Cardiogenic shock with wide complex tachycardia and poor LV function in a young woman

A 30-something woman presented with CP and SOB.  She was hypoxic and intubated.  She had very poor LV systolic function on bedside echo.  There were no B-lines and the RV was normal.

The following ECG was recorded:

Wide complex regular tachycardia at a rate of 140, no P-waves
What do you think?
What do you want to do?

This ECG was texted to me on my iPhone without any clinical information, with the question: "VT or SVT with aberrancy?"

Here was my response:

"Tough one, as they always are.  Looks like SVT with LBBB (LBBB morphology strongly supports SVT).  Lead  aVR is all negative.  I am going to say SVT and I would try adenosine."

Alternatively, it is sinus tachycardia with LBBB and P-waves are not visible.  Always consider Lewis leads when this is a possibility, as they are likely to exaggerate and uncover otherwise hidden P-waves.

Further analysis, with magnification of V2 and V3:

This is typical LBBB morphology.

When VT has its origin in the RV, it can have an LBBB-like morphology, but there are differences.  Except in the case of fascicular VT, VT starts in the myocardium (not in conducting tissue) and therefore the initial part of the QRS is not rapid (it is slow).   Thus, when it is VT with LBBB morphology, the onset of the LBBB-like QRS is more prolonged. 

Thus, if it were VT: 

1) the R-wave in right precordial leads would typically be greater than 30 ms.

Here it is about 20 ms

2) the onset of the R-wave to the nadir of the S-wave would be greater than 70 ms.  In fact, it would usually be greater than 100 ms.

Here it is about 60 ms

Thus, this is very likely SVT with aberrancy (or with baseline LBBB), and the SVT is possibly sinus tachycardia with P-waves that can't be discerned.

If the rate varies over time, sinus becomes more likely.

If it is paroxysmal SVT, Adenosine may convert it.

All ECG findings aside, severely decreased LV systolic function does make VT more likely.  But these ECG findings are pretty convincing.

Case Continued

The physians thought they were dealing with ventricular tachycardia (VT)
--Cardioversion at 200 J biphasic was attempted without success.
--K was slightly low, so K and Mg were given.
--Amiodarone was given, 150 mg x 2.
--Cardioversion x 3 was apparently unsuccessful

    Comment: Cardioversion would usually be effective whether SVT or VT.  The question in my mind would be this: was the patient converted to sinus tachycardia (still with LBBB), at a similar rate, such that it that looked nearly identical to the SVT and the providers were unaware that the cardioversion actually worked?

--Lidocaine was given, after which patient became hypotensive.
--CXR showed pulmonary edema.
--Cardiac function on echo was very poor, prompting initiation of chest compressions.
--After 3 minutes of CPR, and 1 mg of Epi, there was ROSC with hypertension and improved cardiac function.
--The wide complex continued, but rate was down to 120, suggesting that the rhythm had indeed converted to sinus tach, but there was uncertainty as to the presence of P-waves at this point.
--A trans-esophageal echo (TEE) probe was placed by the emergency physicians in the ED.  This revealed coordinated atrial followed by ventricular contraction at a rate of 120, suggesting sinus tachycardia.  (Not proving it, as SVT could have atrial before ventricular contraction)

The patient remained in cardiogenic shock due to severely decreased LV systolic function.  The remainder of the management is beyond the scope of this blog.

Later in the day, this ECG was recorded:

Sinus with LBBB.

So the LBBB is definitely baseline.  This is the same morphology that she had while in tachycardia, proving that the rhythm was supraventricular.

The patient recovered neurologically, but with a persistently very low ejection fraction (20%, due to new cardiomyopathy).  She also had very frequent ventricular ectopy, with short runs of VT.    In order to protect against dysrhythmic sudden death, she was discharged on a "Life Vest". (2)

The diagnosis in retrospect was SVT with aberrancy in the setting of severe cardiomyopathy and acute decompensated heart failure, with later runs of ventricular tachycardia.

Learning Points:

1. If it looks just like LBBB or RBBB, it is probably supraventricular.

2. In a regular wide complex tachycardia, use adenosine if you think it is SVT.  If you're wrong and it is VT, adenosine is safe.

3. VT can have a morphology similar to LBBB, but in VT the initial part of the QRS should be prolonged, such that the septal R-wave is wider than 30 ms and/or the onset of the R- to nadir of the S-wave is greater than 70 ms.(1)

4. In a critically ill intubated patient in shock, ED transesophageal echo (TEE) can help to guide management in many ways.  It can especially help to continuously monitor LV function during a resuscitation.  In this case it also helped to verify sinus tachycardia.

5.  A "Life Vest" (Wearable External Cardioverter Defibrillator) can be used for those who only temporarily need such a device, or as a bridge to a later implantable defibrillator (see full text article below for details, if interested).

References with links to full text

1.  Wellens Hein JJ.  Ventricular tachycardia: diagnosis of broad QRS complex tachycardia.  Heart 2001;86:579–585

2.  Zishiri ET.  Chung MK.  The Role of the Wearable Cardioverter-Defibrillator in Contemporary Clinical Practice.   The Journal of Innovations in Cardiac Rhythm Management.  May 2011.

Starting a list of some of the best blog cases here....

1. I just remembered this one:

Chest Pain and Cardiogenic Shock with Profound ST Depression & STE in aVR. Activate the Cath Lab?

2. 

Chest pain and Concordant ST Depression in a patient with aortic valve and previously normal angiogram

60-something presents with acute onset of chest pain.

His pain was accompanied by shortness of breath.  It awoke him from sleep.

Here is the prehospital ECG:

What do you think?

The rhythm appears to be atrial fibrillation.  There are no pacing spikes and the morphology is not right for a paced rhythm.  There is a wide complex that appears to be RBBB + LAFB.  There is excessive ST depression in V1 and V2.  Where normally RBBB would manifest a large R'-wave in V3, the lead may have been placed to far lateral and, instead, there is an S-wave.   In RBBB, a lead with a prominent S-wave, as is normal in V5 and V6, should not have ST Elevation or Depression.  This is all but diagnostic of posterior STEMI.

Then we see V4-V6 which have very broad, wide, "bulky" T-waves.  These by themselves are all but diagnostic for lateral hyperacute T-waves.

When you put the posterior and lateral together, it spells an occlusion of the circumflex territory.

The medics were concerned for STEMI but not certain enough to activate the cath lab, but did give ASA and NTG x 3, and the pain diminshed from 10/10 to 6/10.

On arrival, this ECG was recorded:

What do you think?

The same thoughts apply here.  The concordant ST depression in V3 is all but diagnostic of posterior STEMI.

There was a previous ECG available from one week prior:

This one is paced, with appropriate ST segments, though the concordant T-waves are slightly unusual

So what is going on?

The patient had a normal angiogram 1.5 years ago.  Could he have an acute STEMI now?

The cardiologist on call did not think so.  He suggested looking for other etiologies of chest pain.

The INR returned at 1.8.

The initial troponin I returned at 0.011 ng/L (normal: LoD = 0.010, 99% = 0.030).  This "negative troponin" seems to support the cardiologist, no?

A nitroglycerine drip was started but had to be stopped for hypotension.

Another ECG was recorded 30 minutes later:

Now there is the typical R'-wave in V3 and the concordant ST depression is in V4.
It still looks like a STEMI.

The pain pretty much fully dissipated.

The patient was treated medically, and a 2 hour troponin returned positive at 0.30 ng/mL.  4 hours into his stay, a third troponin returned at 23.5 ng/mL (quite high, and typical of a STEMI), at which time this ECG was recorded:

ST changes are much less pronounced.
This suggests reperfusion, either by lysis of thrombus or through collaterals.

Angiogram showed a lesion in the 2nd obtuse marginal off the circumflex.  Interestingly, at this point it was only 90% occlusive with TIMI-2 flow (this explains the relief of pain).  It could not be aspirated.  Presumably, it was 100% occlusive during pain.

Peak troponin 33.6 ng/mL

The impression was that this was an embolus from the aortic valve or from left atrial appendage (due to atrial fibrillation).

Echocardiogram: Previous echo EF = 56%; Now = 50%

TEE (Transesophageal echo): showed a thrombus on the mechanical aortic valve.

Myocardial infarction with previously normal coronary arteries.

I could not find any studies that looked at patients who had a previous normal angiogram and present with what appears to be acute coronary syndrome.

But there are at least several studies of patients with STEMI who normal coronary arteries at the time of the event.

This one has a nice figure showing the etiologies:

Myocardial infarction with normal coronary arteries: a conundrum with multiple aetiologies and variable prognosis: an update

Note that "concealed atherosclerosis" is one of them.
Even if there is no previous atherosclerotic stenosis on a standard angiogram, there can be significant occult atherosclerosis.  Most atherosclerotic lesions are "extraluminal" and can only be see with intravascular ultrasound or with CT coronary angiogram.  These lesions are very prone to ulcerate and thrombose.

The following study was also based on the angiogram at the time of the myocardial infarction.

Prevalence of normal coronary angiography in the acute phase of suspected ST-elevation myocardial infarction: Experience from the PRAGUE studies

The observed prevalence of normal coronary angiography in patients presenting with acute chest pain and ST elevations was 2.6%. Most of these cases were misdiagnoses, not infarctions. A normal angiogram during a biochemically confirmed infarction is extremely rare (0.7%) and was not seen during the ongoing symptoms of ischemia.

This is the best study I could find:

Clinical and Therapeutic Profile of Patients Presenting With Acute Coronary Syndromes Who Do Not Have Significant Coronary Artery Disease  (full text)

In this large study of 5767 NSTEMI patients, 88% of patients with acute coronary syndrome had significant CAD (any stenosis greater than or equal to 50%), 6% had mild CAD (any stenosis of 0% to ≤50%), and 6% had no CAD (no stenosis identified).  This shows that even patients with no angiographic coronary stenosis can have unseen extraluminal plaque that ruptures and causes thrombosis and ACS.

Here is a great review in the New England Journal of Medicine:

Mechanisms of Acute Coronary Syndromes and Their Implications for Therapy. 
New Engl J Med 368(21): 2004-2013; may 23, 2013; 

Quote from article:

"Surprisingly, serial angiographic studies have revealed that the plaque at the site of the culprit lesion of a future acute myocardial infarction often does not cause stenosis that, as seen on the antecedent angiogram, is sufficiently severe to limit flow. Angiographic monitoring of responses to thrombolytic therapy has shown that after lysis of the offending thrombus, the underlying stenosis is often not the cause of the critical stenosis of the artery. In a prospective angiographic study involving patients undergoing percutaneous intervention for coronary artery disease, only half the subsequent events arose from lesions with sufficient stenosis to have warranted intervention at the time of revascularization. (CT) angiography, which permits evaluation of the arterial wall (not just the lumen), has shown that the characteristics of plaque associated with acute coronary syndromes include low attenuation (i.e., little or no calcification) and outward expansion of the artery wall, a process that tends to accommodate the growth of plaque while minimizing luminal encroachment.6-8  Intravascular ultrasonography has shown that in acute coronary syndromes, the culprits often lie proximal to the sites of maximal stenosis — the traditional targets of revascularization therapies."

Learning Points

1. A previous normal angiogram decreases the probability that any event is due to ACS, but by no means eliminates it.

2. Acute coronary occlusion may be due to other etiologies than ACS, such as embolism.  Coronay embolism is an indication for PCI.  The embolus can often be aspirated or broken up with the wire.

3. Learn the ECG features of coronary occlusion in the setting of RBBB

Inferolateral ST elevation, vomiting, and elevated troponin

Another post written by Pendell Meyers, with edits from Dr. Smith:

A male in his late 40s presented with nausea, vomiting, and epigastric abdominal pain of several hours duration. An ECG was recorded from triage:

What is your interpretation?

The ventricular rate is 160 bpm and regular with narrow complex. Rhythm differential is therefore sinus tachycardia, SVT (AVRT, AVNRT, etc), or atrial flutter. There is clear ST elevation present in V4-V6, as well as II, III, and aVF. No clear reciprocal changes in aVL, however with this distribution you could consider a very rare case in which high lateral STE cancels out reciprocal STD.

Because of many prior examples of this phenomenon on this blog, this ECG was immediately recognized by two separate physicians who reviewed this ECG shortly after his presentation. The cath lab was not activated. Rather, they started to treat the patient's atrial flutter (as well as the underlying cause of his pain and vomiting).

Atrial flutter causes undulating of the baseline, frequently simulating ST elevations and depressions.

See these other cases where atrial flutter mimicked ST elevations or depressions:

Is this inferor STEMI?

Atrial Flutter with Inferior STEMI?

What is the Diagnosis?

Atrial Flutter Mimicking ST Depression

If this diagnosis did not come easily to you, here is how they knew:

Here are some general principles:

First, STEMI generally does not cause tachycardia unless there is cardiogenic shock. 

While normal heart rate has zero predictive abilities for ACS, a rapid heart rate in ACS means there is compensation for low stroke volume (low ejection fraction).  This should be readily evident on bedside echo.  If there is normal or hyperdynamic function, then there is something else going on.

Second, tachycardia often distorts the ST segment, mimicking STEMI.

Third, demand ischemia (type 2 MI) can have such severe ischemia that it results in ischemic ST elevation that is NOT due to ACS.  So you have to identify and treat that other problem (dysrhythmia?  bleeding? dehydration? sepsis?  PE?) first and then re-evaluate.

Fourth, the ST elevation may not really be the ST segment, as in this case.

What the physicians saw:

With a regular narrow complex tachycardia at 160 bpm, you should immediately begin trying to differentiate ST vs. SVT. vs. atrial flutter. Go to the bedside and watch the rate and the monitor. SVT and atrial flutter generally will show constant rate, whereas sinus tachycardia will float up and down. In atrial flutter, you will occasionally glimpse a single dropped beat in the rhythm (brief 3:1 instead of 2:1), exposing a tiny flutter wave for just an instant that you may see on the monitor. Vagal maneuvers such as the REVERT maneuver offer a quick and feasible diagnostic maneuver at bedside. Lewis leads are another option.

Look closely at the ECG. In general lead V1 and the inferior leads will show the clearest evidence of atrial flutter. In atrial flutter, the P-waves in V1 are often fully upright, which cannot happen in sinus rhythm (sinus rhythm always has a negative component due to left atrial depolarization because the impulse from the SA node must travel away from V1 to reach the left atrium).  Atrial flutter typically has fully upright P-waves in V1, as here. 

Fully upright P-waves in V1.

Furthermore, you must train your eyes using these examples to be able to "subtract the QRS complexes out", and see what pattern emerges without them. Below are some close-ups using different methods to explain this.

Red arrows indicate flutter waves at exactly twice the ventricular rate.

QRS complexes have been removed and replaced with a line showing what would be consistent with flutter waves. The influence of the superimposed T-waves cannot be edited out, and this is the only reason the flutter waves do not appear perfectly symmetric after the QRS (as they do in the ECG later in the case).

A repeat ECG is slightly more obvious, but still 2:1 conduction throughout:

The treating physicians were convinced of atrial flutter. They were about to give diltiazem when the patient had an episode of severe vomiting, and a rhythm change was noted with each bout of vomiting, so this ECG was recorded:

Increased vagal tone to the AV node in the setting of vomiting is likely responsible for this brief increased AV block. Clearly the diagnosis of atrial flutter is confirmed in leads V4-V6 during the break in the rhythm.

The patient received several rounds of diltiazem IV pushes, but continued to have 2:1 flutter, and ultimately required a diltiazem drip. On the drip another ECG was recorded:

Atrial flutter with variable AV block.

Initial troponin I was barely elevated at 0.03 ng/mL (0.01 is considered "elevated" for our assay). Potassium was 3.1 mEq/L.

CT scan confirmed the clinical suspicion of small bowel obstruction. The atrial flutter was treated by treating the underlying causes of bowel obstruction, repleting electrolytes, and temporizing with AV nodal blockade. Repeat troponins were all unchanged at 0.03. The patient did well.


Learning Points:

1) Atrial flutter can mimic ST elevations or depressions.
2) Atrial flutter can be determined based on a combination of ECG and bedside clinical characteristics, as well as bedside diagnostic maneuvers such as Lewis leads, vagal maneuvers, and adenosine.
3) When there is apparent ST elevation in a patient with tachycardia, look for other causes than ACS.

Chest pain and a "normal" ECG

This is another case written by Pendell Meyers (who is helping to edit the blog and has many great recent posts)

Case

A 45 year old man was driving to work when he experienced acute onset sharp left sided chest pain with paresthesias of the left arm. He received aspirin en route via EMS, and no EMS ECGs are available.

Here is his ECG on presentation to the ED, approximately 45 minutes after onset of pain, but with pain improving since onset:

What is your interpretation?

I sent this ECG with no clinical information to Dr. Smith. He replied:

"If acute chest discomfort, then this is likely an acute proximal LAD occlusion
STE in V2 with a Q-wave
Subtle ST depression in III, aVF. down-up in aVF
Subtle STE in aVL"


Baseline ST elevation is common in the anterior leads, but to be called normal STE it must have a normal QRS. The QRS in this case is NOT normal. There is very poor R-wave progression, with no R-wave in V2, and tiny R-waves in V3 and V4. The Q-wave in V2 is followed by STE and large (though not quite hyperacute) T-waves. Therefore this STE cannot be called normal.

We would then look for reciprocal changes in the inferior leads to further confirm the hypothesis that this is abnormal STE in the anterior leads. There we find a relatively normal QRS with abnormal ST segments and T-waves which do not agree with their QRS complexes (which supports them being acute changes). There is minimal STD in III and aVF. There is a fully inverted T-wave in III, and "down-up" morphology in aVF.

This is very subtle, and only long-time readers and experts will see this as a easily-recognizable pattern. Luckily there are some equations which approach the skill of experts for this particular question, which only require a few simple measurements. There is a Q wave in lead V2 which technically prevents the use of these formulas, but for the sake of interest here is what happens if the formulas are applied anyway:

Both formulas predict LAD occlusion, even with the most conservative (small) values for STE 60 V3 used.

The initial ECG was interpreted as "normal" by the computer and "no acute ischemic changes" by the ED physician. The initial troponin was negative (drawn approximately 1 hour after onset of symptoms).

Side note: contemporary troponin drawn 1 hour after acute LAD occlusion should usually be negative, unless the event has been going on longer than the patients symptoms. The assay at my institution, for example, is frequently negative until 4-6 hours after acute coronary occlusion.

The patient had been chest pain free since shortly after arrival, and was sent to the observation unit for serial ECGs, troponins, and CTCA. One hour after arrival, while the patient was awaiting CTCA, he started to have returning chest pain.

A repeat ECG was recorded with pain 2/10:

Not much change. Maybe even improvement in the reciprocal changes in the inferior leads.

This was brought to the ED physician who interpreted this as unchanged from initial ECG.

10 minutes later the patient became diaphoretic with worsening pain. Another repeat ECG was performed:

No caption needed!

Shortly after this, the patient had a VF arrest. He was shocked out of VF twice, and just before the second shock this ECG was captured:

Although this is often erroneously called "Torsades (de Pointes)," it is really ventricular fibrillation.   It should have been shocked at least 10 seconds ago. 

After the second defibrillation the patient had an organized rhythm:

Bradycardic escape/agonal rhythm, with large ST deviations. Beats 4, 6, and 7 are narrow, as the rhythm is trying to resume from above the ventricles.

This rhythm reportedly produced no palpable pulse, and CPR was continued. 30 seconds later, however, the patient began spontaneously moving and CPR was discontinued.

A repeat ECG was done:

Obvious anterolateral wall STEMI. (Proximal LAD occlusion with dramatic ST Elevation)

The patient was intubated and taken to the cath lab. On arrival his BP was 70s/40s, so an intra-aortic ballon pump was placed. They found a 100% acute thrombotic proximal LAD lesion. Here are the cath images before and after intervention:

Serial ECGs after PCI show improvement in ST segments, but also some ongoing ST elevation implying active injury after cath (this could mean downstream small vessel occlusion):

There are also hyperacute T-waves.
Smith likes to say: "Hyperacute T-waves occur 'on the way up,' and 'on the way down.'"
This means that they occur shortly after onset of occlusion, but also may be the last remaining sign of ischemia after ST elevation resolves (after reperfusion).

T-waves less hyperacute, though ST elevation remains

Echo showed EF ~40%, with severe hypokinesis of the mid anterior septum and apex. Troponin T was recorded at 1.41 (very high), and was still climbing but no further measurements were available.

He recovered and was discharged 5 days later.

2 days after discharge, he awoke at 3am with sudden severe chest pain. He presented immediately to the ED and had this ECG:

There is large anterolateral STE with hyperacute T-waves, and reciprocal STD in III. This is diagnostic of re-occlusion. This ECG cannot be present 7 days after a single persistent acute occlusion.

The patient was taken back to the cath lab, where 100% proximal in-stent rethrombosis was found and treated.

Repeat ECG after PCI:

LAD occlusion resolving.

Take Home Points:

1) Computers are not currently sufficient to detect important ECG abnormalities

2) Dangerous LAD occlusion can be very subtle

3) "Normal ST elevation" in the anterior leads requires a normal QRS and R-wave progression

4) Use the LAD occlusion formulas

5) Don't confuse VF with torsades

30 yo woman with chest pain and a "normal ECG" by the computer, this one prehospital

This was sent by paramedics in the Northwest Ambulance Service in the UK.  James Alameddine credits his partner, Gary Wilson.

Case

A 30 year old woman complained of chest pain and called 911.

She had a prehospital 12-lead ECG recorded:

As you can see, the computer interpretation is "normal"
What do you think?

This very perceptive medic noticed that the T-wave in V4 is far too tall for the QRS.  Very abnormal.  But computers are not programmed to find all abnormalities, including many that are dangerous.  This is this one.

How about ST Elevation?

There is (as the computer measures -- at the side) more than 1 mm of STE in V2 and V3, but not the 1.5 mm that would trigger "STEMI" in a woman.

Thus, you have to decide if this STE is due to normal variant or due to ischemia.  Normal Variant ST Elevation always has good R-wave progression, and here the R-wave in V4 is only 3 mm.

If we use the 3-variable formula, with STE60V3 = 2 mm, QTc = 413, and RAV4 = 3, the value returns at 25.8 which is clearly diagnostic of LAD occlusion.

The 4-variable formula which includes the QRS amplitude in V2 turns out to be: 20.6 (most accurate cutoff is 18.2), so both formulas predict LAD occlusion.

The T-waves in V4-V6 should never be taller than the R-wave and should even be far less tall.

They should look like this:

Here are some more examples of hyperacute T-waves in V4-V6:

An elderly man with severe chest pressure......

Ventricular Fibrillation, Resuscitation, and Hyperacute T-waves: What does the Angiogram show?

Chest pain in a 42 yo, relieved by Maalox and viscous lidocaine 

This one was also called "normal" by the computer (but in this case, also by the physician)


Case continued:

Because of this hyperacute T-wave, the medic continued to record serial ECGs over the next 20 minutes:

Now there is subtle ST depression in lead III, seen by the computer

Clear ST Elevation in I, aVL, V4-V6, with reciprocal ST depression in II, III, aVF

Obvious Proximal LAD occlusion

The medics activated the cath lab and the patient went straight to the cath lab and had an LAD occlusion opened and stented.

The medics were unable to get any other information such as troponins or echo.

Here are more cases of "normal" ECGs, posted on September 28:

Just a few cases that the computer called "normal"

Question: How would you like it if there was a policy that patients with "normal" ECGs do not need it to be reviewed by the physician?

This young woman with chest pain would be listed as "very low risk" and would sit in triage for many hours until she arrests or loses half of her myocardium.

Just a few cases that the computer called "normal"

This article has been discussed on Twitter today.  

It purports to show that you don't need to read the ECG if the computer says "normal".  Many on Twitter seem to agree.

Safety of Computer Interpretation of Normal Triage Electrocardiograms

The confidence intervals were 97-100%.  Would you like to be 97% sure you're not missing an emergency?

So I just looked through a few of my blog cases that were read as "normal" by the computer.

Just as an aside: we are just finishing a manuscript studying a deep neural network EKG algorithm.

We compared the new deep neural network (DNN) from Cardiologs technologies(DNN) to Veritas conventional algorithm: Veritas: 364 "normal"; 5 missed emergencies. DNN: 493 normal; 2 missed.

So things will get better as technology advances.

We are not there yet.

Here are the cases:

Subtle Dynamic T-waves, Followed by LAD Occlusion and Arrest

How unreliable are computer algorithms in the Diagnosis of STEMI?

Chest Pain Diagnosed as Gastroesophageal Reflux

It is easy to be led astray by the computer....

This case which I posted on June 12 2017 in response to the article was not my case:

Should Emergency Physicians be interrupted by ECGs that are read as "Normal" by the computer?

A 50-something with chest pain and minimal precordial ST elevation

A 50-something with diabetes presented with 3 hours of sharp chest pain radiating to the left hand, with dyspnea and diaphoresis; it was worse with exertion and with lying flat.

He had this second ECG, which was texted to me and I looked at it on my iPhone.  At the time of this ECG, the patient had received NTG and the pain was decreasing.

ECG-1:

There is 1 mm of ST elevation at the J-point in both V2 and V3 (within normal limits).
Computer interpretation is normal
Cardiologist overread is normal
What do you think?

More description: There is also poor R wave progression, with small R waves in V4. The T waves are slightly broad and large, but probably could not be called hyperacute. There is minimal STD in aVF.

One of our interns had texted this ECG-1 to me, with the message:

"3 hours of chest pain, QTc = 415 ms, 3 variable formula is 25.3.  What do you think?"

__________

[The 3-variable formula for differentiating normal variant ST elevation from the ST elevation of subtle LAD occlusion can be accessed by clicking on the link at the top of the page and entering the values into the online excel applet.  Values are: 1. ST elevation at 60 ms after the J-point in lead V3.  2. R-wave amplitude in V4. 3. computerized QTc.  See also the free iPhone app "SubtleSTEMI".  See also MDcalc.]

A value greater than 23.4 is very worrisome for LAD occlusion.

__________

I responded: 

"Not LAD occlusion.  What do you think?  Do the 4-variable formula."  (I just did not think it looked like an LAD occlusion)

I showed it to Pendell Meyers, and he said: To me it looks like it could be "on the way down" from LADO. The only way to prove it is with serial ECGs and the rest of the clinical story.   

Very perceptive.

__________

[The 4-variable formula adds the entire QRS amplitude in lead V2 and is more accurate than the 3-variable formula.  It is: (1.062 x STE at 60 ms after the J-point in V3 in mm) + (0.052 x computerized QTc) - (0.151 x QRSV2) - (0.268 x R-wave Amplitude in V4 in mm).  It can also be accessed at the top of the page, with value entry into the excel applet.]

The publication of the formula can be found here: A new 4-variable formula

A value greater than 18.2 is quite sensitive and specific for LAD occlusion. 

___________

The calculated value was 19.2

I suggested serial ECGs, which were done:

ECG-2: This one is about 50 minutes later:

Not much change

The first troponin I returned undetectable.

At about 3 hours after ECG-1, the second troponin I returned at 0.097 ng/mL.

At this time, the patient became pain free.

ECG-3. Here is the ECG in the pain free state:

Now there is less than 0.5 mm of ST Elevation.
Some people have nearly zero ST elevation at baseline.
For such patients, LAD occlusion may only manifest 1 mm of STE 

ECG-4. One hour later, this was his ECG (still pain free):

There is still only minimal STE.
T-waves in V2 and V3 are slightly less tall.
This suggests further resolution. 

ECG-5.  Later I discovered that there was an even earlier first ECG, recorded 50 minutes prior to ECG-1.

This has a lot of artifact.
It was called normal except for artifact.

But this is very interesting:
notice the T-wave in V2 is 8 mm, whereas it is 5 mm in the first ECG above.

As it turns out, the ECG at the top (ECG-1) was done after nitroglycerine, and the patient's pain had diminished "from 6/10 to 4/10." 

Here are all the V1-V3 leads, side by side:

                            1300               1350, pain decreasing               1430                  1700, pain free       1800, still pain free

This shows that the T-waves (which never were quite hyperacute), are deflating and may have been hyperacute prior to arrival.

Outcome:

The third troponin I, drawn 4.5 hours after presentation, returned at 4.2 ng/mL.

The patient went for angiogram and had an 80% mid-LAD thrombotic stenosis and proximal LAD disease, as well as a 90% diagonal lesion.  He went for Coronary bypass (CABG). 

This outcome is perfectly consistent with all the ECGs.

Learning points:

1. Pay attention to diminishing T-wave amplitude during diminishing pain.

2. The formulas are very accurate.  I have always thought that I can do better than my formulas, but now I'm in doubt.

3.  Some patients have near zero ST elevation at baseline. Any ST elevation in these patients is abnormal.  In such patients, LAD occlusion may result in very subtle ST elevation.