Friday, March 16, 2018

Are these Wellens' waves?

This ECG was sent to me by one of my residents, who was puzzled by it:

This ECG is from a 21 yo M with PMH of poly-substance abuse.  He presented with nausea and vomiting after drinking the night before.  He denied any chest pain or shortness of breath.  He has no other significant medical history he does not take any medications.

This one was read by the computer as "Acute STEMI" (!!)
What do you think?
My resident thought this looked like Wellens' pattern in lead V2

Some hours later, this was recorded:
Now there is resolution of the inverted T-wave in V2

Electrolytes were normal.

My response:

I looked at the ECGs before reading anything.

The one read as acute STEMI was clearly early repol to me.  

What particularly confuses one would be the T-wave inversion in V2.  However, also notice that there is an rSr' in both V1 and V2.  Notice that in the second ECG, these are gone and the T-wave inversion is not present.  Both of these findings (rSr' and T-wave inversion in lead V2) are seen if V1 and V2 are recorded too high on the chest, which is a very common recording error, but not well known among physicians.  The second ECG is normalized.  I strongly suspect that they were not recorded with the leads in the same position.  Or the patient was lying down for the first one and sitting up for the second, which changes the position of the heart in the chest.

I showed this to Brooks Walsh, see below.  He added this important aspect:

There is one complication: normally, the P-wave in V1 is biphasic.  When the leads are placed too high, the P-wave in V1 is all negative, because all atrial depolarization is moving down, away from the highly placed leads.

In this case, there are all upright P-waves in V1 in both ECGs.  But look also at limb leads: the P-wave is inverted!  Thus, in this case, there is an ectopic atrial rhythm, not sinus rhythm.  This ectopic atrial rhythm accounts for the upright P-waves in V1 and V2, even though the leads were placed too high.

In other words, if you depend on P-wave morphology in lead V1 to tell you if the leads are placed too high, you would be misled!

Learning Points:

1. rSr' in lead V1 is often a result of leads placed too high

2. this also results in T-wave inversion in lead V2.

3. this should also result in an all negative P-wave in V1, unless there is a co-existing ectopic atrial rhythm, as in this case.

My friend, co-author and frequent blog poster, Brooks Walsh, just wrote a great article on this topic.

Here it is:

Wednesday, March 14, 2018

Syncope, History of Coronary Disease, and ST Elevation: Should Medics Activate the Cath Lab?

A 60-something male had a syncopal episode.  911 was called.   The patient had no complaint of chest pain or shortness of breath. A prehospital ECG was recorded:

Limb leads
Precordial Leads
There is ST Elevation in V1-V3, and in aVL, with reciprocal ST depression in II, III, and aVF.
There is also some ST depression in V5 and V6, and ST elevation in aVR.
What do you think?

The medics interpreted the ST elevation, with reciprocal ST depression, as STEMI, and activated the cath lab.

Note that you cannot see the entire QRS on the prehospital ECG.  The R-waves in leads II and III are cut off.  The S-waves in V1-V3 are cut off.  There is likely to be very high voltage that is cut off.

It is important to remember that not all ST elevation with reciprocal ST depression is a manifestation of STEMI.   LVH, LBBB, and WPW can all have ST Elevation with reciprocal ST depression. Especially LVH.

On arrival, I looked at the ECG and immediately knew it was a false positive due to LVH.

An ECG was recorded in the ED:
This confirms high voltage. QRS is 118 ms.
There is no evidence of STEMI.
All ST deviation is a result of LVH with secondary repolarization abnormalities
These are secondary to abnormal depolarization due to LVH, with high voltage.
These are expected ST-T abnormalities given the high voltage abnormal QRS.
They are not "primary" ST-T abnormalities of ischemia.

This ECG has similarities to Left Bundle Branch Block (LBBB), but it is NOT LBBB because the QRS is not long enough and there is not enough delay from onset of the QRS to peak of R-wave in lateral leads.  Q-waves in V5 and V6, and absence of monophasic R-wave in aVL also argue against LBBB.  See more on LBBB and LVH at the bottom of the post.

The cath lab was de-activated.

There was further history:

The patient had not anything to eat or drink all day long and felt subjectively dehydrated. He had been walking much of the day, then went to the bathroom and after urinating became light headed and fell w/ brief loss of consciousness.

There was never any chest pain or dyspnea.

He had a history of CABG and ischemic cardiomyopathy.

A repeat ECG 3 hours later was not different.


The troponins were slightly positive, peaking at 0.52 ng/mL (not consistent with STEMI).  Cr. was elevated, consistent with dehydration.

Echo showed:

Decreased left ventricular systolic performance, moderately-severe, EF about 35%, with LV enlargement.
Asynchronous interventricular septal motion consistent with left bundle branch block (although the ECG did not show LBBB).
Regional wall motion abnormality-distal septum and apex.
Evidence for dilated left ventricle with regional dysfunction in the LAD distribution. 
Markedly dysynchronous septal motion consistent with LBBB.

Thus, there is echo evidence of myocardial infarction (new or old), thought to be old.  Syncope could have been vasovagal (neurocardiogenic, triggered by dehydration), but with poor LV function, it could also have been due to ventricular tachycardia.  Acute type I MI is much less likely.  Troponin elevation is probably due to type II MI: underperfusion in the setting of chronic coronary disease.

The patient refused further investigations and was discharged.

Learning Points:

1. Syncope alone is an uncommon presentation of STEMI.  Any ECG finding with ST elevation should be approached with skepticism if there is no chest pain or chest discomfort.

Corollary: It should be very unusual for medics to activate the cath lab for syncope alone, without chest pain, as any associated ST Elevation is likely to be a false positive.

2. LVH is a common cause of false positive ST elevation, and often has reciprocal ST depression.

LBBB has recently been re-defined:

Strauss DG, Selvester RH, Wagner GS. Defining left bundle branch block in the era of cardiac resynchronization therapy. Am J Cardiol. 2011;107(6):927–34.

Here is a quote from the abstract: 

"Three key studies over the past 65 years have suggested that 1/3 of patients diagnosed with LBBB by conventional electrocardiographic criteria may not have true complete LBBB, but likely have a combination of left ventricular hypertrophy and left anterior fascicular block. On the basis of additional insights from computer simulations, the investigators propose stricter criteria for complete LBBB that include a QRS duration ≥140 ms for men and ≥130 ms for women, along with mid-QRS notching or slurring in ≥2 contiguous leads. Further studies are needed to reinvestigate the electrocardiographic criteria for complete LBBB and the implications of these criteria for selecting patients for CRT." 

One more very short article with full text: 

Int Cardiovasc Res J. 7(2):39-40.LBBB: State of the Art Criteria.

Monday, March 12, 2018

A crashing patient with an abnormal ECG that you must recognize

Written by Pendell Meyers, with edits from Steve Smith

Let's consider this nearly pathognomonic ECG without the clinical context (because sometimes the clinical context will not be as easy as in this case).
What is the answer?

This ECG is diagnostic of hemodynamically significant acute right heart strain. Notice I did not say "pulmonary embolism," because any form of severe acute right heart strain may produce this ECG. This includes, but is not limited to, PE, asthma/COPD exacerbation, hypoxic vasoconstriction from pneumonia, acute pulmonary hypertension exacerbation.  It has even been seen anecdotally in acute cessation or discontinuation of continuous IV pulmonary vasodilator.

The findings include sinus tachycardia, characteristic QRS morphology most diagnostic in V3 with a small R wave followed by a very large S wave with a convex upward ST segment morphology, ST segment strain morphology in the inferior and anterior leads leading to deep symmetric T-wave inversion.

Why is it not Wellens??? (Wellens pattern is a term which refers to coronary reperfusion morphology in the anterior leads)

The best answer is because the entire gestalt of the ECG shows acute right heart strain instead, and just does not look like Wellens after you've seen Wellens hundreds of times. It is true that the morphology of the T-wave inversions can be very similar in anterior reperfusion syndrome (Wellens). It is also true that anterior and inferior T-wave inversion could be consistent with reperfusion of a type III wraparound LAD occlusion, despite the fact that Kosuge et al showed that T-wave inversion in lead III is much more likely to be PE than ACS if your differential contains nothing else.  However, in reperfusion (Wellens'), the symptoms are resolved at the time of the ECG.  Thus, it is critical to compare the ECG with the symptomatic state of the patient!  

Differences of Pulmonary Embolism T-waves from Wellens' T-waves:
1. Wellens' is a syndrome of a painless period following an anginal (chest pain) event.  Coronary reperfusion changes on ECG should be accompanied by significant reduction or resolution of symptoms. In this case we have a crashing patient while T-wave inversion is ongoing!

2. Acute coronary occlusion (especially during reperfusion) is very rarely accompanied by tachycardia.  When there is tachycardia, the patient is in cardiogenic shock with very poor LV function on bedside echo.

3. The T-waves simply look different in Wellens'.  Here is an example of Wellens'.  We hope you can see the difference:

See these cases for more examples: 

Syncope, Shock, AV block, Large RV, "Anterior" ST Elevation....

Please notice in particular the morphology in V2-V3, as I believe this is particularly helpful to describe as evidence of acute right heart strain, including:

- Generally much bigger S-wave than R-wave
- Usually either isoelectric J-point or some small J-point elevation followed by convex upward ST segment elevation rollercoastering into T-wave inversion
- Usually some ST segment depression in the more lateral leads V4-V6 and the inferior leads, also with T-wave inversion
- Please note that these QRS characteristics will not apply in the not-uncommon scenario that the patient develops acute RBBB because of the strain on the RV

Here are the blown up images of V2-V3 from several of the cases on this blog with acute right heart strain (all but one of which was due to pulmonary embolism, and the other was due to acute severe asthma exacerbation)

Now that we've learned the lesson, let's watch this very interesting case play out:

A female in her 40s with history of HTN and obesity presented with progressively worsening dyspnea with mild exertion, and now with dyspnea at rest over the past 4 days. She also complained of generalized weakness, lightheadedness, diaphoresis, chest pain, and cough. On initial exam she appeared acutely ill, with initial vitals showing tachycardia, hypoxia, and borderline hypotension.

Here is her initial ECG, followed by her repeat ECG approximately 15 minutes later:

Bedside echo was done.  This one is from a previous case on this blog,  but is similar to this patient:

This shows impressively obvious right heart strain.  The LV is small (underfilled) with good function. 

She was appropriately anticoagulated immediately with heparin before going to CT scan.
There are filling defects in both main pulmonary arteries. The pulmonary artery trunk is dilated at 35mm per radiology report.

Filling defects are seen to extend to bilateral lobar, interloper, and segmental branches diffusely throughout both lungs. This is a very large clot burden. Radiology commented that the inter ventricular septum is bowed towards the left ventricle, suggestive of right heart strain.

Troponin T returned elevated at 0.12 ng/mL. NT pro BP returned at 10,676 pg/mL.

Despite heparin and supportive care, the patients mental status and blood pressure worsened. She was diagnosed with massive PE and given intravenous tPA with rapid improvement in hemodynamics and mental status.

She had an uneventful ICU course and improved steadily over the course of a week. She was discharged and did well.

Here is her ECG on day 2 after much improvement in hemodynamics and oxygenation:
Tachycardia has resolved. ST and T-wave abnormalities evolving appropriately.

Here is her ECG on day 4:
Almost entirely back to normal.

 Learning Points:

1) The history and exam will not always be this obvious, yet in cases this severe, the ECG findings often are obvious if you know what to look for.

2) The cells of the right ventricle do not know why they are having such a hard time when they report their acute strain on the ECG. Whether it's a PE or a severe asthma attack, the cellular physiology of these cells is acutely the same. Therefore the ECG is also indistinguishable between acute right heart strain etiologies.

3) Reperfusion T-wave inversion should be present in the pain free state. These T-wave inversions in the anterior and inferior leads during pain are likely to be due to acute right heart strain from PE.

Primer on the ECG in Pulmonary Embolism:
These are findings of acute right heart strain, and could be seen in any condition which results in a rapid rise in pulmonary artery pressure. This includes hypoxia because of "pulmonary hypoxic vasoconstriction" 

The ECG is not sensitive for PE, but when there are findings such as S1Q3T3 or anterior T-wave inversions, or new RBBB, then they have a (+) likelihood ratio and the S1Q3T3, or even just the T3, may help to differentiate Wellens' from PE. 

Stein et al. found normal ECGs in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE.  Today, however, that number would be higher because we diagnose more of the submassive PEs that have minimal symptoms.

This is a paper worth readingMarchik et al. studied ECG findings of PE in 6049 patients, 354 of whom had PE.  They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. 

What is an S1Q3T3?  Very few studies define S1Q3T3.  It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV).  In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS.  In this study, (quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

Witting et al. looked at consecutive patients with PE, ACS, or neither. They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6% of controls.  This does not contradict the conclusions of Kosuge et al. that when T-wave inversions in the right precordial leads and in lead III are indeed present, then PE may indeed by more common.  In my experience, this is true, but needs validation in a study of similar methodology. Supporting Kosuge, Ferrari found that anterior T-wave inversions were the most common ECG finding in massive PE. 

Friday, March 9, 2018

A patient with a "seizure" and a completely "normal" ECG

I happened on this ECG while walking by, and read it with no clinical information, remarked on it, and discussed it with the physicians caring for the patient.
The computer read the ECG as completely normal.

I heard this clinical information: This patient presented with a "seizure," and was to be worked up by neurology for new onset of seizures.

What do you think?

The computer measured the QT at 420 ms, and QTc at 445 ms.

Let's magnify V2 and V3:

Here I put lines in at the onset of the QRS and end of the T-wave (or is it a U-wave?)
Approximately 595 ms

Here I point out an apparent U-wave in V1
So it is possible that the T-wave is really a U-wave
A long QU interval is just as dangerous.

The K returned at 2.5 mEq/L and it turns out that the patient had been having diarrhea.

There was a previous ECG recorded with K = 3.6 mEq/L
Much more normal, although has some nonspecific ST depression

The patient did not likely have a seizure, but more likely had an episode of VT (Torsades de Pointes) which resulted in tonic clonic activity.

Even after the K returned low, no clinician went back to look at the ECG to see if there were any findings.  No clinician questioned the symptom of "seizure."   The faculty physician involved is one of the smartest and best clinicians I've ever worked with, and very good at ECG interpretation.  Yet he did not scrutinize the ECG.

This is the problem with computerized interpretations.  People tend to trust them implicitly, and turn off their critical faculties.

Learning Points:

1. Always look at the QT interval.  If it looks long, you must measure it.  Do not trust the computer.  On the other hand, when it looks normal, it is usually accurate.  (That is why it works in the formula for differentiating subtle LAD occlusion from normal variant ST elevation.)

2.  A long QT could be a long QU interval (prominent U-wave), but the danger of polymorphic ventricular tachycardia (Torsades de Pointes) is just as high.

3.  Even when the computer states the ECG is completely normal, it may be very abnormal.

There was a paper last year contending that if the computer reads the ECG as normal, the physician need not look at it, at least not in triage.

I discuss this paper here:

A middle-aged woman with chest pain and a "normal" ECG in triage

Read these:

In depth on QT correction and QT in general:

QT Correction Formulas Compared to The Rule of Thumb ("Half the QT")

I just posted this case yesterday.  Both of these cases were this week.

Thursday, March 8, 2018

Alcohol withdrawal and sinus tachycardia

This patient with alcohol withdrawal and tachycardia had an ECG recorded:
What do you think?

There is sinus tachycardia.

Look at the QT interval: it is far more than half the QT.  The computer reads the QT at 386 ms, and QTc of 462 (proprietary correction formula unknown!)

Read this article: 

QT Correction Formulas Compared to The Rule of Thumb ("Half the QT")

I measure the QT at 440 ms.  RR interval is 470 ms.  It is possible that what we are seeing is a fusion of the T- and U-wave, but the consequences are similar.

Here is the QTc:
Very long QT !!
(Fridericia is best; at heart rates over 60, Bazett results in a QT that is too long)

The magnesium returned at 1.2 mEq/L  (low).

There was also a profound metabolic alkalosis, with K = 3.0 mEq/L.

The patient is at high risk of Torsades.

Learning Point:

Do not trust the computer measurement of the QT interval when it looks long!

Monday, March 5, 2018

To activate or not to activate?

Written by Pendell Meyers, with edits by Steve Smith

I was texted this ECG with no clinical information:
(This will be called ECG-2)
What do you think?

I replied "Actually I think this might be a false positive."

The ECG shows sinus rhythm with relatively normal QRS complex followed by large STE in V1-V3, with ~4mm STE in V2. There are no pathologic Q-waves, no terminal QRS distortion. I do not think there is any STD in the inferior leads; there is a tiny amount of PR depression (normal) and the J-point is exactly on line with the PR interval. In lead III the T-wave does slope downward at first, but I just didn't think this was convincing morphology to be called reciprocal STD.

I was left with concerning anterior STE which may be a normal variant or may be LAD occlusion, so I used the SubtleSTEMI app on my phone:

3 variable


I sent it immediately to Dr. Smith with no clinical information. He saw it on his phone without the QT (so could not use the formulas), and responded: "That is a really tough one. But I think it is actually a normal variant. My best guess, but I am not sure. Did you use the formulas?"

It turns out this was from a male in his 50s with history of smoking and HTN but no known CAD who presented due to chest pain radiating to the right cheek and right arm, which had awoken him from sleep early in the morning. By the time he arrived in the ED, his pain had apparently spontaneously resolved.

Here was his initial ED ECG earlier that morning (ECG-1):

There is a small amount of STE in V1 and V2, but much less than the ECG above. This ECG is easily within normal limits.

The patient had an initial undetectable troponin and was placed in the observation unit for serial troponins and CTCA vs. stress test.

While waiting in the observation unit, the patient suddenly complained of returning chest pain.  This is when ECG-2 was recorded; here it is again:

The following ECG (ECG-3) was recorded 10 minutes later:
Similar findings with dramatic STE in V2. There is no reciprocal STD.

The treating clinicians interpreted his return of pain with dynamic ECG changes and dramatic STE in the anterior leads as a "STEMI," and activated the cath lab (appropriately).

Here is the result:
Normal left circulation (except for a 40% D1 nonculprit stenosis according to the report).

Normal right circulation.

Non-obstructive CAD, no coronary occlusion. Repeat ECG after cath was unchanged. Serial troponins were all undetectable. Echo was done and was unremarkable.

What do you think the final diagnosis was in the chart?

"Pericarditis," of course. He was treated with colchicine and discharged. This patient likely did not have pericarditis. It is much more likely that this ECG is simply a normal variant. Normal variants can change dramatically and dynamically as above. It is an unfortunate truth that we have shown on this blog many times.

Let me be clear: we are not advocating that this patient should not have been cathed emergently. Any patient with a concerning clinical picture or ECG may deserve emergent cath. Dynamic and dramatic STE in general does in fact have a significant rate of true positive acute coronary occlusion. Additionally, diagnostic cath (without any coronary intervention) is a very low risk procedure. But expert ECG interpretation can often predict the false positives in the group of dramatic ECG findings.

Would I have activated the cath lab? Assuming his clinical appearance was as concerning as it sounds on paper, I still think it would have been perfectly reasonable to do so, although in the back of my mind I would suspect a false positive. And that is completely acceptable and likely good care, because the ECG cannot identify all acute coronary occlusion. I would make sure that I am not overlooking the possibility of other dangerous etiologies of chest pain including dissection and PE before letting the patient roll away to the cath lab.

When this specific population (benign early repolarization vs. subtle LAD occlusion) was studied, R-wave amplitude in V4 was the most important predictor variable, more important than STE. QRS amplitude in V2 and QTc were also as important as STE. This is because acute coronary occlusion does not follow the rules of the "STEMI criteria." Instead, you must become expert in ECG interpretation by learning from cases such as these.

Smith comment: 

1. Is there an alternative to activating the cath lab if you suspect normal variant?  Yes. If you can get a rapid high quality, bubble contrast enhanced echocardiogram, read by an expert, and, while the patient has symptoms and ECG findings, it shows no wall motion abnormality (WMA), then you can be certain that it is normal variant.

2.  Caveat: However, frequently clinicians do such an echocardiogram after symptoms and ECG findings have resolved. This is hazardous! Although there is usually some residual stunning (WMA),  sometimes the ischemia was so brief that the wall motion completely recovers.  This would be a false negative echo and leave the patient with an unstable plaque and thrombus in the coronary artery that would then not be intervened upon.

Friday, March 2, 2018

Scary ST Elevation. What is it?

911 was called for an 18 year old who had altered mental status after using K2 (a recreational drug).  The medics put the patient on the monitor and saw ST elevation.  They then recorded a prehospital 12-lead (not shown, as it is identical to the ED ECG), which showed marked ST Elevation.  The computer diagnosed "Pericarditis."  They were very worried, and brought the patient to the "Stabilization Room" for critically ill patients.

On arrival, I looked at the prehospital ECG (again, identical to the ED ECG shown below):
What did I think?

I immediately said "Normal Variant ST Elevation," and directed the patient to our "Special Care Unit" for altered mental status from drugs and alcohol.

This is not pericarditis, nor is it STEMI.  Get to know this pattern just like you would get to know a friend.  I called him "Jack," and told the residents to get to know Jack.

Jack often has high voltage QRS, has marked J-waves (they look almost like Osborn waves).  There is a relatively short QT interval.  The ST Elevation is towards leads II and V5.  Thus, there is no reciprocal ST depression in aVL. [In fact, these could be Osborn waves, but they were not: the patient was not hypothermic.]

Although the T-wave is negative in aVL, it is NOT T-wave inversion, as the QRS-T angle is narrow (QRS axis is 85 degrees, almost directly inferior; T-wave axis is 68 degrees -- angle is only 17 degrees.  Both these measurements are accurately made by the computer algorithm.)

How do I know it is not pericarditis?  First, the patient denied any chest pain!  Second, normal variant STE is far more common that pericarditis.  There are J-waves, no PR depression, and no Spodick's sign (downsloping T-P segment -- of questionable reliability).

It is very common for Normal Variant STE to be misdiagnosed as pericarditis.  Does this have adverse consequences??  It may.  Take a look at this case that was written by Pendell Meyers when he was a medical student: due to misdiagnosis of the ECG as "pericarditis", a patient's chest pain was misattributed to pericarditis and the correct diagnosis of pulmonary embolism was ignored:

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

Wednesday, February 28, 2018

ST-Elevation in aVR with diffuse ST-Depression: An ECG pattern that you must know and understand!

This case comes from Sam Ghali  (@EM_RESUS). 

A 60-year-old man calls 911 after experiencing sudden onset chest pain, palpitations, and shortness of breath. Here are his vital signs:

HR: 130-160, BP: 140/75, RR:22, Temp: 98.5 F, SaO2: 98%

This is his 12-Lead ECG:

He is in atrial fibrillation with a rapid ventricular response at a rate of around 140 bpm. There are several abberantly conducted beats. There is ST-Elevation in aVR of several millimeters and diffuse ST-Depression with the maximal depression vector towards Lead II in the limb leads and towards V5 in the precordial leads.

ECG reading is all about pattern recognition. And this particular pattern of ST-Elevation in aVR with diffuse ST Depression is a very important ECG pattern that you must be able to recognize. But what's probably more important than being able to recognize the pattern, is understanding what it represents. There appears to be a common misconception that the ST-Elevation in aVR in this case possibly represents "STEMI", or acute transmural (full-thickness) ischemia. If this were the case the patient would most likely be dead or at the very least in profound cardiogenic shock. The key to understanding what this pattern represents lies in understanding that the ST-Elevation in aVR is reciprocal to the diffuse ST-Depression - and that this diffuse ST-Depression represents global subendocardial ischemia!

So the real question that you must answer is: 
What is causing the global subendocardial ischemia?

It is critical to realize that more often than not the cause is global myocardial strain from a Non-ACS etiology! (profound sepsis, tachycardia, anemia, hypoxemia, etc). It is also very important to understand that in these Non-ACS settings, you can see this pattern with or without underlying coronary artery disease.

But of course it could be ACS. And if it is, then you are dealing with Left Main, Proximal LAD, or even multi-vessel plaque instability. But keep in mind that even if it is ACS you are still dealing subendocardial and not transmural ischemia.

Here is a subcostal view of the bedside Echo obtained from our patient in the ED:
There is good global function

So what is causing the diffuse subendocardial ischemia in our patient? 

 When the heart rate is significantly elevated as in this case, it is reasonable to suspect that the ischemia is likely tachycardia-induced, or "demand ischemia." So given the normal EF noted on Echo, (and by the way I would strongly recommend assessing the EF of any patient before deciding to give any negative inotropic medications) the decision was made to administer a Diltiazem bolus and infusion and to reassess after rate control was established. Rate controlled was gained as the patient's heart rate came down very nicely into the 80's. He felt much better and his symptoms were all but completely relieved.

Smith comment: it is also critical to assess volume before giving negative inotropes and negative chronotropes.  This tachycardia could be a response to poor LV filling.  Indeed the neither LV nor RV appear to be filling very well.  If the atrial fib with RVR is resulting in a rate so fast that the rate is the cause of poor LV filling, then there should be some increased filling pressures, possible pulmonary edema, and evidence of fluid overload.   Assessment of IVC filling would be helpful, and, if it is collapsed, then administration of fluids first (or blood if this is a GI bleed) is indicated.  If this does not result in a slower heart rate, then an AV nodal blocker is indicated, such as Diltiazem.  

Furthermore, since this patient has no history of atrial fib, and it is a critical situation, electrical cardioversion is both safer and more effective than an AV nodal blocker such as Diltiazem.

See these 2 posts

Atrial fibrillation with RVR: use POCUS to assess volume; then sinus vs. SVT: use of Lewis leads

Here is the repeat ECG obtained 25 minutes after the first one:
The rhythm is still A-Fib. The heart rate has come down more than 65 points. But despite the dramatic decrease in heart rate, the pattern of global subendocardial ischemia persists! (ST-Elevation in aVR with diffuse ST-depression that has a maximum depression vector towards leads II and V5)

If this repeat ECG had shown resolution of the global subendocardial ischemia pattern, it would be reasonable to conclude that it was likely the result of a-fib with an uncontrolled ventricular response. But because this pattern persisted after rate control and in the absence of any other evidence of clinical causes, one must assume that the etiology of the pattern is indeed ACS - meaning there has been acute plaque instability in either the left main coronary artery, Proximal LAD, or multi-vessel involvement. 

The patient was started on heparin in addition to the aspirin he received en route and the Cardiology team was consulted. (Of note, it is important not to start these patients on dual anti-platelet therapy as there is a high likelihood that they will require CABG.) The decision was made to proceed urgently to the cath lab for angiography. 

Cardiac Cath Results:

Left Main: There is a 90-95% stenosis of the distal left main including the ostium of LAD and Left Circumflex arteries.  
LAD: There is a focal 80% stenosis just after the takeoff of the first diagonal branch.

Circumflex: Severe disease at its ostium and moderate disease in the remainder of the proximal segment.

RCA: 100% chronic total occlusion at its proximal segment.

In discussion with the interventional cardiologist who performed the cath there was thought to be evidence of likely a component of acute thrombus at the 90-95% left main stenosis, suggesting Left Main ACS!

Case Resolution:

The patient was referred for CABG and ended up doing quite well.

Take Home Points:

1. The key to ECG reading is pattern recognition. The pattern of ST-Elevation of at least 1mm in lead aVR + diffuse ST-Depression with a maximal depression vector towards leads II & V5 is a pattern you must know. It represents global subendocardial ischemia.

2. When you see this pattern you should divide the differential for the diffuse subendocardial ischemia into two main categories: ACS vs Non-ACS. Do not automatically assume that it is ACS. I have seen this mistake made many times as ACS becomes the focus, at the expense of appropriate resuscitation addressing the underlying cause. It is very important to keep in mind that the etiology is far more likely to be Non-ACS than ACS!

See this case: 

Diffuse Subendocardial Ischemia on the ECG. Left main? 3-vessel disease? No!

3. The key to determining the etiology is through history, physical exam, clinical picture, laboratory data, Echo, and vigilant monitoring and frequent reassessment.  If you have identified and addressed potentially reversible causes of the ischemia, and the ECG pattern persists then you are dealing with ACS until proven otherwise.

4. Refrain from using dual-antiplatelet therapy in these patients as there is a high likelihood they will require CABG.

5. Remember that if this ECG pattern does represent ACS, the ST-Elevation in aVR is not the result of direct injury (or transmural ischemia) and that the ST-Elevation in aVR is reciprocal to the diffuse ST-Depression. Therefore these ACS cases do not represent "STEMI".  However, while there is not great data to guide the timing of cath for these patients, I would advocate going to the cath lab with a much stronger sense of urgency than for other "NSTEMIs".  The reasoning is that ACS is a very dynamic process and without the advantage of optimal medical therapy (a second platelet inhibitor should be withheld) there is a higher chance of the culprit vessel suddenly occluding and evolving to transmural ischemia. If this happens in the Proximal LAD, Left Main, or in the setting of Multi-vessel involvement the myocardial territory in jeopardy is so large that there is a good chance the patient will arrest and die before any reperfusion can be established!

6.  Smith comment: With diffuse subendocardial ischemia, you may not see any wall motion abnormality.  Global function can even be normal, although it may be globally depressed as well.  A normal bedside echo does not help in: 1) differentiating the cause of the STE in aVR 2) ruling out ACS.

Here is the section on aVR written by Smith in: Miranda et al. "New Insights into the Use of the 12-lead ECG in Acute MI in the ED" (Canadian J Cardiol 34(2):132-145; Feb 2018)

Lead aVR in ACS 62

Many experts consider the ECG pattern of STE in aVR, with diffuse STD elsewhere (referred to herein as the aVR STE pattern), to be representative of LM ATO.7 The 2013 ACC/AHA STEMI guidelines consider this a STEMI equivalent,in which thrombolytic therapy is not contraindicated (evidence level B, no specific class of recommendation).  18 However, these conclusions are on the basis of studies in which LM lesions were not true subtotal or complete occlusion (ie, TIMI 0/1 flow).62,63 The interventional community defines occlusive LM disease as >50% according to fractional flow reserve, or 75% stenosis,64 but urgent or emergent intervention on lesions not meeting these thresholds is only imperative if it is a thrombotic lesion and the patient has refractory ischemic symptoms (ie, not resolved by nitrates, antiplatelet, and antithrombotic therapies; see 3 examples in Supplemental Fig. S7).

Although nearly half of patients with 1 mm STE in aVR due to ACS will require coronary artery bypass surgery for revascularization,62 the infarct artery is often not the LM, but rather the LAD or severe 3-vessel disease. More importantly, such ECG findings are frequently due to nonocclusive etiologies (eg, baseline LVH, demand ischemia secondary to respiratory failure, aortic stenosis, hemorrhagic shock). Knotts et al. reported that only 23% of patients with the aVR STE pattern had any LM disease (fewer if defined as 50% stenosis). Only 28% of patients had ACS of any vessel, and, of those patients, the LM was the culprit in just 49% (14% of all cases).57 It was a baseline finding in 62% of patients, usually due to LVH.

Thus, a number of expert reviews emphasize the low specificity of the aVR STE pattern, preferring to label it as circumferential subendocardial ischemia; in this syndrome, STE in aVR is reciprocal STE, reciprocal to an STD vector toward leads II and V5.10,12,62 

The aVR STE pattern is also not sensitive for LM ATO. However, anterior STEMI with combined new right bundle branch block and left anterior fascicular block is highly suggestive of LM ATO (see example 12-lead ECG in Supplemental Fig. S8).65,66

It should be re-emphasized that true LM ATO (ie, TIMI flow 0) is rare in the ED, because most either die before arrival or are recognized clinically because of cardiogenic shock. Thus, reported specificities of STE in aVR for LM ATO result in very low positive predictive values. Of those who do get to the ED, many present with clear STE.62,65,66

The ACC/AHA states that thrombolytics are not contraindicated for diffuse STD associated with  STE in aVR.  Because of the poor specificity of this pattern for LM ATO, we suggest that thrombolytics should only be considered for those with profound STD that is clearly due to ACS, is refractory to all other medical management, and only when PCI is completely unavailable.

Lead aVR in STEMI
 Some patients whose ECGs already meet conventional STEMI criteria might also have STE in lead aVR. This finding does not alter the need to pursue emergent reperfusion, although it might suggest a poorer prognosis.62,67  In a patient with otherwise diagnostic STE, additional STE in aVR does not represent LM ATO and is not helpful in diagnosing the infarct-related artery or the site of occlusion.68  Less than 3% of anterior STEMI has LM ATO, and most are recognized clinically because of cardiogenic shock.69,70


62. Smith SW. Updates on the electrocardiogram in acute coronary syndromes.  Curr Emerg Hosp Med Rep 2013;1:43-52.

63. Jong GP, Ma T, Chou P, et al. Reciprocal changes in 12-lead electrocardiography
can predict left main coronary artery lesion in patients with acute myocardial infarction. Int Heart J 2006;47:13-20.

64. Stone GW, Sabik JF, Serruys PW, et al. Everolimus-eluting stents or bypass surgery for left main coronary artery disease. N Engl J Med 2016;375:2223-35.

65. Fiol M, Carrillo A, Rodriguez A, et al. Electrocardiographic changes of ST-elevation myocardial infarction in patients with complete occlusion of the left main trunk without collateral circulation: differential diagnosis and clinical considerations. J Electrocardiol 2012;45:487-90.

66. Widimsky P, Rohac F, Stasek J, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J 2012;33:86-95.

67. Kukla P, Bryniarski L, Dudek D, Krolikowski T, Kawecka Jaszcz K. Prognostic significance of ST segment changes in lead aVR in patients with acute inferior myocardial infarction with ST segment elevation. Kardiol Pol 2012;70:111-8.

68. Kosuge M, Ebina T, Hibi K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol 2011;107:495-500.

69. Zoghbi GJ, Misra VK, Brott BC, et al. ST elevation myocardial infarction due to left main culprit lesions: percutaneous coronary intervention outcomes. J Am Coll Cardiol 2010;55:A183.E1712.

70. Kurisu S, Inoue I, Kawagoe T, et al. Electrocardiographic features in patients with acute myocardial infarction associated with left main coronary artery occlusion. Heart 2004;90:1059-60.

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