Electrophysiological curiosity. Can you spot it?

        Written by Magnus Nossen (with comments and laddergram by Ken Grauer)

The patient in today’s case is a man in his 60s — who presented with palpitations and lightheadedness. He had no history of syncope. The patient had hypertension, but was otherwise healthy. Due to the reported symptoms, he was admitted for observation and put on telemetry monitoring. Below in Figure-1 is a tracing obtained from the in-house telemetry. 

• The rhythm strip in Figure-1 shows four ECG leads. (aVF, III, V1 and V5). The paper speed is 25mm/s. There is a bigeminal pattern with every other QRS complex being wide. Can you explain what is going on in this tracing? Do you notice anything unusual in this rhythm strip? 

Figure-1: The initial rhythm strip in today’s case.

Below in Figure-2 is another tracing from the same patient. Beat #9 is wide, and manifests a different QRS morphology than the other wide beats. What is the likely explanation for this?

Figure-2: A 2nd rhythm strip from today’s patient.

COMMENT:

Both rhythm strips show sinus rhythm with premature ventricular complexes (PVCs). Following most of these PVCs — there is retrograde conduction that begins from the ventricles, and then travels backward through the AV node and the atria (VA conduction). Because the atria are captured in retrograde fashion — the P waves are negative (with these retrograde P waves being partially hidden within the ST segments of the preceding PVC).

Of note is variation in the RP interval! (ie, the distance from the beginning of the PVC — until the retrograde P wave).

• There are 2 different RP intervals. This can be explained by having dual AV conduction pathways in the retrograde direction. One of these pathways conducts significantly slower than the other.
• When the retrograde impulse travels through the slower pathway — conduction time and RP interval is longer. 
• The opposite occurs when retrograde conduction is through the faster pathway (ie, faster retrograde conduction results in a shorter RP interval).

Because of added complexity in the 2nd tracing — I have labeled this 2nd rhythm strip in Figure-3:

• Green arrows point to sinus P waves in Figure-3 — with normal sinus conduction of beats #1,3,5,7 and 10.
• Beats #2,4,6 and 8 are PVCs with a similar (albeit not identical) QRS morphology. These PVCs most probably originate from the same ectopic site in the ventricles.
• The Orange arrow points to a retrograde P wave with a longer RP interval (295 msec.) — that is conducted from PVC beat #2.
• The Blue arrow points to a retrograde P wave with a shorter RP interval (170 msec.) — that is conducted from PVC beat #4.
• There is no retrograde conduction following the PVC beat #6.
• The Red arrow points to a retrograde P wave with a longer RP interval — that is conducted from the PVC beat #8. Note that this retrograde RP interval from beat #8 is slightly longer than the RP interval from beat #2 (330 msec. vs 295 msec.).

Figure-3: I’ve labeled Rhythm #2.

What about Beat #9?

• Note that beat #9 is wide — but with a different QRS morphology when compared to wide beats #2,4,6,8 (ie, Beat #9 manifests a predominantly negative QRS in all 4 monitoring leads).
• Beat #9 follows after the longest RP interval in this rhythm strip. The reason beat #9 looks different — is that beat #9 is a ventricular “echo” or reciprocal beat. The mechanism operative for this reciprocal beat in Figure-3 — is illustrated in Panel C of Figure-4.

Figure-4: Illustration of the mechanism for reciprocal (echo) beats. (Adapted from Strasberg et al — Am J Cardiol 48(4): 639-646, 1982 ).

KEY Clinical Point (Grauer):

The importance of Figure-4 — is that it shows the mechanism for initiation of many reentry SVT rhythms! (ie, See My Comment at the bottom of the page in the March 6, 2020 post in Dr. Smith's ECG Blog — in which I illustrate near the very end of my March 6, 2020 Comment the initiation of "fast-slow" form of AVNRT by what we see here in Panel B).

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Returning to the mechanism in Figure-3 of today's case:

Grauer: For clarity in Figure-5 — I've kept the same color coding, and illustrate Dr Nossen's above explanation of reciprocal beating in a Laddergram that concentrates on lead III from Figure-3.

• GREEN arrows and lines in the laddergram — show normal sinus-conducted beats.
• Beats #2,4,6 and 8 are PVCs (The PINK circles schematically show origin of these PVCs from the ventricle).
• The ORANGE dotted line — shows PVC beat #2 conducting backward to produce a retrograde P wave with an RP interval = 295 msec.
• The BLUE dotted line — shows PVC #4 conducting backward over the slower AV nodal pathway, to produce a retrograde P wave with an RP interval = 170 msec.
• PVC #6 — fails to make it all the way back to the atria.
• But — PVC #8 not only conducts backward, here over the slower AV nodal pathway to produce a retrograde P wave (the RED dotted line in the laddergram, leading to the RED arrow) — but because of its longer RP interval (330 msec.) — the faster AV nodal pathway has enough time to recover forward conduction properties — and therefore produces beat #9 (in PURPLE) — which is an "echo" beat that is conducted with rate-dependent aberrancy because beat #9 occurs so soon after beat #8.

Figure-5: My proposed Laddergram illustrating the mechanism of the "echo" beat in Figure-3.

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The CASE Continues:

The patient had many episodes of NSVT (Non-Sustained Ventricular Tachycardia) — like the one shown below in Figure-6. He experienced palpitations — both when having PVCs, as well as during his episodes of NSVT and VT. 

• Can YOU identify atrial activity in Figure-6?
•    Why does beat #3 prove that the wide beats are ventricular?

 

Figure-6: Subsequent 5-lead rhythm strip with an episode of NSVT.

Atrial Activity in Figure-6:

The rhythm in Figure-6 begins with a series of regular sinus P waves (GREEN arrows in Figure-7).

• It could be easy to overlook the 2nd and 3rd GREEN arrows — because they are partially hidden within the ST-T waves of beats #2 and 4. 
• The KEY is to recognize the 4th, 5th and 6th GREEN arrows — and to note that the P-P interval is fairly constant for these 3 P waves.
• Setting your calipers to approximately this P-P interval — should facilitate finding the 2nd and 3rd GREEN arrow P waves!
• Remember — Since the 1st beat in Figure-6 is sinus-conducted, It is logical for the underlying atrial rhythm to be regular, at least for the beginning of this tracing. So, we are looking for signs of an underlying regular atrial rhythm (with perhaps slight sinus arrhythmia) — and it is much easier to find this when you know what you are looking for! (and using calipers makes the partially-hidden P waves so easy to find! ).
• 
  
• We know beats #2 and #4 are PVCs — because these beats are wide, very different-looking from sinus-conducted beats, and these beats are not preceded by a premature P wave.
• 
  
• Isn't beat #3 intermediate in its QRS morphology? — compared to the morphology of sinus-conducted beat #1 and PVCs #2 and #4? The reason for this intermediate QRS morphology — is that beat #3 is a Fusion beat! ("F") — and this proves that all of the beats that look like #2 and #4 are also of ventricular etiology! (See "Lesson #3" in My Comment at the bottom of the page of the April 2, 2022 post for more on the diagnostic value of fusion beats).
• 
  
• Finally, knowing that today's patient shows a tendency for ventricular beats to conduct retrograde — I suspect that the YELLOW arrows in Figure-7 represent retrograde P waves following ventricular beats in the run of NSVT.

Figure-7: I've labeled Figure-6.

CASE Conclusion:

Today's patient had a structurally normal heart and a normal cardiac catheterization. A permanent pacemaker was placed and the patient was atrial paced at 60bpm. After pacemaker placement — a ß-blocker was initiated. The  hope was that the increased heart rate (from atrial pacing) combined with ß-blocker treatment would suppress most ventricular ectopic activity and the runs of NSVT. When these measures did not work — the patient underwent PVC ablation, which did achieve a good clinical result.

Learning points:

• Dual AV physiology in the retrograde direction does not necessarily mean there is dual AV conduction in the antegrade direction. 
• Dual AV physiology is necessary for AVNRT and reciprocal or "echo" beats. 
• 
  
• As shown above in Figure-4 — Echo beats provide a common mechanism for initiation of reentry SVT rhythms! (and — understanding the mechanism to produce "echo" beats provides insight for understanding how a run of NSVT may even produce a subsequent run of reentry SVT à la Panel C in Figure-4). 

 

 

Can you treat Non-STEMI with thrombolytics if it is OMI (Occlusion MI)? Of course!

This case was sent by an old residency friend, Kirk Lufkin.  He works in a small hospital in Northern Michigan.  

Case

A 61 year old female. hypertension no other past history presented with 30 minutes of fluctuating non-radiating heaviness in chest, with diaphoresis and nausea. VS normal. No cardiac past history. 

Here is her ECG:

What do you think?

There are inferior hyperacute T-waves (diagnostic of inferior OMI), with 1) reciprocal ST depression in aVL, 2) a reciprocally inverted hyperacute T-wave in aVL, 3) ST depression in V2 (diagnostic of posterior OMI) and 4) large lateral T-waves which are probably hyperacute.

So this is acute OMI.  But it does not meet the ridiculous "STEMI criteria" since there is not 1 mm of STE in any lead.

What does the Queen of Hearts say? (Dr. Lufkin did not need her)

OMI with High Confidence

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Dr. Lufkin gave thrombolytics, with a "door-to-needle" time of 24 minutes.  The standard of care is < 30 minutes.

Minutes later, the pain resolved and this ECG was recorded:

Complete resolution of ST Elevation and of V2 ST depression, and of V4-6 hyperacute T-waves.

Later, the first troponin I returned at 0.057 ng/mL (4th generation, not high sensitivity). 

The patient was transferred to a hospital with PCI capability.

Here is the angiogram:

Very tight stenosis in circumflex, but with TIMI-3 flow, thanks to thrombolytics.

Here is the circumflex after stenting:

Wide open

The cardiologist called Dr. Lufkin back and said "Great call!!"

Learn to read the ECG for sublte OMI, and get the Queen of Hearts.

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MY Comment, by KEN GRAUER, MD (11/1/2024):

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The beauty of today's case is its simple efficiency. Working in a smaller emergency facility — Dr. Lufkin considered the history ( = new-onset, severe CP in a 61-year old woman) — correctly interpreted the initial ECG (which I've reproduced and labeled in Figure-1) — and, given time constraints and distance from a PCI-capable center — he expediently initiated thrombolytic therapy ("door-to-needle" time = 24 minutes).

• When promptly administered — thrombolytic therapy may be very effective (witness relief within minutes of this patient's CP — with marked improvement in ECG abnormalities).

As per Dr. Smith — the initial ECG is diagnostic of acute infero-postero-lateral OMI (consistent with acute LCx occlusion). I highlight KEY findings in Figure-1:

• My "eye" was immediately drawn to the obviously hyperacute T wave in lead III (within the RED rectangle). Equally hyperacute are T waves in the other 2 inferior leads (RED arrows in leads II and aVF) — with each of these 3 leads featuring hypervoluminous T waves "fatter"-at-their-peak and wider-at-their-base than expected given QRS amplitude in each respective lead.
• Confirmation in this 61yo woman with new CP that these inferior lead findings are "real" — is forthcoming from mirror-image opposite reciprocal ST-T wave depression in lead aVL (within the BLUE rectangle), and to a lesser extent in lead I.
• Additional confirmation is seen in lead V2 (within the RED rectangle in the chest leads) — with pathognomonic downsloping ST depression and biphasic T wave with terminal positivity (RED arrow in lead V2). Neighboring leads V1 and V3 are consistent with ongoing posterior OMI (T wave inversion in V1 — and ST straightening with depression in lead V3).
• In view of the above findings — I thought the T waves in leads V5 and V6 were "bulkier" than expected (given modest size of the R wave in these leads).
• 
  
• BOTTOM Line: As emphasized by Dr. Smith — the above findings are absolutely diagnostic of acute infero-postero-lateral OMI. With practice — these diagnostic ECG findings can (and should) be recognized within seconds. Dr. Lufkin appreciated these findings, and given the worrisome history — he needed no more testing and no additional ECGs to justify immediate initiation of thrombolytic therapy.

Figure-1: I've labeled the initial ECG in today's case.

What about the Rhythm in Figure-1?

Did YOU notice the irregularity in today's rhythm? I'll preface my remarks by acknowledging that the rhythm in Figure-1 does not follow "the usual rules".

• There appears to be some sort of group beating — initially with 4 sinus beats, and then 3 groups of 2 beats.
• Upright P waves precede each of the 10 beats in the long lead II rhythm strip. That said — P wave morphology varies in no particular pattern, and to a greater extent than is usually seen in a normal sinus rhythm.
• Given the acute infero-postero MI — I looked for AV Wenckebach, which is so commonly seen in this clinical setting. But I see no non-conducted on-time P wave after beats #4,6,8 and 10.
• I also do not see any evidence of blocked PACs — as the T waves of beats #4,6,8 and 10 look identical to the T waves of other conducted beats.
• The fact that there is variation in the R-R interval for the first 4 sinus-conducted beats suggests the possibility of a marked sinus arrhythmia — but I would not expect this degree of variable P wave morphology and such group beating.
• The rhythm could represent Type I SA block with underlying sinus arrhythmia — but again, I would not expect this degree of variable P wave morphology (and in my experience — true SA block is rare).
• 
  
• By Default: I thought some form of unusual marked sinus arrhythmia, with uncharacteristically variable sinus P wave morphology to be the best I could come up with for the rhythm diagnosis.
• The "Good News" — Normal sinus rhythm with consistent P wave morphology resumed following successful thrombolytic therapy. Perhaps the highly unusual initial rhythm in today's case was simply the result of SA nodal ischemia that resolved following coronary reperfusion.

Chest pain and Saddleback STE. For Which of these 6 Cases should we Activate the cath lab? And how does the Queen of Hearts perform?

Smith Introduction:

Saddleback ST Elevation is often an OMI mimic, so one needs to scrutinize these ECGs!!

Written by Magnus Nossen

Below are ECGs from six different patients. All of the patients contacted EMS due to acute onset chest pain. Imagine you get these ECGs in real time and you are asked whether or not the cath lab should be activated? All ECGs in this case have saddleback ST elevation. Which of the ECGs represent OMI? 

 

ECG #1

Case 1. The above ECG is from a 70 something male with chest pain. The ECG was originally recorded at 50mm/s paper speed. It has been compressed on the X-axis so it looks like it was recorded at 25mm/s. What do you think?

ECG #2

Case 2: The above ECG was obtained from a diabetic 45 year old smoker with chest pain. What do you think of the ECG changes here?

ECG #3

Case 3. This ECG (above) was recorded from a 55 year old male patient with acute onset chest pain and diaphoresis. How would you interpret this ECG?

 

ECG #4

Case 4: The above ECG belongs to an 80 something male with acute onset chest pain radiating to the back. How would you assess the ECG changes here?

ECG #5

Case 5: The above ECG was obtained from a 50 something male with chest pain and epigastric pain. Are these ECG changes benign or not? 

ECG #6

 

Case 6: The above ECG was obtained from a 70 something male with vague pressure like chest discomfort. What do you think?

Discussion: When a patient presents with chest pain and ST segment elevation we need to evaluate whether or not the ST elevation is ischemic in nature. The ST-segment and beginning of the T-wave in a non-ischemic ECG usually have a slightly upward concave appearance. Ischemia often produces a straightening of the ST segment and sometimes upward convexity. Saddleback ST segments are usually not ischemic in origin, but as with all other «rules», there are exceptions. In today’s post we have shown six ECGs out of which three were OMI and three were not. 

Case #1 OMI, Queen gets it right

The ECG shows sinus rhythm with a narrow complex QRS. There is ST elevation with saddleback morphology in the inferior leads (II, III and aVF). The inferior leads do not have a distinct J-wave. The T waves are bulky and appear hyperacute. Moreover the high lateral leads aVL, and I both show reciprocal discordant ST depression and T wave inversions. When looking at the precordial leads there is appreciable slight ST depression in lead V2 and inappropriately isoelectric ST segment i lead V3. All of these findings together makes this ECG diagnostic of inferior and posterior occlusion myocardial infarction (OMI)

The patient is this case was treated as if he had an ongoing OMI. Primary PCI was not feasible and therefore the patient was given thrombolytics by EMS. He arrived in our ED with the below ECG pain free. As you can see the ECG has changed dramatically with the thrombolytic therapy. There is now reperfusion of the artery.

Post thrombolytics ECG

As you can appreciate, the ST elevation in the inferior leads is gone. There is still hyperacute looking T waves in the inferior leads and ST depression V2-V4. Following the improvement in the ECG the patient's pain too improved drastically.  This of course proves that the initial ECG was OMI and that the artery has reperfused. At cath later the same day, a proximal 99% RCA culprit lesion was stented. Troponin T peaked at 4051 ng/L. (ref < 14ng/L)

If the ECG after thrombolytics shows normalization of the ST segment and T wave changes and the patient is pain free, there is no need for urgent CAG. It is reasonable to wait a few hours after lytics if you are sure that the artery is reperfused. The GRACIA-2 trial showed that PCI is safe 3-12 hours after thrombolysis. Of course, the reperfused artery can re-occlude at any time, so these patients need to be on ST-guard and taken for immediate catheterization if they re-occlude. The QoH interpretation (below) was OMI with high confidence for ECG #1.

Case #2 FAKE (Mimic), Queen Version 2 gets it right

The second ECG in today’s case was obtained from a 45 year old male with a history of tobacco use. I was shown this ECG by a colleague who asked for my opinion. I said I thought it looked like a fake (in other words an OMI mimic). I sent this ECG to the EKG Nerdz group. You can see some of the answers below.

The patient ruled out with serial troponins being negative. Echocardiography was without wall motion abnormality. A previous ECG was later obtained that showed similar findings. ECG #2 does have ST depression and an inverted T wave in lead aVL just as in the first ECG in today’s case. Why is this reciprocal ST depression not suggestive of ischemia you may ask?. The ST segment and T wave in lead aVL are concordant to the QRS complex. This is a significant difference and the T wave inversion seen in aVL therefore cannot be given the same significance as in the first case in today's post. (See Dr. Smith comment below for more insight). Also there are no signs of posterior ischemia (ST depression) in leads V2-V4. 

Smith: There is some reciprocal STD in aVL. Reciprocal STD in aVL is seen sometimes in non-ischemic ECGs, but is almost never seen in pericarditis (Bischof et al.).  Moreover, the T-wave inversion in aVL is a normal finding because the QRST axis is normal; this means that the QRS axis and T-wave axis are close to each other.  The QRS axis is approximately 110 degrees and the T-wave axis is approximately 80 degrees (this is best assessed by lead I, which has S-wave > R-wave (right axis deviation) but T-wave upright (more towards lead I than away from lead I).  The difference is only 30 degrees and up to 45 degrees is normal.  True "T-wave inversion" has a wide QRST angle.

The Queen of Hearts AI model version 1 interpreted ECG #2 as OMI high confidence. Version 2.0 (not yet released) was shown the exact same ECG and the interpretation was not OMI. 

The image below shows that QoH version 1 interprets the ECG as OMI with high confidence (value close to 1 on the top line). Version 2 interprets the ECG as not OMI with high confidence (value close to 0 on the second line). It is remarkable how much the AI model has changed its interpretation of the same ECG. It now correctly and confidently identifies ECG #2 as not OMI

Case #3 OMI, Queen gets it right

This ECG shows sinus rhythm with a narrow QRS complex. There is an incomplete RBBB (rSr` in V1). There is left anterior hemi-block (QRS negative in lead II). Lead V2 shows saddleback ST-elevation. In leads V2-V5 there is ST elevation and (very impressive) hyperacute bulky T waves. In the inferior (II, III aVF) and lateral (I, aVL and V6) leads there are hyperacute T waves. This ECG is absolutely diagnostic of anterior and inferior OMI and is compatible with a wrap around LAD supplying the anterior and inferior wall. 

Smith: The vast majority of saddleback STE in lead V2 is NOT due to acute OMI.  I have only 2 such cases on this blog up until now (now 3!).  This one is obvious, luckily!

Case #4 FAKE (Mimic) Queen gets it right

I was on call when I received this pre-hospital ECG. The patient is an 80 year old man with acute onset chest and back pain. The ECG shows significant ST elevation. I was somewhat concerned that the ECG represented OMI and activated the cath lab. The ECG shows qR complexes in leads V2-V3 with upward concave ST segment elevation. Saddleback ST elevation in V2 is rarely due to OMI. A much more common cause of saddleback ST elevation in V1-V3 is that the leads have been placed too high on the chest and this should always be checked. Here the P wave polarity in V1 and V2 are consistent with correct lead placement. (If V1 and V2 are placed too high, P waves are often of negative polarity in these leads)

I thought for a moment that the ECG might represent LVH, but I would expect slightly more (appropriately) discordant ST elevation in the inferior leads. I was concerned that the ECG represented some strange anterior OMI with inferior reciprocal isoelectric ST segments. I was not convinced that the ECG changes represented OMI, but I figured I had to prove it was not. It would be a terrible mistake to miss this as occlusion.

CAG showed significant LAD disease in the mid-segment. However, there was no thrombotic component and there was TIMI III flow in all coronaries and their main branches. In conclusion, CAG was interpreted as showing significant atherosclerotic disease, but it was not deemed likely to be causing the ECG changes. PCI was performed as the lesion was significant. The post-PCI ECG did not change. Troponin T drawn five hours after the onset of symptoms was 17ng/L. Troponin levels did not increase significantly. Below you can see the post PCI ECG and echo. A CT scan was done as part of the work up, but no definite cause of the patient's chest pain was identified. 

Below: ECG recorded post PCI

The Queen is Amazing!

Case #5: FAKE (Mimic), Queen gets it right.

This patient presented with abdominal discomfort. Inferior wall MI is slightly more likely to produce abdominal symptoms than infarction of other myocardial territories. The ECG shows ST elevation in the inferior leads. There is minimal T wave inversion in lead aVL. One would expect much more pronounced reciprocal change in the lateral leads if this was an inferior wall MI (contrast case #1). Also, leads II and aVF have quite distinct J-waves which generally are more common with non-ischemic ST elevation. This patient ruled out by serial troponins. Below is the QoH interpretation. 

Case #6: OMI, Queen gets it right

This ECG shows sinus rhythm at about 60 bpm. There is saddleback ST elevation in leads V1 and leads V2. T waves throughout the precordium are hyperacute with a DeWinters appearance in lead V3-V4. The P waves in lead V1 and lead V2 are mostly negative which indicates that the saddleback STE in these two leads are caused by wrong (too high) lead placement. 

Regardless, the main findings in this ECG are the giant (hyperacute) T waves in the precordium and reciprocal ST depression in the inferior leads. This ECG is absolutely diagnostic of LAD occlusion. These findings were appreciated and the patient was taken straight to the cath lab were a fully occluded proximal LAD was opened. High sensitivity troponin T peaked at close to 15.000ng/L (ref <14ng/L). Below is the Queen of Hearts interpretation. 

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Learning points: 

• Thrombolytic therapy is recommended if primary PCI is not an option. Thrombolytics are more efficient the sooner they are given after symptoms onset. 
  
  
• Thrombolytics will produce TIMI III flow in the culprit artery in just above 50% of the patients at 90 minutes. 
  
  
• Most cases of saddleback ST elevation is not ischemic, but some are and it is our job as health care professionals to identify the patients with an occluded coronary artery
  
  
• Always consider (too high) lead placement as a cause of saddleback ST-E if present in leads V1-V2

Gonzalez, P. E., Omar, W., et al (2020). Fibrinolytic strategy for ST-Segment–Elevation myocardial infarction. Circulation Cardiovascular Interventions, 13(9). 

Dudek, D., Rakowski, T., Dziewierz, A., & Kleczynski, P. (2008). PCI after lytic therapy: when and how? European Heart Journal Supplements, 10

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MY Comment, by KEN GRAUER, MD (10/30/2024):

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In today’s case — Dr. Nossen challenges us to decide on whether or not we would immediately activate the cath lab for a series of 6 ECGs, taken from 6 patients with symptoms that led them to contact EMS. I thought I’d add another perspective on how I approached this challenge.

• Those of us used to some form of “objective competence testing” — probably approached today’s challenge in similar fashion as I did — that it is likely that some (but not all) of these 6 tracings represent acute OMIs in need of prompt cath — but a few don’t, and that there may be “equivocal findings" (to potentially throw us off) inserted along the way.

More than just forcing ourselves to commit to a rapid “binary” decision (ie, either acute OMI with need for prompt cath! — or — not an acute OMI, therefore no need for immediate cath lab activation) — I’ll suggest an additional clinical option, namely — What would YOU do? (ie, if you were clinically charged with the management of each of these 6 patients?).

• My reason for suggesting this additional clinical approach to today’s ECG challenge is: i) All 6 of these ECGs show “saddleback” ST elevation and other remarkable ECG findings that need to be recognized; and, ii) The decision of “What to do?” — is not a “binary” one (ie, of OMI or no OMI ) — but rather includes a 3rd option of us not yet being able to exclude a potential acute OMI.

KEY Point: The most glaring error I’ve seen during the 7+ years that I’ve been privileged to review ECG cases submitted to Dr. Smith’s ECG Blog — has been seeing providers do nothing for hours (or longer) in patients with symptoms whose initial ECG is not “normal” (albeit not yet satisfying criteria for an obvious STEMI ).

• It is “OK” — to not necessarily recognize all of the subtle acute findings that we highlight on Dr. Smith’s ECG Blog.
• It is “not OK” — not to recognize higher risk patients with abnormal initial ECGs that mandate immediate additional evaluation until such time that a definitive decision can be made regarding whether or not to activate the cath lab.
• 
  
• Reminder: Even the experts will not always know with 100% certainty whether an initial ECG represents an acute OMI in progress. As a result — We need to remember the 3rd option, in which our goal is to identify patients for whom the initial ECG could be an acute OMI in progress — for whom we need to expedite additional evaluation to arrive at a definitive determination as fast as this is possible.

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It is with the above principles in mind — that I reviewed these 6 challenging ECGs. 

ECG #1:

• The limb leads suggest an acute inferior STEMI — already with a large Q wave in lead III (hard to tell if there is a Q in aVF — or if this is an rsR' complex).
• The "magical" finding that we often emphasize of mirror-image opposite ST-T wave changes in leads III and aVL — confirms the diagnosis of acute inferior STEMI (reciprocal changes also being seen in lead I ).
• That the RCA is the "culprit" artery — is suggested by: i) ST elevation in III > II; — ii) Marked ST depression in aVL; and, iii) Lack of ST elevation in V6 (as might be expected with a LCx culprit).
• For me — 99+% certainty of OMI was attained by the associated presence of acute posterior OMI (ST flattening and depression in leads V2,V3). 

ECG #2:

• Despite inferior lead Q waves with ST elevation — I thought this was a "fake" because: i) The QRS in lead aVL is predominantly negative — so the relatively shallow T wave inversion is not necessarily abnormal (vs much deeper ST-T wave depression in lead aVL for ECG #1); — ii) Lead I suggests a right axis (which is far less common with simple inferior MI) — and there is no reciprocal change at all in lead I; — iii) There is no suggestion of posterior involvement; — and, iv) The ST-T waves in leads V3,V4,V5,V6 all look virtually the same as the ST-T waves in leads II,III,aVF — with V4,V5,V6 having a virtual identical appearance of leads II,III,aVF with Q wave and identical-looking ST-T elevation/peaking. In contrast — acute OMI usually localizes! (and is less likely to yield a near-identical QRST picture for 7/12 leads! ).
• Note that Drs. Nossen, Meyers, Smith and Frick all thought this was probably a "fake" — but that all of us emphasize less than 100% certainty based on this single ECG.
• That said — the important point is that a few simple actions are all that is needed for us to attain 100% certainty in a very short period of time (ie, finding a prior ECG on this patient for comparison — serial troponins — stat Echo — and repeating this ECG within 10-to-20 minutes).
• 
  
• NOTE: This ECG #2 is not a normal tracing. Instead of acute OMI — I initially suspected acute myocarditis given the diffuse Q waves with ST elevation without localization. This would be a patient for whom I would want to find out WHY this non-OMI ECG looks so abnormal. 

ECG #3:

• This one was easy (ie, Took me less than 5 seconds) because: i) The history is classic ( = 55yo man with acute onset CP and diaphoresis); — ii) Not only are there giant-amplitude positive T waves (≥18 mm in V3,V4) — but these hyperacute T waves are extremely wide at their base; — iii) Counting the inferior leads — there are 9/12 leads with hyperacute T waves + anterior lead ST elevation + loss of R wave from lead V2-to-V3 + Incomplete RBBB with LAHB — which in this patient with new severe CP is 100% diagnostic of acute proximal LAD OMI.

ECG #4:

• This case is a perfect example of a non-binary answer — in that while I did not think this ECG represented an acute OMI — I was not 100% certain (which is OK as long as we quickly rule out an acute event — which was done in this case by cardiac cath that showed significant LAD disease, but no acute OMI ).
• LVH is clearly present by voltage (markedly increased R waves in leads I,aVL and the overly deep S in lead III ) — with LV "strain" definitely seen in lead aVL, with a "strain equivalent" in lead I.
• The deep Q waves in leads V2,V3 are definitely abnormal, in association with marked ST elevation in these leads (and to a lesser extent in lead V4).
• That said — the overall picture to me did not "look" acute — and the history of "chest pain radiating to the back" in this 80-something man with marked LVH — made me strongly consider an aortic dissection as a more likely cause.
• Without a prior ECG for comparison — there would be no way to know IF the above ECG changes were new or old. And, even if there was acute aortic dissection — the dissection could result in occlusion of a coronary artery. As a result, even though I thought acute OMI as a primary event was less likely based on this single ECG — additional evaluation would be needed to confirm my impression. (Aortic dissection was apparently ruled out by a negative CT scan).

ECG #5:

• This case illustrates another example of a non-binary answer — in that while I did not think this ECG represented an acute OMI — I was not 100% certain. As a result — additional evaluation was needed (which ruled out an acute event).

Reasons I did not think this ECG represented an acute OMI were: 

• i) The shape of the ST elevation manifests an upward concavity (ie, "smiley"-configuration). 
• ii) As per Dr. Nossen — there is J-point notching in lead II — and a terminal "slur" in leads III and aVF (which as per My Comment in the October 15, 2024 and May 23, 2022 posts — often serves as a J-point notch "equivalent" sign of a repolarization variant, especially when associated with rapid upsloping of the ST segment).
• iii) An isolated Q wave in lead III (as we see here) — is not necessarily abnormal.
• iv) The very shallow T inversion in this lead aVL (in which the QRS is almost biphasic) — does not qualify as "reciprocal" ST depression.
• v) The QTc is not at all increased.
• vi) There is no sign of posterior OMI (ie, There is slight, gently upsloping J-point ST elevation in leads V2 and V3 — as should occur normally).
• vii) R wave progression is normal, with good R wave amplitude.

ECG #6:

• This ECG is obviously abnormal because: i) There is ST depression in all 3 inferior leads (with a down-up biphasic T wave in III and aVF); — ii) There is ST elevation in lead aVL (with potentially a hyperacute T wave); — iii) There is ST elevation in leads V1 and V2 — with very tall, upright T waves in leads V2,V3,V4.
• IF the history had been "sudden onset of severe chest pain" — I would have instantly thought acute LAD OMI with need for prompt cath.
• That said — the history we were given says, "70-something male with vague pressure-like chest discomfort". No "onset" of symptoms is provided. As a result — this is a case for which I'd want to quickly gather more information to verify if despite only "vague" chest discomfort — an acute event was in progress. 'Sometimes ya just gotta be there!" — and it may be that a 2-second glance at the patient would have immediately conveyed acuity.
• In any event — the findings in ECG #6 are so striking that no more than minutes should be taken to order stat Troponins — repeat the ECG (and search for a prior tracing) — and do bedside Echo.