Monday, May 29, 2017

Chest Pain Diagnosed as Gastroesophageal Reflux

A 50-something male presented to a clinic for one day of intermittent substernal chest and jaw pain.  He had had several episodes of pain since onset; it was described as pressure-like and lasts about 5-15 minutes and resolves spontaneously.  He had been pain free for about an hour.   He had some "pre-diabetes," but no h/o hypertension, no known family history of heart disease, and he smokes about 1-2 cigarettes per day. 

An ECG was recorded:
The computer read:
Normal ECG
What do you think?

Smith Comment:

This is definitely not a normal ECG.
There is less than 1 mm of ST depression in II, III, aVF, and in V3-V6.
The STD is nearly 1 mm in III and V6.
There is a tiny amount of ST Elevation in aVL
The ST vector is around -60 degrees, so that there is some STE in aVL and a bit in I, and zero in aVR

What is a normal ST segment?

--First, one must be sure that the QRS is normal.  An abnormal QRS (abnormal depolarization), such as in LBBB, LVH, RBBB, or RVH, may result in abnormal ST-T (abnormal repolarization).  In this case, the QRS is normal: normal axis, duration, and amplitude, without abnormal Q-waves.

When the QRS is normal
--The normal ST vector is towards leads II and V5 (anterior and leftward)
--Leads I, II, and aVF should not have any ST depression, as the normal ST vector is leftward and anterior.  It is common to have some normal variant ST elevation in these leads, often called "early repolarization."
--Precordial leads also usually have normal ST elevation, not ST depression.  
--Up to 0.5 mm of ST depression can be normal, though it is unusual.  It should not be assumed to be normal unless there are previous ECGs that confirm it.

Causes of ST Depression with a normal QRS:
1. Normal Variant
2. Ischemia
3. Hypokalemia
4. Digoxin

It is very likely that the "inferior ST depression" is due to high lateral MI.  The ST depression in precordial leads suggest still more widespread ischemia, so the exact culprit is not at all clear.

Case continued

He was diagnosed with reflux and treated with a proton pump inhibitor and given nitroglycerin.

He presented to the ED 1 day later:

He stated that he had continued episodes of chest pain and then it became constant that morning (about 8 hours prior).  The NTG had not helped.  There is no change in symptoms with exertion, the pain is not pleuritic, positional, or reproducible by palpation.

An ECG was recorded:
The ED ECG has some differences: there is more ST depression, there is some T-wave inversion in aVL.   There may be new Q-waves in V2 and V3 and there is also some apparent change in the ST-T of V2 and V3.  However, there is so much artifact that this is indeterminate.

Here is yesterday's for direct comparison:

The patient was given aspirin and his first troponin returned at 4.94 ng/mL.  The pain spontaneously resolved.  He was given heparin and metoprolol, with a plan to go urgently to cath if his pain recurred.

Another ECG was recorded at t = 46 minutes:
There is less ST depression

This was recorded at T = 105 minutes
There is a suggestion of terminal T-wave inversion in V2, suggestive of Wellens' waves

The next AM, this was recorded before the angiogram:
What is the culprit artery?

Here is the troponin profile:

The angiogram showed a 100% thrombotic mid-LAD occlusion with faint left to right and right to left collaterals.

Here is the post cath ECG:

So that very subtle terminal T-wave inversion were indeed subtle Wellens' waves.

In Wellens' original studies, every case had either an open artery (LAD) or collateral circulation.  Wellens' waves imply reperfusion, but it might be due to collaterals, not due to reperfusion of the infarct-related artery.

Learning Points

1. Beware ST depression
2. Never assume chest pain is reflux.  They cannot be differentiated without troponin.  (The ECG could be entirely normal in MI, though in this case it was NOT normal)
3. Wellens' syndrome is due to reperfusion or good collateral circulation
4. Ischemia that resolves need not go to the cath lab emergently as long as there is very close monitoring.

See this case:

Chest pain relieved by Maalox and viscous lidocaine

Friday, May 26, 2017

You're busy at triage and another ECG is flashed before your eyes.....

4 second video EKG from Stephen Smith on Vimeo.

Here is the computer read: 

You are working in triage where there are 30 patients vying for your attention and more coming in every minute.  The nursing assistant hands you an ECG every few minutes, wanting to know if the patient needs emergency placement.  She flashes the one above before your eyes.

What is your immediate impression?

The triage emergency physician saw the lateral T-wave inversions and told the assistant that there was no STEMI and to have the patient wait for the next available bed.

Here is the ECG again:
There is subtle ST Elevation in leads III and aVF, with reciprocal ST depression in aVL
This is diagnostic of inferior MI
There is very low voltage in the limb leads, so the ST segments are proportionally very abnormal.

There are also fairly well-formed Q-waves in II, III, and aVF, so this could be subacute or even possibly old (with persistent ST elevation -- aneurysm)

Case continued

The patient was placed in the ED on non-emergent basis.

Here is the history:

Patient has no previous cardiac history and presents to the ED with midsternal CP that radiates to the left and started 14 hours prior.  It was intermittent, but became constant 7 hours prior.  The patient also endorses SOB.   He denies N/V, fevers, chills or cough.  He smokes 5 cigarettes a day.  He states that it feels as if something is stuck in his chest when he swallows anything.

The faculty physician inside the ED had a better look at the ECG and immediately recognized the acute (subacute) inferior MI.

She activated the cath lab.

Another ECG was recorded 39 minutes after the first, before leaving for the cath lab:
There is some subtle evolution in V3-V6


1. Thrombotic occlusion of mid circumflex/second obtuse marginal with faint left to left collaterals
2. 70% stenosis of small First Diagonal
3. Diffuse 60-70% stenosis of the mid-RCA, but with TIMI III flow beyond

Here is the post-cath ECG:
The ST elevation in inferior leads is resolved.
T-wave inversion is deeper, consistent with reperfusion T-waves

Here is the troponin profile:

This is a very large MI.
Troponins have only modest correlation with infarct size because so much is dependent on reperfusion, but a Troponin I over 100 is very large.

The highest troponin I ever saw was 500 ng/mL in a case of left main occlusion.  That was BEFORE reperfusion,
The highest that my troponin research colleague, Fred Apple, has ever seen, is 1000!
A 4 month old with a cardiac arrest had an initial (and peak) troponin was 762 ng/mL!

Here is the formal contrast echo the next day:

Large inferolateral WMA
Decreased left ventricular systolic performance-moderate.
The estimated left ventricular ejection fraction is 35-40%.
Regional wall motion abnormality-anterolateral, akinetic.
Regional wall motion abnormality-inferolateral, akinetic.

Later, the triage physician told me about the case.  He said he was overwhelmed with patients at triage, pulled in many directions, and realizes he did not look at the entire ECG after seeing the T-wave inversions in lateral leads.  The obvious abnormalities stood out and distracted him from the more subtle ones.

Learning Points:

1.  Do not let the computer read fool you.  Do not even look at it until you have scrutinized the ECG.
2.  Don't let the obvious abnormalities prevent you from systematically scrutinizing the entire ECG.
3.  Large MIs often show only subtle (or no) ECG findings

Thursday, May 25, 2017

Chest pain, Dynamic ST Elevation and T-waves, and High Voltage

A 20-something had sudden severe chest pain while smoking marijuana at a party.  After approximately 40 minutes, other people there convinced him to call 911.  The patient told the medics that he had had this pain on other occasions and it is because of an "enlarged heart."  He denied SOB, N/V, or other recent illness.  His vitals signs were relatively normal.

The medics recorded a prehospital ECG which could not be found, but they activated the cath lab based on that ECG.

On arrival, the patient was very agitated and would not allow any IVs or blood draws.

He stated he had a history of pericarditis and that this feels similar.

He had this ECG recorded:
There is sinus tachycardia.
There is very high voltage.
There is strange ST elevation in inferior leads which is not generally seen in STEMI.
There is ST elevation in V2-V4 which is typical for LVH


I was shown this ECG in a conference, with no knowledge of the outcome.  I asked if the patient was thin and athletic.  The answer was yes.  Such high voltage in a 20-something is common in thin athletes.

There is also a large R-wave in V1, which is suggestive of hypertrophic cardiomyopathy (HOCM).

Case continued:

The physicians recognized that this was false positive ST Elevation due to LVH.  They de-activated the cath lab.

A Point of Care Cardiac Ultrasound was normal.

He was taken out of the critical care area and remained anxious, hyperventilating, and diaphoretic.

Another ECG was recorded about an hour later:
Much more ST Elevation.  It is changed
What do you think?

Smith Comment:

Obviously, ST Elevation like this must be take seriously.  But it should also be remembered that very high voltage (abnormal depolarization) can have very strange ST-T waves (repolarization).  And these can be dynamic.

When I was shown this in conference, I said: "This is not due to a coronary event."

Mostly, I just recognize this morphology as typical of LVH or Benign T-wave Inversion (even with its dynamic changes) and atypical of LAD occlusion.

Of course, I can't be 100% certain that it is not LAD occlusion, but there are clues that make me quite certain:

1. There is massive voltage: lead V2 has 55 mm of voltage.
2. Leads V4 and V5 are typical of benign T-wave inversion:
There is high voltage, a distinct (though small) J-wave in V4, a prominent J-wave in V5, with ST elevation that turns down to T-wave inversion in a very particular way.

It reminded me of this ECG which combined LVH and Benign T-wave Inversion:
A Baseline ECG of LVH + Benign T-wave Inversion, a variant of Early Repolarization

Here are other examples of Benign T-wave Inversion:

Young African American Male with Atypical Stabbing Chest Pain

Benign T-wave Inversion: view video or read text

Changes like this in the setting of LVH can happen from stress, takotsubo stress cardiomyopathy, drugs, elevated blood pressure or any number of non-ACS etiologies.

If I were caring for this patient, I would get an emergent formal echocardiogram.  That does, of course, require IV bubble contrast, which requires an IV.

Case continued:

Not inappropriately, the physicians activated the cath lab.  It was complicated because of patient unwillingness to agree with the plan.  He still had not allowed any blood (i.e., troponin) to be drawn.

Another ECG was recorded about 30 minutes later:

Still more evolution
My opinion was that this was still typical of LVH and unlikely to be due to LAD occlusion.

The patient was ultimately taken to the cath lab, but one more ECG was recorded before he left:
No major change

The angiogram was normal

A formal echocardiogram was also normal (not even with LVH or HOCM!)

Here is the troponin profile (3 out of 4 below the level of detection):

The patient refused further workup, including an MRI of the heart.

Learning Points:

1. Electrocardiographic LVH can mimic STEMI
2. Electrocardiographic LVH can have dynamically abnormal ST elevation and T-wave inversion.
3. In Retrospect, knowing that the echo was normal, this is more likely just a normal variant ST elevation similar to the ones in this post:

8 year-old with report of "syncope and an abnormal ECG".

Monday, May 22, 2017

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

I received this case from:
Dominic Larose MD CCFP(EM) FACEP
Alain Vadeboncoeur MD CSPQ
Montreal Heart Institute

Hi Steve,

Here is a case I had a while ago. The patient was seen on the street, with sudden LOC. An off duty fireman was a bystander, so the cardiac arrest was recognised and immediate CPR was begun at 11:58. First responders arrived afterwards, and the patient was shocked twice with an AED.  ALS crew arrived 6 minutes later, and ACLS protocol was performed. The patient was in recurrent VF with wide complex PEA in between. Epinephrine and amiodarone were given. Seven shocks were given. The patient was transported from the scene 32 minutes post arrest.

The patient arrived in the ED 44 minutes post arrest in VF, was shocked and PEA followed. EtCO2 was 25 mmHg with ongoing manual CPR, and with a Combitube that was in place, with good air entry bilaterally. VBG at arrival: pH 6,95, K 4,4 mmol/L, lactate 8,2 mmol/L. First high sensitivity troponin T (hs) was 11 ng/L, the second one two hours later 723 ng/L.

[Smith translation: although all assays are different and will have slightly different results, but one can estimate that, in terms of the contemporary assays used in the U.S., this is approximately equivalent to 0.011 ng/mL and 0.723 ng/mL -- by convention, contemporary trops are stated in ng/mL and high sensitivity (hs) in ng/L. Troponin T values are far lower than cTnI, so this is (very) roughly equivalent to a hs cTnI of 10,000 ng/L (contemporary cTnI of 10.0 ng/mL. Strict troponin officionados would faint at such an attempt at equivalence, but there is literature to support this and I find it very useful, especially in EKG research.]

I decided to activate the ECMO team at 45 minutes post arrest, three minutes after arrival in the ED, for this middle aged man seemingly in previous good medical condition.

The cardiologist, perfusionist, intensivist and cardiac surgeon were on site and the cannulation procedure started 60 minutes post arrest. The procedure was somewhat difficult but 3 L/min flow was obtained 90 minutes post cardiac arrest.

Cannulation during CPR.

But here is where it gets really interesting: the patient regained a rhythm.   Here is the 12-lead ECG, recorded 5 minutes after the start of extracorporeal circulation.
The cardiologist thinks this a non-specific wide complex ECG, and tells me he will get the patient to a hospital bed after going to the head CT. I disagreed! Being a regular reader of this blog, in fact I thought the ECG show a RBBB with “shark fin” STE. There is also RAD with positive QRS in lead 1, and negative QRS in lead 2.

Smith Comment: Here is an analysis of the ECG:
There is probably atrial fibrillation (no P-waves, irregular).
It is too irregular to be ventricular tachycardia.
There is a tall R-wave in V1 indicating right bundle branch block.  There is a tall R-wave in aVL, and negative waves in II, III, aVF.  This indicates Left anterior fascicular block.
The lines indicate my determination of the end of the QRS, and thus beginning of ST segment.
As you can see, there is ST Elevation in V1, V2, (V3 missing), V4, V5, and in aVL with reciprocal ST depression in II, III, aVF.
This is diagnostic of STEMI.
It is common for this to be missed, even in such a dire situation!
I have seen many cases in which the cardiologist did not see the STEMI
This is always due to left main or proximal LAD occlusion.

Dominic Larose continues:

So it is a RBBB + LAFB with STEMI. This is either a total or subtotal LM occlusion or a proximal LAD occlusion, as discussed before on the blog.

So the cardiologist agreed to take the patient to the cath lab. Here are the findings:

It was read as a 80% LM disease with a lot of vasospam, with 100% proximal occlusion of Cx artery and 80% stenosis of proximal LAD. Large doses of intracoronary nitroglycerin is given, with thrombus aspiration then a lesion is stented.

Here is the situation later:

RCA with the large venous ECMO cannula seen:

At 18h00 on the same day, the patient had cardiac standstill on echo, a transvenous pacemaker was attempted, but did not result in any contractility, so the ECMO circuit was turned off and the patient pronounced dead.

I have reviewed 14 cases of E-CPR for ED patients at our site, done in the last two years and we have had 6 survivors/14 (43%) discharged in good neurological condition. Not bad I think!

Learning Point:

1. Watch out for RBBB + LAFB STEMI, and recognise the “shark fin” pattern as STEMI!
2. Start an ECMO program (Extracorporeal Life Support).  It can save patients who have refractory ventricular fibrillation due to coronary occlusion or even pulmonary embolism.

This case illustrates similar ECG findings is great detail:

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

Friday, May 19, 2017

Hours out of the OR for valve replacement surgery: patient with paced rhythm becomes hemodynamically unstable

This case was sent to me yesterday, coincidentally on the same day we presented data at SAEM on the Utility of the Smith-Modified Sgarbossa Criteria in the Diagnosis of Acute Coronary Occlusion in Ventricular Paced Rhythm.

Sent by Brendan Michael Riordan, a PA working in Cardiothoracic Critical Care:
Twitter: @concernecus


A 73 y/o with hx of bicuspid aortic valve and recent cholecystitis developed increasing shortness of breath and was found to have severe aortic insufficiency as well as complete heart block. He was admitted to the CCU and diagnosed with endocarditis with an aortic root abscess, then taken to the OR where he had a relatively unremarkable operative course for a surgical AVR and aortic root reconstruction (short bypass time, no major arrhythmias, etc.). Post-CPB TEE showed preserved biventricular function (LVEF ~65%) but several distinct RWMA (septal and inferior hypokinesis with paradoxical septal hypokinesis). 

He had an immediate post-op ECG:
There is a ventricular paced rhythm with normal discordant ST segments
No evidence of ischemia

The surgeon attributed the wall motion abnormalities to a small amount of air in the right coronary artery and it improved following a short-term administration of Epinephrine. 

The patient arrived to ICU on no infusions with good hemodynamic parameters. He developed hypoxia and a focused TTE was completed overnight for persistence of this hypoxia, with concern for possible MR causing pulmonary edema, but all of the valve functions were intact. 

Notably though, the LVEF had decreased from 65% to 35% and the previous RWMAs were still present. The patient was started inotropes again to maintain good hemodynamics. 

The next day, the patient remained on inotropes with better oxygenation, but hemodynamics were borderline, and something did not feel right about the clinical situation. The patient remained sedated and intubated and unable to provide any subjective data. 

The original post-op EKG (#1) was reviewed (V-paced), and there was initially some concern that the STE in lead V3 met modified Sgarbossa Criteria for STEMI.  

Smith comment: I don't think so.  I get 3 mm divided by 17, which is a ratio of about 0.17.  This does NOT meet the modified Sgarbossa criteria, but it is a high ratio.  It is important to remember that a normal maximal ratio for V1-V4 is about 0.11.  A ratio of 0.20 (20%) is still fairly specific for coronary occlusion.  As the ratio falls below 0.20, the specificity drops some.  I would not call this positive. 

This was reviewed but not thought to be solid enough evidence. A repeat EKG was recorded:


Smith comment:  This shows (new) excessively discordant ST Elevation in lead II and V4, and concordant ST Elevation in leads V5 and V6.  This is diagnostic of acute coronary occlusion.

The providers suspected STEMI and though the patient was reliant on pacing for hemodynamics, they briefly turned it off in order to get a 12-lead without pacing:
Now there is complete heart block and bradycardia (the reason for the pacing) and the ST elevation persists in V4-V6.  It is not seen now in lead II.

Case continued

While a non-paced EKG (#3) was performed (the patient had very tenuous hemodynamics without pacing support), a Code STEMI was called. Both General and Interventional Cardiology reviewed the case and determined that there was enough of a good story to warrant a cath. 

Ultimately, the patient was found to have a 100% acute thrombotic occlusion of the RCA, which was stented open with restoration of TIMI 3 flow. The patient made a substantial recovery following intervention. 

STEMI in Ventricular Paced Rhythm

We have some preliminary results of the PERFECT study, presented today at the Society for Academic Emergency Medicine.

The short version: They work!!

Here is the long version

Paced Electrocardiogram Requiring Fast Emergent Coronary Therapy (PERFECT) Study Identifier:

Performance Characteristics of the Modified Sgarbossa Criteria for Diagnosis of Acute Coronary Occlusion in Emergency Department Patients With Ventricular Paced Rhythm and Symptoms of Acute Coronary Syndrome

Thursday, May 18, 2017
1:39 PM - 1:51 PM
Room: Celebration 14: Convention Level

Kenneth W. Dodd, MD - Hennepin County Medical Center
Kendra D. Elm, MD - Hennepin County Medical Center
Michael Hart, MD - Hennepin County Medical Center
Rehan Karim, MD - Hennepin County Medical Center
Deborah L. Zvosec, PhD - Hennepin County Medical Center
Keith G. Lurie, MD - St. Cloud Hospital/Hennepin County Medical Center
Brett Boggust - Mayo Clinic College of Medicine
Adesola Oje - Thomas Jefferson University
Bayert Salverda - Hennepin County Medical Center
Jennifer L. White, MD - Mayo Clinic College of Medicine
Anna Marie Chang, MD, MSCE - Thomas Jefferson University
Stephen W. Smith, MD - University of Minnesota/Hennepin County Medical Center

Background: The ECG diagnosis of acute coronary occlusion (ACO) in the setting of ventricular paced rhythm (VPR) is purported to be impossible. However, VPR has a similar ECG morphology to LBBB. The validated Smith-modified Sgarbossa criteria (MSC) have high sensitivity (Sens) and specificity (Spec) for ACO in LBBB. MSC consist of ≥ 1 of the following in ≥ 1 lead: concordant ST Elevation (STE) ≥ 1 mm, concordant ST depression ≥ 1 mm in V1-V3, or ST/S ratio < -0.25 (in leads with ≥ 1 mm STE). We hypothesized that the MSC will have higher Sens for diagnosis of ACO in VPR when compared to the original Sgarbossa criteria. We report preliminary findings of the Paced Electrocardiogram Requiring Fast Emergency Coronary Therapy (PERFECT) study (#NCT02765477).
Methods: The PERFECT study is a retrospective, multicenter, international investigation of ED patients from 1/2008 - 12/2016 with VPR on the ECG and symptoms suggestive of acute coronary syndrome (e.g. chest pain or shortness of breath). Data from four sites are presented. Acute myocardial infarction (AMI) was defined by the Third Universal Definition of AMI. A blinded cardiologist adjudicated ACO, defined as thrombolysis in myocardial infarction score 0 or 1 on coronary angiography; a pre-defined subgroup of ACO patients with peak cardiac troponin (cTn) >100 times the 99% upper reference limit (URL) of the cTn assay was also analyzed. Another blinded physician measured all ECGs. Statistics were by Mann Whitney U, Chi-square, and McNemar’s test.
Results: The ACO and No-AMI groups consisted of 15 and 79 encounters, respectively. For the ACO and No-AMI groups, median age was 78 [IQR 72-82] vs. 70 [61-75] and 13 (86%) vs. 48 (61%) patients were male. The median peak cTn ratio (cTn/URL) was 260 [33-663] and 0.5 [0-1.3] for ACO vs. no-AMI. The Sens and Spec for the MSC and the original Sgarbossa criteria were 67% (95%CI 39-87) vs. 46% (22-72; p = 0.25) and 99% (92-100) vs. 99% (92-100; p = 0.5). In pre-defined subgroup analysis of ACO patients with peak cTn >100 times the URL (n = 10), the Sens was 90% (54-100) for the MSC vs. 60% (27-86) for original Sgarbossa criteria (p = 0.25).
Conclusions: ACO in VPR is an uncommon condition. The MSC showed good Sens for diagnosis of ACO in the presence of VPR, especially among patients with high peak cTn, and Spec was excellent. These methods and results are consistent with studies that have used the MSC to diagnose ACO in LBBB.

Thursday, May 18, 2017

Weakness and Hypotension, with Bradycardia.

This dialysis patient called 911 for weakness.  Medics found the patient to be hypotensive and bradycardic.

The patient was taking carvedilol and amlodipine, but denied overdose.

The medics recorded this ECG:
The medics were considering external pacing.
What is a better initial therapy?

The patient was stable enough that no therapy was needed, but the correct therapy would be IV Calcium.  This ECG represents hyperkalemia until proven otherwise and, if it is due to hyperK, it will often respond immediately to calcium therapy.

He arrived and had this ED ECG recorded:
There are no visible P-waves. Rate is 35.
There is a narrow complex bradycardic rhythm.
It appears to be junctional.

Hyperkalemia can abolish atrial activity and eliminate P-waves, even though the sinus node may still be generating a rhythm.  So, in this case, there may be an underlying sinus rhythm that is generating the impulse we see. Or it could be a slow junctional rhythm.  The distinction is academic.

Note the T-waves are only minimally peaked (II, and V4-V6 especially) and would not even be noticed by many observers.

We administered Calcium Chloride 1 gram x 3 as well as atropine, and the pulse increased to 60 beats per minute.

We gave calcium chloride because there is a shortage right now of calcium gluconate.  Had we given gluconate, it would have required 9 grams to obtain the same molar amount.  Calcium chloride is safe to give through a peripheral vein if it is a high quality IV and it is given slowly.  I gave it for years as a young physician with no adverse events.  It does cause skin necrosis if it infiltrates.

The K returned at 8.1 mEq/L.

We also gave albuterol, insulin, and dextrose, as well as bicarb (the patient was not fluid overloaded).

The heart rate increased and he went immediately to dialysis.

It is wise to place external pacing pads!

Learning Points:

1. Bradycardia is hyperkalemia until proven otherwise because it is very common, very easily ruled in or out with a K level, and very easily and safely treated with calcium.

2.  The only ECG sign of severe and life threatening hyperK may simply be bradycardia.  There may be no QRS widening or peaking of T-waves.

Saturday, May 13, 2017

An intoxicated, agitated, 20-something with chest pain

Here is a one hour lecture on the topic of subtle coronary occlusion, especially on the left anterior descending coronary artery

Case 1:

The outcome of this case is at the far bottom.

A thin, athletic young African American male presented by private transportation to the ED after use of "ecstasy" and alcohol and other drugs.  He complained of severe chest pain and was extremely agitated, so much so that he was throwing chairs in triage.  He had an ECG recorded and was brought to a room.  Here is the ECG:

Figure 1:
Sinus rhythm.
What do you think?

Figure 1 shows marked ST Elevation (STE) at the J-point relative to the PQ junction:
1.5 mm in V2
3.0 - 3.5 mm in V3
2.0 mm in V4

The size of the T-wave relative to the QRS in lead V2 is concerning; it is due to very low QRS voltage.

Technically, the STE meets STEMI criteria because there is greater than 2.5 mm STE in V3 and greater than 1 mm in an the adjacent lead V4 (even though V2 does not meet criteria of 2.5 mm).

But this is a thin athletic 20-something and since such STE can occur in this population, it is easy to dismiss it.  The normal upper limit for ST Elevation in lead V2 (as measured at the J-point, relative to the PQ junction) in males under 30 years is 3.0 mm and 3.5 mm in 20 year old males.

How about using the LAD-early repol formula to help differentiate normal variant ST elevation from the ischemic ST elevation of LAD occlusion?

The formula comes from this paper:

In this complex paper, we compare Subtle LAD occlusion to early repolarization (now known as "normal variant ST elevation"").  All early repolarization ECGs had to have at least 1 mm of ST elevation in V2 and V3 (of 242 cases of early repol, 71 were excluded due to absence of sufficient STE), at the J-point, relative to the PQ junction.

Among LAD occlusions, "Subtle" meant we excluded those ECGs we defined as obvious:
1) greater than 5 mm ST elevation in at lead one lead
2) just a single lead of V2-V5 with a straight or convex ST segment
3) any ST depression (inferior or anterior)
4) any Q-waves in V2-V4.
5) T-wave inversion in any of V2-V6

These ECGs were excluded from the study as "obvious" LAD occlusion, and the formula was not derived or validated on those patients, and therefore should not be applied.

On this blog, the warning is this:
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 study as obvious anterior STEMI.

The formula is also at MDCALC:

iPhone app
There is a free iPhone app called "SubtleSTEMI".  (Sorry, no Android)  When you open the app, this caution comes up:

If you click on "show warning," this comes up:

You must click this in order to proceed.

Then you must answer all these questions.  If the answer to any is "Yes", you cannot trust the formula.

Then you must answer all these questions.
If the answer to any is "Yes," you cannot trust the formula.

If the answer to all these is "NO," then the formula can be applied.
But still the formula was not perfect: it was about 90% sensitive (86% actually, at the most accurate cutoff of 23.4) and 90% specific.

Because normal variant ST elevation is far more common that LAD occlusion, especially among 20-somethings, the negative predictive value in this population is indeed very high.

The NPV is even higher for a young athletic male who presents with drug use and agitation!
The Fourth Question: Terminal QRS distortion:

Notice the 4th Question: "Is there terminal QRS distortion?".  This is confusing to people, but is very important: 20% of our exclusions were due primarily to terminal QRS distortion.  

Terminal QRS distortion (TQRSD) is something I noticed long ago in LAD occlusions, and did not see in normal variant ST elevation.  That is why we excluded patients with this finding. 

Definition of TQRSD: Absence of S-wave and J-wave in either of leads V2 and V3.

Last year, we studied it among the 171 patients with proven Normal Variant ST Elevation:
We found that, indeed, none of 171 cases of Normal Variant ST Elevation had TQRSD.
90% had an S-wave in both of leads V2 and V3
Of the 10% without an S-wave in both leads, all had a J-wave of at least 0.5 mm.

An S-wave was defined by a deflection that is negative relative to the PQ junction
J-wave was any deflection of at least 0.5 mm at the J-point
Thus, if there is TQRSD, assume LAD occlusion until proven otherwise.

What is a J-wave?

Figure 2.
These are J-waves (V3-V6).
Notice that there is a very well-formed S-wave in V2, but no true S-wave in V3.
However, there is a marked J-wave at the J-point in V2.
There are of course very well-formed J-waves in V4-V6 also, but these are not sufficient to satisfy the rule.
To use the formula, there must be an S-wave or J-wave in BOTH V2 and V3.
The J-wave in V3 satisfies the criterion, and the formula may be used.The presence of S-waves and J-waves (absence of QRS distortion) does NOT preclude LAD occlusion.  In our study, most cases of LAD occlusion did NOT have terminal QRS distortion, and many had J-waves
(J-waves do not make early repol definite!!) 

In the Figure 2 ECG, there is also

1) Upward concavity in all of V2-V6
2) No inferior ST depression (it is important to note that inferior ST depression is absent in 50% of acute LAD occlusion).
      Reference: [Walsh BM.  Smith SW.  Differences in electrocardiographic Findings Between Acute Isolated Right Ventricular Myocardial Infarction and Acute Anterior Myocardial Infarction.  JAMA Internal Med 2016 Dec 1.; 176(12)1875-1876.]
3) no STE of at least 5 mm
4) no T-wave inversion
5) No Q-waves in V2-V4

Thus, the formula may be used in the Figure 2 ECG.
This is a graphic from the paper (Figure 3):
The complex in V3 on the left:
The end of the R-wave does not descend below the PQ junction, therefore no S-wave
There is no J-wave.
No case out of 171 proven early repolarization cases had this morphology.
It is LAD occlusion until proven otherwise.

On the right:
There is both an S-wave and a minimal J-wave (although this is barely 0.5 mm)
Although this was indeed a case of early repolarization, it could be STEMI.

TQRSD rules out early repol.
Absence of TQRSD does not establish early repol!!

Case 2

Here is a case of a patient with chest pain:
See magnification below

Here is V1-V6 magnified:
There is a well-formed S-wave in V2, but this is not sufficient to rule out TQRSD
There is clearly no S-wave and no J-wave in V3.Hence, there is TQRSD.
LAD occlusion until proven otherwise; do not use the formula!

This case was immediately recognized as LAD occlusion and went to angiography.  A 100% LAD occlusion was opened.  The post cath ECG is here:
Notice that the S-wave has been re-constituted with reperfusion of the LAD.

Some time later, reperfusion T-waves developed (analogous to Wellens' waves):

Case 3

Here is a case of a 30-something otherwise healthy male with chest pain:
There is neither an S-wave nor J-wave in lead V3.
This was a proven LAD occlusion.

Case 1 progression

Let us return to the case at hand:
There is a tiny S-wave (tiny QRS!) in V2
There is no S-wave in V3 (remember, only 10% of early repol do not have this!)
Is there TQRSD?

Here are V1-V6 magnified:

And here magnified even more:
There are indeed tiny deflections, but with all the noise there and the lead-to-lead variability, these are unlikely to be J-waves.
In only 1 of 3 complexes (middle) could you say that the noise reaches 0.5 mm (0.05 mV).
So this is TQRSD: no S-wave or J-wave in one of leads V2 and V3 (in this case, V3)

When in doubt, assume LAD Occlusion until proven otherwise!!
So, this noise should not be considered TQRSD, and then the formula should not be used.

In any case, the patient needs at a minimum serial ECGs and perhaps a formal echocardiogram.

Case progression:

The providers interpreted this as early repolarization.  Not recognizing the exclusion, they used the "SubtleSTEMI" formula and the value was low:

= (1.196 x STE60V3) + (0.059 x QTc) - (0.326 x RAV4)

--QTc = computerized QTc  
                     (here it was 391 ms)
--RAV4 = R-wave amplitude, in mm, in lead V4.  
                     (here it is 21.5 mm)
--STE60V3 = ST elevation measured at 60 milliseconds after the J-point in lead V3, relative to the PQ junction, in millimeters.
                     (here it is ~3.5 mm)
The formula value then = 20.25.  

This value is very low and is well below 23.4, which is the most accurate cutoff.  But 20 out of 143 had a value less than 23.4.  It is also below the safer value of 22.0.  

Only 6 of 143 LAD occlusions had a value below 22.0 (sensitivity, 96%).  But still, six had values below 22.0!  No test is perfect, and this test has been particularly valuable in changing the diagnosis from early repolarization to MI.  It's greatest value is in warning you that a case you thought was benign is not benign.


The patient was given sedatives for agitation and he did calm down.  His chest pain resolved.  Another ECG was recorded:
This is now unequivocally diagnostic of LAD occlusion!
That is to say: this ECG proves that the first one was indeed LAD occlusion.

The ECG was seen only a bit later by the provider.  As he was alarmed by it, he went to the patient who now was having recurrent pain, then suddenly went into cardiac arrest (ventricular fibrillation).  A prolonged resuscitation ensued but the patient could not be resuscitated.  ECMO and cath lab were not available.

Autopsy showed proximal LAD thrombus with 100% occlusion.

What happened?
That first ECG represents 100% occlusion.  As with many thrombi, it autolysed and the artery spontaneously reperfused, resulting in pain resolution.  The thrombus is "hot," however, and can propagate.  It propagated again resulting in 100% occlusion with recurrent pain and then ventricular fibrillation.

Transient STEMI should always have the cath lab activated, or patient transferred to PCI capable facility.  Antiplatelet and antithrombotic therapy is essential:
I have mentioned this case many times:

Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death

How about the new 4-variable formula?

We recently published a new formula based on the same data as the first study.  This was done because I noticed that false positives would happen when there was high voltage in lead V2 and negatives when there is low voltage in lead V2.

The new formula was significantly more accurate, with an area under the curve of 0.9686.

The same exclusions apply, but this case had very low voltage in lead V2, and maybe it would have performed better in spite of the exclusion?

--QTc = computerized QTc  
                     (here it was 391 ms)
--RAV4 = R-wave amplitude, in mm, in lead V4.  
                     (here it is 21.5 mm)
--STE60V3 = ST elevation measured at 60 milliseconds after the J-point in lead V3, relative to the PQ junction, in millimeters.
                     (here it is 3.5 mm)
--QRS V2 = 
                     (here it is 4 mm)

Formula0.052*QTc-B - 0.151*QRSV2 - 0.268*RV4 + 1.062*STE60V3

Value: = 17.68

At a cutoff of 17.75, the formula was 90% sensitive, missing 14 of 143.  This value is slightly below 17.75, so it has

 Learning Points:

1.  I think this is the most difficult diagnosis in emergency medicine.

2.  The vast majority of the time, ST elevation in leads V2-V4, especially in young men, is NOT due to LAD occlusion.  You have to find this needle in a haystack.

3.  The formula should only be used if the exclusions are met.  Terminal QRS distortion is one of the exclusions.

4.  Even if the exclusions are met, and the formula used, like all tests it has false negatives and false positives, and all results must be viewed with skepticism.

5.  Resolution of ST elevation with resolution of chest pain makes the diagnosis.

6.  Even if ischemic ST elevation is resolved (Transient STEMI), activate the cath lab or transfer to PCI capable facility. The artery can close again with very bad outcomes.  Antiplatelet and antithrombotic therapy is essential.

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