Update to: 78 yom CC: "Chest heaviness"

Lots of interesting comments on this case.

Here is the update.

I opted to treat this patient as a presumed monomorphic ventricular tachycardia which is hemodynamically stable. I placed an 18 ga catheter in his left AC at a TKO rate. At approximately 1005 I administered 130mg (1.5mg/kg) of Lidocaine slow IV push which had no effect. At approximately 1010 the patient started vomiting profusely in a projectile fashion. He complained that he now hurt everywhere and he had a headache. At this point we decided to move to the truck even more rapidly than we already were. Enroute I gave him a second dose of Lidocaine this time 65mg (0.75mg/kg) with again no effect at approximately 1015.

At 1017 we arrived in the ER driveway and as my partner was placing the vehicle in park the patient went semi-conscious with a GCS of 9 (E3 V2 M4) and an absent radial pulse. We rapidly unloaded him to the already pre-alerted and waiting ER team. Within several minutes they successfully cardioverted the patient after one shock with a resultant bradycardic sinus arrythmia from 48-56 for a HR. He was subsequently transferred without incident to the regional tertiary care centre for ICD insertion.

Here are the serial ECGs that were captured en route to the hospital.


This case was handled very well, in my opinion. If you’ve read my tutorial on the differential diagnosis of wide complex tachycardias, then you know I believe that wide complex rhythms should be considered ventricular until proven otherwise!

I might not have given a second dose of lidocaine if the patient started projectile vomiting after the first dose, but it’s impossible to know the proximate cause.

Here are some recent comments on the case left by a reader named Billy.

Although VT should be the default diagnosis for a wide complex tachycardia, what sort of criteria do you suggest be used other than QRS morphology?

What sort of criteria to determine that a wide QRS rhythm is supraventricular? That’s an interesting question. Personally, I would require an old ECG for comparison, irregularity to suggest atrial fibrillation, the appearance of flutter waves, or a spontaneous slowing of the heart rate that reveals the rhythm to be sinus tachycardia.

What do you mean by VA conduction not being able to be differentiated from AV conduction? Are you saying that VT can produce retrograde conduction to the atria, resulting in a P wave after the QRS complex originating from the ventricles?

That’s exactly what I’m saying!

Also, I didn’t mean to say that because there appears to be a bifascicular block that makes it SVT. I was wondering why you thought that was unlikely in the first place for this patient, which would suggest VT.

Not to beat a dead horse, but “wide and fast” suggested VT prior to identifying the QRS morphology. VT can mimic virtually all intraventricular conduction defects! I thought RBBB/LPFB was unlikely because the RBBB morphology was atypical in lead V1 (with serial ECGs it became more typical). “Wide and fast” meant VT before we learned how to identify RBBB, LBBB, and bifascicular blocks. Unfortunately, many paramedics seem to throw that right out the window once they learn how to recognize these patterns! It’s very dangerous thinking.

I am interested to how akroeze ended up treating this patient. Regardless, I think amiodorone would be a good choice. Correct me if I’m wrong, but I believe amiodorone works on many mechanisms, including Ca, K and Na channel blocking, as well as beta blocking, which makes it effective on both VT and SVT’s. In these types of situations where a wide complex tachycardia might be SVT amiodorone should treat the arrhythmia no matter where the pacemaker is, making it a safe choice, whereas cardizem would be a better choice in narrow complex SVT’s since its Ca channel blocking is more pronounced.

I agree with that! Amiodarone would have been a perfectly acceptable antiarrhythmic to try in this scenario. In the absence of amiodarone, lidocaine was a viable option.

I would also like to present a “chicken vs. egg” question: What if this is in fact an MI? If you use the 220-age rule then this patient’s maximum heart rate is 142. With the heart rate being 180 I think it’s pretty clear this patient’s problem is an arrhythmia and not an MI (though we might see an MI once the arrhythmia is corrected). Suppose the patient was a bit younger and the heart rate is borderline at about 140 or so, with the same morphology in all leads. I think you can make an argument for inferior ST depression with elevation in the lateral leads. So, do you treat the tachycardia, or for ACS?

Tachycardia in the setting of acute STEMI is bad. For sinus tachycardia you treat the underlying cause. I’ve seen several cases of sinus tachycardia and acute STEMI mimicking a wide complex tachycardia, so you’re wise to consider it. It’s also not unheard of for STEMI patients to experience VT, so you could easily see an acute injury pattern coexistent with VT. All I can tell you is that no one said our job was going to be easy! Sometimes the best thing we can do for our patients is recognize our own limitations.

7 Comments

  • Billy says:

    Hey Tom–Thanks for addressing my comments. I would just like to say that I hope I didn't come off sounding condescending or too argumentative with your interpretation of the EKG. I really appreciate what you do here and visit your site daily. I really feel like some of your posts have helped me be a better EMS provider.

  • Billy says:

    I have been reviewing the serial EKG's that were taken after the lidocaine administration and I think it's interesting to review the heart's response to the drug. As we know, lidocaine blocks fast Na channels which results in a prolonging of the QT interval on the EKG. In comparison to the initial 12 lead that was taken at 10:04, in the next one after lidocaine administration, taken at 10:12, I see taller R waves in I and more pronounced Q waves in III (I'm not sure about the significance of this though) and V1 seems to have taken on the morphology of V2-V6 in the previous EKG, where as V2-V6 now seem to be doing something completely different. I think it's neat to note that V1 now has a positive deflection and V6 now has a negative deflection, which is what we would expect with a ventricular pacemaker. There also seems to be a global widening of the QRS, which can be seen well in III and aVF. Clearly the drug is doing something, and I'm wondering if these are typical responses that you would see with VT after administering lidocaine, or would you expect to observe these changes with SVT? I must admit that during my time as an ALS provider (~1 year) I still haven't given any of the big cardiac drugs and don't have much experience documenting the heart's response to these drugs.Check out the last 12 lead taken at 10:19. It's fascinating too! Did anyone else notice that aVR is now a negative deflection, whereas it was positive in the previous two EKG's? What does this mean? We also see that with the exception of V2, all the precordial leads are returning to their original morphology that we saw in the first EKG taken at 10:04. Also notice that the computerized interpretation of the strip says that the QT interval of this third strip is .322 seconds as compared to .256 seconds in the first strip. Since this third strip was taken only 7 minutes since the second one, and since the half life of lidocaine is at least 1-2 hours, it couldn't just be wearing off, so methinks it was ineffective and this might have been an SVT.What does everyone else think? Would you expect to see these types of changes in serial EKG's after lidocaine administration if the patient was in fact in VT?Again, let me reiterate that I'm not saying that treating this as a wide complex tachycardia is a bad idea, as that is what I would have done also, but since hindsight is 20/20, I think it's interesting to try to figure out what the initial rhythm was with the help of the heart's response to the lidocaine. After all, if it turns out this was an SVT, giving lidocaine to a bifascicular block probably isn't a good idea.Man I'm afraid that was a long rambling mess…hopefully you can all derive a little sense out of that. Thinking about EKG's this hard makes my head spin!

  • Tom B says:

    Billy – Not at all! I didn't think you were being argumentative, at least not for the sake of being so.We're just discussing ECGs, which is a favorite pastime! :)Tom

  • Tom B says:

    Billy -It's been a while since I've studied cardiac action potentials, but I do know that lidocaine is one of the few antiarrhythmics that is actually supposed to shorten the QT interval!You wrote:"I think it's neat to note that V1 now has a positive deflection and V6 now has a negative deflection, which is what we would expect with a ventricular pacemaker."Be careful! Failure to rule-in VT using QRS morphology does not rule it out! What we expect with a ventricular pacemaker is a wide QRS complex. Some morphologies are highly specific for VT, but that doesn't mean that other morphologies are likely to be SVT!I agree that differential diagnosis of wide complex tachycardias is interesting, but the truth is that it's an abstruse topic that does not avail itself of an easy solution.It worries me that so many paramedics (in so many forums) will look at rhythms like this and say "SVT with some kind of bundle branch block."You're better off calling it an undifferentiated wide complex tachycardia (presumed to be VT until proven otherwise) and the burden of proof should be high, because the consequences of a misdiagnosis are high.Tom

  • Christopher says:

    My only question would be were the leads taken off and put back on again? If not, I really enjoyed seeing the progression of the rhythm through the 12L's! Crazy stuff.

  • akroeze says:

    Mr. Watford,The electrodes were left in place for the duration of the call, no new ones were needed to be placed.

  • Tom B says:

    Alex – If I may ask, what is the exact nature of the dispute where you work? Is it whether or not the rhythm is VT or SVT with aberrancy?Tom

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