Thursday, February 22, 2018

Shoulder pain after lifting a heavy box

Written by Pendell Meyers, edits by Steve Smith


This will be too easy for most long-time readers, but if you are at that level, sit back and enjoy noticing how few milliseconds it takes to recognize this thanks to so many prior examples on this blog!

I was sent this ECG from EMS with only the information that it belonged to a middle aged male with left shoulder pain.
What do you think?











There are hyperacute T-waves in leads V1-V6, as well as in leads II, III, aVF. The J-points are all at baseline with the exception of leads V2-V3 which show a small amount of STD (which makes de Winter morphology in the presence of hyperacute T-waves).

How can you explain that the most obvious findings are in the anterior leads, yet the inferior leads are also hyperacute??

The occluded vessel must supply the anterior wall and also the apex and/or inferior wall. The most common variant that satisfies this is a type III "wraparound" LAD. This is a large and long LAD that wraps around the apex of the heart, supplying the apex and sometimes even parts of the inferior wall.

By ECG, this acute coronary occlusion is predicted to be of very short time duration, with very high acuity and very high viability. As shown in our reference diagram below, hyperacute T-waves generally exist only within a few hours of persistent acute coronary occlusion, or immediately after reperfusion ("on the way up, and on the way down," as Dr. Smith says).








We activated the cath lab based on this EMS ECG, because it is obviously diagnostic of acute coronary occlusion involving the anterior, lateral and inferior walls. When I make this decision prospectively on this particular highly diagnostic ECG, I estimate that the likelihood of acute coronary occlusion as the etiology of these ECG findings is approximately 99%, with the remaining 1% being the occasional takotsubo cardiomyopathy with indistinguishable ECG findings, and which can only be differentiated by angiogram.


The patient arrived in the resuscitation bay at the same time as the cardiologist.

He was a middle aged man with history only of HTN who called EMS for "soreness" of the left shoulder while working in his garage. He stated he lifted a box weighing approximately 75 lbs, then set it back down, then noticed severe pain in his left shoulder described as "soreness" and "pressure." He stopped working, but the pain persisted. He waited 2-3 hours at home before calling EMS thinking the pain might simply go away.

Here is his initial ED ECG:
Essentially the same findings, hyperacute T-waves without dramatic ST segment changes.




The cardiologist was somehow not impressed by these findings. He also thought that the pain was musculoskeletal because it started around the time of lifting a heavy box. Yet on exam the patient had full range of motion without any change in his constant severe shoulder pain.

I advised the cardiologist that this patient must be taken immediately for cath and intervention. He stated that this ECG does not meet STEMI criteria. I said that the patient has an acute coronary occlusion based on the hyperacute T-waves, the same pathology as an obvious STEMI. The only difference being that there is even more viable myocardium to save than a classic obvious STEMI because there is not yet STE.

Note: The reason there is even more myocardium to save than classic STEMI is because acutely ischemic myocytes first "register" in the T-wave and create increased area under the T-wave, then as they start undergoing the process of death they register in the ST segment, and finally when they are stunned or dead they cannot conduct the action potential and register in the Q-wave. As far as I know this is not proven on a cellular level but is well supported by my experience and hundreds of cases on this blog.

He asked me: "did you write a case report about this or something?"

I replied "yeah, lots of them actually."

He asked me where I thought the lesion was based on the ECG, and I said "mid LAD or higher, and the LAD will be a type III wraparound."

I stood by the monitor, getting repeat ECGs every 5 minutes for the next 20 minutes while trying to convince the cardiologist, expecting the repeat ECGs to show evolution to frankly obvious STE. But the ECGs did not change - hyperacute T-waves were present non-stop for approximately 45 minutes (from EMS ECG to my last ED ECG). The patient stated that his pain had been exactly the same for 3-4 hours, with no episodes of decreasing and then returning pain.

In my experience (and Dr. Smith agrees), it is unusual for hyperacute T-waves to last this long without progression or evolution. Most cases we have on this blog show evolution to obvious ST elevation, or you see the predictable progression of reperfusion and reocclusion with hyperacute T-waves in both directions. It is possible that there was reperfusion and then reocclusion between the EMS ECG and the ED ECG, although this is less likely because the patient denied temporary improvement in symptoms. Interestingly, Dr. Smith notes that de Winter himself stated that his characteristic morphology was stable for several hours, although Dr. Smith's opinion is that de Winter's data did not actually support that assertion.

It is possible that he had some very small source of collateral flow which was just barely enough to prevent progression, keeping him on the upper end of the de Winter pathology spectrum. It is also possible that the patient had recurrent brief episodes of reperfusion and reocclusion which did not have enough time to show the progression of ECG findings before reversing.



My fellow resident performed a bedside US showing a very dense anterior and apical wall motion abnormality, further confirming the diagnosis.






Thankfully, the cardiologist took the patient to the cath lab at this point.

Here's what they found!

100% mid-LAD occlusion.

With red arrows at the site of occlusion.


Mid-intervention, you can see the occlusion has been opened and there is a very large territory of myocardium supplied by the previously occluded LAD.



After intervention with good flow. This LAD is large and long such that it cannot be captured in one frame, and is seen extending down further in other images (not shown), wrapping around the apex of the heart. This confirms wraparound LAD.


Here is his post-cath ECG approximately 2 hours after the above ED ECG (no ECGs available between my ED ECGs and this one):


What do you think?












This ECG shows progression of acute myocardial infarction to almost complete transmural anterior wall loss. There are new deep wide pathologic Q-waves in V1-V5, with persistent STE and some loss of T-wave hyperacuity. Hyperacute T-waves in the inferior leads are now much less hyperacute than seen in the prior ECG.



But we're done, right? The angiogram confirms successful reperfusion, right?

WRONG.

The ECG is much better at confirming or denying reperfusion than the angiogram. The reason is that epicardial large vessel flow does not necessarily ensure that the actual myocytes downstream are receiving blood flow. The epicardial vessel obviously branches into innumerable smaller branches to provide capillary circulation to the cells. The ECG measures the viability of the cells rather than the flow through the epicardial coronary vessels. Expert ECG interpretation is better than angiogram, better than troponin, even better than patient reported symptoms for determining the state of occlusion and reperfusion!

"No reflow" phenomenon is described when a patient seemingly has successful reperfusion on angiogram but persistently progressing myocardial infarction. This is usually evidenced by ECG changes that progress along the occlusion progression below, and looks similar to the progression seen in patients who receive no intervention at all. This is thought to be due to downstream showering thrombi and platelet aggregates into the microcirculation or other unknown pathophysiology.

So knowing that this patient had relatively good door to balloon time, good angiographic result, and hyperacute T-waves just prior to emergent cath, what do you expect to see for his peak troponin over the next 24 hours?







Answer: Very very high, because despite the angiographic result the ECG shows complete infarction.


Indeed, his peak troponin T was 8.89 ng/mL (very highly elevated). Echo showed EF 35% with dense anterior and apical wall motion abnormality.

Here is the next day ECG:
T-waves further deflating as expected in the course of subacute total LAD occlusion infarction. Remember, when this QRS morphology is present the T-wave becomes almost the only reliable indicator of progression/reocclusion/reperfusion, and is in fact the main consideration used in decision aids to differentiate acute LAD occlusion versus persistent STE (LV aneurysm morphology).


These ECGs are unfortuantely an excellent example of the progression to "LV aneurysm morphology" (see below for reference). The ECG will likely remain similar to the above indefinitely. It is critical to recognize this morphology as this patient is at highest possible risk for the classic complications of transmural infarction including anatomic LV aneurysm, mural thrombus with subsequent stroke, free wall rupture, VSD, Dressler's syndrome, etc. He is also at risk of another complication that gets less discussion: misdiagnosis of his new baseline ECG! He will likely have persistent STE which will be alarming to his future providers, yet the T-waves will likely be the most reliable electrocardiographic feature to tell us whether he is experiencing further acute coronary occlusion affecting his anterior wall. He is at risk of mismanagement in both directions. Should he unfortunately suffer a pulmonary embolism or pericarditis or simply GERD or chest wall pain, for example, he may present with chest pain and this ECG, prompting premature diagnostic closure and immediate catheterization rather than further workup for other causes. Should he suffer another acute coronary occlusion, diagnosis may be missed or delayed because his ST segments are not appreciated as different from his baseline ECG which will now have STE forever.




The patient recovered and did well. Long term outcome unknown.




Learning points: 

1) You MUST be able to recognize hyperacute T-waves such as these. They are common early in the course of acute coronary occlusion.

2) You must learn and advocate for your patients, as these ECG findings are not widely taught or known since our current guideline-promoted strategy focuses only on the misguided STEMI criteria. 

3) Hyperacute T-waves and/or de Winter morphology may be present for hours without obvious evolution, but in most cases you can find evidence of progression with serial ECGs. They may even represent complete occlusion with ongoing necrosis (infarction)!

4) Type III Wraparound LAD is a common anatomic variant which produces anterior and inferior findings on ECG.

5) The ECG is the most accurate measure of occlusion and reperfusion, even better than angiogram, laboratory values, or patient symptoms.

6) You must become familiar with the ECG findings of complete full thickness infarction, as well as the clinical syndromes and complications that ensue.





Monday, February 19, 2018

Altered Mental Status, Bradycardia

911 was called for an elderly woman who fell and was confused.  Medics found her unresponsive, with "convulsive" movements.  They could not find a pulse.  They performed CPR, gave epinephrine, and intubated the patient and regained a pulse, at which time she became responsive. 

On arrival, heart rate was 87 and she was hypotensive at 52/21, with a palpable pulse and cardiac function present on echo.  She was intubated (by medics), but awake and alert and nodding to questions, shaking her head "no" to chest pain, headache, or SOB.  Repeat pulse was slow and irregular.  She was non-focal and followed commands.

Her heart rate dropped back down and an ECG was recorded:
Thoughts??









First, there are very sublte regular P-waves at a rate just over 100, seen best in lead II across the bottom.  The ventricular response is irregular and dissociated, and narrow, so there is complete AV block with variable junctional escape.

And one other finding.   At conference, one of our smart faculty, Dr. Richard Gray, immediately made the diagnosis without any other clinical information, though it is very subtle.  What is it?

This magnification of lead III may help, though it is still very subtle:
What is that bump at the end of the QRS?


The diagnosis was not suspected based on either clinical or ECG grounds.  The patient was given atropine 0.5 mg x 3 with no response.

Labs were:
VBG: 7.21/59/39/23
Lactate: 4.8
Hgb: 13.7
Na: 138
Cl: 109
K: hemolyzed at 8.1
CO2: 23
Cr: 2.62

After ketamine sedation, transcutaneous pacing was begun at a rate of 70, with capture at 48 milliamps.

It was found that the patient was on metoprolol and diltiazem, so Calcium gluconate 3 grams was given for both possible hyperkalemia and calcium channel blocker (CCB) toxicity.  Glucagon 1 mg was given for possible BB toxicity.

High dose insulin (HDI) was started at 1unit/kg for probably CCB and BB toxicity.

At 60 minutes, transcutaneous pacing was stopped and another ECG was recorded:
The finding is still very subtle.








It is very small Osborn waves.  In the second ECG, it is most apparent in lead V6, though still extremely subtle.

This is a diagnosis that should be made clinically.  One would think that you don't need an ECG to diagnose hypothermia, but sometimes the temperature is not easy to get.

In this case, they had trouble obtaining a rectal temperature.  This alone is a clue that it may be very low.  When they finally did get a temperature by urinary catheter probe, it was 29 degrees C, or 84 degrees F.

In this case, the ECG had atrial fibrillation with a very slow ventricular response.  One should not only suspect hypothermia, but also hyperkalemia and drug toxicity.  All three contributed here.  Transcutaneous pacing and treatment for all 3 disorders was undertaken with success.

Ultimately, the patient was found to be uroseptic.

Tiny Osborn waves.

If you don't believe the finding in lead III, look at this series of ECGs that start at 23 degrees and end at 29 degrees.  Look at lead III on the 4th (last, at 29 degrees) ECG.

Massive Osborn Waves of Severe Hypothermia (23.6 C), with Cardiac Echo



Learning Point:

1. Always obtain an accurate temperature in critically ill patients.  Rectal temp may not record accurately.  If the temp does not record, consider that it is too low.  Or get an EKG (just kidding).

2.  Use transcutaneous pacing when bradycardia results in cardiac output that is insufficient (shock, in this case manifested by ).

Everything you need to know about transcutaneous pacing:

Emergency Transvenous Cardiac Pacing





Thursday, February 15, 2018

A female in her 60s who was lucky to get expert ECG interpretation

Submitted and written by Alex Bracey, with edits by Pendell Meyers and Steve Smith:

I was walking through the critical care section of the ED when I overheard a discussion about the following ECG. I had no history on the case and no prior ECG for comparison.

What do you think?




Here are inferior leads, and aVL, magnified:
A closer inspection of the inferior leads and aVL
Sinus bradycardia. 
The T-wave in lead III is slightly tall and broad (increased area under the curve) compared to its QRS complex. In isolation, this probably could not be called a hyperacute T-wave, but you may suspect it.   
There is T-wave inversion (TWI) in aVL.  

T-wave inversion in aVL: when is it abnormal?

There is no LVH or LBBB on which to blame the TWI (i.e., the QRS is normal). While T-wave inversion in aVL may be normal in the presence of a normal QRS, this is only true when the T-QRS angle is small. That is to say, when the T-axis and QRS axis are similar. In other words, if the QRS is negative, the T-wave may be negative. However, here QRS axis is about 35 degrees and the T-axis is about 85 degrees. Thus the T-QRS angle is 25 - 85 = (-60) degrees, which is abnormal. Any absolote value greater than 45 degrees is suspicious for T-wave inversion (however, this is very complex; see table posted at the bottom of this post.)

Now that we know the T-wave inversion in lead aVL following a normal QRS complex is abnormal, it helps to confirm that the T-wave in lead III is indeed hyperacute. The flattened T-wave in V2 suggests likely posterior involvement.

The cath lab was not activated based on this initial ECG. The patient was a female in her 60s with history of HTN and smoking who presented for chest pressure x1 hour. The initial ECG was taken at 0839. Based on the initial ECG and presenting complaint, the attending involved in the case opted to keep the patient in our critical care unit for close monitoring and serial ECGs.


She went on to describe her chest pain as a "buffalo sitting on my chest" and a "weird" sensation in her jaw for 1 hour prior to arrival, associated with lightheadedness and diaphoresis.


The patient was given fentanyl initially for chest pain with minimal effect and then vomited which was followed by zofran and famotidine. Initial troponin T from 0840 was less than 0.010 ng/mL (undetectable).


The following ECG was obtained at 0910:


Repeat ECG recorded 30 minutes after initial ECG. The patient still had chest pain.
Magnified:
Again, a close up of the interior leads and aVL





Sinus rhythm with borderline 1st degree AV block. There has been interval marked increase in the area under the ST-segment and T-wave in leads II, III, and aVF, with concomitant increase in the area above the inverted T-wave in aVL, all confirming that that these truly represent inferior hyperacute T-waves. The STE in the inferior leads is larger. There is now TWI and small STD in lead V2, highly suspicious for posterior MI. 


This ECG is diagnostic of an acute coronary occlusion of an artery supplying the inferior and posterior walls.


The cath lab was activated following this ECG and the cardiology fellow came to the bedside. The patient was given aspirin and ticagrelor and was scheduled for urgent cath.


In the cardiac cath holding area, a repeat troponin T was 0.01 ng/mL (positive). The following ECG as recorded at 1206:


Pre-cath right sided ECG. V1 and V2 are unchanged from the normal 12-lead sytem; V3-V6 are actually V3R-V6R.
The T-waves are even more hyperacute. Right sided leads (V3-V6 on this ECG correspond to V3R-V6R) have STE and hyperacute T-waves indicative of RV infarction.

Progression of Inferior leads and aVL

In this magnified arrangement you can see progression of subtle changes including the progressively increasing area underneath the hyperacute T-waves. Even at ~4 hours into her acute coronary occlusion there is barely any ST Elevation. 

Also notice that the ST segments in this example are concave, which is often erroneously mythologized as a non-ischemic pattern.  



Progression of V2 showing posterior involvement.



The patient was then taken to the cath lab an found to have a proximal RCA 100% thrombotic occlusion which was successfully stented.


100% occluded RCA with TIMI 0 flow

Post drug-eluting stent placement with TIMI 3 flow


While in the cath lab, she transiently developed complete heart block and became hypotensive requiring transvenous pacemaker placement and transient pressors. A right heart cath revealed increased right heart pressures and a similarly timed echo revealed mild right heart failure.

Peak troponin T was 3.00 ng/mL (highly elevated).

Post-cath ECG with resolution of acute changes.


The transvenous pacemaker was removed the following day and pressors were not required again. She was discharged to home 2 days later without further complications.

Learning Points:

1) As we have previously demonstrated, aVL was once again the key initial clue to diagnosing subtle RCA occlusion.

2) Contemporary troponins only start to rise 4-6 hours after the onset of acute coronary occlusion. Relying on troponin elevation to diagnose acute coronary occlusion after at least 4 hours of infarction when the ECG can identify it immediately is poor choice.

3) STEMI criteria failed to identify this acute coronary occlusion, like many others. Only expert ECG interpretation combined with strong clinical suspicion were able to identify this case. Remember that some acute coronary occlusions will present with totally normal serial ECGs, and some patients with extremely concerning symptoms warrant emergent cath lab activation even without ECG findings.


Normal QRS-T angle

From this article: Ziegler R and Bloomfield DK.  A study of the normal QRS-T angle in the frontal plane.  Journal of Electrocardiology 3(2):161-167; 1970.  

Yes, there are valuable articles from 50 years ago! 

For each QRS angle on the left column, Ziegler and Bloomfield have found the normal range of T angles. You can see that, for a QRS angle of 25, as in our patient, the normal range of T angles would be 2-69. So our patient really does have an abnormal T axis at 85 degrees, and the "inverted," or negative, T-wave really is abnormal inversion. A negative T-wave in aVL must have an angle of greater than 60 degrees.


Sunday, February 11, 2018

Is there Wellens' syndrome in left bundle branch block? Or in inferior and lateral leads?

Written by Pendell Meyers, with edits by Steve Smith


A male in his 80s old had acute onset of chest pain.  Here is his first ECG, time zero:
What do you think?









Sinus rhythm with left bundle branch block. There is concordant STE in leads II, V5, and V6. It may not reach a full millimeter, but the QRS is so small that we should make an exception here. It is proportionally large concordant ST elevation!


The cath lab should be activated, but apparently it was not.  Instead, another ECG was recorded at time 46 minutes:
Now there is more than 1 mm of concordant ST elevation in leads II, V5, and V6.
In addition, there is now excessively proportionally discordant (more than 25% of preceding S-wave) in leads III, and aVF.
So there is a definite inferior and lateral MI.  There is no ST depression in lead I, which suggests a circumflex lesion as the culprit.

The cath lab was activated and a circumflex occlusion was opened and stented, with a door to balloon time of 3 hours.


Here are ECGs recorded after reperfusion:
ST deviation has resolved. There is already terminal T-wave inversion in leads III and aVF.




T-waves are inverting in the affected leads.
This is analogous "Wellens' waves" of the inferior and lateral leads, in the presence of LBBB!


As an explorative substudy of our validation of the modified Sgarbossa criteria, we studied T-wave inversion. We looked at serial ECGs on patients with acute coronary occlusion ACO) who underwent reperfusion and compared to serial ECG on patients without ACO. Unfortunately, as a result of our multisite study in which ACO came from many institutions and controls from one institution, only 6 of 45 patients with ACO and reperfusion had serial ECGs available, and all 245 patients without ACO had serial ECGs available.

When this pattern was retrospectively defined as being either 1) present in at least two
contiguous anterior or inferior leads in at least two consecutive ECGs prior to reversal or 2) deeper than 3 mm in two contiguous leads (requiring only one ECG), it was found to be predictive of reperfused ACO (either spontaneously prior to catheterization or with mechanical reperfusion) with derived sensitivity and specificity of 5 of 6 [83% (95% CI 36–99%)] and 241 of 245 [98% (95% CI 96–99%)]. This is preliminary low-level evidence which suggests that terminal T-wave inversion as a sign of reperfusion is sometimes still applicable in the setting of abnormal QRS such as LBBB and likely ventricular paced rhythm as well.


Meyers HP.  Jaffa E.  Smith SW.  Drake W. Limkakeng AT.  Evaluation of T-Wave Morphology in Patients With Left Bundle Branch Block and Suspected Acute Coronary Syndrome.  Journal of Emergency Medicine 51(3):229-237; September 2016.


We (Meyers and Smith) also published a case of Wellens' syndrome (involving the LAD) in LBBB:

Dynamic T-wave inversions in the setting of left bundle branch block


As a very brief review for new readers, terminal T-wave inversion is an expected finding with reperfusion of acute coronary occlusion which is well established in the presence of normal QRS conduction (no LBBB, paced rhythm, etc). It was first described by Wellens and colleagues in the anterior leads in the setting of an acute proximal LAD stenosis, and later it was more fully understood as a transient phase of reperfusion soon after acute coronary occlusion. When it was first described, it was initially divided into "pattern A" and "pattern B", characterized by biphasic terminal T-wave inversions then full, symmetric T-wave inversions, respectively. In reality these are not separate presentations of the disease but simply two different time periods during the progression (see progression below).

Furthermore, though Wellens described this pattern only in LAD leads, it is clear that it occurs in inferior and lateral leads as well.
See this case of inferolateral Wellens' syndrome, with subsequent re-occlusion and pseudonormalization of T-waves.






See this post: Classic Evolution of Wellens' T-waves over 26 hours

See these posts for Pseudonormalization of Wellens' waves (re-occlusion):

This one is EXTREMELY subtle: 

A Middle-Age Male with Chest Pain that Recurs in the ED


Pseudonormalization of Wellens' Waves


Subtle LAD Occlusion with Pseudonormalization of Wellens' Waves.


This one shows why patients with Wellens' syndrome who do not go immediately to the cath lab need continuous 12-lead ST Segment monitoring:



Thursday, February 8, 2018

New paper by Smith: New Insights Into Use of the 12-Lead ECG for Diagnosing Acute MI in the Emergency Department


We just published this paper in the Canadian Journal of Cardiology.  The February 2018 issue is on "Advances and Controversies in Cardiac Emergency Care:"

New Insights Into the Use of the 12-Lead Electrocardiogram for Diagnosing Acute Myocardial Infarction in the Emergency Department


It is a very comprehensive update, concentrating on the ECG diagnosis of acute coronary occlusion and its look-alikes.

Unfortunately, it will be difficult for many to get full text.

https://www.sciencedirect.com/science/article/pii/S0828282X1731173X


Syncope and Prehospital Cath Lab Activation for Posterior STEMI

A middle-aged man had syncope.

This ECG was recorded prehospital; here are the limb leads:
What do you think?







Notice that there are inverted P-waves and a very short PR interval.  This is a junctional rhythm with retrograde P-waves that come slightly before the QRS.  Otherwise, it is unremarkable. 


Here are the Precordial leads:
What do you think?





Here is what the computer read:
Why did it read this?






The computer sees ST depression in V3 and V4, which normally is indeed nearly diagnostic of posterior STEMI.

Is it posterior STEMI?

The computer measures ST elevation or depression at the J-point, relative to the PQ junction.  There is indeed quite a bit of ST depression relative to the PQ junction, but the PQ junction is artificially elevated as an artifact of the P-wave, which is fused with the QRS:

The black arrow shows the PQ junction.  Note that the P-wave occurs just prior to the QRS and is fused with the QRS.  This artificially elevates the PQ junction.  The red arrow shows where the PQ junction really should be.  The blue arrow shows the J-point.
So there really is zero ST depression.



We saw this and de-activated the cath lab immediately.

Learning points:

1. When the patient does not have chest pain, scrutinize the ECG even more closely.  There should always be some suspicion for a false positive when syncope only is the presenting complaint.

2. Read the entire 12-lead ECG.  Our eyes always want to look for ischemia by looking at ST segments and T-waves.  But abnormalities, or apparent abnormalities, of repolarization may be entirely a result of abnormal rhythm or abnormal QRS.




Wednesday, February 7, 2018

ST Elevation after Stab Wound to the Heart

A young man presented after a stab wound to the chest.  Rapid ED diagnosis of cardiac penetrating trauma was made by ED ultrasound, and the patient went to the OR and had a wound to the right atrium repaired.  There was no laceration of any coronary vessel.  He did well.  Because of tachycardia, this ECG was recorded at day 3:

There is sinus tach with diffuse ST elevation, and a bit of ST depression in lead III.  There is PR depression, especially in leads II and V5.  QTc is 383 ms.
This diffuse ST elevation is clearly due to pericarditis, especially given the clinical scenario.  It is slightly unusual, though: The ST vector is directly lateral (highest STE in lead I, with some reciprocal ST depression in lead III).  

[It is unusual to have any ST depression in percarditis, and, if the scenario is one of possible ACS, it would not be wise to assume that diffuse ST elevation is pericarditis without first considering high lateral MI.]

Other ECG factors also support pericarditis: short QTc, significant PR depression, and especially the high ST elevation to T-wave amplitude ratio (in other words, the T-waves are relatively flat, thus non-ischemic).  There is no Spodick's sign (downsloping TP segment).

2 weeks later, his ECG had evolved:
There is resolution of ST elevation, except in V1-V3, and there is now T-wave inversion in V1-V3.

This looks a lot like a common normal variant, and it may actually be, even if it is not seen on the 4 month ECG below.

4 months after the stab wound, it was all resolved:


2 months later (6 months after the stab wound), he again presented with pain typical of pericarditis:
This is more typical: inferolateral ST elevation (ST vector towards lead II), with no reciprocal ST depression.  PR depression is again present.

He was treated with colchicine and NSAIDs, and discharged.

Monday, February 5, 2018

Chest pain and a non-diagnostic ECG. No worries, right?

A middle-aged male complained of chest pain and called 911.  3 prehospital ECGs were recorded.


Here is the time zero ECG:
Just some non-diagnostic T-wave abnormalities  
T-wave inversion in V2 is a bit abnormal, and frequently seen in posterior MI, but not diagnostic. 
 There is tiny bit of ST depression in V3 and V4 which is nonspecific and could be normal.  
There is a large T-wave in lead II which is also nonspecific.  

Here is the repeat at t = 9 minutes:
Lots of artifact, but no apparent change


Here is the t = 25 minute ECG:
Again, no significant change except that the ST segments in V3 and V4, which previously showed some minimal ST depression, are no longer depressed.











The patient arrived in the ED and, before another ECG could be recorded, he had a V Fib arrest.

He was defibrillated, then taken to the cath lab and had a 100% circumflex occlusion.

He did well.

MI in the setting of a normal or nondiagnostic ECG:

This is very common.  Approximately 30% of MI have no diagnostic STE, STD, or T-wave inversion; in other words, they have no ECG findings specific for ischemia.  It is also true that  approximately 25-30% of complete occlusions do not have diagnostic ST elevation (but most have some evidence of ischemia!).

This is the reason we do not rely on the ECG to rule out MI!   Over the years, I have shown you many ECGs that show evidence of MI that might not be seen by everyone, or evidence of coronary occlusion that might not be seen by everyone.

This one has no clear evidence of occlusion, and no reliable evidence of MI at all (occlusive or non-occlusive).

Learning Point: patients can have MI with a normal or nondiagnostic ECG, and they can even have complete occlusion!

That said, I showed it to Vince DiGiulio and he wrote back:

Going into this I figured the ECG showed ischemia since you shared it, but I'm being honest that I didn't look at the outcome when I formulated my opinion (I sound like Ken). My thoughts were:
  • My pretest probability of ischemia is high since Steve Smith sent this. I consider it similar to the patient coming in with a good story and positive Levine sign.
  • There is slight ST-depression in V3 relative to the PR, but absolutely no ST-depression in V6. In my experience, when there is a decent pretest probability, that correlates highly with isolated posterior MI and is almost always due to LCx culprit. If the patient came in with belly pain I wouldn't pay it might mind, but typical CP and this ECG has me thinking LCx until proven otherwise.
I wasn't at all surprised to hear it was a 100% LCx.

The circumflex territory is the most "electrocardiographically silent" of the three epicardial arteries.  50% of circ occlusions do not show diagnostic ST elevation, but most do show some ST elevation less than 1 mm, or some ST depression.

Many circ occlusions result in only ST depression in leads V1-V4 [formerly known as isolated "posterior MI", but now the echo and MRI societies want to call them all lateral or inferior -- (a mistake if you ask me, but more on that later)].  If you do suspect occlusion but see no ST depression or elevation, try posterior leads V7-V9.  Remember that the voltage of the QRS and of the ST segment and T-wave are diminished by the impedance of the lungs between the posterior wall and the posterior leads.  Thus, data supports a cutoff of 0.5 mm of ST elevation (not 1 mm) when there is posterior ischemia.  Like all other distributions, millimeter cutoffs have very imperfect sensitivity and specificity, and do not capture the changes of ACO that can be seen by a skilled interpreter.

Also, posterior leads are not sensitive enough to rule out posterior MI; frequently patients with right precordial ST depression from acute posterior MI do NOT have any posterior ST elevation.  So if you make the diagnosis on the 12-lead, do not reverse your diagnosis based on absence of STE in posterior leads.

In any patient, if you strongly suspect ACS and the patient has continued, refractory pain, the European Society of Cardiology AND the ACC and AHA all recommend urgent (less than 2 hours) angiogram.  However, this makes it very easy to have false positives, as we know that many patients have ongoing noncardiac chest pain.  So this requires great clinical skills (or luck)!   A positive troponin, or stat echocardiogram, or continued serial ECGs (or a cardiac arrest!) may help to identify these patients.

It should be rare that you activate the lab in the absence of all of these!

Thursday, February 1, 2018

This ECG was shown to the doctor with no clinical information

Written by Pendell Meyers, with edits from Steve Smith



I was charting at my computer on a busy overnight shift when a triage ECG was placed between my face and computer screen, asking for my signature. Here it is:
What do you think?











--Sinus rhythm.
--There is a tiny amount of STE in the inferior leads, with lead III having possibly a large T-wave compared to its QRS complex.
--Lead aVL clinches the diagnosis with a very small normal QRS complex followed by minimal ST depression and a proportionally massively inverted T-wave.
--Lead I also shows reciprocal STD.
There is obvious STD in V2-V4 which indicates posterior involvement.
This ECG is diagnostic of acute coronary occlusion affecting the inferior and posterior walls.


Let's look at the magnified limb leads:
Now the findings are more clear


And the magnified precordial leads:
Note clear ST depression in V2, subtle in V3

Subtle ST depression in V4


I asked the triage nurse to bring him back into a room in my zone immediately, and to perform serial 15 minute ECGs as well as labs and cardiac monitor. Although these changes are clear to me, I knew this would be somewhat difficult to convince the cardiologists and I may have to get serial ECGs until more obvious findings are present.

I went to assess the patient. I found out the ECG belonged to a male in his 40s with hypertension who presented with chest pain that woke him from sleep. He stated he had similar chest pain last night which subsided, and he was able to go to sleep only to be awoken several hours later by recurrent pain.

Here is his previous ECG on file:
This further confirms that the findings in the presentation ECG are real and acute.


At this point I got a repeat ECG (approximately 20 minutes after arrival):
This shows increased STE in the inferior leads, increased STD in aVL, increased STD in V2-V4. All indicative of progression of acute coronary occlusion.

I activated the cath lab.

He was taken for emergent cath:
Patent RCA.

This is the so-called "spider view," in which you can see the clean bifurcation of the left main coronary artery into the LAD and the LCX. Soon after the LCX splits off, it quickly branches into two vessels. The larger caliber vessel shows complete proximal occlusion with TIMI-0 flow.  
This was diagnosed as a 100% thrombotic occlusion of the (very large) proximal segment of OM1.  PCI was performed and was able to reduce the stenosis to 50%.

The first troponin T returned highly elevated at 1.33 ng/mL. No more troponins were available.

This is a surprisingly high Troponin T.  It suggests that the patitent's infarct has been going on longer than one would have thought, or that the pain the patient had experienced earlier in the night had resulted in significant myocardial infarct (permanent injury).

Here is his ECG after cath:
ST segment and T-wave findings have almost all resolved.
There are new Q-waves, with T-wave inversion, in lead III.
The T-wave in aVL is now upright.

Learning Points:

1. Lead aVL once again holds the key to the interpretation of subtle findings in the inferior leads.

2. If you weren't convinced by limb leads (although you should be), ST depression in precordial leads make this even more certain -- they complete a pattern of coronary distribution.  Any artery that supplies the inferior wall (could be either RCA or Circumflex) also often supplies the posterior wall.

3. Serial ECGs are always helpful.

4. Acute coronary occlusion frequently does not manifest the classic STEMI criteria.








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