47 year old male CC: Crushing chest pain – Conclusion

Here is the conclusion to 47 year old male CC: Crushing chest pain.

You may want to go back and read the original case presentation to see how we got to this point.

When we left off we had this rhythm on the monitor and surprisingly the patient was conscious and talking! 

As usual there was an excellent discussion in the comments.

I certainly agree that the first step is to check the leads. I've seen artifact mimic VF before! When I worked in the Critical Care Stepdown Unit as a cardiac monitoring technician this would sometimes happen when a patient brushed their teeth.

However, this time it was the real McCoy (hyperlinked explanation of this idiom for my international friends).

  • This has the general appearance of Torsades de Pointes.
  • It's fast, wide and polymorphic.
  • There appears to be a "streamer" effect.
  • The patient is conscious.

However, several features point away from Torsades de Pointes.

  • The ventricular rate (using the small block method) is 375
  • The QTc of the underlying rhythm is 447 ms

The rate of TdP is typically in the 150 – 300 range. A QTc of 447 while technically prolonged is still < 500 ms which is generally considered to be "safe"

It seems to go against everything we've been taught but could this patient have been conscious with VF on the monitor?

The answer is "Yes!" There are two reasons for this.

First, the onset of VF is often course and slow (relatively speaking). A ventricular rate of 375 is a lot different from a ventricular rate of 720. We like to think of VF as if it's all the same and it usually is from a treatment standpoint. But there is quite a lot of variability as I'm sure anyone who has worked on VF detection algorithms could tell you.

The second reason is that forward blood flow continues for several minutes after the onset of cardiac arrest. That's because there is a pressure gradient between aortic pressure and central venous pressure.

This chart from a white paper on the LUCAS device helps illustrate the point.

This is a busy chart but you will note that it takes several minutes for aortic pressure and central venous pressure to merge together after the onset of VF.

Mark Glencorse over at the (retired) 999Medic.com blog presented another case of transient VF where we had the same lively debate as to whether or not we were dealing with Torsades de Pointes.

Some of you are probably thinking, "It's not VF! It's polymorphic VT!" I will simply ask, isn't VF a form of polymorphic VT? At what rate does polymorphic VT become VF?

From a treatment standpoint it doesn't matter in this case because I'd treat both rhythms exactly the same. I'd apply the combo-pads and I'd give 2 g of magnesium sulfate while I was waiting to see if the patient lost consciousness. Tim Noonan (Scallywag Medic) will be disappointed in me for saying so but you really can't hurt a patient with MgSO4 and it might help.

In this case the treating paramedic didn't carry magnesium sulfate but he did apply the combo-pads.

About a minute and a half later the patient lost consciousness.

Now I think we'll all agree that the patient is in VF and we'll also agree on the treatment! 

After another 2 cycles the patient was shocked back into a perfusing rhythm. Interestingly, the patient "woke up" several times during chest compressions.

The patient regained consciousness after return of spontaneous circulation.

Another 12-lead ECG was captured.

Now we're back where we started! (Okay, it's a little worse.)

Advanced notification was given to the receiving hospital and the cardiologist was waiting for the patient. He was taken directly to the cardiac cath lab where angiography revealed a 100% occlusion of the proximal LAD.

The lesion was successfully stented and the patient made a full recovery.

Congratulations to Phil, the Intensive Care Paramedic from Australia (and his crew) for a job well done!

Got an awesome case? Submit it to the EMS 12-Lead blog at ems12lead@gmail.com


  • Rose says:

    Tom, This was an excellant case review.   I was thinking the rhythm as Torsades and had alot of questions. 
    As much as I learn from the case comments, the case review always seems to answer my concerns and I gained additional knowledge.
    Again Thank you sir for your help & knowledge.

  • It's our pleasure, Rose! Thanks for reading.

  • Troy says:

    Oh Tom,

    I can’t agree with your choice to delay defibrillation on this patient. Id rather give him MgSO4 when he’s in a sinus rhythm than when he’s in polymorphic VT. Yes, I know that in TdP it will be refractory to defibrillation but probably not in that light of hypomag (if he has any).

  • Troy – In spite of my previous disagreements with Rogue Medic on this point I'm not a big fan of shocking conscious, talking patients without sedation. Of course I'm also not a fan of dead patients. This was a tough situation.

  • Troy says:

    I agree with you as far as not shocking a conscious, unsedated pt. I’m just saying 5mg IN versed doesn’t really affect BP and is great for light sedation. Then….ZAP!

  • VinceD says:

    Troy, I agree with your idea, but problem with that course is that in a region such as mine you need to call medical control for sedation prior to cardioversion, which can result in you waiting several minutes for a doc to be available (if you even get through the first time), in additionion to the usual roulette that keeps you wondering which doc will pick up the phone. Maybe they'll agree with sedation, or maybe they'll say, "Just shock him," or even, "Just bring him here." That pretty much forces you into two scenarios: in one the patient is stable enough to wait for med control orders, drawing up the med, pushing it, waiting for it to work, and then cardioversion, in which case you may as well just wait to treat him at the department where they're better equipped to handle conscious sedation. The other path, where the patient simply can't wait that long and needs zapping, is not ideal and I wish more regions had standing orders for what you describe, but they don't and so many prehospital providers are left making black or white decisions in a situtation filled with grey zones.

  • Ken Grauer says:

    TOM – Truly an interesting case with excellent graphics.  Good points made about the differential diagnosis between VF & Torsades – though my understanding is that a preceding long QT is NOT essential for Torsades (and your QTc of 447ms IS prolonged, even though under the QTc range at which Torsades risk is greatest). So while good to keep in mind the rate characteristics (Torsade usually slower than VF) – your "bottom line" (= treat with Magnesium) I read as acknowledging the "at the bedside" judgement that given QRST morphology of the rhythm in question, it is truly difficult to know for sure that the rhythm is not Torsades (and as you emphasize, there is no downside to IV Mg++, and it could be lifesaving if the rhythm really was Torsades …. ).  Otherwise – I don't know that one would remain alert and conscious despite true VF for "several minutes" (which is what I think you were implying).  I reviewed the white paper from where the chart you provided on the LUCAS device came from – and although truly an interesting paper – it does have the bias of "data" that comes from the manufacturer of the device (and to my admittedly skeptical mind, the paper reads as an advertisement … ). I didn't see statement in the paper of specific amount of time that alertness could be maintained for a patient in V Fib (best my memory recalls is from an old JAMA article describing a number of well documented cases in the cath lab, with the longest maintenance of consciousness during VF being ~90 seconds for a patient who was told to cough forcibly and repetitively until he could be shocked) – so I'll buy that selected patients may remain awake and alert despite ongoing VF for a short period of time, but respectfully request more documentation before I'd accept ongoing consciousness despite VF for a period of several minutes.  All of that said – this was a FASCINATING CASE with great rhythm strips that spurred excellent discussion.  THANK YOU for sharing! – Ken Grauer, MD (ekgpress@mac.com)

  • I'm just as comfortable saying that it was very rapid (> 350) polymorphic VT. This is just semantics. As for the LUCAS white paper, you're correct that it's essentially an advertisement. I was only interested in the graphic (taken from Stig Steen et al, Resuscitation, 58 (2003) 249-25) to emphasize that some forward blood flow continues after the onset of VF, at least in a swine model. The QTc may have been ever-so-slightly prolonged in this case but that's not unusual for a patient experiencing STEMI and it's barely prolonged by 7/1000 of a second! I doubt that's clinically significant but you are correct that I would give MgSO4 just in case because I see no downside. I guess I would ask you the same question I have asked others. At what rate does polymorphic VT become VF? That's a rhetorical question of course because had the patient been unconsicous I'm guessing you'd have no quarrel with calling it VF. Right? Thanks for the comments!

  • Davison says:

    I ran this same call 2 weeks ago, 62 y/o women.

  • AW says:

    Fantastic case, thanks for all the info.  I agree what we decide to call this rhythm matters less than the patient's tolorance to it as it will evolve into, or look more like each of the VT/VF choices along the call timeline.  Here we don't require orders for sedation/cardioversion if the medic deems the time spent will be to the pts detrament.  However the rule is strict on all patients that have a pulse always getting sedation and syncronised cardioversion.  No just zapping them here unless they are in arrest.  The options of cardioversion or drug first would be the discussion point if the time is taken to call the EP.

  • very interesting. this discussion reminds me of the is-it-VT-or-aberrent-SVT discussion.

  • Christopher says:

    One key takeaway from this case is polymorphic VT is more commonly found in conjunction with ischemia or infarction than Torsades. Useful if you have a "borderline ACS" 12-Lead ECG followed by a run of polymorphic VT/VF.
    Another key takeaway is that polymorphic VT or primary VF (i.e. induced by ischemia/MI) is very ameniable to defibrillation. This is also in contrast to Torsades, which likely will require pharmacological intervention as well. That being said, Tom is right in that as long as you don't push the MgSO4 like adenosine, it will not likely hurt cases of PVT.

  • Andy J says:

    I'm not sure I would be comfortable with waiting for the pt to lose consciousness prior to defibrillation, as what appears to have happened in this case (1.5 mins before his was shocked).
    If the pt was in VT and was conscious, then of course sedation would be appropriate prior to cardioversion, but this pt is in VF and I think the best chance for first shock sucess would be to defib him straight away without any prior sedation when he still has good coronary artery perfusion. He might wake up with a sore chest, but he should revert with the first shock. The pt in this case gets a couple of shocks as well as chest compressions in between, so I'm sure he would be in more pain than if he were shocked straight away.
    IMHO, the priority would be to get the pt out of this life threatening rhythm as soon as possible and if the pt is still aware when you're ready to defib, then it's just unlucky for them.
    I had a similar pt not too long ago who went into VF in front of me secondary to STEMI and still had a GCS of 12 and answering my questions when I shocked him with no sedation. He had no recollection of the defibrillation, and this is consistent with other pts I've had in similar situations.

Leave a Reply

Your email address will not be published. Required fields are marked *