Monday, October 24, 2016

Anaphylaxis and ST Elevation

This was written by one of our excellent 2nd year residents, Nathan Ansbaugh, with some editing and commentary by Smith.

An otherwise healthy middle-aged male age presented as an outpatient for a routine MRI. Immediately after receiving the IV contrast load, he became anxious, nauseous, flushed, and proceeded quickly to become apneic and pulseless.

The emergency response team arrived approximately 2 minutes later and found the patient pulseless and in presumed cardiac arrest. They began CPR. They gave 1mg epinephrine with immediate ROSC and the patient was transported to the Emergency Department for further stabilization and further treatment of presumed anaphylaxis.

An initial ECG was recorded shortly after arrival:
There is sinus tachycardia. There is right bundle branch block (RBBB) with additional left posterior fascicular block (LPFB). Aside: As for LPFB, note the small inferior Q-waves and the rightward axis to approximately +140 degrees, even when disregarding the last 40 ms of the QRS, which is due to the late depolarization of the right ventricle due to RBBB.) Most concerning is the ST elevation in inferior leads, concordant to the majority of the QRS in leads III and aVF, with concordant reciprocal ST depression in I and aVL. This is diagnostic of inferior STEMI.

The prior ECG from 3 months prior was obtained for comparison:
The RBBB and LPFB are old, but this ECG shows no sigificicant ST elevation.
Therefore, the ST elevation on the presentingn ECG is new.

RBBB should not have any significant ST elevation. And here we confirm that it is new relative to the old ECG. So this is new (ischemic) ST elevation.

Should the cath lab be activated?

Approrpiately, the cath lab was not activated.

Instead, the ECG was repeated 10 minutes later:
There is still mild ST elevation the inferior leads but this appears to be somewhat improved.

ECG repeated at 20 minutes:
Inferior ST elevation has essentially fully resolved at this time.

Is this transient thrombosis? Or is it type 2 MI that is resolving as the supply and demand issues improve? It could be either, but type 2 MI is more likely. Both are reported in the literature (see references below) in the context of epinephrine to treat anaphylaxis.

Cardiac arrest can also, of course, lead to type 2 MI, or type 2 STEMI, due to poor perfusion. [Aside: pulselessness is not good evidence of cardiac arrest. Rather, in this case, it is likely that there was severe shock and hypotension such that pulses were hard to palpate. There was no bedside ultrasound to assess cardiac function, and, as far as I know, no monitor showing asystole or wide complex. Probably, there was a narrow complex tachycardia with extremely weak pulses.]

In any case, such poor perfusion can lead to ischemic ST elevation, mimicking ACS STEMI.

Due to the possibility that it was thrombosis, cardiology was contacted for possible angiography +/- PCI.

The patient was admitted to the MICU for anaphylaxis and evaluation for possible ACS. The peak troponin was 1.710 ng/mL. The patient underwent coronary angiography prior to hospital discharge and this showed only mild plaque without angiographic evidence of significant obstructive CAD or cultprit lesion or thrombosis. Echocardiography did not demonstrate wall motion abnormality, and showed normal systolic function and normal EF.

Learning Points:
1. Cardiac Arrest or hypotension can result in ischemic ST elevation without coronary thrombosis
2. Anaphylaxis treated with epinephrine is associated with ischemic ST elevation without coronary thrombosis.
3. Not all electrocardiographic STEMI is due to ruptured plaque and thrombosis. Only the clinical scenario +/- angiography can determine the etiology of the ischemic ST elevation.

Selected Literature

STEMI due to spasm after epinephrine for anaphylaxis:

STEMI with thrombus after epinephrine for anaphylaxis:

Supply/Demand Type 2 Myocardial Infarction: should we be paying more attention?
Yader Sandoval, Stephen W. Smith, Fred S. Apple
JACC 63(020); May 2014.

Myocardial Infarction and Type 2 Myocardial Injury
Yader Sandoval and Kristian Thygesen
Clinical Chemistry (online now)

Here is a classification of Acute Myocardial Injury:

Saturday, October 22, 2016

Sepsis with Pulmonary Edema and Elevated Right Sided Pressures

I was reading from our list of unconfirmed ED ultrasounds and saw a cardiac ultrasound with good LV function, but with B-lines of pulmonary edema, pleural effusions, and a very dilated inferior vena cava. 

So I went to look at the chart.

It was a chronically ill patient with sepsis, a heart rate of 120, presumed sinus tachycardia, and did not have chronic renal insufficiency.

But there was no ECG recorded.

It did not make sense to me that someone who was septic would have ultrasound evidence of fluid overload unless they had renal failure, which this patient did not.

Then it turned out that an ECG was recorded upstairs, but only after admission:
What is it?

This is atrial flutter at a rate of 120.
This was not only recorded late, but misread as sinus tachycardia.
The giveaway is the upright P-wave in lead V1.
Sinus P-waves always have a negative component.  The right atrial component comes first and is upright, the left atrial component comes next and is negative, such that the P-wave in V1 should be biphasic.  Upright P-waves in V1, as in this ECG, are classic for atrial flutter.

See these posts for slow atrial flutter:

--Tachycardia with Pericardial Effusion

The clinicians probably did not consider that tachycardia at a rate of 120 in a septic patient might be something other than sinus tachycardia.  

Just recording a 12-lead on an ill patient may reveal the unexpected.  Atrial flutter commonly comes in atrial rates as slow at 240 (and ventricular rates as slow as 120), and even slower in the presence of sodium channel blocking drugs.

Also, pulmonary edema should raise high suspicion of a cardiogenic cause, and this is due to either pump function (systolic vs. diastolic), valvular dysfunction, or dysrhythmia.  The patient had good pump function, and sepsis usually leads to volume depletion, or relative volume depletion.  Thus, the pulmonary edema had to be either noncardiogenic (or pneumonia), or due to either dysrhythmia or valvular disease.

Most dysrhythmias are easily diagnosed by ECG.

Learning Points:

1. Always record a 12-lead on a sick patient
2. Flutter can be at rates much lower than you expect.
3. Flutter often mimics sinus tachycardia
4. Fluid overload must be explained, and a cardiac cause is very likely.  This is especially true in clinical situations in which volume depletion is expected.

Friday, October 21, 2016

Atrial Flutter. What else??

A 50-something presented with bradycardia.  No other history is available.  Here is the EKG:
There is obvious atrial flutter.  The ventricular rate is 29.
The QRS has the morphology of Right Bundle Branch Block (RBBB) and Left Anterior Fascicular Block (LAFB)

There is also a very long QT, primarily due to a long ST segment
What is really going on?

This is NOT really RBBB and LAFB.  The flutter waves are not conducting through the AV node.   This is not Flutter with 7 or 8 to 1 conduction. Instead, there is third degree (complete) AV block.

How do I know?  When atrial flutter conducts, the QRS should occur at the same part of the flutter wave for every QRS.  Every time the flutter circuit goes around the atrium it arrives at the AV node at the same part of the wave and, if the AV node is ready to conduct, that is when it conducts.

If you look closely, this does not happen:
On beat 1, the QRS starts at the peak.
On beat 2, it starts earlier
On beat 3, it starts earlier still
On beat 4, it starts just after the peak
Beat 5 looks like beat 2.
Instead, there is a very regular escape rhythm

Thus, there is complete AV dissociation.

[There are times when there is atrial flutter and Wenckebach, and the lengthening PR interval changes this otherwise fixed relationship between flutter waves and QRS, but it is far more rare than complete block AND it does not occur with 6:1 block.]

So this is atrial flutter with complete AV block and a regular escape rhythm.

Is it a junctional escape?  A junctional escape should be around a rate of 40, and it should be narrow, unless there is a junctional escape + RBBB + LAFB.  This is possible.

Much more likely is that this is a ventricular escape.  Then why the RBBB and LAFB morphology? Because the escape is originating in the posterior fascicle.  When there is a supraventricular rhythm with RBBB and LAFB, the impulse gets to the posterior fascicle only, then spreads to the ventricle from the posterior fascicle.  Thus, RBBB + LAFB also, in a sense, originates from the posterior fascicle.  In this case, there is no supraventricular stimulus.  There is only the automatic escape, and it originates from the posterior fascicle.

Diagnosis: Atrial Flutter with complete, third degree, AV block.  The long ST segment is probably due to hypocalcemia.  Consider hyperkalemia.

Consider reversible causes (especially hyperkalemia or drug effect from beta blockers or calcium channel blockers before pacing).

Tuesday, October 18, 2016

LAD occlusion or Early Repolarization?

This male in his 20's presented with chest pain:
There is sinus rhythm with a PVC.
There is 2.5 mm ST elevation at the J-point, relative to the PQ junction, in both of leads V2, V3.
This meets the ACC/AHA criteria (for age less than 40) for anterior STEMI.
The ST segments in V2 and V3 are not upwardly concave (they are straight).

Is it STEMI?  Is it Early Repolarization (Normal Variant ST Elevation)?

We have derived a formula to help with this:

Go here for the formula:

Here is the study, a derivation and validation:

It is critical to use it only when the differential is subtle LAD occlusion vs. early repol. Thus, there must be ST Elevation of at least 1 mm. If there is LVH, it may not apply. If there are features that make LAD occlusion obvious (inferior or anterior ST depression, convexity, terminal QRS distortion, Q-waves), then the equation MAY NOT apply. These kinds of cases were excluded from the LAD occlusion group as obvious anterior STEMI.


--Bazett-corrected QTc is the computer measurement.
--RAV4 = R-wave amplitude, in mm, in lead V4.
--ST elevation (STE) is measured at 60 milliseconds after the J-point, relative to the PR segment, in millimeters.

Formula that was derived and validated:
(1.196 x STE at 60 ms after the J-point in V3 in mm) + (0.059 x computerized QTc) - (0.326 x R-wave Amplitude in V4 in mm).
A value greater than 23.4 is quite sensitive and specific for LAD occlusion.

A value less than 23.4 might still be LAD occlusion, but it is unlikely.  A value less than 22.0 is extremely unlikely to be LAD occlusion.

I and at least hundreds of other with whom I have been in contact have used this with a high degree of accuracy.

How to use it?  It does not rule in or rule out LAD occlusion.  Rather, it serves as a warning to evaluate intensively with use of clinical skills, serial ECGs, stat echo and, if needed, angiography.

For this ECG: Strictly speaking, the formula may not apply, as there is a straight ST segment in V2 and V3.  Thus, if we had seen such an ECG in the LAD occlusion group, it would have been excluded as "obvious" STEMI, as early repolarization should have upwardly concave ST segments.  

Unfortunately, there are exceptions to this rule.

Therefore, let's try to apply the rule.  But be very careful with the result.

If we do apply the formula, the numbers are:
--QTc = 410
--STE60V3 = 4.0
--RAV4 = 18
Score = 23.1, which is less than 23.4 and therefore most compatible with early repolarization.

It would be appropriate to do serial ECGs, troponin, and emergent echocardiogram to look for anterior, septal, and apical WMA.


The patient ruled out for myocardial infarction.  This ECG manifests an unusual early repolarization variant.

Monday, October 10, 2016

A patient with a ventricular paced rhythm and chest pain

One of my residents who just graduated saw this patient and sent the case:

This 80-something patient presented with chest pain.  He had recently had a pacer placed for complete heart block and had not had an angiogram at that time.  Ischemia had not been suspected.

He had this ECG recorded:
There is sinus rhythm.  There is clearly a DDD pacer that detects the sinus activity and then paces the ventricle (necessary when there is complete AV block).  The pacing is in the right ventricle (all QRS negative in V1-V6, showing that the lead is in the apex of the RV).
There is some concordant ST elevation in aVL (but not 1 mm).  

There is reciprocal ST depression in II, III, aVF.
There is discordant ST elevation [opposite to a negative QRS (i.e. S-wave)] in V1-V5.
The cardiologist interpretation was "concerning for ischemia."
Is it excessively discordant ST elevation?
In V1, the J-point is 4 mm above the PQ Junction and the S-wave is 14 mm:

The ratio is 28%

We do not know for certain what excessive is in paced rhythm.

The Smith-modified Sgarbossa criteria were derived and validated in Left Bundle Branch Block, which is similar to, but not the same as, ventricular paced rhythm.  For LBBB, an ST/S ratio greater than 25% is very specific and sensitive for acute coronary occlusion. 

Can we apply the rule to paced rhythm?

I don't know for sure, but I do it and we are in the middle of a large multi-center study to try to figure it out.

Here it isPaced Electrocardiogram Requiring Fast Emergent Coronary Therapy (PERFECT) Study.

Importantly, 50% of physicians who care for patients with chest pain believe that you cannot diagnose STEMI in the presence of paced rhythm. This is definitely not true and an old teaching that should be thrown away.

The emergency physician activated the cath lab.  He writes that "Cardiologist thought you could not see the ischemic changes on paced ECG."

In the meantime, an old ECG was found:
The change is obvious and makes the first ECG diagnostic.
The discordant ST elevation in V1-V3 in this old ECG is proportional.
The patient had an acute 100% LAD occlusion.

Smith EKG lectures next year (2017).....Schedule

I will be speaking at these conferences next year:

1.  Oregon ACEP's 2017 Annual Conference in SunRiver will be January 28th- February 1st.

2. Rocky Mountain Winter Conference on Emergency Medicine:  Please Join Us at the 2017 Rocky Mountain Winter Conference at the Copper Mountain Resort, February 25 to March 1, 2017

3. EM conference in Boise, ID.  June 22, 2017.  Details to be announced.

4. DasSMACC (invited, not yet confirmed): Berlin, Germany, EKG workshop half day.  June 26, 2017.  Social Media and Critical Care.

5. 2017 Controversies and Consensus in Emergency Medicine, September 20-21, Northampton, MA

Monday, September 19, 2016

Non-Vagal Syncope and Saddleback Morphology in V2

This is another case provided by Mustafa Alwan, an internist from Jordan and very talented ECG enthusiast.  He posted it on Facebook EKG Club, and I am reposting with his permission.

This is a 26 year old male who presented after having had 2 episodes of syncope in 1 day.  Both episodes started with palpitations, then dizziness.  He had no family history of sudden death.    

Vital signs: normal 

Initial ECG :
This is suggestive of Type 2 Brugada morphology because of the Saddleback in lead V2
At first glance, the beta angle looks wide.
See this post for a review of Type 2 Brugada.
The method is to draw a line from the peak of the R'-wave down along the downslope of the R'-wave, as shown.  At a point which is 5 mm below the peak, you draw a line across and if the distance to the S-wave is greater than 3.5 mm, it is a wide beta angle.   This is equivalent to a 35 degree angle, or 0.61 radians (calculated as the inverse tangent of 3.5/5, or 0.7).

Dr. Ken Grauer, the ECG master who runs this site:, measured the beta angle here: 

So the beta angle is not wide enough to meet type 2 Brugada morphology criteria

For those wanting more — go to minute 21:19 in Ken's ECG Video on Brugada Syndrome. Here is the link to this specific point in the video — 

Type 2 Brugada morphology (in contrast to syndrome) is really quite common, and if you rely on the morphology alone, without the other criteria for syndrome (see below), you will have a lot of false positives.

Diagnosis of Brugada Syndrome requires both:

1. Brugada pattern ECG (either Brugada Type 1, or the newly defined Brugada Type 2 morphology)
Findings may be dynamic and are sometimes concealed; findings may be observed only in certain circumstances such as fever, intoxication, electrolyte imbalance, presence of sodium channel medications/drugs, or vagal stimulation.
2. At least one of the following:
(a) survivor of cardiac arrest,
(b) witnessed/recorded polymorphic ventricular tachycardia (VT),
(c) history of nonvagal syncope,
(d) familial antecedents of sudden death in patients younger than 45 years without acute coronary
(e) Type 1 Brugada pattern in relatives.

This patient only had (c), and no other criteria.

So this ECG did not even meet the criteria for Type 2 Brugada morphology (because the beta angle was too small).  These criteria were developed in a comparison of Brugada syndrome patients with athletes who have an Rsr' saddleback, and they were about 90% sensitive and 90% specific, so they weren't perfect.  

Presumably because this patient had 2 episodes of non-vagal syncope, he was admitted for observation and the admitting cardiologist referred him for Ajmaline challenge test (a sodium channel blocker) in the electrophysiology (EP) lab.

Here is the resulting ECG:
Now there is clearly Brugada morphology.


Does this establish Brugada syndrome?  

One cannot clearly state that there is, or is not, Brugada syndrome due to response to Ajmaline or other Na channel blockers.  One can only risk stratify for future arrhythmic events.

The considerations for ICD implantation are far beyond the scope of this article and all such patients should be evaulated by an electrophysiologist.

Not all emergency and primary care physicians, and even some general cardiologists, recognize these important issues:

This paper (full text) discusses the risk of arrhythmia in patients who have spontaneous vs. drug induced (e.g. ajmaline) type 1 morphology.  If the patient only has a history of syncope (like our patient), the risk of future arrhythmic events is 0.6%-1.9%.  If the patient with only drug-induced Brugada morphology is asymptomatic (unlike this patient), the risk of future arrhythmia is extremely low.

They reference this paper which shows that ICD implantation has a high rate of inappropriate shock and that the ICD's record a low annual rate of dysrhythmia.  

Moreover, the authors of this study, (Outcome After Implantation of a Cardioverter-Defibrillator in Patients With Brugada Syndrome) found that the best cutoff for the beta angle is wider than 35 degrees.  It is 58 degrees, which corresponds to a triangle base width of 8 mm (not 3.5 mm!!).

Here are the latest recommendations from this 2014 publication (full text: HRS/EHRA/APHRS Expert Consensus Statement on the Diagnosis and Management of Patients with Inherited Primary Arrhythmia Syndromes): 

Unfortunately, the situation of our patient is not reflected here:
Symptomatic with drug induced Type 1 ECG, but no family history

Here are the full recommendations:
Class I
  • 1.
    The following lifestyle changes are recommended in all patients with diagnosis of BrS:
    • (a)
      Avoidance of drugs that may induce or aggravate ST-segment elevation in right precordial leads (for example, visit,
    • (b)
      Avoidance of excessive alcohol intake.
    • (c)
      Immediate treatment of fever with antipyretic drugs.
  • 2.
    ICD implantation is recommended in patients with a diagnosis of BrS who:
    • (a)
      Are survivors of a cardiac arrest and/or
    • (b)
      Have documented spontaneous sustained VT with or without syncope.
Class IIa
  • 3.
    ICD implantation can be useful in patients with a spontaneous diagnostic type I ECG who have a history of syncope judged to be likely caused by ventricular arrhythmias.
  • 4.
    Quinidine can be useful in patients with a diagnosis of BrS and history of arrhythmic storms defined as more than two episodes of VT/VF in 24 hours.
  • 5.
    Quinidine can be useful in patients with a diagnosis of BrS:
    • (a)
      Who qualify for an ICD but present a contraindication to the ICD or refuse it and/or
    • (b)
      Have a history of documented supraventricular arrhythmias that require treatment.
  • 6.
    Isoproterenol infusion can be useful in suppressing arrhythmic storms in BrS patients.
Class IIb
  • 7.
    ICD implantation may be considered in patients with a diagnosis of BrS who develop VF during programmed electrical stimulation (inducible patients).
  • 8.
    Quinidine may be considered in asymptomatic patients with a diagnosis of BrS with a spontaneous type 1 ECG.
  • 9.
    Catheter ablation may be considered in patients with a diagnosis of BrS and history of arrhythmic storms or repeated appropriate ICD shocks.
Class III
  • 10.
    ICD implantation is not indicated in asymptomatic BrS patients with a drug-induced type 1 ECG and on the basis of a family history of SCD alone.
     But what about symptomatic patients with drug-induced type 1 ECG??

Sunday, September 18, 2016

A Patient with Vomiting and Abdominal Pain

This patient complained of prolonged vomiting and abdominal pain.
With this history, the ECG is pathognomonic.
What is it?

First, there are narrow J-waves that are similar to Osborn waves.  The temperature was normal.  I am not certain, but I believe these are just exaggerated J-waves with nonspecific etiology.

More importantly, there are large U-waves best seen in leads V3 and V4.    You can also see that lead II has no visible T-wave but only a large U-wave.  (If you look at V3 directly above lead II, you see both a T-wave and U-wave.  If you follow that down to lead II below, you see no T-wave corresponding to the T-wave in V3, only a large U-wave.  This is also true for V5 and V6.)  Thus, what appears to be a long QT interval in these leads is really the QU interval.

This is nearly pathognomonic for hypokalemia.  The K was 2.4 mEq/L.  Magnesium was normal.

Wednesday, September 7, 2016

An Alcoholic Patient with Syncope

A middle-aged male had sudden syncope.  There was head injury and he was intoxicated with alcohol, but he stated "I've been way more intoxicated than this; I have no idea why I passed out."

He denied any kind of chest discomfort or dyspnea or jaw or shoulder pain or epigastric discomfort.

He was completely asymptomatic.

He had a head CT that was normal, a breath alcohol of 0.10% and had this ECG recorded:

What do you think?

As is very common, the computer did not adequately measure the QT interval.  The computer did find a long QT, but greatly underestimated it.
(See this post, which also links to others: Syncope and Bradycardia)

I showed this ECG to the residents and they could not identify the abnormality.  To me, it shouts in my face "long QT!"  This demonstrates how important experience is to Gestalt, and how, if one does not have that experience, one must force oneself to systematically read the ECG.

You must look at every ECG, and if the QT looks long, then measure it yourself.  A good rule of thumb is that if the QT is more than half the RR interval, then measure it and correct for heart rate.  Importantly, at high heart rates (short RR interval), the half-the-RR rule of thumb tends to label too many QT’s as abnormal. At low heart rates (long RR interval), the rule of thumb tends to label too many as normal.

I measured the QT at 530 ms, which results in a Bazett corrected QTc of 620 ms, and that is how I interpreted the ECG at the time:

Here is the old ECG for comparison:

Since the patient is alcoholic and has a long QT, one must consider hypomagnesemia and hypokalemia.  One must also consider medications, and as it turns out, the patient was on 2 psychiatric drugs which can prolong the QT.

Also, I always give any alcoholic 2 g of Mg if they are sick enough to get an IV, so we administered 2 g Mg.

He was also given IV fluids for possible dehydration.

Another ECG was recorded before the Mg was administered:

Again the QT is not correctly measured by the computer
I get 500 ms, not 467.
The correct QTc would then be approximately 610 ms.

There are also very large inferior T-waves, consistent with inferior hyperacute T-waves.
The patient continued, however, to be asymptomatic, serial ECGs showed no change, and bedside echocardiography showed no wall motion abnormality.
Therefore, I attributed these T-waves to the long QT and not to ischemia

The Mg level returned at 1.3 mEq/L (low but not terribly low, reference 1.4 mEq/L)) and K returned at 3.4 mEq/L (low but not terribly low).  2 g of Mg were administered, and then the patient was admitted, after which he received another 2 g of Mg.

The next AM, the Mg was 2.2 mEq/L and this ECG was recorded:
Near normal QTc

The patient was taken off the QT prolonging medications.

The next AM (1.5 days later) a final ECG was recorded:
The patient still has large T-waves, but the QT is normal


Whether this patient had Torsades de Pointes (due to long QT) as the etiology of his syncope is uncertain, but such a prolonged QTc certainly puts him at high risk.  The longer the QTc, the higher the risk, and that risk gets significant when the QTc is greater than 500 ms and becomes very high risk at 600 ms.

Neither the ED treating resident, nor the inpatient team, saw this long QT.  The inpatient team was skeptical of my manual measurement.  They were going to attribute the syncope entirely to dehydration and alcohol intoxication.  I had to personally consult the cardiologists to redirect the evaluation, even though my formal interpretation stated that the QTc was 620 ms.

Physicians want to believe the computer's inaccurate measurements!

Learning Points:

1.  The computer will not consistently accurately measure a very long QT.
2. Look at every ECG and visually estimate the QTc by using the half the RR interval rule of thumb.
                    --If it appears long, manually measure it yourself!  
3. Correct for heart rate using Bazett’s formula: QTc = QT / √RR  (QT divided by square root of the preceding RR interval)
4. A prolonged QT can make T-waves look very large and unusual
5. Check for QT prolonging medications or drugs.  See these two posts.
6. Check Mg and K, and give Mg to patients who drink ethanol daily.
7. Even obvious very long QT may go unrecognized without systematic interpretation.

Sunday, September 4, 2016

40-something with severe CP. True + vs. False + high lateral MI. ST depression does not localize.

This was sent by Jason Winter of the Facebook Page Clinical Electrocardiology 

This post presents one new case, then reviews some interesting aspects of high lateral MI and of ST Depression in "inferior" leads.  Down below are 3 more cases and a discussion of how to differentiate false positive isolated STE in aVL from True positive.


A 47 year old male called 911 for severe chest pain.  He was clammy and looked unwell.  He had a previous MI with cardiac arrest 2 years prior.  

This is his prehospital ECG:
There is very subtle ST elevation in I and aVL, with very subtle ST depression in III and aVF.
Is this due to coronary occlusion?

Jason asked me if I thought it is due to occlusion (without either of us knowing the outcome), and this was my answer:

This is a posterolateral MI.  Probably due to occlusion of the circumflex or one of its obtuse marginal branches.

Why did I say this?

1.  The inferior ST depression is reciprocal to high lateral subtle STE
2.  There is a down-up T-wave in aVF.   Down-up T-waves in inferior leads are almost always reciprocal to ischemia in the territory underlying aVL.
3.  ST segment in V2 has minimal ST elevation and is very flat, and the one in V3 is actually subtly downsloping.  This is not normal and is a tip off that there is posterior ischemia accompanying the ischemia in aVL.  Together they strongly suggest a circumflex lesion.

The medic activated the cath lab but was refused by the interventionalist, who did not believe that this ECG represented acute coronary occlusion.

Later, the patient was taken to the cath lab.  The artery was occluded. It was opened and stented.  I could not get details on which artery, but I'm sure it was the circumflex.

Important Learning Point:

"STEMI" is defined by millimeter criteria (1 mm in limb leads), which this does not meet.  Therefore it is not a STEMI.  But what we truly care about is coronary occlusion, for which STEMI is just a surrogate that is only about 75% sensitive for occlusion.

"Inferior" ST Segment Depression

It is important to understand that "inferior" ST Depression is not due inferior wall ischemia.  Data from stress testing proves that the ST depression of ischemia does not localize.  See this article:

Relation between the electrocardiographic stress test and degree and location of myocardial ischemia

When there is ischemic ST depression localized to the "inferior" leads, it is more likely to be reciprocal to ST elevation that localizes to the high lateral wall (aVL), even though that ST elevation may be nearly invisible.  The ST depression may be the most visibly obvious sign of STEMI.

Here is a case that demonstrates this very well:

Isolated "Inferior" ST Segment Depression: Not a Sign of Inferior Ischemia

Here is the most viewed post of all time on Dr. Smith's ECG Blog, with nearly 100,000 views:

Five Primary Patterns of Ischemic ST depression, without ST elevation. Some are STEMI-equivalents.

True Positive ST elevation in aVL vs. False Positive ST elevation in aVL

Case 1.  

A woman in her 60s with no prior history of CAD presented with 3 hours of sharp, centrally located chest pain with radiation to the anterior neck, with associated nausea. She had known HTN and DM.  She appeared to be in distress.  She was given sublingual NTG with improvement, but there was not complete resolution.

Here was here initial ECG:
There is ST elevation in I and aVL, with inferior reciprocal ST depression in all of II, III, and aVF, and a down-up T-wave in aVF (a sign that is very specific for ischemia).  There is also ST depression in V3-V6.  This ECG is diagnostic of ischemia.

It is important to compare this one with the false positive case #3 at the bottom; that one is a case which could fool you.

There was an old ECG for comparison:
One year prior with no ST segment abnormalities

A bedside cardiac ultrasound was done by the emergency physician.  Here is the parasternal short axis view:

There is an anterior and lateral wall motion abnormality.

This still helps to show the wall motion abnormality:
Arrows point to area of wall motion abnormality

The Cath Lab was activated, and here are the results:

1. LM: No significant stenosis.
2. LAD: luminal irregularities with a 40% stenosis at the take-off of a D3. D3 has a 95% tubular ostial stenosis. (Culprit, stented)
3. LCX: Luminal irregularities, no significant stenosis. Two OM branches without significant stenosis.
4. RCA: dominant. Luminal irregularities without significant stenosis.  Supplies a small RPDA and RPLA.

After cath lab activation, her initial troponin returned at 0.124 ng/mL (99% level = 0.030 ng/mL)

This was the post-cath ECG:
After reperfusion: aVL shows resolution of ST elevation and inverted (reperfusion) T-wave.  There is also some terminal T-wave inversion in anterior precordial leads

A large Diagonal artery may supply both the lateral wall and part of the anterior wall.

Case 2: Another subtle lateral MI, from this post:
A male in his 60's presented 30 minutes after the onset of crushing substernal chest pain.  Medics recorded 2 ECGs, one before and one after sublingual NTG, and both are similar to the first ED ECG.  The patient had never had pain like this before.  The pain improved from 9/10 to 3/10 after NTG.  Here is the initial ED ECG:
There is subtle ST elevation in I and aVL with subtle reciprocal ST depression in III.  Look at aVF.  There is a downsloping reciprocal ST segement followed by an upright T-wave ("down-up" T-wave).  This morphology is highly suspicious for ischemia.   There are also symmetric anterior T-waves with very poor R-wave progression.  T-waves in V4-V6 are taller than normal (compare to ECG in case 3 below)

This ECG, especially along with the very typical history, was very worrisome, but not absolutely diagnostic of, ischemia.  Several serial ECGs showed no change, even after the pain finally resolved to 0/10 after NTG.

He was given aspirin,
clopidogrel, IV nitroglycerine, and heparin, the general cardiologist was called and notified that this patient was very high risk and needed close attention.  He readily agreed, and the plan was to admit for close observation, serial ECGs and troponins, and to scrutinize for any recurrence of pain or change in the ECG.

The first troponin I then returned at 0.063
ng/ml (upper limit of normal = 0.025 ng/ml).  Repeat ECG remained unchanged.
--He remained pain free and the plan remained to admit with a diagnosis of Non-STEMI on medical therapy with plan for angiogram in the morning.
--Just before admission to the hospital, the patient admitted to recurrent pain and appeared uncomfortable.  Therefore, the
cath lab was activated urgently.
--The suspicion was for a circumflex (or obtuse marginal branch) or diagonal artery occlusion or subtotal occlusion.
cath, there was a 95% proximal LAD stenosis with TIMI-II flow, proximal to a large diagonal.  A stent was placed and the patient became pain free.

Case 3: False positive
And here is a similar one that is NOT MI.  How do we tell the difference?
There is ST elevation in I and aVL, with reciprocal ST depression in lead III.   

Just so you don't think I'm cheating by using a retrospectoscope, this was sent to me without any outcome, and I read it as "no MI" with a high degree of certainty.  This is because:
1. The remainder of the ECG is normal.  No poor R-wave progression, no other ST depression, no symmetrical T-waves, no large T-waves, no down-up T-waves, typical early repol in anterior leads
2. The reciprocal ST depression is in lead III only.  Not in leads II and aVF.
3. There are distinct J-waves in the two leads with ST elevation.  This is highly suggestive of early repolarization in these leads.
4. The T-waves in I and aVL are not large (this was also true with the MI case 1 at the top, but that case had many other suspicious findings (many leads with ST depression and no J-waves)
5. There is ST elevation in V2-V4 that is clearly due to early repol.  Early repol in aVL should be accompanied by early repol in the "anterior" leads.

When there is ST elevation in aVL, with reciprocal ST depression in III:
1. Look for:
    a. J-waves
    b. Other ST depression
    c. Large T-waves
    d. Symmetric T-waves
    e. Down-Up T-waves
2. Compare with an old ECG
3. Use ED Echo if available 
4. Use formal Echo 
5. A positive troponin is helpful (a negative one is not)
6. Angiogram if necessary.  You don't want to miss an occlusion.

Recommended Resources