Monday, December 19, 2011

Ventricular fibrillation on a 12-lead ECG

A 54 year old male suddenly collapsed.  He had not complained of symptoms prior to this.  He received bystander CPR, then was defibrillated when the medics arrived.  He arrived in the ED awake. The following ECG was recorded:
There is sinus tachycardia with diffuse ST depression (I, III, III, aVF, V2-V6), with obligatory ST elevation in aVR (ST depression maximal in leads II and V4 establishes the ST vector as upward and rightward; there must be ST elevation in aVR).

This is typical of NonSTEMI with ischemia from acute 3-vessel ischemia or left main stenosis.  It establishes ongoing ischemia, though sometimes may be residual after cardiac arrest.  So a repeat ECG should be done a short time later in order to establish whether there is, indeed, ongoing ischemia.  Thrombolytics are never given for such an ECG, but angiogram and PCI are indicated if medical therapy alone does not control the ischemia.

Amiodarone 150 mg was given, along with aspirin, heparin, and eptifibatide.  Because of tachycardia and thus a risk for cardiogenic shock, no beta blocker was given.  BP was adequate and so nitroglycerine drip was started.  Clopidogrel (or any thienopyridine) was not used because the ST elevation in aVR makes the probability of CABG high.

15 minutes later, the patient was awake enough to take a history.  He stated that he had ongoing chest pressure, strongly suggesting ongoing ischemia.  The leads were placed for a repeat 12-lead ECG, and we were talking to the patient when the ECG tech said, "Hey, guys, uh......"  We looked up and this is what we saw:

12-lead ventricular fibrillation.  Not seen very often!!  Notice how similar ventricular fibrillation is to torsadeBy the way, the computer read: sinus tachycardia with frequent multiform PVCs!!!!

The patient was awake but becoming obtunded when he was defibrillated successfully with one shock; he did not remember it.

Recurrent v fib in the setting of ischemia is diagnostic of ongoing and uncontrolled ischemia.  The only way to control this is with PCI, if angiogram shows a lesion amenable to therapy.

A second 150 mg dose of amiodarone was given.

Angiogram showed 3-vessel disease and 3 lesions in the LAD which were stented.  He did well.


  1. Tell me again how this is Vfib?? Looks like torsades in lead II. Waaaay too regular (most of the time) in lead II.

  2. Torsade is, by definition, only in the presence of a prolonged QT. There is no prolonged QT. Polymorphic VT is either torsade or non-torsade. There are some who might argue that this is non-torsade polymorphic VT. But it was pulseless, so it really makes no difference. V fib frequently looks like torsade. That is the point I'm trying to make. They can look identical.

  3. 12-lead number ONE is very scary to me! Would you say that patients with this pattern have a propensity for cardiac arrest?

    I know I have had one with this pattern that arrested in front of me.


  4. They are certainly at high risk of arrest because of widespread ischemia.

  5. OK makes sense about the QT. So what is the comparison (physiology ) of polymorphic vtach that isn't torsades as compared to torsades. I know the appearience and such but what makes it different?

    Sorry having a hard time phrasing my question.

  6. they look the same but one is caused by things that prolong the QT, the other by ischemia mostly.

  7. The R-R interval in the second strips seems regular to me, so it looks more like some kind of pulseless VT.
    I find it hard to measure the QTc on the computer screen, but at least on V2 the Q-T interval seems more than half the R-R interval, which is a clue for prolonged Q-T. Can you please re-consider the option of torsades?

  8. Again, torsade is by defintion polymorphic VT in the context of a long QT on the baseline ECG. The first ECG did not have a long QT. So this can by non-torsade pulseless polymorphic VT. There is no practical difference between non-torsade polymorphic VT and V Fib. Same etiology in this case (ischemia) and same treatment (electricity).

  9. Would also suspect that the amiodarone, administered after the first ECG shown, prolonged the QT and lead to polymorphic VT, which really looks like torsades... Dr. S, my understanding is the indication for amio here is for shock-refractory VF, which he didnt have. So why was amio given so early?

  10. Good thought,but improbable. The QT is 295 ms, QTc 440ms. it would be highly unusual for a single dose of amiodarone to increase the QT to the length necessary to cause torsade, especially in tachycardia.

    What I find interesting is that clinicians everywhere seem to be fascinated and obsessed with torsade, and frequently desire a chaotic rhythm to be torsade. Most rhythms that look like torsade are really fib. Especially if they occur in the setting of ischemia.

    1. Definitely my feeling also. Coarse VF looks like torsade. But never self terminates, which is very often the case with torsades. I wonder if there is good litterature on this.

    2. Excellent case. I didn't found any literature on the recognition from VF and PMVT. If someone had found any studies on this, I will really appreciate to see it. Thanks :)

    3. you might like these posts:

  11. On rare occasions, V Fib can convert spontaneously. See this case:

  12. No way it is vfib and the patient is awake "becoming obtunded". Zero cardiac output with vfib.


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