50 yo with V fib has ROSC, then these 2 successive ECGs: what is the infarct artery?

A 50 yo was resuscitated from ventricular fibrillation.  

He had a prehospital ECG recorded after ROSC: 

What do you think?

This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL.  Although one may have all kinds of ischemic findings as a result of cardiac arrest (rather than cause of cardiac arrest), this degree of ST elevation and HATW is all but diagnostic of acute proximal LAD occlusion.

This prompted cath lab activation.

On arrival to the ED, this ECG was recorded:

What do you think?

There is profound ST depression maximal in V1-V4.  This usually represents posterior OMI, but in tachycardia and especially after cardiac arrest, this could simply be demand ischemia, residual subendocardial ischemia due to the low flow state of the cardiac arrest.  But without seeing that first prehospital ECG, I would call this: "Posterior OMI until proven otherwise."

Of course the Queen of Hearts also sees OMI:

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Another ECG was recorded 13 minutes later, well after ROSC and with more stable vital signs:

The heart rate is down to 114 beats per minutes

What do you think?

This is diagnostic of posterior OMI.

Of course the Queen of Hearts sees OMI on this one as well:

Click here to sign up for Queen of Hearts Access

Posterior leads were recorded.  It was unusual that the leads that were shifted around to the back, as V7-V8, were V1-3 (usually one puts V4-6 on the back)

V1-V3 (really V7-V9) show the typical low voltage of posterior QRS, with ST Elevation.  

V4-5 continue to show STD.  

V6, which is still in the V6 position, is close to the posterior wall and continues to show trace STE with hyperacute T-wave.   

This rules out subendocardial ischemia and is diagnostic of posterior OMI.

How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later?

The angiogram explains it:

Culprit for OOHCA/VF is an acutely occluded mid-Circumflex Patient is incidentally noted to have chronic occlusion of the mid LAD with robust R > L collaterals.

In other words, the LAD distribution is supplied by the RCA.

LMCA:

Left main is a large caliber vessel

 

LCx: Circumflex is a medium-large caliber vessel that is occluded in the mid-segment on initial angiography.  TIMI-0 flow. 

On follow up angiography, there was a large OM1 and small AV groove Cx/LPL

visible as the vessel re-canalized

LAD is noted to have diffuse 50% stenosis in the proximal segment and is

occluded immediately beyond a small D1

 

RCA is a medium-large caliber vessel and supplies a medium rPDA, medium rPLA1, and three small rPLA branches.

There are well developed R > L septal collaterals that fill a majority of the mid and distal LAD

Explanation:   

The acute circumflex occlusion caused the arrest.  The arrest caused extreme hypotension which rendered the RCA incapable of continuing to supply the distant LAD.  This caused a type 2 anterior STEMI.   

In other words, with a chronic total occlusion of the LAD and collaterals from the RCA, the collaterals were not sufficient to supply the LAD distribution while the patient was in arrest.

Peak troponin I > 60,000 ng/L

Formal Echo

Normal left ventricular cavity size, mildly increased wall thickness, and moderately to severely reduced LV systolic function. The estimated left ventricular ejection fraction is 29%.

---Regional wall motion abnormality--entire apex dyskinetic, mid anteroseptum, mid anterior wall akinetic.

---Regional wall motion abnormality--anterolateral akinesis.

---Regional wall motion abnormality--mid and distal inferolateral wall

akinesis.

In other words: 1) infarct of the LAD territory (much of which could be old) and 2) inferior-posterior-lateral infarct.

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MY Comment, by KEN GRAUER, MD (9/29/2024):

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I found today's case insightful for a number of reasons.

• Today's case reminds us of the intuitive logic that if a patient has a shockable arrest (ie, VFib) — and following successful defibrillation shows evidence of acute OMI (even if STEMI criteria are not necessarily fulfilled) — that such patients have much to gain from immediate cath with PCI. (See Discussion in the June 29, 2024 post of Dr. Smith' ECG Blog).
• 
  
• Although predicting the "culprit" artery of acute coronary occlusion is often straightforward (ie, based on the distribution of leads with ST elevation and leads with reciprocal ST depression) — this is not always the case.
• The LIST of reasons why prediction of the "culprit" artery may not be straightforward include: i) Anatomic variants; ii) Multivessel disease; iii) Unusual patterns of collateralization (which are usually associated with multivessel disease); and, iv) The diagnosis may be wrong (ie, the patient may have Takotsubo cardiomyopathy — SCAD [Spontaneous Coronary Artery Dissection] — coronary artery spasm — acute pulmonary embolism — or something else).
• Relevance to Today's CASE: As per Dr. Smith — Trying to predict the "culprit" artery in today's case was confusing. The dramatically changing distribution of ST-T wave elevation and depression first predicted one — and then soon after, another "culprit" vessel. Learning from the results of cardiac catheterization that 2 of the reasons in my above LIST [multivessel disease and unusual collaterization pattern] account for this difficulty — helps us to understand the ECG findings in today's tracing.

KEY Point: Prediction of the "culprit" artery is more than just an academic exercise:

• I believe trying to predict the culprit artery improves our ability at ECG interpretation — because it forces us to correlate ECG findings in all 12 leads with the clinical situation. For example, once we're able to appreciate if the ECG(s) in front of us does or does not clearly suggest a specific "culprit" artery — we know whether to contemplate one of the 4 reasons I cite in my above LIST.

The other important benefit derived from routinely trying to predict the "culprit" artery — is that doing so may help us clinically. For example:

• The September 9, 2024 post by Dr. Frick illustrates how trying to predict the "culprit" artery helped the interventionist — because knowing that the initial ECG strongly suggested Precordial "Swirl" (therefore diagnostic of a proximal LAD OMI) — meant that despite only minimal intraluminal narrowing of the LAD on cath, IVUS (IntraVascular UltraSound) would be needed for definitive diagnosis (and IVUS confirmed the culprit location suggested from the initial ECG).
• The April 8, 2022 post by Drs. Fetterolf and Meyers illustrates how recognizing the South African Flag Sign, in which there is ST elevation in only 1 chest lead ( = lead V2) — strongly suggested that despite lack of STEMI criteria (that require sufficient ST elevation in 2 consecutive leads) — OMI from acute occlusion of either the 1st or 2nd Diagonal Branch of the LAD was almost certain to be present.
• The September 23, 2024 post by Dr. Frick showed RBBB with ST elevation in leads V1 and V2 that might easily suggest either proximal LAD occlusion or proximal RCA OMI with acute RV involvement. But because Dr. Frick's assessment of the remaining 10 leads on this tracing was not consistent with OMI from acute occlusion of any specific coronary artery — consideration was given to an alternative diagnosis. Prompt identification of acute PE may not have happened if the clinician had not followed through the thought process in searching for a specific "culprit" artery.

In Summary: 

We learn from trying to predict the "culprit" artery. Our understanding of the interaction between symptoms and serial ECGs changes is enhanced — especially in cases like today's presentation, in which the angiogram explains an otherwise confusing set of findings.

• Especially important for emergency providers — our presentation to a doubting interventionist becomes more convincing, when despite being passed off as a "NSTEMI" — we are able to predict what the catheterization that eventually gets done will show.

 

Healthy 45-year-old with chest pain: early repolarization, pericarditis or injury?

Submitted by Dr. George Mastoras (Twitter @georgemastoras), written by Jesse McLaren

It’s a busy day in the ED when you’re sent another ECG to sign off from a patient at triage. A healthy 45-year-old female presented with chest pain, with normal vitals. The computer interpretation was “ST elevation, consider early repolarization, pericarditis or injury.” What do you think? Only one of these options is concerning, so should the patient stay in the waiting room until a bed becomes available, or do they need to be seen immediately?

There’s normal sinus rhythm, normal conduction, borderline right axis, and normal voltages. Anterior R waves are small, but leads may have been placed too high as P waves are inverted in V1 and biphasic in V2. There’s mild concave ST elevation and hyperacute T waves in V3 and especially V4, with more subtle hyperacute waves inferiorly. There’s TWI in aVL but this is concordant to its QRS.

The final cardiology interpretation confirmed the computer interpretation of “ST elevation, consider early repolarization, pericarditis or injury”. But which one is it? 

1. Early repolarization/normal variant has ST elevation and T waves proportional to tall voltages. But here the voltages are normal and the ST elevation and T waves are disproportionately large relative to the QRS – including a T wave almost as big as the entire QRS in V4 - so this isn’t normal

2. Pericarditis has primary diffuse ST elevation without affecting the T wave – but here there are hyperacute T waves localized to an antero-inferior distribution - so this isn’t pericarditis

3. OMI: the ECG was not marked as ‘STEMI’ because there is only borderline ST elevation, and no inferior reciprocal change often associated with anterior STEMI. But inferior reciprocal change in LAD occlusion is mostly seen when the occlusion is proximal to the first diagonal, whereas mid LAD occlusion often has no effect on inferior leads, and distal LAD occlusion can produce inferior ST elevation/hyperacute T waves as in this case 

So this patient with chest pain has hyperacute T waves in II, III, aVF and V3-V5, which excludes early repolarization and pericarditis and is diagnostic of OMI - with a distribution that suggests distal LAD. This is apical OMI -- both inferior and anterior, usually due to a distal LAD, often one that wraps around to the inferior wall, a "wraparound LAD".

Dr. Mastoras immediately recognized the hyperacute T waves, and brought the patient into a room for further assessment. The patient was previously healthy, with no atherosclerotic risk factors, and developed chest pain after an episode of stress. The pain was crushing retrosternal, radiated to the arms and was associated with lightheadedness. During initial assessment the patient received nitro and aspirin, with resolution of symptoms, and had serial ECGs:

The hyperacute T waves have deflated – proving this was transient OMI, and not early repolarization or pericarditis. 

Then the patient suddenly became unresponsive while another ECG was being recorded:

Polymorphic VT preceded by a normal QT interval. So not “torsades” (polymorphic VT + long QT) but ischemic polymorphic VT. The patient was immediately cardioverted back into sinus rhythm and regained consciousness.

Smith comment: Ventricular Fibrillation looks just like polymorphic VT. So whether it is one or the other would depend on 3 factors: 1) preceding long QT, 2) spontaneous conversion, and 3) presence or absence of pulses. An unconscious patient probably has no pulses and so this is VF. On the other hand, when there is not pulse, there is no difference in treatment: it should be difibrillation (not synchronized cardioversion).

Here is the post shock ECG:

Cardiology was called stat for ischemic VT, query SCAD vs thrombotic occlusion vs coronary vasospasm.

Cath lab was activated: There was no coronary artery disease, but there was spontaneous coronary artery dissection (SCAD) of the distal LAD, which was narrowed by 95%, and treated medically. Echo showed EF of 50% with akinetic apex. First trop was 90 ng/L (normal <16 in females) and peak was 7,400 ng/L. Discharge ECG showed antero-inferior reperfusion T wave inversion:

Had the initial ECG been signed off as “STEMI negative” the patient could have arrested in the waiting room, with a poor cardiac and neurological outcome. But because Dr. Mastoras recognized the hyperacute T waves, the patient was immediately seen, the polymorphic VT was immediately defibrillated, and the patient was rapidly diagnosed and treated. 

Without clinical context, the Queen of Hearts identified OMI with high confidence, based on the hyperacute waves.

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Take away

1. LAD occlusions can be missed when there is minimal and concave ST elevation and no inferior reciprocal change

2. Hyperacute T waves help exclude normal variant or pericarditis and identify STEMI(-)OMI

3. Distal LAD occlusion produces antero-inferior STE/hyperacute T waves
4. Young women without atherosclerotic risk factors are at risk for delayed diagnosis of MI, yet this is the classic group to develop MI secondary to SCAD

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MY Comment, by KEN GRAUER, MD (9/27/2024):

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Important question posed above by Dr. McLaren — namely, if working a busy shift in the ED and presented with the initial ECG in today's case (that I've reproduced in Figure-1) — Does this patient need to be seen immediately? 

To take Dr. McLaren's question to another level:

• How long should it take you to know that this previously healthy 45-year old woman with new CP (Chest Pain) is having an acute OMI — at least, until you can prove otherwise?

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

How Long Should It Take?

As per Dr. McLaren — OMI was correctly diagnosed in today's case. The point of my Comment — is that it literally took me less than 5 seconds to know that prompt cardiac cath was going to be needed. I based this on the following:

• The History is Worrisome: This previously healthy 45-year old woman developed sudden, crushing retrosternal pain radiating to her arms, with associated lightheadedness. 
• On learning this history, and then on seeing ECG #1 — my attention was immediately drawn to the ST-T wave in lead V3 (within the RED rectangle in Figure-1). We should instantly recognize that the shape of the ST-T wave in this lead is "off". That is — the T wave in V3 is overly large, "fatter"-at-its-peak and especially wider-at-its-base than it should be given relative size of the QRS in this lead. 
• To assure myself that the abnormal appearance of the ST-T wave in lead V3 was "real" (and not the result of artifact or a repolarization change) — my "eye was next drawn to the ST-T wave in neighboring lead V4 (within the BLUE rectangle in Figure-1) — which showed a clearly disproportionate ST-T wave large enough to "swallow" the modest-sized R wave in this lead.

Conclusion: 

• Given the history of severe, new-onset CP and the presence of hyperacute-looking T waves in leads V3 and V4 — I knew there was no way that this patient was not going to need full evaluation, and most likely prompt cath. 
• Total TIME to Reach this Conclusion: Literally, less than 5 seconds.

Clearly, there are other findings of concern in this initial ECG (that I review below). But the point of my Comment is that Dr. Mastoras (who provided us with today's case) — was quickly able to recognize the hyperacute T waves, that in a patient with sudden, new and severe CP — mandate immediate further assessment.

A Picture is Worth 1,000 Words:

Why then in this patient with new CP — are the T waves in leads V3,V4 of Figure-1 hyperacute? The answer should be immediately apparent on looking at Figure-2:

• The ST-T waves for leads V3,V4 on the left (GREEN border leads) — are from a normal tracing. There is slight J-point ST elevation, with a gently upsloping ST segment that ends with a slender, upright T wave.
• In contrast to the normal ST-T wave appearance in the GREEN border leads — is the appearance of the ST-T waves from leads V3,V4 of today's initial ECG (taken from Figure-1). Aren't the ST-T waves within the RED and BLUE rectangles obviously more "bulky", with a much wider T wave base than would be expected given modest QRS amplitude in these leads? In a patient with worrisome CP — these are hyperacute T waves suggestive of OMI until proven otherwise.

Figure-2: Comparison of normal vs hyperacute ST-T waves.

Return to Figure-1: What are the Other ECG Changes?

Hyperacute T waves are "hypervoluminous". They are larger than what we expect given relative amplitude of the QRS complex in the lead(s) we are looking at.

• Given the hyperacute changes we identified in leads V3 and V4 of Figure-1 — I like to look next at neighboring leads.
• If any doubt remained about the abnormal appearance of the ST-T wave in lead V3 — it should be removed on seeing how flat the ST-T wave is in neighboring lead V2. There simply is no way the transition between the flat ST-T wave in V2 — to what we see within the RED rectangle in lead V3 — is going to be normal.
• Given the hyperacute appearance in lead V4 — I thought the T waves in neighboring lateral leads V5,V6 were both "fatter"-at-their-peak than what is normally seen. And despite the tiny size of the QRS in lateral lead I — Isn't the T wave in lead I wider than you would expect? 
• To Emphasize: I might not think the ST-T wave appearance in leads V5,V6 was abnormal if everything else on the tracing was normal. But in the context of the hyperacute neighboring leads V3,V4 — Doesn't the appearance of the ST-T waves in leads V5,V6 look like a tapering off of the same process?
• Similarly — upright BLUE arrows in each of the inferior leads highlight "bulkier"-than-expected T waves.
• Finally — lead aVL shows reciprocal T wave inversion to the inferior lead hyperacute T waves. This is subtle — but isn't the inverted T wave in lead aVL wider-than-expected given small amplitude of the QRS in this lead. 

BOTTOM Line: In today's patient (who presented with severe new-onset CP) — recognition of hyperacute T waves in leads V3,V4 can be made within seconds. As described above — increased scrutiny elsewhere on the tracing reveals ST-T wave abnormalities in virtually all remaining leads. As capably recognized by Dr. Mastoras — the need for prompt cath quickly became obvious.

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P.S.: Of interest — the previously healthy 45-year old woman in today's case was found to have SCAD (Spontaneous Coronary Artery Dissection) of the distal LAD, with resultant 95% narrowing of the involved area.

• As per Dr. McLaren — the above demographic for today's patient is typical for a much higher-prevalence group for having SCAD as the cause of their acute event. Whereas SCAD is found in ~1-4% of all angiograms performed for ACS — this percentage increases to over 30% in middle-aged women. The risk of SCAD is even higher in pregnancy — accounting for over 40% of angiograms performed for ACS during the peripartum period.
• Clinically — the importance of recognizing SCAD as the cause of ACS — is that the approach to management is different, in that a conservative approach (without PCI) is often favored in hemodynamically stable patients with good TIMI flow. (For more on this topic — See discussion in the October 24, 2019 and July 31, 2018 posts in Dr. Smith's ECG Blog).

 

The Computer and Overreading Cardiologist call this completely normal. Is it?

This is another case sent by the undergraduate (who is applying to med school) who works as an EKG tech.  The undergraduate is now willing to identify himself: Hans Helseth.

A 56 year old male with a history of diabetes, dyslipidemia, hypertension, and coronary artery disease presented to the emergency department with sudden onset weakness, fatigue, lethargy, and confusion. He was admitted to the hospital for evaluation of these symptoms — but no ECG was done at that time. 

On the second morning of his admission, he developed 10/10 chest pain and some diaphoresis after breakfast. 

An EKG was taken at 0917:

The conventional computer algorithm (Marquette 12 SL) diagnosed “Normal Sinus Rhythm, Normal ECG”:

What do you think?

This EKG is very subtle, but it is diagnostic of LAD occlusion.

The T waves in the anterior leads, especially in V2 and V3, are hyperacute. While they only show about 0.5 mm of ST elevation, the T waves are symmetrical, have a straightened upstroke, and are bulky in proportion to their QRS complexes. Some may note the lack of reciprocal change, but it is important to remember that the reciprocal territory to the anterior wall is the posterior wall. Posterior leads would show reciprocal changes, but an LAD occlusion on the standard 12-lead EKG often does not manifest with reciprocal ST depression.

There was also an old EKG on file from a year prior:

This is clearly very different, and confirms that the above ECG has hyperacute T-waves.

See the side-by-side comparison at the bottom

The consulting cardiologist noted no change between this EKG and the latest, confirming the computer's “normal” read and calling the latest EKG “unremarkable” in the consult note. The anterior T waves are now, however, noticeably bulkier than in the old ECG.

The Queen of Hearts does not see the hyperacute T waves.  She reads Not OMI with high confidence:

Smith: I am very surprised that she did not see these hyperacute T-waves.  She is usually incredibly good at recognizing them!  On some occasions, expert humans are better than the Queen of Hearts!

The patient was given opiates which improved his chest pain to 7/10. At 1010, the first troponin I (URL 0.034 ng/mL) returned elevated at 0.4 ng/mL. 

At 1321, a repeat troponin I returned at 0.62 ng/mL. Another EKG was taken at 1454:

It is unclear whether or not the patient had pain at this point, but the EKG suggests reperfusion of the anterior wall. The T waves have deflated significantly and V2 shows the terminal T wave inversion typical to reperfusion.

Smith: These are pathognomonic in this clinical situation, and identical to Wellens' Pattern A biphasic T-waves

The conventional computer algorithm diagnosed “nonspecific T wave abnormality.”   The cardiologist noted “T waves appear flatter in precordial leads.”

The Queen of Hearts again diagnosed Not OMI with high confidence.

Smith: Again, I am very surprised by the Queen.  I suspect that Version 2 would do better and that will be released soon.

The consulting cardiologist wrote in their note:

“Could be cardiac chest pain. EKG initially negative but repeat shows a few T wave abnormalities… There is a chance this could be non-cardiac pain”

At 1518, an echocardiogram showed normal LV size and systolic function with hypokinesis of the mid and distal anterior wall and the mid and distal septum.

A plan was made to put the patient on heparin and continue to trend troponins. At 1605, another repeat troponin resulted at 5.271 ng/mL. The patient received a diagnosis of “NSTEMI” and angiography was scheduled for the next day. 

At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high). An EKG was repeated around midnight:

By itself, this ECG is not diagnostic of anything besides sinus tachycardia, and could be called normal (although there is ST segment straightening in the anterior leads, which should always prompt suspicion). 

But in the context of the previous EKGs, it suggests re-occlusion of the LAD culprit. This is pseudonormalization. The patient’s pain status at this point is also unclear, but one might expect that his pain has returned based on contextual evidence of re-occlusion.

The patient’s angiogram should have been expedited, but the EKG change was not recognized as recurrence of transmural ischemia. 

The conventional computer algorithm called “sinus tachycardia, otherwise normal EKG”. The cardiology overread wrote in comparison to the EKG taken at 1454, “QT has lengthened, nonspecific T wave abnormality is resolved”.

Smith: The Queen of Hearts diagnosed Not OMI with high confidence.  The computer algorithms do not have the advantage of "seeing" the previous ECG.  Not yet anyway.

At 1742 the next day, a final EKG was taken before angiography:

This EKG again shows reperfusion of the anterior wall. Notably, the precordial R wave progression has worsened, suggesting infarction of the anterior wall.

These are Wellens' Pattern B waves (deep symmetric).  Pattern A evolves into Pattern B.  

See this post: Classic Evolution of Wellens' T-waves over 26 hours

The Queen of Hearts recognized reperfusion here, diagnosing OMI with low confidence.

Smith: Version 1 diagnoses OMI even if it is reperfused OMI.  Version 2 will not do this.

Finally, at 1823 on the patient’s third day of admission (33 hours after the first diagnostic EKG) the patient was taken for angiography:

RAO Cranial view

This is the RAO Cranial view. 

The red arrow points to a 90% stenosis in the proximal segment of the LAD. The lesion had TIMI III flow on angiography, consistent with the spontaneous reperfusion seen on the last EKG before cath. 

RAO Caudal view:

This is the RAO Caudal view. The red arrow indicates the culprit lesion in the proximal LAD. 

RAO Caudal View Post PCI

This is the RAO Caudal view after thrombectomy and stent placement. The proximal LAD is now widely patent.

The rest of the patient’s hospital stay was uneventful and he was eventually discharged. This photo shows the series of occlusion and reperfusion the patient underwent during his hospital stay as seen in the right precordial leads:

Not only are T wave changes apparent, but the R waves can be seen to decrease in size.

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MY Comment, by KEN GRAUER, MD (9/25/2024):  

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Today's case serves as a reminder of some important principles to follow in the evaluation and management of a chest pain patient.

• Regular readers of this ECG Blog will be well familiar with many of these points. Nevertheless, cases like the one presented today — illustrate the continued need for review of these points that are KEY to attaining a good outcome.
• For clarity in Figure-1 — I've put together today's initial ECG — with this patient's baseline ECG done a year earlier.

Review of the CASE:

Dr. Smith has reviewed today's case in step-by-step detail. I focus my comments on some additional aspects of this case regarding interpretation of the initial ECG — and regarding initial evaluation and management. Consider the scenario in today's CASE:

• This 56-year old man with risk factors including diabetes and known coronary disease — presented to the ED on Day #1 with new weakness, fatigue, lethargy and confusion.
• No ECG was ordered on Day #1.
• On the morning of Day #2 — the patient suddenly developed 10/10 CP (Chest Pain) shortly after breakfast. This prompted the ordering of the patient's 1st ECG ( = ECG #1 done at 9:17am — as shown in Figure-1).
• Cardiology was consulted — and interpreted ECG #1 as "unremarkable". Cardiology agreed with the computer interpretation that said, "Sinus rhythm; Normal ECG".
• Cardiology gained access to the patient's baseline tracing ( = ECG #2) — and said there was "no change" in today's initial tracing compared to the baseline ECG done a year earlier.
• The patient was treated with opiates for his 10/10 CP. Use of opiates resulted in reduction of the patient's CP to a severity score of 7/10.
• At 10:10 am ( = 53 minutes after ECG #1 was done) — the 1st Troponin came back elevated = 0.4 ng/mL (upper normal = 0.034 ng/mL).
• The 2nd ECG on this patient was not obtained until 14:54 ( = 4+ hours after the elevated 1st Troponin value — and 5+ hours after the 1st ECG).

I will stop here — as I wanted to focus on this initial portion of today's case. (Dr. Smith’s review above covers the entire case).

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TEST Yourself: 

There are errors of omission and commission that are associated with each of the above 8 bullets in my review of today's CASE.

• How many of these errors can YOU identify?

Figure-1: Comparison between today’s initial ECG — with the baseline ECG from ~1 year earlier.

What Went Wrong in the Case:

Looking at each of the above 8 bullets — I thought the following:

• An ECG should be routinely ordered at the time the patient is admitted to the hospital whenever the patient presents with new symptoms (such as the weakness — fatigue — lethargy — and confusion that were noted in today’s case). More than simply “ordering” an admission ECG — the treating clinician should look at this admission ECG when examining the patient. Doing so in today’s case might have expedited recognizing the need for cardiac cath by more than a day!
• As I periodically highlight in Dr. Smith's ECG Blog — the entity of “silent” MI is much more common than is often appreciated (See My Comment in the August 19, 2023 post, among many others). Framingham taught us that ~1/2 of all “silent” (ie, non-CP) MIs have “something else” (ie, some other non-CP symptom). This is relevant to today's case — because a history of new weakness — fatigue — lethargy — and/or confusion — have each been known on occasion to be the presenting symptom of a “silent” MI.

An ECG was finally done at 9:17am on the 2nd hospital day. The reason this ECG was done was the sudden development of 10/10 CP.

• Given that today's patient has known coronary disease — sudden development of 10/10 CP immediately places this patient in a much higher-prevalence group for having an acute coronary event. As a result — regardless of whether the initial ECG and initial Troponin values come back normal — additional evaluation will be needed to rule out an acute event. This was not done (ie, The 2nd ECG was not obtained in today's case until 5+ hours after the 1st ECG — whereas the 2nd ECG should have been obtained within 10-30 minutes after ECG #1). 
• In a patient with new-onset 10/10 CP — the initial ECG in today's case can not be interpreted as "normal" or "unremarkable" (as it was by Cardiology). Instead — a subtle but-clearly-seen straightened ST segment takeoff is present in all 3 anterior leads (within the RED rectangle — being most marked in leads V2, and V3, but also seen in lead V1). Especially in leads V2 and V3 — the T wave is "fatter"-at-its-peak and wider-at-its-base than should be expected given relative QRS amplitude in these leads. As per Dr. Smith — these findings are diagnostic of acute LAD OMI. The cath lab should have been immediately activated at this point!

If there was any doubt about the diagnosis of acute LAD OMI after seeing ECG #1 — that doubt should have been removed as soon as the initial ECG was compared with the prior tracing that was done a year earlier.

• As I have often emphasized in this ECG Blog — unless serial ECGs are placed side-by-side when they are compared — important findings will be missed. In Figure-1 — Isn't the shape of the ST segment takeoff and the relative volume of the ST-T waves in leads V1,V2,V3 clearly different when comparing the 3 leads within the RED and BLUE rectangles? This is because in a patient with new CP — the ST-T waves in leads V1,V2,V3 of ECG #1 are hyperacute (ie, indicative of acute LAD OMI until proven otherwise).
• In any case — the ECG in today's case should have been repeated within 10-30 minutes.

Today's patient was then treated with opiates in an attempt to relieve his CP (with severity of his CP decreasing from 10/10 to 7/10 after this treatment).

• Opiates should not be used to treat CP until: i) The decision has been made to immediately activate the cath lab; — or, ii) A definitive diagnosis of a non-cardiac cause of CP has been made that merits treatment with narcotics (ie, if CP turned out to be the result of cancer). The reason is that if opiates relieve the CP of acute coronary occlusion — then the needed cardiac catheterization for PCI might not get done if the patient's CP was gone. (For more on use of Opiates with acute ischemic CP — See the January 6, 2023 post in Dr. Smith's ECG Blog).
• That said, in today's case — CP was only modestly reduced by opiates (ie, from 10/10 to 7/10). Even if the initial ECG would have been normal (which it wasn't) — persistence of 7/10 CP that is thought to be ischemic — by itself would be indication for prompt cath.

At 10:10am — the 1st Troponin came back elevated = 0.4 ng/mL (upper normal = 0.034 ng/mL).

• The fact that the 1st Troponin came back elevated further supports the previous bullet — which states, that even if the initial ECG would have been normal — persistence of ischemic CP in the face of an elevated Troponin is indication for prompt cath.
• IF for any reason the initial ECG (that was done at 9:17am) had not yet been repeated — return of an elevated Troponin (at 10:10am) should have immediately prompted repeat ECG.

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BOTTOM Line: 

• There are many lessons to be learned from today's case.