Unresponsive and Acidotic: OMI? Acute, subacute, or reperfused? What is the rhythm? Why RV dysfunction? Can CT scan help?

This was written by one of our really fine 3rd year residents, Katie Buerk.

This case was a 69 year old male, brought in by ambulance, after being found unresponsive in bed by family earlier that day. He had last been seen 3-7 days ago. For the medics, he was bradycardic in the 20-30s. They were unable to obtain a blood pressure.

 

On arrival to the ED, he was breathing spontaneously, had faint pulses, and was cool to the touch. His heart rate was in the low 20s and we were also unable to obtain a blood pressure. His temperature was 32.8 C. A quick POCUS which showed significantly reduced ejection fraction and trace B lines. He was given 50 mcg epinephrine with good response in both heart rate and blood pressure.

 

His rhythm on telemetry seemed to be sinus bradycardia vs junctional rhythm. Telemetry also showed possible ST elevation and peaked T waves, so he was given 2 g calcium gluconate empirically.

 

What do you think?

 

There is a regular wide complex rhythm without P waves at a rate of less than 100.  Thus, this could be junctional, but is far more likely to be accelerated idioventricular rhythm (AIVR).  AIVR is often a reperfusion rhythm.  The AIVR has an RBBB configuration; thus, it is originating from the LV.  There is also left axis deviation; thus it is originating in the inferior LV.  The ST segments in AIVR can be analyzed similarly to LBBB (excessively discordant ST Elevation or Depression/concordant STE or STD).  

In this case, there is excessively discordant STD in V2 and concordant STD in V3.  Thus, it is diagnostic of Posterior OMI.  

The AIVR suggests that it is a reperfused posterior OMI, and that is certainly possible, but I think one must assume it is active until proven otherwise.

The PMCardio Queen of Hearts AI Model thinks it is a reperfused OMI:

Case continued:

Initial EKG demonstrated ST depression in V1-V4, concerning for posterior OMI. Cardiology was consulted.

His heart rate had improved to the 80s after epinephrine administration. Subsequently, he became increasingly bradycardic and was noted to have myoclonic movements. At that time, he had no pulses and was in asystole on the monitor. CPR was initiated and he underwent 1 round of ACLS (CPR + 1 mg epi). During CPR, he started moving all four extremities spontaneously. During first pulse check, ROSC was achieved. We proceeded with intubation using ketamine and rocuronium. He was given 2 amps of bicarb empirically prior to intubation due to concern for profound acidosis. Norepinephrine started after intubation due to persistent hypotension.

 

Post intubation we obtained: 

This still shows AIVR with excessively discordant ST depressions in V1-V4.

 

 

His initial labs returned notable for pH 7.01, bicarb 10, and pCO2 41. His lactate was 22. His blood gas demonstrates profound metabolic acidosis, driven by the lactate, with insufficient respiratory compensation. He was noted to have a glucose of 591 and an anion gap of 30. Potassium was 3.7.

 

His potassium was replaced, he was given 300 mg rectal ASA, and an insulin drip ordered. He was hyperventilated at a rate of 28 to provide some compensation for the metabolic acidosis.

 

He was persistently bradycardic, requiring 2 x 50 mcg epinephrine to maintain HR >60. Epinephrine drip was started and norepinephrine was discontinued. He was given vancomycin and cefepime empirically, though we overall had low concern for sepsis as the etiology of his presentation.

 

At this time, there had been multiple discussions with cardiology team, who were debating taking this patient to the cath lab. They felt that the asystolic arrest suggested a different etiology of cardiac arrest. With the severe acidosis and absence of ST elevation, they felt there was more likely to be a non-cardiac etiology of his presentation. Cath lab had not yet been activated, so he was taken to CT for a head and chest/abdomen/pelvis angiogram to rule out other causes of cardiac arrest.

It did not show pulmonary embolism or intra-abdominal pathology, but it did show this:

See the dark area at the bottom of the image?  This is the posterior wall and there is no contract perfusing that posterior wall.  

There is Transmural ischemia of Occlusion MI.

Spectral CT

This spectral CT image really highlights the dense transmural ischemia of the posterior wall.

Here you can also see that there is dense ischemia of the RV.

 

CT showed hypoperfusion of the right ventricular wall and the posterior wall, as well as significant calcifications of the LAD. There were no other radiographic findings to explain his presentation.

 

Third EKG obtained 100 minutes after the first:

Same interpretation: AIVR with excessively discordant ST depression.

 

Initial troponin returned and was 42,747 ng/L.

This very high initial troponin tells us that the infarct is subacute and much, or most, of the damage is already done.

The patient went to the cath lab relatively quickly, at 160 minutes after arrival.  He received an additional 300 mg rectal aspirin and 5000 unit heparin bolus in the ED. 

Coronary Angiography 

 

--First Diagonal occluded

--RCA: 95% distal disease with total occlusion of RPAV with the vessel small and no PCI option to RCA or RPAV RPDA severe diffuse disease, small vessel

 --Ramus: Small vessel with severe diffuse disease

There was no possibility of PCI/stent

 

Echo:

Decreased left ventricular systolic performance mild to moderate.

The estimated left ventricular ejection fraction is 40-45%.

Probable anterior and anterolateral wall hypokinesis.

 

Right ventricular enlargement.

Decreased right ventricular systolic performance.

Assessment:

Cardiology thought this was cardiogenic shock from RV dysfunction.

Smith Comment: the RV was very ischemic on the CT scan and dysfunctional on echo, and this does explain the shock.  But I'm not sure how to explain the RV ischemia based on either ECG or angiogram.  There was no pulmonary embolism.

Case Continued

The post cath course was very complicated with cardiogenic shock and severe dysrhythmias that were eventually controlled, but he did not recover neurologically.

 

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MY Comment, by KEN GRAUER, MD (4/6/2025):

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As per discussion above by Dr. Smith — the patient in today's case did not survive. His case was complicated by failure to respond to intense treatment efforts (as described above by Dr. Smith). 

• I focus my comments on the series of the 3 ECGs that were done in this case, each of which are extremely challenging — yet richly illustrative with important principles for the interpretation of difficult tracings in a critically ill patient.

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In Summary: Today's case regards a 69-year old man, who was found unresponsive in bed by his family. Given that the patient was last seen "3-to-7 days earlier" — it is likely that he was in the critical state noted on arrival in the ED for a prolonged period of time.

• On arrival in the ED — he was breathing spontaneously, but hypothermic, markedly bradycardic and without an obtainable blood pressure. In short — with a very guarded likelihood for a positive outcome.
• Telemetry initially was interpreted as showing sinus bradycardia vs a junctional rhythm. Because of peaked T waves — the patient was appropriately treated empirically with IV Calcium (No rhythm strips of this available).
• Subsequent serum K+ came back = 3.7 mEq/L (which given this patient's profound acidosis — suggests a true serum K+ significantly lower than 3.7).
• The patient was warmed and treated with vasopressor agents — which succeeded in improving his heart rate and blood pressure.

Around this time — an initial ECG was obtained (which I have reproduced in Figure-1).

• Clinician notation regarding interpretation of this tracing was, "Initial EKG demonstrated ST depression in V1-V4, concerning for posterior OMI. Cardiology activated via Pathway B".

QUESTION: 

• How did YOU interpret the initial ECG in today's case? 
•    — Please take another LOOK at this tracing. Do you agree with the clinician notation of their interpretation?

Figure-1: The initial 12-lead ECG obtained in the ED.

MY Thoughts on ECG #1:

To emphasize — clinicians appropriately suspected hyperkalemia, and treated the patient with IV Calcium. But serum K+ was not elevated (ie, The returning lab value = 3.7 mE/L was probably falsely elevated by the severe underlying acidosis). 

• I completely agree that my initial concern on hearing this case and seeing this initial ECG — was that QRS widening and the large, peaked T waves represented hyperkalemia. But this patient was not hyperkalemic!
• I also completely agree that it looks like in addition to RBBB — there is excessive ST depression in anterior leads V2,V3 of Figure-1 — which given the clinical scenario would suggest the possibility of a large, ongoing posterior OMI.
• 
  
•  QUESTION: How did YOU interpret the rhythm?

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MY Thoughts regading the Rhythm in ECG #1:

Although one might easily consider a bifascicular block ( = RBBB/LAHB) — We do not see P waves.

• There is marked baseline artifact in this initial ECG — perhaps the result of tremor or shivering in this hypothermic patient. 
• That said, the overall rhythm in Figure-1 is fairly regular — with obvious QRS widening. And even though marked artifact complicates assessment of atrial activity — I don't see P waves.
• And although the all upright R wave in lead V1 could be consistent with RBBB conduction — and the marked left axis could be consistent with LAHB — the complete lack of a triphasic complex in V1 — and the entirely negative QS complexes in each of the inferior leads are both against this rhythm being supraventricular!
• In addition — the all negative (QS complexes) in leads V4,V5,V6 are virtually never seen in a supraventricular rhythm. And while hyperkalemia may widen the QRS and negate the presence of P waves (with a sinoventricular rhythm) — the serum K+ was not elevated.
• BOTTOM Line: The rhythm in Figure-1 is not supraventricular. Instead — this rhythm is AIVR (Accelerated IdioVentricular Rhythm).

QUESTION:

• Did YOU notice beat "X" ( = beat #6) in Figure-2?

ANSWER:

• Support that the rhythm in today's initial ECG is AIVR is forthcoming from the presence of beat "X" — because: i) This beat occurs earlier-than-expected; — and, ii) Beat #6 is clearly narrower than all other beats in Figure-2, with a much straighter (steeper) S wave descent — which strongly suggests that this beat is supraventricular (in distinction to the other wider 13 beats in this tracing — that therefore must be ventricular).

Learning Points: I have seen the best of cardiologists and emergency clinicians skip assessment of the rhythm (therefore not realizing the rhythm they are looking at is not the usual sinus rhythm). 

• BEST way to avoid overlooking important landmarks of the cardiac rhythm — is to begin your interpretation of every ECG you encounter, by spending 3-4 seconds letting your "educated eye" focus on the long lead II rhythm strip — to ensure that upright P waves precede each QRS with fixed PR interval. If you do not see this — then the rhythm is not sinus.
• The BEST clue to the etiology of a challenging rhythm that for the most part is regular — is to look for the "break" in the rhythm! Beat #6 clearly occurs earlier than any other beat in Figure-2 — which should "catch" your eye, and entice you to look closer.
• P.S.: Even though ECG #1 represents AIVR — I completely agree with the clinician concern that the disproportionate amount of ST depression in leads V2,V3 may represent acute ongoing posterior OMI — so this tracing once again illustrates that on occasion, acute infarction may be suggested by ventricular beats.

Figure-2: I've added an "X" to today's initial ECG. What does this "X" indicate?

The CASE Continues:

Some time later in the management of today's case (ie, after an asystolic episode — from which the patient was successfully resuscitated) — a 2nd ECG was obtained, which I have reproduced in Figure-3.

• Clinician notation regarding interpretation of ECG #2 was, "This ECG continued to demonstrate ST depression in leads V1-thru-V4".

QUESTION: 

• How did YOU interpret this repeat ECG in Figure-3?
•    — Please take another LOOK at this tracing — and compare this ECG #2 with ECG #1 (that was shown in Figure-2). Do you agree with the clinician notation of their interpretation of ECG #2?

Figure-3: Repeat ECG obtained after ROSC from an asystolic episode.

MY Thoughts on ECG #2:

One of the most common oversights that I see repeated by even experienced cardiologists and emergency providers — is the failure to compare lead-by-lead serial tracings.

• Comparison of ECG #1 with ECG #2 should reveal: i) That QRS voltage has dramatically decreased in ECG #2 (especially in the limb leads); ii) That the QRS is clearly more narrow than it was in ECG #1; — and, iii) That there is now predominant positivity of the QRS in leads V4,V5 — whereas the QRS in these leads was entirely negative in ECG #1.

Learning Points: 

• If you did not initially recognize that ECG #1 was not a supraventricular rhythm — the dramatic change in QRS width and appearance that we now see in ECG #2 should have clued you into this.
• The tiny voltage that we now see in this supraventricular rhythm in ECG #2 is a poor prognostic sign — that in today's case probably represents cardiac "stunning" with significantly reduced cardiac output.
• P.S.: I fully acknowledge that I do not know what the rhythm in Figure-3 is. I believe the above points indicate this is a supraventricular rhythm — that manifests QRS widening consistent with RBBB conduction, but without P waves that I can see (with amplitude so greatly reduced that I have no idea if P waves are or are not somehow present).

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The CASE Continues:

Some time later in the management of today's complicated case (ie, after multiple therapeutic interventions) — a Troponin value of ~40,000 apparently prompted the recording of a 3rd ECG (which I have reproduced and labeled in Figure-4).

• I do not see any clinician notation regarding interpretation of ECG #3.

QUESTION: 

• How did YOU interpret this 3rd ECG that I have labeled in Figure-4?
•    — What is the rhythm?
•        — HINT: What are the arrows pointing to? What about beats #13,14,15?

Figure-4: The 3rd ECG — obtained after return of a Troponin ~40,000.

MY Thoughts on ECG #3:

I found it helpful to interpret ECG #3 in the context of knowing this patient was previously in both AIVR (in Figure-2), as well as in a supraventricular rhythm of uncertain etiology (in Figure-3).

• My "eye" was immediately drawn to beats #13,14,15 in the long lead II rhythm strip — as QRS morphology of these beats is clearly different from the previous 12 beats in this tracing.
• Beat #13 clearly occurs earlier-than-expected — so this should clue us in that something else is occurring.
• I believe we are for the first time seeing some P waves (RED arrows in the long lead II). To emphasize that the amplitude of this atrial activity is tiny — but we do see similar signs of atrial activity in simultaneously-recorded leads II,III; and V4,V5,V6 (PINK arrows) — so I believe these are indeed P waves. 
• In further support that these colored arrows are highlighting atrial activity — is that QRS morphology of beat #15 is intermediate between QRS morphology of the first 12 beats — and of beats #13,14.
• Now although the QRS in the long lead II does not look overly wide for the first 12 beats — simultaneously-recorded lead V1 tells us that the QRS for these first 12 beats is actually very wide!
• And — the fact that the first sinus P wave (1st RED arrow in the long lead II rhythm strip) manifests a PR interval that is too short to conduct before beat #2 — tells us that the rhythm for the first 12 beats must be ventricular (ie, AIVR).
• Support that this assumption is correct is forthcoming from the slightly longer PR interval before beat #15, which is a fusion beat between supraventricular beats #13,14 — and the AIVR that we see for the first 12 beats. It is because the PR interval before beat #15 is longer than the PR interval before beat #2 — that there is enough time for this P wave to partially traverse a portion of the ventricles (and thereby produce a fusion beat).
• Note that in contrast to the AIVR that we saw in Figure-2, in which there were completely negative QS complexes for leads V4,V5,V6 — there is a small, but-definitely-present initial R wave before beats #13,14 in leads V4,V5,V6 — whereas there is no initial R wave before beat #15 in leads V5,V6.

Learning Points: 

• As noted — it is all-too-easy to overlook subtleties in a complex rhythm if you do not religiously spend those 3-4 "magic" seconds taking an "educated look" at each beat in the long lead rhythm strip (assessing for atrial activity — and looking for any "break" in regularity of the rhythm).
• Today's patient was in persistent shock. While I do not believe that any additional intervention could have saved this unfortunate patient — persistence of AIVR (especially if unrecognized) may exacerbate persistent hypotension.

 

 

Will this case be flagged for Quality Improvement in the STEMI/NSTEMI Paradigm?

Written by Jesse McLaren

A 40 year old presented with 90 minutes of midsternal chest pressure, radiating to bilateral arms, with shortness of breath. Below is the first ECG, signed off by the over-reading cardiologist agreeing with the computer interpretation: “ST elevation, consider early repolarization, pericarditis, or injury”. What do you think?

What do you think?

There’s normal sinus rhythm with normal conduction, right axis and delayed R wave, and normal voltages. There’s ST elevation in V3-4 which meets STEMI criteria, which could be present in either early repolarization, pericarditis or injury. But there are also hyperacute T waves (HATW) in V4-5, which exclude early repolarization and pericarditis, leaving only LAD occlusion for this patient presenting with classic symptoms of ACS.

 

Here’s the PMCardio Queen of Hearts AI Model interpretation:

This is great example of how the Queen uses proportionality to identify hyperacute T waves: the T waves in V3 and V4 are almost identical, but in V3 they are proportional to its large QRS whereas in V4 they tower over its small QRS; the T wave in V5 is much smaller, but relative to its QRS it is large and bulky.

 

So using the OMI paradigm and its AI, this patient would have had immediate cath lab activation before the first troponin result. Let’s see what happens in the current STEMI paradigm.

 

Emergency physician: ‘STEMI neg’ but with elevated troponin = Non-STEMI

 

The first ECG was signed off. After only 90 minutes of chest pain, the first troponin was unsurprisingly in the normal range at 11ng/L (normal <26 in males and <16 in females), so the emergency physician waited for repeat troponin. After it rose to 150ng/L two hours later a repeat ECG was done:

What do you think?

There’s now a Q wave in V3 and a smaller T wave in V3-V4, proving this is LAD occlusion. Hyperacute T-waves remain in V3 and V4.  There’s the same degree of ST elevation, but this time the computer calls it STEMI. But it was interpreted as no acute ischemia and the patient was referred to cardiology as Non-STEMI. 

 

Nurse notes: the silent scream of the heart

 

The emergency nursing notes document the patient complaining of chest pain refractory to nitro, with a rising trop:

 

            2200: ECG shown to ED MD

            0020: repeat ECG shown to ED MD, patient complain of midsternal chest pain

            0520: nitro x 3. Chest pain still persists. Cardiology aware. Repeat troponin ordered

            0630: lab called for high troponin 3900. Paged cardiology

            0800: patient complains of chest pain. Repeat blood work and ECG

            0845: repeat trop over 7000. Cardio aware

            1030: repeat trop sent, no change in chest pain

            1100: heparin drip started

            1130: transfer for cath, still complains of chest pain

 

Here’s the ECG repeated at 0800

There’s now Q waves V3-4. T waves have deflated and inverted in V3-4 suggesting some degree of reperfusion, but the patient still complained of ongoing chest pain. Troponin rose to 12,000 before cath.

 

 

Cardiology: delayed cath = Non-STEMI

 

Here’s the interventional cardiology note describing the ECGs, management and outcome:

 

“He has had transitory peak T-waves, ST-segment elevation, and biphasic T-waves during recurrences of pain. This morning, he was also found to have a rising troponin. He was thus referred for emergent invasive assessment. Code STEMI was called…Mid LAD had serial 70 and 60 percent lesions and was occluded in the distal segment…An excellent result was achieved. The total occlusion was recanalized and stented from 100 to 0%.”

 

Here's the discharge ECG, with ongoing Q waves and reperfusion T wave inversion:

 

Peak troponin was 47,000 ng/L and echo showed an akinetic apex with EF 45%.

 

What should the discharge diagnosis be, and why does this matter?

 

The patient had an ECG with ST elevation (and hyperacute T waves), activation of code STEMI, a 100% LAD occlusion on angiogram, a massive peak troponin, and an akinetic wall. The discharge diagnosis should reflect the underlying pathology of Occlusion MI, regardless of whether the ECG was interpreted to show STEMI criteria, and regardless of time to reperfusion. But because of the delayed reperfusion, the discharge was Non-STEMI.

Thus, a case with more than 12 hours of delay for reperfusion will not be flagged for review. 

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Smith: we have an article under review that shows that the variable most closely associated with the final diagnosis of "STEMI" vs. "Non-STEMI" was a door to balloon time less than, vs. greater than, 90 minutes.  Not whether there was or was not Acute Coronary Occlusion.  Not whether the ST segments met STEMI millimeter criteria.

_______

The problem is not just for this patient, and simply changing the discharge diagnosis in this case from "Non-STEMI" to "STEMI" is not the solution. This is just an example of the broader problems of the STEMI paradigm for research and quality improvement. 

 

For research, 12 hours to PCI is deemed ‘early intervention’ for Non-STEMI. If two of the same patients were part of Non-STEMI trials like TIMACS, and randomized into ‘early’ (16 hours) vs ‘delayed’ intervention (52 hours), there would appear to be no benefit to the ‘early’ intervention, because the damage was already done. But clearly this 'Non-STEMI' patient with OMI would have benefited from immediate cath lab activation on arrival, when their first troponin was 11ng/L, rather than after after it rose to 12,000ng/L after 12 hours of refractory ischemia.

 

For quality improvement, the discharge diagnosis also matters. Classifying as STEMI vs Non-STEMI can be more reflective of reperfusion time than ECG findings or patient outcomes, which allows cases like these to be normalized. Instead, if patients are classified by the actual outcome of OMI vs NOMI, then this patient clearly had a missed OMI. This is not to assign blame but to identify multiple opportunities for improvement:

1.     ECG: using OMI signs and AI, to activate the cath lab on arrival, before waiting for the troponin

2.     POCUS for complementary regional wall motion abnormalities for subtle OMI

3.     Clinical: patient alerts for refractory ischemia (refractory chest pain), and empowering nurses to advocate for patients

            4.     Troponin: troponin is a rear-view mirror that shows damage that has already happened, so the first troponin is unreliable with acute symptoms and serial troponin will lag behind the damage of ongoing occlusion. But refractory ischemia with rising troponin is an indication for cath lab activation regardless of the ECG.  

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MY Comment, by KEN GRAUER, MD (4/4/2025):

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As an Associate Editor on Dr. Smith's ECG Blog for the past 7+ years — I found today's post by Dr. McLaren among the more (most) difficult that I have reviewed. It's not that today's oversights are unique — but rather that: 

• i) The errors of omission and commision in today's case are multiple and preventable.
• ii) Since it is now 7 years since initial publication of the OMI Manifesto (See the April 18, 2018 post in Dr. Smith's ECG Blog) — We would have expected that emergency providers (especially cardiologists!) would by now accept the expanding body of literature demonstrating that at least 1/3 of all acute coronary occlusions are missed by clinicians "stuck" on the outdated millimeter-based STEMI protocol (our every expanding OMI Literature Timeline — being readily accessible in the upper Menu Bar Tab at the top of each page in this ECG Blog).
• iii) Cardiologists are all-too-often rewarded for misclassifying all-too-many MIs as a "NSTEMI" — often in cases in which there is foolproof evidence of acute coronary occlusion that should have been recognized many hours earlier. Take today's case, in which Dr. McLaren highlights how despite more than 12 hours of delay for reperfusion — the interventionist note indicates "an excellent result was achieved". Especially concerning is that for data-keeping (research) purposes — this 12+ hour delay until PCI was finally achieved, will end up being viewed not as an unfortunate delay — but as a beneficial "early" intervention by the irony that this event was misclassified as a "NSTEMI". 

Dr. McLaren details these problems from today's case in his above discussion. These problems include erroneous interpretation of several ECGs (as well as the failure to repeat the initial ECG for over 2 hours) —  not acting on Troponin elevation (with progressively rising Troponins throughout the patient's course) — and allowing the patient to continue having CP (Chest Pain) without expediting cardiac catheterization.

• MY Thoughts: While fully acknowledging that I viewed today's initial ECG in the comfort of my home office in front of my large screen computer — there are findings on this initial ECG, that in a patient who presents with new-onset severe CP have to be recognized!

I've labeled in Figure-1 — KEY findings on this initial ECG.

Figure-1: Today's initial ECG.

The Cath Lab should have been Immediately Activated!

As per Dr. McLaren, on seeing today's initial ECG — the cath lab should have been immediately activated!

• There is no need to wait for Troponin results — and not even any need to repeat the ECG prior to activating the cath lab.
• And, as soon as the decision is made to activate the cath lab — IV morphine could have been given to relieve this patient's chest pain (that the patient had to experience for more than 12 hours).

The initial ECG is diagnostic of LAD OMI!

• After identifying that the initial rhythm in Figure-1 is sinus — my "eye" was immediately drawn to the hyperacute T wave in lead V4 (within the RED rectangle). Although true that some repolarization variants may be marked by tall, peaked T waves — the disproportionate enlargement of this T wave in lead V4 (that is no less than 13 mm tall!) in this patient with severe new-onset CP clearly exceeds the dimensions reasonably expected for a repolarization variant.
• In the context of this hyperacute T wave in lead V4 — the T wave in neighboring lead V5 has to be also interpreted as hyperacute (clearly "bulkier"-than-it-should-be given modest size of the R wave in this lead).
• Any doubt that may have existed about the acuity of these lead V4,V5 findings — should be alleviated on seeing the ST-T wave in lead aVL (While the T wave inversion in aVL may sometimes be a normal finding when the QRS is predominantly negative — there should not be ST segment coving with slight elevation in this lead as we see in ECG #1). 

Additional (more subtle) findings in ECG #1: 

• As per Dr. McLaren, although the T wave in lead V3 is equally tall as the T wave in lead V4 — it is associated with a much deeper S wave. In the context of ST-T wave appearance in the other 5 chest leads — I still interpreted this T wave in lead V3 as hyperacute, but I would have been less certain of that interpretation if other chest leads were normal.
• In the context of ST-T waves in leads V3,V4,V5 — I interpreted the coved and elevated ST segment in lead V2 as an acute change (I thought the amount of J-point elevation in lead V2 to be more than is normally seen in this lead).
• Similarly — I interpreted the ST segment coving and slight elevation in neighboring lead V1 as abnormal (while fully acknowledging that as an isolated finding — I would not interpret the ST-T wave appearance in lead V1 as abnormal).
• Finally, in the context of the other 5 chest leads — I thought the T wave in lead V6 to be "fatter"-at-its-peak and wider-at-its-base than I would normally expect given the modest R wave amplitude in this lead.

What about the Frontal Plane Axis?

Today's case features a total of 4 ECGs. Each of these tracings manifest a similar degree of marked RAD (Right Axis Deviation).

• QRS morphology in lead I is that of an rS complex.
• QRS morphology in leads II,III,aVF is that of a qR complex.
• This QRS morphology in these 4 limb leads is completely characteristic of LPHB (Left Posterior HemiBlock). Although it is rare to see LPHB as an isolated conduction defect (LPHB almost always occurs as a bifascicular block, in association with RBBB) — this patient's ECG is otherwise diagnostic of acute LAD OMI, so this could be a new conduction defect occurring in association with acute LAD OMI (ie, There is no baseline ECG to compare this limb lead morphology to — so we cannot tell if this is or is not a new conduction defect).
• Because the left posterior hemidivision is typically a thick, diffuse fascicular bundle (as opposed to the much thinner, and much more easily injured left anterior hemifascicle) — acute LPHB is a potentially serious conduction disorder (that potentially might need pacing if this LAD OMI is not treated in a timely manner).
• Failure to recognize potentially new LPHB is yet one more oversight in today's case.