Look at this ST Depression

October 2, 2019, 10:14 am

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≪ Previous: A man in his 70s with chest pain during a bike ride

A healthy 30-something presented with 2 days of chest heaviness. He had some risk factors for pulmonary embolism, but none for ACS.

There was no SOB.

He had some reasons to be dehydrated.

He had taken a run that day and was symptom free during the run.

He was very well appearing.

Here is his initial ECG:

What do you think?

Interpretation:
Sinus tachycardia with what appears to be ST depression, especially in V2-V5 and ST Elevation in aVR.

But if you look more closely, you'll see that there is a very depressed PR segment (and elevated in aVR). This is a deep atrial repolarization wave, and can mimic ST depression. The deepest part of the wave is frequently just after the J-point.

Here I outline the atrial repol wave with my crude pen:

There was initial strong suspicion of ischemia among providers until I pointed this out.

We did a bedside cardiac ultrasound, which confirmed a small RV and hyperdynamic LV:

The patient's heart rate diminished after we put him supine on the cart. He was orthostatic. He was given IV fluids and the heart rate came down.

D dimer and 2 troponins were undetectable. Hemoglobin was normal and there was no evidence of bleeding.

Here is the post hydration ECG:

Completely normal
The atrial repolarization wave is gone.

You might think there is T-wave inversion in leads III and aVF.
But a negative T-wave does not mean there is T-wave inversion.
The T-wave axis, which is measured by the computer, is -12 degrees.
The QRS axis is 6 degrees.
So the QRST angle is only 18 degrees and anything less than 45 is normal.

He was asymptomatic after fluids and was discharged.

Discussion

Atrial repolarization waves are recognized by a downsloping PR segment and are a common cause of false positive stress tests. They are augmented by tachycardia.

See this paper:
Sapin PM et al. Identification of false positive exercise tests with use of electrocardiographic criteria: a possible role for atrial repolarization waves. JACC 18(1):127-35; July 1991. (link is full text)

Link to abstract: http://www.onlinejacc.org/content/18/1/127.abstract

Here is a schematic from my book, The ECG in Acute MI (this is a link to a free pdf)

Learning Points:

1. Recognize the atrial repolarization wave. It can mimic ST depression.
2. A patient with chest pain who takes a run while symptomatic and feels well during his run is unlikely to have ACS or pulmonary embolism.
3. Look for the QRST angle
4. The problem of the atrial repolarization wave is one of the reasons why the guidelines suggest that measuring ST Elevation should be at the J-point, relative to the PQ junction, NOT relative to the TP segment.

In fact, there is no validated way to measure the ST segment that is highly sensitive and specific for Occlusion Myocardial Infarction.

Here is more on the atrial repolarizaton wave.

Here is more on the QRST angle

↧

Shark Fin morphology recognized only by EM physician

October 4, 2019, 11:03 am

≫ Next: A 40-Something male with a "Seizure," Hypotension, and Bradycardia

≪ Previous: Look at this ST Depression

Case submitted by Alex Bracey, Written by Alex Bracey and Pendell Meyers

A man in his 70s complained of acute chest pain followed by witnessed cardiac arrest. He received immediate bystander CPR prior to EMS arrival. EMS found him in VF and administered 4 shocks, multiple doses of epinephrine, and amiodarone with intermittent ROSC, however he was in arrest on arrival to the ED with ongoing CPR via LUCAS device. Overall down time was 35 minutes from the time of arrest to arrival at the ED.

First rhythm check in the ED showed PEA with a wide complex at a rate of approximately 30 bpm. Calcium and epinephine were given at CPR was restarted. He was intubated, and arterial and central venous access were established. The next rhythm check revealed a wide complex rhythm at 78 bpm with a pulse on the arterial line. Norepinephrine was initiated to maintain blood pressure.

An ECG was obtained immediately:

What do you think?

There is a regular wide complex rhythm at a rate of about 85 bpm. The QRS complex is another example of the "shark fin morphology", composed of RBBB and LAFB, with superimposed massive STE in the anterolateral leads.

As you remember from our recent post,

When the QRS is wide, the J-point will hide.

Your next move, of course, is to:

Trace it down and copy it over.

Here is the result:

Meyers comment: Alex sent me this ECG with no clinical information and my immediate response was: "Shark fin! This patient is likely post-ROSC or peri-ROSC, right? LAD occlusion." I then sent it to Dr. Smith who said: "Just another shark fin. Should be obvious."

The cath lab was activated immediately based on this ECG.

iStat labs revealed hypokalemia of 2.2 mEq/L and pH 7.08 (VBG). He was given 300 mg rectal ASA and loaded with 4000U heparin.

Soon after establishing a perfusing rhythm, the patient was gagging and coughing against the endotracheal tube indicating intact brainstem reflexes.

He had recurrent VFib several times requiring defbrillation with ROSC each time. Epinephrine drip was added for additional inotropy.

The cardiology team arrived and another repeat ECG was obtained:

Similar to first ECG. It has been 20 minutes since sustained ROSC, therefore the findings are likely not simply due to low flow during arrest (assuming the patient has had at least several minutes of at least decent coronary perfusion pressure, and this patient had a MAP >65 on low doses of epinephrine and norepinephrine during this time).

In total, four cardiologists felt that these ECGs "did not represent a STEMI," and they felt that the ECG abnormalities were likely attributable to "hyperkalemia" (until the K returned at 2.2 mEq/L), "metabolic disturbances" and "down time." When the ED physician attempted to show them where the J-point was, highlighting massive anterolateral STE, it was simply not accepted at first in the setting of the wide QRS complex.

The ED attending advocated persistently that the ECG and clinical picture were diagnostic of proximal LAD or even left main occlusion, having seen this pattern several times before on this blog.

Of course, the initial troponin T was undetectable, less than 0.01 ng/mL, which made the ED attending's job even more difficult.

Side note: in our recent study of 467 high risk ACS patients over 6 months, we found 108 with proven OMI. Of those 108, 25% had initial undetectable troponin! The results were even more interesting when stratified by the patient's reported duration of symptoms (see below). Our contemporary troponin T assay does not seem to elevate until at least 3 hours after persistent Occlusion.

Data presented in abstract form at SAEM and ACEP, in review for publication.

After 30 minutes of discussion, another ECG was obtained:

In this ECG the QRS is slightly more organized, and it seems that the ED attending was finally able to convince the cardiologists where the J-point was.

The patient finally went for emergent cath which revealed acute, thrombotic, proximal LAD occlusion (100%, TIMI 0 flow), which was stented with excellent angiographic result. Diffuse CAD otherwise was also noted, but there were no other acute culprits or interventions.

Does angiographic reperfusion guarantee actual downstream reperfusion of the myocardium? No! As we have shown many times including this popular post:

Shoulder pain after lifting a heavy box

So here is the ECG after reperfusion, decide for yourself whether the actual myocardium is reperfused:

This shows a more organized QRS complex, persistent RBBB but no longer LAFB, and reduced STE in the anterolateral leads with terminal T-wave inversion in aVL, V1-V3, all indicating reperfusion downstream.

Several more serial ECGs were recorded over the next 24 hours which show the progression of reperfusion:

Next morning:

Less than 24 hours after presentation, he was following commands and recognizing his family.

Peak troponin T was 13.06 ng/mL (very large MI). Echo showed EF 30-35%, but views not good enough to assess wall motion abnormalities.

These ECGs clearly have STE meeting the classic STEMI criteria (assuming you interpret the wording of the guidelines to say that the criteria apply in this QRS scenario, which I do but just barely). Thus, this is a STEMI(+) OMI. I personally have been told by more than one cardiologist that scenarios like this do not apply to the STEMI criteria because, similar to their outdated view on LBBB, "you can't tell if there's a STEMI in a QRS like this."

Despite the clearly met STEMI criteria, the diagnosis on the chart and in the cath note is "NSTEMI".

Learning Points:

You absolutely must be able to recognize OMI in the context of wide complex rhythms, because the current STEMI vs. NSTEMI paradigm and current mainstream ECG education has little to offer for such patients.

When the QRS is wide, the J point will hide, so trace it down and copy it over.

Please memorize this "shark fin" STE morphology so that it becomes instantly recognizable, because these are some of the sickest patients who need emergent cath the most. Shark fin is a fusion of QRS and ST elevation, and in some other cases on the blog, although the QRS is wide, the greatest part of the width is ST segment. In this case, most of it was indeed the QRS. Here are other examples:

"Shark Fin": A Deadly ECG Sign that you Must Know!

"Shark fin" ECG in I, aVL, V4 and V5. Which artery? Hint: patient is in shock and was put on ECMO

Refractory V FIb Arrest, put on ECMO, regains an organized rhythm, and a 12-lead is recorded.

Giant R-waves. What are they?

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

Massive LAD and or LM occlusion often produces bundle branch blocks, classically RBBB + LAFB or RBBB + LPFB, making the QRS wide and the ST segment deviations more difficult to see.

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Comment, by KEN GRAUER, MD (10/4/2019):

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

Our THANKS (!) — to Drs. Bracey & Meyers for this important post that illustrates the Shark Fin morphology of acute STEMI with marked QRS widening. Tremendous credit to the team managing this patient for an incredible save! From an ECG perspective — I limit my Comment to an observation about the cardiac rhythm ...

There are 8 tracings shown on this post. The 2nd tracing shown added vertical lines to indicate location of the J-point — so this 2nd tracing was not a “new” ECG. This means that a total of 7 ECGs were done in this case.

For clarity — the numbering for the ECGs done that I refer to omits the tracing with the vertical lines drawn in to label the J point.

NOTE: We do not see any P waves until the 5th ECG that was done. I always look for P waves first in lead II — because sinus rhythm is defined by the presence of upright conducting P waves in this lead. My search for P waves next goes to lead V1 (generally the 2nd-best lead for identifying P waves) — and then to the other 10 leads on the tracing. P waves are absent until the 5th ECG ...
The wide QRS rhythm is fairly regular for the first 3 ECGs that were done.
The rhythm then becomes irregularly irregular for the 4th ECG that was done — without significant change in the wide QRS morphology.
Sinus P waves are clearly seen beginning with the 5th ECG. The rhythm is again regular with this 5th ECG — and, this is associated with some narrowing of the QRS complex, with significant change in QRS morphology (ie, less left axis; development of frank Q waves in high lateral and anterior leads, all in association with RBBB).
A regular sinus rhythm persists for the last 2 ECGs ( = ECGs #6 and #7) — without further change in QRS morphology.

BOTTOM LINE: I’m not sure what the original rhythms were … — but they were not sinus. Shark fin morphology was present — which allowed recognition of acute STEMI despite marked QRS widening.

↧

A 40-Something male with a "Seizure," Hypotension, and Bradycardia

October 7, 2019, 6:48 am

≫ Next: Do you understand these T-wave inversions?

≪ Previous: Shark Fin morphology recognized only by EM physician

This is by one of our outstanding 3rd year residents, Aaron Robinson, with some edits and comments by Smith

EMS responded to a reported seizure in a 42 year old male. Per bystanders, he went down after some intense sporting activity, and had “shaking” type movement. He reports no personal or familial history of seizures.

One of our EMS Fellows along with a Senior EM Resident were on duty that evening, and arrived on the scene with the Fire Department. When the physicians approached him, he was ashen, diaphoretic, and appeared in shock. Fire was able to obtain a BP of 60/palp and a pulse in the 40s. The physicians quickly recognized that this was not a seizure and likely cardiac in nature.

When the paramedics arrived, they obtained a 12 lead ECG and confirmed the unstable vital signs. EKG is pictured below:

What do you think?
There is an obvious inferior STEMI, but what else?
Why is the patient in shock?

Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. He was in profound cardiogenic shock.

Smith comment: I suspect lead reversal of V2 and V3: the STE is high in V1, lower in V2, and high again in V3. This STE is diagnostic of Right Ventricular STEMI (RV MI). In fact, the STE is widespread, mimicking an anterior STEMI. It really is an anterior STEMI, but of the Right Ventricular Anterior Wall, not the LV anterior wall.

When there is inferior and anterior STE, the differential is:
1. inferior + RV MI due to RCA occlusion vs.
2. LAD occlusion in a "wraparound LAD" (wraps around to the inferior wall).
In this case, the inferior STE is the most exaggerated, and the anterior STE is highest in V1 and V2. Both of these features make inferior + RV MI by far the most likely (Pseudoanteroseptal MI is another name for this)

There is also sinus bradycardia and the patient is in shock with hypotension. Although the shock is no doubt partly a result of poor pump function, with low stroke volume, especially of the RV, it should be compensated for by tachycardia. Cardiac output is stroke volume x rate, so this patient needs a higher heart rate.

This is a perfect indication for atropine. Atropine may succeed in increasing the heart rate in any narrow complex bradycardia, especially sinus bradycardia, but also with AV block, as AV block with a narrow complex QRS may be a junctional escape. A narrow complex bradycardia without any P-waves is also likely to respond to atropine, as it may be a junctional rhythm.

RCA ischemia often results in sinus bradycardia from vagal reflex or ischemia of the sinus node. In fact, in inferior MI, sinus bradycardia may be further evidence of Proximal RCA occlusion, which is the occlusion location that results in RV MI. Here is full text of this article.

Case continued

EMS immediately transported, activated the cath lab and gave 324 mg aspirin en route. It was about a 7 minute transport time. EMS also quickly administered 1L of NS to optimize preload and hopefully boost perfusion. They did not have an ultrasound on the ambulance (some local crews are starting to utilize POC limited US in our service areas).

EMS obtained a second ECG one minute later:

It appears the patient’s inferior STEMI has reperfused, as there is resolution of the inferior STE.

The patient arrived at the Emergency Dept critical care area and had this ECG recorded:

The sinus bradycardia persists. As you can see, the STE has returned in the inferior leads and there is now ST depression in the anterior leads concerning for posterior involvement. A right sided ECG was not recorded. STE in V1 with an inferior STEMI is moderately sensitive for right-ventricular involvement but this is only if there is no ST depression in V2! If there is STD in V2, the STE in V1 may be artificially normal! See this paper by Smith et al. Of note, despite the classic teaching, ST depression in Lead I is NOT reliable for the diagnosis of R-sided MI.

A bedside cardiac US was performed and showed an overall decrease in systolic function.

Also, the RV appears large and hypokinetic

The patient kept having recurrent syncopal episodes in the ED and was subsequently intubated for stabilization and airway protecting prior to going to the cath lab. Before transport, a final ECG was recorded:

There is, again, inferior reperfusion, but persistent marked anterior STE.

He was taken to the cath lab and underwent emergent intervention:

Thrombotic stenosis of the proximal RCA (95% with evidence of plaque

rupture) is the culprit for the patient's inferoposterior STEMI. He was successfully stented. This also confirms right ventricular infarction (RV MI)

A follow up TTE demonstrated a normal LVEF with a “regional wall motion abnormality-posterolateral hypokinetic mild, probable.” His troponin I peaked at 6.107 ng/mL. He was discharged neurologically intact and did very well. He has a history of sudden cardiac death in his family. The patient never arrested during his time at the hospital and his prognosis is good.

Learning Points:

1. It is easy to mistake syncopal episodes with associated myoclonus as seizures, so have a high index of suspicion for syncope as the etiology. This patient’s shock state upon arrival didn’t fit with seizures and it was quickly recognized.

2. Recognize Right Ventricular STEMI by inferior MI with shock (and clear lungs), sinus bradycardia, and ST elevation in Lead V1 (but it may also be V2 and beyond, with maximal STE in V1 and V2).

3. STE in V1 in inferior MI is moderately sensitive for RV MI (if there is no posterior MI "pulling the ST segment down"). Plus STE in V1 in inferior MI is very specific for RV MI.

4. If time allows, a right sided ECG may help to recognize RV MI, but even this can be falsely negative in the presence of posterior MI (see below).

5. Give atropine for narrow complex bradycardia with hypotension.

6. Give a moderate fluid bolus for Hypotension in RV MI

7. Give norepinephrine for hypotension in spite of the moderate fluid bolus.

I (the senior resident on scene with the EMS Fellow) had a discussion with Dr. Smith regarding this case. During transport, I had debated giving atropine for his bradycardia and cardiogenic shock, but was worried about making an already profoundly ischemic heart more ischemic, and chose instead to optimize preload with pressure bagging 1L NS. Dr. Smith pointed out that while atropine may may result in slightly more oxygen demand, the increase in cardiac output and in blood pressure would increase overall coronary perfusion and decrease ischemia. This is particularly true of RV MI: LV coronary perfusion is dependent on diastolic pressure because the myocardial pressure is too high for perfusion during systole. But RV systolic pressure is low, so the RV perfuses during BOTH systole and diastole. Higher mean arterial pressure improves RV perfusion. Norepinephrine can be very useful adjunct to shock from RV MI, as hypotension is so detrimental to RV perfusion.

So when I find myself in this position again prehospital, I will administer atropine.

V4R in Right Ventricular MI

As in the Smith study of lead V1 in RVMI, Kosuge et al. studied lead V4R in the context of posterior involvement and found that RVMI was associated with a high rate of STE in V4R in the absence, but not in the presence, of posterior MI. STE V4R had sensitivities of 34% and 96% (p b 0.001), and specificities of 83% and 82% (NS) in the presence and absence of PWI, respectively. They did not study lead V1. Like our study, they used angiographic criteria for RVMI [13]

Kosuge M, Ishikawa T, Morita S, et al. Posterior wall involvement attenuates predictive

value of ST-segment elevation in lead V4R for right ventricular involvement in

inferior acute myocardial infarction. J Cardiol 2009;54(3):386–93.

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MY Comment, by KEN GRAUER, MD (10/7/2019):

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

What I like most about this case — is that cath confirmation of acute proximal RCA occlusion as the “culprit” artery allows us to optimally appreciate ongoing events on sequential ECGs done in this case. As such — this case provides unique insight into the interplay between RV vs posterior wall ST-T wave changes from acute occlusion — followed by reperfusion — followed by re-occlusion ...

For clarity — I’ve put the 4 ECGs done in this case together in Figure-1.

Figure-1: A sequential look at the 4 ECGs in this case (See text).

MY THOUGHTS: In the setting of acute proximal RCA occlusion that produces acute inferior STEMI — it is difficult to predict the net effect of simultaneously-occurring RV and posterior wall infarction.

Looking first at ECG #1 — As per Dr. Smith, there is an obvious acute inferior STEMI. Acute RCA occlusionas the “culprit” artery is suggested by markedly more ST elevation in lead III > II — and, by an equally marked amount reciprocal ST depression in lead aVL.
There is also a relatively modest amount of ST elevation in the lateral chest leads (V4, V5, V6) of ECG #1. This can be seen with acute RCA occlusion when there are large postero-lateral branches from the PDA (Posterior Descending Artery) branch of the RCA that supplies the lateral wall. In contrast, when there is infero-postero-lateral MI from acute LCx (Left Circumflex) occlusion — ST elevation in lead V6 tends to be greater than ST elevation in the lead III.
There is also marked ST elevation in leads V1, V2 and V3 in ECG #1. In the setting of acute inferior STEMI, in which the greatest amount of ST elevation is seen inferiorly (ie, in leads III and aVF) — this anterior ST elevation strongly suggests acute RV MI. And, since the RCA but not the LCx supplies the RV (Right Ventricle) — the diagnosis of acute RV MI confirms that the RCA is the “culprit” artery!
PEARL: Reasons why Dr. Smith strongly suspected lead reversal of lead V2 with lead V3 in ECG #1 include: i) QRS morphology (Wouldn’t R wave progression be much more logical IF lead V3 was lead V2?); and, ii) ST-T wave morphology (IF lead V3 was lead V2 — Wouldn’t the progression of marked ST elevation in V1, V2 from acute RV MI — with transition to more modest ST elevation by V3 — make much more physiologic sense?).
BOTTOM LINE: ECG #1 shows bradycardia + marked ST-T wave deviation from acute infero-lateral STEMI + acute RV MI — both being the result of acute RCA occlusion. NOTE: Although we know that acute posterior MI very often accompanies acute inferior STEMI — we would not have known there is posterior involvement if all we had to look at was ECG #1.

ECG #2 was obtained just 1 minute after ECG #1 ...

QUESTION: What if ECG #1 had not been done — and the initial ECG in this case was ECG #2?

ANSWER: If the initial ECG in this case was ECG #2 — then we would not yet have had a definitive diagnosis of acute RCA occlusion. Instead — I would have suspected an LAD “culprit” from the peaked T waves in leads V1-thru-V4 of ECG #2, that without the context of ECG #1 would look like hyperacute anterior changes ...

BACK to sequential evolution in this case.

In light of ECG #1 — How would you interpret ECG #2?

As per Dr. Smith — ECG #2 shows complete resolution of the inferior wall ST elevation that we saw in ECG #1.
There is also: i) resolution of high-lateral reciprocal ST depression (in leads I and aVL); ii) resolution of the ST elevation in lateral chest leads (V4,V5,V6); and, iii) beginning T wave inversion in leads III and aVF. These changes strongly suggest spontaneous reperfusion of the occluded RCA.
In addition — the anterior ST elevation from acute RV MI has also resolved. In its place — we now see T wave peaking in leads V1-thru-V4. MY THOUGHT: Given that the anterior leads show a mirror-image view of the posterior wall of LV — the shape of the ST-T waves that we now see in the anterior leads of ECG #2 to me are most consistent with reperfusion changes from acute posterior MI (that now become visible because ST elevation from acute RV MI has resolved).
PEARL: Note increased R wave amplitude in leads V2, V3 and V4 of ECG #2 (compared to ECG #1). This is consistent with evolving posterior MI.
REFLECTION — Isn’t it interesting how quickly the ECG picture can change in the space of 1-minute (the time between ECGs #1 and #2) when there is: i) acute reperfusion of the “culprit” artery; and, ii) interplay between opposing ST-T wave forces of acute RV and acute posterior MI.

Looking at ECG #3:

As per Dr. Smith (and compared with ECG #2) — there is once again ST elevation in the inferior leads in ECG #3. This is associated with return of reciprocal ST-T changes in the high-lateral leads (leads I and aVL). This strongly suggests re-occlusion of the RCA.
Although the absolute amount of ST elevation in the inferior leads of ECG #3 is not as much as it was in ECG #1 — it is of interest that once again, the amount of reciprocal ST depression in lead aVL is virtually the mirror opposite of the amount of ST elevation we see in lead III of ECG #3. This reflects that “magic” mirror-image picture for ST-T wave changes in leads III and aVL that is so commonly seen with acute inferior STEMI.
It is interesting to note that in the chest leads of ECG #3 — the changes of acute posterior infarction now predominate! These include: i) increase in R wave amplitude in leads V2 and V3 (compared to R wave amplitude for these leads in ECG #1); and, ii) the “shelf-like” shape of ST depression in leads V2 and V3 that is so typical of acute posterior MI.
NOTE: There is no indication at all from ECG #3 that there was acute RV involvement just a little while earlier ...

Finally (ie, just before this patient was taken to the cath lab) — ECG #4 was obtained:

Limb lead changes once again suggest spontaneous reperfusion of the inferior wall (ie, resolution of inferior ST elevation and high-lateral reciprocal ST depression between ECG #3 and ECG #4).
BUT in the chest leads for ECG #4 — there is once again ST elevation in leads V1-thru-V4 (most marked in leads V2 and V3). Given that we know from results of cardiac cath that the LAD was not a culprit artery — this means that this return of anterior ST elevation in ECG #4 has to reflect loss of perfusion to the RV.

REFLECTION — So WHY does the shape of anterior ST-T waves look so different in leads V1, V2 and V3 of ECG #1 compared to ECG #4? I think the answer is that in ECG #1 — anterior chest lead ST-T wave changes were dominated by acute RV MI. In contrast, by the time ECG #4 was obtained — we were seeing a combination of ST elevation from acute RV MI + reperfusion changes in the posterior wall (ie, precisely what you might expect to see if you fused the ST-T wave picture for leads V1, V2 and V3 from ECG #1 and ECG #2)!

Bottom Line: I think it fascinating to reflect on how quickly ST-T wave changes may occur when there is spontaneous reperfusion, which is then followed by re-occlusion of the culprit artery. The ECG picture becomes that much more intriguing when there is interplay between opposing electrical forces, as occurs with acute RV and posterior MI evolving at different tempos.

Our THANKS to Dr. Smith for presentation of this fascinating case!

↧

Do you understand these T-wave inversions?

October 10, 2019, 4:01 am

≫ Next: What could this rhythm be? And what is going on after it breaks?

≪ Previous: A 40-Something male with a "Seizure," Hypotension, and Bradycardia

Case submitted and written by Alex Bracey, with edits by Pendell Meyers

A man in his 50s without prior medical history was sent to the emergency department from an urgent care facility for concern of an "abnormal ECG" after he had complained of chest pain earlier in the day. He was symptom free at the time of arrival.

Here is the triage ECG at the Emergency Department (we did not immediately have access to the urgent care ECG just yet):

ED ECG#1

What do you think? What do you think his urgent care ECG (done during pain) will show?

This ECG shows sinus bradycardia with terminal ST depressions in II, III, aVF, V3-V6, with reciprocal changes in aVL and I. These findings indicate reperfusion of the inferior and lateral walls, implying that an ECG during active symptoms would likely show OMI.

Note: This is the same pathophysiology and electrophysiology involved in Wellens syndrome, which is simply the name given to reperfusion of anterior wall OMI when the patient is in the pain free state of reperfusion and has not yet lost the anterior wall (requires persistent R-waves to be classic Wellens syndrome). This pattern occurs in any wall of the heart, whichever wall is currently reperfused from a prior occlusion.

On this note, "type A" and "type B" Wellens are useless distinctions that arose before we realized that reperfusion is a progression of findings starting with terminal T-wave inversions ("type A") and progressing to full T-wave inversions ("type B"). My analogy for this misunderstanding of Wellens syndrome that I tell my residents is this: "Imagine you were an alien looking through a microscope and you discovered Earth. You zoom in to a city and look at a single street and you see humans, which happens to be a woman walking with her small child. You watch them for a few hours and then report your findings to your fellow aliens: you declare that there are two types of humans: type A (smaller, helpless ones) and type B (large, smarter ones). If they simply had more knowledge and experience with humans, it would be easy to understand that type A and type B are not different types at all, rather different points along the same progression. If you only look at individual snapshots in time, they appear to be different types, however if you follow them for the full course of their progression the pattern becomes clear.

To make type A and B even more useless, they are misnomers applied by someone who had not carefully read Wellens' papers. They called terminal T-wave inversion type B and deep inversion type A. Wellens called terminal T-wave inversion "Pattern A" and deep "Pattern B."

He reports that today while sitting outside he developed sudden onset bilateral arm “burning” and an “odd feeling” though he was not able to further describe it. He had no chest pain, heaviness, or discomfort at any point and was never short of breath during today’s events. When pressed, he recalls that last week he traveled to Denver where he experienced dyspnea on exertion, though he attributed it to the altitude.

He was alarmed by these symptoms today and presented to an urgent care where this ECG was recorded:

Urgent Care ECG (this was done before arrival to ED, during active symptoms):

STE in II, III, and aVF (which probably barely does meet STEMI critiera) with hyperacute T waves in II, IIII, aVF and reciprocal negative hyperacute T-wave in aVL, with STD in V1-V2

Small R waves in II, III, aVF

This is diagnostic of inferoposterior OMI. The most likely culprit vessel would be the RCA.

Back to the present, in the ED, asymptomatic:

Given that the patient was now asymptomatic in the ED with ED ECG#1, I asked for serial ECGs to be recorded every 30 minutes and for any acute changes in discomfort or clinical condition.

At our facility we have a process to promptly evaluate patients for urgent or emergent PCI that present with ECGs concerning for acute coronary occlusions that do not meet STEMI critieria (OMI) called Heart Alert. We activated this process and the cardiology fellow presented to the bedside.

A thirdECG was record at this time with no change, persistent reperfusion pattern.

During this time I received a call from the interventional cardiologist. I discussed the case with him as he reviewed the ECG. We agreed that there were dynamic changes; however, he did not feel that it could represent acute coronary syndrome as the patient did not have chest pain at any time during his prior symptoms.

This is clearly false.

The patient then reported another episode of diaphoresis. An ECG at this time was recorded:

Redemonstration of small STE in II, III, aVF (not meeting criteria in this ECG) and reciprocal changes in aVL, V2. This ECG demonstrates reocclusion of the affected coronary vessel.

At this time the cardiology fellow again contacted the interventionist who agreed to take the patient for urgent PCI at this time.

His initial troponin T was 0.02 ng/mL.

Here is what they found on cath:

100% mRCA with TIMI 0 flow

Post DES RCA with TIMI 3 flow

His formal echo performed the next day revealed an EF of 50% and Septal, lateral, and apical wall motion abnormalities.

His troponin T continued to climb over the next day with a peak of 1.4 ng/mL.

He had an uncomplicated post-PCI course and was discharged 3 days later.

Teaching Points:

We must understand the ECG patterns of occlusion and reperfusion because they are not currently taught or understood in the classic STEMI paradigm.

Serial ECGs greatly increase the chances of finding diagnostic features of OMI on ECG.

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What could this rhythm be? And what is going on after it breaks?

October 16, 2019, 5:13 am

≫ Next: 60-something with 2 days of intermittent epigastric pain. Why does the cardiologist disagree?

≪ Previous: Do you understand these T-wave inversions?

Written by Pendell Meyers, edits by Steve Smith

A man in his 30s with no prior medical history presented with palpitations. His vitals and exam were within normal limits with the exception of his heart rate.

Here is his initial ECG:

What do you think? What is the differential?

This shows a regular narrow complex tachycardia, thus the differential is sinus tach, SVT (including AVNRT most commonly, AVRT [which is SVT in the setting of WPW with an accessory pathway] next most common, then atrial tachycardia, etc.) or atrial flutter.

It it were atrial flutter, and because it is regular at a rate of 210, the flutter would have to be conducting 1:1 to the ventricle. There are no definite atrial waves, although the negative deflections in V1 before the QRS complexes could be atrial in origin, or the entire baseline may appear to have a sawtooth pattern in lead II - it is not clear in my opinion. 1:1 atrial flutter seems unlikely because, as it would have to be 1:1 conduction, the atrial flutter rate would have to be a very slow 210 bpm (normal would be 300). The ventricular rate of roughly 210 bpm makes sinus tachycardia unlikely in a 30 year old (max sinus rate theoretically 190ish according to 220-Age rule of thumb).

Aside: if the atrial flutter rate were 300 bpm, it could not be conducted by the AV node, and the ventricular rate could only be 300 if there were an accessory pathway or a peri-AV node bypass tract that inserts into the bundle of His. In the former case, there would have to be a wide QRS (due to the preexcitation of the delta wave), but in the latter case, the QRS would be narrow.

The REVERT vagal maneuver was performed with a change in rhythm.

A repeat ECG was performed:

What do you think?

There is now a regular rhythm with wider QRS complexes than during the tachycardia above, almost imitating LBBB. There is an extremely short PR interval, such that the wide QRS takes off from the end of the P-wave. The takeoff of the QRS complex is not the most obvious delta wave, but overall this appears consistent with accessory pathway conduction, or WPW.

See these two similar cases:

A 40-something woman with no medical history presented with 2 days of chest pain

What do you think about this Left Bundle Branch Block?

Now that we suspect the patient has an accessory pathway, the most likely rhythm responsible for his paroxysmal narrow complex regular tachycardia in the first ECG is orthodromic AVRT, in which the action potential is conducted down the AV node (causing a narrow QRS complex) and then up the bypass tract, and so on.

The patient was referred to EP for an EP study and possible ablation.

Learning Points:

You must easily be able to think through the differential of tachycardias based on the categories of narrow vs. wide QRS and regular vs. irregular rhythm:
- Narrow & Regular
- Narrow & Irregular
- Wide & Regular
- Wide & Irregular

After conversion from a regular, narrow complex tachycardia, you should always obtain a post-cardioversion ECG to look for the presence of underlying causes of the tachycardia, most commonly WPW syndrome.

WPW can distort the QRS complex and mimic bundle branch blocks or other conduction abnormalities, without showing the classic delta wave into an otherwise normal, narrow QRS complex. The risk in this case is that WPW is missed due to the confusing QRS morphology.

Some bypass tracts are "concealed" meaning they do not conduct during normal sinus rhythm and thus leave no evidence on the resting sinus ECG.

↧

60-something with 2 days of intermittent epigastric pain. Why does the cardiologist disagree?

October 20, 2019, 6:48 am

≫ Next: Is this ST depression due to "lateral ischemia"?

≪ Previous: What could this rhythm be? And what is going on after it breaks?

One of our residents who just graduated 3 months ago texted me this ECG:

"Hey Steve, would be grateful for any thoughts on this EKG. 60-something with 2 days of waxing and waning epigastric pain and diaphoresis. Also diffuse abdominal tenderness."

Presenting ECG:

What was my answer?
What is the management?

My Answer: "Inferior and lateral OMI"

Detailed Interpretation: Sinus rhythm. Left axis deviation, but not quite LAFB (no r-wave in inferior leads; no q-wave in aVL). There is less than 1 mm STE in inferior leads, with reciprocal ST depression. There are hyperacute T-waves in inferior leads. There are hyperacute T-waves in V2-V6.

His Reply: "Thanks. On his way to cath now but not before plenty of guff from cardiology...."

Outcome:

Initial troponin I = 52.0 ng/mL. 100% proximal RCA occlusion. Severe RV dysfunction on echo.

My Question: "Did my response help you persuade the interventionalist?"

His Answer: "The troponin actually came back before your response and that's what did it....although the fact that it happened in the daytime on a weekday did not hurt. I imagine it would have been more of a struggle if it had been 2 AM."

My Question:"How could they give you lots of "condescending guff" with a troponin like that?"

His Answer:"The cardiologist said: 'Hard to call this "acute" if he has a couple of days of pain and there are Q waves, isn't it?"

My response:"Well the literature would say that if there is continued ST elevation and/or continued pain, and it is less than 48 hours (persistent ischemia), that they should go to the cath lab. The presence of Q-wave or elevated troponin is NEVER a reason to not pursue reperfusion. Besides, no one knows when his MI really started. "Waxing and waning pain, etc.""

His Answer: "That's good to know. He also had active pain which I thought was a good indication. They also steadfastly refused to see any ST Elevation on the EKG. Even after I got a second one that was more pronounced."

Even if you knew the patient's MI was less than 24 hours old, immediate intervention is still indicated:

The below article shows that even asymptomatic patients with STEMI that is 12-48 hours old have much more myocardial salvage with immediate PCI than those who have PCI on an as needed basis (recurrent symptoms, etc.)

Learning Points:

Expert ECG interpretation is much more accurate than clinical symptoms for measuring viable, endangered myocardium in OMI.

When taking a careful history, you must distinguish off and on pain (which can be repeated occlusion and reperfusion) from constant, persistent pain.

Schomig et al demonstrated smaller infarct size (and an underpowered trend toward reduced mortality) for even asymptomatic STEMIs between 12 and 48 hours of symptom onset.

Important Article

Schomig A et al. Mechanical Reperfusion in Patients With Acute Myocardial Infarction Presenting More Than 12 Hours From Symptom OnsetA Randomized Controlled Trial.

jin Ndrepepa, MD; Christina Markwardt, MD; Francesco Di Pede, MD; Stephan G. Nekolla, PhD; Klaus Schlotterbeck, MD; Helmut Schühlen, MD; Jürgen Pache, MD; Melchior Seyfarth, MD; Stefan Martinoff, MD; Werner Benzer, MD; Claus Schmitt, MD; Josef Dirschinger, MD; Markus Schwaiger, MD; Adnan Kastrati, MD; for the Beyond 12 hours Reperfusion AlternatiVe Evaluation (BRAVE-2) Trial Investigators

JAMA. 2005;293(23):2865-2872. doi:10.1001/jama.293.23.2865

Full text:

https://jamanetwork.com/journals/jama/fullarticle/201080

Abstract

Context No specifically designed studies have addressed the role of primary percutaneous coronary intervention in patients with acute ST-segment elevation myocardial infarction (STEMI) presenting more than 12 hours after symptom onset. Current guidelines do not recommend reperfusion treatment in these patients.

Objective To assess whether an immediate invasive treatment strategy is associated with a reduction of infarct size in patients with acute STEMI, presenting between 12 and 48 hours after symptom onset, vs a conventional conservative strategy.

Design, Setting, and Patients International, multicenter, open-label, randomized controlled trial conducted from May 23, 2001, to December 15, 2004, of 365 patients aged 18 to 80 years without persistent symptoms admitted with the diagnosis of acute STEMI between 12 and 48 hours after symptom onset.

Interventions Random assignment to either an invasive strategy (n=182) based predominantly on coronary stenting with abciximab or a conventional conservative treatment strategy (n=183).

Main Outcome Measures The primary end point was final left ventricular infarct size according to single-photon emission computed tomography study with technetium Tc 99m sestamibi performed between 5 and 10 days after randomization in 347 patients (95.1%). Secondary end points included composite of death, recurrent MI, or stroke at 30 days.

Results The final left ventricular infarct size was significantly smaller in patients assigned to the invasive group (median, 8.0%; interquartile range [IQR], 2.0%-15.8%) vs those assigned to the conservative group (median, 13.0%; IQR, 3.0%-27.0%; P<.001). The mean difference in final left ventricular infarct size between the invasive and conservative groups was −6.8% (95% confidence interval [CI], −10.2% to −3.5%). The secondary end points of death, recurrent MI, or stroke at 30 days occurred in 8 patients in the invasive group (4.4%) and 12 patients in the conservative group (6.6%) (relative risk, 0.67; 95% CI, 0.27-1.62; P = .37).

Conclusion An invasive strategy based on coronary stenting with adjunctive use of abciximab reduces infarct size in patients with acute STEMI without persistent symptoms presenting 12 to 48 hours after symptom onset.

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

MY Comment by KEN GRAUER, MD (10/20/2019):

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

I find it difficult to believe that the Cardiologist Attending On Call did not allow for the possibility that the OMI in this case was either acute and/or ongoing.

MY Question: Was this the opinion of the Attending Cardiologist — or a Resident, or less experienced Cardiology Fellow? If it was the experience of anyone but the Attending Cardiologist — then my suggestion would be to directly consult with the Attending Cardiologist assigned to this case (and to ensure that he/she has directly viewed this ECG before rendering their decision).

For clarity — I’ve reproduced the ECG in this case in Figure-1. I’ll focus My Comments on addressing the following points.

How should you date the infarction(s) that we see in Figure-1?
Do you agree with the Cardiology team that “steadfastly refused to see any ST elevation” on this tracing? If YOU disagree — in which leads is there ST elevation?
Is QRS morphology in the inferior leads consistent with LAHB? — with inferior infarction? — or, potentially with both?
Is the appearance of the QRS complex in lead V1 normal? If not — is QRS appearance in lead V1 of this tracing potentially relevant to this case?

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

Descriptive Analysis of the ECG in Figure-1: As always, I advocate routine use a Systematic Approach to each and every ECG that you interpret (More on this in My Comment on Dr. Smith’s 6/28/2019 Blog post). Not to routinely use a Systematic Approach invites missing potentially important findings (See below — as no one mentioned QRS appearance in lead V1 of this tracing ... ) — CLICK HERE for more on MySystem.

The Rate and Rhythm for the ECG in Figure-1 is sinus at ~75/minute.
All Intervals (PR, QRS duration, QTc) are normal. NOTE: Measurement of all intervals should be from that lead in which you can clearly see the onset and offset of the interval — and in which the interval is longest! Although the QRS complex looks a bit longer-than-usual in a number of leads (ie, leads V1, V6) — the QRS does not measure more than half a large box in duration in any lead (ie, not more than 0.10 second) — so the QRS complex is therefore not prolonged!
There is marked left Axis duration (Note QS complexes in each of the inferior leads)! That said (as highlighted by Dr. Smith) — QRS morphology in the limb leads is not typical for simple LAHB (Left Anterior HemiBlock) — because instead of a qR complex in lead I with rS complexes in each of the inferior leads — there is no initial q in lead I, and no initial r in the inferior leads.
PEARL: The finding of QS complexes in each of the inferior leads could be due to: i) Inferior MI; ii) LAHB; and/or, iii) Inferior MI + LAHB. There is simply no way to distinguish between these 3 possibilities on the basis of the single ECG shown in Figure-1. My hunch (given the overall appearance of this ECG), is that the QRS complexes we see here in each of the inferior leads reflects both inferior MI + LAHB — but I can’t prove this.
There is no Chamber Enlargement.

Regarding Q-R-S-T Changes:

As noted — there are QS complexes in each of the inferior leads. There are also Q waves in leads V5 and V6. Especially in view of the tiny QRS amplitude in lead V6 — the Q wave in this lead V6 is most definitely abnormal (ie, it is not a “normal” septal q wave)!
Regarding R Wave Progression — the tiny QRS complex in lead V1 is all positive. This is not normal — since the normal QRS complex in lead V1 should be predominantly negative (reflecting the fact that depolarization of the left ventricle should be viewed as moving away from right-sided lead V1). The finding of a Tall (or predominant) R wave in lead V1 should prompt consideration of a short list of diagnostic entities (CLICK HERE— for Review of this LIST). In this particular case — there is a small-but-definitely-present narrow terminal s wave in both leads I and V6. In view of the narrow QRS + rr’ configuration for the QRS complex in lead V1 — ECG criteria are satisfied for IRBBB (Incomplete RBBB). NOTE: This raises a question as to whether a form of bifascicular block that could be new, may be present in ECG #1 (ie, IRBBB/LAHB) — which is relevant, given our consideration of recent/acute/ongoing OMI.

Returning to the ECG in Figure-1 for assessment of the last 2 parameters in my Q-R-S-T assessment = ST-T Wave Abnormalities:

As per Dr. Smith — there are hyperacute ST-T waves in multiple leads — including the 3 inferior leads +leads V2-thru-V6. The peak for the T waves in each of these leads is fatter-than-it-should-be and, the T wave base is broader-than-expected. While one might question the “hyperacute” nature of the T waves in leads V2 and V3 (if these leads were viewed alone) — there can be no question that T wave amplitude (relative to QRS amplitude in the same lead) is disproportionately tall in leads V4, V5 and V6. By the concept of “neighboring leads” — since the T waves in V6, V5 and V4 are obviously hyperacute — the rounder-and-fatter T wave peak appearance in neighboring leads V2 and V3 are almost certainly part of this process!
I still have trouble believing that an experienced Cardiology Attending would “steadfastly refuse to see any ST elevation” in ECG #1. The horizontal RED dotted lines that I have drawn in no less than 7 leads in Figure-1 demonstrate a small-but-definitely-present amount of ST elevation in each of the infero-lateral leads (as well as probably also in lead V2).
As we have emphasized numerous times in this Blog — the presence of the “magic” mirror-image opposite view for the shape of the ST segments in leads III and aVL tells us there has been recent (if not acute) inferior OMI until you prove otherwise!
The ST segment in lead I is also not normal! Note how straight this ST segment is — which makes for abrupt angulation at the point where the ST segment joins the small upright T wave in lead I. A normal ST segment should be gradually upsloping, with imperceptible transition from the ST segment to the upslope of the T wave.
PEARL: The last abnormality that I see on this tracing is the small-but-upright T wave in lead V1. Given the presence of IRBBB — we should normally expect a negative ST-T wave in lead V1. In addition — the RED horizontal line in lead V2 of Figure-1 suggests a small amount of ST elevation in this lead. While I was admittedly not initially certain of the significance of these findings — my hunch was that it was part of the overall acute process (See below).
Bottom Line: No less than 11 of the 12 leads on this ECG (all leads except lead aVR) show abnormal ST-T waves — as well as the above noted possibility of bifascicular block.

Clinical Impression of this ECG: We need to remember the History of this patient = 2 days of “waxing and waning epigastric pain and diaphoresis” in a 60-something year old.

While admittedly, this patient did not specifically have chest pain — the Framingham Studies long ago taught us that at least 1/4 (if not 1/3) of all MIs are “Silent MIs” = not associated with chest pain (ie, instead associated either with some other “chest pain equivalent”, such as shortness of breath, mental status changes, “flu-like” syndrome, GI pain — or without any symptoms at all). Therefore, the history in this case is potentially consistent with a recent or new event over the 2 days prior to presenting to the ED!
As per Dr. Smith — the ECG in Figure-1 is consistent with infero-lateral OMI. In addition — I would add the qualification of OMI of uncertain age, which could possibly be acuteorongoing. Granted, the inferior QS complexes suggest that this may be a completed event — BUT — there is an unmistakable small-but-definite amount of ST elevation in multiple leads + hyperacute ST-T waves in multiple leads + mirror-image reciprocal changes in lead aVL + possible bifascicular block of uncertain age in a 60-something adult with a 2-day history of new symptoms that could be a “chest pain equivalent” — which to me means there is no way to rule out a recent (if not acute or ongoing) event on the basis of this initial ECG.
Retrospectively — we are told that acute cath showed 100% proximal RCA occlusion — and, that Echo showed severe RV dysfunction. Considering the IRBBB, and the fact that there should usually be ST-T depression in anterior leads with this finding + our usual expectation of associated posterior MI (with anterior ST depression) in association with acute inferior MI — I bet the upright T wave in lead V1 and the ST elevation we see in lead V2 are both reflective of acute RV involvement!
BOTTOM LINE: The onus of proof in this case should be to demonstrate that prompt cath is not indicated — rather than the other way around. It is difficult to conceive that the Cardiology team would not at least actively consider this, even prior to learning that serum troponin was elevated ...

Our THANKS to Dr. Smith for presenting this case!

↧

Is this ST depression due to "lateral ischemia"?

October 21, 2019, 6:30 am

≫ Next: A young peripartum woman with Chest Pain

≪ Previous: 60-something with 2 days of intermittent epigastric pain. Why does the cardiologist disagree?

This patient who presented with acute heart failure has a history of heart failure and atrial fibrillation:

This was interpreted as "lateral ischemia".
The patient's previous hospital admission had been predicated on this "ischemia."
What do you think?

There is atrial fibrillation with a controlled ventricular rate. There is scooped ST depression in II, III, aVF and especially in V5, V6.

There are 4 categories of etiologies of ST depression in the context of a normal QRS:
1. Ischemia
2. Hypokalemia
3. Digoxin
4. Baseline/non-pathologic

--When the QT interval is very short, think digoxin.
--When the patient has atrial fibrillation with a controlled ventricular rate, it is not unlikely that the patient is on Digoxin for rate control.
--When the ST depression is what I call "scooped", think Digoxin.

When I suggested this as the likely etiology of the ST depression, and asked if she is on Digoxin, the resident said "That is so old school"!!

Well, it turned out she was on Digoxin, and there was no ischemia.

I showed this with no info to one of our young but very smart toxicology faculty and she instantly said "Dig", proving that this is not "old school."

Finally, it is important to remark that this is Dig effect and NOT Dig toxicity.

"Salvador Dali's mustache"
Some have likened the scooped ST depression of digoxin effect to "Salvador Dali's mustache" (for those of you who are young, Salvador Dali was the archetypal Surrealist painter).

This image comes from Life in the Fast Lane. I'm not sure they created it. https://litfl.com/digoxin-effect-ecg-library/

Steve — I believe Dale Dubin first popularized the image of Salvador Dali's mustache as a representation for the "scooped" shape of Digoxin effect (Ken Grauer, MD).

Some other interesting posts on Digoxin:

Looks like a Posterior STEMI. Is it?

This one is pathognomonic of Dig toxicity.
There is an accelerated junctional rhythm
Note the ST depression has a very short QT; hence cannot be ischemia

Coved ST elevation with reciprocal ST depression: what is the diagnosis?

Here the scooped ST depression is in aVL.
Note the very short QT

ST segment depression: what is the etiology?

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

MY Comment by KEN GRAUER, MD (10/21/2019):

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

Excellent post by Dr. Smith to highlight potential causes of ST depression on ECG. While I immediately had the same initial thought about this case as Dr. Smith (ie, “Is this patient on Digoxin?” ) — I’d like to expand on his comments.

For clarity — I’ve reproduced the 1st ECG shown in this case (Figure-1).

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

Pertinent points regarding the interpretation of ECG #1 include:

Descriptive Analysis of the ECG Findings: The rhythm in ECG #1 is AFib with a fairly slow ventricular response (ie, the rate dips below 60/minute in several places). All intervals are normal (as per Dr. Smith — the QTc looks short). The frontal plane axis is normal at +60 degrees. There is normal standardization — and clearly no sign of ventricular hypertrophy by voltage. Regarding Q-R-S-T Changes — there are small septal q waves (in leads aVL, V6) — transition is slightly delayed (occurs between V4-to-V5) — with the most remarkable finding being appearance of ST-T waves.
NOTE #1: This ECG was apparently “interpreted” as showing “lateral ischemia”. This “interpretation” suggests premature closure regarding the diagnostic possibilities — so there is little wonder that the correct diagnosis was initially overlooked. We are still in the Descriptive Analysis phase, rather than “interpretation”. The way in which I would describe ST-T wave appearance in this ECG is that there are, “diffuse, nonspecific ST-T wave abnormalities” with (as per Dr. Smith) — ST segment “scooping” with a short QTc, that is most prominent in the lateral chest leads.
NOTE #2: More than just the infero-lateral leads — virtually all leads on this tracing (except perhaps aVR and V1) show ST-T wave abnormalities (if not ST “scooping” — then nonspecific ST-T wave flattening).
Clinical Impression: Optimal interpretation of ECG #1 should indicate that there is AFib with a fairly slow ventricular response + nonspecific ST-T wave flattening that includes ST segment “scooping” with a short QTc in several leads. Clinical Correlation is then needed to assess which one (or more) entities is (are) most likely to be responsible for this ST-T wave appearance (Figure-2).

Figure-2: Common causes of ST-T wave depression (See text). This Figure was taken from my ECG Blog #166.

Causes of ST-T Wave Depression: There are actually over 50 causes of ST-T wave changes on ECG. Although many of these causes are cardiac-related — there are also many that are not cardiac-related. Among the many non-cardiac causes of ST-T wave changes are hyperventilation; temperature extremes (excessive heat or cold exposure); anxiety or emotional stress; anemia; tachycardia; sleep deprivation; pulmonary disease; electrolyte abnormalities; central nervous system disorders; certain medications; and severe medical illness (among others). KEY Point — Many of the 50+ potential causes of ST-T wave abnormalities on ECG are non-cardiac!

BOTTOM Line: Rather than attempting to commit to memory an exhaustive list of conditions that may predispose to ST-T wave changes — it suffices to appreciate the variety of entities that may produce changes on ECG.
NOTE #3: In general — causes of T wave abnormalities (including T wave flattening or frank T wave inversion) are similar to potential causes of ST segment depression.

We favor remembering the short LIST of entities that we show in Figure-2. Our purpose in making this List, is to simplify your task as the interpreter. As soon as you recognize generalized ST-T wave changes on an ECG — Consider the short LIST of Potential Causes in Figure-2:

NOTE #4: Often — more than a single cause may be operative. For example — the patient in this case had a history of heart failure and AFib — so we can presume this patient was probably taking at least a few medications. As a result — the patient might be taking Digoxin and/or a Diuretic (which might contribute to electrolyte disturbance). The patient has heart failure — so the abnormal ST-T wave changes may reflect LV “strain” (or a strain equivalent). And despite a history of recent chest pain — the ST-T wave changes we see in ECG #1 could reflect chronic ischemia. BOTTOM Line — Except for tachycardia, each of the other potential causes of ST-T wave depression in Figure-2 might be contributing in varying degree to the ECG picture we see in Figure-1.

PEARL: The Shape of the ST-T wave may suggest which one (or more) of the 6 entities in our LIST is (are) most likely to be operative in a given patient (See bottom half of Figure-2):

Ischemia — is suggested by symmetric T inversion (RED arrow in Panel B) — especially when seen in two or more leads of a given lead group (ie, in leads II, III and aVF — or in both leads I and aVL).
Strain — from LVH, is suggested by asymmetric ST depression occurring in one (or more) of the lateral leads (less often in the inferior leads). Note the initial slow sagging of the ST segment with LV “strain” (BLACK arrow in Panel A) — with more rapid return to the baseline. “Strain” is more likely to be the cause of ST depression when ECG voltage for LVH is present. NOTE #5: On occasion, there may be Echo-verified LV enlargement with ST-T wave changes suggestive of “strain” on ECG — but without accompanying voltage. This point may be relevant to the patient in this case — as asymmetric ST-T wave depression is most marked in lateral leads in this patient with chronic heart failure (that predisposes to LV enlargement) — but who does not satisfy any ECG voltage criteria for LVH in ECG #1.
"RV strain"— is suggested IF the picture in Panel A of Figure-2 is seen in right-sided leads (leads II,III,aVF; or V1,V2,V3) in a patient with RVH.

Use of Digoxin may affect ST-T waves in any one of 3 ways: i) There may be “scooped” ST depression in multiple leads (that simulates an inverted ice cream cone, as in Panel D of Figure-2). This is often associated with a relatively short QTc; or, ii) Digoxin “effect” may produce a "strain"-like pattern (identical to Panel A); or, iii) Despite use of an appropriate amount of Digoxin — there may be little-to-no effect on the ST-T wave.

NOTE #6: In my experience (from correlating ECG ST-T wave appearance to serum Digoxin levels over the 3 decades that I worked closely with PharmDs at our institution) — the serum Digoxin level correlates poorly with the amount of ST-T wave scooping or depression. Thus, despite even high serum Digoxin levels — some patients fail to manifest ST-T wave abnormalities — whereas other patients show marked ST-T wave changes despite surprisingly low serum Digoxin levels.

Finally — Panel C in Figure-2 shows a non-specific ST-T wave pattern, in which the T wave and ST segment are flattened (if not slightly depressed). This pattern is called “nonspecific” — because any of the many potential causes of ST-T wave abnormalities may be operative.

BOTTOM Line (regarding ST-T wave changes in ECG #1 for this case) = Clinicalcorrelation is needed:

As per Dr. Smith — the “scooped” ST segment appearance in several leads (most remarkable in leads III, V5, V6) with noticeably shortened QTc make inquiring about whether the patient is on Digoxin the 1st priority.
That said — the other entities on the LIST in Figure-2 should also be considered — as they may be contributing to the ST-T wave changes we see. Reviewing the patient’s medication list — serum electrolyte values (especially serum K+ and Mg++) — and, obtaining a prior ECG for comparison purposes would all be helpful.
The “good news” in this case — is that the ST-T wave changes we see in Figure-1 do not look acute. In the absence of a history of worrisome, new-onset chest pain — it is highly unlikely that the ST depression in ECG #1 reflects acute ischemia.

↧

A young peripartum woman with Chest Pain

October 24, 2019, 11:11 am

≫ Next: 40-something male in a head-on Motor Vehicle Collision and Splenic Injury

≪ Previous: Is this ST depression due to "lateral ischemia"?

This is written by Brooks Walsh.
https://twitter.com/BrooksWalsh

A 30 year-old woman was brought to the ED with chest pain.

It had started just after nursing her newborn, about an hour prior, and she described it as a severe non-pleuritic “pressure” radiating to the back.

She had given birth a week ago, and she had similar chest pain during her labor. She attributed the chest pain to anxiety and stress, saying "I'm just an anxious person."

A CXR and a CTA for PE were normal.

The ECGs

An initial ECG was obtained as the pain was rapidly resolving:

Minimal upsloping ST Elevation in III, with a steeply biphasic T wave, and with reciprocal ST depression in leads I and aVL.
There is also a Q-wave in III.
This strongly suggests reperfusing RCA ischemia.

There is also subtle STD in V3-V5.
(Inverted T in V2 is likely due to lead misplacement -- this is evidence by the inverted P-wave)

A second ECG was obtained 6 hours later (pain-free):

Aside from a slightly biphasic T wave in lead III, the findings from the first ECG are now resolved.

This dynamic findings, especially when correlated with the patient’s resolving symptoms, are not“non-specific.” The biphasic T wave is consistent with recent reperfusion of an occluded coronary artery supplying the inferior region. The initial STD depression in aVL and V3-V5 (later resolved) further supports a very recent occlusion affecting this area.

Troponins, echocardiogram

An echocardiogram showed inferobasilar hypokinesis, further supporting a diagnosis of regional ischemia, likely of the area supplied by the RCA.

The initial troponin I was elevated at 0.75 ng/ml (99th %-ile URL = 0.04 ng/ml), and rose to 12 ng/ml six hours later. This rate and height of troponin rise strongly suggested a type 1 MI.

Angiography

Angiography was performed after aspirin and heparin were started.

Here’s the angiogram of the RCA:

No thrombus or plaque rupture in the RCA (or any coronary artery) was found.
However, a smooth tapering of the mid-RCA was seen, highlighted in red below:

How do we explain the MI if no sign of CAD was found? This MI wasn’t caused by a ruptured plaque of CAD - it was a coronary artery dissection of the RCA.

Spontaneous coronary artery dissection

Dissection of a coronary artery may occur in the context of atherosclerosis, or be iatrogennic during angiography or angioplasty. In the absence of these factors it is termed spontaneous coronary artery dissection (SCAD).

This case occurred 10+ years ago. At that time the literature suggested:

SCAD was rare,
Mostly related to pregnancy,
Seen on angiography as a dissection flap, and
Managed similarly to MI caused by CAD (ASA, BB, lytics/PCI).

However, in the intervening years there have been marked changes in the understanding of SCAD. Many of these issues were described in a prior post by Dr. Angie Lobo (@aloboMD)

(Foropen-access reviews of this literature, see Saw 2016, Saw 2017, or Hayes 2018.)

See also this fascinating case:

An athletic 30-something woman with acute substernal chest pressure

Five takeaways about SCAD:

1. SCAD isn’t rare, especially in women

Historically SCAD had been identified in < 1% of angiograms performed for ACS. However, contemporary studies find it in up to 4% of ACS, and in > 22% of ACS cases in women. A recent study found that SCAD causes almost 20% of STEMI in young women.

2. Pregnancy is not a common cause of SCAD

When ACS occurs in the peripartum period, SCAD is responsible in 43% of cases. However, pregnancy-associated spontaneous coronary dissection (PA-SCAD) is still pretty uncommon, and accounts for less than 5% of SCAD cases overall. Fibromuscular dysplasia is a much more common trigger for SCAD.

3. SCAD can have subtle angiographic features, and coronary CTA is unhelpful.

SCAD was originally thought to show a characteristic dissection flap and and false lumen(s) ion angiography. However, this “classic” pattern ( “Type 1”) only occurrs in about 25% of cases. Most SACD does not create a flap, and shows instead a long smooth narrowing of the true lumen. Type 2 is seen in almost 70% of cases. Our patient had a type 2 lesion.

Type 2 is more difficult to appreciate on angiography than type 1. The relatively poorer resolution of cardiac CTA makes it especially inappropriate to rule out SCAD. Often, intravascular ultrasound or intravascular optical coherence tomography is requeried to make the diagnosis.

4. You don’t just treat it like ACS caused by CAD

Aggressive intervention may cause more problems than the original SCAD lesion. Guidewires for PCI may be difficult to thread through the weak, twisty arteries, and may rupture the false lumen. Heparin hasn’t been shown to help or hurt, but could theoretically promote expansion of an intramural hematoma. Fibrinolytics have been associated with devastating complications. While there isn’t good evidence that aspirin and beta-blockers help, there are few concerns about their safety, and they are generally recommended.

5. Coronary lesions often resolve without intervention, but PCI has role

Treatment of SCAD requires a different risk-benefit calculation than ACS caused by typical atherosclerotic disease, as shown by two studies form this year.

On the one hand, most SCAD lesions resolve with only conservative treatment, and PCI is not required. A study byHassan et al. provided evidence that PCI/CABG was unnecessary for most SCAD, and should be considered for only high-risk presentations.

On the other hand , high-risk lesions appear to do well with aggressive treatment.Lobo et al.examined SCAD presenting as STEMI (unlike Hassan et al. where more than 3/4 of cases were NSTEMI). The SCAD cases in Lobo et al. were pretty sick, with mostly LM/pLAD lesions and high rates of cardiogenic shock. Despite this, there was a high rate of PCI success.

Outcome of our case

Once the type 2 SCAD was identified, the heparin drip was stopped. No PCI was performed, and only conservative medical therapy was pursued. No evidence of a connective-tissue disease such as FMD was found. She did well, and was ultimately discharged from her cardiologist’s care years later!

References

Lobo AS et al. Revascularization in Patients With Spontaneous Coronary Artery Dissection and ST-Segment Elevation Myocardial Infarction. JACC 2019 Sep 10;74(10):1290-1300.

Hassan S. et al. Natural History of Spontaneous Coronary Artery Dissection with Spontaneous Angiographic Healing. JACC Cardiovascular Interventions 2019 Mar 25;12(6):518-527.

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40-something male in a head-on Motor Vehicle Collision and Splenic Injury

October 27, 2019, 3:39 pm

≫ Next: How do you interpret this ECG?

≪ Previous: A young peripartum woman with Chest Pain

A 40-something male presents to the stabilization room for evaluation following head on motor vehicle collision (MVC). Pt was reported restrained driver, hit at city speeds, with + airbag deployment.

The MVC was unquestionably caused by the other car, not by this driver.

The patient complained to EMS of chest pain and a prehospital EKG en route was concerning for STEMI.

The patient was at all times hemodynamically stable, without evidence of any profuse bleeding.

He had an ECG recorded on arrival to the ED:

Anterior and Inferior STEMI with diffuse hyperacute T-waves.

This ECG really can't be anything else.
Takotsubo is on the differential of anterior and inferior STE, but takotsubo just looks different (see some cases below).

This must be an occluded "wraparound"LAD (wraps around the apex to the inferior wall) and one would expect an apical wall motion abnormality, as well as probable septal, anterior, and inferior wall motion abnormalities.

But acute STEMI in this situation is not necessarily due to plaque rupture and/or thrombus. It could be due to the trauma, and contusion of the LAD with thrombus or dissection.

Further patient history revealed that the chest pain started following the crash, and that he had no chest pain previously. Brief review of chart showed no h/o known CAD. DDx was possible aortic dissection or injury, cardiac contusion, LAD dissection, or type I MI w/ plaque rupture.

They performed a bedside ED cardiac ultrasound:

With this ECG, there must be a wall motion abnormality if the ECG and echo are done at the same time.

If you do not see a wall motion abnormality, it is because:
1. ultrasound, or your technique or expertise, is not good enough.
2. The artery reperfused quickly enough, such that all wall motion recovered.

It is possible to have a normal echo if, immediately after the ECG:
1. The artery reperfuses and
2. The duration of ischemia was short.

This shows an apical wall motion abnormality
This is consistent with anterior/inferior MI due to wraparound LAD, and also with takotsubo.

However, this was the provider's interpretation:

"Further bedside ultrasound of cardiac function w/o demonstration of significant WMA or impaired function."

The patient went to pan scan, with CT of chest/abd/pelvis. It showed a splenic laceration and pelvic fracture, and also this:

Just the heart is shown from the CT of chest/abdomen/pelvis, with contrast

Shows a clear apical area without any perfusion (dark, no contrast gets to this myocardium)

Slightly different CT technique:

Again, apical area without contrast

These images further confirm the diagnosis of acute STEMI.

When the patient returned to the ED, he had another ED cardiac ultrasound:

Now there is no clear wall motion abnormality, but these can be very difficult to appreciate.

This echo was done with Speckle Tracking, Strain Echocardiography. This was done by one of the most expert ED echocardiographers in the world:

Good contraction is measured by a large negative value. The light green is the most negative, and this would represent the most wall contraction, and represents the lateral wall. Red, which is the apex, has moderate contraction, so there may be a subtle apical wall motion abnormality still.

But it is very hard to appreciate with the naked eye, without speckle tracking.

At this point, another ECG should have been recorded, but was not. It would almost certainly have shown resolution of the STEMI findings (due to spontaneous reperfusion).

Should the cath lab have been activated?

This is a tough question. PCI usually requires antiplatelet and antithrombotic therapy, but a persistently occluded LAD must be opened, even if such medications cannot be given. Plain old balloon angioplasty without these meds can temporarily open the artery.

I asked our chief of cardiology, Gautam Shroff:"Plain old balloon angioplasty (POBA) requires at least one antiplatelet agent indefinitely and 2 of them for 30 days, or else it clots off. Heparin is also needed during the cath. For a head bleed I would sacrifice the anterior wall. Perhaps the best approach for this case would be splenectomy (or Interventional radiology to stop the bleed?), then POBA or bare metal stent?? No good options and risk benefit has to be weighed."

So Cardiology consultation is essential, and coordination with trauma surgery and interventional radiology.

Fortunately for this patient, as you'll see below, and unbeknownst to the providers, the artery quickly spontaneously reperfused.

FINAL ED DIAGNOSES:
1.MVC
2.Splenic laceration
3. Pelvic fracture
4.ST elevation w/ chest pain

The patient was admitted to the hospital. He did have serial troponins:

First 3 troponins

Notice the last one shoots up, which is typical with reperfusion (artery opening, resulting in sudden troponin release).

At this point (8 hours later), the 2nd ECG was recorded:

ST Elevation is gone. There are Q-waves in V2-V4. The LAD has reperfused.

Formal echo was done:

Normal left ventricular cavity size.
Normal estimated left ventricular ejection fraction - 70%.
Regional wall motion abnormality- apex, distal septum and inferior segments.

This demonstrates that a bubble contrast echo, read by an expert, is superior at identifying subtle wall motion abnormalities than an ED echo.

Another 24 hours of troponins were recorded, starting at time 1504:

This was recorded another 24 hours later:

Terminal and symmetric deep T-wave inversion (reperfusion T-waves), with Q-waves (not exactly Wellens' waves, which should have R-wave preservation)

All troponins

It is really not necessary to get all these troponins, but they are interesting.

Angiogram, 5 days later:

--Culprit for the patient's "NSTEMI" (!) [comment: It is really a transient STEMI) is plaque rupture or traumatic coronary dissection in the distal LAD. It is a wraparound LAD to the inferior wall.
--While there is residual 80-90% stenosis, there is TIMI III flow beyond
--Will initiate treatment with clopidogrel (300 mg give post-procedure), without PCI at this time, given potential inability to tolerate DAPT in the setting of splenic laceration/rupture.
--Can proceed to PCI if patient tolerates anticoagulation and develops angina prior to discharge or would plan for staged re-look angiography and PCI in 4-6 weeks.

Summary:
So this was a brief LAD occlusion, with transient STEMI. It may have been a dissection related to the trauma, or coincidental plaque rupture, which could be triggered by the stress of the trauma.

Here are several cases of Takotsubo with ST Elevation that could mimic STEMI.

Many takotsubo have on T-wave inversion, in which case emergent cath lab activation is not critical (though it could mimic Wellens')

Diffuse ST Elevation with Apical Ballooning: is it Takotsubo Stress Cardiomyopathy?

COPD exacerbation, what do the ECG and bedside echo show?

Takotsubo Stress Cardiomyopathy, with Echocardiogram

Two more Cases of Takotsubo Stress Cardiomyopathy

Here are some cases of myocardial contusion

Blunt Trauma in a Child

Gunshot wound to the chest with ST Elevation

A Child with Blunt Trauma -- this one has to be seen

↧

How do you interpret this ECG?

November 1, 2019, 8:27 am

≫ Next: A man in his 50s with witnessed arrest and ST elevation in aVR

≪ Previous: 40-something male in a head-on Motor Vehicle Collision and Splenic Injury

Late in an evening shift, during a lull in care, I was reading a list of ECGs, one after another, on the computer queue and saw this one, which had been recorded 12 hours earlier in the day:

What do you think?

I thought to myself:

"Hmmm, there is terminal T-wave inversion in V2, and the suggestion of it in V3. But the QTc interval is too short for Wellens (377 ms)," so I confirmed the computer interpretation of "non-specific ST-T abnormalities," and moved on. I still think that, by itself, this ECG is not diagnostic.

There had been an ECG recorded 110 minutes earlier, but I did not notice that and did not look at it. Here it is:

What do you think?

Interpretation: some minimal ST Elevation in V2. The ST segment is straight, which is might be very suspicious for MI, but here it does not strike me as significant. aVL and III are also suspicous, but not diagnositic.

The computerized QTc was 394 ms. If we do the 4-variable formula, it comes to 15.11 which is extremely low. At a cutoff of 17, the formula is > 95% sensitive.

So each ECG, on its own, is negative.

But if you see them side-by-side, and in the right clinical context, one would now highly suspect that the first ECG presented (the 2nd recorded) is Wellens', and the 2nd presented (the 1st one recorded) was an LAD occlusion.

The patient indeed presented with chest pain:

"A 30-something male with 2 days of worsening chest pain that he describes as pressure. He endorses associated SOB and pain radiating down his left arm as well. He has some increased pain with deep inspiration it denies pain with movement or palpation. He denies history of cardiac disease."

The patient's pain on the 2nd ECG had been resolved (this is consistent with Wellens' syndrome). It appears that the triage MD saw the first ECG (which is non-diagnostic), and the 2nd providers saw only the 2nd ECG, which is also non-diagnostic.

In this case, 2 non-diagnostic ECGs make for a diagnostic pair of ECGs. But no one saw them both at once!

The first troponin I returned elevated at 0.101 ng/mL. The patient's pain returned and so a NTG drip was started. The bed became available before anyone knew if the patient's pain was resolved. And he left for his inpatient bed.

Fortunately, when he arrived, the MDs upstairs saw him immediately and realized he had uncontrolled pain on the NTG drip, so they activated the cath lab immediately.

Here is the angiogram result:

90% hazy stenosis of the proximal LAD, no improvement

with Intracoronary NTG x 100 mcg, 200 mcg, 300 mcg - suggestive of plaque

rupture/culprit

Impression and Recommendations:

Culprit for NSTEMI is a 90% thrombotic stenosis of the proximal LAD.

Stented.

Here is the post cath ECG:

There appears to be pseudonormalization of the T-waves!
I suspect they were pseudonormalized BEFORE the angiogram, when the pain had recurred, and that this is residual after opening the artery.
It often takes hours for the reperfusion T-waves to evolve after reperfusion, or (as in this case) to be re-established after re-reperfusion(see below).

And the next AM:

Typical reperfusion T-waves

Learning Points:

1. Always look at all the EKGs. By themselves, they may appear nearly normal. But seen in evolution, they may be diagnostic

2. Always assess the response to therapy before deciding the patient does not need the cath lab now.

↧

A man in his 50s with witnessed arrest and ST elevation in aVR

November 3, 2019, 9:06 am

≫ Next: A healthy 30-something presented with nausea, vomiting, benign positional vertigo and atrial fibrillation

≪ Previous: How do you interpret this ECG?

Written by Meyers, edits by Smith

A 50-ish year old man was working construction when he suddenly collapsed. Coworkers started CPR within 1 minute of collapse. EMS arrived within 10 minutes and continued CPR and ACLS, noting alternating asystole and sinus bradycardia during rhythm checks. He received various ACLS medications and arrived at the ED with a perfusing rhythm.

Initial vitals included heart rate around 100 bpm and BP 174/96. Here is his initial ECG, very soon after ROSC:

What do you think?

Sinus tachycardia. There is incomplete RBBB (QRS duration less than 120 ms). There is diffuse STD, maximal in V4-V5 and lead II. There is a tiny bit of STE in aVL, and there is a significant amount of reciprocal STE in lead aVR, and less so in V1.

Comment/Refresher on Lead aVR:

Remember: think of lead aVR this way: "aVR = the aVerage Reciprocal lead to the rest of the ECG". There is no wall of the heart that corresponds to the direction of lead aVR, but rather it is the opposite direction of the main average vector of depolarization and repolarization of the heart, opposite leads V4-V6 and lead II. It is not really possible to have Occlusion MI that affects a myocardial wall and causes primary STE in lead aVR. Instead, lead aVR simply reflects any ECG finding which is found diffusely throughout the ECG, especially those findings which are directed opposite of it (V4-V6 and lead II).

Thus, anything that causes widespread STD will always come with STE in aVR, and the differential of widespread STD is enormous, including any process that causes diffuse supply/demand mismatch but NOT complete lack of blood flow (as seen in Occlusion MI with no collateral circulation). One of the rarest causes of this pattern would be acute but non-occlusive left main ACS (or any single vessel ACS in the setting of preexisting triple vessel disease), which of course would benefit from emergent angiography and intervention. However, non-ACS causes are by far more common overall.

See our many other posts on aVR for more details.

Among other considerations in this case is whether this arrest was caused by ACS. As above, widespread STD with STE in aVR has many etiologies, not just ACS. If the arrest itself caused ischemia, then stabilization and supportive care may lead to resolution, so serial ECGs remaining ischemic support ACS, while those which resolve generally support another etiology (however, of couse, even ACS is dynamic, with thrombus propagating and lysing, so an improving ECG may just be lysis of a thrombus that could later re-propogate from that ruptured, exposed plaque.)

Also, the circumstances of the arrest are a strong clue to etiology. A shockable rhythm is far more likely to be due to ACS than a non-shockable rhythm, which is what we appear to have here.

Case continued:

The team recognized the diffuse STD and decided to repeat it every 5-10 minutes while stabilizing the patient and assessing for any other modifiable factors to explain diffuse supply/demand mismatch.

Here is the ECG 10 minutes after sustained ROSC and normal-to-high blood pressure (without any continued vasopressors needed).

Similar findings, but slightly less pronounced.

They got another repeat ECG 15 minutes later:

Continued diffuse STD with obligatory STE in aVR.

It has now been at least 25 minutes with continued ROSC and reasonable vital signs, and the diffuse STD with reciprocal STE in aVR have persisted despite no clear reversible reason for increased demand or indequate coronary perfusion. Thus, the wide differential has narrowed significantly, and ACS is still on the differential since we have not found any other reversible reason for supply demand mismatch.

The team considered activating the cath lab for these ongoing ECG findings despite resuscitation.

However, they also noticed minimal signs of neurologic activity despite short low-flow time, and began to suspect a possible intracranial source.

So before activating the cath lab they took the patient for a head CT, which showed:

Massive subarachnoid hemorrhage.

The patient did not undergo cath, and ultimately expired.

Here is another case written by Smith:

I saw this patient many years ago: She was a 40-something year-old woman who suddenly collapsed at a bus stop. Medics found her comatose and in VT. She was cardioverted and brought to the ED with a GCS of 3.

Looks like a high lateral STEMI with STE in V2-V6, I, and aVL. Because there is widespread STE, aVR must show some reciprocal STD (because aVR = aVerage Reciprocal).
Is this a STEMI?

What bothered me was that she had become instantaneously comatose from VT. Such immediate coma is of course common with VF, but not VT. Furthermore, she was quickly resuscitated and remained a GCS of 3.

Therefore we scanned her head and she had a lethal intracranial hemorrhage.

It was NOT a STEMI. It was stress cardiomyopathy from intracranial hemorrhage.

Learning Points:

Lead aVR = the aVerage Reciprocal lead to the rest of the ECG

Diffuse STD which is maximal in V4-V6 and lead II, MUST come with reciprocal STE in aVR, and this represents diffuse supply/demand mismatch, for which the differential is enormous but does rarely include ACS which may benefit from emergent reperfusion. The key to distinguishing these rare patients with STE in aVR who need emergent cath lab activation is:

1) First make sure that the patients symptoms and presentation are consistent with ACS.

2) Make sure that you identify and correct all reversible non-ACS causes of increased demand (atrial fibrillation with rapid ventricular rate, increased afterload from extreme hypertension, aortic stenosis, ICH, etc) or decreased myocardial oxygen supply (hypotension, hypoxemia, anemia, etc.)

3) If no other clear source of supply/demand mismatch can be found or corrected, then ACS is a likely cause of decreased supply and the patient may benefit from emergent cath.

4) Non-shockable initial rhythm makes it unlikely that ACS was the cause of cardiac arrest.

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

MY Comment, by KEN GRAUER, MD (11/3/2019):

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

Informative post by Drs. Meyers and Smith — regarding the entity of diffuse ST segment depression that occurs in association with ST elevation in lead aVR.

As per Dr. Meyers — the presence of these ECG findings represents diffuse supply/demand mismatch.

I limit my comments to a number of points regarding ECG findings in the initial 12-lead tracing.

I have labeled this initial ECG as ECG #1. For clarity — I have lightened this tracing and optimized resolution in Figure-1.

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

The important ECG findings in ECG #1 are the following:

There is sinus tachycardia at ~110/minute. Regarding intervals — the PR interval looks to be normal. Although the QRS looks a little wide, I measure it no more than half a large box in duration (ie, ~0.10 second). The QTc appears prolonged, though it is difficult to precisely measure, and to assess the clinical significance of the QTc here, given the increased rate and marked ST-T wave changes.
As per Dr. Meyers — there is incomplete RBBB because: i) there is a QR’ pattern in lead V1 (with an rSr’ in lead V2); ii) there are terminal s waves in left-sided leads I and V6; and, iii) the QRS complex is not wide enough to qualify as “complete” RBBB.

Regarding ST-T Wave Changes — the alteration in QRS morphology from the incomplete RBBB makes assessment of the amount of ST elevation and depression challenging. To facilitate this — I’ve added short colored horizontal lines in Figure-1 to illustrate what I chose as my “baseline” for assessing ST segment deviation.

Diffuse ST segment depression is seen here in no less than 8 leads (RED horizontal lines serving as the baseline I used to assess ST depression). As per Dr. Meyers — ST depression is most marked in leads II, V4 and V5.
ST elevation is most marked in lead aVR — but it is also seen in leads aVL and V1 (BLUE horizontal lines serving as the baseline I used to assess ST elevation).
There is minimal ST segment deviation in lead V2 — with this being the only lead without clear ST elevation or depression.

NOTE — Opinion is divided as to whether the optimal “baseline” for assessing the amount of ST segment elevation or depression should be the PR or TP segment.

In practice, this gets complicated — since the PR segment tends to shorten with tachycardia — PR segment depression and/or elevation may sometimes be present (this occurs not only with pericarditis! — but also with other entities, as is seen here) — there may be baseline wander (due to patient movement, tremor, pain, shortness of breath, etc.) — and, in cases like the ECG shown in Figure-1 — the limits of the TP segment are not always clear.
While I generally favor use of the PR segment as my baseline — I always survey the entire tracing, and often end up using a combination of PR and TP segments in various leads. (CLICK HERE and watch the next 3 minutes of this ECG video — if interested in “My Take” on how I decide on the ST-T wave baseline). I acknowledge that others may differ with the baselines I chose in Figure-1 to assess ST segment deviation.

MY Preference in Terminology: Realizing that supply/demand mismatch represents the underlying pathophysiologic process responsible for the findings we see in ECG #1 — I favor use of the term diffuse Subendocardial Ischemia for the words I use to describe these ECG findings in my interpretation:

As per Dr. Meyers — the differential diagnosis of entities that may produce diffuse subendocardial ischemia is large. It includes tachycardia, severe anemia, septicemia, hypoxemia, shock, serious arrhythmias, cardiac arrest, “sick patient”, and significant underlying coronary disease, to name a few.
The History is KEY for suggesting the most likely cause(s) for the case at hand. Significant coronary disease (ie, multivessel, proximal LAD or LMain disease) — is not rare under the right clinical circumstances.
The case presented here is different — as this 50-ish year old man had sudden collapse (without preceding chest pain) — the initial rhythm was non-shockable (alternating between bradycardia and asystole) — and, despite return of reasonable vital signs, neurologic activity remained severely depressed.
The astute clinicians in this case ordered a head CT prior to activation of the cath lab — and this revealed massive subarachnoid hemorrhage. PEARL — CNS catastrophes (stroke, bleed, trauma, tumor, sudden coma, etc.) are notorious for causing among the most abnormal (and sometimes bizarre) ECG findings. Pseudo-infarct patterns are common with CNS catastrophes — and may manifest Q waves, diffuse ST segment elevation and/or depression — often with a markedly prolonged QTc. This patient’s massive subarachnoid hemorrhage with associated tachycardia, could certainly have caused the ECG picture seen in Figure-1.
NOTE: The entity of diffuse subendocardial ischemia has been discussed on multiple occasions in Dr. Smith’s ECG Blog. I’ll simply reference the February 28, 2018 post as a nice review of this entity.

Our THANKS to Drs. Meyers and Smith for presenting this case!

↧

A healthy 30-something presented with nausea, vomiting, benign positional vertigo and atrial fibrillation

November 5, 2019, 9:35 am

≫ Next: A 41 year old with chest pain and a Nondiagnostic Triage ECG. Thrombolytics prior to transfer for PCI.

≪ Previous: A man in his 50s with witnessed arrest and ST elevation in aVR

A healthy 30-something presented with nausea, vomiting, vertigo and atrial fibrillation. The vertigo is triggered by head movement and relieved by holding still. He has severe nausea with it, and epigastric discomfort.

He had an ECG recorded because epigastric discomfort can be due to inferior MI:

This patient is healthy and on no medications.
His electrolytes are normal.
He does not drink alcohol or use drugs.
Thyroid was not checked, as A Fib from thyroid would be very rapid.

What is unusual here, and why?
What is the likely cause of the atrial fibrillation?

There is no real evidence of ischemia.
There is atrial fibrillation.

--First, it is unusual that a young healthy person develops atrial fibrillation.
--Second, a young person should have a rapid ventricular response if there is a healthy AV node and no AV nodal blockers.

Why is the ventricular response below 100 beats per minute?

This patient had no idea that he was in an abnormal rhythm, so it was impossible to say for certain how long he had been in it.

I learned from this case, from our electrophysiologist (Rehan Karim) and from one of our very smart hospitalists, who is particularly smart at cardiology (Meghan Walsh), that extreme vagal tone can BOTH cause atrial fibrillation and then, correspondingly, be associated with a relatively slow ventricular response because of that high vagal tone.

This happens particularly in young healthy athletic men.

So this young man got benign positional vertigo, then severe nausea, which made for high vagal tone, which converted him to atrial fibrillation with a relatively slow response.

His Benign Positional Vertigo was managed successfully with an Epley maneuver.

He ultimately converted back to sinus rhythm spontaneously.

For more, see this article:

Paroxysmal Atrial Fibrillation: A Disorder of Autonomic Tone?

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

MY Comment, by KEN GRAUER, MD (11/5/2019):

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

This is an important case, in that it brings up a number of underappreciated concepts regarding Atrial Fibrillation (AFib).

The most common sustained cardiac arrhythmia by far is atrial fibrillation. When assessing the patient with new-onset AFib — once you have ensured hemodynamic stability, sequential priorities optimally include: i) Finding the cause; ii) “Fixing” the cause (if at all possible); iii) Slowing the rate; iv) Converting the rhythm; and, v) Preventing thromboembolism.

Most patients with new AFib will not be hemodynamically unstable as a result of the AFib. If they are — then immediate synchronized cardioversion is in order!
Once you’ve ensured that the patient is stable — the reason I suggest considering the above 5 clinical priorities in the sequence that I list them — is that IF you can “find and fix” the cause of new-onset AFib — then you may at the same time slow the rate, convert the rhythm and reduce the chance of stroke (ie, if the cause of new AFib is heart failure — then diuresis may facilitate conversion).

It’s helpful to keep in mind the Common Causes of AFib. There are many ... The 3 most common causes of AFib are:

Heart failure/cardiomyopathy.
Acute ischemic heart disease (acute MI/acute coronary syndrome).
Hypertension (especially when longstanding, because of structural alteration of the heart that longterm hypertension produces).

Among the many other potential causes of AFib are the following:

Valvular heart disease
Hyperthyroidism (which overall is not a common cause of AFib — but which is still very important, because there is a specific treatment).
Drugs (ie, cocaine, sympathomimetics, alcohol use)
Pulmonary embolus/hypoxemia
Other significant medical illness
Sleep apnea
Sick sinus syndrome
“Lone” AFib (ie, when AFib occurs in a patient under 50-60 years old in the complete absence of underlying heart disease [ie, not even hypertension]).

PEARL #1: Today’s case emphasizes the need to actively consider an additional entity:

Vagotonic AFib (discussed more below).

PEARL #2: Description of the rhythm that the patient in this case had as “atrial fibrillation” would be an incomplete description of his cardiac rhythm. WHY ???

ANSWER: The reason that simply saying this 30-year old man presented with “atrial fibrillation” is an incomplete description of the rhythm — is that this description provides NO indication of the average rate of the ventricular response. Knowing the ventricular response of AFib instantly tells you so much about how to proceed with diagnosis and treatment!

Figure-1 shows 4 examples AFib. For each of the rhythms shown — there is an irregular irregularity without indication of sinus P waves. The QRS complex is wide in the last example.

QUESTIONS:

How would you describe each rhythm in Figure-1?
What diagnostic and treatment considerations should be immediately suggested for the examples of AFib that you see in Rhythms A, B, C and D?

Figure-1: Four examples of AFib. How would you describe each of these? (See text).

ANSWERS:

Rhythm A in Figure-1:

This is AFib with a rapid ventricular response — which I define as AFib with a rate averaging over ~120/minute (Note that the R-R interval varies between 2-to-3 large boxes in duration — which is consistent with an average rate of ~120-130/minute). Rapid AFib is by far the most common ventricular response for new-onset AFib.
The reason new-onset rapid AFib in an older population is so commonly associated with heart failure is due to: i) loss of the “atrial kick” (which provides between 5-40% of cardiac output — but typically closer to the higher range in patients with longstanding hypertension who have resultant diastolic dysfunction); and, ii) the rapid rate disproportionately shortens the period of diastolic filling, which greatly reduces cardiac filling, and resultant cardiac output.

Rhythm B in Figure-1:

This is AFib with a controlled ventricular response — which I define as AFib with a rate averaging between ~70-110/minute. Attaining rate control is one of the principal goals of treating new-onset rapid AFib with antiarrhythmic medication.
Occasionally, an otherwise healthy older adult will present in new AFib with a controlled ventricular response that falls within this rate range. But, as emphasized by Dr. Smith — We should not expect an otherwise healthy young adult (as in this case) to present in AFib with an average heart rate under 100/minute — unless something else (in this case, vagotonic AFib) was going on.

Rhythm C in Figure-1:

This is AFib with a slow ventricular response — which I define as AFib with a rate averaging less than ~50-60/minute.

PEARL #3: It is unusual for new-onset AFib to present with a slow ventricular response! When this is seen — it should immediately prompt a different set of diagnostic considerations. These include:

Use of rate-slowing drugs (ie, digoxin; ß-blockers; verapamil/diltiazem; amiodarone; sotalol; clonidine; various herbal preparations). Ask about all pills that the patient is taking — including herbal preparations (you may need to look up which of these may be rate-slowing ...). PEARL #4 — Don't forget to ask about eye drops! (ie, ß-blocking eye drops are partially absorbed — and may produce significant bradycardia that resolves when the eye drops are stopped!)
Acute ischemic heart disease (ie, from ischemia/infarction; acute coronary syndrome). Recent MI may present with slow AFib without any history of chest pain.
Hypothyroidism (abnormal thyroid function may predispose to arrhythmias).
Sleep apnea (which is commonly overlooked as a potential cause of bradyarrhythmias).
SSS (Sick Sinus Syndrome) — which can only be diagnosed after ruling out causes in the 4 bullets above this! PEARL #5 — Almost by definition, a patient older than 60-70 years old who presents with new-onset slow AFib, but who is not on any rate-slowing drugs — has no acute or recent ischemia — does not have sleep apnea — and has normal thyroid function — will have SSS!

Rhythm D in Figure-1:

This is AFib with a very rapid ventricular response. The usual rate range for “rapid” AFib is between ~110-180/minute. This is because the intrinsic refractory period of the normal AV node generally does not allow conduction of more than 200-220 impulses per minute.
PEARL #6 — IF ever the rate of AFib is significantly above this (ie, >200-220/minute) — the patient probably has an AP (Accessory Pathway) that is bypassing the AV node (ie, WPW = Wolff-Parkinson-White Syndrome).
Note in Panel D of Figure-1 — that the QRS complex is wide. AFib in patients with WPW will almost always be antidromic (traveling first down the AP instead of through the AV node, as the path to the ventricles). This is because of the shorter refractory period of the AP. As a result, the QRS complex is typically wide in patients with WPW who develop AFib. As seen in Panel D— the irregularly irregular tachyarrhythmia is characterized by periodic slowing of the rhythm in some places, while attaining exceedingly fast rates that may approach 250-300/minute in other places (CLICK HERE— for more on the arrhythmias commonly seen with WPW).

MORE on Vagotonic AFib:

Autonomic dysfunction often figures prominently in the onset of AFib. In most instances, there is excessive sympathetic activity — but on occasion, increased vagal tone may trigger AFib episodes (Vagal stimulation shortens the atrial effective refractory period — and therefore enhances the ability of a single PAC to induce AFib).
Vagotonic AFib — is most commonly seen in younger males (ie, 30-50 years old). Active participation in endurance sporting activities (ie, cycling, long-distance running, cross-country skiing, etc.) predisposes to longterm increases in resting vagal tone.
IF episodes of AFib most often occur at rest, after meals, or during sleep — these episodes of AFib are more likely to be vagally stimulated.
Episodes of vagotonic AFib are more likely to resolve in the morning or during periods of exercise (ie, when sympathetic tone is increased).
AFib recurrence is commonly precipitated by episodes of coughing, intense nausea or vomiting — or after ingestion of cold food or drinks (all potential stimulators of vagal tone). Sometimes, simply eating a meal may precipitate episodes.
If 24-hour Holter monitoring is done — there will often be a period of sinus bradycardia prior to onset of AFib.
Episodes of vagotonic AFib typically manifest a relatively slow ventricular response.

BACK to THIS CASE — It is of interest that this patient was totally unaware that he was in AFib! That said — he apparently converted to sinus rhythm after his vertigo was successfully treated with an Epley maneuver.

Given this history — I suspect this patient has frequent episodes of vagally-induced AFib — that spontaneously resolve when vagal tone decreases. The fact that he is unaware of AFib episodes when they occur complicates management. Nevertheless — Holter monitoring with a DIARY may prove insightful for indicating which activities of daily living are most likely to precipitate episodes. There may be certain precipitants that can be avoided, or at least minimized.
Rate-slowing drugs, such as ß-blockers should be avoided in treatment — because these may result in further imbalance of parasympathetic tone (since sympathetic tone is reduced).
Antiarrythmic medications that reduce vagal tone (such as flecainide, disopyramide) may be effective.
Ultimately, if episodes of vagotonic AFib are frequent and persistent — referral to EP cardiology may be indicated. Some patients require ablation for control of vagotonic AFib ...

Our THANKS to Dr. Smith for this interesting case!

↧

A 41 year old with chest pain and a Nondiagnostic Triage ECG. Thrombolytics prior to transfer for PCI.

November 8, 2019, 6:47 am

≫ Next: High-Sensitivity Troponin is not a Myth, and “Myth-busting” is often another Myth to be Busted

≪ Previous: A healthy 30-something presented with nausea, vomiting, benign positional vertigo and atrial fibrillation

This was sent by Tom Fiero, from Merced CA, and an avid reader of the blog.

"A 41 yo man presented with sudden severe chest pain, onset 1 hour prior to arrival."

"Here is the first ED ECG at 2242:"

What do you think?

"My partner was shown the ECG and he was not impressed."

"30 minutes later, I picked up the patient and saw this ECG, and I was concerned."

"I was worried about the slight ST depression in lead aVL, and the morphology of aVL."

"I sought a previous ECG and found one from 9 months prior:"

Smith analysis:

Much different
However, much of the difference may be due entirely to the QRS axis.
1. QRS axis = approximately 45 deg in the old ECG, but 90 degrees (vertical) in presentation ECG.
2. T-wave axis is 30 degrees in the old ECG and 90 degrees in the presentation ECG.

Old ECG: QRST axis = ~15 degrees
Presentation ECG: QRST axis = ~ 0 degrees

So there really is no significant change in the QRST axis, which measures T-wave inversion, but there is a change in both the QRS axis and the T-wave axis, and I don't really know the significance of this. Nevertheless, I agree with the reader that aVL looks suspicous, but not diagnostic.

Dr. Fiero continues:
"At this point, the patient was also diaphoretic. I ordered aspirin and heparin bolus. BP was 220/110. I ordered sublingual NTG. I would order a NTG drip, but it holds up stat ground transfer because it requires a critical care nurse. So I ordered labetolol."

Then I ordered another ECG at 2316

"This is now obvious."
Smith: Agree. Clearly an Inferior OMI

"I ordered TNK-tPA (Tenectaplase), since the transport time is too long to rely on PCI alone."

Smith comment:
1. If first medical contact to balloon time is greater than 120 minutes, which happens in more than 50% of transfers, then give thrombolytics and transfer for immediate PCI upon arrival.

Stated otherwise:

2. If door (at referring hospital) to balloon (at receiving center) time is greater than 90 minutes, then give thrombolytics. When transport time is greater than 30 minutes, door to balloon time is greater than 90 minutes in more than 50% of cases.

Fiero
"The patient was still having chest pain."
"Door to needle is greater than 90 minutes, hence TNK."
"And I recorded the 3rd ECG:"

2322

More obvious still

"At this point, the patient was looking and feeling better. We loaded him up and sent him."

"Before leaving, he admitted to amphetamine abuse about 10 hours prior to presentation."
"I thought I was maybe over-reacting with first ECG."
"Then I got the old EKG, and he looked ill, and I realized I was not overreacting."

The patient reperfused his RCA and had a good outcome.

Smith comments

A couple further points on thrombolytics prior to transfer:

1. Clopidogrel is a good idea and proven beneficial when giving thrombolytics for STEMI. The dose in this situation is 300 mg.
-----Neither Prasugrel nor Ticagrelor have been studied, nor clopidogrel at a dose of 600 mg.
2. ASSENT-3 showed that the best antithrombotic for STEMI who are receiving thrombolytics is enoxaparin.

This is the dosing regimen:

STEMI with thrombolytics:

Enoxaparin is the optimal choice:

If less than 75 y old: 30 mg IV bolus, followed in 15 min by 1 mg/kg subcutaneous (SC) (max 100 mg for the first dose)
If over 75 y old: No bolus, 0.75 mg/kg SC (max 75 mg for the first dose)

Transfer of patients with STEMI and use of thrombolytics

Dr Meyers and I wrote the ACS chapter in the upcoming EmRap “CorePendium” (Compendium of Emergency Medicine, an online Textbook). Here is the section on Transfer of STEMI patients which I wrote.

Transfer for PCI-only vs. thrombolytics prior to transfer for STEMI

If delay from first medical contact to PCI will be greater than 120 minutes (and it almost always is)

Then Thrombolytics first

If delay is less than 120 minutes, then transfer for PCI without thrombolytics

Facilitated PCI (thrombolytics) with full adjunctive antithrombotic therapy and P2Y12 inhibition, when patient cannot get PCI within one hour for STEMI

STREAM study (Armstrong et al. 2013). Patients presenting to non-PCI hospital. All transferred.
Randomized to:

1) TNK-tPA before transfer

Standard dose bolus tenecteplase (½ dose in patients over 75 years of age) with clopidogrel 300 mg and enoxaparin (30 mg IV + 1 mg/kg subcutaneous) before transport to a PCI-capable hospital.

2) No TNK-tPA before transfer

PCI-only group:

Patients in the PCI-only group were treated very fast, with 100 minutes from symptom onset to sheath insertion (Armstrong et al. 2013)

Thrombolytic before PCI group:

Emergency coronary angiography was performed if fibrinolysis failed (this was measured by resolution of pain and ST-segment elevation on the ECG).

Thus, it is analogous to planned rescue PCI (see Rescue PCI below)

Otherwise, angiography was performed 6 to 24 hours after randomization.

The primary endpoint was a composite of death, shock, congestive heart failure, or reinfarction up to 30 days.
Results:

36% of lytic patients required urgent PCI. Mean time from randomization to angiography for these patients was 2.2 hours, vs. 17 hours for the other 64%.
The primary end point occurred in 116 of 939 patients (12.4%) in the fibrinolysis group with rescue, and in 135 of 943 patients (14.3%) in the primary PCI group (p=0.21
Intracranial hemorrhage was 1.0% for TNK-tPA vs. 0.2%.

Conclusion: Transfer for PCI without thrombolytics is best if PCI at receiving facility can be done in less than 120 minutes from first medical contact, or less than 90 minutes from STEMI diagnosis in first ED.

Thrombolytics prior to Transfer to a PCI capable facility, then rescue PCI if no reperfusion for STEMI

TRANSFER AMI (Cantor et al. 2009).
High risk STEMI: BP less than 100, HR greater than 100 Killip class II, III, ST depression of at least 2 mm in precordial leads, ST elevation in right precordial leads (right ventricular MI
All patients get TNK-tPA.
80-90% received clopidogrel 300 mg (75 mg for age over 75).
Enoxaparin (not for age over 75) or UFH (50-50). Doses not specified, presumably standard doses.
Patients randomized to:

1) Standard Rx:

Transfer only if there is persistent ST elevation (less than 50% ST resolution)
No transfer if there is reperfusion (ST resolution)

2) Transfer with immediate PCI regardless of reperfusion.

Results: Intervention group had PCI a median of 2.8 hours after randomization

30-day severe adverse outcomes 17.2% vs. 11.0% (NNT = 16)

Conclusion: All high risk STEMI should be immediately transferred after thrombolytics

Thrombolytics prior to transfer to a PCI capable facility, then routine PCI regardless of reperfusion for STEMI

CARESS-in-AMI (Di Mario et al. 2008)

Patients: High risk STEMI, had at least one high risk feature treated initially at non-PCI hospital

Extensive ST elevation, new LBBB, previous MI, Killip class greater than or equal to 2, LVEF less than 35%

½ dose reteplase, abciximab, heparin, aspirin, only 1 in 6 received upstream clopidogrel, but this is probably not so important because they did receive DAPT using abciximab.
Randomized to:

Immediate transfer for PCI or
Standard therapy: Transfer for rescue PCI only if needed

PCI in 85.6% of immediate group; rescue PCI in 30.3% of standard group
Median time from thrombolytics to transfer = 110 minutes in immediate group vs. 180 minutes in rescue group.
Composite of all-cause mortality, reinfarction, and refractory myocardial ischemia within 30 days (4.4% versus 10.7%, p = 0.004) in the immediate PCI group vs. standard care/rescue PCI group (NNT=17).

No significant differences in major bleeding at 30 days (3.4% versus 2.3%, P0.47) or stroke (0.7% versus 1.3%, P0.50).

Meta-analysis including both high risk and non-high risk patients

Concluded that all patients should be transferred for early routine PCI after thrombolytics (Borgia et al. 2010).
Early was defined as less than 24 hours. However, the figure below from an editorial (Granger 2011) representing the 7 trials in the meta-analysis shows that the time to PCI was usually very short.

Conclusions:

All high risk patients who receive thrombolytics prior to transfer should have immediate angiography +/- PCI at the receiving facility, regardless of reperfusion status (in other words, not only the patients who need rescue PCI).
Among non high risk patients who do not need rescue PCI, also consider immediate angio +/- PCI after a delay of 2-3 hours (O’Gara et al. 2013).

Half dose thrombolytics prior to transfer to a PCI capable facility for STEMI

Half dose thrombolytics prior to transfer appears to be a attractive option, without an increase in major bleeding. (Larson et al. 2012)

Not a randomized trial
STEMI receiving center, with some referral hospitals are more than 60 miles distant
Compared to STEMI patients presenting directly to the receiving hospital
All received aspirin, clopidogrel, and unfractionated heparin (UFH)
Those presenting to hospitals ≥60 miles away also received half-dose fibrinolytic with transfer for immediate PCI.
Total 2634 consecutive STEMI patients from all sources

660 transferred from remote hospitals utilizing half-dose tenecteplase (TNK-tPA)
600 patients who presented directly to the PCI centre.
Door to balloon time for direct vs. transfer: (mean +/- CI): 62 (44-83) vs. 122 (100-147)
No significant differences in 30-day mortality (5.5 vs. 5.6%; P= 0.94), stroke (1.1 vs. 1.3%; P= 0.66), major bleeding (1.5 vs. 1.8%; P= 0.65), or re-infarction/ischaemia (1.2 vs. 2.5%; P= 0.088) in patients receiving TNK vs. those presenting directly to the PCI centre, despite a significantly longer door-to-balloon time

Summary: Combination Reperfusion Strategies (Thrombolytics + PCI)

First, it is important to realize that only a small percentage of STEMI patients who do not receive thrombolytics are actually transferred for PCI in a timely fashion, and thus thrombolytics prior to transfer should be strongly considered.

When drive time is over 30 minutes, only 42% of patients achieve first door to balloon time in less than 120 minutes. Recommended time is first medical contact to balloon of time of less than 120 minutes (Vora et al. 2015).

Thus, according to the ACC/AHA, immediate transfer after thrombolytics is recommended:

For all failed reperfusion (for rescue PCI), ST resolution at least 70%
For all high risk patients
For all other patients, it is reasonable to transfer

For these patients, PCI should be delayed for 2-3 hours after thrombolytics (O’Gara et al. 2013)

Finally, Half dose thrombolytics prior to transfer appears to be a attractive option, without an increase in major bleeding. (Larson et al. 2012)

↧

High-Sensitivity Troponin is not a Myth, and “Myth-busting” is often another Myth to be Busted

November 10, 2019, 7:49 am

≫ Next: What is this Regular SVT?

≪ Previous: A 41 year old with chest pain and a Nondiagnostic Triage ECG. Thrombolytics prior to transfer for PCI.

This is published simultaneously in Emcrit

Emergency Medicine News has now published 2 “Myth-Busting” articles by Rory Spiegel which dispute the value of high-sensitivity troponin. We call them “Fake News,” (as they cherry-pick and misrepresent several studies) and EM News would not allow rebuttal.

The bottom line: the value of high-sensitivity troponin is NOT a myth; it helps to rule out and rule in acute MI earlier (but it is complex, and there is a lot to know).

Stephen W. Smith*

Alexander Limkakeng**

Frank Peacock***

Disclosures:

*Dr. Smith has researched the Abbottt Architect high-sensitivity assay with the Hennepin Healthcare Research Institute’s Biomarkers Research Lab, which has received funding from Abbottt. He has no personal disclosures.

**Dr. Limkakeng:

Has done research into high-sensitivity troponin funded by Roche, Abbott, and Siemens.

***Dr. Peacock’s disclosures:

--Research Grants: Abbott, Boehringer Ingelheim, Braincheck, CSL Behring, Daiichi-Sankyo, Immunarray, Janssen, Ortho Clinical Diagnostics, Portola, Relypsa, Roche, Salix, Siemens. --Consultant: Abbott, Astra-Zeneca, Bayer, Beckman, Boehrhinger-Ingelheim, Ischemia Care, Dx, Immunarray, Instrument Labs, Janssen, Nabriva, Ortho Clinical Diagnostics, Relypsa, Roche, Quidel, Salix, Siemens.

--Expert Testimony:Johnson and Johnson.

--Stock/Ownership Interests:AseptiScope Inc, Brainbox Inc, Comprehensive Research Associates LLC, Emergencies in Medicine LLC, Ischemia DX LLC.

This piece is in response to an article in Emergency Medicine News, in the series "Myths in Emergency Medicine":

Myths in Emergency Medicine: Hoopla Aside, hs-cTnI is Not Catching Missed MIs.

Spiegel, Rory, MD

https://journals.lww.com/em-news/Fulltext/2019/02000/Myths_in_Emergency_Medicine__Hoopla_Aside,_hs_cTnI.1.aspx

Dr. Spiegel was responding to this very complicated article in Lancet:

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)31923-8/fulltext

We wrote our rebuttal, and then Dr. Spiegel doubled down this month by publishing another “Myths in EM” piece in EM News: “Is hs-cTnT Worth the Downstream Testing?.

Rebuttal to the First Article

Stephen Smith, of Dr. Smith’s ECG blog, wrote this rebuttal: Smith SW. Letter to the Editor: hs-cTnI’s True Intent. Emergency Medicine News; 41(5):28-49; May 2019. https://journals.lww.com/em-news/Fulltext/2019/05000/Letter_to_the_Editor__hs_cTnI_s_True_Intent.39.aspx

Alex Limkakeng and Frank Peacock also responded:

https://journals.lww.com/em-news/Fulltext/2019/05000/Letter_to_the_Editor__hs_cTnI_s_Value_is_High.40.aspx

Here is the Smith response:

Note that units in contemporary assays are reported in ng/mL, and in high-sensitivity (hs) assays as ng/L (cTnI of 0.030 ng/mL is comparable to hs cTnI of 30 ng/L)

To The Editor:

I believe Rory Spiegel, MD, misinterpreted the study in his article, “Hoopla Aside, hs-cTnI is Not Catching Missed MIs.” (EMN 2019;41[2]:1; http://bit.ly/2Bv4FUd.) The high-sensitivity troponin (in this case, Abbott Architect hs troponin I) reclassified 1771 patients as acute MI (about 600 type 1) not identified by the (Abbott) contemporary assay (cTnI), and their ultimate outcome was not different from those not reclassified. (Lancet2018;392[10151]:919; http://bit.ly/2Erob73.)

This makes it seem that the hs assay has no value, that it simply leads to more investigations without improving outcomes. The reason for this is not increased test sensitivity but the threshold used for the test's upper reference limit (URL). It also ignores the intended value of the test: earlier MI rule in or out.

The definitions of normal vs. increased for both assays are based on the 99^th percentile of a normal population, which may result in varying cutpoints for normal. The upper reference limit must also be accompanied by a low coefficient of variation (CV), which statistically measures the reproducibility of the test and should not exceed 10% at the 99^th percentile. Different labs have different CVs and URLs; the laboratories used in the study had a 10% CV at a relatively high URL of 40 and 50 ng/L, higher than it would be in many labs. The URL for the same (Abbott Architect) contemporary cTnI assay in the Hennepin County lab is 0.030 ng/mL, and the CV is less than 10% at this value. The higher URL would result in the cTnI assay being less sensitive in the study than it would otherwise. The hs assay uses different thresholds for women (16 ng/L) and men (34 ng/L). This is likely why women were reclassified in the study more often.

These factors may account for the differences in reclassification. Data from the UTROPIA study, in which the URL for cTnI was 0.030 ng/mL (hs-cTnI used 16 ng/L for women, 34 for men), showed fewer positive assays with the hs-cTnI than with the cTnI; that is, it resulted in fewer false-positives. (Am J Med 2017;130[12]:1431.)

It is also important to remember that “high-sensitivity” means analytical, not clinical, sensitivity. All positives and negatives are determined arbitrarily by the 99^thpercentile of a “normal population” without ACS symptoms; thus, as long as the 2 “normal” populations on which the 2 assays’ normal values were defined are comparable, the two assays cannot be different in the proportion of MIs identified except for the different thresholds used and the number of hours of serial troponins measured.

I like to call high-sensitivity assays “high-precision” assays because they can accurately quantify low levels of troponin, far below the 99^th percentile cutpoint. This means that troponin changes at low levels can be detected in order to rule in or rule out MI earlier by using low thresholds or delta values. Small changes at low values are true changes, not just analytical noise. A single extremely low value, which can now be quantified, can all but rule out MI in patients with at least two hours of chest pain. (JAMA 2017;318[19]:1913; http://bit.ly/2MVSsMT.)

The Lancet study used values at six to 12 hours after symptom onset to diagnose myocardial injury. The contemporary (not high-sensitivity, hs) assay (cTnI) is excellent and just as sensitive as hs assays at six to 12 hours after symptom onset. The use of these late measurements negated the value of the hs assay, which is that it helps in earlydiagnosis of MI and early rule out. It is true that the hs assays will not catch missed MIs, but that was never the intent.

Stephen W. Smith, MD. Minneapolis, MN

Here is the response of Drs. Limkakeng and Peacock:

To the Editor:

The headline and publication reviewed in the EMNarticle, “Hoopla Aside, hs-cTnI is Not Catching Missed MIs” are misleading. (2019;41[2]:1; http://bit.ly/2Bv4FUd.) Rory Spiegel, MD, wrote, “Despite our hopes, it would appear that the introduction of hs-cTnI added very little to the workup of patients presenting with symptoms concerning for ACS.” On the contrary, a wide body of published research demonstrates that hs troponin can positively affect ED evaluation of ACS if properly implemented.

Our European and Asian colleagues have shown us for years that the value of a high-sensitivity troponin assay is not to identify more MIs but to identify patients who can be safely discharged home faster. Indeed, the literature is rife with examples of how this can be done. (Circulation 2017;135[16]:e923; http://bit.ly/2tzs02Q; Eur Heart J 2016;37[44]:3324; http://bit.ly/2NjMFAO.)

Our early experience at Duke University Hospital has confirmed this experience (manuscript in preparation). Thoughtful high-sensitivity troponin implementation strategies that incorporate structured risk stratification and disposition pathways significantly reduce length of ED stays, admission and stress testing rates, and costs without a concomitant increase in hard cardiovascular outcomes such as MI and death in those discharged. Note that these outcomes cannot be achieved simply by changing your troponin assay. They require an evidence-based, multidisciplinary change in the practice of ACS evaluation.

We agree that it is unfortunate that these assays have been termed high-sensitivity because their real value is high precision and reproducibility. This allows for accurate serial measurements in a short time. They also allow more precise identification of extremely low (undetectable) levels that can allow safe discharge after one lab draw in select patients who present several hours after symptom onset.

Alexander T. Limkakeng Jr., MD

Durham, NC

W. Frank Peacock, MD

Houston

Dr. Spiegel responded to all of us:

Thanks to Drs. Smith and Limkakeng and Peacock for their insightful comments. Both are well versed in their understanding of the literature surrounding the use of high-sensitivity troponins, and both argue that the results of Shah, et al., discussed in my EMN article are discordant from the remaining literature which demonstrates that high-sensitivity troponin assays can be used to safely discharge patients home from the ED without increasing the number of patients identified as positive for an acute myocardial infarction. They go on to cite a number of studies to support these claims.

While a number of studies have demonstrated that the introduction of a high-sensitivity assay allowed clinicians to send more patients home from the ED without increasing the number of patients diagnosed with AMI, an equal number have demonstrated the opposite. (Acad Emerg Med 2017;24[3]:388; http://bit.ly/2Nuefvl; Heart 2014;100[20]:1591; Emerg Med J 2012;29[10]:805; Acad Emerg Med 2014;21[7]:727; http://bit.ly/2IzUcg5.) Multiple studies have found that the use of high-sensitivity troponin is at best no better than the standard assay or at worst increases downstream testing.

In fact, all the studies that support the use of a high-sensitivity troponin are observational in nature. Their results are promising, but they are highly vulnerable to bias because of their observational design. The only other RCT I am aware of comparing the use of standard to high-sensitivity troponin assay found the high-sensitivity assay offered no clinical value over and above the standard assay. (Circ Cardiovasc Qual Outcomes 2016;9[5]:542; http://bit.ly/2U7kHuR.) The results presented by Shah, et al., are even more concerning. They suggest not only that the assay is not beneficial, but also that it may lead to more downstream care with no recognizable benefit.

Both Drs. Smith and Limkakeng offer logical reasons why the Shah results do not represent the true value of a high-sensitivity assay, and they may be correct. Shah's results may be due to how the assay was deployed rather than the assay itself. But it is just as likely that the results are a representation of what will occur when high-sensitivity assays are introduced into the clinical arena. These results should not be written off because they are discordant from a sampling of observational data supporting the use of high-sensitivity assays. Rather, it is our responsibility to empirically demonstrate the clinical value of the high-sensitivity assay before welcoming its widespread use in EDs across the country.

Drs. Smith, Limkakeng, and Peacock responded with the following, but EM News would not print it.

So here it is:

Real Myth-Busting for high-sensitivity Troponin

Recently, in Emergency Medicine News, Rory Spiegel wrote in his "Myth Busting" column about the HighSTEACS study (1) and claimed that “the introduction of hs-cTnI added very little to the workup of patients presenting with symptoms concerning for ACS”.

This position could not be more wrong.

We countered his piece with reference to the mountains of data which contradict the idea that hs troponin adds little. He responded by stating "While a number of studies have demonstrated that the introduction of a high-sensitivity assay allowed clinicians to send more patients home from the ED without increasing the number of patients diagnosed with AMI, an equal number have demonstrated the opposite."

In fact, the 4 articles he references do not show the opposite at all, and the 5th study, and RCT, was also mischaracterized. These are addressed point-by-point below.

His response ignores a decade of research detailing how high-sensitivity assays can beneficially impact ED patients. There are many systematic reviews, meta-analyses, and prospective randomized trials from dozens of countries and tens of thousands of patients on use of high-sensitivity troponin for safe rapid ED discharge (just for example, Zhelev Z,et al. BMJ. 2015 Jan 20;350:h15. Than MP, et al. Circ 2018; 137 (4): 354-63, Twerenbold R, et al. Eur Heart J. 2016 Nov 21;37(44):3324-3332) The literature is replete with data showing how properimplementation of high-sensitivity troponin can avoid increased workups and downstream testing, while at the same time decreasing ED length of stay and costs.

The HighSTEACS article referenced had several flaws. Most importantly, the advantage of hs troponin is its precision, which allows it to quantify very low levels of troponin, and accurately measure very small changes. Thus, it is used for early rule-in or rule out of MI. Measurements at 6-12 hours, as done in the HighSTEACS trial, would not be expected to result in improvements over the contemporary assay; at this time period, contrary to conventional thinking, hs troponins are neither more sensitive nor less specific. Moreover, the finding of an increase in workups without improvement in outcomes was due to a “positive” cutoff, defined as the assay’s 99^th percentile. The 99^th percentile may be used to rule out MI, but not rule it in. This common error has been recognized for years. See the “10 Commandments of Troponins” (Jaffe, AS. Heart 2011 97: 940-946 doi: 10.1136/hrt.2009.185751). This should be considered a well-established standard for improving the clinical utility of biomarker.

It is important to remember that the most important use of hs troponin is the earlyrule out and rule-in of MI (early rule-in by very high levels or large deltas). Protocols for both rule out and rule-in always have an intermediate range of values for which it is necessary to use delta troponin and other clinical data in order to make the diagnosis.

In fact, there are hundreds of articles that show the utility of hs troponins, and below we describe the 4 articles which he purports show the "opposite."

(Acad Emerg Med 2017;24[3]:388; http://bit.ly/2Nuefvl; This paper actually shows that a single hs troponin (measured at time of arrival in the ED) which is below the level of detection, especially with a normal EKG, has a 99.1% sensitivity for acute MI. It supports our argument fully; it does not show the "opposite."

Notice how all the other studies (the 3 below) cited by Dr. Spiegel are from 5 or more years prior (even 2012!), most of them gathering data from before 2010 (2007, 2008) when hs assays were not very sensitive or precise.

Heart 2014;100[20]:1591; https://heart.bmj.com/content/100/20/1591 (data from 2008-2010).

This study is downright dangerous. The cutoff used for the contemporary assay (0.200 ng/mL) was far higher than the 99th %-ile (0.070 ng/mL). Many patients should have been diagnosed with MI (by the contemporary assay) who were not. In other words, the researchers used the diagnostic cutoff for the high-sensitivity assay, but a much higher cutoff (thus not sensitive) cutoff for the contemporary assay. This would obviously lead to more "positives" for the high-sensitivity assay. The authors set the cutoff for the contemporary assay such that many patients who actually were having an acute MI (by definition) were not diagnosed with MI. Their conclusion might be that, because the 6 month MACE is the same in both groups, one need not diagnose every myocardial infarction.

But with a study this small and with only a 6 month followup, and results which contradict all other studies on acute MI, it no doubt underestimates the adverse events. All other data would show that missed MI, even with troponin values at less than 5x the upper reference limit, does lead to adverse events. See JAMA reference below by Mills Nicholas L et al.,*** in which 39% of patients with MI whose troponin levels were between 0.05 and 0.19 ng/mL had death or MI within one year, vs. 7% of those with troponin less than 0.05 ng/mL. Indeed, elevated troponin in the lower range from any cause is associated with worse outcomes. Thus, this study should be ignored. Furthermore, the high-sensitivity assay is a previous generation hs-cTnT which is not as precise as the one produced today, and so has more false positives.

Emerg Med J 2012;29[10]:805; Could not get full text. This very old study does not compare the "hs" troponin with any other strategy. In fact, it showed fairly good sensitivity at 2 hours. This article does not show the "opposite."

Acad Emerg Med 2014;21[7]:727; http://bit.ly/2IzUcg5.) This study had a total of 24 myocardial infarctions. No more need be said.

***Mills study, referenced above, showing that minimally elevated contemporary troponins are associated with much worse outcomes in MI:

https://jamanetwork.com/journals/jama/articlepdf/895839/joc15019_1210_1216.pdf

Mills, Nicholas L., Antonia M. D. Churchhouse, Kuan Ken Lee, Atul Anand, David Gamble, Anoop S. V. Shah, Elspeth Paterson, et al. 2011. “Implementation of a Sensitive Troponin I Assay and Risk of Recurrent Myocardial Infarction and Death in Patients with Suspected Acute Coronary Syndrome.” JAMA: The Journal of the American Medical Association 305 (12): 1210–16. https://doi.org/10.1001/jama.2011.338.

Spiegel: “The only other RCT I am aware of comparing the use of standard to high-sensitivity troponin assay found the high-sensitivity assay offered no clinical value over and above the standard assay. (Circ Cardiovasc Qual Outcomes2016;9[5]:542;http://bit.ly/2U7kHuR.) “

Circ Cardiovasc Qual Outcomes 2016;9[5]:542; used 99%ile dichotomously “normal: less than or equal to 14 ng/L and greater than 14 ng/L: myocardial injury]”

However, again, among patients classified as low or no risk by Heart Foundation Criteria, a higher rate of discharge from the ED was observed in the hs-report group (hs-report: 168 of 253 patients (66.4%) versus std-report: 148 of 263 patients (56.3%); P=0.010),

“There was no difference in angiography (hs-report: 11.9% versus std-report: 10.9%; P=0.479). . . . However, among those with troponin levels less than 30 ng/L, a modest reduction in the primary end point was observed (hs-report: 2.6% versus std-report: 4.4%, [hazard ratio, 0.58; 95% confidence interval, 0.34–0.1.00; P=0.050).

High-sensitivity troponin reporting alone is associated with only modest changes in practice. Clinical effectiveness in the adoption of high-sensitivity troponin may require close coupling with protocols that guide interpretation and care.”

In other words, there was clinical value:10% increase in discharges and 2% decrease in 1 year death or recurrent ACS in the subset expected to be stratified best by the hs trop, both statistically significant.

Finally, there is now a very large prospective trial that was presented at the European Society of Cardiology in August 2019. It is the HiSTORIC trial and is by the very same HIGH-STEACS group who published the Lancet study that generated all this controversy.

_______________

Mills NL et al. high-sensitivity cardiac Troponin at presentation tO Rule out myocardial InfarCtion (HiSTORIC): a stepped-wedge cluster randomized controlled trial.

New Protocol:

Abbott Architect hs-cTnI

Exclude patients with STEMI and clearly ischemic ECG

--If presentation value less than 5 ng/L and time to presentation greater than 2 hours, then low risk.

--If less than 2 hours, or hs-cTnI greater than or equal to 5 ng/L, then obtain 3 hour troponin. If delta greater than or equal to 3, then admit for peak test.

--If presentation value greater than 99th percentile gender specific value, admit for peak test.

Compared to standard Evaluation:

--Hs Troponin less than 99th percentile at presentation if greater than 6 hours of symptoms, or

--Serial testing 6-12 hours from symptoms onset

(This protocol is no different from using contemporary troponin because at this late time period, as cTnI and hs-cTnI are not significantly different).

Outcomes:

--30-day death or MI

--Proportion discharged from ED

--Secondary safety endpoint: 1 year MI, cardiac death, unplanned revascularization, re-attendance

31,492 patients overall: standard pathway - 14,700; Early rule out 16,792

Results:

Reduced length of stay by 3.3 hours (10.1 vs. 6.8 hours)

Increased discharge from ED by 57%

One year MI and cardiac death higher in the standard group.

Conclusion: Early rule out protocol is effective and safe.

We refer interested readers to the following excellent reviews of high-sensitivity troponin implementation:

Twerenbold, R. et al. JACC70 (8): 996–1012.https://doi.org/10.1016/j.jacc.2017.07.718.

Yader S. et al. 2016. Am J Med 129 (4): 354–65.https://doi.org/10.1016/j.amjmed.2015.12.005.

Response to the 2nd “Myth-busting” article

Interestingly, on Nov 5, Dr. Spiegel published another “Myths in EM” piece in EM News: “Is hs-cTnT Worth the Downstream Testing?. The piece assesses a new randomized trial of the Roche hs -cTnT (not the Abbott Troponin I, which is what was studied in the above Lancet study). [Here is the full text of this randomized trial: A Randomized Trial of a 1-Hour Troponin T Protocol in Suspected Acute Coronary Syndromes.]

Spiegel’s piece starts by conceding that “hs assays....will soon replace the 4th generation assays currently being used.”

This hs-cTnT study randomized potential ACS workups to a 0/1 hour hs-cTnT protocol vs. standard care. In the standard care arm, 0/3 hour troponins were used and the providers were blinded to any value less than 29 ng/L (the rationale for hs-cTn is to be able to precisely measure such small quantities, so this study was testing the value of knowing, vs. not knowing, the precise value of all such low troponin measurements). The study showed that more patients are discharged (45.1% vs. 32.3%), and discharged earlier (4.6 vs. 5.6 hrs), with hs-cTnT 0/1 hour protocol.

Somehow, Dr. Spiegel, in his zeal to bust “myths,” manages to dismiss these findings!!

As expected with hs-cTn, the overall number diagnosed with MI was not different because that is not the function of hs-cTn — it is to diagnose or rule out acute MI earlier. Moreover, the protocol ruled out MI in 72.1% with an NPV of 99.6%; in other words, 27% of patients were not discharged even though the protocol would safely allow for it. No doubt the rate of early discharge would have been higher if providers had felt comfortable enough with the new protocol to consistently follow it, a common problem when introducing a new pathway.

By 30 days, among all 3288 patients, the hs-cTnT group (n=1646), compared to the standard group (n=1642), had less functional testing (11.0% vs. 7.5%), but the same number of angiograms, CT coronary angiograms, coronary interventions and revascularizations. However, among the 1493 with an initial cTnT less than 29 ng/L, there were slightly more revascularizations in the group using hs-cTnT [38/1515 (2.2%) vs.15/1493 (0.9%)], partly because there were more index acute MI diagnosed (1.1% vs. 0.5%).

The number of acute MI, unstable angina, and revascularizations following the index hospitalization were the same in both groups. Thus, it would seem that the use of hs-cTnT diagnosed a few more patients at the index visit, without leading to any decrease in adverse 30-day outcomes after the visit. The rate of “non-MI myocardial injury” diagnosis was also slightly higher in the hs-cTnT group (1.6% vs. 1.0%); given than acute myocardial injury is associated with high mortality, detecting it is not necessarily a bad thing.

From the article: “The major downside of noninvasive testing are the downstream invasive testing and interventions it leads to, both of which were higher in the rapid diagnostic strategy group.” But the difference is only 1.3%, or only 23 more over 3.5 years!!

Dr. Spiegel criticizes this tiny bit of higher rate of revascularization: “What have we really accomplished if hs-cTnT leads to a decrease in noninvasive testing but increases the number of diagnostic catheterization and revascularization procedures?”

It seems obvious to us that what we have accomplished is the diagnosis and treatment of a few more acute MI, and possibly also the diagnosis of unstable angina that would need revascularization. Apparently, the interventionalists caring for these patients thought that their patients’ angiographic coronary disease would benefit from revascularization, probably because they opined that it was indicative of ACS. It is also possible that some patients of the patients had stable coronary lesions, which often do not need revascularization.

But Dr. Spiegel seems to be implying that the revascularization undertaken according to the judgment of those patients’ interventionalists was unnecessary; why would he imply that?

Similar to his criticism of the earlier article, this criticism also depends on the notion that one need not treat all acute MI nor all unstable angina, nor even diagnose them.

It is very likely that these patients had their lives saved by this procedure.

Spiegel’s criticism apparently assumes that because there was an absence of difference in death or acute MI at 30-days, that those interventions were unnecessary. But studies of invasive vs. conservative management of ACS, most of which show benefit, show that benefit at 1 year, not at 30 days[1] . A 30-day outcome is used for this trial to show that it is safe to discharge the patient if he/she can get follow up within 30 days. If coronary disease is discovered and treated in the interim, that is not an adverse outcome.

The fact that there were more revascularizations is a benefit of hs-cTn, not a complication. It implies that hs-cTnT helped to find signficant coronary disease. If interventionalists saw ruptured plaque on angiogram, and this was the reason for the revascularization, then it is clear that the hs-cTnT was beneficial. They may well have found other coronary disease that was NOT revascularized, as it was 1) not thought to be ACS or the etiology of the symptoms, or 2) was thought to be ACS but not thought to require revascularization. Certainly not all presumed ACS with coronary disease requires revascularization (see the ICTUS trial). But whether there is coronary intervention or not, there are other interventions for coronary disease that are very effective, mostly statins. In fact, we know from a large CT coronary angiogram study that diagnosing non-ACS coronary disease does benefit the patient because more preventive therapies are adhered to.

In other words, one need not do a coronary intervention in order for it to be worthwhile to make the diagnosis of acute MI or of coronary disease.

In summary, more information is better if the provider knows what to do with it. As we all get more experience with hs-cTn, and there are more clinical trials and observational studies to guide us, the more precise information provided by high-sensitivity troponin will be beneficial to patients and to patient flow.

Myth Busting

Myth-busting is popular and fun, but it is rarely good science. It's fine and good to approach any field of knowledge or any dogma with skepticism. And it is great to really overturn untrue dogma. But to turn skepticism into myth-busting, it is essential to comprehensivelyreview the existing literature. If you set out intent to bust a myth, then you can easily find one or two counterexamples to a prevailing heuristic and write a "Gotcha!" piece on the topic. However, if those who advertise themselves as myth busters are not primary researchers in the area they are myth-busting, there is a risk that they will not fully understand the topic and write a misleading review based on cherry-picked studies that amounts to fake news. Many venues will be eager to publish these pieces since it will attract attention both by those interested in learning something new and by those seeking to correct the inaccurate portrayal of the literature. However, our medical publications should seek to disseminate reliable information and better vet pieces that proclaim propositions that run counter to the vast majority of existing evidence.

Good myth busting in EM:

Here are very nice examples of well substantiated myth-busting by Salim Rezaie at Rebel EM: https://rebelem.com/tag/mythbuster/.

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This is evolving literature, but there is also some who believe that stenting even stable lesions can improve patient-oriented outcome of improved symptoms and function. (I think the ORBITA study? still a little controversial).

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What is this Regular SVT?

November 12, 2019, 8:17 am

≫ Next: A 50-something with left shoulder pain and diffuse ST elevation

≪ Previous: High-Sensitivity Troponin is not a Myth, and “Myth-busting” is often another Myth to be Busted

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MY Comment by KEN GRAUER, MD (11/12/2019):

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

My appreciation to Kenneth Khoo for this case. This patient was hemodynamically stable. There was debate among providers in his institution as to what the rhythm in this ECG was (Figure-1).

What do YOU think the rhythm is?
What is the differential diagnosis?
Why can you be virtually certain what this rhythm is even before treating and before any diagnostic maneuvers?

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

My Approach to this Rhythm: I reviewed the basics for rhythm interpretation in the October 16, 2019 Case from Dr. Smith’s ECG Blog. In brief — once you’ve assured that your patient is hemodynamically stable (as this patient was) — We need to assess the remaining 5 KEY parameters. I favor this memory aid, “Watch your Ps, Qs and the 3 Rs”:

NOTE: It does not matter in what sequence you address these 5 KEY parameters — and I often change the sequence I use depending on the tracing (ie, Which of these 5 parameters is easiest to assess in the tracing in front of you?).
For the tracing in Figure-1 — the rhythm is perfectly Regular. The R-R interval is almost exactly 2 large boxes — which means that the ventricular Rate is 300/2 ~150/minute. The QRS complex is narrow — so this rhythm is supraventricular! Normal atrial activity is not seen — because there are no clear sinus P waves (ie, the P wave is not clearly upright in lead II …).

QUESTION: What does the above analysis suggest to YOU thus far?

ANSWER: We’ve established that this patient is hemodynamically stable. The rhythm in Figure-1 is a regular SVT (SupraVentricular Tachycardia) at ~150/minute without clear sign of sinus P waves. The principal differential diagnosis is similar to what we derived in the October 16, 2019 Case: i) Sinus Tachycardia; ii) Reentry SVT (either AVNRT if the reentry circuit is contained within the normal AV nodal pathway — or AVRT if an accessory pathway is involved); iii) Atrial Tachycardia; or iv) Atrial Flutter.

PEARL #1: The major difference between this case and the case we presented on October 16 — is that the ventricular rate is very close to 150/minute. The most commonly overlooked sustained cardiac arrhythmia (by far) is AFlutter! Over the years — I’ve seen numerous cardiologists overlook this rhythm (especially those cardiologists who do not routinely use calipers for assessment of complex arrhythmias). I fully acknowledge that I’ve overlooked AFlutter. The BEST way never to overlook the ECG diagnosis of AFlutter is to: i) Think of this diagnosis often! — and, ii) To assume that any regular SVT rhythm in which clear sinus P waves are not seen is AFlutter until you prove otherwise — especially IF the ventricular rate of this regular SVT rhythm is close to 150/minute (ie, ~140-160/minute range).
PEARL #2: The reason the ventricular rate for AFlutter is so often close to 150/minute — is that: i) The atrial rate for untreated AFlutter is almost always close to ~300/minute (ie, 250-350/minute range) — and, ii) Untreated AFlutter most often conducts with a 2:1 ventricular response (ie, atrial rate ~300/minute — therefore ventricular rate ~300/2 = ~150/minute).
PEARL #3: The expected atrial rate for flutter is likely to change IF the patient has been “treated” — in which case the ventricular rate in AFlutter with 2:1 AV conduction may be slower (if the patient is on antiarrhythmic medication) — or possibly even faster (if he/she has been treated by ablation).

QUESTION: We said that normal sinus P waves were not seen for the rhythm in Figure-1 — because there is no clearly upright P wave in lead II.

Does this mean that there is no atrial activity in Figure-1?

ANSWER: There appear to be lots of “extra deflections” in a number of leads in ECG #1 ...

PEARL #4: The BEST way we know to quickly determine if the “extra deflections” that we seem to be seeing in ECG #1 represent atrial activity — is to use Calipers!

We show the result of using calipers in Figure-2.

Figure-2: RED arrows indicate that the “extra deflections” are indeed regularly occurring in multiple leads (See text).

Looking for Flutter Waves: The diagnosis of AFlutter can be established in a regular SVT at ~150/minute — IF you are able to identify regular atrial activity at ~300/minute. Nothing else results in a regular atrial activity at this fast of a rate (Atrial tachycardia will rarely be faster than 250/minute ... ).

PEARL #5: The way I look for flutter waves is to carefully set my calipers at precisely HALF the R-R interval of the regular SVT (since IF the rhythm is AFlutter — then the atrial rate should be twice the ventricular rate if there is 2:1 AV conduction). RED arrows in Figure-1 confirm that there is indeed 2:1 atrial activity in this tracing — which tells us even before application of a vagal maneuver or administration of Adenosine (or other AV blocker) that the rhythm is virtually certain to be AFlutter.
PEARL #6: My “GO TO” leads for identifying atrial activity are: i) Lead II — which is typically the BEST lead for identifying atrial activity. In AFlutter — leads III and aVF also usually provide ready evidence of 2:1 atrial activity; ii) Lead V1 — next to lead II, lead V1 is often the 2nd-best lead in my experience for identifying atrial activity. With AFlutter — one will often see positive deflections similar to those seen in Figure-1 in this V1 lead; iii) Lead aVR is often surprisingly helpful for identifying atrial activity (RED arrows in ECG #1); and, iv) IF none of the above leads suggest atrial activity — then I’ll survey the remaining 7 leads as I look for atrial activity. That said, AFlutter will almost always provide ready evidence of atrial activity in one or more of my “Go To” leads.
PEARL #7: On occasion — atrial activity may not be readily apparent in a hemodynamically stable patient with a tachyarrhythmia. In such cases — use of an alternative lead system, such as a Lewis Lead may enhance atrial activity and facilitate rhythm determination. Figure-3 reviews how to use a Lewis Lead. The March 20, 2018 post on Dr. Smith’s ECG Blog illustrates application of a Lewis Lead in a patient in a regular SVT rhythm.

Figure-3: Use of a Lewis Lead (See text).

Our THANKS to Kenneth Khoo (from Malaysia) for sharing this case with us!

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A 50-something with left shoulder pain and diffuse ST elevation

November 14, 2019, 11:54 am

≫ Next: Status epilepticus. What is this ECG pathognomonic of?

≪ Previous: What is this Regular SVT?

A 50-something presented with left shoulder pain.

He had an ECG recorded:

What do you think?

There is a huge amount of ST Elevation, but to my eye it was typical of normal variant. One might say there is terminal QRS distortion, but, although there is indeed absence of S-waves in BOTH V2 and V3, there is in fact very clear notching at the end of the QRS in both V2 and V3.

Fortunately, there was an ECG from about a year prior:

And here is one from about 10 years prior:

You can see here that the computer says "suggests pericarditis" but that I changed it to early repolarization.

Just because there is diffuse ST elevation does NOT mean it is pericarditis.
The most common etiology of diffuse ST elevation is, by far, early repolarization.

The patient had musculoskeletal shoulder pain.

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MY Comment by KEN GRAUER, MD (11/14/2019):

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A subject well worth periodic review — is the concept of Terminal QRS Distortion (T-QRS-D). Prior to working with Dr. Stephen Smith — this concept was unknown to me. When present — T-QRS-D may provide invaluableassistance for distinguishing between early repolarization vs acute OMI (ie, When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI). To review:

T-QRS-D — is defined as the absence of both a J-waveandan S-wave in eitherlead V2orlead V3. Although simple to define — this finding may be subtle! I fully acknowledge that it has taken me a while to become comfortable and confident in its recognition.

A picture is worth 1,000 words. I’ve taken the lead V3 examples in Figure-1 from previous cases posted on Dr. Smith’s ECG Blog:

TOP in Figure-1— Despite marked ST elevation in this lead V3— this is not T-QRS-D, because there is well-definedJ-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
BOTTOM in Figure-1— This isT-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).

Figure-1:Comparison between ST elevation in lead V3 due to a repolarizationvariant (TOP— from4/27/2019) — vsacuteOMI (BOTTOM— from9/20/2015), which manifests T-QRS-D(See text).

Regarding the current case — I have put together the first 2 ECGs that were shown above (Figure-2).

Isn’t it tempting to say there is T-QRS-D in the initialECG that was done in the ED ( = ECG #1inFigure-2)?After all, there is no S wave in lead V3 ...

Figure-2:The first 2 ECGs shown in this case (See text).

COMMENT on ECG #1: The patient in this case was a 50-something man, who presented with left shoulder pain. As per Dr. Smith — there is markedST elevation in lead V3— with a lesser amount of ST elevation in inferior and lateralchest leads.

The reason the ST-T wave appearance in lead V3 of ECG #1 does not qualify as T-QRS-D — is that despite lack of an S wave in this lead, there isJ-point notching (or at least J-point slurring) that is characteristic of repolarization variants.
Other ECG features in ECG #1 in favor of a repolarizationvariant instead of acute OMI include: i) A relatively short QTc interval andtall R waves in the mid-chest leads; ii) Lack of reciprocal ST depression; iii)A similar “look” to the peaked T waves that we see in at least 9 of the 12 leads in ECG #1 (compared to a more localized ST-T wave picture that is typical with acute infarction); and, iv)J-point notching or slurring that is typical for repolarization variants in no less than 7 of the 12 leads in ECG #1(BLUE arrows inFigure-1).

BOTTOM Line: While the composite of the above features makes it more likely that ECG #1 does not reflect acute OMI — there nevertheless is a significant amount of ST elevation in multipleleads in this 50-something man who presented with new symptoms.

Therefore — moreinformation was neededto attain greater certainty (ie, stat Echo looking for wall motion abnormality; additional ECGs on this patient; serial troponins).
In this case — finding a priorECGon this patient from a year earlier was revealing (ECG #2inFigure-2). Neither the lack of S wave in lead V3, nor J-point notching or slurring were new findings (RED arrows inECG #2). This confirmed the impression that the ST-T wave appearance in ECG #1 reflected a longterm repolarization variant in this patient.

Our THANKS to Dr. Smith for presenting this case!

For additional examples illustrating distinction between T-QRS-D vs repolarization variants — Review of the October 6,2015 post may prove insightful.

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Status epilepticus. What is this ECG pathognomonic of?

November 18, 2019, 7:30 am

≫ Next: A man in his 30s with chest pain

≪ Previous: A 50-something with left shoulder pain and diffuse ST elevation

This patient presented with status epilepticus.

Here is the ECG:

The computer reads a long QT at 449 ms, and a Hodges QTc of 506 ms.
What do you think?

In lead V2, you can see distinct T-wave and U-wave. Thus, you can see that the QT interval is not very long. Really, it is 280 ms, for a Hodges corrected QT of 350 ms.

But there are prominent U-waves in all leads.

In many leads, you do not see the T-wave, but ONLY the U-wave: II, III, aVF, and V4-V6. What you might think is a QT interval is really a QU interval. (But a long QU is also dangerous)

This is pathognomonic for hypokalemia.

The K was 1.6 mEq/L.

Of course this is not a difficult case because one will always measure the K in such a case, but it does show that the K is markedly affecting cardiac electrical activity.

Case outcome

The Na was 109. This was the etiology of seizures.

He was treated with hypertonic saline.

Volume was down, and so repleted.

But volume repletion will shut off anti diuretic hormone release, and allow for free water excretion, which can result in rapid rise in Na.

Thus, the patient was also treated with DDAVP to moderate the rise in Na and prevent central pontine myelinolysis.

From EMCrit:

Taking control of severe hyponatremia with DDAVP

An ECG recorded 2 days later with a K of 4.1:

No more abnormal U-waves

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A man in his 30s with chest pain

November 20, 2019, 5:52 am

≫ Next: Persistent Ventricular Fibrillation, ED ECMO, ED TEE, ROSC, Shark Fin ECG (also called "Giant R-wave"), Postinfarction Regional Pericarditis. What a Case!

≪ Previous: Status epilepticus. What is this ECG pathognomonic of?

Written by Pendell Meyers, submitted by Siva Vittozzi-Wong

A man in his 30s with history of hypertension, hyperlipidemia, and diabetes presented with chest pain which started 12 hours prior to presentation. The pain was described as pressure, constant for 12 hours, radiating to the jaw, with left arm numbness. Initial vitals were significant for bradycardia at 45 beats per minute.

Here is his presenting ECG with active pain:

What do you think?

Here was the prior EKG on file:

The emergency medicine resident (who has received lectures from me on hyperacute T-waves, suble OMI, etc) documented the following interpretation:

"Initial EKG showed hyperacute T-waves in the inferior leads, in particular lead III. These findings are suggestive of an RCA occlusion which is supported by bradycardia due to SA node ischemia. Compared to an old EKG on file, these are all new findings."

Meyers comment: So proud. Spot on. Inferior hyperacute T-waves, with negative hyperacute T-wave in aVL. The lateral leads also have minimal STE and hyperacute T-waves. Even without having the baseline ECG, I would say the inferior hyperacute T-waves are still diagnostic. With the baseline ECG in hand, it is all much easier and much more diagnostic, and you can see that the lateral leads are clearly hyperacute as well. Of note, the inferior leads may actually have STE that just barely meets criteria - it is just barely under a full 1 mm in two consecutive leads, and I believe that almost every cardiologist I've ever met would say it does not meet criteria.

After seeing this ECG, the resident immediately called an emergent consult to express concern of an acute RCA occlusion. The initial troponin was not yet back. Cardiology promptly evaluated the patient and did not recommend cath lab activation. Even though the pain was still active, it seems that they were most interested in the fact that the patient had had 12 hours of constant pain and did not meet STEMI criteria.

Meyers comment: There has NOT been 12 hours of persistent Occlusion MI per the ECG! This shows very very high "Acuteness", with no significant Q-waves and hyperacute T-waves. There is maximal myocardium left to save! As we have said many times on this blog, the ECG is much much better at determining duration and salvage conditions than are patient reported symptoms.

Just like the ECG would suggest, the first troponin came back undetectable (because there hasn't been 2-6 hours of occlusion to be picked up by our contemporary troponin T assay). The patient was admitted to the cardiology floor as per cardiology.

The second troponin was also undetectable. The third troponin T came back positive at 0.10 ng/mL. Heparin drip was started. There are no ECGs at this time. The fourth and fifth troponins continued to rise at 0.19 and 0.26 ng/mL, during this time we do not know if the patient still had active pain. Then an EKG was checked at 4am:

Looks slightly less hyperacute than initial presentation, but no signs of reperfusion such as terminal T-wave inversion or ST resolution. Without signs of reperfusion, and with persistent T-wave inversion in aVL, I would still be concerned for ongoing occlusion, though it looks improved.

Another ECG was done at 8am (still no indication in the chart whether there was ongoing pain):

Very similar.

After the troponin went up to 0.60 ng/mL, no more troponins were ordered.

The patient finally underwent angiography and they found:

Culprit lesions of the mid and distal RCA each with 95% stenosis (no TIMI flows documented), and the patient received 4 stents in the RCA. There was also non-acute CAD in the LAD (60% stenosis).

Here are the cath images below. Pay attention to the ECG recording in green at the bottom of each image:

Poor flow prior to intervention, but no complete occlusion during this snapshot in time. Notice the ECG lead looks similar to prior leads, perhaps lead II.

After the intervention the angiographic flow in the main course of the RCA seems much more robust. But look at the ECG tracing across the bottom of the image! Although these monitor strips often exaggerate STE due to different filtering, we should pay attention to them. What do you think this means?

The rhythm strip shows large STE with hyperacute T-wave. Despite no obvious occlusion of the main RCA on the angiogram, this means that a side branch must have become occluded during the intervention, or else a large amount of plaque embolized downstream into downstream vessels.

Like we always say, the ECG is superior to the angiogram for determining actual tissue perfusion.

There is no comment in the cath note about possible adverse events from the intervention, no recognition of the new STE during the procedure. The RCA is documented as having "TIMI 3" flow after the procedure.

An ECG was performed several hours later:

Obvious STEMI with hugely hyperacute T-waves.

Interestingly, no action was taken at this time. I suspect this means they already knew that something became occluded during the cath and it simply was not fixable. If they did not recognize it during the cath, then this ECG would have made them take the patient back to look for immediate in-stent stenosis of the new stent, but they did not take the patient back to the lab, so I must intuit that they understood what happened initially.

No more troponins were ordered at that time.

On day 3 he had another ECG recorded:

Progression likely to full thickness OMI with large wide Q-waves in the inferior leads and persistent STE with persistent upright T-wave, suggesting minimal reperfusion of the infarcted tissue.

Another ECG 7 days later:

Now T-wave inversion in the affected leads. It is unclear to me whether this means any reperfusion happened, or whether this is simply the progression of T-waves expected at 7 days post full thickness OMI. I favor the latter based on the appearance of the previous ECG.

The patients course was apparently uncomplicated in the hospital. He was discharged without further events.

Learning Points:

With the right training, emergency medicine physicians and residents (and any other human with eyes and a brain open to new ideas!) can outperform entire cardiology teams for detecting OMI while we are still stuck in the STEMI / NSTEMI era.

Train your eyes to see the inferior T-waves in this case as hyperacute, and to see their reciprocal finding in aVL.

Expert ECG interpretation is better than patient-reported symptoms to determine viability of myocardium in OMI.

Expert ECG interpretation is better than the angiogram to determine the actual success of reperfusion therapy in OMI. (see literature below)

Here is some older but very interesting literature on TIMI myocardial perfusion grade and ST resolution:

1. Claeys MJ, Bosmans J, Veenstra L, et al. Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction: importance of microvascular reperfusion injury on clinical outcome. Circulation 1999;99(15):1972-7.

2. Gibson CM, Cannon CP, Murphy SA, et al. Relationship of TIMI myocardial perfusion grade to mortality after administration of thrombolytic drugs. Circulation 2000;101(2):125-30.

3. Shah A, Wagner GS, O'Connor CM, et al. Prognostic implications of TIMI flow grade in the infarct related artery compared with continuous 12-lead ST-segment resolution analysis. Reexamining the "gold standard" for myocardial reperfusion treatment. J Am Coll Cardiol 2000;35(3):666-72.

4. van't Hof AW, Liem A, de Boer MJ, et al. Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction. Zwolle Myocardial Infarction Study Group. Lancet 1997;350(9078):615-9.

5. van't Hof AW, Liem A, Suryapranata H, et al. Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade. Zwolle Myocardial Infarction Study Group. Circulation 1998;97(23):2303-6.

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Persistent Ventricular Fibrillation, ED ECMO, ED TEE, ROSC, Shark Fin ECG (also called "Giant R-wave"), Postinfarction Regional Pericarditis. What a Case!

November 22, 2019, 6:07 am

≫ Next: Global ST depression with ST elevation in aVR - what is the cause?

≪ Previous: A man in his 30s with chest pain

A 40-something suffered witnessed ventricular fibrillation, had bystander CPR, but could not be defibrillated after 4 attempts.

He was transferred to the ED and put on extracorporeal life support (ECLS, ECMO).

A series of ED Transesophageal echos (TEE) was done over 23 minutes before an ECG was recorded.

We usually do not get ROSC before angiography in these cases, and recording the ECG is not as important as usual, because we send them all to the cath lab by our ECMO protocol.

This is before another defibrillation attempt, during chest compressions:

Orientation:
The probe is in the esophagus, right next to the left atrium. so the chamber at the top of the image is the left atrium. Directly below that is the left ventricle.

Flow on ECMO was successfully initiated.

13 minutes later, the patient was successfully defibrillated. This was the immediate TEE:

Minimal organized activity, and you can see good blood flow in the chamber due to ECMO

Another 4 minutes later:

There is organized activity, but very slow and with poor contractility

Another 6 minutes later (TEE with short axis):

Contractility and heart rate are better

An ECG was recorded:

"Shark Fin"
Diagnostic of Coronary Occlusion.
I and aVL are involved, so this is a proximal LAD.

Here are 2 more examples of Shark Fin on this blog.

The patient was taken for immediate angiogram:

Do you see the occlusion?

Here I point it out with a red arrow:

It was opened and stented:

Excellent flow

An ECG was recorded after PCI:

This appears to be a junctional rhythm (narrow) with a PVC (wide, complex 7)
The resolution of ST Elevation is a very reliable sign of reperfusion.
The narrow beats have T-wave inversion in V1-V5 and aVL, also signs of reperfusion

This was recorded the next AM:

There are QS-waves with some persistent ST Elevation
It would not be surprising if the patient ended up with an LV aneurysm (persistent STE after previous MI)

Last troponin I measured was 107 ng/mL at about 12 hours after presentation.

In the literature, this morphology has been called:

"Shark Fin". See here for search.

and also:

"Giant R-wave."

This was recorded 48 hours after ECMO started:

Less persistent STE, but QS-waves persist

Formal echocardiogram at about 24 hours after the event:

Amazingly, the ejection fraction was 55%! (there was an apical wall motion abnormality)

At 72 hours, he developed some chest pressure. He was also hypoxic with pulmonary edema. This ECG was recorded:

There is re-elevation of ST segments, and new upright T-waves, suggesting re-occlusion, but also consistent with postinfarction regional pericarditis.

There was thus worry for in-stent thrombosis, and the patient was taken back for repeat angiogram, but it showed open arteries.

What could account for these ECG findings? One possibility is postinfarction regional pericarditis, described below.

This was recorded at day 6:

There is some restoration of r-waves and some persistent STE.

The patient awoke without neurologic deficit.

Postinfarction Regional Pericarditis (not to be confused with Dressler's syndrome, which happens later)

Oliva et al. (1) strongly associated myocardial rupture with postinfarction regional pericarditis (PIRP), and associated PIRP with persistent upright T-waves.

He found 2 patterns of atypical T-wave development in PIRP:

1) persistently positive (upright) T-waves 48 hours after AMI onset, diagnostic of PIRP; and
2) premature, gradual reversal of inverted T waves to positive (upright) deflections by 48 to 72 hours after MI onset in the presence of well formed QS-waves.

The wide Q-waves suggest "transmural" MI (completed MI with infarction of the entire thickness of the ventricle). This was common in the days before reperfusion of STEMI, but still happens in patients who present late and therefore do not get timely reperfusion therapy, or who have very severe MI.

When there is MI extending all the way to the epicardium (transmural), that infarcted epicardium is often inflamed (postinfarction regional pericarditis, or PIRP). In addition, when there is full thickness infarction, especially with inflammation, the myocardium is at risk of "rupture." (2) The term "rupture" makes it sound like some sort of explosion or massive blowout, but it is usually a small, slow leak that, over time, can cause tamponade and death. Rupture can be either free wall rupture (causing tamponade) or septal rupture, causing ventricular septal defect with left to right flow and resulting pulmonary edema and shock.

If detected early by ultrasound, the patient can be saved. Our own Dave Plummer of HCMC reported on survival of 2 of 6 patients with free wall myocardial rupture diagnosed by bedside ultrasound in the ED.(3)

1. Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis: ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction. Circulation 1993;88(3):896-904.

2. Oliva PB, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 1993;22(3):720-6

3. Plummer D, Dick C, Ruiz E, Clinton J, Brunette D. Emergency department two-dimensional echocardiography in the diagnosis of nontraumatic cardiac rupture. Ann Emerg Med 1994;23(6):1333-42.

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MY Comment, by KEN GRAUER, MD (11/22/2019):

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Excellent case by Dr. Smith that details superb management with resultant miraculous save of this 40-something man with cardiac arrest. The Echos and cath films speak for themselves.

I limit my comments several advanced ECG interpretation concepts that I found fascinating. None of these ECG findings altered clinical results in this case — but they are worthy of mention, since awareness of these intriguing ECG findings may indeed be helpful in other cases.
For clarity and illustrative purposes — I’ve reproduced and labeled 3 of the 6 tracings shown in this case in Figure-1.

Figure-1: Three of the 6 ECGs that were done in this case (See text).

Comment on ECG #1 — As per Dr. Smith, the initial ECG in this case (ECG #1) — manifested a dramatic “Shark Fin” morphology that was diagnostic of acute proximal LAD occlusion.

Shark Fin morphology has been discussed a number of times on Dr. Smith’s ECG Blog. As per Dr. Meyers (ECG post from Oct. 4, 2019) — “When the QRS is wide, the J-point will hide. So, your next move is to Trace it down, and Copy it over”.
Following Dr. Meyers’ directive reveals how narrow the QRS complex actually is in ECG #1. I started by looking at leads V1,V2,V3 in this tracing — since I thought the R’ in lead V1, and the change in slope in the dramatic Shark Fin seen in leads V2 and V3, provided a good landmark for defining the end of the QRS complex (vertical DARK BLUE line in ECG #1). Tracing this DARK BLUE line down to the lead II rhythm strip complex suggested to me that the extra “hump” to the right of this BLUE line (RED arrow) was an Osborn wave!
“Copying over” this point where the DARK BLUE line under the 2nd complex in leads V1,V2,V3 intersected at the end of the QRS in the other 3 sets of simultaneously-recorded leads — yielded the LIGHT BLUE vertical lines in ECG #1. To me, this suggested the presence of prominent Osborn waves in multiple leads! (RED arrows).

OSBORN Waves: The Osborn wave has been described as a deflection with a dome or hump that occurs at the point where the end of the QRS complex joins with the beginning of the ST segment. This is the J-Point (ie, it Joins the end of the QRS with the beginning of the ST segment) — so Osborn waves are exaggerated J-point waves. They’ve also been called the “camel-hump” sign.

Osborn waves are most commonly associated with significant hypothermia (usually not seen until core temperature is below 90°F).
PEARL #1 — It is important to appreciate that other conditions may also be associated with this prominent J-point deflection. Osborn waves have been reported with hypercalcemia, brain injury, subarachnoid hemorrhage, Brugada syndrome, cardiac arrest from VFib — and — severe, acute ischemia resulting in acute MI (as in this case! ). The development of Osborn waves in association with acute ischemia/infarction may be a marker of impending VFib.

Comment on ECG #2 — There are several advanced ECG concepts associated with ECG #2.

The rhythm is not sinus! That’s because there is no upright P wave in lead II. In fact, there is no more than perhaps the tiniest negative “dip” of a P wave in lead II (GRAY arrow).
Note that P waves are more noticeable in the other 2 inferior leads (GRAY arrows highlighting negative P wave deflections in leads III and aVF).
Definite positive P waves are seen in leads I and aVL (BLUE arrows in these leads).
All of the above noted P waves are conducting — because the PR interval remains constant. This is a normal PR interval (~0.16 second).
PEARL #2 — The combination of P waves conducting with a normal PR interval — with a null or negative P wave deflection in the inferior leads — and positive P waves in leads I and aVL — suggests that rather than a junctional rhythm, there is a low atrial (or coronary sinus) rhythm in ECG #2.

Recognition of definite P waves in ECG #2 is important in helping to define what the wide beat ( = beat #7) in leads V1, V2 and V3 is.

I’ve labeled with the letters a, b, c — the 3 P waves that we see in lead V1 of ECG #2 (BLUE arrows in this lead). Note that this low atrial rhythm remains regular throughout (P waves a, b, c are all right on time) — which tells us that the initial tiny positive deflection in front of the wide beat (beat #7) is the initial part of an on-time P wave!
Beat #7 is clearly of ventricular etiology. But given that an on-time P wave precedes it with a shorter-than-expected PR interval — beat #7 is almost certainly a Fusion beat (ie, with delayed and partial conduction of the P wave labeled “b” — that “fuses” with the ventricular beat).
I like to distinguish further the type of “PVC” that beat #7 is. Yes, it is “premature” — because it occurs slightly before where the next normally conducted sinus beat would be seen. But this is a “late-cycle” (ie, end-diastolic) PVC — which is important, because it carries the same clinical significance as the rhythm AIVR (Accelerated IdioVentricular Rhythm) does in a patient with acute MI — namely, that it is a marker for reperfusion! As per Dr. Smith — the resolution of ST elevation + T wave inversion in ECG #2 are other markers of reperfusion in this case. That said = PEARL #2 — Sometimes the onset of either AIVR and/or late-cycle PVCs may suggest there has been acute reperfusion before you see resolution of ST elevation and T wave inversion!
Finally — Note that prominent Osborn waves are still present in many leads in ECG #2 (RED arrows).

Comment on ECG #4 — I believe ECG #4 supports my previous comments regarding how narrow the QRS complex actually was in ECG #1 — as well as that RED arrows in the prior tracings did in fact represent prominent Osborn waves.

Using the vertical lighter and darker BLUE lines in ECGs #1 and 2 as the end point of the QRS complex — it appears that this very narrow QRS morphology remains consistent through all tracings! This supports that the “extra hump” (RED arrows) were indeed prominent Osborn waves — which finally resolve (light GREEN arrows) in ECG #4 as the patient improves.

Our THANKS again to Dr. Smith for this fascinating case with positive clinical result!

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Global ST depression with ST elevation in aVR - what is the cause?

November 26, 2019, 9:08 am

≫ Next: A 50-something Australian with sudden severe epigastric and chest pain presented looking extremely ill.

≪ Previous: Persistent Ventricular Fibrillation, ED ECMO, ED TEE, ROSC, Shark Fin ECG (also called "Giant R-wave"), Postinfarction Regional Pericarditis. What a Case!

Written by Pendell Meyers

An elderly patient with cardiac history presented with shortness of breath. This ECG was brought to me with concern for diffuse ST depression and STE elevation in aVR.

What is your response?

Flutter waves are simulating diffuse ST depression, and therefore there must be the reciprocal finding of apparent STE in aVR.

The ventricular rate is slightly greater than 100 bpm, with 2:1 block. This means an atrial flutter rate of 200 bpm, which is somewhat unusual unless the patient has a very large, dilated left atrium and/or antidysrhythmic medications which slow the speed of action potential conduction (typically class 1, Na channel blocking agents).

AV nodal blocking agents were given and the rhythm changed to atrial flutter with slower, variable block (strip not available unfortunately).

The patient did not have ACS. Three troponins were negative. The patient was treated for atrial flutter and did well.

Learning Point:

Atrial flutter can mimic diffuse ST depression, which always must cause reciprocal ST elevation in lead aVR. It can also mimic ST elevation, or conceal true underlying ST deviations. See these other cases for examples: