A woman in her 70s with bradycardia and hypotension

Submitted by Anonymous, written by Pendell Meyers



A woman in her 70s with HTN and DM had been experiencing lower chest / upper epigastric pain off and on for approximately one week until it acutely worsened, with diaphoresis and extreme fatigue. Her family called EMS and EMS recorded hypotension and this ECG:

What do you think?

This is an obvious inferoposterior OMI. There is STE in III and aVF which does not meet STEMI criteria due to insufficient STE in lead aVF. There is reciprocal STD in I and aVL. There is STD in V1-V5, maximal in V2-3, which is diagnostic of the posterior component. The quality is not perfect, but I believe this is sinus rhythm at about 100 bpm with prolonged PR interval.

It is impossible to determine from this ECG if there is also a right ventricular MI, but there is a suggestion of RVMI: the STD in V2 is very deep and yet minimal in V1. STD in V2 from posterior MI can "pull down" the STE in V1 and negate it.

On arrival in the ED, she was profoundly hypotensive, nearly obtunded, and bradycardic.  Resuscitation was initiated and this ECG was obtained:

Likely AFib (irregularly irregular) with bradycardia. ST changes persist, however this ECG shows some signs of reperfusion including terminal T-wave inversion in the inferior leads with tall posterior reperfusion T-waves in V2-4. 

Of course, the electrical and mechanical aspects of reperfusion are not always perfectly coincidental - just because there appears to be transient electrical reperfusion pattern does not mean that the inferior and posterior walls (or the SA and/or AV nodes) are functioning.

The cath lab was activated. The interventionalists insisted that the ECGs did not meet STEMI criteria and cancelled the activation, stating that they would consider urgent cath after further stabilization.

Atropine produced no response. The patient was placed on pressors and transcutaneous pads (which failed to capture). She was intubated and a transvenous pacemaker was inserted with good capture. She received PR aspirin.

Bedside echo showed obvious inferior wall motion abnormality and good TVP placement, no effusion.

At about 30 minutes after presentation, the patient had acceptable vital signs with the TVP and low dose epinephrine drip. Another ECG was obtained during pacing:

Mostly paced rhythm with PVCs (#3, #6, #9, #12). The PVCs have obvious STE in III and aVF and V6, with STD in I, aVL, V2-3. The paced beats show a clear OMI pattern as well, by the modified Sgarbossa criteria: lead III for example has 3.5 mm STE with 9.5 mm QRS = 37%, well over 20-25% as we have described. Proportionally excessive discordant STE is present in II, III, aVF, and V6. V5 has a barely concordant appearance, probably not a full millimeter.

The ED team again pointed out the evidence of inferoposterior OMI, this time by the modified Sgarbossa criteria. The cardiologists were not familiar with this and insisted that the ECG in paced rhythm could not be used to "look for a STEMI". After some discussion, cardiology insisted that they would need a native rhythm ECG to evaluate for STEMI criteria.

So they paused the TVP and obtained this ECG:

First beat is paced, then the rest are native. There appear to be very small possible P waves which may be conducting with huge PR interval and heart block, but this is irrelevant clinically. The QRS is narrow and shows a clear inferoposterior OMI pattern like all the ECGs before.

The ED team believed that this ECG met STEMI criteria, however the cardiologists felt that there the inferior leads had significant J-waves at the J-point, followed by STE that does not meet STEMI criteria.

At this point it was approximately 90 minutes after patient arrival.

Cardiology requested a head CT before cath for unknown reasons, which was negative. First troponin T was positive at 0.06 ng/mL.

Cardiology then requested 2U PRBC transfusion for Hgb 7.5 prior to cath, which was started.

During this time, the patients blood pressure continued to decline, requiring 4 pressors to sustain hemodynamics.

The patient expired approximately 2.5 hours after arrival, before cath was performed.



Learning Points:

We must not let STEMI criteria prevent identification and/or treatment of Occlusion MI. We must hold ourselves and our consultants to a higher standard to protect our patients.

Use the modified Sgarbossa criteria to detect OMI in the setting of ventricular paced rhythm.

Consider thrombolytics for OMI when PCI is not an option.

What is the infarct artery????? And have you ever seen a troponin this high?

An elderly woman with h/o stroke and aphasia seemed different to her daughter, and was pointing all over her body as if in pain.

They called 911.

She had a history of PCI to the circumflex and also of severe mitral regurgitation, status post bioprosthetic valve replacement.  Also a h/o LV aneurysm with thrombus, on anticoagulation, as well as a dual chamber pacemaker. 

On arrival, the BP was 60/30.

Here is the initial ECG:

There is atrial pacing and Right Bundle Branch Block (RBBB)
There is STE in I and aVL, V5, V6, with reciprocal STD in II, III, aVF
There is appropriately discordant ST depression in V1-V3 (appropriate to RBBB) 

The RBBB is new and the previous ECG had no ST elevation 

What is the infarct artery?

The cath lab was activated.

Here is the bedside echo (POCUS): Short Axis

Extremely poor LV function and massive wall motion abnormality

Long Axis

Extremely poor LV function and massive wall motion abnormality
Dr. Dick Asinger and Gopal Punjabi (@spectralCT) also points this out:

The parasternal long axis isn't tough--there is a pseudo aneurysm of the inferior wall with thrombus--likely from old circ infarct.
See the outpouching at the bottom of the image.

At 20 minutes, just before cath, another ECG was recorded:

More (worsening) STE

Her initial troponin I returned at 0.341 ng/mL (URL = 0.030 ng/mL) (not per L, not high sensitivity)

Lactate was 3.7 mEq/L

Her BP with pressors came up to 80, then 100.

Angiogram showed a 99% left main thrombotic occlusion with TIMI-1 flow (this is considered "occlusion" even though there is some flow.  It was opened and stented with resulting TIMI-3 (normal) flow.

The  stent to LCX is patent.  OM1 is occluded and OM2 has 60% stenosis.  Her RCA is a medium caliber vessel with tandem, at least moderate stenosis in the mid segment.

A balloon pump was placed.

Post cath echo:
left ventricular wall thickness and severely reduced systolic function.
The estimated left ventricular ejection fraction is less than 10 %.
Regional wall motion abnormality-anterior, anterolateral and inferolateral, akinetic/dyskinetic.
Aneurysm of the mid-portion of the lateral and inferolateral wall. No evidence for LV thrombus, probable.

Previous EF had already been low at 15%

Troponin profile:

This is in ng/mL (NOT ng/L !!!). 
This is equivalent to over 2 million ng/L.
The highest troponin I that I had ever seen prior to this was 500 ng/mL.
This is more than 4x as high!
A Huge Infarct

Left Main occlusion can have many different ECG patterns.  Here are many other examples:

How does acute left main occlusion present on the ECG? (Many example ECGs of true left main occlusion)

ST Elevation in Lead aVR, with diffuse ST depression, does not represent left main occlusion

ST-Elevation in aVR with diffuse ST-Depression: An ECG pattern that you must know and understand! (not left main occlusion

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MY Comment by KEN GRAUER, MD (1/16/2020):

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I did not correctly identify the “culprit artery” in this case. When I didn’t — I went back to the August 9, 2019 Post that Dr. Smith references in his comments above. It makes for impressive reading.

• It will not be often that emergency providers encounter patients with acute LMain occlusion — simply because survival of most of these patients is so limited. Because time until treatment is so critical — it is worth reviewing lessons learned regarding the ECG presentation of patients with acute LMain occlusion.

I have summarized the major points from Dr. Smith’s 8/9/2019 post in Figure-1. The KEY Take Home Points are as follows:

• There is no “single” ECG presentation for patients with acute LMain occlusion. Quite literally — You can see almost anything!
• The reason for this highly variable ECG presentation, is that multiple territories may be involved to varying degrees — making it impossible to predict how much ST elevation you will see — and how much opposing (reciprocal) ST depression will attenuate (if not completely cancel out) these initial ST segment vector forces.
• The ST-T wave appearance in lead aVR can be anything when there is acute LMain occlusion.

Figure-1: Reasons for the varied ECG presentation of acute LMain occlusion — excerpted from Dr. Smith’s 8/9/2019 post (See text).

Figure-2: The initial ECG in this case (See text).

I then took another look at the initial ECG in this case ( = ECG #1 in Figure-2). I noted the following:

• As per Dr. Smith — there is atrial pacing, with conduction of paced P waves in the form of RBBB. There is also LAHB (predominant negativity of the QRS in each of the inferior leads).
• The QRS complex is markedly prolonged (to over 0.16 second) — with marked and unusual fragmentation. This amount of QRS prolongation + fragmentation defines the presence of severe underlying heart disease — which is not at all surprising given the patient’s advanced age + history of coronary disease, valvular heart disease, history of LV aneurysm + permanent pacing.
• In addition to the fragmentation — there is evidence of prior infarction in the form of deep and wide Q waves in high lateral leads I and aVL (consistent with prior PCI to the LCx).
• There is suggestion of small initial q waves in leads V1 and V2 — consistent with likely prior septal infarction.

With all of this evidence of severe preexisting heart disease — it can be very challenging to look at an initial ECG (when no prior tracing is available) to determine, What is New vs Old? I was impressed by several observations I made in Figure-1:

• The shape of the ST-T wave in each of the inferior leads of ECG #1 clearly looks acute! The “scooping” we see toward the end of the depressed ST segment (especially in leads II and III) — then rising to a terminally peaked and enlarged T wave is simply not a longstanding finding.
• The nearly mirror-image opposite ST-T wave picture in lead aVL (compared to lead III) + the ~2mm of J-point ST elevation with ST segment straightening in the other lateral leads (ie, leads I, V5, V6) — suggested LCx (Left Circumflex) occlusion — but WHY so much inferior reciprocal change?
• As per Dr. Smith — the ST-T wave depression seen in leads V1 and V2 is perfectly consistent with appropriate discordance from the RBBB. BUT — WHY then is there more J-point ST depression in lead V3 (within the dotted PURPLE rectangle) than there is in leads V1 and V2 that typically show the most marked appropriate discordance with simple RBBB?
• I was struck by the shape of the depressed ST-T wave in lead V3. Isn’t the shape of this depressed ST-T wave in lead V3 (within the dotted PURPLE rectangle) a virtual mirror-image opposite of the shape of the ST-T wave elevation that we see in lateral chest leads V5 and V6? (Compare mirror-image views of these ST-T waves in leads V3 and V6 within the inserts outlined in PURPLE).

Putting It All Together: I fully acknowledge that I did not predict acute LMain occlusion as the “culprit artery” in this case. That said — considering the relationships summarized by Dr. Smith in Figure-1 — what we are seeing in ECG #1 could be consistent with a number of ECG findings of acute LMain occlusion:

• New bifascicular block (RBBB/LAHB).
• Marked acute STEMI changes in no less than 4 lateral leads.
• Disproportionately marked reciprocal ST-T wave changes in all inferior leads.
• Probable cancellation of oppositely-directed forces in anterior leads V1 and V2. I wouldn’t expect J-point ST depression to be more in lead V3 than in V1 and V2 (nor would I expect the mirror-image opposite ST-T wave picture in lead V3, compared to leads V5 and V6) — unless some of the anterior ST elevation from acute LMain occlusion was being cancelled out by acute posterior involvement.

A 40-something with sharp chest pain, worse with lying down, better leaning forward

A 40-something y.o. male with only PMH of DM and tobacco use presented with chest pain.  

Patient complained of 2 days of sharp, constant, sternal chest pain, 10/10, waxing and waning, worse with laying down and improved with leaning forward or walking.  

He has not had pain like this before.

Here is his ED ECG:

Diffuse ST Elevation.
The only reciprocal depression is in aVR
There is a lot of PR depression.
The inferolateral T/ST ratio is low (i.e., T-waves are not large in spite of STE)

What do you think?

This was texted to me and my answer was this:

"This looks like myo- or pericarditis, but you diagnose myopericarditis at your peril."

Since pain has been present so long, then troponin should be elevated in either MI or myocarditis.  If elevated, the patient needs the cath lab to be certain it is not acute coronary occlusion (occlusion myocardial infarction -- OMI).

Initial troponin I was 23.11 ng/mL (see profile below).

Here is the formal echo:

Regional wall motion abnormality-inferolateral.

Since it could not be definitively proven that this was myocarditis and not acute MI, the cath lab was activated.

Angiogram:

Culprit Lesion: Hazy, 70% stenosis of the mid-OM3; Successful PCI with excellent angiographic results, with normalization of flow post-PCI

Learning Points

How is this possible???
How can acute MI have positional and pleuritic chest pain??
How can the ECG in acute MI look exactly like myo- or pericarditis??

2 reasons:

1.  The clinical presentation of acute MI can be protean.  (Those who think that it cannot present like myocarditis have not been around long enough.)   It can present with pleuritic chest pain, positional chest pain, NO chest pain, or just about any other symptom!

See this case:

Should Troponin be a Vital Sign? Perhaps, but only if Interpreted Using Pre-test Probability.

2. Acute MI can result in post-MI pericarditis.

Follow up

In this case, the final clinical diagnosis was presumed acute MI with post infarction pericarditis.


How can you make the diagnosis short of an angiogram?

1.  If there is no new wall motion abormality on a high quality contrast echo, then it is not OMI.  If there is, then it may be either OMI or myocarditis.

2.  MRI, but this takes some time.

3.  Clear pericardial friction rub

4.  Pericardial effusion.

5.  Clear viral syndrome, elevated CRP change the probability, but do not rule out OMI.

Finally: Among these options, only MRI and angiogram will rule out post infarction pericarditis.


Myocarditis is not so common that, if you do an angiogram on all cases, that you will be doing hundreds of unnecessary angiograms.  Furthermore, although PCI has a significant complication rate, angiogram has a vanishingly low complication rate, especially in patients who are previously healthy.

So why risk missing an acute MI (an OMI)?


You diagnose pericarditis and myocarditis at your peril (actually, at your patient's peril).

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MY Comment by KEN GRAUER, MD (1/14/2020):

===================================

If I ever decided to write another ECG textbook — I would want to use the ECG in this case for illustrative purposes because: i) It shows a number of ECG findings that are highly typical for Acute Pericarditis; and, ii) It also shows features that are not typical for simple acute pericarditis.

• For clarity — I have reproduced and labeled the ECG in this case in Figure-1.

NOTE: Although we have frequently discussed distinction between acute pericarditis — acute myopericarditis — repolarization variants — and acute MI — differentiation between these entities remains problematic in practice. Hopefully the points emphasized in this case will assist simplifying the task of the emergency care provider.

• By way of reference — I reviewed the 4 ECG Stages of Acute Pericarditis (including assessment of the ST Segment/T Wave Ratio) in My Comment, at the bottom of the 12/13/2019 SSmith ECG Blog post.
• I further reviewed ECG findings of Acute MyoPericarditis (including recognition of Spodick’s Sign) in My Comment, at the bottom of the 1/10/2020 SSmith ECG Blog post.

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

QUESTION #1: Which ECG findings in Figure-1 are typical for simple Acute Pericarditis?

ANSWER: Typical ECG findings for acute pericarditis that are seen in ECG #1 include the following:

• There is diffuse ST elevation (ie, in almost all leads — except for right-sided leads III and aVR).
• There are no more than trivial Q waves (ie, and very narrow septal q waves in several lateral leads).
• There is no reciprocal ST depression (as is usually seen when there is acute infarction).
• The ST-T wave appearance in lead II looks similar to what is seen in lead I. In contrast, with acute MI — the ST-T wave appearance in lead II tends to resemble lead III.
• There is an increased ST/T wave ratio in lead V6 — because T wave amplitude in this lead is modest, and there is a relatively large amount of ST elevation in this lead.
• There is significant PR depression in multiple leads (GREEN arrows in Figure-1). The amount of PR depression is especially marked in leads V2 and V3. In addition — there is marked PR elevation in lead aVR (PURPLE arrow).
• Finally — there are aspects of the History that are clearly consistent with a diagnosis of acute pericarditis (ie, chest pain is positional — being exacerbated by lying supine, and relieved by leaning forward).

QUESTION #2: Which ECG findings in Figure-1 are NOT typical for simple Acute Pericarditis?

ANSWER: As typical as the history initially sounded in this case — demographics of this patient do differ from the most common presenting scenario of acute pericarditis.

• Although there are numerous potential causes of acute pericarditis — an acute viral etiology in a previously healthy younger adult would be the most typical presenting scenario. The patient in this case was somewhat older (ie, in his 40s) — and he had a history of diabetes + longterm smoking. Clearly, he might be predisposed to developing coronary disease.
• PEARL #1: Despite the above noted ECG findings that are typical of acute pericarditis — the dramatic amount of T wave peaking (especially in lead V3) is much more suggestive of the hyperacute T waves of impending coronary occlusion than of simple acute pericarditis.

PEARL #2: A distinguishing feature between Acute Pericarditis vs Acute MI is that with pericarditis — T waves tend not to invert until after ST elevation has returned to the baseline.

• In contrast, with acute MI — it is not uncommon to see residual ST elevation while T waves have begun to invert. Therefore, another feature against simple pericarditis in ECG #1 — is the fact that beginning T wave inversion is seen in multiple leads (RED arrows) in which ST segments are still at least slightly elevated.

PEARL #3: When in addition to Pericarditis, there is also Myocarditis (ie, acute MyoPericarditis) — Distinction from Acute MI becomes even more difficult! Troponin elevation by definition implies at least some degree of acute myocarditis.

• Potential ECG findings of acute Myocarditis (or MyoPericarditis) are many — and they may be identical to the findings of acute MI. Often, there is a combination of ECG findings suggestive on the one hand of acute pericarditis — and, on the other hand, of acute MI (such as we see in Figure-1!).

In SUMMARY — Among KEY POINTs which have been emphasized numerous times by Dr. Smith:

• You diagnose acute pericarditis (and acute myopericarditis) at your peril (that is, at your patient’s peril)!
• Neither ECG findings nor clinical history are totally reliable for distinguishing between acute myopericarditis vs acute MI.
• As was seen in this case — sometimes both conditions may coexist! Thus, the patient in this case had acute MI and then developed post-infarction pericarditis.
• Sometimes, diagnostic cardiac catheterization may be needed to distinguish between these entities. It is perfectly fine if cardiac cath is sometimes needed to be certain of your diagnosis.