Friday, January 27, 2017

Grouped Beating, What is it?

This is a case seen by one of my great partners at Hennepin County Medical Center Dept. of Emergency Medicine, Dr. Ashley Strobel, @AStrobelMD.


A patient was found down and was quite ill and in shock.  The POCUS of his heart showed very poor contractility.

Here is his initial ECG:
It is a supraventricular rhythm, with grouped beating.
What else?

Here is a rhythm strip (10 seconds of all leads):
Again, there is grouped beating.
What else do you see?

When she showed me this ECG, I was at first distracted by the rhythm, and did not immediately see the life threatening finding.  It took me a minute before I looked beyond the rhythm.

What is it?

The QRS is slightly wide, greater than 120 ms.  Leads V1 and V2 have domed ST Elevation with T-wave inversion that is very similar to Brugada pattern ("Brugada phenocopy"), similar to my last post.

Brugada pattern should make you think of either hyperkalemia or sodium channel blockade.  Additionally, there is T-wave peaking in many leads.

Dr. Strobel suspected hyperkalemia and treated with Calcium and shifting. She was right.  The K returned at 7.1 mEq/L.

Here is another post with many cases of Brugada phenocopy due to hyperkalemia:

This ECG is NOT Pathognomonic of Brugada Syndrome

Here are other etiologies of Brugada phenocopy:

Analysis of rhythm

Here is Ken Grauer's analysis:

"While there most definitely is a repetitive pattern of group beating (which is a feature of Wenckebach) — this is NOT completely typical of Wenckebach conduction — because the pause containing the dropped beat is NOT less than twice the shortest R-R interval. That’s not to say there can’t be some component of Wenckebach conduction out of the AV node — but rather to recognize that lack of this above “footprint” is indeed a bit atypical …. and under normal circumstances is often a clue that the mechanism may not be Wenckebach despite group beating ...

"That said — T waves in many leads are tall, peaked and pointed with symmetric upstroke and downstroke and narrow base in a number of leads in this somewhat widened QRS rhythm with group beating but no P waves. This strongly suggests hyperkalemia (which may also be responsible for the Brugada-like V1,V2 findings as well).

"It’s been my experience that most of the time it is NOT worth one’s while to contemplate arrhythmia mechanisms when the underlying problem is hyperkalemia — because this electrolyte abnormality “does not follow the rules” — and because whatever arrhythmia abnormality we see will “go away” once you fix this underlying problem of hyperkalemia. Sounds like this is precisely what happened in your case."

Learning Point:

Always be on the lookout for hyperkalemia.  It comes in many form and can mimic many pathologies.

Wednesday, January 25, 2017

A Patient with Cocaine Chest Pain and Prehospital Computer interpretation of ***STEMI***

A 20-something male drank heavily of ethanol and used cocaine, then was involved in a stressful verbal altercation, at which time he developed chest pain.

911 was called and the medics recorded this ECG (unfortunately, leads V4-V6 are missing)
Due to marked ST Elevation, the computer read was ***STEMI***
What do you think?

He arrived in the ED and had this ECG recorded:
Very similar to the prehospital ECG.
The Mortara (Veritas algorithm) Interpretation was:

 ***ACUTE MI***
What do you think?

The ECG shows Brugada morphology in V1 and V2, and the typical normal variant ST elevation in lead V3.

Brugada morphology can be caused by baseline Brugada morphology, including Brugada syndrome, or by hyperkalemia or Sodium channel blockade.

Cocaine not only has effects on dopamine neurotransmission, but is also a sodium channel blocker, as are all "-caine" local anesthetics.  Cocaine is well known to result in Brugada morphology.

See this post and associated case reports:

Cardiac arrest, severe acidosis, and a bizarre ECG

The patient was admitted and ruled out for acute MI by serial troponins.

Below are subsequent ECGs, showing resolution of the Brugada morphology as the cocaine metabolizes.  Cocaine metabolism is rapid.  After approximately 3-4 hours, the cocaine and its effect are gone.  Testing for cocaine is for the inactive metabolite Benzoylecgonine, and this inactive metabolite is present for days.  So a positive screening test for "cocaine" does not imply persistent intoxication.

Here are the serial ECGs:
Time 1 hour:
Cocaine Brugada Effect is still present

Time 4 hours:
Minimal effect is still present

Time 10 hours:
The ECG only shows some slight abnormalities in V1 and V2, with minimal residual saddleback morphology in lead V2.

The vast majority of cocaine chest pain is NOT due to myocardial ischemia or infarction, and most is in young males with normal variant ST Elevation or LVH, so it often looks scary on the ECG.

As there was no personal history of syncope or family history of sudden death, the patient was discharged with cardiology followup.

Sunday, January 22, 2017

A very fast narrow complex tachycardia in an Infant

Case 1

A 4 month old infant with known co-arctation of the aorta and reflux presented with respiratory distress.

Here is the ECG:
A Narrow Complex Tachycardia with a rate of 218.
What is the rhythm?

Answer: there are clear P-waves in nearly every lead.  Notice the intervals are very short, which is typical of infants.  Infants can have very fast sinus tachycardia, easily reaching a rate of 220.  Most SVT in infants is faster than 220.

Throughout this case, the patient was on a cardiac monitor and the rate drifted up as high as 246, still in sinus (not recorded)!

The tachycardia turned out to be a result of disease (pneumonia), not a cause of it.

Case 2

This newborn presented to the ED for some exudate on the umbilical stump. There was no fever.  The infant was very well appearing.  The palpated heart rate at triage was 140.  There were no respiratory symptoms.

The ECG was performed because, on auscultation, the heart rate was far higher than palpated by pulse.
Narrow complex tachycardia at a rate of 300.

This shows how fast SVT can go in an infant and how well tolerated it might be.  This infant was completely without any signs of illness.

There is also electrical alternans, which is a normal finding in PSVT.

If you see this in sinus tachycardia, it indicates tamponade.

It was converted to sinus with adenosine.

Learning points

This shows how well a newborn/young infant tolerates a very fast heart rate, and that sinus tachycardia of 218 is not unusual, and may even go as high as 240!

If in doubt, use Lewis leads to find otherwise hidden P-waves

I don't have a case of use of Lewis leads in pediatrics, but here is a nice one in an adult:

Wide Complex Tachycardia. What is the Diagnosis? Use of the Lewis Lead.

Friday, January 20, 2017

Do patients with LBBB and STEMI, when reperfused, develop T-wave inversion (reperfusion T-waves)?

The case below was contributed by Pendell Meyers, an EM G1 at Mt. Sinai (the case did not come from Mt. Sinai though!)
Pendell is the lead author on our Modified Sgarbossa Criteria Validation Study.

Meyers HP.  Limkakeng AT.  Jaffa EJ.  Patel A. Theiling BJ. Rezaie SR. Stewart T. Zhuang C.  Pera VK.  Smith SW.  Validation of the Modified Sgarbossa Rule for Diagnosis of STEMI in the Presence of Left Bundle Branch Block. American Heart Journal 170(6):1255-1264; December 2015.

Before the case, a few comments:

Pendell and I just published a case report of a patient with left bundle branch block who presented with chest pain that then resolved.  His ED ECG showed his baseline LBBB, with no evidence of MI.  Over the ensuing hours, he developed classic T-wave inversion of Wellens' syndrome, but in the context of LBBB!  Troponins were then positive, and the angiogram revealed a 99% LAD lesion with thrombus.  The case demonstrates that Wellens' syndrome can occur in the context of LBBB.

Here is a link to the case report:

Dynamic T-wave inversions in the setting of left bundle branch block

Though Wellens' syndrome was described in the LAD territory, I have shown cases demonstrating that it occurs in any coronary distribution.  That is to say, that reperfusion results in terminal T-wave inversion even if the involved territory is the inferior or the lateral wall.

Today's case shows how, even in the context of LBBB, reperfusion of the inferior and lateral walls, just as with the anterior wall, can result in typical reperfusion T-waves (which is what Wellens' waves represent).

Wellens' syndrome represents a post (spontaneous) reperfusion state.  This is why the patient is always pain free.  The ST elevation is implied but was never recorded because the patient did not have an ECG during pain.

This is worth a look (7 serial ECGs showing evolution of Wellens' over time):

Classic Evolution of Wellens' T-waves over 26 hours


An 82 year old had the acute onset of chest pain.  Here is his first ECG, time zero:
There is concordant ST elevation in leads II, V5 and V6.  It may not reach a full millimeter, but the QRS is so small that we should make an exception here.
It is proportionally large concordant ST elevation!

The cath lab should have been activated at this point, but apparently it was not.  Instead, another ECG was recorded at time 46 minutes:
Now there is more than 1 mm of concordant ST elevation.
In addition, there is now excessively proportionally discordant (more than 25% of preceding S-wave) in leads III, and aVF.
So there is a definite inferior and lateral MI.  There is no ST depression in lead I, which suggests a circumflex lesion

The cath lab was activated and a circumflex occlusion was opened and stented, with a door to balloon time of 3 hours.

Here is the first ECG recorded after reperfusion:
ST deviation has resolved. 
There is T-wave inversion in III and aVF, typical of "Inferior Wellens'"
There is no T-wave inversion yet in the lateral leads.
There is increased T-wave amplitude in V2 and V3: these represent posterior reperfusion T-waves, or Wellens' syndrome of the posterior wall.

2 Examples of Posterior Reperfusion T-waves

(these are in the context of normal conduction, not LBBB)

Here is our formal study of posterior reperfusion T-waves, written by me and lead author Brian E. Driver (Hennepin) and published in Emergency Medicine Journal:

Posterior reperfusion T-waves: Wellens' syndrome of the posterior wall

Here is a still later ECG after reperfusion:
There is evolution of T-wave inversion (deeper) in the affected leads.
This is analogous "Wellens' waves" of the inferior and lateral leads, in the presence of LBBB!

Peak troponin T was 3.71 ng/mL, which is indicative of a large MI (Troponin T peaks are far lower than troponin I).  Earlier recognition of the concordant ST elevation could have saved more myocardium.

With reperfusion, T-wave inversion even occurs in LBBB:

As an explorative substudy of our validation of the modified Sgarbossa criteria, Pendell and I and others studied T-wave inversion.  We looked at serial ECGs on patients with acute coronary occlusion ACO) who underwent reperfusion and compared to serial ECG on patients without ACO.  Unfortunately, as a result of our multisite study in which ACO came from many institutions and controls from one institution, only 6 of 45 patients with ACO and reperfusion had serial ECGs available, and all 245 patients without ACO had serial ECGs available.

When this pattern was retrospectively defined as being either 1) present in at least two
contiguous anterior or inferior leads in at least two consecutive ECGs prior to reversal or 2) deeper than 3 mm in two contiguous leads (requiring only one ECG), it was found to be predictive of reperfused ACO (either spontaneously prior to catheterization or with mechanical reperfusion) with derived sensitivity and specificity of 5 of 6 [83% (95% CI 36–99%)] and 241 of 245 [98% (95% CI 96–99%)]. 

Meyers HP et al. Evaluation of T-Wave Morphology in Patients With Left Bundle Branch Block and Suspected Acute Coronary Syndrome

Another very illustrative case:
Here is a case of transient LAD occlusion that resulted in transient LBBB.  After reperfusion, Wellens' waves are evident:

Chest pain and LBBB. LBBB resolves and there is V1-V3 T-wave inversion.

Tuesday, January 10, 2017

Wide Complex Tachycardia and Cyanosis

This case was sent by a former HCMC resident:

A 20-something non-English speaking woman with a history of some sort of congenital heart defect collapsed at home and EMS found her with a regular wide complex tachycardia around 200 bpm. They attempted cardioversion with adenosine, unsuccessfully (dose was uncertain, thought to be 12 mg, but this would be an unusual initial dose).

She was cyanotic and minimally responsive on arrival here, and had a healed sternotomy scar.  There were no records immediately available.

Her blood pressure was normal throughout the case.  O2 sats were 70s and 80s on high flow O2, but there was no evidence of pulmonary edema.  They did notice "clubbing" of the fingers.

A relative was able to state in broken English "single ventricle."

Here is the initial 12-lead ECG:
There is a regular, wide complex tachycardia at a rate of 160, with no P-waves. 
There is a monomorphic Right Bundle Branch block pattern with QRS duration of between 140 - 160 ms (is it difficult to ascertain the exact beginning and end of the QRS)
Is it Ventricular Tachycardia (VT) or SVT with aberrancy?
What else can be said about it?
What should be done?

Full interpretation is at the far bottom of the post


If the patient is unstable, just cardiovert with electricity.  Her altered mental status may be due to hypoperfusion (shock), in spite of the normal blood pressure (non-invasive blood pressures are unreliable in sick patients).  Thus she must be considered unstable, so use electricity 

One might call this patient unstable because of the low saturations, but a patient with a known single ventricle is likely to have cyanotic heart disease and to have baseline O2 saturations that are very low, even on high flow O2.  This is especially true if there is no evidence of pulmonary edema on chest X-ray or bedside ultrasound.  Clubbing is further supportive evidence.
Thus, it is very likely that the patient has uncorrectable hypoxemia due to shunt physiology.

If the patient had been stable (conscious), then there would have been a few minutes to think:

First, if one can easily find old ECGs that are in sinus rhythm, then one can compare the QRS morphology at baseline with this one in tachycardia.  If identical, then this is supraventricular (which includes sinus tachycardia).  To diagnose sinus tachycardia, one can use Lewis leads in order to uncover hidden P-waves.  This takes about 30 seconds.  Here are the instructions for recording Lewis leads.  It is done with the monitor, not the 12-lead.

Second, in most young people without structural cardiac disease, SVT is more likely.  However, this patient does have structural heart disease, so VT is not at all unlikely.

Third, assuming it is truly NOT sinus tachycardia, either adenosine at a higher dose or electrical cardioversion works well.  Even if it is sinus tach, neither of these therapies is terribly dangerous, but they will not benefit the patient.

Fourth, is there any evidence from the QRS that this is SVT vs. VT?  There is a "northwest" axis (between -90 and 180, with a large monophasic R-wave in aVR).  This implies origination at the apex (the ventricle, where VT originates) with propagation towards the base of the heart ("base" meaning upper right). On the other hand, the first part of the QRS (initial depolarization) is very rapid, even in that upright R-wave in aVR.  Look at lead V5: that first part is comprised by the onset of the R-wave to nadir of the S-wave, and it is less than 60 ms.  Thus, SVT with aberrancy is not at all unlikely.

Thus, in a stable patient: As it is easiest, I would try a larger dose of adenosine.

Case continued:

"We intubated the patient, then consulted cardiology and decided to do an electrical cardioversion at 200J biphasic.  This was successful."

"I found records which were limited but suggested congenital heart deformity, and that her baseline O2 sats were in the 70-80% range."

Here is the post cardioversion ECG:
What does this post cardioversion ECG tell you about the initial rhythm?

There is clearly sinus rhythm, with exactly the same QRST morphology as the first.
This proves that the original was indeed SVT with aberrancy.

Airway, Breathing, Circulation (ABC)
We are always taught to use this sequence, but we often get it confused.  Sometimes the issue with the airway and breathing is really a circulation problem (shock with altered mental status).  I would cardiovert first, which will usually solve the problem.   Intubate if it does not.  Also, when the patient is obtunded (stuporous), it is both dangerous and unnecessary to sedate before cardioverting. Our research at HCMC shows these critically ill patients do not remember such events.

A Primer on Wide Complex Tachycardia

First, use electricity on unstable patients.

What is instability?  Severe shock, cardiac ischemia, or pulmonary edema.

If stable, you can take a bit of time to think.

Differential Diagnosis of Wide Complex Tachycardia

When assessing for the rhythm in wide complex regular tachycardia, these are the assessments I make, though no method is foolproof:

--Sinus with aberrancy -- Aberrancy can be due to toxins (wide complex from the many drugs which have sodium channel blocking effects and prolong the QRS) or to hyperkalemia.
--SVT with aberrancy.  This can be either 1) AVNRT with abnormal conduction to the ventricles, or 2) antidromic AVRT (AV reciprocating tachycardia) with the impulse going down an accessory pathway and up through the AV node)
--Ventricular Tachycardia (VT)

Assess pretest probability:
--Majority of wide complex tachycardia is VT
--If h/o MI, cardiomyopathy, low Ejection Fraction, VT more likely still
Assess the ECG:
--P-waves in front of QRS? --Sinus
--Irregularly irregular? Atrial fib 
                    (VT is regular, except for polymorphic VT which must have a polymorphic QRS)
--Regular? --then: sinus / atrial tach / flutter / PSVT / VT)
--Rate gradually changes or always the same?
              Gradual: sinus or other automatic rhythm (some atrial tachycardias, junctional tach)
              Unchangingreentrant rhythm such as: flutter vs. PSVT (incl AVRT) vs. VT

Wide, monomorphic QRS, and regular without P-waves (or retrograde P-waves)
1. SVT with aberrancy 
           (including antidromic AVRT using an accessory pathway)
2. VT (though it may have P-waves that are dissociated, or retrograde P-waves)

VT vs. SVT with aberrancy

5 Algorithms to differentiate SVT with aberrancy from VT - in my opinion, only Sasaki's is usable in the ED:

1. Brugada
2. Vereckei 1
3. Vereckei 2 (uses aVR only)
4. Sasaki (see below) (Sasaki K.  Circulation 2009; 120:S671) had 86% sensitivity and 97% specificity among 107 cases of wide complex tachycardia.  It has not been validated; this is important: Brugada's rule fared much better in the initial study than in subsequent validation studies.
5. New algorithm (Jastrzebski et al.): more complex but more accurate (full text link):
The ventricular tachycardia score: a novel approach to electrocardiographic diagnosis of ventricular tachycardia. In this very complex scoring system, derived in 512 proven cases of VT and 276 proven cases of SVT, the specificity for a score greater than or equal to 3 was 98%, but with a sensitivity of only 66%.  This is clearly not something that can be easily done in the ED.


Below I have listed what I consider usable features of the algorithms.

If you're not sure, but you are pretty sure it is not sinus tach
Sedate/Cardiovert (or Adenosine)
Adenosine if you suspect SVT:
---Older, with known absence of structural heart disease
---Young age, unless known heart disease
---QRS duration less than 140 ms
---No obvious signs of VT
       concordance, fusion beats, AV dissociation
---Unequivocal rapid depolarization of the initial part of the QRS (e.g., normal LBBB or RBBB)
--safe in VT
--safe in WPW, if regular rhythm
--Unsafe in WPW with atrial fib (irregular, RR intervals less than 250 ms, polymorphic QRS)
--converts reciprocating tachycardia, whether orthodromic or antidromic
    --these depend on the AV node for re-entrance 
--converts one kind of fascicular VT (RV outflow tract VT) 

1) Look for hidden p-waves before each QRS.  Don't miss sinus rhythm.  Use Lewis Leads.
2) QRS duration: VT usually (but not always) has a QRS duration of greater than 140 ms.  A prominent exception is fascicular VT.  The wider the QRS, the more likely it is to be VT.  
3) Is there RBBB or LBBB morphology and is the initial part of that BBB narrow?  Then it is very likely to be SVT.  
4) Do a quick look for obvious fusion beats and AV dissociation.  If found, then VT.   
5) Do a quick look for concordance (in precordial leads, all QRS's in the same direction -- this is not the same as concordance of ST segments in LBBB).  Concordance means there is no RS. 

A concordant QRS in the precordial leads comes in two varieties: 
1) Upright QRS in V1 (RBBB type). 
         This is almost always VT or AVRT (antidromic, lateral accessory pathway) 
2) Negative QRS in V1 (LBBB type). 
         This is VT at least 90% of the time, but not 100%.  

6) Finally, because it is easy to apply, I like Sasaki's rule 

Sasaki's rule

Step 1: Initial R in aVR?  

This means is there a large single (upright) R-wave (not a small r-wave) in aVR.  This indicates that the beats originate and propagate from the apex to the base, so that it must be coming from the ventricle, hence VT.
--If yes, then rhythm is VT. If no, step 2.  

Not here.  See ECG with line below.  Although at first glance there appears to be a monophasic initial R in aVR, the line shows that there is actually a 30 ms delay.
Step 2: In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100 msec (0.10 sec)?  See image below.  
--If yes, then rhythm is VT. If no, step 3.  Not here.

Step 3: Initial r or q ≥ 40 ms in any lead?

If there is, this means that, for the first 40 or more milliseconds, conduction is slow as would occur through myocardium (left ventricle, VT), not through conducting fibers, as would occur in SVT)
--If yes, then it is VT.   If no, then it is SVT.  "No" here, therefore it is SVT

Although there appears to be an initial R in aVR, there is actually about 30 ms of hesitation before the R-wave initiates.  I have drawn a line at the beginning of the QRS.
Thus, there is also only a 30 ms r- or q- wave at the beginning of the QRS.

This Sasaki rule was quite accurate in derivation, but never validated, at least not to my knowledge.

My interpretation is that the initial deflections are of very short duration and therefore unlikely to be VT.  But I only saw it after knowing the outcome (too biased!)

So I showed the ECG blindly to Ken Grauer (one of the masters, here is his site):

"Bizarre morphology, which of course makes one consider VT — but:
1) check leads (all positive in aVR); and
2) Could very well be supraventricular with some severe form of underlying heart disease (cardiomyopathy; congenital heart disease if young)"

"So I'd really want to know the clinical situation....Several leads looked like they might be supraventricular (ie, very slender narrow initial r-wave in predominantly negative lead I and aVL — rather than being all negative) — slender initial r-wave in V4 with very steep downslope — and the Q in lead III looked like it may be pathologic rather than an all neg axis Q as VT would have."

Friday, January 6, 2017

LVH with secondary ST depression??

This was sent by Michael Macias (Twitter: @EMedCurious), a 4th year EM resident at Northwestern in Chicago.


An elderly man with end stage renal disease and coronary disease presented with chest pain.

Here is his ECG:
See the computer interpretation above.
What do you think?

Dr. Macias' interpretation is here:

Significant elevation in aVR with diffuse ST depression. Hemoglobin was 7.0 g/dL. I thought this was likely triple vessel disease with subendocardial ischemia, but we activated the cath lab given impressive ECG and his history.

Smith interpretation:

The computer reads LVH with repolarization abnormality. There is high voltage, and you expect some discordant ST depression, but this ST depression, although always discordant, is way out of proportion to the QRS voltage. Moreover, the ST depression is NOT maximal in V5 and V6, as it should be with LVH repolarization abnormalities.

So this is ischemic ST depression.

Whether it is diffuse subendocardial ischemia or posterior STEMI is more problematic.

As the STE is most profound in V3 and V4, NOT V5 and V6, posterior STEMI is more likely. However, the STE in aVR (which is reciprocal STE, reciprocal to the ST depression vector towards the apex), is more typically seen in diffuse subendocardial ischemia. ST depression due to subendocardial ischemia is most commonly caused by demand ischemia. One cause of demand ischemia is severe anemia, but a Hgb of 7.0 does not qualify, especially without any tachycardia.

So this must be assumed to be due to ACS.

In fact, the ST depression in V5 and V6 is not all due to ischemia: it is a combination of LVH repolarization and ischemia; the ischemia component is only one portion and so there is less ischemic STD here than one might at first think. This means that the ischemic ST depression is significantly more profound in V3 and V4.

So this is most likely a posterior STEMI pattern, superimposed on LVH. Activating the cath lab is indicated!


100% acute circumflex occlusion, opened.

Learning Points:

1. Again, the computer algorithm cannot be trusted.
2. Posterior STEMI has more ST Depression in V3 and V4. Subendocardial ischemia is maximal in V5 and V6.
3. Know the expected amount of repolarization abnormality in the presence of LVH.  I don't have a calculated ratio.   Below are two examples of LVH with repolarization abnormalities.  These are both baseline ECGs without any active ischemia.  Notice the proportional amount of ST depression, and that it is maximal in V5 and V6.

Recommended Resources