Prehospital ECG looks very suspicious to the paramedic

This was sent by an anonymous paramedic.

"One of the paramedics at my work approached me the other day and asked for my opinion on two ECGs from a 50s male with sharp chest pain radiating to the back."

What do you think?

The medic asked for my opinion: "This is diagnostic of LAD occlusion, either mid or distal."

Paramedic thoughts: "I was concerned with the size of the T-waves in V4-V6 and of the STD in the inferior leads with slight STE in aVL."   

Smith comment: These T-waves in V4-V6 are all but diagnostic for being hyperacute.  When you combine this finding with the STE in I and aVL and the reciprocal ST depression in III, this is diagnostic of coronary occlusion.

See this post: 

Ten cases of hyperacute T-waves in V4-V6

Paramedic continues:  "Although your formula differentiating normal ST elevation from LAD occlusion should not be applied due to the ST Depression in leads II, III, and aVF, I decided to apply both formulas for the fun of it with the following values:" 

Note from Smith: the formulas really are intended to differentiate STE in V2-V4 that is normal from that which is due to occlusion.  This ECG does not have any appreciable STE in V2-V4.  The leads in question are V4-V6 and only because of T-waves, not ST elevation.

Paramedic continues

"For ECG 1: Computerized QTc: 394ms, STEV360ms: 0. R-wave V4: 4mm. QRSV2: 5mm. This received a positive 4-Variable value of 18.66." 
"For ECG 2: Computerized QTc: 404ms, STEV360ms: 0. R-wave V4: 2mm. QRSV2: 5mm. This received a negative 3-Var Value of 23.18, and a positive 4-Var Value of 19.72"


The medic recorded another ECG 21 minutes later:

No great change

Paramedic: "The ED that this patient was transported to almost never looks at pre-hospital ECGs unless transmitted prior to patient arrival (this one was not), so it is almost guaranteed that the findings would not be appreciated by the receiving physician."

"Anyway, after expressing the concerns that I had, the paramedic told me that the patient waited 90 minutes in the ED prior to being sent to the cath lab. (I did not ask, but I’m assuming that either troponin or serial ECG changes were responsible for the activation)."

Outcome:

"100% LAD occlusion stented. Patient is doing well. If I remember correctly, it was mid-LAD."

This comment is gratifying:

"On another note, I have been following this blog for just over a year now and I can say, without doubt, that i would have missed the subtle findings had it not been for your invaluable knowledge. For that, I sincerely thank you."

Ed Burns (from Life in the Fast Lane) sent me this one....

Ed Burns (who is the creator of the incredible, fantastic, Life in the Fast Lane ECG library) sent me this one....


This is a from a patient with chest pain:

What do you think?
There is very little ST elevation, only 1 mm at the J-point in V2 and V3

Ed's message was this:

Hi Steve,

A colleague sent me this ECG today.

I responded saying that it was a STEMI...

I thought the STs were a little too straight in V2-3 and the T waves a little tall, plus the reciprocal changes in lead III.

Can you improve on my assessment a little?

What is it that definitively makes the diagnosis of STEMI in this case?

Cheers!

Ed

Here was my response:

Ed,

Good call!

There are several features:

First, as you said, there is a nearly straight ST segment.  It is very rare to have non-concavity (convex or straight) in any one of leads V2-V6 in normal variant ST elevation

Second, the QT appears slightly long for early repol.  Remember early repol is called early repol because repolarization comes early (relatively short QT)

Third, there is not enough R-wave amplitude in V4 for the T-wave size

Fourth, there is not enough QRS amplitude in V2 for that T-wave size.

The 3- and 4-variable formulas take the second, third, and fourth issues into account (see below):

Leads III and aVL are indeed somewhat suspicious; however, there really is no ST depression in III and a negative T-wave is normal, especially in the presence of a negative QRS (QRST angle is very small, less than 30 degrees)

Thanks for sending!

Steve
_______________________

One more comment: I would not call it a STEMI, as this diagnosis is associated with ST Elevation "criteria" which this ECG does not meet.  One might call it:

1. Subtle STEMI
2. "Semi-STEMI"
3."Subtle occlusion" (in this case, subtle LAD occlusion)

Formulas use the following measurements

QTc =  (manually measured)                                                      = 400 ms  

ST Elevation at 60 ms after the J-point in lead V3 (STE60V3) = 2.5 mm

R-wave amplitude in V4 (RAV4)                                               = 9.5 mm

QRS amplitude in V2 (QRSV2)                                                 = 17 mm.

3-variable (STE60V3, RAV4 and QTc) = 23.48 (greater than 23.4 predicts LAD occlusion)

4-variable (adds QRSV2)                       =18.34 (greater than 18.2 predicts LAD occlusion)

These 2 cutoffs are the most accurate, not the most sensitive, nor the most specific.  

At 23.4, 3-variable formula had sens, spec, and acc of 86%, 91% and 88%
At 18.2, 4-variable formula had sens, spec, and acc of 89%, 95%, and 92%

The 4-variable is better for both but only in a derivation sample (needs validation!  Anyone??).

The patient did indeed have an LAD occlusion.

Final note on T-wave size: how do the formulas take T-wave size into account??   In our study, T-wave amplitude was not significantly greater for LAD occlusion vs. normal variant ST elevation (early repol also has large T-waves).  But large T-waves are only normal when there is high QRS voltage, as in normal variant.  ST elevation at 60 ms after the J-point is a measure of the slope of the ST segment; the higher the STE60V3, the steeper the slope. A steep slope correlates with a large T-wave and a flat slope with a smaller T-wave. 

Links to articles

3-variable formula: http://www.annemergmed.com/article/S0196-0644(12)00160-6/pdf

4-variable formula: http://www.jecgonline.com/article/S0022-0736(17)30107-3/pdf

See what happens when one fails to diagnose STEMI in LBBB and Paced Rhythm

Written by Meyers, edits by Smith:


A female in her 60s presented complaining of 2-3 days of fatigue and shortness of breath. She called EMS when her symptoms acutely worsened while she was shopping. EMS arrived and recorded a heart rate of 27.

On arrival to the ED she was noted to be in complete heart block. She was given atropine with transient increase in HR to 80s.

This ECG was recorded after response to atropine:

What do you think?

Rhythm

Sinus rhythm with 2nd degree type 1 (Wenckebach) AV block, best visualized in lead I.

Note: Wenckeback AV block occurs at the AV node (as opposed to the His bundle or below). Complete heart block that responds to atropine is also high (AV node, not His bundle or below). The AV node blood supply comes from a branch of the RCA.

On the other hand, 2nd degree type II and third degree (complete) block are likely to be due to LAD ischemia (in third degree block, especially if the escape is wide), and are unlikely to respond to atropine.

So the Wenckebach rhythm alone, and its response to atropine, can provide important information as to the etiology of the block.


How about the QRST?

LBBB is present with concordant ST elevation in leads III and aVF, with excessively discordant reciprocal ST depression in aVL. There is also concordant ST depression seen in the second QRS complex in V2. These findings meet both the original and modified Sgarbossa criteria, and are diagnostic of inferior and posterior wall acute coronary occlusion.

As a reminder or review for new readers, the modified Sgarbossa criteria are designed to identify acute coronary occlusion in the setting of LBBB, and are considered positive if any of the following three criteria are met in any lead when measuring ST elevation (at the J-point, relative to the PR interval):

1) Concordant ST elevation of 1mm or greater in any lead
2) Concordant ST depression of 1mm or greater in leads V1-V3
3) Excessively discordant ST elevation in any lead, such that the STE is 25% or greater of the preceding S-wave amplitude (20% was also still quite specific and even more sensitive)

There is a second rule which is less sensitive but very specific:
Any single lead with proportionally excessively discordant ST elevation or ST depression that is at least 30% of the previous S- or R-wave

See this post for further details on the modified Sgarbossa criteria.

The AV block is almost certainly attributable to the fact that the RCA almost always supplies the AV node.  Her prior recorded heart rate of 27 before atropine suggests she was in complete heart block at that time (no tracings available).

These findings were apparently not noticed in the setting of LBBB. A transvenous pacemaker was placed as the heart rate continued to drop.

What do you think?

Now there is a paced rhythm, as expected.  Do ST segments meet the modified Sgarbossa criteria?  In other words, are the ST segments either 1. concordant or 2. proportionally excessively discordant?  (See the third component of the first rule, or the second rule).

1. The STD ratio in lead I is indeed excessive by the second criteria (one lead with STE or STD greater than 30% of the preceding S- or R-wave).

2. Moreover, the first complex in lead III appears to 4.5 mm of ST Elevation with a 19 mm S-wave, for a ratio of 23.7% (almost 25%). The second complex appears to have a lower ratio (3mm/20mm = 15%).

3. The first complex in aVF seems to have 3mm STE / 14 mm S wave = 21%.

So the third criterion (excessively proportionally discordant STE at 25% of preceding S-wave) is almost met. Remember that, in the validation study, the rule using the third criterion at a 25% ratio was 99% specific and 84% sensitive, but a criterion of 20% was still 80% specific (and 94% sensitive) and thus is almost always due to occlusion.

So although the ischemia is much less visible in the paced rhythm, it is still diagnostic.

Look at lead V2: it is the transition lead in this case (where the QRS transitions from mostly negative to mostly positive), and the positive component of the QRS is slightly larger than the negative component. Thus, one expects ST depression in V2, and in order to indicate ischemia, it has to be proportionally excessive ST depression. Since the R-wave is 8 mm, and excessive STD is 30%, the ST depression would have to be at least 2.4 (2.5) mm to be ischemic. I don't believe it is.

This ECG by itself is be diagnostic of inferior and posterior acute coronary occlusion.

However, in this case, you get the benefit of seeing the ischemic findings both with and without pacing. For the vast majority of our chronic pacemaker patients, we don't get to see this, but they still deserve immediate diagnosis and treatment.

The initial troponin I was elevated at 0.44 ng/mL. After temporarily improving the heart rate with transvenous pacemaker, she was noted to be hemodynamically stable and to have "decreased shortness of breath but persistent fatigue." Coronary ischemia apparently was still not considered the most likely etiology at this time. Electrophysiology consult was placed, and together the physicians felt that the situation was more likely explained by acute renal failure and hyperkalemia (despite the fact that the highest potassium level measured was 5.9 mEq/L). Her second troponin I drawn 3 hours later was 0.38 ng/mL, which was interpreted as reassuring. She was admitted to the CCU and consented for a permanent pacemaker planned for the following morning.


Another ECG was recorded that night, with no mention of what symptoms prompted it:

This shows a huge amount of inferior ST elevation (ST/S ratio 1.0 or greater!) with reciprocal depression in aVL and I. This confirms ongoing transmural infarction of the inferior wall. The ST segment in V2 is inappropriately isoelectric (it should be elevated), suggesting ongoing posterior infarction.

Repeat troponin I around this time was rising at 0.68 ng/mL. Another troponin 4 hours later was 3.04 ng/mL. Unfortunately there is no available documentation about the thought process throughout the evening and night concerning the worsening ECGs and rising troponins. It seems that they scheduled her for cath the next morning.

Her last recorded troponin at 1:30am returned at 181.23 ng/mL!

At 7:45 am the next morning she went into asystole. She received CPR, atropine, epinephrine and was then noted to be in ventricular fibrillation. She was shocked once with return of spontaneous circulation, however her blood pressure continued to trend downward over the next 10 minutes. She was placed on dopamine and epinephrine drips, as well as receiving further hyperkalemia therapy (hyperkalemia had resolved on labs at this point). Another VF arrest was corrected with defibrillation. The patient remained critically hypotensive on multiple drips.

Finally the patient was taken to the cath lab where she was noted to have a completely occluded proximal RCA. Thrombectomy was performed with excellent angiographic result, however the patient continued to deteriorate despite balloon pump placement and continued pressors.

She expired on the cath lab table.



You may think this case is rare, that you and your colleagues would never miss ECG changes like the ones in this case, when the clinical scenario is so obvious. Yet I find these cases far too often. I cannot comment on the clinical decision making about NOT doing angiography when such patients have obvious clinical and ECG indications. What I can help with is helping clinicians to know what ECG findings to look for in the setting of LBBB and/or paced rhythms.

In one online quiz in Medscape, 50% of physicians believed the STEMI cannot be diagnosed in the presence of a paced rhythm.

The modified Sgarbossa criteria have been validated as the most accurate criteria currently available for identifying acute coronary occlusion in the setting of LBBB (but like all other criteria, are not perfect). We believe (based on cases like this and many others) that they are also applicable in paced rhythm, and are currently in the process of studying this. Preliminary results are positive, and the full multicenter results are on the way.

Serial ECG recordings are essential: paramedic makes a great call!

This case was sent by Andrew, an Intensive Care Paramedic from Melbourne, Australia.

Case

We were dispatched to a female in her 50's who had been experiencing L) sided, intermittent chest heaviness, radiating to her L) arm for the past ~24 hours. 

She had a past Hx of IDDM, hypertension, high cholesterol and was an ex-smoker. She had called the ambulance today as the pain was more severe and persistent than it had been previously. She had never experienced symptoms like this in the past.

When we arrived, she was c/o 8/10 pain and was mildly diaphoretic, but not looking overly unwell. I recorded this ECG.

I read this as normal

The pt was given 300 mg aspirin and 300 mcg sublingual GTN, with the pain reducing to 5/10.

A few minutes later, her pain then increased to 7/10 and she appeared a bit more diaphoretic. I took the following ECG.

Now there is new ST elevation in V2-V4, with tiny new Q-waves

I was concerned with the 1mm STE she developed in V2 and 0.5mm in V3-V4 as well as the presence of small Q waves. The T waves also looked bigger and fatter to me when compared to the initial ECG. Unsurprisingly, the computer interpretation failed to recognize these changes.

Her pain then reduced to 3/10, which prompted me to record another ECG. 

All the segments have returned to isoelectric, the Q waves and T waves also appear smaller and are consistent with the initial ECG.

Based on the presence of dynamic ST segments and T waves, I chose to bypass two smaller hospitals and transport her to a PCI centre with a STEMI notification. 

Throughout the transport to hospital, there was no change in the ECG from #3, but upon arrival at ED, she was pale and profusely diaphoretic, and still complained of 1/10 pain post IV analgesia.

The ED consultants were skeptical of my read.

About an hour after our arrival, she became agitated and hypotensive and the final ECG was taken.

Obvious Anterior STEMI

The pt was taken to Cath Lab where her LAD was stented. There was minimal rise in her troponin and CK and she was doing well the following day.

Are These Wellens' Waves??

This is a repost.  I've received a few questions like this, so wanted to re-inforce the idea of down-up vs. up-down T-waves

Case:

One of our residents texted me this ECG and was worried about Wellens' waves.

A middle-aged male presented with vomiting.  Here was the initial ED ECG:

What do you think?

Here is my response:  "What is the Potassium?"

Wellen's waves are always Up-Down T-waves, not Down-Up T-waves as here.  Down-Up T-waves in V2 and V3 have only 3 causes, as below.

Moreover, the QT interval is impossibly long at about 560 ms, with a corrected QT of 593 ms (Fridericia correction, which seems to be the best; QTc(Bazett) = 611 ms.

When the QT is impossibly long, think that the "T-wave" is actually a U-wave, not a T-wave.

Here the U-waves are highlighted:

1. In lead V6, one can discern discrete T-waves (red arrow) and U-waves (black arrow).
2.  Go down to rhythm strip lead II across the bottom, identify T- and U-waves there.
3. Go 3 beats earlier in lead II to identify the U-wave there (green line).
4. Draw the green line up to show the U-waves in leads V1-V3

So these are indeed U-waves, not T-waves

1) Posterior MI with some reperfusion (reciprocal to Up-Down T-waves of the posterior wall, analogous to Wellens' of the posterior wall as recorded from the anterior wall). 
See case below
2) Hypokalemia (in which case the upright component is really a U-wave).  In this case, V6 is pathognomonic: you can see a clear large U-wave following the T-wave.  It must be hypokalemia.  Notice also the very long QT, which is really a long QU-wave.

Other down-up T-waves:

3) Reciprocal findings between leads III and aVL in post-ischemic (Wellens' type) T-waves:
             In lead III: reciprocal to up-down (Wellens' type) post-ischemic T-waves in aVL.  
             In lead aVL: reciprocal to up-down (Wellens' type) post-ischemic T-waves in III.



The K was 2.0 mEq/L.

For contrast: Here are classic Wellens Pattern A (biphasic) waves:

Notice they are biphasic Up-Down.

Clinical Course

The patient had all serial troponins below the level of detection.  Potassium was repleted.  Here is the ECG after normalization of K at 3.5 mEq/L:

Here, again, the previous ECG at K = 2.0 mEq/L:

Here is an example of a Down-Up T-wave from Reperfusing Posterior MI.
It comes from this fascinating post:

Series of Prehospital ECGs Showing Reperfusion of Inferior-posterior STEMI:

See this too:

Classic Evolution of Wellens' T-waves over 26 hours

Learning Points

1. Wellens' waves (Pattern A) are biphasic Up-Down.  

                            (Pattern B is deep symmetric inversion)
2. Down-Up waves in V2, V3 should make you think of reperfusing posterior MI or hypokalemia. 
3. A very long QT (really a QU) should make you suspect hypokalemia.
4.  Look for clear U-waves in other leads.
5.  Finally, Wellens' syndrome is a SYNDROME that requires 1) typical anginal chest pain 2) Resolution of the chest pain 3) ECG recorded after resolution.

A 70-something woman with syncope and a wide complex

This case was written by Andy Lichtenheld (https://twitter.com/ALichtenheld), a really smart 2nd year resident here at our Emergency Medicine program at Hennepin County Medical Center.  

Here is some shameless promotion of our residency, which was started in 1972 and which we think is second to none:

Learn why our current residents chose Hennepin.

Case

A 70-something woman with a history of CAD arrived by EMS after a syncopal episode. She had been in her usual state of health when she suddenly became lightheaded and collapsed. She regained consciousness prior to EMS arrival and arrived in the ED confused but gradually clearing. She had no chest discomfort, shortness of breath, arm pain, jaw pain or any other symptoms.

An initial ECG was recorded:

What do you think?

The computer has identified it as sinus with a Mobitz I AV block with a LBBB.   

However, both the rhythm and QRST appear to be more complicated.  

Rhythm: Regular P-waves can be seen throughout the rhythm strip. Without using calipers and without using more thought than necessary in an emergency, it is hard to say whether this is first or second degree AV block with conduction to a left bundle branch block, or if it is third degree (complete) heart block with an escape from the right ventricle.  Beats 3 and 5 are PVCs.   

Smith: After scrutinizing at leisure, I do think it is complete heart block with an RV escape, but it is complicated.

What else?

There is excessively discordant ST elevation in V1 & V2.  ST/S ratio in V1 is 5/15 = 33%.

There is excessively discordant ST elevation in aVR.  The ST/S ratio is 3/8 = 37%.

There is also excessively discordant ST depression in lead I (ST/R ratio = 100%) and V4 (ST/R ratio = ~60%).

If you accept, as Dr. Smith does, that the Smith Modified Sgarbossa criteria can be used not only in LBBB, but also in ventricular escape rhythms, then any one of these findings meets those criteria.  The STE in V1 as well as the STD in I and V4 are particularly specific for occlusion.

Furthermore, there is an abnormal amount of STD in V5 and V6 (ST/R ratio almost 20%).

Smith Modified Sgarbossa Criteria for LBBB and Ventricular Paced Rhythms

Rule 1: (80-90% sensitive, 95% specific for occlusion)

Any one of:

1. 1 mm concordant STE in any one lead

2. 1 mm concordant STD in any one of V1-V3

3. At least 1 mm discordant STE that is ≥25% of the preceding S-wave in at least one lead

Rule 2: (Only 64% sensitive, but 98% specific for occlusion)

Any one lead with proportionally discordant STE or STD of at least 30% of the preceding R- or S-wave

Smith comment: 

One more finding!!   PVCs!!!!   The 5th beat is a PVC and has an RBBB morphology (large R-wave in aVR with wide S-wave in V5).  This implies a PVC originating in the left ventricle.  RBBB morphology PVCs should never have an ST segment that is concordant to the QRS, as it is here in lead aVR.  This is diagnostic for STEMI.

See these cases:

STEMI Seen Best in PVC, Diagnosed by Medic, Ignored by Physician

Look at the PVCs!!

Look at the PVCs (again)!!

Case continued

A previous ECG was obtained:

There is a preexisting LBBB with proportionally normal discordant ST elevation, which makes the ST changes in the new EKG obvious by comparison.

This also suggests that the rhythm in the first ECG is supraventricular, because the QRS morphology is LBBB.  However, if you look closely at V5 and V6 in the first ECG, both have a very narrow peak compared to this old ECG which is much more typical LBBB.

Smith comment: I am still not completely certain as to whether the first ECG is supraventricular with left bundle branch block, or with RV escape.  But it does not matter: the patient has a coronary occlusion until proven otherwise.  She needs immediate pacer pad placement and angiography/PCI.

Case Continued

The clinicians caring for the patient were concerned about an acute coronary occlusion. The cardiologist was in hospital and was paged to the resuscitation area. Over the course of the following few minutes, the patient gradually recovered to her normal mental status. She remained normotensive and entirely asymptomatic. 

As the cardiologist arrived, a change in the QRS morphology was noted on the monitor and a repeat ECG was obtained:

What is your interpretation?

Now there is definitely complete heart block with a ventricular escape:

--The predominant QRS morphology is now RBBB + LAFB with interposed PVC's, which indicates a dominant escape focus now in the left posterior fascicle.

--The ST elevation in V1 and V2 with reciprocal ST depression are now obvious.  It is RBBB morphology with ST elevation concordant to the R-wave, similar to the PVC mentioned above.  This does not happen without ischemia.

--There is marked ST depression in lead II which is then attenuated in aVF and then entirely absent in lead III.  

Smith comment: What is the infarct artery???  With STE in V1 and aVR, one might think this is LAD or left main. Such a conclusion would be consistent with the diffuse ST depression.  

The ST axis is exactly towards aVR, which is what you expect with diffuse subendocardial ischemia (ST depression vector towards I and II, with a reciprocal ST elevation vector towards aVR).  However, the ST elevation is so much more pronounced than the ST depression.  

Is there something else going on??

Andy Lichtenheld wrote: "This is also consistent with inferior and large RV MI due to proximal RCA occlusion."

Case continued:

The initial troponin I returned elevated at 4.5 ng/mL.

She was taken to the cath lab where a 90% proximal RCA lesion, proximal to the RV marginal branch, was stented and a temporary pacemaker was placed.

The next day echo showed very poor LV function with an inferior wall motion abnormality.

Smith comment: 

So Dr. Lichtenheld was correct.  It was an inferior + right ventricular (RV) STEMI.

This pattern of ST elevation and depression is often due to LAD or left main.

I can't fully explain why there was no ST elevation in the inferior leads, especially lead III.

See this case: 

Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6

More on ECG in inferior and RV MI:

http://hqmeded-ecg.blogspot.com/2014/05/inferior-and-posterior-stemi-what-else.html

http://hqmeded-ecg.blogspot.com/2014/03/the-ecg-told-whole-story-but-no-one.html


Here are comments from Ken Grauer:

ECG Interpretation

Fascinating case, about which we’ll probably never know the mechanism of the rhythms for certain. I’ll make a few speculations. I suspect that ECG #1 was not complete AV block — because of the clear irregularity of the ventricular response. In most cases with complete AV block — the ventricular response will be more regular. We see this in ECG #3, in which there clearly IS complete AV block. Returning to ECG #1 — the atrial rhythm is NOT regular. Initially P waves are buried within the ST segment of the first few beats. If you follow out atrial deflections carefully with calipers — the P-P interval varies in a difficult-to-predict manner in some parts of the parts of the tracing. This can happen with atrial infarction, though we really do not see P wave ST segment deviation … QRS morphology in ECG #1 I believe is consistent with LBBB (albeit with lots of fragmentation) — with beats #3 and #5 being PVCs. As per Dr. Smith — the situation is extremely complex. I suspect there may be atypical Wenckebach (PR intervals increasing to quite long toward the end of the tracing) — though R-R interval periodicity is clearly atypical. What IS apparent (as per Dr. Smith) — is that ST-T wave morphology that we see in ECG #1 is abnormal regardless of the etiology of the QRS complex. This ST-T wave abnormality in ECG #1 was confirmed when the baseline LBBB tracing was obtained. NOTE — The first 2 beats in ECG #2 conduct with a NARROW QRS complex — which suggests that this patient’s “baseline” ECG had a rate-related LBBB! I believe that theory is confirmed in ECG #3, which as per Dr. Smith now definitely DOES show complete AV block — with regular escape rhythm and now clearly much more regular atrial activity than we saw in ECG #1. I believe we may have an AV nodal (junctional) escape rhythm in ECG #3 — as the escape rate is ~50/minute, and QRS morphology looks VERY supraventricular given well definite RBBB-morphology in anterior leads and sharp/narrow initial deflections in lateral leads with wide terminal S waves. The heart rate is slower — so the rate-related LBBB has now resolved. We are left with a pattern of marked ST elevation in V1,V2,V3 — with maximal ST elevation in lead V1. As astutely pointed out by Dr. Lichtenheld — this pattern is consistent with isolated acute RV infarction! Of note — virtually all other leads on ECG #3 show significant scooped ST depression (actually a “mirror-image” shape opposite to the coved ST elevation in V1,V2,V3 — so my thought is that in addition to acute RV infarction — there was diffuse subendocardial ischemia. Note however, that there IS suggestion of ST coving in lead III on ECG #3, as well as relatively LESS ST depression in lead aVF — so perhaps the reason we did not see ST elevation in the inferior leads, is that this was essentially cancelled out by the diffuse subendocardial ischemia ST depression seen in virtually all other leads except V1,2,3? Finally — If we go back to ECG #1 (when there was rate-related BBB) — we actually DO see the same type of ST segment deviations that we see in ECG #3 — with the difference being that these ST deviations in ECG #1 were partially masked by the underlying rate-related LBBB. That is, marked ST coving in lead III, ST elevation in V1,2,3 — and dramatic ST depression (beyond the amount expected for LBBB) in all other leads. GREAT case! Thanks for presenting!