Wellens' syndrome, no culprit, what happened?

A 55 yo male with h/o smoking complained of 4 days of intermittent chest pain lasting up to a few hours each day.  He presented to the ED pain free and had the following ECG at 1332:

There is a suggestion of terminal T-wave inversion in V2, highly suggestive for early Wellens' syndrome.  There is T-wave inversion in I and aVL diagnostic of ACS.

The first troponin returned with "minor increase" on a qualitative troponin I, so another quantitative troponin was sent and it was elevated at 0.325 ng/ml.  The patient remained pain free.  

Another ECG was recorded at 1555:

The T-wave inversion is more pronounced in V2, an evolution diagnostic of Wellens' syndrome.  TWI in aVL again is clearly ischemic.

See here for classic evolution of Wellens' waves.

The patient was admitted to the hospital late on a Friday, and put on antithrombotics and antiplatelet agents.  His troponin I peaked at 1.05 ng/ml that day.

On day 2, he had an echo which was suggestive of anterior wall motion abnormality.  He had no ECGs that day.

Sunday AM at 0800, he had another episode of severe chest pain, waxing and waning.  He had the following ECG recorded, and it is unclear whether he was having the pain at the time of the ECG.

Now there are deeper and more symmetric Wellens' waves.  Is this just evolution of the waves seen 2 days ago? 
Or did something new happen?

Troponin rose again that day (day 3).  So the patient was taken to the cath lab.  He had no culprit, but a 50-60% narrowing of the proximal LAD.  

Fractional Flow Reserve was performed across the lesion and it was 0.88 to 0.90 (negative, showing no blockage of flow).  

Intravascular ultrasound revealed that the lesion had a minimal luminal diameter of 2.3 mm but a large plaque burden.  Nevertheless, it did not appear to the angiographer to be the cause of the symptoms.

The patient went back to the wards.  He had an identical episode of pain the next morning (day 4).  It turns out that the patient was on an ST segment monitor and it had not been checked on day 3 after the previous episode of pain.  

So the interventionalist went and had it printed out.  Here it is, a 12-lead monitor strip:

Obvious anterolateral STEMI.

This illustrates what Wellens' syndrome is: it is always recorded when the patient is pain free, after an episode of chest pain.  The artery is always open, or the territory is supplied by good collaterals, but there is an LAD lesion that is at high risk of re-occlusion (as in this case).  

Wellens' is the aftermath of occlusion that has reperfused.  The inverted T-waves are "reperfusion T-waves."

In this case there was no clear LAD lesion.  It is uncertain whether this was spasm or a case of plaque rupture with thrombosis and complete lysis.  

However, aftert they went back and stented the LAD, all symptoms resolved, suggesting ruptured plaqe.

Four anterior STEMIs: acute and reperfused vs. won't reperfuse, subacute and reperfused vs. not reperfused

These 4 recent cases illustrate acute and subacute MI with reperfusion and absence of reperfusion (or failed reperfusion).  QS-waves and depth of T-wave inversion are very helpful in determining the duration of injury (the "acuteness" of the ECG), the viability of the myocardium, and patency of the infarct-related artery.  Persistence of ST elevation helps to determine state of the myocardium after reperfusion.

Definition: total loss of R-wave means there is a QS-wave (a single deep deflection).  Preservation of R-wave may mean and initial Q-wave followed by an R-wave (this is called a QR-wave.  Upper case vs. lower case Q (q) or R (r) is used to designate smaller or larger waves. 

1.  This 57 yo diabetic male presented with generalized fatigue, myalgias, and arthralgias, mild subjective fever and chills, and nausea.  He also stated his arms and head feel "heavy" and he had a headache, dry heaves, and dizziness, and some "indigestion" in his chest "like acid". His pulse was 114.  Exam was otherwise normal.

There are QS-waves in precordial leads with some preserved R-wave in V2 (Qr-wave).  There is persistent ST elevation, but no T-wave inversion. T-waves are not tall (tall, hyperacute T-waves are markers of ischemic but viable myocardium).  The fact that they are not present here suggests that the MI is complete.  That they are not inverted tells us that the artery is still closed.  But the presence of a bit of R-wave gives some hope that there might be some viable myocardium left. [STE in lateral leads, with inferior reciprocal ST depression, tells us it is a proximal LAD ]

Cath showed a 100% proximal LAD and other disease.  It was opened.  Initial troponin I was > 50 ng/ml; followups are not available.  Echo on the day after admission showed EF of 30-35% and antero-apical wall akinesis with an LV thrombus [these frequently form in complete or near complete (no early reperfusion) anterior STEMI because of akinesis/stasis]

2 more days later, this was recorded:

ST elevation is still present.  Persistent ST elevation 3 days after a nearly transmural MI portends possible LV aneurysm.

Echo at this time showed some improvement in EF to 40%, but persistent akinesis and thrombus.



2. This 42 yo diabetic male presented with cough and foot pain.  He had been awakened by cough at 3 AM 2 days earlier.  In spite of aggressive questioning, he denied chest pain, but he did tell one triage nurse that he had had some chest burning, and so he underwent an ECG:

There are deep Q-waves and QS-waves in precordial leads V2-V3, with a bit of R-wave left in V4.  ST segments are greatly elevated and T-waves are deeply inverted.  There is also T inversion in I and aVL (Proximal LAD) and a Q-wave in III.

Symptoms have been prolonged but intermittent, and there has been little chest pain, if any.  So all duration of injury must be estimated from the ECG.  Even when there is chest pain, the ECG is a more reliable indicator of injury duration than are symptoms.  Here there are some QS-waves, telling us that there has probably been a significant amount of completed infarction, but there is also persistent R-wave in lead V4 suggesting some viable myocardium.  The deep T-wave inversion also tells us that there is a significant amount of viable myocardium left and that the artery is most likely open.   It is very unlikely to be LV aneurysm morphology when the ST elevation is so high and the T-Wave inversion is so deep.

Cath showed a 95% LAD with flow.  Echo showed anterior wall motion abnormality.  Peak troponin I was 52 ng/ml (significant myocardial loss, but not the whole anterior wall)



3. This 67 yo male with h/o HTN and GERD only presented with 60 minutes of diaphoresis and GERD symptoms.  He had a prehospital ECG:

Obvious anterolateral acute STEMI

The patient received aspirin only and his pain immediately resolved:

Clear resolution of all ST elevation, with only some residual T-wave inversion in I and aVL.  The LAD has reperfused early.

An open 90% LAD was stented.  Peak troponin I was 0.3, so almost no myocardium was lost.

Here is the ECG the next AM:

There was so little infarction that there are lateral, but no anterior reperfusion T-waves (normally, there would be Wellens' type waves after LAD reperfusion).  The T-waves are smaller than they were immediately after reperfusion, illustrating how hyperacute T-waves are present BOTH shortly after occlusion (when ST segments are on the way up) and shortly after reperfusion (when ST segments are on the way down).

4. A 51 year old male with h/o stent presented with 30 minutes of chest pain:

Obvious anterolateral very acute STEMI with hyperacute T-waves

He went for immediate PCI, with successful reperfusion of a 100% occluded proximal LAD, and a door to balloon time of 35 minutes.  This was recorded 2.5 hours later, after PCI:

There is a significant QS-wave in V2, with some persistent ST elevation, suggesting incomplete small vessel reperfusion and significant infarction.

The patient continued to have ischemia after PCI, and in fact had an episode of polymorphic VT shortly after while in the ICU.   This was recorded the next AM:

There are QS-waves in V2 and V3, with rather shallow T-wave inversion, both indicative of  significant myocardial loss.

Peak troponin I was 84 ng/ml and there was a large anterior wall motion abnormality, in spite of very fast treatment and a symptom onset to balloon time of 65 minutes.

Sometimes, even with very fast reperfusion, there is significant myocardial loss because of downstream obstruction of small vessels.  This can be seen on angiogram as an absence of "myocardial blush" and is measured the the TIMI myocardial perfusion grade (TMP grades 0-3, just like TIMI flow grades 0-3).

As it turns out, the best measure of reperfusion is TMP (not TIMI flow) and the best noninvasive measure of TMP is the ECG, as measured by resolution of ST elevation on the ECG ("ST resolution"), with 70% resolution associated with high TMP grade.  The ECG, as it turns out, is the best predictor, better the TMP grade because TMP measures microvascular patency, and the ECG measures cellular viability (see this full text article and this abstract).


I will specifically discuss acuteness on the ECG in a future post.


Here is some older but very interesting literature on TIMI myocardial perfusion grade and ST resolution:

1.  Claeys MJ, Bosmans J, Veenstra L, et al. Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction: importance of microvascular reperfusion injury on clinical outcome. Circulation 1999;99(15):1972-7.

2. Gibson CM, Cannon CP, Murphy SA, et al. Relationship of TIMI myocardial perfusion grade to mortality after administration of thrombolytic drugs. Circulation 2000;101(2):125-30.

3. Shah A, Wagner GS, O'Connor CM, et al. Prognostic implications of TIMI flow grade in the infarct related artery compared with continuous 12-lead ST-segment resolution analysis.  Reexamining the "gold standard" for myocardial reperfusion treatment. J Am Coll Cardiol 2000;35(3):666-72.

4. van't Hof AW, Liem A, de Boer MJ, et al. Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction.  Zwolle Myocardial Infarction Study Group. Lancet 1997;350(9078):615-9.

5. van't Hof AW, Liem A, Suryapranata H, et al. Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade.  Zwolle Myocardial Infarction Study Group. Circulation 1998;97(23):2303-6.

Wide complex tachycardia in a 36 year old

A 36 year old male presented with palpitations.  He has had these many times for many years, episodes lasting 30-60 minutes, without syncope or pre-syncope.  He has a bit of chest pressure, but is otherwise comfortable.  He has no other medical history and is on no significant medications.

There is a wide complex tachycardia at a rate of 179 bpm.  The QRS duration is 139 ms.  The frontal axis is 180 degrees.


What action do you want to take?  Answer below.


But first:
If this is ventricular tachycardia (VT), is it likely to be a dangerous type?  No.  With no history of any structural heart disease, no syncope or pre-syncope in spite of many prolonged episodes, and no other medical problems, this is unlikely to be a life-threatening dysrhythmia.  This does not mean that it cannot be VT.  Some VT is not life threatening, and most of these are called "idiopathic."   The most well known of these are: 1) posterior fascicular, verapamil sensitive, "idiopathic" VT or 2) right ventricular outflow tract (RVOT, adenosine sensitive) idiopathic VT.  Both of these entities occur in a structurally mostly normal heart with fairly normal ejection fraction.  In terms of danger, they act more like SVT.  Two other more rare types are: idiopathic propranolol-sensitive (automatic) VT (IPVT), catecholaminergic polymorphic VT (CPVT).  See this excellent full text online review.

There are ECG instructors who warn against using adenosine for wide complex tachycardia.  They warn that, if it converts, it might be the adenosine-sensitive VT, and you might discharge to home a patient with a diagnosis of SVT when in reality it is VT.  I do not subscribe to this for three reasons: first, these are comparatively rare; second, these are not dangerous and it is ok to send the patient home; third, because it is wide complex, you will have the patient follow up with a cardiologist. 


Why would any physician give adenosine rather than just sedate and cardiovert?  While most recently trained emergency physicians routinely give propofol for sedation, there are many other physicians who are not so comfortable with it.  For them, cardioversion may not be so safe.

FYI: I posted this case of SVT with aberrancy last month and many readers thought it was RV outflow tract VT.  The reason that RVOT VT was very unlikely is that RVOT starts in the outflow tract and propagates inferiorly; therefore, inferior leads are all positive.  In this case, there was an initial Q-wave in inferior leads. I'm sorry I do not have a case (yet) of RVOT VT.

--Best answer: sedate and cardiovert
--Acceptable answer: give adenosine (but it would not work)
--You are brilliant and very sure of yourself: verapamil
               --If you have the diagnosis right (idiopathic VT), this will work.
               --If it is non-idiopathic VT, verapamil is dangerous.


Let's take a close look at this one using Sasaki's system to diagnose wide complex tachycardia:

Step 1: Initial R in aVR?
--This means is there a large single (upright) R-wave (not a small r-wave) in aVR, indicating 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.
 

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

However, this is one of the exceptions.  This is VT that looks like SVT.  Why?  Because this is VT that originates in conducting fibers of the ventricle; therefore, the initial impulse is conducted quickly through conducting fibers, just as in SVT.  So the initial part of the QRS is narrow, and the entire QRS is less than 140 ms (normal VT is usually greater than 140 ms).  Andrade FR et al. [J Cardiovasc Electrophysiol January 1996; 7(1):2-8] found in all their 11 cases of fascicular VT that the QRS duration was 105 to 140 ms, and the RS interval, which in normal VT is more than 100ms, was always less than 80 ms.

In this case, there is a fast depolarization at the initial part of the QRS, just as you would see in SVT with aberrancy.  However, there is also an RBBB morphology and a rapid narrow depolarization towards leads II and aVL, and a subsequent wide depolarization towards inferior lead III, with aVF relatively isoelectric.  The axis is directly to the right.  This is typical of an idiopathic fascicular VT.  The most common form of fascicular VT originates in the left apical inferior septum, corresponding to the posterior fascicle, and therefore has an RBBB morphology with a leftward axis, as in RBBB + left anterior fascicular block.  Less commonly, it originates in the anterior fascicle and has a rightward axis.  So this would appear to be due to the less common variety.  Fascicular VT is apparently due to "false tendons" which are conducting and which can be seen on transesophageal echo.  See this excellent full text article (Thakur RK et al.  Anatomic substrate for idiopathic left ventricular tachycardia. Circulation 1996;93:497-501.)


Further historical information: this patient had been to EDs many times, and received adenosine several times without success.  He had been electrically cardioverted successfully several times.  On this occasion, he was cardioverted, with this subsequent ECG:

Notice T-wave inversions in II, III, aVF and V3-V6.  It is typical for the baseline ECG of patients with idiopathic VT to have some shallow abnormal T-wave inversions like this in inferior and lateral leads.

The patient was diagnosed with verapamil sensitive idiopathic fascicular VT.   He was put on verapamil SR 240 mg per day, and this only partly controlled his symptoms.

Therefore, he underwent an EP study.  This did not show the typical abnormalities one finds in posterior fascicular type (near the septum), but rather possible "false tendons" on the lateral wall.  These were ablated and the patient has had relief from the frequency and severity of palpitations, but not complete.

Here is his baseline ECG after ablation:

Normal ECG, T-wave inversions are gone.

What is the diagnosis? A nearly pathognomonic ECG.

A 50 year old woman complained of shortness of breath, but on closer questioning she seems to be weak.  An ECG was recorded immediately.  What is the diagnosis?

Answer below.

Notice large U-waves (arrows).  One is tempted to think that the long hump after the QRS (between the two vertical lines) is the T-wave.  Whenever you see this, you should think about both long QT and U-wave.  But if you look closely, you see there are 2 bumps, so the second one must be a U-wave.

The diagnosis of hypokalemia was made 1 hour prior to return of the lab value. K was 1.8.




This patient presented with hypotension, shock, acidosis, hgb of 8.  He stated he had been vomiting all day.

There is scooped ST depression in V4-V6, possibly due to ischemia, but mostly it is highly suspicious for hypokalemia.  The K was 2.6.

ST elevation (Saddleback), is it STEMI?

This 56 year old male presented with atypical chest pain and left arm numbness off and on for one week, worse on the day of presentation:



There is saddleback type ST elevation in leads V2 and V3, and diffuse T-wave inversion.  But there is also very high voltage  especially in V4 (35mm, sorry it is cut off) and V5 (27 mm).  The QTc was 426 ms.



Answer is below:

This ECG was shown to me by a colleague, and I immediately said: "You thought it was a STEMI, but it is not."  He had, in fact, activated the cath lab, and the coronaries were clean and the patient ruled out.

Saddleback ST elevation, in my experience, is rarely due to STEMI.  I will not say it is never due to STEMI because I know of no research on this topic.  It is usually a form of early repolarization that also usually meets criteria for type II or III Brugada pattern (see this post).  I will post more on this topic later.  In this case, it may be related to the LVH or be simultaneous early repolarization and LVH.  The diffuse (both inferior and precordial) T-wave inversion is somewhat atypical of LVH. 

Echocardiography confirmed marked concentric LVH. 

In this case, you might want to try applying the early repol/anterior STEMI equation rule posted on the sidebar.  However, it is not validated in the presence of LVH).  You would get a value of 16.11, which is very low and argues strongly against LAD occlusion.

Inferior ST Elevation: what is the Diagnosis?

You can read this post here, or watch a video presentation of it:

https://hqmeded.com/inferior-st-elevation-2/

I was handed this ECG, without any clinical information, while on my way to see another patient:

There is sinus rhythm.  There is ST elevation diffusely: 2 mm in V2, 3.5 mm in V3, 2.5 mm in V4, 1.5 mm in V5, and 1 mm in V6, 1.5 mm in lead II, 1 mm in leads III and aVF.  R-waves are well formed, and in fact there is high voltage.  T-wave to ST ratio is greater than 4 in lead V6, making pericarditis unlikely (also there were no symptoms of pericarditis).  The computerized QTc is 386 ms.   There are marked J-waves in II and V4-V6, with slurring of the R downstroke in III and aVF.  There is no reciprocal ST depression anywhere except aVR; in particular, there is none in aVL.  Not only is there no ST depression in aVL, there is actually a bit of STE in lead I.   These are all classic signs of early repolarization.

I immediately recognized this as early repolarization of inferior, lateral, and anterior leads, and went on my way. Some time later, I found out that the residents had initiated an aggressive workup because they were worried about the ECG.

It turns out that this was a 27 yo African American male who presented with pressure-like (non-pleuritic) chest pain and dyspnea.  He appeared very anxious and was hyperventilating and he had just had an episode of what sounds like carpal spasm.  Clinically, he was having a panic attack.  His ECG did not worry me.

Is there LVH on the ECG?  By voltage there does seem to be, but this was a young thin male and high voltage without LVH is common in this situation.


Most early repolarization is in precordial leads, where it is so common that it is considered normal to have baseline ST elevation on the ECG.  I have put up many posts on this topic, and on differentiating ER from LAD occlusion. But there is also early repolarization in inferior or lateral leads, and when present, it is virtually always present in anterior leads as well.


Here is a case of a 45 year old with chest pain:

There is ST elevation in inferior leads only, with no reciprocal ST depression in aVL.  There is a slight T-wave inversion in aVL.

Inferior MI was diagnosed by the emergency physician and the patient needed to be flown by helicopter to the cath lab.  The arteries were clean.  There was no MI.  This was the patient's baseline ECG.   It was a false positive.

How would you be able to know this from the ECG alone?  If there are no changes in aVL, it is highly unlikely to be inferior STEMI.  If there is simultaneous lateral MI, it is possible that aVL may be silent, but in this case V5 and V6 have very minimal ST elevation.  Would you be certain that it is not STEMI?  No, but you should suspect that it is a false positive.  If you have immediate echocardiography available, you could prove that it is early repolarization by showing good contraction of the inferior wall.  Serial ECGs may be useful.  Or perhaps you need to just activate the cath lab and risk a false positive.

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation.  Elevations in inferior leads were less than 0.5mm in 18 of 20 cases.  Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.

Is there danger to early repolarization itself?

Haïssaguerre et al. performed a case control study of patients with idiopathic ventricular fibrillation, and found that many more of these patients than of controls had baseline inferior or lateral early repolarization.  Tikkanen et al. performed a longitudinal community study, following people for a mean of 30 years.  They found early repol pattern in inferior and/or lateral leads in 3.5% and 2.5% a , respectively, and in both locations in only 0.1%.  These patients had a small but significant increased long-term risk of death from cardiac causes (Relative Risk = 1.28 for 1mm, 2.98 for 2 mm of inferior STE). 

No one is certain what to do with this information, and it certainly does not impact emergency medicine, in which the problem remains: is it STEMI or not? 


1.  Haissaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med 2008;358(19):2016-23.
2.  Tikkanen JT, Anttonen O, Junttila MJ, et al. Long-term outcome associated with early repolarization on electrocardiography. N Engl J Med 2009;361(26):2529-37.
3.  Kambara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38(2):157-61.

Fusion Beat During Supraventricular Tachycardia: No criterion is absolutely accurate in differentiating wide complex tachycardia

Yesterday, I posted this case of wide complex tachycardia, and some steps to help in differentiating VT from SVT with aberrancy.

One step was this:  
"Do a quick look for obvious fusion beats and AV dissociation.  If found, then VT."  It is generally thought that fusion beats are diagnostic of VT.

This prompted our excellent electrophysiologist, Dr. Rehan Karim, to make the point that no criterion or algorithm can make a certain diagnosis of wide complex tachycardia.  And so he provided me with the interesting tracing below (sorry, no 12-lead because this just happened to occur in the EP lab while they were recording):

There is a wide complex tachycardia; rate was 171.   It was proven at EP study to be SVT.  You can see the RBBB morphology, with rSR' in V1 (green arrow) and a wide S-wave in lateral leads (see lead I, red arrow).   There is a fusion beat (black arrow) which was proven in the EP lab to be due to a PVC occurring in the midst of the SVT!!

Learning point: whatever system or rule you are applying, it is not perfect.  Dr. Karim also wanted to make the point that Brugada's algorithm had very good sensitivity and specificity in the derivation group, but attempts to validate it were not nearly as successful.  This may be just as true for Sasaki's rule. 

Nevertheless, while appreciating the limitations of all algorithms, I like Sasaki's rule because it depends on many of same principles as the other algorithms (principles which, though fallible, are pretty reliable), but is quite a bit simpler to apply.

Wide Complex Tachycardia: Ventricular Tachycardia or Supraventricular Tachycardia with Aberrancy?

Before we start, here is another popular post on wide complex tachycardia.

What is the ECG rhythm diagnosis?

Wide complex regular tachycardia at a rate of 209, so it is not atrial fibrillation. 

First, in regular wide complex tachycardia: when in doubt, just use electricity, even in stable patients!  Electricity is safer than medications and will work no matter the diagnosis.   A small dose of propofol is adequate for the patient to be amnestic to the cardioversion.

But even if you can manage it, it may be useful to determine the diagnosis:

Which is it?
1) VT 

2) SVT with aberrancy (usually AV nodal reentry tachycardia with aberrancy)

3) AV reciprocating tachycardia [antidromic, up through AV node and down through bypass tract, (AVRT)]4) What can you do if you don't know? (Does it matter?)

4) I should briefly mention idiopathic VT, which occurs in structurally normal (or nearly normal) hearts, and is therefore not as dangerous as standard VT; this includes adenosine-sensitive VT (RV outflow tract, with LBBB morphology, monomorphic R-wave in inferior leads) and verapamil-sensitive VT (posterior fascicle, RBBB morphology).  I will discuss this in a future post.



Here is the clinical data: 
26 yo male with chest pain and SOB and no history of structural heart disease.  He was not hypotensive or in shock.

A young person with no cardiac history is likely to have SVT, not VT, but let's consider the ECG alone:

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

1) Look for hidden p-waves before each QRS.  Don't miss sinus rhythm! Not here.

2) If there is a transition from narrow to wide, is the rate the same?  Then it must be SVT.  Not here.
3) QRS duration: VT usually (but not always) has a QRS duration of at least 140 ms.  A prominent exception is fascicular VT.  The longer the QRS, the more likely it is to be VT.  Here it is 155 ms, so it is plenty long for VT.

4) Is there RBBB or LBBB morphology and is the initial part of that BBB narrow?  Then it is very likely to be SVT.  This one has LBBB morphology with a narrow initial R-wave.

5) Do a quick look for obvious fusion beats and AV dissociation.  If found, then VT.   None here.

6) Do a quick look for concordance (all QRS's in the same direction in precordial leads, not the same as concordance when evaluating ST segments in LBBB).  Concordance means there is no RS.  No concordance here: this is easy to see comparing V4 to V6.

7) Finally, because it is easy to apply, I like a new rule better than Brugada's or Vereckei #1 or Vereckei #2 (aVR).  It is Sasaki's rule (Sasaki K.  Circulation 2009; 120:S671), and it had 86% sensitivity and 97% specificity among 107 cases of wide complex tachycardia.  It has not been validated; this is important: remember that Brugada's rule was much better in the initial study than in subsequent validation studies.
 

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.
 

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

Treat without a diagnosing
If you don't know what to do, you can always use electricity, but you can also give adenosine.  As long as the rhythm is regular, not irregularly irregular (atrial fibrillation), adenosine is safe.   It will usually (safely) convert SVT with aberrancy and AVRT (antidromic reciprocating tachycardia) without harming a patient in VT, and may convert a patient with fascicular VT.

Obviously, synchronized cardioversion should be undertaken if the patient is unstable.

If it is irregular with a wide QRS, it could be WPW, in which case an AV nodal blocker could be life threatening (see this post).

Diagnosis: SVT with aberrancy; it resolved with adenosine.

Added Oct 22, 2011: many readers thought this was RV outflow tract VT.  The reason that RVOT VT is very unlikely is that RVOT starts in the outflow tract and propagates inferiorly; therefore, inferior leads are all positive.  In this case, there is an initial Q-wave in inferior leads.

Here is the post-conversion ECG:

There is slight slurring at the beginning of each QRS, suggestive of delta waves, and the QRS is thus 109 ms (borderline wide).  The PR interval is 138 ms, so WPW is very unlikely.  There is also some ST depression which appears to be secondary to this slightly abnormal QRS, and lends some further credibility to some sort of pre-excitation.

There is no further follow-up at this point.