Tachycardia, Fever, and ST Elevation

This patient is approximately 30 years old with some serious baseline illness, and has a history of nonischemic cardiomyopathy.  911 was called for fever and increasing tachycardia.  The patient was too obtunded to report presence or absence of chest pain or discomfort.  The medics recorded this ECG:

There is sinus tachycardia at a rate of 150.  The computerized QTc is 441 ms.  There is 3.0-3.5 mm of ST Elevation at the J-point in V2-V4 (4.5 mm at 60 ms after the J-point) that would normally be called diagnostic of STEMI.

There is no reciprocal ST depression anywhere (which has a poor negative predictive value, but a high positive predictive value).

The medics activated the cath lab.

What do you think?






On arrival, the patient remained tachycardic, was febrile, and was obtunded.  Bedside echo showed very poor LV function.

The patient was not in clinical shock, was warm and well perfused, and did not have pulmonary edema.

There were no previous ECGs for comparison.

An ECG was recorded:

Slightly less tachycardic, and slightly less ST Elevation

What do you think?









We de-activated the cath lab.

The clinical picture did not fit STEMI.  The patient was clearly septic.  There was a previous history of non-ischemic cardiomyopathy.  Tachycardia can greatly exaggerate ST Elevation.

Here is a subsequent ECG:

There is not less tachycardia and less ST Elevation.

The patient ruled out for MI with very low troponin elevations, consistent with sepsis and cardiomyopathy (peak cTnI 0.048 ng/mL with 99% at 0.030 ng/mL).

Learning Points:

1. The ECG must always be interpreted in clinical context.  In a patient with fever one must treat the infection with supportive care and re-evaluate.  When there is no chest discomfort, one must be even more skeptical of ST Elevation and strongly suspect non-ACS etiologies of ST Elevation.
2. Extreme tachycardia can greatly exaggerate ST Elevation
3. STEMI only causes tachycardia to this degree when there is cardiogenic shock
4. Cardiomyopathy can also lead to false positive ECGs.

Chest Pain, ST Elevation, and an Elevated Troponin: Should we Activate the Cath Lab?

This was written by Sam Ghali (@EM_RESUS), with a few edits by me.

52-year-old lady presents to the Emergency Department with 2 hours of chest pain, palpitations & SOB. She is somewhat hypertensive, but her vital signs are otherwise normal. Here is her 12-Lead ECG: 

There’s a sinus rhythm at around 70 bpm. There are Q-waves in the inferior leads (II, III, AVF) with ST-Elevations. These elevations meet STEMI criteria (≥1mm in 2 contiguous leads). However, old MI w/aneurysm morphology (persistent ST-Elevation) can look just like this. Looking closer, we see clear ST depression in the lateral limb leads, I and AVL. While this may be change that is reciprocal to an Acute/Subacute Inferior STEMI, the problem is that LV aneurysm may also manifest with this reciprocal change. [This is further complicated here by the fact that this patient has LVH & strain pattern (R wave in AVL > 11mm) which can also account for these changes]

Is this a Acute/Subacute STEMI or an Old MI with persistent STE/ “Aneurysm Morphology”? 

What are some clues to help us differentiate between the two in this scenario?

1.  Ischemic Hyperacute T waves (Tall, round, symmetric, vs the “pointy” peaked-T’s of HyperK), are often a clue to ischemia. In STEMI, they are generally upright and large in proportion to the QRS. The T-waves here are not upright or particularly large. So this argues against acute STEMI. However, we must also keep in mind that in Subacute STEMI (6 hours duration) Hyperacute T-waves will decrease in amplitude and eventually invert as infarction progresses (indicating less viable myocardium) similar to what we see here. 

 2. There are Qr-waves in the inferior leads with minimal r-wave amplitude. In acute/subacute STEMI, the natural progression is for the Q-waves to increase in size, while the amplitude of the R-waves diminish. These will ultimately develop into a final mature “Qr-waves”. Therefore, catching these waves in their “transition period” would imply an evolving STEMI. Are the waves seen here still in the process of evolution, or is this their final state? It is difficult to answer this question based on this single ECG alone.  A word of caution: while anterior aneurysm almost always has QS-waves or tiny r-waves followed by an S-wave (rS-wave), inferior aneurysm may present with QR-waves (and, of course, Qr-waves)

3. Old MI w/Aneurysm will show moderate ST Elevation, as seen here. We don’t see excessive ST Elevations (“Tombstones”) that would suggest acute STEMI, but clearly acute STEMI can certainly present with moderate ST Elevation as well. 

4. Although not always available a prior ECG is probably the most helpful piece of information in these cases. Without them the diagnosis is often tough and one must often rely on other clinical data-  serial ECG’s, troponin, on-going chest pain, etc.

5. Most, but not all, ECG “aneurysm morphology” is associated with an actual aneurysm on Echo (see this case with ED bedside echo). So a bedside Echo showing a dyskinetic inferior wall may be helpful in this scenario as well, but this wasn't the case here. Bedside echo did show inferior wall motion abnormality, but this isn't helpful in distinguishing the two entities in the differential at hand.

6. Finally, prolonged duration of MI (subacute MI) can mimic LV aneurysm.  This is a case from Dr. Smith's files of a patient with no prior history of MI who presented with 12 hours of chest pain:

There are Qr-waves in inferior leads, and reciprocal ST depression in aVL.
Notice also that no lead has 1 mm of ST elevation.
This turned out to be a subacute inferolateral STEMI.
Immediate angiography showed 100% acute RCA occlusion and 99% circumflex (dual culprit lesions).  Maximum troponin I was 197 ng/mL (huge MI)

Case continued:

So is this patient having a STEMI? Should the cath lab be activated?

This case is tough. I will say that without a previous ECGs, given this patient's active/persistent chest pain and positive troponin, I very likely would have activated the cath lab. In this particular case however, a review of the chart revealed the following ECG from an admission 3 weeks prior:

Comparing the two ECGs, we see that her presenting ECG is largely unchanged.

Therefore, the changes in the inferior leads seem to indicate "persistent ST-Elevation", which is typically the result of an unreperfused, full thickness ("transmural") MI. Naturally, in the reperfusion era, this entity has become much more rare than it used to be.

So why did this patient have this persistent ST-Elevation/Aneurysm morphology?  

Interestingly, in further review of the chart it seems the patient was admitted to the hospital floor 3 weeks prior for an unrelated surgical procedure. She complained of nausea that night and the following 3 ECGs were obtained over a period of 10 minutes:

Just 2 minutes later:

8 minutes after that:

There is an obvious, large inferior STEMI with marked ST-Elevation in II, III, & AVF, along with significant depression in I & AVL. We can see that there is evolution of the elevations, worsening reciprocal change, as well as evolution of posterior involvement (right precordial R-waves with ST depression) 

There was very little documentation surrounding these ECGs. It appears that the patient was not experiencing any chest pain, and therefore unfortunately these ECGs were not acted upon. The following morning on rounds the ECGs were noted and the patient eventually underwent cardiac catheterization (>18 hrs after later!) She was found to have 100% occlusion of the mid RCA(culprit lesion), which gave rise to acute marginal, PDA and PL branches(which explains the posterior involvement). She received PCI with 2 drug-eluting stents in overlying fashion. She had a very large troponin leak. Convalescent Echo showed 30-35% LF EF, inferior wall akinesis, and persistent severe posterior wall hypokinesis. 

Take a look at the patient’s ECG taken the morning during rounds (still prior to cath):

Compared to the obvious STEMI ECGs from the night before, we can see that the degree of inferior ST elevation has diminished, along with the amplitude of the R-waves. These waves are still in the process of transitioning to their mature and final state as Qr-waves. These features are indicative of evolving infarction and of decreasing myocardial viability. Note also the T-wave evolution, from large, tall hyperacute T-waves to smaller biphasic/inverted T-waves. 

Also interestingly, note the increased R-wave amplitude in lead V2. This is a result of posterior wall infarction. The R-wave amplitude in V2 is the sum of the anterior forces from the anterior wall minus the forces of the posterior wall which are directed opposite this lead. Since there are now no opposite forces, the anterior forces predominate even more, resulting in increased R-wave amplitude in V2. What we are seeing is essentially "posterior Q-waves".

To better appreciate the electrocardiographic evolution of this MI, take a look at the chronological progression in the inferior leads:

Note the evolution of the R-waves as we catch them in transition to their final/mature QR wave state. Also note the evolution of the T-waves. 

Back to the patient’s present visit (3 weeks after this initial visit). She was again admitted to the hospital, and there was no further evolution of her ECG. She was maximized on medical therapy, her pain subsided, and her max troponin was only slightly elevated (NSTEMI). After a short stay, she was discharged home.

Learning Points:

1. Acute/Subacute STEMI vs LV Aneurysm can be tough to differentiate. Inferiorly, the distinction can be much tougher than anteriorly. (This is due to the fact that inferiorly we see the development of QR waves as opposed to anterior QS waves). Look at R-wave amplitude, T-wave size and morphology (especially hyperacute, upright T-waves for acute STEMI), and degree of ST Elevation (which should only be moderate in aneurysm morphology). Perform an echo, obtain serial ECGs, and always if possible compare to a prior ECG.

2. If despite taking these measures, the diagnosis is still in doubt: err on the side of cath lab activation!

3. Beware of ACS presenting with atypical symptoms, including absence of chest pain. This is particularly true in women, diabetics, and the elderly. You can see from this case that one can have Massive MI and still not experience any chest pain!

Very young man with chest pain, then cardiac arrest

A very young man, approximately 30 year old, called 911 because of 1 hour of severe chest pain.

The medics got him into the truck and recorded the following ECG:

It starts as sinus rhythm with probable inferior STEMI, but becomes ventricular fibrillation (or polymorphic ventricular tachycardia) halfway through!

He was defibrillated immediately and awoke.

He arrived awake and alert in the ED and had a bedside echo prior to arrival of the ECG tech:

This is a subcostal view and clearly shows the base of the heart with good function, but the apex with poor function.

This made me suspect not only inferior STEMI, but anterior as well, due to an LAD lesion with a wraparound to the inferior wall.

He then had this ECG:

De Winter's T-waves in precordial leads and ST elevation in inferior leads.  There are already QS-waves in V2 and V3. 
This suggests a partly open proximal LAD to a wraparound distal LAD supplying the inferior wall in addition to the anterior wall.

The cath lab was activated and angiography revealed a subtotal occlusion of the LAD (but not 100% - it was probably 100% at the time of the arrest).  There was a large clot burden with some thrombus embolized to the apex (accounting for the inferior STEMI).

He underwent thrombectomy of the proximal LAD and stenting of a residual atherosclerotic lesion.  The distal thrombus could not be removed.

Door to balloon time was less than 60 minutes; symptom onset to balloon time was less than 120 minutes (fast!!).

Here is the ECG after PCI:

Residual ST depression precordial, continued ST elevation inferior, loss of R-waves anterior.

Peak troponin I was over 100 ng/mL, a large STEMI.

Here is the ECG the next morning:

Minimal ischemia, but total loss of anterior depolarization forces (QS-waves).

There was never any ST elevation recorded, though it may have been there on the prehospital ECG if the ventricular fibrillation had not interceded.  And yet the entire anterior wall appears to be infarcted.

When de Winter reported his de Winter's waves, he reported that they were "persistent" and always associated with "occlusion."  However, "persistent" was not defined as having this on multiple serial ECGs; rather, it was reported that patients who had them had them for up to 2.5 hours of chest pain.    "Occlusion" was not defined, so it is unlikely that it was always 100%.

My belief, based on multiple cases with serial ECGs is that de Winter's T-waves represent a subtotal occlusion of the LAD such that it looks like a synthesis of subendocardial ischemia with ST depression AND hyperacute T-waves.  Thrombus is dynamic and is always forming and lysing, so that the angiogram may not exactly represent the state of the artery at the time of the ECG.

See this case.

And see also this case.


Formal echo is consistent with all of this:
Decreased left ventricular systolic performance -- moderately severe.
The estimated left ventricular ejection fraction is 30%.
Regional wall motion abnormality-distal septum, anterior and apex, large.
Regional wall motion abnormality-anterolateral.
Regional wall motion abnormality-distal inferior wall.
No contrast perfusion uptake of septum and apical walls (i.e., continued ischemia in spite of an open artery) 

This would seem to indicate "No reflow" (see this case)]: downstream platelet-fibrin aggregates have occluded small vessels, such that reperfusion is very limited in spite of an open epicardial artery.  "No Reflow" usually implies less than TIMI 3 flow in spite of an open artery.  In this case, the flow in the LAD after PCI was not commented upon.


This was repeated a few days later:
Regional wall motion abnormality-distal septum anterior and apex large.
Regional wall motion abnormality-anterolateral .
Regional wall motion abnormality-distal inferior wall .
Decreased left ventricular systolic performance moderately severe .
Left ventricular hypertrophy concentric .

This ECG is from day 5:

QS-waves are persistent, consistent with the large anterior wall motion abnormality

Learning Points:

1. The LAD can occlude and re-open, and can shower downstream thrombi that occlude more distally, in this case resulting in inferior STEMI also (due to wraparound LAD)

2.  de Winter's T-waves were the only sign of LAD occlusion.  One can miss the ST elevation.

3.  The angiogram may not exactly represent the state of the artery at the time of the ECG.  de Winter's T-waves probably represent a state of subtotal occlusion of the LAD.

4.  The thrombus in ACS is dynamic.

5.  Downstream platelet fibrin aggregates can result in profound infarction, even with rapid reperfusion of the epicardial infarct-related artery.  If it results in less than TIMI-3 flow, it is called the "No Reflow" phenomenon.

Validation of Smith Modified Sgarbossa Criteria Published in American Heart Journal

We have completed and published the external validation of the Modified Sgarbossa Criteria for Diagnosis of Acute Coronary Occlusion in the Presence of Left Bundle Branch Block.

H. Pendell Meyers had just graduated from college when he took this project on.  Now he is a 4th year student at Duke, interviewing for Emergency Medicine Residency Positions.

He did amazing work on this project.

Here is a link to the abstract:
http://www.sciencedirect.com/science/article/pii/S0002870315005918

A quick summary:

Sgarbossa criteria:

1. at least 1 mm of concordant ST elevation in at least one lead (5 points)
2. at least 1 mm of concordant ST depression in at least one of leads V1-V3 (3 points)
3. at least 5 mm of discordant ST elevation in at least one lead (2 points)

Weighted criteria (the actual Sgarboss criteria): At least 3 points required to make the diagnosis of acute MI.  Thus, criterion 3 is not sufficient.

Unweighted criteria: any one of the above

Derived Smith-Modified Criteria, published in 2012 in Annals of EM (amazing work on this was done by Dr. Ken Dodd, who was a medical student at the time and is one of our emergency medicine/internal medicine residents now):

1. at least 1 mm of concordant ST elevation in at least one lead (5 points)
2. at least 1 mm of concordant ST depression in at least one of leads V1-V3 (3 points)
3. at least 1 mm of discordant ST elevation AND an ST elevation to S-wave ratio of at least 25% in at least one lead.

Validation Results:

There were 45 patients with LBBB and acute coronary occlusion and 249 controls:

The Modified Criteria (ST/S ratio of greater than or equal to 25%) was far more sensitive than either the weighted or unweighted Sgarbossa criteria 

Formula positive for LAD occlusion. But echo shows no wall motion abnormality! What is it?

Dr. Josu Abecia Valencia, from Spain, asked me my opinion on this case.  He has a great Spanish language blog.  You can find this case in Spanish at his blog here: https://urgenciasbidasoa.wordpress.com/2015/11/16/caso-201-varon-de-35-anos-con-dolor-toracico-de-10-horas-de-evolucion/

He gave his permission for me to post it here.

A 35 year old complained of typical substernal chest pain:

What do you think?
My opinion is below.
Notice the computer reads early repolarization.

Here is my response:

Dr. Abecia,

This is highly suspicious for LAD occlusion, though not diagnostic.

Have you used my formula?

ST elevation at 60 ms after the J point in lead V3 = 4 mm

computerized QTc = 405

R-wave amplitude in V4 = 14.5 mm

Formula value = 23.9, which is > 23.4 which is pretty specific for LAD occlusion.

I would do frequent serial EKGs, every 15 minutes, for several hours.

I would do an emergent formal contrast echocardiogram.

If still non diagnostic, consider immediate angiography.

What was the outcome? 

Here is the outcome (slightly limited because I don't read Spanish very well):

Time zero: Troponin T drawn, returns later at 43 ng/L (= 0.043 ng/mL, slightly elevated)

Serial EKGs unchanged.

Thoughts: myopericarditis vs. early repolarization vs. possible MI

Time 5 hours: Troponin T returns at 151 ng/mL.

Still thinking myocarditis

Time 11 hours: Troponin T returns at 350 ng/mL

Echo shows EF of 67% and no Wall Motion Abnormality

But symptoms persisted, and with the positive troponin, they sent him for angiogram.  Here are the results:

Occlusion of the very distal LAD.  So in this case, it was a small infarct territory.
The thrombus was suctioned out and it was stented.
Symptoms resolved.

The formula to differentiate benign ST elevation from LAD occlusion worked perfectly, even though it was a small anterior MI.  It outperformed serial ECGs and formal echocardiogram.

One might argue, with good rationale, that such a small MI can wait until the next day for angiogram.  I will not oppose the argument strongly, but the patient did have ongoing chest pain that was relieved by intervention.  

What is the treatment for this subendocardial ischemia?

This elderly patient had an accidental carbon monoxide poisoning.  The patient did not have ischemic symptoms, but we do an ECG routinely to look for ischemia.  Here it is:

There is ischemic ST depression, typical of diffuse subendocardial ischemia.

The CO level returned at 28%.

Carbon Monoxide displaces oxygen from hemoglobin, and thus effectively decreases oxygen saturation, in this case by 28%, down to 72%.  But it also binds with cytochrome oxydase to inhibit ATP formation.  Thus, its effect is the same as ischemia.

We consider cardiac ischemia (on the ECG, or by elevated troponin), by itself, to be an indication for emergent hyperbaric oxygen (HBO) even if there are no other indications such as neurologic disability, loss of consciousness, level greater than 40%, pregnancy, or other indications.

We happen to have one of the world's finest hyperbaric oxygen facilities here at Hennepin County Medical Center (HCMC).  Dr. Cher Adkinson designed and built the center, and it is now run by our director of Hyperbaric Therapy, Chris Logue, MD.

We treat many chronic conditions with , but are open 24/7/365 for emergencies including CO poisoning, air embolism, decompression sickness, and central retinal artery occlusion.

The patient underwent hyperbaric oxygen therapy.  Here is her ECG afterwards:

There is only minimal residual ST depression.

The troponin I peaked at 5.1 ng/mL.

Dr. Adkinson's research here at HCMC, published in JAMA, found that myocardial injury (as indicated by troponin elevation, but also by ischemia on the ECG) is common in carbon monoxide poisoning and is independently associated with an increased risk of mortality at 7-year followup (38% vs. 15%).  A subsequent publication in JACC reported that myocardial injury was not at all predicted by CO level.

Echo after HBO showed:
Normal estimated left ventricular ejection fraction - 65%.
No wall motion abnormality
Normal left ventricular size.

The patient did well.

STE in aVR and diffuse ST depression: It can be ACS or demand ischemia. If ACS, either posterior STEMI or subendocardial ischemia!

A middle-aged male with a history of 2-vessel coronary bypass called 911 because of the relatively sudden onset of severe SOB.  He had had more mild SOB for the past 2 days.  The medics found him in respiratory distress with coarse breath sounds, a BP of 196/132, oxygen saturations of 90%, and a pulse of 130.  They put him on CPAP for respiratory support.  He denied chest pain.

Here is his prehospital ECG:

There is diffuse ST depression, with ST elevation in lead aVR

The patient arrived in the ED and was put on Noninvasive ventilation (BiPAP).  Blood Pressure was 200/110.  A nitroglycerin drip was started and this ECG was recorded:

Same as prehospital

The ischemia could be due to supply/demand ischemia from hypoxia, tachycardia, and hypertension, or it could have been initiated by ACS.  The ECG cannot differentiate.   If ACS, it could be diffuse subendocardial ischemia, or posterior STEMI.  Does that matter?

Bedside echo showed diffuse B-lines of pulmonary edema.

The plan was to completely control the blood pressure and re-assess for ischemia.

BP was controlled to 120/70 with very high dose Nitro, and the patient's respiratory distress was improved, and another ECG was recorded:

Continued ST depression

Now we have controlled the excessive demand but the ischemia persists: the BP is not elevated, the heart rate is only mildly elevated, there is no more hypoxia, the hemoglobin returned normal, and there is no evidence of valvular dysfunction (at least no murmur).

Thus, ACS is very likely the initiating factor.  So we have ACS with both refractory symptoms and pulmonary edema, both of which are indications for cath lab activation.

ST depression in the precordial leads can be either posterior STEMI or diffuse subendocardial ischemia.  Does this matter?  No!  This is ACS that needs the cath lab now because it is refractory to medical management.

There are those who think this ECG pattern in ACS is due to left main occlusion.  This is not accurate.  See this exhaustive post on the topic.

The cath lab was activated.

Normally, a P2Y12 inhibitor (clopidogrel, ticagrelor) would be given, but in this case with STE in aVR and diffuse ST depression, there is high potential for left main insufficiency or severe 3 vessel disease.  Thus, there was approximately a 50% likelihood that the patient would need CABG (surgical bypass), although this probability is less in a patient with previous bypass.  Clopidogrel or even ticagrelor would increase the risk of severe bleeding at surgery.

Thus, eptifibatide was given instead of ticagrelor.  Eptifibatide can be turned off.

The patient could not lie flat and so was intubated.

The patient went to the cath lab and had a 100% mid circumflex occlusion that was opened.  Since bypass would not be needed, ticagrelor was initiated.

The outcome was good except for some bleeding complications, during which time his P2Y12 inhibitor (ticagrelor) needed to be held.

The echocardiogram confirmed a posterior wall motion abnormality.  The troponin I peaked at 20 ng/mL.

Epilogue

The patient returned a few weeks later with the identical presentation: respiratory failure, pulmonary edema, and severe hypertension.  His ECG is shown here:

There is diffuse ST depression and ST elevation in aVR, although not as profound as the first time

After treatment with BiPAP and IV Nitroglycerin, his symptoms greatly improved and this ECG was recorded:

The supply/demand issues are gone and the ST depression is resolved.

Because of the recent stent and the time off of clopidogrel, an angiogram was done and showed no in-stent thrombosis (no new ACS).  The troponin peaked at 1.5 ng/mL and there was no new wall motion abnormality.

This ST Depression was due entirely to supply/demand mismatch, not due to ACS.  The second presentation was purely a type II MI.

Learning Points:
1.  In the setting of ischemia, before diagnosing ACS, manage the oxygen supply and demand issues first.  Use supportive care.  Then re-assess.  If ischemia persists, then it is ACS.

2. If ACS and symptoms are refractory, it does not matter whether it is a posterior STEMI or diffuse subendocardial ischemia.  Emergent angiogram and PCI if indicated should be undertaken.

Slightly Peaked T-waves, What is it?

I saw this as I was reading a large a stack of ECGs:

What do you think?

There is sinus tachycardia.  The T-waves are slightly peaked, suggesting hyperkalemia.  But what is atypical is that the T-wave in V3 towers over the R-wave.  And there is terminal QRS distortion in lead V3 (meaning there is neither a J-wave nor an S-wave).  The QTc is 462 ms.  These are suspicious for hyperacute T-waves and anterior injury.  The formula score is 24.8 (>23.4), also consistent with anterior injury.

The above is what I thought when I saw this, so I went to the chart and found this history:

A type I diabetic aged approximately 35 years old presented with chest pain, nausea, vomiting and diffuse abdominal pain.  The patient was in DKA with an anion gap of 35, a glucose of 1128, and a K of 5.5 mEq/L. 

pH = 7.17, pCO2 = 24, HCO3 =  8.  
Her T-waves were attributed to hyperkalemia, without further investigation.

What do you think of this?

T-waves are much more normal, less peaked, but also with better R-wave amplitude.  The ST segment is back to 0.  Equation value is 23.0.  There is an S-wave in V3 now, although small.

One would not expect such profound T-wave changes from a K of only 5.5.  

The patient did have a serial troponins (they are automatically ordered on critically ill patients) and they rose to a peak of 12.4 ng/ml, which is too high for a typical critical illness without MI.  
Here is her ECG the next day (with a normal K):



Because of the high troponin, echocardiography was done and showed a wall motion abnormality in the anterior, anterolateral, and apical walls, consistent with LAD myocardial infarction.  Therefore, she underwent angiography and had a 95% LAD thrombotic culprit that, fortunately, had reperfused on its own (that's why the troponin was only 12).  It was stented.  Had it not opened on its own, it could have resulted in a very large anterior wall MI.

The possibility of anterior STEMI was not noticed during patient care.  I noticed it much later on looking through a random stack of EKGs.  I mention this only to point out that these findings can be noticed, and differentiated from more benign etiologies, prospectively.  

This is NOT a retrospective finding.

Learning point: 
Hyperacute T-waves and hyperkalemia may be confused, and they may be simultaneous.  Here the potassium was barely high enough to result in a change in T-waves, so one should be especially suspicious in this case.

Is this Coronary Occlusion? Cath lab?

This patient presented with cardiac arrest:

There is RBBB and ischemic ST elevation in V1-V3.  There is ST elevation in aVL and ST depression in III.  This is all consistent with a proximal LAD occlusion.
Should the patient go to the cath lab?

The answer depends on the clinical situation, of course!

This is a young patient who had pulseless, non-shockable cardiac arrest.  He was found with heroin paraphernalia.  He was resuscitated with ventilation and epinephrine.

So this is a type 2 MI with ST Elevation.  Not all ischemic ST elevation is due to plaque rupture.  Only if it is a result of plaque rupture is there an indication for emergent coronary angiogram.


The etiology of cardiac arrest was respiratory, with hypoxia as the etiology.  The ischemia on the ECG is due to a combination of hypoxia from hypoventilation and severe hypotension while in arrest.  It is not due to coronary obstruction. 

New Paper published on Significance of Reciprocal ST depression in lead aVL

We just published this online in the American Journal of Emergency Medicine:

ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis

Johanna E. Bischof

Christine Worrall

Peter Thompson

David Marti

Stephen W. Smith

I've written about this topic many times, but this is the first formal study we have done on the topic.

A few highlights:

1. Any ST depression (it might be as little as 0.25 mm, so be careful!) in aVL was extremely sensitive for any coronary occlusion that resulted in inferior infarction.  Of 426 inferior MI due to complete coronary occlusion, 418 (98%) had an obvious inferior MI and/or had some ST depression in lead aVL.

2.  Even when there was ST elevation in V5 and V6 (35 cases), there was some ST depression in lead aVL in all 35 cases!

3.  No pericarditis case had any ST depression in lead aVL (100% specificity, CI 91-100%) .

4.  We did not compare inferior early repolarization (as defined as benign inferior ST elevation). Some inferior early repol may have some ST depression in lead aVL, but I believe that this is very uncommon.  I have been unable to find a consecutive cohort of proven benign inferior ST elevation to formally study.

5.  ST depression in aVL was more accurate than STE in lead III greater than STE in lead II.    88% of inferior STEMI had STE in III greater than II, but 12% did not.

A couple ECGs: These do not come from the study:

This was a middle-aged man with chest pain (Figure A):

There is diffuse ST elevation, but there is no ST depression in lead aVL
Diagnosis?

The above is a case of a patient with chest pain who did not have MI.  This was early repolarization.

Figure B. Here is a 40-something with chest pain

What is it?

The above (figure B) was a proven occlusion of an artery supplying the inferior wall (in this case, it was a distal occlusion of an LAD that wrapped around the apex and supplied the inferior wall.
Notice the minimal (less than 1 mm) ST elevation in III.  But there is clearly some ST depression in aVL.  This makes it all but diagnostic of inferior MI.


Figure C:

What is this?

Figure C above is proven pericarditis.

Here is the ECG 2 days later (Figure D):

Pericarditis later still

Paramedics make a great call

A middle-aged male called 911 for chest pain.

Here was the first prehospital ECG with pain at 5/10:

Computerized QTc is 418 ms.  There is nondiagnostic ST elevation in V1-V4.
If you use the formula, you get 25.15, (> 23.4, which is all but diagnostic of LAD occlusion).
The medics did not use the formula, as far as I know.

Medics were worried, and gave nitroglycerine, then repeated the ECG at 5 minutes with pain at 2/10:

 Less ST elevation

And they repeated again with pain at 1/10 at 9 minutes:

Near Normal 

Medics asked for physician interpretation on arrival. Physicians were worried and activated the cath lab.   The first (and only) ED ECG is here:

QTc 386.  Most ST elevation is resolved.  Formula value is now down to a very low value of 19.352

A 90% thrombotic LAD lesion was found and stented.  There was pre-procedure TIMI-3 flow (perfect flow)

Door to balloon time was 25 minutes.

Peak troponin I was 17 ng/mL.

Subsequent Echo showed EF of 56% and distal septal, anterior, apical, and

anteroseptal hypokinesis (wall motion abnormality).

Here are post PCI EKGs, this one at 29 minutes after arrival:

You can see the beginning of terminal T-wave inversion in V2 and V3.
Had there been no prior ECGs, this patient who is now pain free would be suspected of Wellens' syndrome

The next one was done at 10 hours after the first:

Evolving T-wave inversion, classic Wellens pattern B morphology

And then the next day:

Full blown Wellens' Pattern B terminal T-wave inversion.

Learning Points

1. This was diagnosed as a NonSTEMI.

2. The artery was occluded, or nearly so, at the time of the first ECG.

3. Serial ECGs demonstrated dynamic changes diagnostic of ACS (transient STEMI)

4. This facilitated rapid treatment of a potentially life threatening LAD thrombus.

5. This also demonstrates how Wellens' ECG morphology is a representation of the post occlusion state, after spontaneous reperfusion (although it also looks that way after therapeutic reperfusion)
6. Finally, Transient STEMI should be taken emergently to the cath lab.  Failure to do so can result in Disaster: Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death
  

Here is a similar case and its learning points, with a reference to an article by my partner, Brian Mahoney, on use of prehospital nitroglycerin:

Wait until after the ECG to give Nitroglycerine

Learning points:
1. NTG may cause reperfusion
2. Record an ECG before NTG
3. Always look at prehospital ECGs
4. Even after STEMI (if reperfused, with small amount of myocardium infarcted), and even when the ECG is diagnostic of ACS (as it was the next day), the simultaneous echocardiogram may be normal.

Here is an interesting abstract regarding NTG after the EKG:

Mahoney BD, Hildebrandt DA, Allegra P. Normalization of Diagnostic For STEMI Prehospital ECG with Nitroglycerin Therapy. Prehospital Emergency Care 2008;15:105, Abstract 24.

 Hypothesis. The decision to take a patient for emergent reperfusion therapy is largely determined by an ECG diagnostic for ST Elevation Myocardial Infarction (STEMI). Hildebrandt et al have proven that  prehospital 12 Lead ECGs followed by an immediate call for reperfusion team mobilization reduce door to balloon times.We hypothesize that prehospital ECGs will normalize in some STEMI patients after  nitroglycerin (NTG)therapy or due to spontaneous reperfusion.  NTG therapy before an ECG, or the absence of a prehospital ECG capacity in some services may lead to missing the early diagnosis of STEMI thus delaying reperfusion therapy. Methods. A prospective analysis of consecutive adult patients  presenting to an urban/suburban two paramedic ambulance service fromJuly 15, 2006, to August 15, 2007, who have diagnostic ECGs for STEMI.  Paramedics managing a possible myocardial infarction patient were instructed to obtain rapidly an ECG prior to treatment with NTG. If the initial ECG was diagnostic for STEMI the paramedic called to mobilize the reperfusion team. A second ECG was done prior to arrival at the ED. The ECGs were later reviewed by emergency physicians and cardiologists who confirmed the presence of a diagnostic prehospital ECG and STEMI.  Results. During the 13 month interval, 87 patients had an initial ECG that was diagnostic for STEMI. These patients received no NTG from the paramedics prior to obtaining the first ECG. An average of 16 minutes 42 seconds later, 3 patients had an ECG that was no longer diagnostic for STEMI and 3 had a partial normalization in their ECG that made diagnosis of STEMI more difficult. Conclusions. Prehospital ECGs diagnostic for STEMI can normalize or become nondiagnostic after NTG administration or due to spontaneous reperfusion or evolution. In the absence of a prehospital ECG, it is possible that 6 of 87 (7%) of STEMI patients in this study would have had reperfusion delayed due to a rapid change in their ECG. Limitations include no control group receiving NTG prior to the first ECG.