Monday, April 30, 2018

Chest Pain, "Negative" Stress Tests, POCUS, & ECG Equations -- A Case from Salim Rezaie (R.E.B.E.L. EM)

This case is posted by Salim Rezaie (@srrezaie)

Chest Pain, “Negative” Stress Tests, POCUS, & ECG Equations

It has some peer review by me at the end, so we're co-posting!!

Chest Pain, "Negative" Stress Tests, POCUS, & ECG Equations

by Salim Rezaie

I was working a busy shift in the ED, like many of us do, and the next patient I was going to see was a 57 year old male with no real medical problems complaining of chest pain.  I remember thinking as I walked into the room this guy looks ashen and diaphoretic….he doesn’t look well.  He is a paramedic telling me how he has been having off and on chest pain for the past several months.  He just had a stress test two months ago that was “negative”.  Today he was working on his pool and developed the same chest discomfort as he had been having off and on the past several months, but today, the pain would just not go away.  In his mind, he thought this might be an ulcer and just needed some Pepcid to help. He got put on the monitor and an ECG was run…
The patient involved in this case has given permission to share the story, and relevant images with the knowledge that this information will be used for the purposes of education.

This was read by the ECG machine as normal sinus rhythm and age undetermined septal infarct.  Looking closer at leads V2 and V3 I can imagine that I am seeing some ST-segment elevation.  

Given he was diaphoretic, I was thinking this was an evolving anterior STEMI.  So I asked for a second ECG and quickly ran to get the ultrasound machine so I could do a bedside POCUS to look for wall motion abnormalities.  

The 2nd ECG was done, but I didn’t get to see it until much later, as a Code Blue was called overhead.  Here is the 2nd ECG by the way…

Again the ECG machine read this as normal sinus rhythm with age undetermined septal infarct, but as you can clearly see there is more ST-segment elevations in leads V2 and V3 when compared to the 1stECG. This is still not an anterior STEMI by definition (no mm criteria met), but it is diagnostic of a coronary occlusion.

I ran back to the room and saw a cyanotic patient, unresponsive getting CPR.  The crash cart was called for and as we were waiting for the crash cart, the patient was intubated without difficulty.  Defibrillation pads were placed on the patient and after one round of CPR (≈2minutes), ventricular fibrillation was seen on the monitor.  The patient was successfully defibrillated with 200J on a biphasic machine…There was asystole on the monitor for about 5 – 10 seconds and then sinus tachycardia with ROSC.

It’s hard to have a great concept of time, but going back and reviewing the chart, all of this transpired within 10 minutes of the patients arrival to the ED.  I finally did get to do the Post-ROSC POCUS at the bedside and sure enough the patient had an antero-septal wall motion abnormality. Lucky for both of us, cardiology happened to be in the department and saw the bedside POCUS.  The patient was quickly taken to the cath lab and found to have a 100% proximal LAD lesion (“The Widow Maker”).  He ended up getting 2 stents.
I went to follow up with the patient the next day and he is doing quite well.  Extubated in less than 24 hours.  

I asked Dr. Smith to give some expert peer review as well: 

Teaching Point #1: Uselessness of “Negative” Stress Tests
Many emergency providers have taken care of patients with true acute coronary syndrome or even primary cardiac arrest despite having had a recent “negative” stress test.  I know I have.  Overreliance on “negative” stress tests can be a common reason for misdiagnosis or delays in patient care.  It is important to remember that coronary artery disease can arise from atherosclerotic lesions that are only mildly stenotic with unstable plaques that rupture and not picked up by standard stress testing. There is a huge misconception about “negative” stress tests in the health care industry and by laypersons. The sensitivities and specificities for stress testing are often reported between 65 – 90% depending on which study you read.  Here are two trials that stress this exact fact:
Trial #1 [1]:This was a retrospective chart review of 164 patients with either a “negative” stress test (122 patients) or a “normal” indeterminate stress test (42 patients) over the past 3 years.  34 patients (20.7%) from the total cohort were determined to have significant coronary artery disease in the next 30 days. Significant coronary artery disease was defined as myocardial infarction identified by positive cardiac markers, subsequent positive stress test of any type, cardiac catheterization requiring intervention, CABG, or death due to medical cardiac arrest.  Here is the troubling part…8/34 (23.5%) had their most recent stress test within 1 month prior to admission 7/34 (20.6%) had their stress test between 1 – 3 months, and 11/34 (32.4%) had their stress test between 6mo – 1 year.  Of the total cohort of 164 patients, 13 patients (7.9%) had an AMI.
Trial #2 [2]:This was a prospective evaluation of 186 patients who had been referred for coronary angiography for suspected stable angina.  All patients had a normal ECG at rest, none had undergone coronary revascularization, or have diabetes mellitus. 50% of women and 25% of men who had reversible perfusion defects on coronary angiography had completely normal exercise electrocardiographic findings.
Teaching Point #1 Bottom Line: Stress testing is used to identify critical stenosis causing obstruction to coronary blood flow, however in the setting of acute myocardial infarction the underlying pathophysiology is plaque rupture and thrombus formation.  Coronary lesions may not have been significant enough to be detected on stress testing.  Therefore a prior “negative” stress test should not be used to determine the disposition of your patients. If you think they are having ACS, then disposition them appropriately regardless of the prior “negative” stress test.
Teaching Point #2: Use POCUS (or as I like to call it Stethoscope 2.0)
For obvious reasons I was not able to get a live recording of this patient’s bedside ultrasound, but thought it would be useful to put up some images and videos describing ultrasound and coronary anatomy as this clenched the diagnosis. So first, let’s start with an ECG and the coronary anatomy and then move on to echo and coronary anatomy.

Image from Marwick TH et al [3]

Teaching Point #2 Bottom Line: Use POCUS liberally, as this will save patients' lives.  I have started putting an ultrasound machine right next to me when I am on shift.  When I go to evaluate patients I am ultrasounding as many hearts and lungs as I can.  I cannot even begin to tell you the number of times, this has changed my disposition or expedited the care my patients received, including the above patient getting to the cath lab.

Teaching Point #3: Steve Smiths Early Repolarization vs “Subtle” Anterior STEMI Equation
Steve Smith over at Dr Smith’s ECG Blog has created a calculation that differentiates early repolarization vs subtle anterior STEMI.  The key is the ratio of the T-wave amplitude to the R-wave amplitude.  In anterior STEMI, the R-wave amplitude is smaller and early repolarization has a shorter QT interval.  One HUGE CAVEAT, is that this equation should not be used in patients with LVH or LV aneurysms as this can cause false positives.
The Calculation:(1.196 x [ST-segment elevation 60ms after the J point in lead V3 in mm]) + (0.059 x [QTc in ms]) + (0.326 x [R-wave amplitude in lead V4 in mm)
Don’t worry, you don’t have to memorize this.  It’s now on MD Calc

The Evidence [4]: A retrospective study of patients  with “subtle” (non-obvious) anterior STEMI and early repolarization at 2 hospitals had ECGs compared.  355 anterior STEMIs were reviewed and 143 of them were non-obvious and compared with 171 early repolarization ECGs.  The generalized findings were: in “subtle” anterior STEMI the R-wave amplitude was lower in leads V2 – V4 and the QTc was longer when compared to early repolarization. Also a value of >23.4 predicted STEMI while a value of ≤23.4 was predictive of early repolarization.  The overall sensitivity, specificity, and accuracy of this equation was 86%, 91%, and 88% respectively.  This had a positive likelihood ratio of 9.2 and negative likelihood ratio of 0.1.

Getting ECG Nerdy:
60 Milliseconds (= 1.5 small boxes) after the J Point in V3

QTc not shown in ECG #1 above was 416ms
R Wave Amplitude in V4

So for the above patient…

(1.196 x [ST-segment elevation 60ms after the J point in lead V3 in mm]) + (0.059 x [QTc in ms]) + (0.326 x [R-wave amplitude in lead V4 in mm)
(1.196 x [2.7mm) + (0.059 x [416ms]) + (0.326 x [4.5mm]) = 26.3 which is suggestive of an anterior STEMI, not early repolarization
Teaching Point #3 Bottom Line:  When you are having difficulty differentiating between benign early repolarization vs “subtle” anterior STEMI don’t forget about the Steve Smith equation to help differentiate between the two in the correct clinical setting.
Clinical Bottom Line & Things I Learned from the Case:
  1. A prior “negative” stress test, even if recently done, should not be used to determine the disposition of your patients. If you think they are having ACS, then disposition them appropriately regardless of the prior “negative” stress test.
  2. In patients having chest pain, use POCUS liberally, as this will save patients' lives
  3. If you are having difficulty differentiating between benign early repolarization vs “subtle” anterior STEMI don’t forget about the Steve Smith equation to help differentiate between the two in the correct clinical setting
Expert Peer Review
Stephen W. Smith, MD
Hennepin County Medical Center (HCMC
Minneapolis, MN
Blog:Dr. Smith’s ECG Blog

I can see the ECGs better now, and also see the computer read.  

There is a Q-wave in lead V2.  Since normal variant ST elevation never has Q-waves in V2 – V4, it must be assumed to be LAD occlusion (OMI – Occlusion Myocardial Infarction) even without using the formula.  

One might think this... there is a QS-wave in V2, therefore this is old MI.  And the computer read is “age undetermined septal infarct.”  But I have a rule for Old MI with persistent ST elevation (LV aneurysm morphology). The rule is based on the fact that acute MI has large T-waves compared to the QRS, and old MI has small T-waves.

ECG Differential May Include: Old anterior MI with Persistent ST Elevation (LV aneurysm morphology)

My rule for differentiating acute STEMI from LV aneurysm really only reliably distinguishes between:
  1. Acute STEMI on the one hand
  2. Subacute STEMI or LV aneurysm on the other
What is the Rule?
  • First, there must be ST Elevation
  • Second, the ECG differential diagnosis must be LV aneurysm (old MI with persistent ST Elevation) vs acute STEMI
  • This rule should not be used for early repol vs acute STEMI.  Conversely, if the differential is LV aneurysm vs acute STEMI, then you should NOT use the early repol formula
When should LV Aneurysm be on the ECG differential diagnosis?
Primarily when there are well-formed Q-waves, with at least one QS-wave, in V1 – V4.  A QS-wave is defined by absence of any R-wave or r-wave of at least 1mm.  (If there is an R-wave or r-wave, we call the whole wave a QR-wave, Qr-wave, or qR-wave, depending on the relative size of the Q-wave vs. R-wave.)

The Rule: If there is one lead of V1 – V4 in which theT/QRS ratio is greater than 0.36, then acute STEMIis the likely diagnosis, though subacute STEMI is also possible.  Since both require the cath lab, if the ratio is greater than 0.36, and the clinical situation is right (i.e. unexplained chest discomfort), then cath lab activation is indicated.  I both derived and validated this formula, for which the cutoff has good sensitivity and specificity.
  • Derivation: Accuracy of Formula = 93.2% (Smith SW T/QRS Ratio Best distinguishes Ventricular Aneurysm from Anterior Myocardial Infarction. Am J Emerg Med 2005. PMID: 15915398)
  • Validation: Sensitivity 91%, Specificity 81% (Electrocardiographic criteria to differentiate acute anterior ST-Elevation Myocardial Infarction from Left Ventricular Aneurysm. Am J Emerg Med 2015. PMID: 25862248)
  • False negatives had pain duration greater than 6 hours.  Thus, it may classify those patients with prolonged chest pain as LV aneurysm when they are really subacute STEMI.
Here is More Data on Stress Tests:
  • Nerenberg et al. Impact of a Negative Prior Stress Test on Emergency Physician Disposition Decision in ED Patients with Chest Pain Syndromes. Am J Emerg Med 2007. PMID: 17157680
  • Smith SW et al. Incidence of Myocardial Infarction in Emergency Department Chest Pain Patients with a Recent Negative Stress Imaging Test. Acad Emerg Med 2005.; 12:51 [Abstract]
    • There were about 600 visits in 300 patients who had a negative stress imaging test within 3 years.  There were 20 MIs, most in patients whose negative stress had been within the last year.  We show that a recent negative stress imaging test is poor evidence that someone who returns to the ED with chest pain is not having an MI.
  1. Walker J et al. coronary disease in Emergency Department Chest Pain Patients with Recent Negative Stress Testing. West J Emerg Med 2010. PMID: 21079714
  2. Hoilund-Carlsen PF et al. Usefulness of the Exercise Electrocardiogram in Diagnosing Ischemic or Coronary Heart Disease in Patients with Chest Pain. Am J Cardiol 2005. PMID: 15619400
  3. Marwick TH et al. Techniques for Comprehensive Two Dimensional Echocardiographic Assessment of left Ventricular Systolic Function. Heart 2003. PMID: 14594869
  4. Smith SW et al. Electrocardiographic Differentiation of Early Repolarization From Subtle Anterior ST-Segment elevation Myocardial Infarction. Ann Emerg Med 2012. PMID: 22520989
For More on this Topic Checkout:

Friday, April 27, 2018

Another Cardiac Arrest - Is it OMI this time? Use your skills from the previous post!

Written by Pendell Meyers, with edits by Steve Smith:

A 49 year old male with history of HTN suddenly complained of shortness of breath, and walked down the street to the fire department, where he walked in the door and collapsed. The fire department crew on scene immediately recognized cardiac arrest and began CPR within seconds. Initial rhythm was VF, shocked into pulseless VT. En route, paramedics shocked him out of VF/VT 5 times, with an intermittent wide complex rhythm between episodes of VF/VT. He arrived in our ED with a perfusing rhythm, intubated and without any spontaneous movements.

Here is his initial 12 lead ECG, approximately 10 minutes after his most recent ROSC:
What do you think?

The computer wrongly diagnosed left bundle branch block, and had no comments concerning ischemia. The computerized QRS duration is stated as 138ms.

The interpretation of this ECG hinges completely on correct understanding of the QRS complex and location of the J-point. Your eyes are drawn to V2-3 and you are tempted to believe that the entire shape represents the QRS complex. If that were true, the QRS complex in V3 would be almost 300ms long! This is not possible, or so unlikely that we must consider it incorrect until proven otherwise.

In reality, the computer is actually correct about the QRS duration of ~138 ms. If you search carefully for the J-point (see annotated ECG below), you'll see there is actually a massive amount of STD in V1-V5, and there is STE in V6, I, and aVL.

Like the case from yesterday, the end of the QRS is obliterated by massive ST segment deviation, mimicking LBBB in the precordial leads.

Should you consider hyperkalemia? Yes of course, as it is wide and bizarre to the less trained eye. So give some calcium if you can't tell, while your resuscitating and sorting it out. If it's hyperkalemia, calcium will usually produce rapid change in the ECG.
With the correctly identified J-point seen above, there is obvious and massive STD in V1-V5, with massive STE in I and aVL and reciprocal STD in II, III, and aVF. This indicates acute and total ischemia of the posterolateral walls.

Remember, this is an immediately post-ROSC ECG. This means that you must consider whether these changes are due to the immediate post-ROSC state, or not.

In my experience, the magnitude and anatomically logical distribution of these ST segment changes makes it less likely to be simply post-ROSC abnormalities, and much more likely to represent true full thickness focal ischemia due to an occluded artery (OMI).

There are still two possibilities:

1) A focal fixed stenotic lesion, combined with the low flow state of cardiac arrest, creating such poor flow through the stenosis that there is effectively an occlusion during the down time.

2) An acute coronary occlusion (OMI).

Obviously the clinical history of this case points toward true OMI. But in many cases it will be more confusing. If you are unsure, get a repeat ECG 20-30 minutes after the initial post-ROSC ECG. If it was #1 (combo of fixed lesion with temporary low flow during down time), then the changes will improve or disappear. If it was #2 (OMI) and the artery is still occluded, the changes will persist.

Here is the ECG 23 minutes after the initial ECG:
Practice finding the J-point and the ST segment deviations before looking at the annotated ECG below.

Annotated ECG showing persistent massive ST deviations, including anterior STD and high lateral STE indicative of persistent posterolateral OMI. 
Conveniently for our education, there are 4 PVCs spaced perfectly to show us that we can see analogous ST changes within the PVCs in all 12 leads, including proportionally excessive discordant ST segment deviations in V5-6, I and aVL, II, III, and aVF, and aVR. There is concordant STD present in the PVCs in leads V3 and V4. The J point is inappropriately isoelectric in V2.

The ECGs are diagnostic of posterolateral OMI.

Unfortunately, the ED physicians and cardiologists all believed these ECGs represented LBBB. It is even documented that "no Sgarbossa criteria are present." (Regardless of the fact that the Sgarbossa and modified Sgarbossa criteria are inapplicable in this case, they are indeed both present). We believe from experience that the modified sgarbossa criteria can be applied to PVCs. This case supports our claim, because almost all 12 leads have a PVC with either concordance or excessive discordance.

Luckily for the patient, the team decided to take the patient to the cath lab because he had complained of SOB before collapsing in front of the firemen and suffering a VF cardiac arrest. The initial positive troponin T of 0.22 (normal less than 0.01 ng/mL) also helped push the patient appropriately to cath lab.

In the cath lab they found severe chronic 3 vessel disease, including chronic appearing stenoses of the left main (40%), proximal LAD (90%), "chronic total occlusion of all diagonals", proximal LCX (75%), mid RCA (80%), with an acute thrombotic 100% occlusion of the mid-distal LCX (the culprit, obviously). A stent was applied to the LCX culprit lesion, with TIMI 0 flow improved to TIMI 3 flow after intervention.

Here are the angiogram images:

The RCA is overall patent but has a lesion at the level of the mid-RCA.
Annotated, with arrow showing the mid-RCA lesion.

This appears to be a diffusely diseased but overall currently patent LAD. There are few to none visible diagonals.

The left main can be seen to bifurcate into the LAD (running horizontally across the top of the image) and the  LCX (running vertically down the middle of the image). The LCX shows several points of stenosis and then is abruptly occluded. See next image for annotation.

Arrow showing the site of the acute thrombotic LCX occlusion.

The wire has crossed the occlusion, preparing to perform the intervention.

After intervention, TIMI 0 flow has been restored to TIMI 3 flow, exposing the long course of the LCX which was previously occluded.

Another view post-intervention.

Here is his ECG about 18 hours later:

His troponin T peaked at 11.78 at around 14 hours after presentation. This indicates a very large MI and portends much worse prognosis.

Next day ECG:

Unfortunately, the patient suffered anoxic brain injury. I do not have the details to explain why this occurred in a patient with short down time, immediate bystander CPR, and appropriately timed reperfusion therapy. The patient ultimately died 2 weeks later.

The ECG pitfalls in this case are common, especially among the sickest patients with OMI. The STEMI vs. NSTEMI paradigm does not prepare us for cases like this. The STEMI vs. NSTEMI paradigm fails even in those with normal-appearing QRS complex, and fails even more as the QRS complex becomes more and more abnormal. Only advanced ECG interpretation and training will help these patients in the cases when the clinical history does not already provide the correct management.

Learning Points:

Finding the end of the QRS complex and the J-point is a basic but absolutely crucial skill.

If you see what appears to be an extremely wide QRS complex (greater than 200ms), then consider hyperkalemia and/or incorrect measurement of the end of the QRS (which is most importantly caused by obliteration of the QRS complex by ST segment deviation)

You must be able to recognize posterior STEMI/OMI, despite the fact that it is downplayed by the STEMI vs. NSTEMI paradigm, and even more downplayed in actual practice by some physicians (EM and cardiology).

Look for supplementary evidence of OMI within PVCs.

Wednesday, April 25, 2018

Cardiac Arrest -- Is it STEMI?

A late middle aged male collapsed while walking and had immediate bystander CPR.  He achieved ROSC at the door of the ED, 30 minutes after arrest.

The CPR provided had been so effective that the patient began to follow commands upon arrival.  Why was it so effective?  Because they used the inspiratory threshold device, ITD (ResQPod) and ResQPump.

Go here for the latest in CPR, a fast evolving field: Lecture by Keith Lurie that includes the latest on head-up CPR.

This was his initial ED 12-lead, with pH 7.09, pCO2 69, and bicarb 19.  K was 2.8 (low K is common after resuscitation due to lots of exogenous epinephrine):
The computer diagnosed atrial fibrillation with left bundle branch block.  
I would have agreed with atrial fib except that the 3rd complex appears to be sinus (see double-peaked P-wave).  So perhaps it is an accelerated idioventricular rhythm?

Is it LBBB?


LBBB should have a slow upstroke ("intrinsicoid deflection") to the R-wave in lateral leads of at least 60 ms.  This is a relatively rapid upstroke of about 40 ms (see red arrows below which show onset and peak of R-wave in lead V5).

Is this a wide QRS?  

Yes, but I believe not nearly as wide as it first appears.

In the annotated version of the ECG (below), I put a short black line in V4 where I believe the QRS ends.

This a QRS that looks very wide because its terminal portion is obliterated by ST elevation.

This is "shark fin" ST elevation

They have also been called "Giant R-waves":  JE Madias.
Full text, with image:

Here is an annotated version with lines and arrows:
The red arrows show the onset and peak of the R-wave in lead V5
The short black line in V4 shows what I believe to be the end of the QRS.
Thus, the QRS duration is about 140 ms. It would be easy to believe that it is 230 ms.

--I then draw a long black line from that same point and extended it down to lead II.
--I then draw that long black line from the corresponding points on other complexes of lead II, up to all other leads.
Now, assuming my estimate of the end of the QRS is correct:
1. You can see concordant ST elevation in I, aVL, V3, V5, and V6.
2. You can see concordant reciprocal ST depression (STD) in II, III, aVF
3. There is also STD in V1 and V2.

In any ventricular rhythm, including PVCs, concordant ST elevation implies subepicardial ischemia (STEMI)

for another example of that downsloping ST elevation, see this case:

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

Management decisions

We are enrolling patients in a study called "ACCESS" ( Identifier: NCT03119571).  It is a randomized trial of early angiography/PCI for cardiac arrest victims who do not have "STEMI" or "STEMI equivalent."  (The research question is: do patients with shockable rhythms who do not have STEMI need emergent cath lab activation?)

So the ECG interpretation is critical to whether this patient gets:
1) immediate angiography as if he is a STEMI patient or 
2) randomized to early angiography vs. angiography later, as indicated by other data.

If you believe that:

A)  This is a simple post arrest ECG with very wide QRS and no ST elevation or depression
Then the patient is randomized and not automatically studied with immediate angiography.

B) The QRS really is much shorter and only appears to be wide due to ST elevation and depression which obliterates the end of the QRS
Then, you activate the cath lab and do not enroll the patient in this randomized trial.

I was convinced that it was ST Elevation and Depression.

We activated the cath lab based on this ECG, with the knowledge that this subepicardial ischemia may simply be a result of cardiac arrest alone.

ECGs Immediately after Resuscitation from  Cardiac Arrest

Any ECG recorded immediately after cardiac arrest can be wildly abnormal.  During the 30 minutes of cardiac arrest, even if there is no acute MI, or even without any coronary disease, there can be severe ischemia from the low-flow state of cardiac arrest , as well as alterations from acidosis.(Cardiac output and blood pressure during CPR chest compressions is a fraction of normal.)

If there are fixed coronary lesions, the flow beyond that stenosis may be exceedingly poor, and the ischemia may be focal.

Thus, one should always record another ECG after the patient stabilizes.  We recorded this one 25 minutes later:
Sinus rhythm.
Typical hypokalemia ECG.
There is some residual STE in aVL and reciprocal STD in inferior leads

What do you think?

Three Options:

1.  The QRS really was very prolonged, and there is and was no focal ischemia
2.  There was a thrombosis, probably of the LM or LAD, and it spontaneously reperfused (autolysis)
3.  There is a fixed stenosis in the LM or LAD.  During cardiac arrest, and shortly thereafter, there was profound ischemia in that territory, resulting in ST Elevation (a type 2 STEMI).

Further history came to light:

The patient had recently been experiencing exertional angina. He had a stress test a few days prior that was markedly positive, and was scheduled for an angiogram on the following day.

This suggests presence of a fixed stenosis.

What happened?

1. Maybe that stenotic plaque ruptured and thrombosed.
2. Maybe the stress of walking was enough to cause exertional ischemia and then ventricular fibrillation.

The patient went to the cath lab: 

A 95% stenosis of the proximal LAD was found.  The lesion did not appear to be acute (no ulcerated plaque and no thrombus).  The lesion was reduced to 0% with intervention and stenting.

Peak Troponin I = 19 ng/mL (STEMI is greater than 10 ng/mL in about 70% of cases)

Formal Echo
Normal left ventricular size and thickness.
Mildly decreased left ventricular systolic function with an estimated EF
of 45%.
There is hypokinesis of the mid anterior wall.

It looks as though Option 3 was the correct one.


This is a type II STEMI due to fixed stenosis in the LAD which, in the setting of very low flow state of CPR resulted in severe hypoperfusion to the anterior wall, a wide QRS, and ST elevation and depression consistent with STEMI.  The arrest was caused by exertional ischemia in the setting of a very tight fixed, non-thrombotic, LAD stenosis.

However, the discharge diagnosis was "NonSTEMI."

In retrospect, this patient could have been randomized in the ACCESS trial.  He did not need immediate intervention, though he did get it.

Learning Points:

1. It is critical to find the end of the QRS before concluding that there is not STE or STD.

2. In the presence of a fixed stenosis, exertion can lead to ischemia and ventricular fibrillation.  Stress tests are always done with resuscitative equipment available!

3. Low flow of cardiac arrest can lead to severe cardiac ischemia, especially in the presence of fixed coronary stenosis

4. The ECG immediately after cardiac arrest is often very abnormal. Wait 15 minutes after stabilization to record another one

5. We don't know if everyone who has cardiac arrest from a shockable rhythm needs emergent angiography.  My bias is to send them, but the ACCESS trial's goal is to find out.

More on Type 2 STEMI:

You Must Read the ECG in Clinical Context....

Monday, April 23, 2018

A 33 year old male with acute back pain radiating to the chest

Written by Pendell Meyers, with edits by Steve Smith


I was called to the EMS control room to answer an RMA (Refusal of Medical Advice). After the call was over, just before I was about to go back to the grind in our acute emergency department, my fantastic EMS colleague paramedic Jess Boyle asked me for an opinion on these 2 ECGs from a single patient, one done immediately after the other, without any other clinical information:

What do you think?

Both of the ECGs show sinus rhythm with normal QRS complex morphology. There is ST segment depression in leads III and aVF with inappropriate large "volume" T-wave inversion. This is reciprocal to a small amount of ST elevation in lead aVL, with suspiciously large amount of area underneath the ST segment and T-wave, suspicious for hyperacute T-waves. In the context of the inappropriate (inappropriate for the QRS) STE in aVL with reciprocal inferior STD, these T-wave must be considered truly diagnostic for hyperacute T-waves. In the first ECG, take a close look at the PVC that occurs in leads aVR, aVL, and aVF just before the precordial leads start. What do you notice?

There is concordant ST elevation in that PVC in lead aVL. PVCs, like any other form of abnormal conduction (LBBB, ventricular paced rhythm, etc) generally follow the rule of appropriate discordance (which states that the ST segment and T wave will deviate away from the majority of the abnormally conducted QRS complex). So in the absence of superimposed ST elevation, the PVC in aVL should have an isoelectric or depressed ST segment following that large, abnormally conducted R wave. Instead, the J point is clearly above the baseline. This is concordant ST elevation, and we believe based on much experience with this exact question and many prior cases showing this, that this is also diagnostic of acute transmural ischemia just as it has been shown to be in LBBB (and soon, ventricular paced rhythm).

So this ECG is diagnostic for the fact that the high lateral wall has very recently lost its blood supply. The ECG reports the acute transmural thickness of the myocardium at the cellular level, and the cells do not know or care why they have acutely lost blood supply - any etiology of acute coronary occlusion, or even small vessel ischemia such as is seen in takotsubo stress cardiomyopathy, or in "No Reflow" phenomenon after opening of an occluded coronary artery, will produce the same ECG changes. On a population level, by far the most common etiology for acute coronary occlusion is type 1 ACS (plaque rupture causing acute thrombotic occlusion). But remember, the ECG just shows the fact that there is an occlusion, not the etiology of the occlusion.

Back to the case:

The EKG had been sent to medical control approximately 15 minutes prior to my review, and my paramedic friend had been worried by it so he took it immediately to an ED physician for review. Although he mentioned that he was worried about aVL and the inferior reciprocal changes, the reviewing attending disagreed and did not think that it warranted prehospital cath lab activation.

I was immediately worried about what might happen to the patient. I asked him which hospital the patient had been transported to (our medical control services oversees many different hospitals). Luckily, he responded that the patient had just arrived in our ED! So I went to find him and make sure that the receiving team had gotten copies of these prehospital ECGs.

As it turns out, the receiving team had not gotten a copy of these prehospital ECGs. I gave them the ECGs, told them my concerns, and asked for some info about the patient:

He was a 33 year old male with history of asthma and smoking who called EMS for sudden onset chest pressure beginning 1 hour prior to arrival. He stated he had just finished urinating when he was reaching to flush the toilet when he suddenly felt a cramping pain in his mid back. When he went immediately to lay down, the pain radiated into the center of his chest. He took tylenol with no improvement, then called EMS. EMS administered ASA, NTG, and 5mg morphine with improvement in pain. He adamantly denied any ingestions, drugs, cocaine, etc.

Here was his first ECG in the ED, during this time he supposedly had 2/10 pain which was improved since onset:
The findings are much more subtle compared to the prehospital ECGs, but still present. There is also a tiny new Q wave compared to the priors. Because the findings have decreased, but the T-wave is still upright, it is hard to say whether the artery is still fully occluded or whether we might be witnessing the beginning of the changes of reperfusion. 

If the artery is reperfusing, we should soon see complete resolution and/or the classic reperfusion sequence of terminal T-wave inversion followed by full T-wave inversion over time. 

Usually, improvement in pain is very helpful in this decision, however morphine may confound your assessment in the setting of ACS. Unlike aspirin, NTG, or other ACS medications, which improve pain by treating the underlying cause, morphine does not treat the occlusion, and unfortunately may be effective in masking the pain of acute coronary occlusion, inspiring less frequent serial ECGs and serial examinations of a sick patient. "Masking" of ischemia may be the reason that morphine is associated with worse outcomes in ACS (

Overall, the treating team interpreted the clinical picture as improving, and did not immediately activate the cath lab but instead continued aggressive bedside evaluation and serial ECGs.

There was no appreciable wall motion abnormality upon bedside echo without contrast.

The iStat point of care troponin I returned at 0.38 ng/mL (elevated, normal less than 0.08 ng/mL). In general, iStat troponins can be unreliable, although the higher the result the more likely it is true. The initial troponin T returned at 0.04 ng/dL (also slightly elevated from normal which is less than 0.01 for this assay).

At this point, only ~20 minutes after arrival, they activated the cath lab.

The patient was taken immediately for cathetization, which showed "mid to distal 1st diagonal branch revealed 90% stenosis and mid-distal segment attenuated and appears in spasm, unresponsive to intracoronary NTG and intracoronary nicardipine." The RCA and LCX were normal. See the cath images below.

Normal RCA.

In this view you see the LAD (largest vessel coming down the center of the screen), with the large 1st diagonal  branching off and appearing robust until approximately halfway down its length, when it suddenly is extremely narrowed and then followed by downstream low attenuation. See next picture for annotation.

The arrow points out the beginning of the spasm of the D1.

The cath report states that he had improvement in symptoms and ECG findings despite the fact that the angiographic appearance was not improved after the intracoronary administration of NTG and nicardipine. Given this improvement and the suspected spasm as the etiology, they did not place a stent, but instead planned to treat the patient with medical therapy including amlodipine and NTG as needed.

His serial troponin T rose from initial 0.04 to 0.43 to 0.66, then started to trend back downward.

Here is his first post-cath ECG:
There appears to be no resolution of active injury on the ECG. Rather, it appears as though there is ongoing injury and progression along the classical pattern of OMI. This is concerning for persistent downstream ischemia despite an open artery angiographically.

Two more hours later. Now you can see the development of larger Q waves in lead aVL. There is persistent STE in aVL with reciprocal STD in III and aVF.

No longer any R wave in aVL, replaced entirely by Q wave. This does not necessarily mean that the full thickness of the high lateral wall has infarcted, because stunned but viable myocardium may also produce a Q wave and later recover.

The cardiologists plan on repeat catheterization in several weeks after medical therapy to reassess whether any other intervention will be necessary.

Learning Points:

Make sure you have a system in place so that your EMS ECGs get delivered to the receiving ED team every time, even when they are originally interpreted as normal.

The ECG cannot tell you the etiology of OMI. By the numbers, the etiology must be assumed to be one treated by immediate reperfusion therapy (in the absence of a specific known alternate cause). This is not a "false positive" OMI, rather this is one of the few patients who has something other than thrombus causing the OMI. The only appropriate way to differentiate occlusive spasm from occlusive thrombus is by performing an emergent angiogram. See our other cases of spasm here.

This patient never met the "STEMI criteria", like many other very significant acute coronary occlusions and near occlusions.

Young people can have acute MI.

Don't forget to look for the signs of OMI within PVCs.

I believe that even transient OMI/STEMI should ideally be taken to the cath lab if feasible, because it is unlikely that the patient will get serial ECGs and close monitoring enough to recognize reocclusion before more myocardium is lost, or worse, even in the best of hands.

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