in at least two anatomically contiguous leads).
902 patients were enrolled in the study. Of those, 202 patients (22.4%) had ST segment elevation on their initial 12 lead ECG. Of those, only 31 patients (15%) had a discharge diagnosis of STEMI. In other words, 171 patients (85%) had a non-AMI cause of ST segment elevation on their initial 12 lead ECG.
So what were the other causes of ST segment elevation?
Left ventricular hypertrophy (LVH) – 51 cases (25%)
Left bundle branch block (LBBB) – 31 cases (15%)
Benign early repolarization (BER) – 25 cases (12%)
Right bundle branch block (RBBB) – 10 cases (5%)
Nonspecific BBB – 10 cases (5%)
Ventricular Aneurysm – 5 cases (3%)
Pericarditis – 2 cases (1%)
Undefined or unknown cause – 35 cases (17%)
44 patients had AMI as the final diagnosis of whom 31 showed ST segment elevation on presentation to the ED. In 2 of 31 (6%) cases of STEMI, the ST segment waveform was atypical for acute infarction.
“AMI is not the most common cause of ST elevation in ED chest pain patients. LVH is most often responsible for electrocardiographic STE followed by AMI and LBBB which occur at equal frequencies.”
As a side note, I find it a bit unusual that paced rhythms are not mentioned (unless they fell into the nonspecific BBB category for some reason). It also seems strange that RBBB is listed as a cause of ST segment elevation. In my experience RBBB does not distort the ST segment the way LBBB does. That’s not to say that it’s always easy to identify STEMI in the setting of RBBB, just like it’s not always easy to identify STEMI in the absence of bundle branch block.
*** Update 12/20/08: I recently saw an ECG with sinus tachycardia and RBBB that appeared to show ST segment elevation. The patient was emergently cathed and no culprit artery was found. The absence of a well defined TP segment as a baseline for comparison was a confounding factor. ***
Regardless, the message is clear. It’s not enough to discover ST segment elevation on the 12 lead ECG of a chest pain patient. A monkey could do that. We need to specifically discover the ST elevation of AMI.
Consider Sejersten et al. Comparison of the Ability of Paramedics With That of Cardiologists in Diagnosing ST-Segment Elevation Acute Myocardial Infarction in Patients With Acute Chest Pain (Am J Cardiol 2002 Nov 1;90(9):995-8):
“Paramedics diagnosed over half of patients as having ST elevation AMI, when in fact they did not. One reason for this may be that the paramedics were concerned about missing patients with this condition. The number of false-positive diagnoses may also have been increased due to the problem of differentiating ST elevation AMI from other electrocardiographic abnormalities that result in ST-segment elevation…”
“The paramedics’ diagnosis of ST elevation AMI was confirmed in 55 patients (45.5%) by acute angiography. In an additional 4 patients (3.5%) who did not undergo angiography due to high-risk assessment or other causes, the diagnosis was confirmed clinically by typical electrocardiographic changes in evolving ST elevation AMI accompanied by transient elevation of creatine kinase-MB. Thus, the paramedics’ true positive rate was 49% (n = 59). The paramedics’ decision was not confirmed in the 23 patients (19%) with no thrombus at angiography, and in the 38 (31%) who did not undergo coronary angiography because the attending cardiologist judged them not to have an evolving ST elevation AMI [...] The false-positive rate by paramedics was 51% (n = 62)…”
The authors also observe:
“The incidence of poor quality ECGs recorded by the paramedics was calculated to determine the paramedics’ performance in electrocardiographic acquisition. In 13 of 124 patients (10.5%), the ECGs were characterized as poor quality…“
Amazingly, they refer to this as “acceptable.” I guess their standards are low! They’re either satisfied with the care of 1 in 10 patients being compromised by poor data quality, or they think that’s all EMS is capable of.
“This study concludes that paramedics’ true-positive rate of ST elevation AMI diagnosis is high in patients presenting without confounding factors, but decreases when the ECG has confounding factors. This is in contrast to an experienced cardiologist whose true-positive rate was high and not affected by confounding factors. The results demonstrate that before implementation of electrocardiographic transmission directly to a cardiologist’s handheld device, there is a need to provide education and training to paramedics responsible for acquiring and interpreting prehospital ECGs, with special emphasis on confounders…“
To all the paramedics out there who feel offended that they’re being asked to transmit the 12 lead ECG to the emergency department for physician interpretation, do you know how to identify all of the mimics of acute myocardial infarction? Do you know how to identify acute myocardial infarction in the presence of baseline abnormalities?
We’ve been taught that identifying acute STEMI on the 12-lead ECG is easy! And so it is… to a point. Identifying ST segment elevation that is not STEMI… that’s the trick.
It’s false positives that cause the most problems!
Here’s a final thought from Otto and Aufderheide, Evaluation of ST segment elevation criteria for the prehospital electrocardiographic diagnosis fo acute myocardial infarction (Ann Emerg Med 1994 Jan;23(1):17-24):
“Fifty-one percent of patients whose prehospital 12-lead ECG met 1 mm or more ST segment elevation criteria had non-myocardial infarction diagnoses. ST segment elevation alone lacks the positive predictive value necessary for reliable prehospital myocardial infarction diagnosis. Inclusion of reciprocal changes in prehospital ECG myocardial infarction criteria improved the positive predictive value to more than 90% and included a significant majority (62% to 86%) of acute myocardial infarction patients with ST segment elevation who received thrombolytic therapy within five hours after hospital arrival. ST segment elevation criteria that include reciprocal changes identify patients who stand to benefit most from early interventional strategies.“
Thanks to ncline7 for reminding me that you can test your ability to identify the mimics of acute STEMI by taking the ACC-D2B ECG Challenge!