Differential diagnosis of wide complex tachycardias – Part VI

Let’s take a look at a couple of rhythms you never want to see on the monitor.

First, from ABC of clinical electrocardiography – Broad complex tachycardia Part II, BMJ 2002; 324:776-779:

This is an irregular and polymorphic wide complex tachycardia that appears to show a streamer effect, or “turning of the points.”

Is it Torsades de Pointes?

The answer is, it’s impossible to tell from this rhythm strip!


Because the key distinction between polymorphic VT and Torsades de Pointes (which is a form of polymorphic VT) is that Torsades de Pointes will have a prolonged QT interval in the underlying rhythm!

This rhythm strip doesn’t show the underlying rhythm, so it’s impossible to diagnose as Torsades de Pointes, unless you can derive something useful from the history that would make you reach for the magnesium sulfate instead of the amiodarone (or defibrillator).

Since a normal QT interval varies with heart rate, what we’re really talking about is a prolonged QTc interval (the small ‘c’ stands for ‘corrected’ and normalizes the QT interval for the heart rate).

Most of the books I’ve read suggest that a QTc > 460 ms is prolonged and > 500 ms is clinically significant.

Dr. Wes has an interesting case of Torsades de Pointes here.

There are some very interesting YouTube videos that show Torsades de Pointes here and here.

Here’s another from ABC of clinical electrocardiography – Junctional tachycardias, BMJ 2002; 324:662-665:

This is an irregular and slightly polymorphic wide complex tachycardia. It’s also very fast! Anytime a tachycardia approaches 250 beats/min., you should be very suspicious of an accessory pathway (or Wolff-Parkinson-White Syndrome).

What else makes this rhythm different from the first? All of the “points” of the QRS complexes are pointing the same direction (in this case down). Familiarize yourself with this rhythm! These patients are rare, but they’re out there!

If you have atrial fibrillation on the monitor, and the shortest R-R interval is 6 small blocks or less, then you should treat it like WPW, and stay away from antiarrhythmics!

Atrial fibrillation in the presence of WPW is a very dangerous rhythm, and one of those occasions where you can kill your patient by selecting the wrong medication. The only safe drug for AF/WPW may be procainamide.

Consider this interesting transcript from Amal Mattu M.D.’s December 2008 podcast at EMedHome.com (thanks for the tip, Maciek!):

Another concern that you need to be aware of is, if you have a patient who has AF with WPW, stay away from amiodarone. Even now, AHA continues to list amiodarone as a viable option, but it’s not a viable option. In fact, the only published reports on using amiodarone in rapid AF and WPW have indicated that amiodarone is associated with adverse outcomes. There’s a handful of case reports of patients that had rapid AF and WPW. They got amiodarone and they decompensated. There are, to my knowledge – and I’ve looked through the literature in detail multiple times – and I have yet to find even a single case report or a single case series or a published study saying, “I had a patient with rapid AF and WPW, I gave him amiodarone, and they did well.” Not a single publication that I can find. The only publications on that particular scenario that have ever been published in the literature are “patient did worse” so my recommendation and a handful of other peoples’ recommendations also; “Stay away from amiodarone if you’re taking care of a patient with rapid AF and WPW.”

Remember the first rule of medicine!

If your patient is hemodynamically stable, then transport the patient to the emergency department for cardioversion. It’s probably the safest option.

You can see an example of what I’m talking about here and here.

Do you noticed any similarities between these two case studies? Look carefully!

See also:

Differential diagnosis of wide complex tachycardias – Part I

Differential diagnosis of wide complex tachycardias – Part II

Differential diagnosis of wide complex tachycardias – Part III

Differential diagnosis of wide complex tachycardias – Part IV

Differential diagnosis of wide complex tachycardias – Part V

Differential diagnosis of wide complex tachycardias – Part VI


  • PQRST says:

    So, if Polymorhphic VT and Torsade is only differentiated with exact measure of QTc (which is impossible in such tachycardias), then neither of these can really be diagnosed from a surface ECG?

  • Tom B says:

    Both are polymorphic VT.Torades is a subtype of polymorphic VT. If it’s sustained, it should probably be defibrillated. You’ll note that I said defibrillated and not cardioverted. The computer will have a very difficult time tracking R waves with a polymorphic VT.Most of the time, Torsades will be intermittent, so you’ll have an opportunity to see the underlying rhythm, and consider whether or not a prolonged QTc is present.So, according to the AHA ECC 2005 guidelines for stable irregular wide complex tachycardias, you should consider expert consultation (remember that AF/WPW is a possibility) and give magnesium sulfate for polymorphic VT if the underlying QTc is prolonged, and amiodarone if it is not.You should also attempt to identify the underlying cause of the prolonged QT. For example, hypokalemia, poisoning, prescription drugs, etc.

  • PQRST says:

    Ah, I see. The preceding/underlying QTc, of course. Hm. I just got myself a Torsade case that I thought I’d post to the blog. Now I gotta study it closer.. Thanks for thorough and excellent information as always..!

  • Alison says:

    I’m confused as to why the patients who presented with wide-complex tachycardias were treated with adenosine as a first-line medication (especially the irregular ones)…In our system, a patient presenting with stable, regular WCT would be treated with amiodarone as the first medication, while the patient with stable, irregular WCT would usually be assumed to be in AF with some aberrant conduction, and the decision to proceed with cardizem/amiodarone/procainamide would be made in concert with medical control.Perhaps it has to do with the way standing orders are written in NJ, but we automatically bypass adenosine for WCTs as it is only permitted for treatment of narrow-compex tachycardias unless medical control is contacted. It seems pretty darn risky to give WCTs adenosine in the regular treatment pathyway.

  • Tom B says:

    Alison – Sometimes, AF/WPW appears to be narrow. In the “old” guidelines, stable wide complex tachycardia of unknown origin received L-A-P-B (lidocaine, adenosine, procainamide, bretylium).Contacting medical control isn’t a bad idea, but even they should “consider expert consultation” per the ECC 2005 guidelines.I wouldn’t give a patient with a suspected accessory pathway adenosine, diltiazem, or amiodarone, even with orders from online medical control.As my colleague (and EMS attorney) Gene Gandy, LP JD is fond of reminding me, “following orders” will not protect non-physicians from liability when performing negligent acts.See Columbia Medical Center of Las Colinas v Bush (122 S.W. 3d 835, Texas, 2003).

  • Brian S says:

    Tom, I found this series very interesting, thanks for posting. I especially found the WPW with atrial fib interesting. The links (and other research) says Adenosine causes v. fib, and cardizem causes a faster rate.
    In the PA protocols, we give cardizem for a stable irregular narrow complex tachycardia (need to call med command first). For a stable irregular wide complex tachycardia, we give amioderone (again, have to call medical command first). Lidocaine's only indicated for a stable regular wide complex tachycardia, but it's still written to "try amioderone first." I also don't recall ever being taught about this dangerous condition in classes. Following our protocols could make the patient condition much worse, so I think more attention should be brought to this issue.

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