Wednesday, December 31, 2014

A woman in her 20s with syncope

A young woman had what sounded like vasovagal syncope.  This ECG was recorded:
There is incomplete RBBB (QRS = 110 ms).  There is some ST depression and T-wave inversion in V1-V3, but remember this is the normal repolarization pattern for RBBB.
What else?

















It looks like a very long QT.

Is it?

You can clearly see the peak of the T-wave in lead II across the bottom.  So let's find where the peak is on other leads:
There is sinus rhythm with inverted P-waves (low atrial pacemaker, of no clinical significance). The blue line shows the peak of the T-wave in II.  Drawn up to V1-V3, you can see that the large wave is AFTER the T-wave.  It is thus a U-wave, not a T-wave, and the QT is not long.  The arrows point to U-waves in other leads


The patient had a previous ECG:
It turns out she had had unspecified cardiac surgery in the past and had incomplete RBBB at baseline.  As you can see, there were no U-waves on that previous ECG.




Her K was 2.9 mEq/L.  This is not terribly low, but can certainly result in ECG abnormalities.

She had K replaced to a level of 3.9 mEq/L.  Then, 2 hours, 40 minutes later this ECG was recorded:
U-waves are still present but not as prominent.
The treating physicians interpreted this as normalized back to baseline ECG; clearly this is not so.


Why are U-waves still present?

1. She may have some other unspecified reason for U-waves
2. Recurrent hypokalemia: Her K may have dropped back down after replacement.  For every 1 mEq/L of low potassium, there is a 200-400 mEq total body deficit.  So K may shift to the intracellular space soon after replenishment, and the serum K may drop within hours after administration.


The syncope and the ECG are probably completely unrelated, though it is possible that this resulted in ventricular dysrhythmias.

Here is another case of hypokalemia in RBBB.

Monday, December 29, 2014

All this teaching makes a difference! And a new paper on subtle ST Elevation.

One of my residency grads sent this.

A male in his 50's with h/o CAD presented with 2 days stuttering chest pain (also with nausea, diaphoresis, and SOB).  The chest pain had been constant for 2 hours.

"His first ECG was reviewed by a partner [who has not had as much training in ECGs) who said it was ok for the patient to wait in triage.  When he was roomed I took a look at his initial ECG."

Here it is:
This was his assessment:
"I saw the T-wave in inferior leads and immediately 'freaked out.'  Then I saw the subtle but non diagnostic ST elevation, but mostly it was the look of aVL which I've heard you talk about a million times now as being specific for inferior ischemia."


He got a repeat right away (24 minutes after the first):
"This showed STEMI, so I activated the cath lab."


Outcome:

The patient had severe diffuse CAD with a 99% thrombotic stenosis culprit in the circumflex, with TIMI-1 (very slow inadequate) flow.  It was stented.

Peak troponin was 53.5 ng/mL.

He is scheduled for CABG in 2 weeks.


What is the outcome of patients with MI who present with subtle ST elevation?  

Is it more benign than those with diagnostic ST Elevation?

This Spanish paper published this month in American Heart Journal by Marti et al. suggests that it is not more benign.

The authors have a very aggressive policy of taking patients to the cath lab immediately even for low suspicion of STEMI.  They studied 504 consecutive patients who were taken to the cath lab for suspicion of coronary occlusion.   86% were found to have TIMI 0 or 1 flow.  18% of these patients did not have any lead with at least 1 mm of ST elevation measured at the J-point.   These patients more frequently had multivessel disease and longer delays to reperfusion.  They had the same incidence of subsequent death or re-infarction.

Their study underestimates the number of subtle STEMI because they used 1 mm even in V2 and V3. The guideline recommended cutoff for these leads is 1.5 mm for women, 2.0 mm for men age greater than 40, and 2.5 mm for men aged less than 40.

Their conclusion was: "Subtle STEMI is frequent in clinical practice and is usually associated with acute total coronary occlusion.  Therefore, it should be diagnnosed and treated in the same expeditious manner as marked STEMI.  (Marti D et al.  Incidence, angiographic features, and outcomes of patient presenting withsubtle ST-elevation myocardial infarction.  Am Heart J 2014; 168:884-90.)

Learning point:

It is important to recognize subtle ST elevation myocardial infarction.  These patients are frequently not recognized and not taken for cath until the following day.  This study shows that patients with coronary occlusion frequently have minimal ST elevation.






Saturday, December 27, 2014

Very Fast Very Wide Complex Tachycardia

A male in his 60's called 911 for dizziness and chest pain, onset with exertion.  He was pale and diaphoretic (in shock) with a thready radial pulse.

Here is his initial rhythm strip (it is not a full 10 seconds):
Wide complex tachycardia, rate 235
This is a very wide complex regular tachycardia at a rate of 235.  It should be considered to be Ventricular Tachycardia and treated as such.


Here is the 12-lead:

By any analysis, it is most likely VT: There is slow depolarization of the initial deflections of the QRS.  However, this is a very fast VT.

The patient should be safely sedated and electrically cardioverted.

The paramedic instead gave adenosine, which is not contraindicated, and will not harm a patient in VT.  It is now part of the ACLS protocol.

If it is VT, as suspected, it will not work (RV outflow, adenosine sensitive VT is likely to respond, but this is NOT such a benign VT as it is too wide and does not have the right morphology).

If it is SVT with aberrancy, it is likely to work.

If it is AV reciprocating (antidromic WPW), adenosine is likely to work.

If it is slow Atrial flutter with 1:1 conduction, it should slow the conduction and reveal the flutter waves.  This is the exact rate one expects with slow atrial flutter and it is why slow atrial flutter can be so dangerous: it conducts 1:1, with fast ventricular rates.

Here are the monitor leads during and after adenosine:

During adenosine:
Lead II is monitored.  The rate starts at 222 with a wide complex.  It is uncertain to me why the initial rate is slower than the rate above; it is clear though that it is the same rhythm because lead II has the same morphology.  In the middle of the second strip, there is a minimal pause, after which the complexes are narrow, and after which there are visible flutter waves at a rate of 228.  There is mostly 2:1 conduction, but some 1:1  

After adenosine:

The strip continues: now the flutter waves are easily seen at a rate of 240 (almost exactly the same rate it started with) with 2:1 conduction and a relatively narrow complex QRS (less than 120 ms).



















2 12-lead ECGs were recorded within the next 3 minutes:
Rate 118, flutter rate 236: One can see the flutter waves in lead II, and an upright P-wave in V1 confirms that this is flutter.  Some of the ST depression is due to flutter waves, but there is also significant subendocardial "demand" ischemia.  ACS is of course possible.

Rate 120, flutter rate 240.  Still more ST depression.


So what happened?

One might speculate that the patient co-incidentally converted from VT to atrial flutter at the time of the adenosine.  But I think that this atrial flutter was just slow enough to conduct through the AV node but too fast to use the conducting system, so if conducted through the ventricles VERY aberrantly and, the first time that there was AV conduction delay (2nd line of rhythm strip during adenosine), the conducting system recovered (was no longer refractory) and was able to conduct such that the QRS is a relatively narrow complex.  

How do I know (or think I know) it was atrial flutter with aberrancy?

Because the rates before and after the change in conduction are nearly exactly the same.  Again, see line 2 of rhythm strip during adenosine.  It is clearly atrial flutter after, so it must have been atrial flutter before

Did adenosine convert anything?  

No, but it appears to be associated here with a slight increase in atrial flutter rate and thus subsequent 2:1 conduction with slower ventricular response (atrial flutter 240, faster, but ventricle at 120, slower).

Learning points:

1.  Sometimes it is better to be lucky than right.
2.  Generally, adenosine is safe in VT
3.  If it looks like VT, treat it like VT.  Don't count on being lucky.
4.  Slow atrial flutter can produce VERY FAST ventricular rates.
5.  Very fast ventricular rates may conduct very aberrantly and be very wide.
6.  Sometimes what appears to unequivocally be VT is not


Comments appreciated.


Tuesday, December 23, 2014

Chest pain relieved by Maalox and viscous lidocaine

An otherwise health male in his early 40's presented with "burning" in his epigastrium that radiated to his throat and was relieved with Maalox and lidocaine.  He had an ECG recorded:
Sinus Rhythm.  This was read as normal by the emergency physician and by the computer.  QTc is 400 ms.  What do you think?  See below.


























There are a few subtle signs of coronary occlusion here.  

First, look at V4-V6.  The T-wave is almost as tall as the R-wave.  This should not be.  Here is a normal relationship:

Second, look at aVL.  It has a massive T-wave compared to the size of the QRS.  There is also a tiny amount of ST elevation but, again, it must be considered in the context of a very small amplitude QRS.


Sometimes the T-wave can appear to be relatively large because the QRS axis is perpendicular to the lead (so the QRS looks small) but the T-wave axis is parallel.  However, here are the two axes:


Finally, look at lead III:

There is minimal ST depression.  Although the T-wave appears also to be inverted, we know from the above graphic of T-wave axis, that there is not an abnormal T-QRS axis (they are nearly equal), which is what defines T-wave inversion.

None of these findings are diagnostic of ischemia, but they should give you a high index of suspicion and prompt serial ECGs at a minimum.

Formula: There is not enough ST elevation in V2-V4 to be applying the LAD/early repol formula, but if it is applied, one gets 1.5 mm of STE at 60 ms after the J-point in lead V3, 400 ms QTc, and 6 mm of R-wave amplitude in V4.  The formula results in 23.43, just above the 23.4 cutoff!



The patient was diagnosed with esophageal reflux and was being discharged by the nurse when he had a cardiac arrest. He was defibrillated.  



Here is his post resuscitation ECG:
Now the diagnosis is obvious.  Anterolateral STEMI.  
The rhythm is sinus with PVCs that occur after a P-wave but before it conducts.  In V1, it appears to be alternating RBBB and normal conduction with high ST elevation.  However, the 1st, 3rd, and 5th complexes in V1 are PVCs with RBBB morphology.  The 2nd and 4th are sinus with normal conduction with deep QS-waves (not LBBB).  Notice how visible the ST elevation is in the PVCs. 


He underwent PCI and had a good outcome.

Learning Points:

1. T-wave size must be assessed relative to the QRS amplitude
2. Ischemia comes and goes.  It may incidentally go away with antacids!





Friday, December 19, 2014

Beware confusing the diagnosis of posterior STEMI by using posterior leads...

Or at least understand their limitations!!


This patient had chest pain and this ECG:
There is no significant ST elevation. But there is ischemic ST depression in V2-V6.  It is maximal in V3 and V4, which represents posterior STEMI until proven otherwise.

(This can be due to subendocardial ischemia, but less likely.  Most subendocardial ischemia is diffuse, with the ST depression vector pointing towards the apex of the heart (II, V5) and thus has maximal ST depression out in V5 and V6.  

The ST elevation vector is clearly away from V3 and V4, towards the posterior wall.  If you put posterior leads on, you MUST get posterior ST elevation.  HOWEVER, it may be of very small magnitude and thus is may be a false negative.

Posterior leads were applied:
V3 is misplaced here, so ignore it.  Notice there is some ST elevation in V7-V9, but it is minimal.  It does not even meet the "criteria" of 0.5 mm in posterior leads.  V2 has the same ST depression in had on the first ECG, confirming that the artery is still closed.

So this gives a false negative.  Posterior leads lead you astray.  The voltage is so small that you might be dissuaded from your diagnosis of posterior MI.

This was indeed a circuflex occlusion with a posterior wall motion abnormality.




So when should you use posterior leads?

There is some literature showing that some posterior MI show up only on anterior precordial leads as ST depression, and some show only on posterior leads.

I think some of this is due to timing.  Arteries open and close and if you don't record the ECGs simultaneous, then you might be recording two different conditions of ischemia.

It may be useful to record posterior leads in a patient in whom you are convinced has an MI but has no significant abnormalities on the standard 12-lead. 

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Wednesday, December 17, 2014

Subtle LAD Occlusion with Pseudonormalization of Wellens' Waves.

Here is another patient I saw a few weeks ago  He is in his 30's and presented with many hours of chest pain.  Here is his initial ECG:
The computerized QTc is 361.  There is ST elevation in V2-V4.  Is it normal ST elevation?  Normal ST elevation should have good R-waves and V2 and V3 have Q-waves.  So this is not normal ST elevation.
STEMI criteria: 2 consecutive leads with ST elevation, defined as 1 mm in V1 and V4-V6, and, for a 35 year old, 2.5 mm in V2 and V3 (at the J-point relative to the PQ junction).   This ECG has at most 1 mm in V2, 1.5-2.0 in V3, and 1.5 in V4, so it does not meet STEMI criteria.  LAD occlusion frequently does NOT present as STEMI on the ECG.

With the presence of Q-waves, one should assume this ST elevation is due to LAD occlusion, not to normal variant.  Do not even use the formula.

Let's go back in time

It turns out he had been in the hospital less than a month prior with a NonSTEMI with Wellens' syndrome.  Here is his ED ECG from that visit, after resolution of chest pain:
Classic Wellens'.  Patient is at high risk of closure of his LAD.

The physicians wanted to do an angiogram, but in spite of pleading with the patient, the patient would not agree to undergo any further testing because he felt fine.  They discharged him on aspirin and clopidogrel.

This was his pre-discharge ECG after having a peak troponin I of 0.78 ng/mL (99% = 0.030 ng/mL)
Notice that much of the T-wave inversion has normalized, but there is residual biphasic T-wave inversion in V4 and V5.

A pre-discharge echo showed LVH, no wall motion abnormality, and an EF of 60%.


Back to the 2nd ED presentation


And then he presented to me with this ECG, which I post again here so that it is in sequence:
I did not see this ECG immediately.  The computer of course read it as early repolarization.  The resident saw it and was worried and ordered a repeat ECG.      

--Had the resident compared with the previous ECG, the loss of R-wave would have made the diagnosis immediately.
--Had the resident seen the pseudonormalization of T-waves (now upright in V4 and V5, all but diagnostic of re-occlusion), the diagnosis would have been made sooner.
--Serial ECGs should not wait an hour



This is ECG #2, 54 minutes after the first:
Obvious anterior STEMI


Angiogram showed a proximal subtotal thrombotic occlusion which was stented.

Here is the post cath ECG:
Marked loss of R-waves with persistent ST elevation.  These may resolve over time but are highly correlated with development of LV aneurysm.

Echo 5 days later showed anterolateral, septal, and apical wall motion abnormalities and an EF of 40%.  Peak troponin I was 176 ng/mL (very high).



Learning Points:

1. As I've endlessly repeated here, LAD occlusion may be very subtle.  Any delay in diagnosis can result in significantly worse outcome.

2.  Wellens' syndrome is the result of reperfusion of a briefly occluded LAD.  That LAD is at high risk for re-occlusion

3. Re-occlusion results in pseudonormalization (see link for other cases) of the inverted Wellens' waves.  The apparently normal, upright, T-waves are in fact NOT normal and are the result of re-occlusion.

Monday, December 15, 2014

It is Far too Early for a Requiem for Unstable Angina

Dr. Braunwald declared that high sensitivity troponins will make Unstable Angina a thing of the past.  That very well may be true, but in the United States we are not yet in the era of high sensitivity troponins.  And we do not know what their effect will be.

Here are many more cases of Unstable Angina.

Unstable Angina

A male in his 50's with no past history presented with new intermittent burning left chest pain, lasting 10 minutes at a time, radiating to the left arm, for 24 hours.  He had chest pain just prior to arrival in the ED, but it resolved prior to physician evaluation.  He did use cocaine a few days prior.  He had blood pressures in the 170/100 range.  Here is his initial ECG:
There is terminal T-wave inversion in V2-V5, highly suggestive of "Wellens' syndrome."
Patient had pain, is pain free, has intact R-waves, and terminal T-wave inversion
(Wellens' Pattern A)

There was no further pain, but a second ECG was recorded 1 hour later:
There is some evolution of T-wave inversion (V3 has a deeper negative deflection), increasing suspicion for Wellens' syndrome.

The ED was concerned about "Wellens' pattern," and gave aspirin, clopidogrel, and heparin.  He was not given anything for his blood pressure.  He was admitted to the hospital. The consultants were very worried as well, and discussed angiogram vs. stress test in the morning.

Comment: when a patient has cardiac ischemia and is hypertensive, the blood pressure should be controlled.  There are many choices. One is metoprolol.  There is an admonition not to use a beta blocker in patients who have cocaine in their system because if may produce "unopposd alpha" effects by blocking the vasodilating effects of beta-2. However 1) that admonition is based on faulty data from combined beta-1 and beta-2 blockade (namely propranolol -- metolprolol has almost no beta-2 blocking effects) and 2) the patient has not had cocaine for days.

The patient ruled out by 4 serial contemporary troponins over 9 hours.

A cardiac echo was normal, showing no wall motion abnormality and EF of 65%.

No more ECGs were done (was there further evolution of T-wave inversion?  Was there resolution?)  In my experience, if troponins are all negative, the T-waves rarely evolve to Pattern B (deep symmetric inversion).  Instead, they often resolve.  Such resolution is NOT pseudonormalization (which is due to re-occlusion of the vessel), but rather due to resolution of ischemia.

The assessment in the light of a normal echo and normal troponins was that this was noncardiac chest pain or cocaine chest pain with nonspecific T-wave inversions.

There had been discussion of a stress test but the patient was discharged.  It seems he had been instructed to go to his primary MD and get a stress test.

Case progression.

Two days after discharge, the patient presented to another hospital ED with the same complaints of intermittent chest pain (3 episodes).  He had not seen his MD nor had a stress test yet.  His last episode of chest pain was just prior to ED arrival and was resolved upon arrival.  Here is the initial ECG:
Classic Evolution of Wellens' Waves


The physician had no access to previous ECGs.

The first troponin was negative.  The physician consulted the on-call cardiologist who thought it was very unlikely that this would be Wellens.'  He did not think it possible that the patient could have 4 days of intermittent chest pain with normal troponins throughout and without wall motion abnormality, and with a normal ejection fraction.

He thought the most likely cause was related to the patient's recent cocaine use and vasospasm. He did agree with the plan for stress test but felt like it could be done as an outpatient.

The patient was told to return for increased or longer lasting pain.

He did return the next day after another episode of pain, and was pain-free on arrival.

Here is the ECG:
More Wellens' Evolution, but with some loss of R-wave amplitude




This time the initial troponin I returned at 1.5 ng/mL.  The peak troponin is not available.

He had an angiogram which showed a 95% thrombotic LAD stenosis with preprocedure TIMI-3 flow.  It was stented.  There was also an 80% proximal LAD stenosis.

Here is the angiogram:


Here is the post cath ECG:
There is loss of R-wave in V2 and V3.  The T-waves have evolved as expected from Pattern A (biphasic) to deep and symmetric (Pattern B). 



A post cath echo showed anterior and apical WMA with EF of 55%.  Will this be permanent?  It is uncertain if there was irreversible loss of significant myocardium.  The loss of R-waves suggests that this is the case.


Learning Points:

1. Unstable Angina still exists.  Contemporary troponins are CERTAINLY not good enough to rule it out.

2.  Regional wall motion recovers rapidly after reperfusion of the infarct artery.  After chest pain is resolved, a normal echocardiogram should not reassure you!

3.  Pay attention to specific ECG findings!

4. Chest pain in a patient who uses cocaine is just as likely to be due to ACS as it is in a patient who does not use cocaine.  See this article and editorial.  

5. Chest pain that occurs more than one day after cocaine use should not be attributed to cocaine.

Friday, December 12, 2014

I was reading a stack of ECGs yesterday, and saw this one, with no clinical information....

I was reading a stack of ECGs yesterday, and saw this one, with no clinical information:
What do you think? (computerized QTc is 429 ms)
See followup below.


















My thought was: "This is an acute LAD occlusion, and I am afraid it would have been missed."

Why did I think that this apparently benign looking ECG represents LAD occlusion?  It is an ECG that does not meet any millimeter "criteria" for STEMI.

I am sorry if I repeat myself too often, but there are many LAD occlusions which are missed at initial presentation because it is thought to be normal variant ST elevation.  That is why I studied it and produced the formula for differentiating benign from ischemic ST elevation in "anterior" leads.  Many are not diagnosed until the patient "rules in" by biomarkers, goes to cath later, and has the artery opened only after the damage is done.  And these get a final diagnosis of "NonSTEMI" because they do not meet "criteria" for STEMI and yet they are due to complete occlusion of the artery. You don't get a message from anyone that you "missed a STEMI."  And yet the patient lost a lot of myocardium unnecessarily.

See these references:
Wang T et al.  Am Heart J 2009;157(4):716-23.
From AM, et al. Am J Cardiol 2010;106(8):1081-5.
Pride YB et al.  JACC: Cardiovasc Interventions 2010; 3(8):806-11.

Almost all of these occlusions can be diagnosed, but only with a high suspicion and with careful investigation, serial ECGs, and high quality echocardiography.

On this ECG there is ST elevation in lead V2, and it must be explained.  Is it benign?  If it were benign, then there should be excellent R-wave progression.  There is not.  In fact, the R-wave gets smaller from V2 to V3.  Furthermore, the T-waves are much more symmetric than the T-waves of early repolarization.  If you plug these numbers into the excel applet on the sidebar:
--ST elevation at 60 ms after the J-point in lead V3
--computerized QTc
--R-wave amplitude in V4

The resulting value is 25.0.  Any value greater than 23.4 is LAD occlusion until proven otherwise.  Less than 4% of LAD occlusion have a value < 22.0.

So I went to the chart:

The patient had acute onset of chest discomfort, called 911, and had this prehospital ECG approximately 15-20 minutes prior:
Besides a PVC, there is no evidence of ischemia.  But the fact that it is so different from the one above tells us that the one above one has evolved injury (ischemic ST elevation).


It turns out that the clinical information made this case much easier than the ECG: the patient looked distressed, was diaphoretic, vomiting, and ill appearing.

The clinicians looked at this first ECG and the prehospital one and did not think much of it.  So they recorded another one shortly thereafter:
The ST elevation has evolved into a definite STEMI.

The cath lab was activated.

There was a 100% occlusion of the mid-LAD.

Here is the post cath ECG:
This is a normal amount of ST elevation, and normal T-waves in V2-V4.  There is some T-wave inversion in V5 and V6.

The management was so fast that the peak troponin I was only 9.2 ng/mL.

Subsequent echo showed:

Left ventricular hypertrophy concentric .
Regional wall motion abnormality-distal inferior wall .
Regional wall motion abnormality-apex.

I suspect there will be nearly full recovery of wall motion because the post cath ECG is nearly normal.

Here is another identical case that did not turn out so well.

Learning Point:

ST elevation must be adequately explained, even if it appears benign.  This case was relatively easy because of the clinical presentation.

Many others are not so easy and require subtle ECG diagnosis.

People often think that I read these with a retrospectoscope.  I do not.  I found this in a "stack" (reading through a list on the computer) of undifferentiated ECGs.  And I do this often.  There are ways to make the diagnosis from the ECG. They can be learned.  And the LAD occlusion, early repol formula can greatly help.

Wednesday, December 10, 2014

Bilateral Arm and Mid Back Pain, BP 250/140, in a 50-something

A 50 something presented with 10/10 bilateral arm and pain between the shoulder blades that started at work.  It felt like a "tearing," and was associated with diaphoresis.

BP was 250/140.  He appeared distressed.

Here is the initial ECG:
This is diagnostic of inferoposterior MI, with acute coronary occlusion.  
There are hyperacute T-waves in inferior leads, ST depression and T-wave inversion in aVL, and ST depression with T-wave inversion in V2 and V3.  There is also ST depression in V4-V6.


Of course the initial fear was aortic dissection, with the classic pain and severely elevated BP.  And it is not uncommon for a dissection to dissect down the coronary arteries, especially the RCA, so one might find an ECG like this in aortic dissection.  (Though only a tiny minority of RCA STEMI are caused by aortic dissection!)

The patient was given labetolol without much effect, then esmolol and nitroprusside until the BP was under control.

He was sent to the CT scanner where no dissection was found.

At this point the ECG findings must be attributed to acute coronary syndrome.  A repeat ECG is indicated to look for evolution or resolution. 

Before another ECG was obtained, the pain resolved.  This was recorded at 90 minutes:
Normalization was attributed to normalization of the severely elevated BP.

The first troponin was slightly elevated.  The ischemia was thought to be due to severe hypertension (a type 2 MI).  The cath lab was not activated.

Only less than 5% of type 2 MI present with subepicardial ischemia (ST elevation).  Demand ischemia from hypertension would be unlikely to manifest such focal STEMI on the ECG.

Progress

While waiting for a bed, he developed chest pain again, and this ECG was recorded at 120 minutes:
Now there is obvious inferoposterior STEMI


The cath lab was activated.

While waiting, the pain subsided again 10 minutes later (recorded at 130 minutes):
ST segments and hyperacute T-waves have normalized.



10 minutes later, the pain recurred again (time 140 minutes):
Obvious STEMI again.


Cath showed a 100% thrombotic occlusion of the RPAV off the RCA, stented.

Reperfusion was so fast that there was no wall motion abnormality the next day.




Friday, December 5, 2014

Transient ST elevation, rules out for MI, what is it?

A 70 year old diabetic complained of 6/10 epigastric pain.  Here is his initial ECG:

There is diffuse ST elevation: II, III, aVF and V3-V6.  There is reciprocal ST depression in aVL.  This is diagnostic of inferolateral STEMI

The emergency physician activated the cath lab and gave appropriate antiplatelet and antithrombotic therapy.

The PCI team came to talk to the patient, and while they were talking, the patient vomited and was pain free thereafter and said he felt much better.  They recorded another ECG:
The ST elevation is resolved.
There can be no other explanation than the patient spontaneously reperfused an occluded coronary artery.


The cath team cancelled the angiogram.  They admitted the patient to a floor bed.  I do not have any insight into what they were thinking.  Did they think it was pericarditis?  If so, pericarditis does not suddenly resolve.  Did just ignore the first one?  Or did they think that since the ST elevation resolved that this did not need emergent cath?

As it turned out, the patient ruled out for MI by serial contemporary troponins.  They were about to discharge him to home when an emergency physician objected.  He called the inpatient team and expressed his concerns, and to at least do a CT coronary angiogram or a stress test before discharge.

They consulted the cardiologists again and this time they took the patient for an angiogram.

Angiogram: 80% thrombotic occlusion of the circumflex, stented.

Imagine what might have happened if the fleeting ST elevation had not been recorded on that one ECG?  There are those who say that Unstable Angina no longer exists and that we should not be doing further testing on patients who rule out for MI.

Eugene Braunwald argues for a Requieum for Unstable Angina.

Here are many other unstable angina cases.


Transient STEMI, or, as in this case, Transient ST elevation Unstable Angina.

I have seen many cases of transient STEMI with negative biomarkers.  Technically, these are not MI by the Universal Definition of MI, which requires at least one elevated troponin, with appropriate rise and/or fall.  They are thus really unstable angina with ST elevation.  In any case, they are very high risk lesions.

See this case where I screwed up and the patient died.  


I am aware of 2 studies on Transient STEMI:

Ownbey M. et al.  Prevalence and interventional outcomes of patients with resolution of ST-segment elevation between prehospital and in-hospital ECG.  Prehosp Emerg Care 18(2);174-9.  Apr-Jun 2014.

They found 293 total cases of prehospital STEMI, but could only find all the relevant records in 83 cases (28%).  ST Resolution (STR) by the time of ED arrival occurred in 18 of 83 cases. There were no differences between STR and non-STR cases in prehospital vital signs or treatments. 95% of patients underwent cardiac catheterization with a mean door-to-needle time of 57 minutes (interquartile range 43-71). Comparing STR and non-STR cases, significant lesions (greater than or equal to 50%) were found in 94 and 97% of patients (p = 0.6), and subtotal or total lesions (greater than or equal to 95%) were found in 63% and 85% (p = 0.1), respectively.


Meisel SR, et al.  Transient ST-elevation myocardial infarction: clinical course with intense medical therapy and early invasive approach, and comparison with persistent ST-elevation myocardial infarction.  Am Heart J 155(5):848.

They studied 1244 consecutive STEMI patients.  63 (5%) had Transient STEMI (TSTEMI): Patients with Transient STEMI were treated with intravenous isosorbide dinitrate, aspirin, and clopidogrel, and/or with glycoprotein IIb/IIIa inhibitors. Coronary angiography performed 1.5 days after admission demonstrated no obstructive lesion or single-vessel obstructive disease in 43 patients (70%). PCI was performed in 48 patients (77%), and 8 patients (13%) were referred to surgery. Left ventricular ejection fraction was within normal limits, and peak creatine kinase was mildly elevated. Transient STEMI was associated with less myocardial damage, less extensive coronary artery disease, higher thrombolysis in myocardial infarction flow grade in culprit artery, and better cardiac function. These data suggest that immediate intense medical therapy with an early invasive approach is an appropriate therapy in patients with Transient STEMI.

The key is that all patients were treated with antiplatelet and antithrombotic therapy, and they generally underwent angiography.


Management of Transient STEMI: My opinion from experience and the literature:

1.  Patients with transient ST elevation should go to the cath lab emergently just as if they had not had resolution of ST elevation.

2. If for some reason the angiogram is delayed, they should get maximal medical therapy, be admitted to an ICU, and continuous 12-lead ST segment monitoring.  This is because re-occlusion is not always accompanied by symptoms.  See this case of asymptomatic re-occlusion.

Tuesday, December 2, 2014

A 50-something with severe chest pain and a normal ECG

A 50 something with no past history presented with sudden severe substernal chest pain with no radiation or associated symptoms.  The clinicians were very impressed with his presentation and were sure he was having an MI.  Here is his initial ECG:
Not very revealing.  They had expected a positive ECG.

A chest x-ray was completely normal.

The first troponin was negative.  

The pain persisted and another ECG was recorded 80 minutes later:
There is now some nonspecific ST depression in V5 and V6.

The second troponin returned negative at 5 hours.  The patient's pain persisted.

The clinicians were certain that something serious was wrong and were not convinced by the ST depression that it was ACS, so they performed a bedside ultrasound.

Here is the parasternal short axis:

There is good function and normal wall motion

Here is the parasternal long axis:

The emergency physician thought he saw a flap in the aorta (the echo free area behind the left atrium (see still image with arrow below):

The arrow points to something that, on the video, is apparently moving inside the aorta on the video























So the emergency physician took a look at the aorta through the suprasternal notch:

You can see a flap in the aorta



Here is a still picture with arrows pointing to the flap:
Here you can easily see the flap



Here is the CT scan:
Here you can clearly see the dissection flap



He went to the operating room and had a successful graft placed.  As I understand it, he was not a candidate for intravascular stent placement.


Learning point:

I don't usually do an ED ultrasound on every chest pain patient.  Maybe one should.  But in this case there were clues that something was wrong:

1.  Sudden pain
2.  Never had before
3.  Looked ill and in distress
4.  Could not be explained by the ECG
5.  Troponins negative.

One could argue that this could simply be suspected and he could get a d dimer, the CT if positive, or simply go straight to CT.

Fair enough.

But this is an easy screening test that one could do on more patients with unexplained chest pain.



Monday, December 1, 2014

Wide Complex Tachycardia: Lewis Leads Do Not Differentiate VT from SVT with Aberrancy

An 83 yo complained of palpitations and dizziness and presyncope.  He had a history of systolic heart failure with an EF of 40-45% and h/o coronary stents.  He is on digoxin and coumadin for atrial fib.   He denied chest pain or shortness of breath.  EMS arrived and noted HR in the 170's.  He was not in shock.  There was no pulmonary edema.  Mental status and blood pressure were normal.

They recorded the following rhythm strips:

V5
A very wide complex regular tachycardia.  By ECG alone (without considering pretest probability), the differential is VT vs. SVT with aberrancy vs. AVRT vs. very fast sinus with aberrancy.
The QRS width and the time from onsent of R-wave to nadir of S-wave is typical of VT (greater than 100 ms).
Here is lead II
This does not add much to the above.


This is a regular wide complex tachycardia.  I see no P-waves, antegrade, retrograde, or dissociated.  The QRS is very wide.

They attempted adenosine, first 6 mg, then 12 mg, with no change.

On arrival, the patient was very stable.  In the ED, this 12-lead ECG was recorded:
What is the diagnosis?



















The diagnosis is VT, for many reasons.  For those who can perform procedural sedation safely, the appropriate therapy is sedation with electrical cardioversion.  In such a stable patient, if sedation cannot be performed safely, an antidysrhythmic such as ajmaline, procainamide, or sotalol (or lidocaine) may work.  None are as dependable as electricity.

See annotated ECG:
--Black lines show the onset of the QRS in all 12 leads, as determined from finding the onset of the QRS in lead I
--Green arrows.  Using the black lines to find the onset, these arrows then illustrate the onset and end of the QRS in V1, such that one can determine the QRS duration is about 200 ms.  This is too long for SVT with aberrancy 
--Blue arrow shows the wide q (lower case)-wave, which indicates prolonged duration of initial depolarization, also consistent with VT
--Red circle shows the right bundle morphology with RR' (first R has greater voltage, unlike true RBBB), also consistent with VT
--Black arrow shows the nadir of the S-wave in V6: from onset of R-wave to nadir of S-wave is at least 100 ms, also consistent with VT.




When determining VT vs. SVT, here is the sequence of analysis I use:

Consider in the context of clinical scenario.  
(None of this applies to fascicular VT or RV outflow VT, which are associated with normal heart structure and originate in or near conducting fibers.  However, these are rare exceptions):

a. VT is more common than SVT among WCT
b. Older patients are more likely still to have VT
c. Any history of cardiomyopathy, MI, structural heart disease, or coronary disease makes VT much more likely

And then consider the ECG.  

The unifying principle of most VT is that the first part of the QRS is initiated in myocardium, NOT in conducting fibers, and thus conducts slowly.  Therefore, the initial part of the QRS changes its voltage SLOWLY (wide).  This is what I look for to diagnose VT:

1. The longer the QRS, the more likely it is VT.  A QRS duration greater than 140 ms is likely VT, though it is not a terribly reliable differentiator.  However, a QRS duration of 200 ms is almost always VT or aberrancy with hyperkalemia.  This case is thus almost certainly VT.
2. Obvious AV dissociation?  Then VT, if not:
3. Obvious fusion beats?  If so, the VT, if not:
4. Leads V1-V6 unidirectional (no RS or SR) and "concordant" (in the same direction)?  Then VT
5. If there are RS complexes (they are not concordant): is there any precordial RS that has a duration from onset of R to nadir of S that is greater than 100 ms?  Then VT.
6. Abnormal LBBB or RBBB pattern (see this link for a figure from the Brugada paper):
----a normal RBBB or LBBB pattern makes SVT very likely: both have a rapid initial deflection, the r-wave in LBBB and the rS in RBBB, followed by a slowly conducting latter part of the QRS.
     a.  If there is LBBB pattern, is the initial r-wave greater than 50 ms?  Or is the onset of the QRS to nadir of the S-wave in V1-V3 greater than 60-70 ms?  If so, this is not true LBBB.  VT.
     b. If there is RBBB pattern, is there a monophasic R-wave?  Or is the first R of the Rsr' larger than the second one?  Then VT.
7. Initial R-wave in aVR (not an r-wave, not preceded by q-wave)?  Then VT
8.  If the initial deflection in aVR is an r-wave or q-wave, is it greater than 40 ms?  If so, then VT


In this case, the physicians were confused by the ECG.  (With some practice, this ECG should not be confusing!)

They placed Lewis leads (see below for instructions).  See this link for graphic instructions on how to use Lewis leads; it is very easy.  Why?  Lewis leads are good for illuminating P-waves.  The physicians wanted to see if there were P-waves, and, if so, whether they were associated or dissociated.   AV dissociation with normal upright P-waves is nearly diagnostic of VT (not 100%), and regular upright P-waves followed consistently by QRS complexes would be nearly diagnostic of sinus tachycardia with aberrancy.  On the other hand, retrograde P-waves would not necessarily differentiate SVT with aberrancy from VT.


  • Place the Right Arm electrode on the patient’s manubrium.
  • Place the Left Arm electrode on the 5th intercostal space, right sternal border.
  • Place the Left Leg electrode on the right lower costal margin.
  • Monitor Lead I.

  • Rhythm strip with Lewis leads:
    There is an axis change that is due to the lead change.  Lead I is the most important lead and it is highlighted below:


    Lead I is the important lead in Lewis leads.  Here is lead I alone:
    The Lewis leads appear to have made the P-waves in lead I more visible.  They are invertedand start after the beginning of the QRS.  They are associated with each QRS.  
    This would rule out sinus as the rhythm, but it still does not differentiate between 1) SVT with aberrancy and retrograde P-waves and 2) VT with retrograde P-waves.  

    They saw these P-waves, but did not understand that they could also be the result of VT.

    So they gave adenosine 18 mg.  It did nothing.  Adenosine is perfectly safe in VT.  However, it will have no effect.

    At this point, they appropriately sedated the patient and electrically cardioverted.

    The post conversion ECG is here:
    Atrial fibrillation with some mild ST depression.  There are inferior Q-waves.


    Clinical Course:

    ECG and Transthoracic Echo confirmed prior inferior infarction.  Angiogram confirmed known severe RCA disease.  There was no new ischemia.

    Thus, this was scar-mediated VT.   An ICD was placed.


    Learning points:

    1. Sometimes it is difficult to differentiate VT from SVT with aberrancy.  In this case, the diagnosis should be clear.  There are multiple variables to look for and many were present here, especially the pretest probability of VT.

    2. Adenosine is safe in VT.  However, you could convert adenosine sensitive RV outflow tract VT and not realize it.  However, these have no structural disease and are safe.

    3.  Lewis leads help to see P-waves.  Associated retrograde P-waves can be present in VT as well as SVT.

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