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Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer.

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I was handed this ECG of a patient with dyspnea:

What do you think?

Computer interpretation: Normal EKG
Physician Overread (Final interpretation): Normal EKG





















The ST segment is very flat, with a sudden rise to the peak of the T-wave.  This makes the base of the T-wave look very narrow.  A narrow-based T-wave is nearly pathognomonic for hyperkalemia.  My diagnosis was hyperkalemia.

The resident I showed it to saw nothing.  I explained all this to the resident, then went to see the patient.

Turns out he is a dialysis patient.

Later, the ECG computer interpretation was overread by another physician, and that physician thought it was normal, but took the step to compare with the most recent previous ECG.  There was no change, so that physician concluded that it was indeed normal and entered "Normal EKG" as the final diagnosis.

However, I looked a bit more in depth, and the previous ECG had also been recorded during hyperkalemia.

The K returned at 6.3 mEq/L.

Let's look at a couple previous ones from 2 years prior:

This was recorded when this patient presented with diaphoresis and muscle cramps:
The formal read was normal except for "possible old lateral MI"
QTc was measured at 484 ms which appears to be accurate, but the statement did not say "long QT"

There are definitely peaked T waves, and a long flat ST segment with an abrupt rise to the peak of the T-waves.

The K was 6.6 mEq/L

What else do you suspect?

This ECG was recorded a few hours later after bringing down the K to 4.8 mEq/L.:
These are now normal T-waves.
Can you see the difference between these and the T-waves in the 1st 2 ECGs?


Computer interpretation AND physician overread:
Normal except for long QT (486 ms)

The other thing you might have suspected is hypocalcemia, as the long QT is long because of a long ST segment (not because of a wide T-wave). 
The (not ionized) Ca on these 2 ECGs was 6.4 mg/dL (very low)
On the first ECG above, the QTc was 402 ms and the Calcium was normal.

The diagnosis was fluid overload and hyperkalemia.  Dialysis fixed both.

Learning Points:

1. Peaking of T-waves can be very subtle
2. Comparison with previous must be done with a previous that is recorded in the presence of a normal K.
3.  Peaked Ts are not necessarily large or tall.  They have a narrow base, and a sharp upstroke.  Often they look as though they would puncture you if you sat on them.
4.  Early repolarization and even LVH can have T-waves that mimic hyperK.
5. Having the physician read every EKG, whether the computer calls it normal or not, is of course only useful if the physician can recognize the abnormality

If you miss hyperK T-waves, your patient may have an unexpected cardiac arrest:

Here is a really interesting post, in which a patient with very subtly peaked T-waves, which are misinterpreted as early repolarization, has a ventricular fibrillation arrest before the K returns high:

HyperKalemia with Cardiac Arrest. 

Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia



===================================
Comment by KEN GRAUER, MD (6/15/2019):
===================================
Instructive case! I focus My Comments on ECG #1 = the initial ECG obtained in the ED (Figure-1). In my opinion, rather than calling this ECG “normal” (as did 2 clinicians and the computer) — there are ECG findings that should be noted: iProlonged QTc; iiLVH, clearly by voltage; iiiST segment straightening in multiple leads; andivTall, peaked (and pointed) T waves with a narrow base in at least 4 of the 6 chest leads. 
  • While I fully acknowledge that some of these ECG findings are subtle — I submit that recognition that this ECG is not “normal” would not have been overlooked IF interpreters had used a Systematic Approach (For “My Take” on how routine use of a Systematic Approach not only improves accuracy, but also speeds you up — See Dr. Smith’s May 7, 2019 Blog).
Figure-1: The initial ECG done in the ED (See text).

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

Beginning with Descriptive Analysis:
  • There is baseline artifact in ECG #1 — which is most marked in the limb leads. That said, this does not prevent accurate interpretation of the key findings.
  • Rate & Rhythm — The rhythm is sinus at ~85/minute. Intervals  The PR interval is normal. The QRS complex is not wide. However, the QTc is somewhat prolonged. I measure the QT = 400 msec (See markings in lead V3). Correcting for the heart rate of 85/minute — I estimate a QTc ~470-480 msec (which is clearly above the upper expected range ~440 msec).
  • Axis  The frontal plane QRS axis is normal (about +30 degrees).
  • Chamber Enlargement — There is no atrial abnormality, and no RVH. But voltage criteria for LVH are definitely satisfied! I have reviewed “My Take” on a user-friendly approach to ECG diagnosis of LVH in Dr. Smith’s April 27, 2019 Blog. For ease of recall — I’ve excerpted the user-friendly criteria I favor in Figure-2. ECG #1 is an example in which the most commonly helpful criteria (35& 12— as per Figure-2) are negative — but both Cornell Criteria (R in aVL + S in V3 ≥28 for a manand especially Peguero Criteria (deepest S + S in V4 ≥28mm for a manare met. NOTE: Short, horizontal BLUE lines in leads V4 and V5 indicate the limits for R wave and S wave amplitude in these leads, in which overlap of complexes makes assessment a bit challenging.
  • Q-R-S-T Changes  There are small, narrow Q waves in leads V5 and V6 (most probably normal septal q waves). R Wave Progression — shows slightly delayed transition (the R becomes taller than the S wave is deep between lead V4-to-V5). ST-T Waves — show ST segment straightening (short PURPLE lines in leads V4,V5,V6) and frank ST flattening (PURPLE lines) in leads V2 and V3. This is not normal — as the ST segment should normally be gently upsloping (Please see My Comment in Dr. Smith’s June 9, 2019 Blog). And, there is even a hint of ST depression in leadsV5 and V6.
  • As noted by Dr. Smith — it is because of this ST segment straightening and flattening in multiple chest leads — that the abnormal shape of the T waves in leads V2-thru-V6 should be noted. As a memory aid — the shape of the Eiffel Tower (= tall and rising to a point at the top, but with a surprisingly narrow base) — should recall the shape of typical hyerkalemic waves (See Figure-1).
Putting this Together to formulate your Clinical Impression:
  • After looking at the ECG in Figure-1 — my thoughts were that we needed to knowmore about this patient! I saw sinus rhythm — a prolonged QTc — definite LVH by voltage — and, ST segment straightening + flattening (and slight ST depression) T waves in multiple leads that strongly suggested hyperkalemia.
  • The fact that the QTc is prolonged in association with hyperkalemia should suggest that there may also be hypocalcemia (these 2 electrolyte abnormalities in patients with renal disease so often go hand-in-hand). Although sensitivity and specificity of the ECG is far from optimal for detection of hypocalcemia — the morphologic picture we see here (ie, with fairly straightened but not elevated ST segments, at the end of which appears a hyperkalemia-looking T wave) should strongly suggest this possibility, especially in a patient with severe renal disease.
  • NOTE  Marked LVH is very common in chronic dialysis patients. The reason why T waves in ECG #1 are not all that tall in multiple leads — and why ST-T wave changes typical for LV “strain” are not seen — might be that these 2 conditions are each attenuating ST-T wave effects of the other (ie, IF on a “baseline” of marked LVH + “strain”, serum K+ then becomes markedly elevated — then you might see exactly the ST-T wave pattern we see here in Figure-1in which there is diffuse ST straightening with slight lateral ST depression + relatively modest T wave height in most leads given the high K+ value = 6.3 mEq/L).
  • P.S.  Very important point emphasized by Dr. Smith! — when going back in the patient’s chart to look for prior tracings — BE SURE (as best you can) to determine the patient’s clinical status athe time the baseline” tracing was done. This is why peaked and pointed T waves looked “unchanged” from the first prior tracing in this case — when the patient’s serum K+ was also high ( = 6.6 mEq/L) at that time.

Figure-2: The user-friendly criteria I favor for ECG diagnosisof LVH (For my source —  CLICK HERE).




More precise interpretation of the results of the 4-variable formula.

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If you haven't heard of the 4-variable formula for differentiating Normal Variant ST Elevation in V2-V4 from Ischemic ST Elevation due to LAD occlusion, then go here:

12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion


I have often said that the closer the formula value is to the cutpoint of 18.2, the more accurate.

But how wide is the variation?

Here I plot the graphs:

Specificity
Specificity is 97% at a cutpoint of  20.7


Sensitivity
Sensitivity is 97% at a cutpoint of 17.0


Accuracy



===================================
Comment by KEN GRAUER, MD (6/17/2019):
===================================
Today’s brief Blog post illustrates insightful sensitivity, specificity and accuracy data for use of Dr. Smith's 4-Variable Formula for differentiating between normal variant ST elevation in leads V2-thru-V4 from ischemic ST elevation due to LAD occlusion.
  • Near the top of the page is a LINK to 12 Example cases. I’m repeating the link to this page — because it provides an excellent opportunity for REVIEW! (LINK to 12 EXAMPLE CASES — from Dr. Smith’s November 3, 2017 Blog).
  • For each of these 12 cases — Dr. Smith provides Formula values and specific commentary on the ECG abnormalities present — followed by “the Answer” (ie, if the ECG turned out to be a case of acute LAD occlusion or a repolarization variant ). It is worth spending a few minutes going through these 12 cases to solidify your understanding and to “hone” your acute ECG diagnostic ability.
MTHOUGHTS: I think Dr. Smith said it BEST in answer to one of the commenters on this November 3, 2017 blog (Figure-1):
Figure-1: Comment by Dr. Smith on November 6, 2017 in answer to one of the commenters (See text).
================

  • Dr. Smith’s formulas serve as an AID. The amount of assistance they provide may vary, depending on the experience of the interpreter. You don’t need the formula — if you recognize that the ECG is clearly abnormal and suggests acute LAD occlusion. Even if the formula were to be “negative” in such a case — this should not dissuade you from acting as if there is acute LAD occlusion.
  • In participating in an ECG study with Dr. Smith — I had the opportunity to interpret 1,000 tracings, in which I was immediately provided with the Formula calculation. To keep myself “honest” — I always interpreted each of these ECGs first — and only then looked at the Formula value. I found knowing the Formula value to be very comforting in my interpretations! When I thought the ECG was negative for acute occlusion — knowing that the Formula value was clearly below the “cutpoint threshold” was exceedingly reassuring, and allowed me much more quickly to move on to the next tracing. On the other hand — learning that the Formula value was near (or above) the cutpoint alerted me to much more closely go back and review those occasional tracings that I otherwise would have thought were negative. As per Dr. Smith in his Comment above (Figure-1) — I too was occasionally surprised by the Formula value! — and on those occasions, awareness of a higher-than-anticipated Formula value was extremely helpful to me!
In my opinion — each of the 12 Example Cases at the above link that were positive manifest morphologic features that should suggest possible acute LAD occlusion even without use of the Formula. We have discussed these features on numerous occasions in this ECG Blog — but it may be helpful to repeat them here: KEY ECG Features that may suggest PossibleLAD Occlusion include the following:
  • One or more of the chest leads show T waves that are disproportionately tall (compared to the R wave in the same lead) — as well as being fatter-than-they-should-be at their peak and/or wider-than-they-should-be at their base.
  • Loss of the normal upward concavity of the ST segment upslope (being replaced by straightening of the ST segment takeoff — or by coving of the ST segment).
  • Poor R wave progression (ie, loss of anterior R wave amplitude, compared to what should be expected).
  • Unexpected ST elevation in lead V1.
  • Reciprocal ST-T wave changes in the inferior leads (including unexpected ST-T wave flattening in these leads).
  • Unexpected ST elevation in lead aVL.
  • NOTE #1: Sometimes the above ECG findings in one or more leads may be subtle. I always lookfirst for those one or two leads in which there is NOdoubt about the abnormality. It often becomes easier to identify more subtle abnormalities in neighboring leads after identifying one or two leads that are clearly abnormal.
  • NOTE #2: The moreleads showing abnormal ST-T wave findings — the greater the likelihood of acute ischemia. In each of the 12 Example Cases at the above link — there were atleast 2 definitely abnormal leads plus several additional leads with more subtle changes.
BOTTOM LINE  For any provider, ready availability of Dr. Smith’s 4-Variable Formula value can be an invaluable aid for teaching, expediting clinical decision-making, and improving accuracy. While I personally prefer to interpret ECGs before I am told the Formula value — others may prefer to use the Formula value sooner, as a “heads up” to alert them to a high likelihood of an abnormal ECG.
  • P.S. — Be aware of EXCLUSIONS for using the Formula.





ROSC: does the ECG rule out OMI? And why does a heart just stop beating? And what rhythm is this?

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A 60-something was outside walking with a friend when he suddenly stated that he "felt weak," without chest pain or SOB or headache, and dropped to the ground, pulseless.  She did CPR and called 911. When medics arrived he was pulseless and the monitor showed a slow wide regular pulseless rhythm.

After several minutes of excellent resuscitation, they achieved ROSC.

In the ED, he was intubated, TTE showed very poor cardiac function, and a TEE was placed, as well as arterial line and central cooling catheter.

Here was the first ED ECG:
There is sinus tach (see the P-waves in V1? The small up-down waves?)
The P-waves in lead II are superimposed on the T-waves.
There is a nonspecific intraventricular conduction delay.
There is no clear evidence of OMI.
There is some ischemic ST depression in V4-V6, but it is not profound.

Here are causes of sudden cardiac arrest, and relevance to this case (H's and T's):
  • Hypoxia --  does not fit
  • Hypovolemia -- Causes would be GI bleed, Rupture AAA, other ruptured vessel such as mesenteric aneurysms. None of these fit for such a sudden arrest
  • Hypothermia -- does not fit
  • Hypo/hyperkalemia -- K was normal
  • Hydrogen ions -- Lactate was 8 in spite of being measure after arrest.  Anyway, life-threatening acidosis does not happen so rapidly
  • Hypoglycemia -- this is a reason to have coma, but not sudden cardiac arrest
  • Thrombosiscoronary or pulmonary -- either of these are likely culprits
  • Tamponade– cardiac -- ruled out immediately by echo
  • Toxins -- is there any toxin that causes arrest so fast?  Cyanide?
  • Tension pneumothorax -- doesn't fit, and patient was ventilating well, had breath sounds, and sliding signs.
  • Trauma -- History doesn't fit.

Coronary or Pulmonary thrombosis
--Pulmonary embolism: did not fit, as the TEE showed a lot of B-lines and the RV was normal
--He had been well until the moment of weakness.

The only explanation in my mind was a sudden massive coronary occlusion, such as left main.  When occluded, the heart can just stop functioning.  The heart might just stop beating, without dysrhythmia (without VT or VF).

How do I know he didn't start with a VF arrest?  Because his initial rhythm was organized. VF does not re-organize itself except in very rare circumstances:
This is an amazing case for many reasons:

Ventricular Fibrillation During Echocardiogram, Then Spontaneous Conversion Without Defibrillation


Case continued

I had just requested a cardiology evaluation for emergent angiogram in the absence of STEMI when he had another arrest.

We resuscitated him again, and he was then more hypotensive and in atrial fib with RVR, so we cardioverted to a regular rhythm, which helped with perfusion.

Here is the 12-lead ECG after re-arrest:
What is the rhythm?  Is it ventricular tachycardia (VT)?
Is there any evidence of OMI?

Rhythm
One might think this is VT, but if you look at beats 15 and 16 across the bottom, they are PVCs, and the 2nd PVC is followed by a P-wave and then a conducted beat, proving that the rhythm is sinus rhythm.
If you assess the PR interval, then go to other complexes, you can see that the P-wave in the first 14 complexes, and in 18-23, is superimposed upon the T-wave.

QRS?

Appears to be RBBB and LAFB 
(a very bad combination, often associated with left main thrombosis)

OMI?
There is no clear ischemic ST Elevation.  
Inferior leads have what may seem to be ST Elevation, which should not occur in RBBB.
And aVL appears to have some ST depression
However, if you look closely, the J-point really is isoelectric
The fact is that the ECG commonly fails to show evidence of OMI.  In this recent large study of consecutive chest pain patients, ST elevation was only 21% sensitive for OMI, and 6% sensitive for any acute MI.  We have submitted a manuscript showing very poor sensitivity of the ECG for OMI in cardiac arrest patients with a shockable rhythm who were resuscitated.

Should all patients with shockable arrest be taken to angiography regardless of STEMI or No STEMI?

There has long been controversy about whether to take patients with a shockable rhythm without ST Elevation to the cath lab, and a recent randomized trial showed no benefitCoronary Angiography after Cardiac Arrestwithout ST-Segment Elevation
This study had a fatal flaw: they did not keep track of all the Non-STEMI patients who were NOT enrolled, but instead were sent for immediate angiogram.  It was done in Europe, where the guidelines suggest taking all shockable arrests emergently to the cath lab.  So it is highly likely that physicians were very reluctant to enroll patients; they did not want them to be randomized to no angiogram.  This strong suspicion is supported by their data: only 22 of 437 (5.0%) patients in this study had OMI.

What percent of shockable arrests without STE have an OMI?  

This large registry in Circulation 2010 reported that at least 1 significant coronary artery lesion was found in 128 (96%) of 134 patients with ST-segment elevation on the ECG performed after the return of spontaneous circulation, and in 176 (58%) of 301 patients without ST-segment elevation

5% vs. 58%!!  So there is definitely enrollment bias.

The etiology of arrest in non-shockable rhythms is much less likely to be OMI (I don't know the exact number here).  

Even though most OMI causes VT/VF, when the ischemia is overwhelming, such as in Left Main occlusion or near-occlusion, the heart may just stop beating.

Seeing no other etiology than OMI, and knowing that the only chance for survival was to find and open a coronary artery, I activated the cath lab.

He was taken to angiogram in a very unstable condition on an epinephrine drip.  The angiogram showed:

LM: 90%
LAD: 100%, probably chronic
RCA: moderate to severe proximal RCA, and acute distal rPLA1 100% (probable acute) occlusion.  Prior to occluding, it was supplying almost the entire territory of the left main through collaterals.

The LM and rPLA1 were stented.

The patient stabilized.

After PCI



Outcome

The patient had an unstable course but did wake up and stabilized but with severe ischemic cardiomyopathy, EF 15%.


Learning Points:

The pretest probability of OMI in cardiac arrest is very high.  In patients with chest pain, only 1-5% have OMI, so the negative predictive value (NPV) of the ECG is pretty high, even though the sensitivity of the ECG for OMI is low.  In shockable cardiac arrest, and in non-shockable cardiac arrest without any other etiology, the pretest probability of OMI is very high, so the NPV of the ECG is very poor.

More literature

In this 1997 NEJM study, 48% of shockable ROSC cardiac arrests were due to coronary occlusion; 1/4 of these had no ST elevation.  Immediate coronary angiography in survivors of out-of-hospital cardiac arrest

We have submitted a study of the ECG in shockable resuscitated cardiac arrest:  My sensitivity and specificity for occlusion on the angiogram was 75% and 85%.  The cardiologist who read the same ECGs had sensitivity and specificity of 62% and 77%.  So even I cannot see 25% of OMI on these ECGs.  

Interestingly, the 2nd ECG, after stabilization, had an overall sensitivity for OMI of only 26%!!

Do you recognize these ECGs? STEMI? LVH? What?

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What do you think of these ECGs?

I came across the first one reading it blind for a study.  I was certain I knew the diagnosis, and went to the chart to confirm.

The first 3 were recorded on one day.

ECG 1:



ECG 2:



ECG 3:




ECG 4, recorded 12 days later:













These ECGs are classic for a benign variant in Black males.  I was certain it would be a relatively young black male without cardiac pathology.

Result from chart:

It was a black male in his 40s.

The first ECG, and then the next two (1-3), were recorded for chest and abdominal pain.  The patient was ultimately diagnosed with biliary colic.

The patient ruled out for MI by serial trops.

The second presentation (ECG 4) was for epigastric pain due to GERD.

After ruling out for MI both times, the formal ECG diagnosis was LVH. But we know that this pattern is nearly always a normal pattern for black men (although one cannot be 100% certain and an echo is important especially to rule out hypertrophic cardiomyopathy).

An echocardiogram was completely normal.  No LVH.


See this article published this month by Brooks Walsh, Smith, and others in Journal of Electrocardiology: 

Distinctive ECG patterns in healthy black adults

Journal of Electrocardiology

Volume 56, September–October 2019, 
Pages 15-23



ST segment concavity is just one small piece of the puzzle that is pattern recognition

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Written by Pendell Meyers

Here are two striking examples from a single shift highlighting the fallibility of the standard "smiley face" or upwardly concave ST segment morphology "rule".

Case 1.
Obvious STEMI and OMI with massive STE in the inferior and lateral leads, even extending back into V3. 
All STE has concave upward (smiley face) morphology. V2 shows STD indicating posterior involvement. 
V1 may be in a tug-of-war between STD from posterior involvement and STE from possible RV involvement. 
Reciprocal STD in I and aVL. 
Sinus bradycardia with first degree heart block present, clearly high risk for worsening bradycardia and/or heart blocks.

I received this ECG via telemetry from an ambulance far from our hospital. There was another cath center closer than our institution, so we agreed they should go there and advised they activate their cath lab immediately. Before our conversation was finished, the patient went into VF arrest and they hung up. I was unable to get back in touch with them for the outcome.


Case 2.
Hyperacute T-waves in V2-V6, I, and aVL. STEMI criteria met by the STE in V6, I, and aVL. Reciprocal STD in III and aVF. V5 has very diminished voltage and poor quality, suggesting some combination of lead misplacement and/or physical object between it and the patient (hair, defibrillation pad, medical cables, clothing, etc.).

I received this also by telemetry, and again we agreed with their plan of the nearest cath center and activated their cath lab protocol. He was found to have proximal LAD occlusion, but other outcome details are not available.





We are taught in medical school that concave upward ST segment morphology is a feature of benign STE, pericarditis, etc.

In actuality, 40-50% of acute LAD occlusion have upwardly concave ST segment morphology in all of V2-V5.


Smith SW. Upwardly concave ST segment morphology is common in acute left anterior descending coronary artery occlusion. Journal of Emergency Medicine 2006; 31(1):67-77.


In anther study of 355 LAD occlusions, only 36 of 355 LAD occlusions were excluded as "obvious" due to non-concave morphology:


Smith SW et al. Electrocardiographic Differentiation of Early Repolarization from Subtle Anterior ST-Segment Elevation Myocardial Infarction. 

https://www.annemergmed.com/article/S0196-0644(12)00160-6/pdf

Brady et al. looked at all sites of MI and found that non-concave morphology had sensitivity and specificity of 77% and 97%, with PPV and NPV of 94% and 88%.


Brady, W. J., et al. 2001. Electrocardiographic ST Segment Elevation: The Diagnosis of Acute Myocardial Infarcton by Morphologic Analysis of the ST Segment. Academic Emergency Medicine 8 (10): 961–67.


Learning Points:

Concavity (aka "upward concavity") is just one small piece of pattern recognition of OMI, and is not reliable to assuage concern by itself.

Up to half of LAD occlusions have concave ST segments, and overall non-concavity (upwardly straight or convex) is optimistically 77% sensitive for OMI of all MI sites (including inferior), but is far less sensitive for anterior OMI.

2 ECGs texted to me. Minimal STE in inferior leads. How important is it?

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These 2 ECGs were texted to me with the words "I think acute MI, but cardiology does not."

I believed these to be 2 serial ECGs:

ECG 1: (later found to be time zero):
Computer read: "minimal ST depression 0.025 mm"
There is a small amount of STE in II, III, aVF
From less than 0.5 mm - 0.5 mm.
There is les than 0.5 mm of reciprocal ST depression in aVL, and an inverted T-wave

And the other: (later found to be time 24 minutes):
Now there is more STE and more STD
One very telling finding are the ST segments in V2-V6:
ST depression has developed in V2-V6, downsloping in V4-V6.
Though minimal, this is very specific adjunctive data for ECG diagnosis of MI.

This was my response:

"It looks like a myocardial infarction...Does the patient have chest pain?"

History:

Syncope in clinic, some vague chest pain.

Not a great history, so we looked for a previous ECG:
From within the last year
No STE, no STD.
This makes the others diagnostic.

Cardiology had wanted the patient to be admitted, but had not seen evidence of acute MI and had not wanted the cath lab activated.

In spite of this, my partner and I agreed the cath lab should be activated, so he did activate.

Just before transport, another ECG was recorded at time 71 min, prior to cath:
Now obvious inferior and posterior STEMI.


The patient had a ventricular fibrillation arrest before the angiogram, and was resuscitated.

Angiogram: 100% distal RCA occlusion.

After cath, next day:
Reperfusion T-wave in III.
STE resolved.


Peak trop 47.4 ng/mL (large MI)


Echo: Regional wall motion abnormality-inferior, EF 60%. 

Learning Points:

1. In the original thrombolytic trials (the only placebo-controlled reperfusion trials!), especially GISSI-1, treatment of inferior MI with streptokinase did not have a measurable effect on mortality outcome.  Here we see what appears to be an electrocardiographically tiny inferior MI, which only later becomes large.  The patient arrests and has a very high troponin.  So don't be fooled by an apparently small inferior MI.
2. Do serial ECGs.
3.  Compare with a previous ECG.
4. You must push to get patients who need it to the cath lab.
5.  Cardiologists have a huge amount they have to know, spanning an enormous specialty.  They do not always have time to learn the subtleties of OMI on the ECG.  
6.  You have to be the expert!!


Serial Evolving ECGs all diagnostic of LAD OMI, but never meet STEMI criteria

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A 60-something called 911 for chest pain.

Medics recorded an ECG at time zero:

What to you think?



There is no ST elevation, but V2 has a definite hyperacute T-wave.  Inferior leads have a tiny bit of ST depression (this is very significant).  aVL has a tiny amount of coved ST elevation in the presence of a tiny QRS.  These are all very very suspicious for proximal LAD OMI.

They recorded another at 20 minutes:
 
Evolving anterior OMI, but with barely any ST Elevation.
 Look at the huge size of the T-wave in V4 relative to the R-wave.
Increasing STE in aVL
Increasing inferior reciprocal ST depression

If you doubted LAD occlusion on the first one, there is no doubt any more.
This is diagnostic
Repeat at 25 Minutes:

Further evolution.
Absolutely diagnostic of acute LAD occlusion.



And another at 30 minutes:

The computer never noticed the myocardial infarction on any of these ECGs.


The patient arrived in the ED.

This is the first ED ECG (at t = 40 minutes):
Computer did not comment on acute MI.
The attending physician brought this to me without any of the other ECGs and asked my opinion:
With 3 seconds, I said:
Acute LAD Occlusion.
It is diagnostic of LAD occlusion all on its own, without even comparing to the others.

This is what my partner thought also, but just wanted confirmation.

The cath lab was activated.

2nd ED ECG 60 minutes
Now there is diagnostic ST Elevation, but barely.
Computer still did not comment on STEMI



A Proximal LAD occlusion was found and stented.

ECG after reperfusion
Typical Reperfusion T-waves, similar to Wellens' waves (and same pathophysiology), but different in that true Wellens' waves have preservation of R-wave.   This has a QS-wave in V2 because of extensive infarction, in spite of rapid reperfusion.


Next day
QS-waves with reperfusion T-waves again

Peak trop I 85.6 ng/mL (very large OMI)

Anterior Wall Motion Abnormality

At no point in time did the computer read a STEMI

Learning Points:

1. Acute LAD occlusion frequently does not manifest ST Elevation that meets "criteria"
2.  Look for hyperacute T-waves (relative to QRS amplitude/voltage)
3. Look for any inferior ST depression, even minimal
4. Do serial ECGs.





















Inferior Subtle ST elevation: straight ST segment, but also no reciprocal ST depression in aVL: which is more important?

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60-something with h/o MI and stents presented with chest pain radiating to the back and nausea/vomiting.

Time zero

What do you think?












There is inferior ST elevation.  Is it normal variant?  Is it ischemic (OMI)?  [Pericarditis? (NOT!)]

There is one finding that argues against inferior OMI (There is absence of reciprocal ST depression in aVL; STD aVL is extremely sensitive for inferior OMI;   Reference: Bischof and Smith). 

However, there is also straightening of the inferior ST segments, and a straight ST segment in aVF; this is extremely rare in normal variant STE).
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There is also terminal QRS distortion in II, III, aVF [absence of S-wave and J-wave (notch)].  The significance of this in inferior leads is unknown, but I suspect it is a marker for inferior OMI vs. normal variant.

Terminal QRS distortion is definitely significant for anterior OMI in V2 and V3:

An intoxicated, agitated, 20-something with chest pain

______

Here is an ECG from one month ago:
There is a definite change in the inferior leads, with new ST elevation.
Previously, all inferior leads had appropriate upward concavity.



The patient was given aspirin, heparin, and IV nitroglycerine.

Another ECG was recorded at 35 minutes:
It is hard to discern a difference


At this point, the first troponin I returned at 0.55 ng/mL (significantly elevated)

A D dimer was also elevated.

Another ECG was recorded at 58 minutes:
Again, no big difference.


There was concern for aortic dissection, so a CT was done and was negative.

The cath lab was activated:

Result: Thrombotic 95% stenosis at the ostium of a small LPL2 with 70% stenosis at the LPL2/LPDA bifurcation in the distal/AV groove Cx Tubular 70% stenosis in the mid-circumflex.  (In other words, inferior MI with some posterior involvement).  It was stented.

For coronary anatomy, see here: https://www.pcipedia.org/wiki/Coronary_anatomy


This is the post intervention ECG:

All ST Elevation is gone (more proof that it was all a result of ischemia)

Formal Echo:

Normal estimated left ventricular ejection fraction - 55%.

Regional wall motion abnormality-mid and basal inferior .

Troponin I peaked at 12.1 ng/mL.

Learning Points:

1. Any inferior ST elevation may be acute OMI, but there are subtle differences between OMI on the one hand, and normal variant on the other.
2. 99% of inferior OMI are either obvious or have some amount of ST depression in aVL.  But 1% may be/have neither!
3. In this case, one might say it is "obvious" MI because of a straight ST segment in aVF.  A straight ST segment virtually never happens in inferior ST elevation that is NOT due to OMI (normal variant, pericarditis)
4. If a patient presents with symptoms of ACS, has an elevated troponin, and has persistent symptoms in spite of medical therapy [antiplatelet, antithrombotic, and anti-ischemic (nitro)], then cath lab activation is indicated regardless of ECG findings.
5. Compare with an old ECG.
6. Record serial ECGs.


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Comment by KEN GRAUER, MD (6/28/2019):
===================================
I like this case because it provides an excellent example of how to use comparison tracings in a patient with a prior history of coronary disease.
  • For clarity — I’ve put the first 2 ECGs shown in this case together in Figure-1. To highlight KEY findings — I’ve enlarged one complex in leads II, III, aVF and aVL, that I’ve placed to the right of each of the 12-leads.
Figure-1: The first 2 ECGs shown in this case — with enlargement of leads II, III, aVF and aVL to the right of each tracing (See text).


The CASE: The patient is a 60-something who presented to the ED with new-onset chest pain. The patient had a prior history of MI stents.
  • KEY Points: This patient has known coronary disease. Therefore: iThe initial ECG may show signs of prior injury; iiECG evidence of new OMI may be subtle; it may be difficult to distinguish “new” from “old” ECG findings from the initial ECG alone (ie, from ECG #1 alone in Figure-1); andiiiFinding a prior ECG on this patient may provide invaluable assistance!


QUESTION:   regarding ECG #1: Before you looked at the prior ECG in this case (which is ECG #2 in Figure-1) — YOU should have seen abnormal findings in the chest leads of ECG #1! — Did you??? —
  • HINT: It would have been EASY to overlook these 3 findings if you were not systematic in your interpretation ...


MTHOUGHTS on ECG #1  The rhythm is fairly regular, at a rate between 55-60/minute.
The QRS is narrow. This is sinus bradycardia.
  • All intervals (PR, QRS duration, QTc) are normal.
  • The frontal plane axis is normal (about +65 degrees).
  • There is no chamber enlargement.
Regarding Q-R-S-T Changes:
  • There are Q waves in multiple leads, including leads I, II, III, aVL, aVF; and in leads V3-thru-V6. Most of these Q waves are small and narrow. Many are unlikely to be clinically significant. That said — although tiny, the in aVL of ECG #1 could reflect lateral MI of uncertain age given how small the QRS is in this lead (Note in the Blow-Up view that the initial deflection in lead aVL of ECG #1 is negative = a Q wave).
  • While the Q waves in leads V4V5 and V6 are narrow — they are a little deeper-than-usual for normal septal q waves. In this patient with documented coronary disease — these q waves could reflect prior lateral infarction (especially in view of the Q in lead aVL).
  • Regarding R Wave Progression —Transition is early! In fact — in lead V1, and this is not a “normal” finding! Because LV (left ventricular) forces predominate in a normal ECG — there is usually no more than a small initial r wave in lead V1, which is normally associated with a fairly deep S wave in lead V1 (this deep negative deflection in right-sided lead V1 results from the normal predominance of LV forces).
  • NOTE: Computer interpretations almost always miss detection of a Tall R Wave in Lead V1. Many (if not most) clinicians also often overlook this important finding if they are not systematic in their approach. This is precisely the reason why I add an R” to my memory aid of looking for Q-R-S-T Changes” — because it is otherwise all-too-easy to forget about routinely looking to see if R wave progression is appropriate.
  • PEARL: Recognition of a Tall Wave in Lead Vshould prompt quick recall of a list of the 6 Common Causes — one of which is posterior MI. This is highly relevant to this case! (CLICK HERE — for discussion on how to distinguish between these 6 entities).
  • For review of “My Take” on the Systematic Approach to ECG Interpretation that I favor — CLICK HERE —
Returning to this case for the last 2 parameters in my Q-R-S-T assessment of ECG #1 = ST-T Wave Abnormalities:
  • We’ve already noted small-but-present-in-all-3-inferior-lead Q waves. The Blow-Up view to the right of 12-lead for ECG #1 shows the features already highlighted above by Dr. Smith = inferior lead ST elevation straightening of the ST segment upstroke in lead aVF terminal QRS distortion (ie, lack of an S wave and J wavein each of the 3 inferior leads. More than this, the ST-T waves in each of these inferior leads just look” acute (with T waves taller-and-fatter-than-they-should-be).
  • The T wave in lead aVL of ECG #1 is not normal. Instead, the entire ST-T wave in lead aVL is flat— and it shouldn’t be.
  • In the chest leads — T waves in leads V2-thru-V5 (if not also in V6) appear taller-and-more-peaked-than-they-should-be. While I doubted hyperkalemia as the cause — I’d check serum K+ to be sure. More likely, these T waves probably reflect ischemia of uncertain age.
MIMPRESSION of ECG #1: In this patient with a history of documented coronary disease new-onset chest pain — one has to assume new inferior OMI until proven otherwise.
  • ANSWER to the aboveQUESION: The abnormal ECG findings in the chest leads of ECG #1 that you should have noted before you looked at ECG #2 are: iThe Tall R Wave in lead V1; iiThe Q waves that begin as early as lead V3, and which are a bit deeper-than-is-usually-seen in leads V4, V5 and V6; andiiiChest lead T waves that are taller-and-more-peaked-than-usual. In view of this patient’s history — the combination of these ECG findings suggests possible infero-postero-lateral Mof uncertain age (probably new-upon-old injury). Of note — cath findings on this patient are consistent with my impression of these 3 abnormal findings.


MTHOUGHTS on ECG #2  ECG #2 was done 1 month earlier on this patient.
  • NOTE: We are not told about what was going on clinically 1 month earlier at the time ECG #2 was recorded (ie, we don't know if the patient was admitted for their initial event during that earlier admission). That said — what we can say, is that there has been NO change in chest lead appearance between the time that ECG #1 and ECG #2 were done.
  • I would have loved to see an ECG on this patient prior to development of coronary disease. I bet that the R wave would not be comparable to S wave size in lead V1 — and, I bet chest lead T waves were not so peaked. I’d also be curious to see if there were Q waves of similar size in leads V3-thru-V6 on a prior tracing.
What is different between ECG #1 and ECG #2 — is easily seen in the magnified leads of the Blow-Up magnifications in Figure-1 to the right of each 12-lead.
  • As emphasized by Dr. Smith — 1 month earlier, there was no ST elevation in any of the inferior leads. This confirms that there is a new inferior OMI in ECG #1!
  • Note that 1 month earlier — the ST-T wave in lead aVlooks very different! Thus, in the Blow-Up of ECG #2 — lead aVL showed slight-but-real ST elevation with an upright T wave. This tells us that the flat ST-T wave in lead aVL of ECG #1 actually was reflective of acute reciprocal change (ie, in response to new inferior lead ST elevation — the ST segment and T wave in lead aVL of ECG #1 was acutely lowered compared to what it was 1 month earlier).
  • Note also that there is now no doubt from the Blow-Up of ECG #2 that an abnormal Q wave was already present in the earlier tracing ( = ECG #2) in lead aVL — most probably reflecting a prior lateral infarction.
Additon Learning Points:
  • Sometimes acute reciprocal changes in lead aVL may be masked by prior abnormalities in an earlier tracing. The flat ST-T wave in lead aVL of ECG #1 actually did represent acute reciprocal change — since a month earlier the T wave in this lead was upright, and the ST segment was slightly elevated.
  • It’s easy to miss abnormal ECG findings if you fail to routinely use a systematic approach. Thus, in ECG #1 — the Tall R in lead V1 the more-peaked-than-expected chest lead T waves all of those lateral lead Q waves were probably all findings reflective of this patient’s prior coronary injury and coronary anatomy (with disease in the posterior and circumflex circulation). The importance of not overlooking these findings — is that we would not be able to exclude the possibility that these were acute changes if all we had to look at was ECG #1. It was only after locating the tracing from 1 month earlier that we were able determine that none of the chest lead findings in ECG #1 were acute.




Two patients with RBBB

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Case 1.

A 60-something woman presented with dyspnea.  She had a history of chronic respiratory disease and hypoxia, but hypoxia was no worse than normal.

ECG:

There is abnormal ST Elevation in I and aVL.
Although as a general rule, there should be no ST elevation in RBBB in the absence of ischemia, there sometimes is ST elevation that looks like this.

Therefore, I went to find an old ECG and it looked the same.







The patient ruled out for acute MI with all negative troponins.
She had a completely normal formal echo.
All previous ECGs were identical.

This was her baseline ST elevation, and I have seen this many times.




Case 2: sent by Dr. James Alva

A man in his 50s with diabetes, hypertension, and hyperlipidemia presented to the ED with chest pain and shortness of breath off and on over the past three days, with associated vomiting. He was slightly tachycardic, otherwise normal vital signs.

Here is his initial ECG (no prior available):


What do you think?


I sent this ECG with no clinical context to Dr. Smith. He commented: "by every measure, this would be RBBB with inferior and lateral STE appearing to be STEMI," but he also noted that there are several features that appear similar to false positives (like the first case above). For example, he noted a lot of what looks like STE in inferior leads in this EKG is really just the end of the QRS complex. "Nevertheless, lead II really does have STE that looks ischemic, and aVR has STD that looks ischemic." There is also much STE in V3-V6, especially V4-V6, that must be considered to be STEMI.

The first troponin (contemporary troponin T) returned at 2.00 ng/mL.

The patient was taken to the cath lab where a 100% occluded OM2 was opened.

Peak troponin was 3.21 ng/mL.

Here is his ECG just after cath:
This is minimally different from the pre-cath ECG. If the ECG findings are truly new compared to a baseline (unavailable), this could suggest persistent ECG findings of ischemia, meaning poor downstream perfusion ("no reflow" phenomenon). Or it may be simply too early after cath, and subsequent ECGs may show resolution of ischemic findings.

Learning Points:

It can be difficult to distinguish true positive vs. false positive ECG findings in RBBB in some cases like these. As a general rule, there is usually no STE in any lead in most normal RBBB. However, some baseline cases of RBBB may sometimes have STE in leads with especially large, slurred S-wave of RBBB (such as V5-6, I, and aVL). When in doubt, these findings should be assumed new until proven otherwise.


Here is an old post with some similar relevant cases:

PseudoSTEMI and True ST elevation in Right Bundle Branch Block (RBBB). Don't miss case 4 at the bottom.

Acute MI, pain onset 24-48 hours ago. Should the patient go for emergent angiogram/PCI?

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Case 1.

A 60-something man with HTN, DM, and hyperlipidemia presented stating he had chest pain starting 48 hours prior to arrival. It was substernal, non-radiating and associated with diaphoresis.  

He stated that he had the symptoms throughout the day. He didn't think much of the pain at the time and took some acetaminophen without much relief.  

He had similar discomfort 1 day prior to presentation.  

Apparently the pain was not continuous.


Patient denies of having any chest pain previously before this episode. No cardiac history.

The patient had no chest pain at the time of arrival.

Here was his triage ECG:

What do you think?
















There is inferior ST elevation with reciprocal ST depression in aVL and I. There is ST depression in V2-V4.  So this is an infero-posterior STEMI.

However, there are deep QS-waves in II, III, aVF and very tall R-waves in V1-V3.  Why?

This ECG correlates perfectly with the history of 48 hours of pain, as this is a classic subacute STEMI.  There is completed infarction.  The tall R-waves are really Q-waves of the posterior wall as recorded from anterior leads.  [For purists, these tall R-waves actually represent "lateral" infarction, (see Bayes de Luna; Journal of Electrocardiology 41 (2008) 413–418.)]

The initial troponin I returned at 11.0 ng/mL. This is a very typical initial troponin for a subacute STEMI. One expects that, after the artery is opened and the trapped troponin is released, that the post PCI troponin will be much higher.

There is significant ST Elevation.

The cath lab was activated even though symptoms were resolved.  Is that necessary?

Angiogram

There were 2 culprits ("co-culprits"):

1. 99% stenosis in the mid RCA with 90% long stenosis in the ostial and proximal RPDA.

2. Also 99% long stenosis in the distal Left Circumflex and 2nd obtuse marginal (OM2).

These were both opened and stented.

Post PCI ECG, next day:
There is less ST Elevation


48 hours
Less STE still.




Echocardiogram:

Significantly reduced LVEF (35-40%) on TTE with large inferior and inferolateral (+ apical) regional dysfunction. 

A STEMI with early reperfusion may these echocardiogram findings due to reversible myocardial stunning, and then recover much or most its function over the ensuing weeks. On the other hand, in a case of completed transmural infarction, as evidenced by Q-waves (and tall R-waves which signify lateral MI, the poor function and wall motion abnormalities are likely to be permanent. 

Fortunately, he did not develop any overt heart failure signs or symptoms while in the hospital, but was initiated on an ACE inhibitor.




Case 2.


A 70-something y.o. male w/PMH HTN, HLD, DM2 presented with malaise. On the day prior, he experienced "crushing" chest discomfort and profuse diaphoresis between 1330-1500, accompanied by some lightheadedness. He went home to rest.

On the day of admission, he experienced occipital headache and some vague epigastric abdominal pain and two episodes of non-bloody emesis.

At triage, this was his ECG:

His family brought him to triage. He had an ECG that was concerning for STEMI, so he was immediately moved to the stabilization room.

He was chest pain free on arrival.

An ECG was recorded at triage:
This again shows inferior Q-waves and large R-waves in V2 and V3.
There has already been significant infarction, completed.
The "coving" (upward convexity with slight STE and inverted T-wave) in inferior leads is diagnostic of inferior MI, and with Q-waves and inverted T-waves, is typical of subacute MI.






















The initial troponin I (which also turned out to be the peak) was 39.5 ng/mL.

Angiogram next morning

Because the infarct had happened the previous day, and the patient was asymptomatic at presentation, he was not taken for emergent angiogram.  He was taken the next day.

There was a 100% mid circumflex subacute occlusion.  It was opened and stented.

Echo:

Decreased left ventricular systolic performance-mild.
The estimated left ventricular ejection fraction is 40-45%.
Regional wall motion abnormality-inferior.
Regional wall motion abnormality-inferolateral.



Discussion

Which subacute STEMI should go to the cath lab?

Simplified:

IF there is subacute STEMI by ECG or other criteria AND:
1. Symptoms onset is within 48 hours AND
2. There are persistent symptoms OR persistent ST Elevation

Then the patient should go for emergent angiogram/PCI.

I think it makes sense to extend this beyond 48 hours because ischemia can be so intermittent.

Schomig et al. randomized patients with:
STEMI
12-48 hours of symptoms
No persistent symptoms
Persistent ST Elevation
No hemodynamic or electrical instability, no pulmonary edema

The patients who received emergent PCI had significantly smaller median left ventricular infarct size (8% vs. 13%, p=0.001) measured by single-photon emission computed tomography study, as well as non-significant but underpowered decrease in the composite of death, recurrent MI, or stroke at 30 days (4.4% vs. 6.6%, p=0.37).


The first patient had no symptoms but did have persistent ST Elevation (and ST depression of posterior MI, which is reciprocal to posterior ST Elevation), so emergent angio was indicated.  The wisdom of this is somewhat demonstrated by the dramatic rise in troponin after opening the artery.

The 2nd patient had BOTH resolved ST segments (no ST deviation) and no persistent symptoms, so angiography could be delayed.  That emergent angio was not indicated is retrospectively supported by the absence of a rise in troponin after artery opening.

Summary: if there is EITHER symptom or ECG evidence of ongoing ischemia, subacute STEMI should go emergently to the cath lab.  
If there is any hemodynamic or electrical instability, or pulmonary edema, the patient should go emergently.
If neither, it is ok to wait.

Reference:

Schomig, A., J. Mehilli, D. Antoniucci, G. Ndrepepa, C. Markwardt, F. Di Pede, S. G. Nekolla, et al. 2005. “Mechanical Reperfusion in Patients with Acute Myocardial Infarction Presenting More than 12 Hours from Symptom Onset: A Randomized Controlled Trial.” JAMA: The Journal of the American Medical Association 293 (23): 2865–72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15956631.




For those wanting even more detailed ECG Analysis, See Below comments below by Ken Grauer:


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Comment by KEN GRAUER, MD (7/5/2019):
===================================
The 2 cases in today’s ECG blog post illustrate how much correlation with the History facilitates clinical interpretation of the ECGs in this Case.
  • I focus my attention on ECG interpretation of the initial ED tracing in each Case (Figure-1).

Figure-1: The initial ECG in each Case (See text).

Extra CHALLENGE: YOU should be able to identify at least 4 different and important ECG findings in assessment of ECG #1What are they?
  • HINT: You are likely to miss at least one of these important findings IF you fail to use a systematic approach ...

MTHOUGHTS on ECG #1  The patient in Case #1 was a 60-something man with hypertension and diabetes, who presented with intermittent chest pain over the 48 hours preceding his arrival in the ED. He was not having chest pain at the time of his initial Etracing ( ECG #in Figure-1):
  • The rhythm is sinus at ~95/minute.
  • The PR interval is normal — and the QRS complex is narrow. The QTc appears at least slightly prolonged, although assessment of QTc duration is more challenging (and often less helpful) at heart rates over 90-100/minute.
  • There is marked LAD (Left Axis Deviation— as evidenced by all negative complexes in each of the inferior leads.
  • There is definite voltage for LVH. This is most evident in lead aVL (R wave amplitude is obviously much greater than the criterion of R≥12 mm— but increased voltage is also evidenced by the very tall chest lead R waves. (CLICK HERE — for the LVH criteria I favor).
Regarding Q-R-S-T Changes:
  • As already noted — there are deep Qcomplexes in each of the inferior leads. No other Q waves are seen.
  • There is a Tall R Wave in Lead V1. I measure 13 mm for the predominant R wave in lead V1 — vs only 3 mm for the S wave in this lead. (CLICK HERE — for Review of Common Causes of a Tall R in Lead V1).
  • Regarding ST-T wave Changes  Each of the inferior leads manifest coved ST elevation of 2-3 mm, followed by fairly deep, symmetric T wave inversionReciprocal ST depression is seen in lead aVL > lead I. In the chest leads — ST depression is maximal in lead V2 — but also present in leads V1, V3, V4 — with ST-T wave flattening (and shallow T inversion) in leads V5,V6.
COMMENT / Clinical Impression: To answer the CHALLENGE I posed earlier — the 4 important findings in ECG #1 are: iRecent acute MI; iiMarked LAD (that is consistent with LAHB Left Anterior HemiBlock); iiiLVHandivTall R Wave in Lead V1.
  • Each of these findings is important and relevant to this case. Considering the History ( new chest pain that began 48 hours earlier, and which has been intermittent since — but which was not present at the time ECG #1 was recorded— the overall clinical picture makes sense.
  • It is quite unusual to see such deep QS complexes in each of the inferior leads as appear in ECG #1. Much more often, you’ll see at least some R wave activity in at least one or two of the inferior leads (as we see in ECG #2). That said — the inescapable conclusion is that there is most likely both LAHB and inferior MI in ECG #1.
  • R wave amplitude far surpasses criteria for LVH in lead aVL (as well as being quite generous across the precordial leads). Without seeing a prior tracing on this patient — I find it impossible to discount a component of LV “strain” (or a strain equivalent) for the ST depression that we see in lead aVL. Given the history of diabetes and hypertension — the inescapable conclusion is that there is LVH.
  • Recognition of the finding of a predominant wave in lead Vshould prompt consideration of the differential diagnosis that we have REVIEWED PREVIOUSLY. Given new chest pain (of 48 hour duration at the time of presentationand the limb lead findings described above — we have to presume the Tall R in V1 is the result of associated posterior infarction.
  • BOTTOM Line: As per Dr. Smith — the findings in ECG #1 are consistent with a subacute infero-postero STEMI. Although it is possible for Q waves of acute infarction to form in as little as 1-2 hours — formation of the deep inferior lead QS complexes and the predominant R wave of posterior MI that we see in lead V1 generally take more time than that to develop (ie, typically at least 12-48 hours). Similarly, the fairly deep inferior lead T wave inversion seen here typically also takes some time to develop. Yet significant ( = 2-3 mm) ST elevation persists in the inferior leads of ECG #1 — which (as per Dr. Smith) was the reason for taking this patient to cath even 48 hours after likely onset of his acute event.
  • P.S. — As I’ve emphasized many times in these ECG blogs — the most common reason I see for capable clinicians overlooking important findings is simple failure to regularly use a Systematic Approach in the interpretation of every tracing they encounter (CLICK HERE — for the System I favor).




MTHOUGHTS on ECG #2  The patient in Case #2 was a 70-something man who experienced “crushing” chest pain the day before he presented to the ED. He was not having chest pain at the time of his initial Etracing ( ECG #in Figure-1):
  • The rhythm is sinus bradycardia at ~55-60/minute.
  • All intervals (PR/QRS/QTc) are normal.
  • There is a leftward frontal plane axis — but not leftward enough to qualify for LAHB. That is — since the QRS complex in lead II appears to be at least slightly more positive than negative — the frontal plane axis is less negative than -30 degrees, which is the minimum required to qualify LAD as LAHB. In addition — QRS morphology (with a QR rather than an rS) in lead II is consistent with inferior infarction, but not with what is typically seen in LAHB.
  • There is no chamber enlargement.
Regarding Q-R-S-T Changes:
  • There are large Q waves in each of the inferior leads. The deep Q waves in leads III and aVF appear to be followed by a tiny r wave. Considering how small QRS amplitude is in lead II — the 2 mm deep Q wave in this lead (which comprises ~40% of the R wave in lead II) qualifies as a “large” Q wave.
  • Transition occurs early in ECG #2 — with abrupt development of a predominant R wave as soon as lead V2. While there is no predominant R wave in lead V1 — the dramatic change in transition seen here should prompt consideration of similar entities as were mentioned in Case #1 for a Tall R in lead V1.
  • Regarding ST-T wave Changes  Each of the inferior leads in ECG #2 manifest ST segment coving — but with no more than minimal ST elevation. This is followed by shallow T wave inversion. Lead aVL manifests ST segment flattening — but really no ST depression. Similarly, there is ST-T wave flattening in leads V4-thru-V6 — but no ST segment deviation. And, although the T waves in leads V1 and V2 look a little-more-peaked-than-expected given QRS morphology in these leads — these are not acute changes.

COMMENT / Clinical Impression: There has been inferior MI. In addition, abrupt early transition with a surprisingly tall R wave already in lead V2 suggests associated posterior involvement. That said — the History (ie, severe new-onset chest pain the day before — that has since resolvedthe non-acute nature of the ST-T wave changes described above — suggest that the onset of this acute MI most probably corresponds to the onset of chest pain 1 day earlier.
  • Lack of ongoing symptoms, and lack of acute ST-T wave changes in Case #2 — were the reason cardiac cath was not done until the following day.





Would you have given thrombolytics to this NSTEMI patient?

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Case submitted by Dr. James Alva

A middle aged male called EMS for chest pain. EMS arrived and confirmed that the patient was complaining of chest pain and shortness of breath.

They recorded this prehospital ECG:

What do you think?







Normal QRS complex rhythm with hyperacute T-waves in V2-V6, I and aVL. Slight STE in V2 only, with significant STD and thus de-Winter pattern in V4-V6. Leads II and III show reciprocal depression of the ST segment (II) and T-wave (III). This is diagnostic of acute myocardial infarction of the anterolateral walls, with the most likely etiology being Occlusion of the LAD. In other words, this ECG shows LAD OMI.

Why was ST depression excluded from thrombolytics in all the guidelines? (except in the American 2013 guidelines, in which it is indicated for 1) STD in V1-V4 of posterior MI and 2) widespread STD with STE in aVR.
The data:
The data on when to give thrombolytics is incredibly scant. All trials of thrombolytics vs. placebo had poorly defined ECG criteria for enrollment.  Those that required ST Elevation had no instructions in the methods of how to measure ST Elevation.  No study analyzed ECGs to determine subgroups that benefit except to classify as STE, STD, or T-wave inversion.  Only ISIS-2, GISSI-1, LATE, and TIMI IIIB enrolled patients with ST depression.  They enrolled those with as little as 1 mm of ST depression in only 1 lead.  There were small numbers of patients.  Very few were enrolled in less that 6 hours from pain onset.  And yet for years thrombolytics have been contraindicated in ST depression (STD).
In intervening years, syndromes of acute coronary occlusion (Occlusion MI-OMI) presenting as ST depression have been identified.  The 2 mentioned above have now been included in the guidelines, but de Winter's T-waves, although now recognized as representative of OMI, have not been included.

We (Smith and Meyers) would give thrombolytics for ACS with this ECG unless PCI is available.




Shortly after this ECG, the patient suffered a witnessed VF arrest. ACLS was started and continued without ROSC to the Emergency Department despite several shocks administered.

He arrived still in VF arrest. Several more shocks were administered with no change out of VF arrest. ECMO was not available at this institution, and it is the policy of interventional cardiology not to perform cath with ongoing chest compressions.

Dr. Alva correctly diagnosed "hyperacute T-waves anterolaterally" on the EMS ECG and decided to give tenecteplase as both ECMO and intra-arrest cath were not an option.

ROSC was achieved after two more rounds of CPR.

Here is his initial post-ROSC ECG:
Obvious huge anterior STEMI (obvious OMI). Assuming you correctly found the J-point!


The cath lab was activated based on this obvious STEMI, however cardiology refused and deactivated the cath lab. The reason given was that "the bleeding risk was too high" due to thrombolytics administration. However, angiography +/- PCI is not contraindicated immediately after administration of thrombolytics, although the incidence of increased bleeding is higher in the first 2-3 hours afterward (see literature review at the end of this post for current applicable STEMI and combination reperfusion strategy guidelines).


Here is his ECG 60 minutes after ROSC:
New RBBB with LPFB, with persistent but improving STE in V2-V5. Decreasing STE and T-wave inversion in leads with STE implies that the artery is open, and reperfusion is in progress.

Rhythm is accelerated idioventricular rhythm, another sign of reperfusion



Here is his ECG 90 minutes after ROSC:
Back to normal QRS complex with continuing improvement of STE. This ECG alone would still be barely diagnostic of hyperacute T-waves in V2-V4 in the right clinical context.



Troponin T rose to 13.0 ng/mL (not ng/L! -- very high) and then was not further trended (peak troponin unknown).

Cardiac catheterization was performed the next day, approximately 24 hours after arrival, and showed a "hazy 80-90% mid LAD lesion" (TIMI flow not listed) which was successfully stented with resultant TIMI 3 flow and excellent angiographic result.

The patient survived.





Brief review and summary of combination reperfusion strategies:

Combination reperfusion strategies (thrombolytics plus PCI) constitute a large topic with many subcategories, however the relevant summary of our 2013 ACC/AHA STEMI Guidelines is:

Immediate transfer and PCI is recommended for:
 - all failed reperfusion ("rescue PCI", ST resolution less than 70%)
 - all high risk patients (hemodynamic / electrical instability)
 - all other patients may be transfered and PCI delayed for 2-3 hours after thrombolytics

Here is a relevant quote from our 2013 Guidelines:

TRANSFER FOR ROUTINE EARLY CORONARY ANGIOGRAPHY AFTER FIBRINOLYTIC THERAPY  

With the introduction of coronary stents and aggressive antiplatelet therapies, there has been renewed interest in immediate and early catheterization after fibrinolytic therapy. The advantage of this approach is that it can be initiated at non–PCI-capable hospitals and affords the healthcare system additional time to arrange a “nonemergency” transfer for angiography and PCI. Routine referral for angiography with the intent to perform PCI is supported indirectly by retrospective analyses from trials of fibrinolytic therapy that suggest that patients treated with PCI during the index hospitalization have a lower risk of recurrent MI and a lower 2-year mortality rate (365–367). The results of RCTs evaluating a strategy of routine catheterization after fibrinolysis are limited by small sample sizes or surrogate endpoints and have provided mixed results. Nevertheless, most trials have demonstrated improvement in clinical outcomes in patients transferred for early catheterization, most notably in higher-risk patients (357– 362,368–371) (Table 8 and Figure 3). In the GRACIA (Grup de Analisis de la Cardiopatia Isquemica Aguda) study (362), early catheterization within 6 to 24 hours of successful fibrinolysis in stable patients was compared with an ischemia-guided approach. It resulted in improved outcomes, including a significantly lower rate of death, reinfarction, or ischemia-driven revascularization at 1 year. The TRANSFER-AMI (Trial of Routine Angioplasty and Stenting after Fibrinolysis to Enhance Reperfusion in Acute Myocardial Infarction) study (360) was the largest (n=1059) of the RCTs evaluating transfer for coronary angiography and revascularization among high-risk patients and showed a significant reduction in the combined primary endpoint of death, recurrent MI, recurrent ischemia, new or worsening HF, or shock at 30 days with immediate transfer for the angiography group compared with conservative care. The findings from this and other studies indicate that high-risk patients with STEMI appear to benefit from immediate transfer for early catheterization, compared with either an ischemia-guided approach or delayed routine catheterization at 24 hours to 2 weeks (360,361). The reported benefits relate to a reduction in the incidence of recurrent infarction or ischemia, thus favoring earlier transfer and revascularization when possible.


In a meta-analysis (359) that included 7 RCTs of early transfer for catheterization, a strategy of routine early catheterization after fibrinolysis was associated with a statistically significant reduction in the incidence of death or MI at 30 days and at 1 year, without an increase in the risk of major bleeding. This meta-analysis was based on a mixture of trials that randomized high-risk patients (360,361,369) and trials that did not mandate the inclusion of high-risk subjects. A meta-regression analysis investigating the relative benefit of an invasive strategy after fibrinolysis according to the baseline risk of the enrolled patients for each trial suggested a larger proportional benefit with early catheterization and PCI in trials enrolling higher-risk patients (359)."






Although there is no specific recommendation regarding a patient who suffered out-of-hospital cardiac arrest, given lytics, and has a STEMI on their initial ROSC ECG, it is clear from the above ACC/AHA recommendations that they would intend for this patient to receive immediate angiography as soon as possible, and at the very least within 2-3 hours.




Learning Points:

This patient had witnessed VF arrest with prehospital ECG showing subtle but definite signs of LAD OMI without STEMI criteria. No literature exists yet on this specific population, but common sense tells us that intra-arrest thrombolytics are a reasonable option when both ECMO and intra-CPR cath are not available.

You must learn to recognize these subtle signs of OMI on ECG.

Immediate PCI after thrombolytics is recommended for all high risk patients, as well as those with evidence of thrombolytic failure. For all other patients, catheterization is recommended within 2-3 hours.

The OMI Manifesto Lecture (1 Hour Video Lecture)

A 40 year old man with chest pain since last night

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Written and submitted by Ashley Mogul, with edits by Pendell Meyers and Steve Smith


A man in his 40s with recent smoking cessation but otherwise no known past medical history presented due to chest pain since the previous evening. The pain has been constant and associated with vomiting and diaphoresis. He decided to present the following day when the pain had not stopped.

Here is the presenting ECG (no prior available):
What do you think?









Relevant findings include slight STE in V1 with an upright T-wave, slightly large T-waves in V2-3 (possibly hyperacute if compared to baseline), and slight reciprocal depression in II, III, aVF, V4-V6.


Meyers: This ECG was texted to me with no clinical information, and my response was: "That looks like a very subtle LAD OMI. If clinical picture was anything compatible with ACS I would heart alert it [Ashley and I trained at Stony Brook where we call a "Heart Alert" on a situation/ECG that doesn't meet STEMI criteria but we are nevertheless worried about the need for emergent cath and emergent ACS workup] and get serial ECGs, unless I had access to an identical baseline (not likely in my opinion). Very very subtle one. What happened?"


These findings are very subtle but suspicious for LAD occlusion, as we have seen in many similar (but less difficult) cases on this blog:

A man in his sixties with chest pain at midnight with undetectable troponin







These findings were not initially recognized. Labs were sent and an initial Troponin I resulted at 2.14 ng/mL. At that time, the patient was given 324 mg ASA and sublingual NTG. Cardiology was called and the patient was taken for urgent catheterization with the time from ED arrival to cath about 1 hour and 45 minutes.

100% proximal LAD thrombotic occlusion with TIMI 0 flow was found and stented with excellent angiographic result and TIMI 3 flow. He also had non-acute CAD of the RCA (50%) and LCX (50%).

Cath images:

Before intervention.

Before intervention with arrows demonstrating the area of occlusion.

After intervention showing the site of prior occlusion.

After intervention.


ECG a few hours later:


Some leads with STD previously have now resolved. The T-wave in lead V1 is no longer upright, with terminal T-wave inversion which is likely due to reperfusion.

Echo showed akinesis of the anteroseptal and anterior walls as well as the apex with an LVEF of 45%. Troponin I elevated to 3.93 ng/mL but was not trended to peak.



Learning Points:

Not all OMI will present as STEMIs. Complete LAD occlusion can be incredibly subtle as in this case. Remember this case and the similar cases (links above) showing this patter of LAD occlusion including subtle STE with upright T-wave in V1-2 with reciprocal STD in lateral and inferior leads. When in doubt, record serial ECGs and watch out for signs of ischemia despite medical management.


===================================
Comment by KEN GRAUER, MD (7/11/2019):
===================================
Our thanks to Drs. Mogul, Meyers and Smith for this illustrative case.
  • I focus my attention on the interpretation of the initial ED tracing ( = ECG #1 in Figure-1). Although the ECG findings are challenging — I feel they should not be missed.
Figure-1: The 2 ECGs in this case (See text).


MTHOUGHTS on ECG #1  The patient is a man in his 40s with a history of smoking — who presented with new chest pain that was ongoing through much of the night, and despite associated vomiting and diaphoresis — this patient would not go to the ED until the next day when chest pain persisted.
  • This is a higher-prevalence History for acute coronary disease. By this, I mean that the onus is on us to rule out that even subtle ECG changes may be acute — rather than the other way around.
Descriptive Analysis of ECG#1:
  • The rhythm is sinus at ~85/minute. The PR, QRS and QTc intervals are normal. The frontal plane axis is normal (about +40 degrees). There is no chamber enlargement.
Regarding Q-R-S-T Changes:
  • There are Qcomplexes in leads V1 and V2. There is notching on the initial part of the downslope of the S wave in lead V2. There may be tiny q waves in lateral chest leads.
  • Transition (where the R wave becomes taller than the S wave is deep) occurs between leads V2-to-V3, which is normal. That said — R wave amplitude is minimal until lead V4 ...
The most remarkable finding in ECG #1 relates to the ST-T wave Changes:
  • Looking sequentially, first at the 6 limb leads — and then at the 6 chest leads — what immediately caught my eye was that the T wave in lead Vlooked taller-than-it-should-be (that is, disproportionate) given the lack of any r wave in this lead.
  • My eye was next “caught” by the appearance of the ST-T wave in lead V3. There is simply NO WAY that the ST-T wave in lead V3 is “normal”. A normal ST-T wave does not have a straight (ledge-like) ST segment as we see in ECG #1, that then abruptly rises to a disproportionately tall T wave (that is 1½ times the height of the R wave in this lead), and which manifests as wide of a T wave base.
  • COMMENT: I will emphasize that despite my detailed, written descriptive analysis above — it literally took me less than 5 seconds to arrive at my ST-T wave assessment — and no more than 2-3 seconds more to assess leads V2 and V3. Even without looking at anything else on this ECG — in a patient with worrisome new chest pain, the ST-T wave appearance in lead V3 the disproportionately tall T wave in neighboring lead V2 is enough (in my opinion), to say that while this may be subtle and we can’t be 100% certain — this patient merits prompt cath.
The more additional leads that we can identify in ECG #1 that show ST-T wave abnormalities — the greater the likelihood that our suspicion for an acute cardiac event (based on this history the ST-T wave appearance in leads V2 and V3is correct:
  • The ST-T wave in neighboring lead Vof ECG #1 is abnormal. It is not normal to see ≥1.5 mm of ST elevation in lead V1 — and, given the ST-T wave appearance in leads V2,V3 — there is little doubt that the ST elevation that we see in lead V1 is part of this process!
Other findings in ECG #1 are more subtle. I probably would not have thought much of them IF the ST-T wave appearance of lead V3 was not so flagrantly abnormal, with associated ST-T wave findings in neighboring leads V1 and V2 (as described above).
  • Considering the hyperacute T wave appearance in lead V3 — it is almost certain that the slight-but-real scooped ST depression and prominent T wave in lead Vis part of the process. Doesn’t the shape of the upper part of the T wave in lead V4 (if not also in V5 and V6) look a lot like the shape of the T waves in leads V3 and V2 that we now know are hyperacute?
  • ST-T wave changes in the limb leads are much less marked. But in the context of chest lead findings just described — the T wave in lead III looks hyperacute (it equals R wave height in lead III, with an extremely wide base considering this tiny R wave). Finally, while there is no ST depression in lead aVL — the ST-T wave flattening we see in this lead is not the normal response when the R wave in aVL is upright.
Taking another look at R wave progression in the chest leads:
  • Notching of the downslope of the S wave of a QS complex (as we see in lead V2 of ECG #1) — increases the likelihood that this QS complex reflects an infarction Q wave.
  • Although a predominant R wave does develop in lead V3 of ECG #1 — this R wave is barely 3 mm tall. This adds further support that the QS in leads V1,V2 (with notched S wave downslope in V2the abnormal ST-T wave changes in lead V1-thru-V4 described above are all part of the same ongoing acute process!
BOTTOM Line: While ECG #1 does not satisfy the definition of a STEMI — as per Dr. Meyers, it really looks like acute LAD OMI. And in a patient with this worrisome of a history — I don’t see how one can justify not calling a heart alert.

Additional LEARNING Points: Among the best ways to enhance appreciation of subtle acute changes — is to compare the initial ECG to one or more post-reperfusion ECGs ( = ECG #2 in Figure-1).
  • To be sure comparison of serial tracings is valid — one must always ensure that frontal plane axis, R wave progression, and QRS morphology are all comparable. And, there are slight differences in this regard when comparing ECG #1 with ECG #2. Thus, several leads (most notably leads I, III; aVR,aVL,aVF) show baseline artifact in ECG #2 that was not present previously. In addition, the frontal plane axis in ECG #2 is a little more vertical (about +75 degrees, compared to an axis of +40 degrees in ECG #1). That said, I believe that for the most part — comparison of ST-T wave appearance between these 2 tracings is valid.
  • There is a difference in QRS appearance of lead Vbetween the 2 tracings. Although impossible to prove — I suspect the return of a predominant R wave in lead V3 of ECG #2 is due to reperfusion of the LAD, rather than to any change in precordial lead placement.
  • Note after reperfusion (ie, in ECG #2) — that: ithere is now no more than trace (if any) ST elevation in lead V1; iithe T wave in lead V2 does not look nearly as disproportionate as it did before PCI; iiieven accounting for the changed QRS appearance in lead V3 — the ST-T wave in V3 of ECG #2 now looks benign; andivthe very subtle suggestion of hyperacute T wave changes in leads V4, V5, V6, as well as lead III — is no longer present in ECG #2. The ST segments in these leads also look better.
  • Final Pearl: I find it ever-so-helpful to look for those 1 or 2 leads in the initial tracing that without doubt are abnormal. Once you find such leads (such as leads V3 and V2 in ECG #1) — it becomes much easier to identify other leads that show more subtle, but clearly abnormal findings.



EXTRA Credit: Go back to ECG #2. Note the artifact in 5 of the 6 limb leads. From which extremity is the problem causing the artifact arising?


ANSWER: There is no artifact at all in lead II of ECG #2. Bipolar lead II is derived from the difference in electrical potential from the foot (F) and the right arm (RA) electrodes. But the left arm (LA) electrode is not involved in derivation of lead II. In contrast, the LA electrode is involved in derivation of both leads I and lead III (which are the leads that show the artifact). That the left arm (LAis the “culprit” extremity is supported by the fact that in the augmented leads, the amount of artifact is greatest in lead aVL, and approximately half this amount in leads aVR and aVF. CLICK HERE — for a brief article by Rowlands et al that explains these concepts in more detail.




A female in her 60s with sudden chest pressure

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Written by Pendell Meyers


A female in her mid 60s with history of SVT and HTN presented with sudden onset 3/10 chest tightness while lying in bed in the early morning. She had nausea and diaphoresis with this event, as well as tightness between her scapula, and a loose bowel movement.

Here is her initial ECG at presentation to the ED at time zero (no prior available):

What do you think?









Sinus rhythm with significant downsloping STD in V1-V3, maximal in V1-V2. There is also subtle STE in V6 with large-area T-wave with straight/convex ST segment morphology. The T-waves in the inferior leads could be large if a prior ECG were available for comparison.

This ECG is diagnostic of acute MI of the posterior and lateral walls. The most common etiology of this condition is Occlusion MI (OMI) affecting these walls, most likely LCX or other artery in this territory including a diagonal or obtuse marginal, or RCA in some cases.

Because the current STEMI vs. NSTEMI paradigm greatly undermines the understanding and recognition of the STD of posterior OMI, this finding was not initially recognized.

Initial troponin returned slightly elevated at 0.02 ng/mL. This triggered a repeat ECG at t = 50 minutes:



The findings above are still present but slightly improved, however there is still active ischemia on this ECG. OMI is ongoing until proven otherwise.

It is unclear whether the patient still had symptoms at this time.

The patient was admitted to cardiology for NSTEMI. There was no bed in the cardiology unit, so the patient was boarding in the ED.

The second troponin returned at 0.13 ng/mL, prompting another repeat ECG at t = 2 hrs:
Further improvement but still not back to baseline.



CT aorta was negative for dissection.

She was started on heparin.

Trop #3 at t = 6 hrs 30 min = 0.41 ng/mL
Trop #4 at 9 hrs = 1.13 ng/mL
Trop #5 at 12 hrs = 1.17 ng/mL

Finally, a note from the admitting team states that she will be taken to cath for ongoing chest pain and rising troponins at t = 15 hrs.


Cath at t = 16 hrs:

Mid LCX 100% occlusion with TIMI 0 flow. TIMI 3 after PCI. Also noted triple vessel disease with RCA 70% and LAD mid 90%.







ECG the next day:




First five measurements were before cath, then you can see the spike as sequestered troponin in non-perfused myocardium is released after reperfusion.

Learning Points:

STD maximal in V1-V4 with a normal QRS complex (not explained by RBBB, etc) is worrisome for posterior OMI until proven otherwise. Posterior leads may be helpful, but lack of clear elevation in the posterior leads does not obviate concern for posterior OMI when the STD on the anterior leads is diagnostic.

Ongoing ischemia (by symptoms, troponin, or ECG) despite medical management is an indication for emergent cardiac catheterization.



A Text Message in the Middle of the night. Do you give thrombolytics?

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I awoke in the morning and discovered a text with this ECG that was sent 6 hours prior by a former resident:

"60 year old with classic chest pain.  The cath lab is occupied for the next 90 minutes.  Cards says "not a STEMI".  Thinking of giving lytics."
What do you think?
What do you do?













I texted back: "Sorry for delay!  Was sleeping.  This is OMI!!  Did you give lytics?  Proximal LAD.  Great catch!"

There is 0.5 mm of ST Elevation in V3-V6.  The T-wave in V4 is far too large for the QRS.  The LAD occlusion formula would be very high due to the extremely small R-wave in V4 and QRS in V2, but without the QT I cannot calculate it exactly.

This ECG is diagnostic of LAD OMI.  Occlusion Myocardial Infarction.

I continued:

"Cards was right.  It is not a STEMI.  But the new paradigm is OMI.  And that is what is important.  ST Elevation is a very poor way to define myocardial infarction. We have a couple articles, one in press and one in review, that we hope will continue to prompt a change in that inadequate paradigm."

More about the case:

History: 60 yo woman w/ history of smoking but no other cardiac risks who presented to triage w/ CP. She had awoken in the morning w/ bilateral arm paresthesias and by evening called a nurse advice line who told her she may be having a heart attack and to go to ED to be evaluated.

While in her car she developed central chest pressure radiating to right shoulder about 20 min prior to arrival.

She was seen in triage where she had an ECG recorded at T0:
What do you think?
(The dx can be made without looking at the baseline ECG, but it is below if you want to see it)?














A baseline ECG was available and is also attached.


Now you know the diagnosis.  Acute LAD occlusion.

But the ED is a busy place:
"She was hypertensive in the 190s-200s systolic but otherwise had normal VS. The ED was very busy and there were no open rooms.

"The triage ECG was shown to a physician, I don't honestly recall if it was me or one of my partners and labs and CXR were ordered by the provide in triage.

"By the time she was roomed and I assigned myself to her care it was about 1 hr later. She remained very hypertensive and had a nursing note that said she had been too anxious to get a repeat ECG and requesting an order for Ativan.

"As I was reviewing her triage information and initial ECG another pt was roomed who appeared to be critically ill with an STEMI.

"I ordered her aspirin, NTG, fentanyl, a repeat ECG and walked into the room w/ the new STEMI pt.

"As I walked into that room that lab called w/ her initial troponin value of 1.0 (LOD < 0.03). The repeat ECG I ordered is attached here as ECG #2 and was done at T+70."

Tough to interpret

"I activated the cath lab for my 2nd pt and was not able to get to her bedside until about 30 min later. Her pain and HTN were improved but she was still having active CP. I ordered more NTG and fentanyl and obtained another repeat ECG."

(ECG 3-2 at T+100 attached here).

This is the ECG at the top


"I activated the cath lab at this point.


"Our cardiologist came back down to the ED looked at the most recent ECG and said, "That's not a STEMI".  I told him I disagreed and thought the patient needed emergent catheterization. He told me that regardless they would be unable to take her for at least 90 min b/c they were just starting the other case I had sent them.

"That's the point at which I texted you. 

"We gave heparin, started nitro gtt and was considering giving thrombolytics but our unit coordinator was able to find an accepting cardiologist at the hospital down the street in about 5 minutes. 

"She went emergently to cath (not able to figure out exact timing from my chart review) and was found to have 100% thrombotic distal LADD1 which was stented. Her troponin I there was >50 (they don't measure higher). No post cath echo yet."



The question still remains (thrombolytics?):

If there is no cath lab, are thrombolytics indicated?  If I were the treating physician, I would give thrombolytics. But that is because I am so certain that this is an LAD occlusion that there is no doubt in my mind that the benefit/risk ratio of thrombolytics favors treatment.

A careful read of all the original thrombolytic literature shows that the "criteria" for giving thrombolytics are extremely inaccurate.  Moreover, there is much recent literature showing that acute coronary occlusion frequently does not meet criteria.  In the best study to date, published last month, ST Elevation was 35% sensitive for adjudicated STEMI (51% on serial ECGs) and 21% sensitive for OMI (30% on serial ECGs).  Cardiologists were 49% sensitive for OMI.

If I diagnose an acute Coronary occlusion, regardless of "STEMI criteria" of an artery that supplies a significant myocardial territory,  and the cath lab is not available, I will give thrombolytics if there are not any really serious contraindications.  I am not going to recommend that everyone do it because it is very dependent on ECG and other skills to be certain of the diagnosis.

Prospective validation of current quantitative electrocardiographic criteria for ST-elevation myocardial infarction


Pendell and I wrote an Editorial on this, but we cannot reproduce it here:
H. Pendell Meyers.  Stephen W. Smith.  Prospective, real-world evidence showing the gap between ST elevation myocardial infarction (STEMI) and occlusion MI (OMI)



===================================
Comment by KEN GRAUER, MD (7/18/2019):
===================================
This case was made especially challenging by small size of QRS complexes, baseline artifact in a number of leads, and continued use of the outdated “stemi” paradigm for defining acute coronary.
  • I focus my attention on interpretation of the ECG that was texted to Dr. Smith ( = ECG #1 in Figure-1).
  • NOTE: There is low voltage in all 12 leads. In my attempt to facilitate interpretation — I’ve relabeled this tracing, and have removed some of the excess spacing in between lead groups. I believe doing so makes it easier to appreciate the acute ST-T wave changes.
Figure-1: The ECG that was texted to Dr. Smith in this case (See text).



MTHOUGHTS on ECG #1: The patient in question was a 60yo woman with typical new-onset chest pain. As per Dr. Smith — the ECG in Figure-1 that was texted to him is diagnostic of acute OMI.

Descriptive Analysis of ECG #1:
  • Low voltage! There is baseline artifact in several limb leads. The rhythm is sinus at ~80/minute. The PR interval is normal. All intervals (PR, QRS, QTc) are normal. The frontal plane axis is slightly leftward (ie, more negative than positive in lead aVF) — but not negative enough to qualify as LAHB (left anterior hemiblock), because the QRS is not predominantly negative in lead II. I estimate the axis to be about -15 degrees. There is no chamber enlargement.
Regarding Q-R-S-TChanges:
  • There are small, narrow Q waves in leads aVL, V5 and V6. These Q waves are of uncertain significance.
  • The area of Transition (ie, where the R wave becomes taller than the S wave is deep) is slightly delayed (ie, it occurs between leads V4-to-V5). More importantly — the R wave remains tiny until lead V5This most probably is related to the acute ongoing process.
As has already been noted — ST-T wave Changes are diagnostic:
  • Considering the tiny size of QRS complex — there is significant Selevation in leads V3-thru-V6. This is associated with hyperacute waves (that are disproportionately taller and fatter-then-they-should-be-at-their-peakin leads V3V4V5, and probably also V6.
  • In the limb leads — there is ST elevation in lead aVL reciprocal ST-T wave changes in each of the inferior leads. While more difficult to appreciate because of artifact and small QRS complex size — the ST segment is conspicuously straightened in leads II and aVF; slightly depressed in lead III; and, associated with disproportionate T wave size in all 3 inferior leads.
  • Personal Observation: Doesn’t doubling the size of the QRST complex in certain leads of ECG #1 facilitate appreciation of a definite acute OMI(See Figure-2).
Figure-2: I’ve doubled the size of 1 complex in leads III, aVL, aVF, and V3-thru-V6. I have not changed proportions of the ECG grid within the RED rectangles. Doesn’t this facilitate diagnosis of acute OMI? (See text).



COMMENT: Regardless of whether the millimeter definition of acute “STEMI” is or is not met — the ECG in Figure-1 is diagnostic of acute OMI in this patient with new onset typical chest pain. Acute reperfusion is indicated.
  • The ECG in Figure-1 is consistent with acute mid- or distal-LAD occlusion — since ST elevation does not really begin until lead V3, and is maximal in leads V4 and V5 (ie, ST elevation typically begins sooner with proximal LAD occlusion).
  • From an ECG terminology standpoint — preservation of the initial r wave in leads V1 and V2 suggests that this is not anteroseptal infarction, but rather anterior infarction (ie, from a terminology standpoint — the initial r wave should be lost in lead V1 when there is “septal” infarction).
  • That said, persistence of no more than a tiny r wave until lead V5, and then no more than relatively small R waves in leads V5 and V6 — is consistent with the extensive area of jeopardized myocardium suggested by the number of leads in ECG #1 that show acute ST-T wave deviation.
  • P.S.: Taking another look at the magnified complexes within the RED rectangles in Figure-2 — perhaps the definition of acute “STEMI” is met after all in this case?

Our THANKS to Dr. Smith for presenting this case!




A man in his 40s with chest pain and syncope after cocaine use

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Written by Pendell Meyers, with edits by Steve Smith


A man in his early 40s with history of MI s/p PCI presented with bilateral anterior chest pain described as burning and belching with no radiation since last night starting around 11pm (roughly 11 hours ago). He also described a syncopal episode just prior to onset of symptoms. He had used cocaine approximately 20 minutes prior to onset of symptoms.

He still had active pain on arrival to the ED.

Here is his triage ECG:
What do you think?






His baseline ECG was on file:




--Sinus rhythm
--Subtle STE in V1-V5, II, III, and aVF
--Q-waves in V1-V5, as well as II, III, and aVF which must be assumed new until proven otherwise
--Possibly large area under the T-wave (concern for hyperacute T-waves) in V4, II, III, and aVF, with reciprocal negative T-wave in aVL
--These Q-waves are so fully developed that it appears to be a nearly completed MI, at a stage when it is likely that all ST elevation is resolved. STE occurs primarily in viable ischemic myocardium; persistent STE after completed infarction is ominous and portends development of an aneurysm.
--There is also an interesting Brugada-like morphology in V1 (also similar to hyperkalemia, which sometimes mimics brugada). This morphology can be cause by or associated with cocaine:

A Patient with Cocaine Chest Pain and Prehospital Computer interpretation of ***STEMI***


This is OMI of the anterior, lateral, and inferior walls until proven otherwise. This distribution is classic for a type III "wraparound" LAD Occlusion.

But it does not meet STEMI criteria and it was not initially recognized. Whereas most STEMI(-) OMI is acute, this one might have had STE at its onset, or earlier in its course. We'll simply never know without ECGs from that time period.

The first troponin T was delayed for several hours for an unknown reason in the lab, and returned at 1.50 ng/mL (very elevated).

This prompted a repeat ECG (we do not have documentation from that time to tell us whether he had persistent, recurrent, or absent pain):  




Progression of anterior OMI to full Q-wave MI with large pathologic Q-waves in V2-V4 with persistent STE which now meets STEMI criteria (after full thickness infarction/stunning).



The cath lab was now activated.

He was found to have 100% mid LAD occlusion. Thrombectomy performed, then stent placed with improvement of TIMI 0 to TIMI 3 flow.

Pre-PCI:


Post-PCI:

In this view you can see the extent of the "wraparound" distal LAD:



Peak troponin T was 35.70 (massive MI, rarely survivors at this level in my 3 years here).




Echo showed EF 30% with anterior, septal, apical, and inferior wall motion abnormalities.

ECG after cath:


Continued STE with anterior wall Q waves (LV aneurysm morphology), combined with extremely high troponin are likely indicative of full thickness irreversible MI (rather than stunning), and are high risk features for resulting LV aneursym. The extremely high troponin and ECG evidence of LVA morphology are very worrisome long term features for resultant morbidity and mortality.

Amazingly, he did not suffer any serious complication in hospital. He recovered and was discharged several days later. Long term follow up is unknown at this point.


Learning Points:

Even if NSTEMI Occlusions (STEMI- OMIs), overall prove to have slightly lower morbidity and mortality than STEMI Occlusions (STEMI+ OMI), there are many cases like this one showing that some of the worst, largest OMIs may not manifest STEMI criteria until far too late, if ever. Again, it is possible that this patient would have had obvious STE earlier in the time course of this MI, but we do not know. What we can say is that his initial ECG was certainly diagnostic and the delay of many hours could have been improved.

Wraparound type 3 LAD Occlusion causes STE in many leads including anterior, lateral, and inferior distributions. This is the most important exception to the classic teaching of "diffuse STE without reciprocal depression is less likely ACS, more likely pericarditis". Always keep in mind the possibility of diffuse STE (and other OMI findings) as being due to a type 3 LAD.


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Comment by KEN GRAUER, MD (7/19/2019):
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I was intrigued by the challenge of clinical correlation posed by the ECGs in this case. The patient is a man in his 40s with a history of prior MI (s/p PCI— who presented to the ED with new chest pain that had begun ~11 hours earlier. His initial ECG in the ED ( = ECG #1) is shown in Figure-1. The patient was still with ongoing chest pain at the time ECG #1 was done.
  • baseline tracing was found on this patient ( = ECG #2).
  • Several hours later a follow-up ECG was obtained in the ED, because the 1st troponin came back significantly elevated ( ECG #3).
Figure-1: The first 3 ECGs that were shown in this case (See text).



CHALLENGE: How did YOU interpret ECG #1 before you looked at ECG #2?
  • As we soon learned in this case — this patient has had a new STEMI. Cardiac cath (which was done soon after ECG #3) told us that this STEMI was the result of 100% mid-LAD occlusion (LAD with wraparound). But the BEST way to enhance one’s ECG interpretation skills is to always interpret the initial tracing in the context of the brief clinical history given (which in this case, was new chest pain that began 11 hours earlier).
  • Strive to interpret this initial ECG before you look at additional information. THEN look for previous tracings in the patient’s chart, repeat ECGs, troponin and Echo results the patient’s clinical course. This sequence of assessment will not slow you down — and it is the BEST way to optimally “grow” as an astute ECG interpreter.
MTHOUGHTS on ECG #(determined BEFORE I looked at ECG #2):
Remember the History a man in his 40s with known prior MI (s/p PCI— who presented to the ED with new chest pain that had begun ~11 hours before ECG #1 was done.

Descriptive Analysis of ECG #1:
  • The rhythm is sinus at a fairly regular rate of ~80-85/minute. The PR, QRS and QTc intervals are all normal. The frontal plane axis appears to be normal — though the axis is difficult to calculate because of nearly isoelectric complexes in 4 of the 6 limb leads (leads I, III, aVL and aVF). There is no chamber enlargement.
Regarding Q-R-S-T Changes:
  • There are multiple Q waves in ECG #1. Although small in size — the inferior Q waves are likely to be significant (ie, indicative of inferior MI at some point in time) — because relative to QRS dimensions, inferior Q waves are both large and relatively widened. There are large Q waves (relative to QRS complex size) in leads V1, V2 and V3. There is marked fragmentation of the Qcomplex in lead V3.
  • PEARL: Although Q waves in leads V4, V5 and V6 become much smaller and narrower — the fact that the wave in lead Vis decidedly larger than the Q waves in leads V5 and V6, tells us that the Q in V4 is significant (ie, part of the infarction process suggested by the Q waves in V1-V3). With normal “septal” q waves — the opposite progression occurs (ie, Septal q waves are uncommon in lead V4 — and when present, a septal Q in V4 should be smaller than the septal Q in V5 and V6).
  • The area of Transition (ie, where the R wave becomes taller than the S wave is deep) is slightly delayed in ECG #1 (ie, it occurs between leads V4-to-V5).
Regarding — ST-T wave Changes:
  • As noted by Drs. Meyers and Smith — there is an interesting Brugada-like morphology to the ST-T wave in leads V1 and V2 (convex down RED line in V1,V2 of ECG #1). There is not enough ST elevation to qualify this as a Brugada-1 pattern — but, the clinical significance of recognizing this pattern is that the slight ST elevation in these leads is more likely to reflect a Brugada “phenotype” rather than acute septal infarction.
(For more on assessment of Brugada ECG patterns — CLICK HERE for a link to my 29-minute video on the subject. If you click on SHOW MORE under the video on the YouTube page — you’ll see a linked Contents to all in the video).
  • Back to ECG #1: As per Drs. Meyers and Smith — there is subtle-but-real Selevation in multiple leads. That said — the almost horizontal elevated ST segments in the inferior leads look less acute than one might have expected. These elevated ST segments are associated with prominent inferior T waves — and, reciprocal (albeit shallow) T wave inversion in lead aVL.
  • Similarly the subtle-but-real ST elevation in leads V3, V4 and V5 has a shape that looks less acute than one might have expected (gently upward concave, as suggested by curved BLUE lines in V3 and V4 of ECG #1).
  • NOTE: The different shape of the slightly elevated ST segments in leads V1,V2 of ECG #1 (curved-down RED lines) — vs the upward concavity ST segments in leads V3-thru-V6 (curved-UP BLUE lines) — in my opinion, adds further support that these are 2 different processes (ie, Brugada-like phenotype for the ST-T waves in leads V1,V2— vs recent acute injury for the elevated ST segments in leads V3-thru-V6).

Clinical IMPRESSION: Before finding this patient’s baseline tracing — I would have been hard pressed to know how much of what I was seeing in ECG #1 might have been due to the prior MI that this patient had — vs what might have developed since the onset of chest pain 11 hours earlier. This is the CHALLENGE I put forth to you earlier! Realizing there is NO way to be certain — these were my thoughts:
  • What we see in ECG #1 probably did not just happen. Although possible to develop new Q waves in as little as 1-2 hours after acute infarction — I thought the size and number of Q waves seen here the fragmentation in lead V3 suggested that at least some of these Q waves were the result of this patient’s prior MI. I would have guessed from the prominent T waves and subtle ST elevation that this patient manifests in ECG #1 — that he had suffered an acute event at the onset of symptoms (ie, ~11 hours earlier).
  • That said — because there is still ST elevation in ECG #1, with inferior T waves that look like they may still be hyperacute ongoing chest pain — cardiac cath sooner-rather-than-later seems indicated to clarify the clinical picture.


At this point in time — Finding a Baseline Tracing on this patient ( = ECG #2) proved invaluable! My thoughts on comparing ECG #2 with ECG #1:
  • I was wrong about my hunch that at least some of the Q waves in ECG #1 were old. Other than lead V1 — there are no Q waves at all in ECG #2! Instead, R wave progression in this earlier baseline tracing was normal — with development of a fairly tall R wave already by lead V3. This means that the extensive Q waves in ECG #1 (including the fragmentation in lead V3) are new since the baseline ECG #2 was done. We have to presume (until proven otherwise) that these ECG findings are new since the onset of symptoms 11 hours earlier.
  • There is virtually no ST elevation in ECG #2. Overall, I don’t see much difference in T wave appearance between ECG #1 and ECG #2. This left me with uncertainty regarding how acute the subtle-but-real ST elevation now present in ECG #1 might be. Did it develop days or weeks earlier? — or, sometime after the onset of symptoms within the 11-hour period prior to presentation in the ED? That said — persistence of chest pain the ECG changes that developed between ECGs #1 and 2 would be indication for acute cath to clarify the clinical picture.


Apparently — the new ST elevation that developed in ECG #1 (compared to the baseline ECG) was not recognized. Several hours later, when the 1st troponin came back elevated — ECG #3 was obtained.
  • I see no significant change in ST-T wave appearance in the limb leads between ECG #1 and ECG #3 done several hours later.
  • However – there has been marked change in ST-T wave appearance in the chest leads in ECG #3! Even accounting for slight change in QRS morphology and amplitude in the mid-chest leads (suggesting some variation in precordial lead placement) — there clearly is now straightening of the ST segment takeoff (slanted BLUE lines in ECG #3with more ST elevation in leads V3 and V4.
  • Beyond-the-Core: The Brugada-like morphology in lead V1 of ECG #3 looks the same as it did in ECG #1 (curved-down RED line). It is interesting that the shape of the elevated ST segment in lead V2 of ECG #3 now manifests a flattened (BLUE-RED line) morphology that is intermediate between the curved RED line in lead V1 — and the upward slanting BLUE line in lead V3. I suspect the reason for this is a “fusion” between the Brugada-like ST segment effect being exerted on lead V2 — with what is now acute ST straightening and elevation in leads V2, V3 and V4 from the actively evolving anterior STEMI.
  • Putting IAll Together  Despite the history of a prior MI (with PCI) — the baseline tracing ( = ECG #2) shows no evidence of prior infarction. From the information available — it’s impossible to know if a 2nd event occurred sometime after ECG #2 was done — but before the onset of symptoms associated with this admission. What can be said — is that regardless of whether this marks a 2nd or 3rd cardiac event, that there is definite ECG and troponin evidence of an acute STEMI that is actively evolving between the time that ECGs #1 and #3 were done.
  • Final Teaching Point: Thoughtful review of serial tracings + clinical correlation may retrospectively facilitate deduction of the timesequence of events.

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


What does this ECG with significant ST Elevation represent?

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These 2 serial ECGs were texted to me recently.  They were recorded 12 minutes apart:

"Hey Steve, 30-something with one week of chest pain, mostly right-sided, better with sitting up.":



What do you think?
QTc's were 330 ms and 373 ms






This is what I texted back:

These look like they are a very pronounced case of Benign T-wave Inversion.  I do not think this is acute occlusion myocardial infarction (OMI).  Get an emergent contrast echocardiogram.


These are reasons why it does not look like OMI: 
1. flat ST segment in V4
2. huge R-wave in V4
3. very short QT interval
4. J-point notching
5. classic early repol in V3
6. classic features of “Benign T-wave inversion” T-waves in V5, V6.  

I would guess the patient is African American.

Would I blow it off?  No.  I would get an echo.  I am 99% certain that it is not OMI.

An emergent echo was done:

Normal left ventricular size, normal wall thickness and mild to moderate systolic dysfunction.
The estimated left ventricular ejection fraction is 43%.

Global hypokinesis.

The first troponin I then returned quite elevated at 9.8 ng/mL.

In the absence of a wall motion abnormality, especially with global decreased ejection fraction, a troponin that is quite elevated like this strongly suggests global myocarditis.  

When does myocarditis mimic OMI?  Often, myocarditis is more focal, has both focal ST Elevation and focal wall motion abnormalities, as well as elevated troponin, and an emergent angiogram must be done to differentiate the two entities.  Definitive diagnosis is by MRI.

I learned more about the history:


30-something African American with 5-7days of sharp R-sided shoulder/scapula/chest discomfort, presented with sinus tachycardia.  This history of a week of constant chest pain is also much more suggestive of myocarditis.  

OMI is generally of more acute onset, unless there is intermittent angina.  OMI it is very unlikely with a week of constant pain.

2 hours later, this ECG was recorded:
This was interpreted as having Wellens'-like reperfusion T-waves.
I would have said they were also likely due to different lead placement or to common hour-to-hour variation in non-ischemic ST elevation.

However, to be certain, the patient went for an angiogram.

Angiogram was normal

C-reactive protein (CRP) returned at 250 mg/L, consistent with myocarditis.

Serial Troponins remained in the 9-11 range, w/o any large rise and/or fall, also atypical for OMI.

He later underwent an MRI:

1) Mildly decreased LV function with no focal wall motion abnormalities
2) Patchy intramyocardial delayed enhancement compatible with myocarditis.
There is also mild pericardial enhancement consistent with pericarditis.
Overall findings are consistent with myopericarditis.


Summary:

It was not benign T-wave inversion, but also not OMI.

When there is worry for OMI, but the ECG and history are just not right, then an emergent contrast echo may be done in lieu of an immediate angiogram.

A wall motion abnormality and elevated troponin may be seen in myocarditis, and then an angiogram must be done to differentiate myocarditis from OMI.

Bizarre T-wave inversions, with Negative U-waves and Very long QT. And a myocardial viability study.

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This 60-something year old male was admitted and his hospital course complicated by GI bleed, hemodynamic instability, and a nadir hemoglobin less than 5 g/dL.  An ECG was relatively normal.

The next AM, his potassium was measured at 2.9 mEq/L, so another ECG was recorded.

He was asymptomatic.
The previous ECG from one week prior had been relatively normal.

There are bizarre inverted T-waves and also inverted U-waves (see the 2nd inverted bump?)
The QT is incredibly long
There is some subtle STE in inferior leads but also STE in I, aVL.
There is STE before the bizarre TU inversion in leads V3-V6.

There are some artifacts that look similar to this.  

Bizarre (Hyperacute??) T-waves


Inverted U-waves are very strongly associated with LAD occlusion.

Besides the Nonspecific T-wave Inversion in aVL, What Else is Abnormal on this ECG?


Bizarre T-wave inversion with long QT is typical of takotsubo.

Bizarre T-wave Inversions in a Patient without Chest Pain


I thought he either had acute MI of the LAD, or takotsubo stress cardiomyopathy.  The team obtained an immediate cardiology consult, a stat formal echo, and serial troponins.

Troponin I was 4.2 ng/mL.
Echo showed: 
Low normal left ventricular systolic function with an ejection fraction of 52%.
Regional wall motion abnormality--akinesis of the apical anterior, mid-anteroseptal, apical septal, apical inferior, and apical lateral segments.
Regional wall motion abnormality--hypokinesis of the mid anterolateral and anterior segments.
Hyperdynamic basal segments.

This is consistent w/ wraparound LAD occlusion or takotsubo; the ECG is consistent with both.

Cardiology consult elicited some brief episodes of chest pain while in the hospital, squeezing, lasting 10 minutes.

The patient went for an angiogram.

Impression and recommendation:
Severe multivessel CAD involving the ostial LAD.
Occlusion of the apical LAD resulting in inferior infarction, chronicity uncertain - decreasing troponin would suggest that occlusion is more than 24-48 hours old.

Given the distal LAD occlusion of uncertain chronicity, TIMI III flow in other vessels and patient restlessness, as above, intervention was deferred.

Here is the ECG after the angiogram:
Some interesting evolution



After all this, it was not certain whether there was ACS (type I MI), type II MI due to GI bleed with anemia and hemodynamic instability, or takotsubo.

Further, if it was MI, was it:
1) a large MI with downtrending troponin or
2) a previous large MI due to the previous LAD occlusion, with superimposed small acute MI, or
3) a small acute MI with a large area of myocardial stunning (large wall motion abnormality)?

Absence of Q-waves on the ECG should argue strongly against a large irreversible infarction.  This was almost certainly a small infarction or takotsubo.

A Thallium Myocardial Viability Study was done.

--Myocardium may not contract because of "hibernation" or stunning, which are reversible, as well as by irreversible infarction.
--This may be assessed by Thallium scintigram myocardial viability study.
--Details of this are beyond the scope of this article, but may be found here (full text, 2019).

FINDINGS:
Review of the rest/redistribution 3 plane SPECT reconstructed scintigram demonstrate normal perfusion on the immediate scintigram except for a small area of reduced perfusion in the apical inferior and mid segments consistent with absence of infarct and normal viability in all vascular
distribution. The 24-hour/redistribution image shows reduced uptake in the apical and mid inferior wall adjustment to significant subdiaphragmatic tracer uptake most consistent with ramp filter artifact.

Impressions:
1. Normal viability of the anterior, anterolateral, septal, and inferolateral walls.
2. High probability of viability in the inferior wall.

This answered the above questions:

Thus, it was not a large infarction with downtrending troponins, or an old infarction with acute MI superimposed.

It had to be either a small infarction (type 1 or type 2), or takotsubo.  And this is evident from the ECG.
















"Long QT" after droperidol

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A patient presented to the ED with intractable hiccups.  He also had "ongoing GERD symptoms with heartburn......but no chest pain"  (Whatever that means).  He was treated with droperidol and benadryl and this decreased his symptoms and he was discharged.  No ECG was recorded (!).

Later, the patient returned with altered mental status and reports of falls.

He had an ECG recorded:
The QT was 504 ms
The computerized QTc (Hodges correction) was listed as 530 ms.
Bazett correction would be 563 ms
The providers were worried that the droperidol had resulted in a long QT.
What do you think?

See below for explanation.














There are huge U-waves, best seen in V1-V3.  These are almost always due to hypokalemia.  Some overdoses can cause this:

Cole JB, Stellpflug SJ, Smith SW: Refractory Hypotension and “Ventricular Fibrillation” With Large U Waves After Overdose (this is a great full text online case of hydroxycholorquine overdose)


Here I have drawn lines at the beginning and end of the U-waves in V1-V3
Then I draw them down to lead II across the bottom
Then I go to sections that are under I-III, aVR-aVF, and V4-V6.
Then I draw the line up through those leads to show where the U-wave is in those leads.
And you can see how what may appear to be a T-wave and a long QT is really a U-wave.

V4-V6 in particular show only one wave which appears to be a T-wave only.  But by showing from other leads where the U-wave vs. T-wave is, we can see that this apparent T-wave is really a U-wave.

Whether it is a long QT or a QU, it may be equally prone to ventricular tachycardia and VF.
However, the etiology of U-waves is different is different from the etiology of long QT.
This would not be drug effect due to droperidol, but more likely hypokalemia.


The K was measured and was 1.7 mEq/L

Learning Points:

1.  When the QT seems impossibly long, consider that it might be U-waves which are mimicking long QT (often with a long QU interval)

The etiologies of long QT and large U-waves are different, even if they both may have the same dysrhythmic consequences.  Therefore, the treatment will be different.

2. Also, patients with intractable hiccups, or who have what they call "heartburn", should usually get at least an ECG, as ischemia could be underlying both of these.

What is the Diagnosis in this 70-something with Chest Pain?

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This is a very commonly missed ECG of a terrible condition.  In this case, it was almost dismissed.  I present many other similar ECGs at the bottom that were indeed missed or dismissed.


Case

I was texted this ECG from a physician assistant who works by himself in several small Emergency Departments.

He is a particularly smart and well trained emergency medicine PA (because he trained at Hennepin).

He added the words:

"What do you think?  70-something male with DM, HTN, no previous MI, with Chest pain"
What do you think?



















Here was my response:

"Definite Huge Occlusion MI (OMI). STEMI! This is a bad one.  There is RBBB with Left Anterior Fascicular Block (LAFB) which is a very ominous sign."

He texted back:

"That's what I thought but the cardiologist (at the receiving facility) was not convinced."

This is an obvious diagnosis to me.  Unambiguous.  Can't be anything else.
There is RBBB with LAFB with huge ST Elevation seen in V2-V4, (also subtle STE in aVL).

(The rhythm is uncertain, but it is supraventricular and probably atrial bigeminy (with P-waves that are not well seen), but the rhythm diagnosis is NOT critical in making the OMI diagnosis.)

Here I have put a line at the end of the QRS and beginning of the ST segment, so that you can assess for ST Elevation:
The image is distorted because it was a photo of a paper ECG.  
That is why the lines are not parallel.
Note that the QRS itself can mimic ST deviation; this is especially seen in inferior lead here.

Also note that the Elevated ST Segments in V2 and V3 are downsloping.  In the many cases of RBBB + LAFB in anterior MI that I have seen, this is the rule rather than the exception.  


Case continued:

The PA transferred the patient and, on arrival, the ECG was reportedly even more obvious.  The patient went to the cath lab:

Proximal LAD: 90% with thrombus
Mid LAD: 80% with thrombus
Distal LAD: 80% with thrombus

3 stents were placed.  Peak hs Troponin T was 23,070 ng/L (equivalent to 23 ng/mL; this is an enormous infarct!).

Echo showed anterolateral and septal wall motion abnormalities and an ejection fraction of 29%.

Comment:

Some ECG findings which are very clear to me are not clear to others.  I try not to post cases that are easy.  This one I would have thought was easy.  But apparently it is not, as ECGs like this are very often missed, by all kinds of providers, including cardiologists.



More similar cases

Other examples of RBBB/LAFB OMI in which the cardiologist contradicted the interpretation of the emergency provider and disagreed with cath lab activation:

I had just resuscitated this patient from VF cardiac arrest after 68 minutes of CPR:

I told the cardiologist that it is a proximal LAD occlusion and he rolled his eyes, and said "Maybe."  It was indeed acute LAD OMI


____________________________


Here is another example in which the cath lab was activated, then de-activated by the cardiologists, with the ST Elevation annotated below it:

This patient died 8 hours after cath lab de-activation.


With markup

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



_________________________

Here is another that was missed:

Resuscitated from ventricular fibrillation: what is the ECG Diagnosis?



________________________

Finally, this one

Here is a case of a young woman who presented with acute pulmonary edema.  The ECG was recorded during the pulmonary edema.  Cath lab was activated, then she arrested, and, after 30 minutes of resuscitation, achieved ROSC but was in severe shock.
Sinus tachycardia (NOT VT!).  See P-waves in lead II across the bottom.
RBBB and LAFB (wide complex)
There is clear STE in aVL, V2, and V3.
There is deep reciprocal ST depression in II, III, aVF.

The cath lab was de-activated.  She died of a 100% left main occlusion and peak troponin I of 500 ng/mL (the highest troponin I have ever heard of).

___________________________

Here is another that was missed by the ED providers:

This is a patient with chest pain and the following prehospital ECG:

Here are lines that mark the end of the QRS and beginning of the ST segment:
This also has RBBB and LAFB with ST Elevation, but more subtle
This STEMI was not recognized and the patient arrested and could not be resuscitated.


Learning Points:

1.  Level of training does not predict ability to diagnose OMI from the ECG. Paramedics and PA's can be outstanding at this.

2.  Beware RBBB with LAFB.  ST Elevation may not be obvious, or it may be.  It does distort the ECG and it confuses many ECG interpreters.






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