A man in his 60s with diaphoresis, vomiting, and inferior STE

Written by Pendell Meyers

A man in his 60s appeared altered and diaphoretic and vomiting to a bystander, who called EMS. EMS personnel agreed that he was altered, possibly intoxicated, and seemed to deny all complaints that EMS inquired about. Vital signs were within normal limits.

EMS performed an ECG:

What do you think?

Raw findings:

 - Sinus rhythm

 - Normal QRS, axis straight down at lead aVF

 - STE in leads II (2.0 mm), III (1.5 mm), aVF (2.0 mm)

 - STD in aVL (1.0 mm)

 - STD in V1 (0.5 mm), STD in aVR (0.5 mm)

Subjective interpretation of those findings:

It is slightly tough to decide whether this is inferior and/or posterior OMI. "Normally", this ECG would trigger the rule that any STE in the inferior leads with any STD and/or TWI in lead aVL (not explained by some other reason, like a QRS abnormality) should be considered inferior OMI until proven otherwise. "Normally", we would teach that STD maximal in V1-V4 (without another explanation e.g. RBBB, juvenile T wave pattern, known prior baseline, etc.) should be considered posterior OMI until proven otherwise. But there is something about this particular ECG and its morphology that matches prior false positives to me. I have a hard time explaining what feature it is, exactly, but I have made lots of mistakes in the past and feel that this one is similar to the last time I saw a false positive like this. One thing I can explain is: Any time there is focal STE in the inferior leads for any reason (whether it is due to acute inferior wall OMI, or whether it is a baseline ECG finding), there MUST BE reciprocal STD in aVL. The fact that there is STD/TWI in aVL does not make the STE in the inferior leads specific for active OMI, it just means that the STE in the inferior leads is indeed focal. If it were diffuse STE on all walls of the LV, it would be very unlikely to have STD in aVL.

Also remember that Dr. Smith's study on STE in the inferior leads and STD/TWI in aVL was only comparing patients with inferior OMI against patients with pericarditis. Normal variants and other reasons for STE in the inferior leads were not in that comparison.

I received this ECG immediately, automatically onto my phone, with no clinical information at all (not even age). I had no idea if the patient had chest pain or any other symptom. I notified the ED that I thought the ECG was likely a false positive, unless the patient has very convincing ACS. But this is a very difficult decision with only this ECG. I was not working at the time, and could not get any more info.

I sent it immediately to Dr. Smith without the outcome or clinical information; he also agreed that he thought it was likely a false positive.  Smith's thoughts: "The ECG is unlikely to represent OMI because it has a combination of 1) high R-wave voltage, 2) J-waves, 3) high STE to T-wave ratio, such that the ST segment is BOTH relatively flat AND upwardly concave, and 4) a "Saddle" appearance, which is usually not due to OMI."

A prior ECG was available in the system:

Does this change your interpretation?

On this prior ECG, we see that the QRS complex is basically the same as the presentation ECG, but with less STE in the inferior leads, isoelectric baseline in aVL, with preexisting but smaller TWI. Some would say that the T waves are smaller in the baseline ECG than the presentation ECG, some would be worried about hyperacute T waves. One of the reasons I think that the inferior T waves in the presentation ECG are not hyperacute is that they are very asymmetric. Hyperacute T waves are usually symmetric. These are not.

Most would say that this prior ECG makes the presentation ECG diagnostic because of a change from baseline. 

Most would say that the inferior STE has gotten larger and therefore is diagnostic. 

This is understandable, and if the patient has ACS clinically then I would call that presentation ECG a STEMI until proven otherwise. However, experienced ECG interpreters know that baseline ECG findings can change, fluctuate, be exaggerated, etc. I always struggle how to teach my residents that baseline ECGs are not always the same day to day, hour to hour. 

All of that said, 

1) if this patient had ACS clinically, I would simply call it STEMI(+) OMI until proven otherwise, and I would have a sneaking suspicion that it would turn out to be a false positive activation. This assumes I do not have access to an emergent high quality contrast enhanced echo (I personally never have this available).

2) if this patient does not have ACS clinically, then I will not be immediately activating the cath lab, but instead will carefully to history, physical, bedside echo, prior ECG checks in system, serial ECGs over the first 10-15 minutes. Then decide. If I still truly think it's a false positive, I could choose to wait for the initial troponin.

Back to the case:

The ED received the ECG, and given the very little information they had at the time of the phone call to discuss the ECG with paramedics, they decided to activate our code STEMI prehospital.

The patient arrived in the ED within about 10 minutes of that phone call, before the cath lab was ready, and so he got evaluated by the ED team. At that point he was able to completely deny any chest pain or shortness of breath, and admitted to large volume alcohol consumption hours prior to his altered behavior and vomiting.

Cardiology arrived, and together ED and cardiology agreed to cancel the cath lab activation.

A repeat ECG was obtained:

In this one, J waves are much more readily apparent in the leads with STE. The same STE and STD is present as before. This one is much easier to identify as normal variant STE in my opinion.

Side note / rant:

All parties involved called this "just J point elevation," which I find to be a term that is almost universal in its usage, but should instead be replaced by describing it as a J wave. A J wave is a discrete wave at the position of the J point. The J point is the point where the QRS ends and the ST segment begins. When there is a wave at the J point, it is a J wave. J waves are frequently seen in benign early repol and benign normal variants. We have a couple examples of clear OMI/STEMI with J waves, but statistically J waves favor benign variants.

It is incorrect to say "J point elevation" in the way that is commonly used. The J point is explicitly where all STE is supposed to be measured (let's talk about whether to use the PR or TP interval as the baseline another day), as stated formally in the Fourth Universal Definition of MI. STE is measured at the J point (unless specified otherwise, such as Dr. Smith's anterior OMI vs. early repol equation), and thus all STE of all the STEMIs you have ever seen are also correctly described by the term "J point elevation." What providers actually mean is "there is a J wave, so I think that is false positive STE."

The distinction is very important because it implies that most physicians do not actually know the formal recommendations for where STE is actually measured (but we already know this is true, as it has been studied: humans cannot agree on how and where to measure STE).

Case continued

The first troponin was negative (less than 6 ng/L).

The second was also negative. No further ECGs were ordered. ED bedside echo was normal

He became sober, without complaints, and was discharged. He did not have ACS in any way.

Learning Points:

In general, if a patient has ACS clinically, then otherwise unexplained STE in the inferior leads with reciprocal STD and/or TWI in aVL is very concerning for inferior OMI. Likewise, ischemic STD maximal in V1-V4 is posterior OMI until proven otherwise in a patient with ACS clinically.

That said, there are always exceptions and false positives to every rule. Experience with cases like this one allow us to build our knowledge of false positive morphology and recognize them better in the future, even if we cannot always express the exact morphology reasons for that suspicion.

"J point elevation" is a widespread term used inappropriately. All providers should know that the Universal Definition of MI recommends the J point is the location to measure STE. All providers should also know the definition of a J wave.

New Paper: Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute OMI.

Just published online today by Meyers and Smith.

@PendellM

This is our best and most important work ever. Another nail in the STEMI/NonSTEMI coffin. Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute OMI. Full text:

https://www.sciencedirect.com/science/article/pii/S2352906721000555

Getting It Right Despite the Wrong Paradigm

Written by Alex Bracey, edits by Meyers and Smith

A 50 something year old male presented to the ED as a transfer from an outside hospital with chest pain. As EMS gave report I looked through the transfer packet for the initial ECG:

Sinus bradycardia with loss of R-wave progression and hyperacute T-waves in V2-V5, slight STE in aVL and I without meeting STEMI criteria. There is a down-up T-wave in lead III, which is a very specific reciprocal finding in high lateral OMI. Very highly suspicious of OMI. Applying the 4-variable formula for detection of subtle anterior OMI would yield: STE60V3 = 2.5, QTc = 360, RV4 = 3, QRSV2 = 5 Formula value = 19.6 which is positive for anterior OMI The most accurate cutpoint for the formula is 18.2. A value above 19.0 is very specific for LAD OMI. See more about the use of the formula here.

As EMS continued, I noticed that this particular hospital plainly forced the physicians to categorize the ECGs into the false paradigm of STEMI or “no STEMI:”

While it is true that this patient did not meet STEMI criteria, it is also true that this is recognizable as OMI and that the patient is in need of emergent reperfusion, ideally by coronary intervention.

EMS reported that the patient arrived at the outside hospital with chest pain radiating to both shoulders. He had an ECG performed (above) that was notable for ‘non-specific ST changes.”

Serial ECGs had been performed that demonstrated dynamic changes, with the following taken 15 and 45 minutes after the initial respectively:

Interval improvement, though persistent hyperacute T waves in the precordial leads with persistent STE in I and aVL with reciprocal depressions in III, and aVF representing spontaneously reperfusion of anterior OMI.

The dynamic nature of the ECG confirms without question that the previous tracing was indeed OMI.

Once again, “No STEMI” was circled.

Interestingly, the likelihood ratio for MI (but not necessarily OMI) of chest pain radiating to both shoulders is 7.1.[1]

Similar to above now with further STE in leads aVL and I

Smith interpretation:

Precordial T-waves are diminishing while high lateral STE is increasing Now it looks like the LAD is open but the first diagonal is getting worse.

The initial contemporary 4th generation troponin I was undetectable (very common).

Given the patient’s pattern of pain, the physician was concerned for aortic dissection and the patient underwent CT angiography that was negative.

The treating emergency physician was apparently concerned enough that this patient had an acutely occluded coronary that thrombolytics were administered, despite lack of STEMI criteria (although STE in I and aVL is close to 1 mm).

EMS reported that this was followed by “slow ventricular tachycardia” for which amiodarone was administered:

An ECG taken moments following thrombolytic administration demonstrating accelerated idioventricular rhythm (AIVR), which is classically seen after reperfusion of OMI. This rhythm is thought to be generated by an ectopic pacemaker below the bundle of His that fires at a faster rate than the SA node. It is often benign and self-limiting and therefore requires no specific therapy. Treatment of AIVR with antidysrhythmics can be dangerous by inhibiting automaticity.

As I interviewed the patient he reported that he still had the same chest heaviness, though it was better than what he had experienced prior to receiving thrombolytics. His pain improved with nitroglycerine. A post-transfer ECG was performed:

Sinus bradycardia with PVCs with slight, persistent STE in aVL and I and STD in V4-V6

A point-of-care echo was performed by my fantastic resident:

Obvious anterior hypokinesis consistent with LAD OMI

Based on the ongoing ischemic symptoms and persistent STE, I contacted the cardiologist for rescue PCI, which he underwent approximately 3 hours after receiving thrombolytics.

Coronary angiogram demonstrating 99% LAD stenosis with TIMI II flow (See the narrow red arrows)

Coronary angiogram after single drug eluting stent deployment with resulting TIMI III flow

Troponin I peaked at 14.26 ng/mL 24 hours after arrival to the receiving hospital, consistent with values seen in STEMI. A formal echocardiogram was performed shortly after PCI which demonstrated an EF of 20-25% with akinesis of the anterior wall. Just prior to discharge, a follow up echo was performed which demonstrated improvement in EF to 40-49% and hypokinesis of the anterior wall. 

This illustrates the concept of "stunned myocardium." Frequently, the mechanical effects of ischemia persist long after the ischemia is resolved; this may last hours to days to weeks, depending on the duration and severity of ischemia, but ONLY if the myocardium remains viable.

There are times when intervention, or CABG, is high risk and it is only worth performing when the myocardium is viable; such "viability studies" can be done with MRI. In this case, of course that is unnecessary, as PCI was not high risk.

He had an uneventful hospital course and was discharged to home two days after PCI.

This case highlights again how the false dichotomy of the STEMI/NSTEMI paradigm fails our patients. We know that in approximately 25% of NSTEMI cases an OMI will be found at the time of cardiac cath and the short and long term morbidity and mortality of these patients is double that of their STEMI counterparts. [2] In this case, this false decision making tree’s limitations were laid bare: the physician at the outside hospital was forced to choose between STEMI (which it was not) and No STEMI, which would not warrant thrombolytic therapy in the current treatment paradigm. However, this person overcame this bias and did the correct thing for the patient, and undoubtedly spared him a larger MI and all the complications accompanying it.

Teaching points:

• STEMI/NSTEMI paradigm is a false dichotomy and should be replaced by the OMI/NOMI paradigm and subjective ECG interpretation

• Serial ECGs are useful in the detection of OMI

• Bedside ultrasonography may identify regional wall motion abnormalities, which can heighten suspicion for OMI. The wall motion abnormality can be profound, as in this case, or more subtle. 

• AIVR is a classic finding following reperfusion of an OMI. It is often self limiting, benign, and requires no specific therapy

• Thrombolytic therapy is not a contraindication to emergent mechanical reperfusion in the cath lab

1. Panju AA, Hemmelgarn BR, Guyatt GH, Simel DL. Is this patient having a myocardial infarction?   JAMA 1998 Oct 14;280(14):1256-63    

2. Khan AR, Golwala H, Tripathi A, et al. Impact of total occlusion of culprit artery in acute non-ST elevation myocardial infarction: a systematic review and meta-analysis. Eur Heart J. 2017;38(41):3082-3089.

Other examples of AIVR on the Blog:

The cardiologist disagreed with cath lab activation. What do you think?

A Wide Complex Rhythm in an Intoxicated Patient

Chest pain and precordial ST depression which resolve, followed by a wide complex rhythm

What is this rhythm?

An adolescent with trauma, chest pain, and a wide complex rhythm

Is this Left Bundle Branch Block? Is there STEMI?

What is the rhythm? And is there new left bundle branch block (LBBB)?

An 80-something with weakness, cough, and CP. Should this ECG provoke a Prehospital Cath Lab activation?

An 80-something called 911 for chest pain, generalized weakness, and cough.

Here is his prehospital ECG:

The medics were worried about this ECG and activated the cath lab

Smith: As in many prehospital ECGs with large voltage, the tracing goes off the image, making assessment of voltage impossible.  Thus, it is impossible to assess the ST Segments and T-waves, which should always be assessed in proportion to the size of the QRS.  I call this "proportionality" and in a non-ischemic ECG, the repolarization should always be proportional to the depolarization.  

Since we can't see the true size of the QRS, we cannot assess proportionality.

So an ECG like this should not precipitate cath lab activation.

On some machines, one can change the settings of millimeters per millivolt and re-record.  Standard measurements are 0.1 mVolt = 1mm (as in this case), but it can be changed on most ECGs to "half standard" which means that 0.1 mV = 0.5 mm and the QRS complexes then are half sized.

When the patient arrived, an ED ECG was recorded:

Rhythm is uncertain but probably supraventricular at a rate of 100.  

There is RBBB and LAFB and Massive LVH.  

No ST segments are out of proportion to the QRS.

A bedside cardiac POCUS was done, short axis: 

This shows very hypertrophied myocardium

 Long axis

Again, very hypertrophied myocardium

There was no previous ECG on file.

Another ECG was recorded shortly thereafter:

Now P waves are visible in lead V1 

(See biphasic wave approximately 200 ms AFTER the QRS.)  

Thus, there is very prolonged PR interval, at approximately 400 ms.  Then RBBB with LAFB is confirmed.

Thus, this is often called Trifascicular Block.  (Bifascicular block PLUS very prolonged PR interval) and it is associated with progression to complete heart block.  

Read more about "Trifascicular block" here: 

Symptomatic Bradycardia. So-called Trifascicular Block. Occum's Razor and Hickum's dictum.

Formal Echo with contrast

--Normal left ventricular systolic function, lower limits of normal; estimated left ventricular ejection fraction is 50%

--Regional wall motion abnormality- mid-inferolateral hypokinesis.

--Marked left ventricular hypertrophy, concentric.

--Normal right ventricular size and function.

The patient turned out to have Covid pneumonia and an elevated hs troponin to 544 ng/L due to type II MI. 

The myocardial diagnosis is hypertrophic cardiomyopathy (HOCM).

Paroxysmal Atrial Fibrillation with RVR, hypotension, volume depletion, good EF, AND pulmonary edema. Strange. Why? What to do?

A 30-something woman presented with a few days of feeling ill.  She had a history of paroxysmal atrial fibrillation, bio-prosthetic mitral valve, and tricuspid valvuloplasty, and was on Coumadin.

Records showed she is usually in sinus rhythm and has normal LV function.

She presented hypotensive (systolic pressure 80), with diffuse B lines, flat IVC, good LV function, and an irregular, fast heart beat.

Here is here ECG:

Atrial fib with RVR and some probable ischemic ST depression in V3-V6

Here is her POCUS:

What do you think?   

There is a small LV with good function and a large left atrium, and moderately large RV.

There is another finding on the ultrasound which I'll explain below.  Do you see it?

Her inferior vena cava was very flat, with respiratory variation, and she had diffuse bilateral B lines

Here is her chest X-ray:

This shows pretty severe pulmonary edema.

Questions:

1. Why does she have severe pulmonary edema, excellent LV function, a small LV, and a flat IVC?

2. What precipitated this acute emergency and why?

3. What do you want to do first?

Clinical Course

The paradoxes of this case were not immediately identified.  At first they had thought, due to the flat IVC and good LV function, that she was septic with pneumonia (thus relatively volume depleted, interpreting the B-lines and X-ray as pneumonia rather than as pulmonary edema). Thus, they had given fluids and antibiotics.  This management did not improve the pulmonary edema.

Comment:

Whether this is sepsis or not, if a patient is usually in sinus rhythm, but presents unstable (hypotension/shock and/or pulmonary edema and/or ischemic chest pain) in atrial fibrillation with RVR, then cardioversion is indicated, especially if the patient is anticoagulated (her INR was 8.8).  Hypotension and pulmonary edema, no matter the etoliogy, will virtually always be improved with electrical cardioversion.  Furthermore, in this case, because the patient is usually in sinus, the cardioversion is likely to be successful.  

Improvement in clinical status is to be expected in sinus rhythm, vs. atrial fib, due to both the restoration of the atrial contribution to ventricular filling, and also potentially due to the slowing of the ventricular rate. 

Clinical Course continued

I arrived late to the case, saw this situation, and said "we need to cardiovert."

The patient was given 10 mg of etomidate and cardiovereted at 200J; she converted to sinus rhythm and immediately felt better.  

Comment: She did not seem to me to be septic, and so the hemodynamics were unusual, and the only way to explain the entire clinical picture was to postulate the there was worsening mitral stenosis, exacerbated by sudden atrial fibrillation:

1. Mitral stenosis leads to poor LV filling, which causes BOTH pulmonary edema AND hypotension but in the presence of good LV function and a small (poorly filled) LV. (All present in this case)

2. Atrial fib worsens the situation in 2 ways: 

     1) There is no atrial contribution to LV filling and 

     2) The rate is very fast, leaving little time for filling. When there is mitral stenosis, the flow from the left atrium to the LV is very slow and the LV needs more time to fill.  Thus, a slower heart rate is beneficial.

3.  Even in the presence of hypovolemia (flat IVC), a patient with severe mitral stenosis can have cardiogenic pulmonary edema.

Look again at the bedside echo. Here is a still photo:

What do you see?

Here I annotate the image:

The blue box shows the very echogenic (thickened) mitral valve

The red arrows show an enlarged left atrium

Case Continued

Cardiology was urgently consulted and a formal contrast echocardiogram was ordered.

____________

Contrast Echo

Left atrial enlargement.

Right atrial enlargement.

Right ventricular enlargement. Decreased right ventricular systolic performance .

 

Normal estimated left ventricular ejection fraction, 77%.

Bioprosthetic mitral valve with severe stenosis (see below).

Also: Mitral valve insufficiency-moderate, eccentric.

Pulmonary hypertension; estimated PA systolic pressure 65 mm Hg + RA.

Inferior vena cava is normal in size with respiratory variation.

 

ADDITIONAL REMARKS

 

Patient in sinus rhythm. Compared to the prior study, there is now evidence for severe, mixed stenosis/regurgitation involving the mitral bioprosthesis (placed in 2006), with markedly elevated mean transmitral gradient of 14 mmHg @ HR 102 bpm and accompanying pulmonary hypertension.

Comment: had this been done during atrial fib with RVR, the transmitral gradient would have been far greater!

 

The mitral prosthesis appears bulky with exaggerated motion throughout the cardiac cycle. 

Mitral Valve

 

Area (PHT): 3.14 cm^2                 Area (continuity): 1.3 cm^2

Peak E-Wave: 2.5 m/s                  Mean Velocity: 1.78 m/s

Peak A-Wave: 1.1 m/s                  Mean Gradient: 14 mmHg

Peak Gradient: 25 mmHg                Deceleration Time: 238 msec

P1/2t: 70 msec

E/A Ratio: 2.36

Summary: Severe prosthetic valve mitral stenosis mean gradient 14 mmHg at heart rate 102 bpm and moderate MR.

____________________

The subsequent cardiology note explains everything very well:

"Past medical history significant for paroxysmal atrial fibrillation, rheumatic mitral stenosis status post bio-prosthetic MVR in 2006 now with evidence of prosthetic valve dysfunction with severe mitral stenosis and moderate mitral regurgitation and resultant RV enlargement and decreased systolic function with severe pulmonary hypertension.  She presented to the ED with 2 weeks of weakness and decreased oral intake and 2 days of palpitations shortness of breath and orthopnea.  She was found to be in atrial fibrillation with RVR.  She was also volume depleted and hypotensive and received fluids.   She underwent cardioversion in the emergency department after she developed pulmonary edema following volume resuscitation.  It appears that she most likely had 1-2 weeks of a nondescript viral syndrome resulting in fatigue and decreased oral intake.  She probably then developed atrial fibrillation with RVR in the last 1 to 2 days which, in the setting of severe mitral stenosis of her bioprosthetic mitral valve, resulted in symptoms of heart failure and flash pulmonary edema due to elevated left-sided filling pressures at a high heart rate.  She markedly improved after cardioversion."

She was given beta blockade with metoprolol to slow the heart rate.

She will need a mitral valve replacement.

Prehospital Cath Lab Activation for inferior STEMI -- do you agree?

A 40-something male complained of 3 days of chest pressure.  He called 911.  He had some pulmonary edema and hypoxia.

Here is the prehospital ECG:

The computer says ***STEMI***

Based on this and the presence of chest pain, the medics did a prehospital activation of the cath lab.

What do you think?

Interpretation: There is clear atrial flutter. Look at the spikes in V1 at a rate over 300, which are flutter waves.  The flutter wave in the inferior leads mimics ST Elevation.  

An ED ECG was recorded:

Confirmed Atrial Flutter

Again, notice the flutter waves manifest are sharp spikes in V1

There is 2:1 conduction.

The atrial rate is over 300, with a ventricular response at a bit over 150

The cath lab activation was cancelled and the patient was electrically cardioverted.

Here is the post cardioversion ECG:

Sinus tachycardia

Look at the P-waves

Notice the very large upright AND inverted portions of the P-wave in lead V1.  

Notice also the large P-wave in lead II.  

These features indicate right and left atrial enlargement and explain the pronounced size of the atrial flutter spike in V1 during flutter.

A man in his 40s with a highly specific ECG

Case submitted by Charles Harris M.D. and Vitaliy Belyshev M.D., with edits by Pendell Meyers

A 43 year old man with no reported past medical history presented with acute onset chest pain and shortness of breath, as well as a syncopal episode. He stated he was walking into his house when he suddenly started coughing and had a syncopal episode. Over the past few days he had been noticing some intermittent central chest pain described as "burning" with associated shortness of breath. He had no cardiac family history, no drug use, no recent COVID infection. His vitals were normal except for mild tachycardia.

Here is his triage ECG (no prior available):

What do you think?

Meyers' comment: I was on a walk with my wife and new baby daughter in the park when I received a text message with this ECG (see below). In our department we have secure channels to ask each others' opinions on ECGs, echos, etc. You can see that I had no knowledge of the patient, not even age. 

After my interpretation, I was told "burning chest pain." There are certain rare ECGs like this one that are so pathognomonic that clinical context is almost irrelevant, or as in the case of the initial clinical context I got here ("burning chest pain"), can even be misleading in the context of a pathognomonic ECG. There is nothing smart or exceptional about this interpretation, it is simply pattern recognition of squiggly lines. I've seen this exact ECG many times (see below for our other posts on this), have followed up the outcome, and learned from the mimics, to the point that I recognize this ECG instantly and pathognomonically. Anyone can do it, and a computer AI / deep neural network could do it much better than I ever could. I later sent this ECG to Dr. Smith, who instantly said "PE."

ECG Interpretation:

Raw findings:

 - Sinus tachcyardia

 - QRS is narrow with RAD and very poor R wave progression

 - Very slight STE in V2, V3 with convex morphology

 - Terminal T wave inversion in V2 and V3

 - Inferior T wave inversion (III and aVF)

 - S1Q3T3

Subjective Interpretation (Meyers):

 - Pathognomonic for acute severe R heart strain (the most common etiology by far being acute PE)

 - V2-V3 have the most important pathognomonic morphology here, with the small R wave followed by large S wave, then slightly convex ST segment followed by terminal-to-whole T wave inversion

 - paired with the classic simultaneous "inferior and anterior" T wave inversion

 - by the way, sure, there is S1Q3T3, which is by far the least important supportive finding of all the above, because it is the least specific

 - Not consistent with anterior reperfusion (Wellens' morphology), it does not have the right morphology of either the QRS complex or the STT waves. This is hard to describe and can really only be learned by comparison: 

Examples of acute right heart strain from PEs vs. Anterior MI (with reperfusion pattern):

Note that, as Kosuge's study found, ALL cases of PE with precordial T-wave inversion have an inverted T wave in lead III and ALL cases of MI have an upright T wave in lead III:

Examples of anterior reperfusion (Wellens):

Notice that this last one (further along in the reperfusion sequence) has some characteristics in V2-V3 similar to the PE pattern I'm describing, but the differences are easy: PE affects the RV, which should have findings proportionally maximal in V2-V3 and usually not extending leftward beyond V4-5, but this example of Wellens shows the T wave inversions in V2-V6, as well as I, II, aVL. The T waves are upright in III and aVF, whereas they are usually inverted in active right heart strain. 

Back to the case:

A bedside echocardiogram was performed by one of our ultrasound fellowship-trained EM faculty, shown below.

The apical 4 chamber view above was interpreted as having RV dilation and McConnell's sign. Color doppler was applied and showed moderate tricuspid regurgitation.

This was followed by a bedside DVT ultrasound, which shows a non-compressible left popliteal vein as shown below.

Based on all the above information, the patient was given 1mg/kg enoxaparin. The CT pulmonary angiogram was performed approximately 20 minutes later, showing "severe pulmonary thromboembolic disease involving the main pulmonary arteries and lobar supply to all lobes. Imaging evidence of associated right heart strain."

CT images shown below:

The patient was activated as a "Code PE" by our hospital protocol, which facilitates rapid consultation with critical care, interventional radiology, CT surgery, as needed. He continue to have normal oxygen saturation on room air, with no respiratory distress, and BNP 477 and high sensitivity troponin T 55 ng/L (URL = 14 ng/L). He was deemed appropriate for non-ICU status in a medical telemetry bed.

He had an unremarkable 2-day hospital stay on the medical floor, without even requiring any oxygen. He had no obvious coagulopathy discovered, but with further outpatient workup planned. He was discharged on a novel anticoagulant.

Three hours later the ECG was unchanged:

Learning Points:

In a very small subset of PE with at least submassive right heart strain, the ECG can be highly specific or even pathognomonic as detailed by the findings above. The ECG is not at all sensitive for all PE.

Don't forget that severe PE can also present with much more difficult findings on ECG, including RBBB and inferior/RV/anterior STEMI mimics.

Use your bedside echo to correlate ECG findings. 

Wellens (anterior reperfusion) can be differentiated from acute right heart strain as detailed above. 

Consider having a (secure, de-identified, approved) channel for you and your colleagues to help one another recognize and interpret ED-based images for which there is no radiologist or other expert, such as the ECG and bedside ultrasound. It may improve patient care, resident education, and departmental camaraderie.

See some of our prior PE cases:

A crashing patient with an abnormal ECG that you must recognize

Chest pain, ST Elevation, and tachycardia in a 40-something woman

A young woman with altered mental status and hypotension

An elderly woman transferred to you for chest pain, shortness of breath, and positive troponin - does she need the cath lab now?

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

Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the Diagnosis?

A 30-something with 8 hours of chest pain and an elevated troponin

Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis

Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis

Answer: pulmonary embolism. Now another, with ultrasound....

Chest Pain, SOB, anterior T-wave inversion, positive troponin

Anterior T wave inversion due to Pulmonary Embolism

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 reading: Marchik 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.