Unusual: Troponin Trajectory to Help Determine Ongoing/Recurrent Infarction vs. Completed Infarction.

A 40-something male with no PMH of any kind presented  to urgent care on a weekend (cath team is at home) with cough starting 2 weeks prior and SOB one week prior.

He underwent a chest x-ray:

As this was consistent with "pulmonary edema vs. viral infection," and he was transferred to the ED

The faculty physician did an immediate cardiac and lung ultrasound:

Many B lines (probable pulmonary edema)

Parasternal short axis cardiac ultrasound:

The anterior wall is closest to the transducer and shows an obvious wall motion abnormality

Further history:

The patient denied chest pain but stated that he had had about 3 episodes of chest pressure, lasting 5 minutes each, in the past week.

The physician was alarmed by these findings and ordered an ECG:

This is diagnostic of Anterior MI, but:

Is this an "old" MI, a completed transmural anterior MI, or is there ongoing myocyte necrosis?

The QS-waves suggest that there is no myocardium left.

  

The T-waves are taller than one would expect in a completed MI, but the highest T/QRS ratio of V1-V4 is still only about 0.33, close to diagnosing acute STEMI, but not quite (see discussion of ratio below).
A ratio less than 0.36 is still consistent with a subacute STEMI.

Is it old, or is it subacute and ongoing?  We usually determine this from ongoing chest pain, but this patient NEVER had chest pain.

The ECG in a true "old anterior MI with persistent ST Elevation," usually associated with an aneurysm, looks like this proven LV aneurysm:

Notice that there is anterior ST Elevation and QS-waves.  This could easily be mistaken for a STEMI.  The difference is that STEMI has a taller T-wave, at least when it is less than 6 hours after occlusion.

I derived and validated a formula to differentiate anterior LV aneurysm from acute anterior STEMI.

This formula depends on the fact that an acute MI has a tall T-wave and that the T-wave is proportional to the QRS.  If any lead from V1-V4 has a T/QRS ratio greater than 0.36, then acute STEMI is most likely, unless the duration of symptoms is greater than 6 hours (as the infarct progresses, the T-wave gets smaller).

So in this case, it is difficult to ascertain symptom duration because the patient never had any pain.  However, he has been SOB for a week, so it is likely that the infarct started 1-2 weeks ago.

However, was it:
1) a completed infarct that is now complicated by pulmonary edema? or
2) a small infarct with a lot of viable, but ischemic and stunned (wall motion abnormality) myocardium, or
3) did he have a small infarct and now a recurrent occlusion with impending transmural infarction?

The distinction is critical, as if there is new, recurrent occlusion, then he needs the artery opened NOW in order to save that myocardium.  If the myocardium is all dead, then there is no great urgency.

The QS-waves suggest that it is completed, but QS-waves are not definitive.

Usually you can tell by the presence or absence of chest pain whether there is ongoing ischemia or not.  But this patient never had and does not have chest pain.  His SOB is due to pulmonary edema, which will be there whether there is active ischemia or not, as his ejection fraction is poor either way.

So how can we get some indication of the trajectory?

We decided to check the troponin trajectory.  This is not usually an accurate way to assess the current state of the artery, and if the troponin is rising, you will not know whether there is ongoing infarction (rising troponin can be from ongoing necrosis or from release of troponin from already infarcted myocardium).

However, if the troponin is falling, then it is likely that there is no more ongoing infarction.

This is NOT the way to approach a case of acute symptoms, as in these cases, the troponin lags far behind the ECG, and waiting for the initial troponin, or especially for a 2nd troponin, takes too long and will result in unnecessary infarction.  For example, the initial troponin is negative in approximately 50% of STEMI cases.  While the 2nd is almost always positive, by that time all the damage is done.


The first troponin I returned at 2.53 ng/mL.

Here is the one hour ECG:

Not much changed

The second trop I returned at 2.417 ng/mL.  So we decided that angiogram could wait for the next day.

He was treated with IV Nitroglycerin and furosemide.

There might even be some advantage to waiting, other than doing it in work hours:  

Occlusions that have organized over days may be difficult to open, difficult to pass the wire.

Some think that heparin therapy for 12-24 hours before angiogram helps in softening the thrombus and thus helps to open the artery (This was conveyed to me by one of our cardiologists. I had never heard it and cannot find any literature on it.  If anyone knows, please forward!)

Here is the 5.5 hour EKG:

T-waves are not as tall.
Does this mean that the artery is opening?  Possibly, but it is more likely due to improving hemodynamics with nitro and furosemide. 

Here is the ECG the next AM:

T-wave are smaller still.
This really looks like an LV aneurysm, though it is really too early to tell whether an aneurysm will form or not.

Troponin profile

Angiogram:

There was indeed a 100% LAD occlusion, and it was very difficult to pass the wire.  The interventionalist estimate from the characteristics of the lesion was of a 2 week old thrombus.

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Comment by KEN GRAUER, MD (9/17/2019):

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Interesting case of a 40-ish year old male with the unexpected finding of recent large anterior MI — despite the absence of chest pain. From an ECG interpretation perspective — I thought the initial ECG offers a number of interesting teaching points that are worthy of mention.

• I’ve reproduced this initial ED ECG in Figure-1. My sequential impressions were as follows:

Figure-1: The initial ED ECG in this case (See text).

DESCRIPTIVE ANALYSIS of ECG #1: The patient was a previously healthy 40-ish year old male with 1-2 weeks of coughing and dyspnea, but no chest pain.

• Rate & Rhythm — Sinus rhythm at a fairly fast rate of ~95/minute.
• Intervals (PR-QRS-QT ) — To my measurement — the longest PR interval is seen in lead I = 0.22 second, which is consistent with 1st-degree AV block. Assessing QRS width is challenging. This is because the QRS complex in leads V2, V3 and V4 clearly looks wider-than-normal. That said, the QRS complex is not more than half a large box in duration in any lead (ie, not more than 0.10 second) — which means that the QRS is narrow. The QTc looks normal (clearly less than half the R-R interval).
• Axis — The mean frontal plane axis is indeterminate! That’s because, other than lead aVF (which is predominantly negative) — the QRS complex in the 5 other limb leads is virtually isoelectric.
• Chamber Enlargement — None! This is also tricky — because overly deep anterior S waves often signal LVH. That said — the reason anterior S waves are so deep on this tracing is most likely not due to LVH, but rather to the loss of anterior R waves from recent infarction. PEARL: It becomes difficult to diagnose LVH on ECG in the presence of anterior infarction — because these 2 conditions produce opposing forces. That is, marked LVH (with increased lateral lead R wave amplitude, and increased depth of anterior S waves) may result in reduction (or even loss) of anterior r waves on ECG. By the same token — loss of anterior forces (ie, loss of anterior r waves) due to anterior MI may result in deeper anterior S waves that simulate LVH.

Q-R-S-T Changes:

• Q Waves in the Inferior Leads? — I stared for a long time at the inferior leads, in my attempt to determine IF there were any inferior Q waves. I believe there are not. There appears to be an initial small positive deflection in lead II (which I’d describe as an rR’S complex). There appear to be small-but-real initial r waves (positive deflections) in both leads III and aVF. I’d describe QRS complex morphology in leads III and aVF as consistent with an rSR’ (or rSr’) pattern. Technically — lack of any clear-cut inferior lead Q waves means we cannot diagnose prior inferior MI with any certainty. PEARL: Given the clinical context of this case — the unusual rR’ pattern in lead II + no more than very tiny initial r waves in leads III and aVF + notching (fragmentation) of the downslope of the S wave in lead aVF in this patient with a large, recent anterior MI may serve as an “ECG infarct equivalent” pattern in the inferior leads. I suspect this patient with total LAD occlusion most likely had a “wraparound” LAD that resulted in inferior wall involvement at the time of his infarction.
• Q Waves in the Anterior Leads? — YES! There is a Qr pattern in lead V1 (perhaps reflecting incomplete RBBB in association with anterior MI?). As noted by Dr. Smith above — there are deep QS complexes in leads V2-thru-V4. R waves finally develop in leads V5 and V6 — but these r waves are TINY (with a fragmented initial r wave in lead V6). PEARL: The finding of deep QS complexes in several anterior leads is not indicative of prior MI if there is complete LBBB. On the contrary — we expect to find small, if not absent r waves in anterior leads in the presence of this conduction defect. But despite “looking wide” — QRS complexes in leads V2-thru-V4 are not more than half a large box in duration — which means that the QRS complex in this tracing is not wide, and there is no bundle branch block. Given that there is no bundle branch block here — precordial lead QRS appearance is therefore diagnostic of extensive anterior (anterolateral) infarction at some point in time.
• ST-T Wave Changes — As per Dr. Smith, ST-T waves in leads V1-thru-V4 look taller-than-expected. Qualitatively — I thought the SHAPE of these ST-T waves did not look acute (ie, rather than coved — there was a clear upward concavity to these ST-T waves). In addition — true reciprocal ST depression was absent from this tracing (I thought the isolated shallow T inversion in aVL was probably not acute). PEARL: Despite my “gut” feeling that ST-T wave changes on this initial ED ECG did not look acute — it's important to appreciate that there was enough unexpected ST elevation to mandate additional information before drawing any conclusions. Considerations included: i) Emphasis on the history (ie, NO chest pain — but increasing dyspnea that could be consistent with anterior MI occurring 1-2 weeks earlier); ii) Search for a prior ECG (I don’t believe any was available); iii) Checking the “troponin trajectory” (discussed in detail by Dr. Smith above); and, iv) Clarifying the anatomy with cardiac catheterization.

Our THANKS to Dr. Smith for presenting this instructive case!

Chest pain, pelvic and abdominal pain, hypotension, and severe ischemia on the ECG

An elderly male was lethargic at the nursing home and complained of some pelvic pain, but then also chest pain and abdominal pain.  He was hypotensive.  His medications include beta blockers.

BP on arrival was 66/31, pulse 80, saturations 90% room air.  The patient was lethargic and shocky.

An ECG was recorded:

There is severe diffuse ST depression of subendocardial ischemia, with the obligatory reciprocal ST Elevation in aVR.
One might also think there are hyperacute T-waves in inferior leads, with reciprocal STD and T inversion in aVL.  

A bedside echo showed good LV function, no pericardial effusion, and normal right ventricle.  There were no B lines and the inferior vena cava looked somewhat flat.

Is this Acute Coronary Syndrome?  What do you think?
















The cath lab had been activated by the time I walked into the critical care area and saw this.

However, I was skeptical that this was ACS.  Not all severe ischemia is due to ACS.  Shock/Hypotension can be the cause of ischemia or the result of ischemia.

How do we differentiate?

If ACS is the cause, then shock/hypotension is cardiogenic shock.  Cardiogenic shock has 3 etiologies:
1. pump failure
2. dysrhythmia (too fast or too slow)
3. valve dysfunction

The rhythm is sinus.  The bedside echo showed good pump function.  There was no evidence of valve dysfunction on our bedside echo.

Because of the above considerations, I thought ACS was very unlikely.  I suspected some other catastrophe as an etiology of hypotension which then caused a decrease in coronary flow and consequent ischemia.

The patient responded to fluids, but also developed pulmonary edema.  Although ACS with valve dysfunction must be considered, this was not the etiology.   (Among the investigations was an aortic CT which was negative.)

Without going into detail, sepsis was discovered as the etiology of hypotension, which in turn resulted in ischemia.  Beta blockers prevented any compensating tachycardia.

In spite of adequate BP, his ECG did not improve by the next AM, but peak troponin I was only 0.200 ng/mL, confirming that acute ACS was not the initiating factor.

Learning Points:

1. When the ECG shows ischemia, it does NOT show the initiating event of the ischemia.
2. If there is good LV function and no dysrhythmia, and no valve dysfunction, then shock is not cardiogenic, and ACS cannot be blamed as the instigating factor.
3.  Thus, you need to look elsewhere for the many etiologies of shock.  Do not fixate on ACS just because there is severe ischemia.
4. ST Elevation in aVR does NOT mean left main occlusion.  Usually it does not even represent ACS.(1)

(1) Knotts RJ, Wilson JM, Kim E, Huang HD, Birnbaum Y. Diffuse ST depression with ST elevation in aVR: is this pattern specific for global ischemia due to left main coronary artery disease? J Electrocardiol 2013;46:240-8.

How does acute left main occlusion present on the ECG?

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Comment by KEN GRAUER, MD (9/12/2019):

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Interesting case! — with the important clinical point “brought home” that not all ischemia on ECG is due to ACS. It is worth memorizing Dr. Smith’s deductive reasoning for why the cause of this elderly man’s marked hypotension — was unlikely to be ACS.

• Apparently the cath lab was initially activated — but we are not told if cardiac catheterization was done … or if the order for cath activation was cancelled. While not needed for effective management of this patient (whose hypotension was found to result from septicemia) — I’d be curious to know what cath would have shown … (See below).

MY THOUGHTS on this ECG: I found the ECG in this case especially interesting — since in my opinion a few of the findings did not “fit”. None of these alter the astute decision-making deductions by Dr. Smith — but in the interest of ECG discussion, I feel the following points worthy of mention:

• There is generalized low voltage. That is, QRS amplitude in none of the limb leads exceeds 5mm — and relative QRS amplitude is small in all 6 chest leads. This is a nonspecific finding — which in this case appears not to be due to pericardial or pulmonary effusion, nor to acute infarction. No mention is made of the patient’s body habitus (obesity is a common cause of low voltage) — and, we know nothing about whether the patient has hypothyroidism or emphysema. Perhaps voltage increased after treatment of septicemia, and after an increase in this patient’s blood pressure … ? (MY POINT is to recognize low voltage — and to at least contemplate potential causes.)
• There could be lead misplacement in the chest leads — since lead V2 looks “out of place”. Wouldn’t the sequence of both R wave and ST-T wave progression look more natural IF lead V2 was lead V3; and lead V3 was lead V2? (Repeat ECG after verifying electrode lead placement might help explain some of the questions I raise below.)

For all of the reasons mentioned by Dr. Smith (especially good pump function with lack of wall motion abnormality on Echo — no evidence of valvular dysfunction — no more than minimally elevated peak troponin) — this ECG should be interpreted not as ACS — but rather as consistent with subendocardial ischemia. However — the typical ECG presentation of diffuse subendocardial ischemia should show significant ST depression (sometimes with T wave inversion) in virtually all leads, with the exception of leads aVR (and sometimes lead V1) that show ST elevation. The ECG in this case does not quite fit with this picture:

• As already noted — there is no more than modest ST depression in lead V3 (Lead V3 looks “out of place”…).
• The T waves in each of the 3 inferior leads look hyperacute! This is most marked in leads III and aVF — in which compared to the QRS complex in these leads, T waves are HUGE, being disproportionately “fat” at their peak and wide at their base. In addition, the ST segment in lead aVF is flat before the onset of the T wave — and, the ST segment “takeoff” in lead III looks like it is about to be elevated.

WHY Might This Be? To answer this question — I’d love to see this patient’s baseline ECG — and if cath was done, I’d love to learn the results ...

• I initially considered that the ST-T wave appearance in the inferior leads (with the mirror-image opposite ST-T wave picture of lead III being seen in lead aVL) — was the harbinger of acute coronary occlusion. But, as per Dr. Smith — results of bedside Echo, troponin and serial ECGs (which apparently did not evolve) — along with clinical confirmation of acute septicemia as the etiology for this patient’s hypotension all negated a theory of acute infarction.
• My GUESS — is that this elderly patient may have had underlying multi-vessel coronary disease — in which hyperacute inferior lead changes might reflect a “cancelling out effect” with what otherwise might have been frank inferior lead ST depression. Could there have been spontaneous reperfusion ...?

Do you recognize this ECG yet?

Case contributed by Dr. David Gordon

See if you can recognize this ECG without the clinical context:

Sinus tachycardia
Wide QRS
Terminal R-wave in aVR, V1, and V2 with STE and coved downsloping ST segments
Slightly peaked T-waves, most evident in V5-6

Together, these features make this ECG consistent only with hyperkalemia or another toxic/metabolic abnormality such as Na channel blockade. Sometimes a patient with profound metabolic acidosis may have this pattern as well, generally in the context of profound metabolic intoxication, usually critically ill, with down time, peri-arrest, post-ROSC, etc. V1-V2 morphology would be consistent with Brudaga pattern, but this should generally be more isolated to V1-V3 and would not generally have findings in all leads as we see here.

The differential of the ECG is short, and the most common, most rapidly deadly, and most treatable etiology is hyperkalemia.


Now for some context:

The patient was a male in his 30s with type 1 diabetes presenting with chest pain and RUQ abdominal pain. His fingerstick read "Hi" and he stated he couldn't remember if he took his insulin the night before. Vitals were within normal limits with tachycardia.

The team recognized the ECG as possibly due to hyperkalemia, especially in the clinical context. Labs were not yet back.

They gave 2 gm calcium gluconate, then recorded this ECG:

The QRS is more narrow, however the peaked T-waves and Brugada morphology in V1-V2 persist.

The team administered another 2 gm calcium gluconate.

The initial K returned at 7.3 mEq/L.

After 4 gm calcium gluconate was adminstered, this repeat ECG was obtained:

Resolution of the peaked T-waves, as well as the STE and Brugada pattern in V1-V2.

Three serial troponins were negative. Hyperkalemia and DKA were effectively treated, and the patient did well.



Learning Points:

Hyperkalemia can mimic almost anything on the ECG, including Occlusion MI, Brugada, etc. However, this pattern of STE in V1-V2 is an especially common and notable variant which we have reported many times on this blog:

You MUST recognize this pattern, even if it is not common

Right Bundle Branch Block with ST Elevation in V1?

ST elevation in aVL with reciprocal ST depression in the inferior leads

"Steve, what do you think of this ECG in this Cardiac Arrest Patient?"

A Tragic Case, related to the last post

Calcium in hyperkalemia should be titrated to ECG normalization, and no there is no upper limit when the patient is critically ill or when the ECG shows severe effects of hyperkalemia.

See this article for more information on hyperkalemia

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Comment by KEN GRAUER, MD (9/9/2019):

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Our THANKS to Dr. David Gordon — for his contribution of this case! The title of this blog post = “Do You Recognize this ECG Yet?”, is indeed an appropriate one — since recognition of the pattern shown here is clinically essential for emergency providers.

• That said — I’ll offer a different perspective on how one might describe the ECG findings in this case, along with differential diagnostic possibilities that this type of ECG pattern should prompt.
• For clarity — I’ve lightened the 3 tracings in this case, and show them together in Figure-1.

Figure-1: The 3 sequential ECGs shown in this case (See text).

MY THOUGHTS: Dr. Ed Burns of Life-In-The-Fast-Lane has an excellent review on the ECG features of Sodium-Channel Blockade (CLICK HERE). These ECG features include:

• Sinus tachycardia.
• QRS prolongation to ≥0.10 second. (I would add that it is especially the terminal portion of the QRS complex that is prolonged with sodium channel blockade.)
• RAD (Right Axis Deviation).
• Addition of a significant terminal R wave component to the QRS complex in lead aVR (that is usually ≥3 mm in amplitude).

NOTE: The initial ECG in this case ( = ECG #1) illustrates each of these features of Sodium-Channel Blockade:

• Sinus tachycardia (seen in ECG #1 at a rate of ~130/minute).
• The QRS complex is clearly prolonged. Most of this QRS widening is a result of widening of the last part of the QRS complex.
• The frontal plane axis is rightward — as demonstrated by predominant negative component to the QRS complex in lead I.
• There is a tall, terminal R wave component in lead aVR.

THEREFORE: As per Drs. Gordon and Meyers — ECG #1 is completely consistent with any toxicity producing Sodium-Channel Blockade (ie, tricyclic antidepressant overdose; proarrhythmia from antiarrhythmics such as flecainide or procainamide — or other agents, as listed by Dr. Burns at the above LITFL link).

Beyond-the-Core: Returning for a moment to ECG #1 — I was not at all certain in my initial assessment of this tracing that there were P waves deforming the terminal portion of the T wave in the inferior leads (BLUE arrows in ECG #1). These deflections were not distinct, and they were not seen everywhere (PURPLE arrow) — so, given QRS widening in ECG #1 without indisputable sign of atrial activity — VT was among my diagnostic considerations for ECG #1.

• That said — other features strongly supported the empiric treatment approach taken — and, without much slowing of the rate at all, clear evidence of sinus P waves emerged in the next 2 tracings ( = ECGs #2 and #3) following treatment with Calcium Gluconate (as shown by RED arrows in ECGs #2 and 3).

As per the title of this blog post by Drs. Gordon and Meyers ("Do You Recognize this ECG Yet?" ) — we need to consider (and, depending on the History — we need to assume!) HyperKalemia as the cause of the findings in ECG #1 until we prove otherwise because:

• The QRS complex is wide — and this widened QRS does not manifest a typical bundle branch block morphology.
• Atrial activity was not clearly seen in ECG #1.
• There is T wave peaking in some of the leads!

PEARL #1: By the time hyperkalemia has significantly widened QRS complexes — there will not always be diffuse, “Eiffel-tower-like” T wave peaking. Instead, you might only see slightly-more-pointed-than-expected T wave peaks in no more than a handful of leads (as suggested by the pointed T wave peaks in leads I, V4, V5 and V6 of ECG #1).

• PEARL #2: As per Drs. Gordon and Meyers — Sometimes with severe hyperkalemia, more than 1 dose of Calcium Gluconate may need to be given!

QUESTION: How do you know when you need to repeat Calcium Gluconate?

ANSWER: You don’t always know! That said:

• If the cause is severe hyperkalemia — the patient may die without more Calcium. So if you suspect this diagnosis — then repeat the Calcium.
• The HISTORY often provides an essential clue. (The patient in this case presented with DKA, without any hint in the history of drug overdose or toxicity — and severe acidosis may result in marked increase in extracellular K+.)
• And — after giving the 1st dose of Calcium Gluconate in this case — the next ECG done shortly thereafter ( = ECG #2) clearly shows improvement, in the form of: i) Less RAD (the S wave in lead I of ECG #2 is not as negative as it was in ECG #1); and, ii) The QRS is less wide (most noticeable in seeing that the S waves in leads I, V4, V5 and V6 of ECG #2 are not as wide as they were in ECG #1).

MY PERSPECTIVE: There is a Brugada-1 ECG pattern in ECG #1, which if anything — is even more pronounced in leads V1 and V2 of ECG #2.

• In my opinion — the ECG appearance of ECG #1 is not hyperkalemia that “looks like a Brugada pattern” — but rather a manifestation of Brugada Phenocopy — in which a Brugada-1 ECG pattern is seen as a result of some other factor. I discuss this distinction in detail in My Comment to the January 30, 2019 Dr. Smith post — and, beginning at 9:17 in my ECG Video on Brugada Syndrome.
• If you want more on Brugada — Check out Josep Brugada’s 2018 State-of-the-Art Review on Brugada Syndrome.
• For another very similar ECG case + related discussion — Please see My Comment on the 8/20/2019 ECG Guru (Scroll to the TOP of that page for the initial ECG).

NOTE: I fully acknowledge that you might call it “semantics” as to whether ECG manifestations that we see in ECG #1 reflect hyperkalemia vs Brugada Phenocopy caused by hyperkalemia — because in either case, these ECG manifestations resolve once hyperkalemia is treated (Note resolution of QRS widening, RAD, T wave peaking, and Brugada-1 ECG changes in ECG #3!). That said — I feel it important that:

• Clinicians appreciate that there is an entity known as Brugada Phenocopy — in which a Brugada-1 ECG pattern identical to that seen in true Brugada Syndrome may be seen as a result of some other cause.
• That among the LIST of potential “other causes” of a Brugada-1 ECG pattern are certain DRUGS (calcium channel blockers; ß-blockers; antianginals; psychotropics; ETOH; cocaine; others …) — acute febrile illness — variations in autonomic tone — hypothermia — electrolyte imbalance (hyperkalemia; hypokalemia) — ischemia/infarction — bradycardia — post-cardioversion/defibrillation. There may be others ...
• That the entities I just listed should be considered in your differential diagnosis whenever you see a Brugada-1 ECG pattern.
• The GOOD NEWS — is that if instead of true Brugada “Syndrome”, the reason for the Brugada-1 ECG pattern in your patient turns out to be Brugada Phenocopy precipitated by one or more of the above causes — and, that IF you find and “fix” the precipitating cause (as was done in this case of hyperkalemia due to DKA) — then longterm prognosis of the patient may not be adversely affected (and an ICD may not be needed, as it would be if true Brugada Syndrome was present)!