78 yom CC: "Chest heaviness"

Here’s an interesting case submitted by Alex Kroeze. He is currently taking a sabbatical from blogging but was kind enough to share this interesting case with me.

Here is the story in Alex’s own words.

78 year old male with a history of MI with cardiac arrest around 1975 as well as diabetes (metformin) and fairly well controlled hypertension. He had no history of dysrhythmia as best as I could determine. This gentleman had a sudden onset at rest at approximately 0900 this day of 2/10 chest heaviness with no radiation/provoke/palliate and it is constant in nature. When he told his wife, she felt his pulse and noted it to be extremely rapid. She wanted to call EMS immediately however he was resistant to this; eventually she decided to call us anyway even though he still didn’t want to.

On arrival he appears in no acute distress. He is calm with no shortness of breath, nausea, or other stated complaints beyond the heaviness. His lungs are clear apices to bases. He has a noticeably variable ‘loudness’ to the S1 heart tone. His apical heart rate is measured to be 180 beats per minute and he has a good strong radial pulse. No Cannon A waves noted on quick inspection. He is placed on the stretcher and oxygen is applied while vital signs and ECG are acquired (see attached files).


I think that’s enough for starters.

What is your interpretation of the ECGs?

Treatment plan?

32 Comments

  • akroeze says:

    Hi all, if you have any questions that Tom doesn't have answers to about the call I can provide them. I will be keeping an eye on this post.I look forward to seeing what everyone "out there" has to say about this as it has sparked quite a bit of discussion/disagreement amongst the colleagues I have shown it to!Alex Kroeze

  • Did the patient have any records on a prior EKG at the hospital? I'm leaning towards BBB on the 12-lead, though I would like to know if it's new onset or not.

  • Tom B says:

    MIFL – What kind of bundle branch block? A right axis deviation is present and the morphology in lead V1 is bizarre.Based on morphology in lead V2 you'd have to say RBBB, which would make this bifascicular morphology (RBBB/LPFB) which seems unlikely to me.There's also the issue of the patient's history….Tom

  • akroeze says:

    MIFL,The patient had no relevant cardiac related charts at the local ER. He had no cardiac events to speak of since his MI in 1975. Hasn't had nitroglycerin prescribed for him since when Johnny and Roy were still on the streets providing care.I questioned him many different ways to determine if he had any history of BBB or any "funny heart beats" or anything and he said no and his wife denied it too and she seemed VERY on the ball about his history.

  • Ryan says:

    Well, heres what I think I know: -Theres just under 2 bix boxes between RR intervals, placing the rate at above 150. -The smallest, possibly biphasic complex is Lead II, placing the axis around 150 (but with the initial positive deflection, a little under 150.) So, RAD. -Theres a regular R to R interval. Not that this rules out A-fib with RVR, but it doesnt rule it in.Heres what Im curious about: -The complex in aVF doesnt have an increased QRS duration, apparently unlike the rest of this tracing. -Is he just a tough old bat, or is his heaviness really that low on the 10 scale? And how is he showing no respiratory distress, regardless of what this rhythm turns out to be? Heres my guesses, in order of what I believe: -Perfusing V-tach -SVT with a RBBB -Some form of AMI with MASSIVE ST changes and T wave inversions. Not extremely likely, but its a thought.

  • Tom B says:

    Ryan – Nice job calculating the axis.As for lead aVF, I would suggest the QRS duration is the same, but that part of the QRS complex is isoelectric in lead aVF.That's why it's a good idea to obtain a 12-lead ECG before treating an arrhythmia!Based on just the rhythm strip, one might easily treat this as a narrow complex tachycardia!Tom

  • Tony says:

    Tom, please tell me if I'm wrong, if lead 2 would be the same as V1 then I would treat it as a V Tach, I think that its lead 2 that gives off a supraventricular morphalogy that makes me think that its not V Tach

  • Tom B says:

    Tony – You should go with the lead that shows the greatest QRS duration. Sometimes part of the QRS appears isoelectric in one or more leads, creating the illusion that the QRS is narrow.Tom

  • Tom B says:

    Would anyone else like to offer a theory or treatment plan for this patient?If not, I'll post some additional 12-leads of the case (which won't necessarily help determine the exact mechanism of the tachycardia).What is the most important rule of thumb for wide complex tachycardias?Tom

  • Christopher says:

    Extremely wide and bizarre complexes in the precordials, I've got the QRSd at somewhere between 150-160ms. The QRSd is >140ms, which is rare for SVT w/ aberrancy. It'd be nice to see an old 12L for comparison. Another thing of note is V1 appears biphasic, while V2-V6 are all predominantly positive. VT should have all positive or all negative in the precordials. I think between II and V1 I have regular P-waves. I have RAD rather than ERAD, and I believe it meets RBBB criteria. The S1 heart tone varies in loudness, common with AV disassociation.Putting all of this together I have almost as much going for SVT as for VT. However given: QRSd, S1 variability, and prior MI, I am going with VT w/ a pulse.Rx: O2, ASAx4, IV, bolus per BP and lung sounds, repeat 12L after bolus. Pt appears to be tolerating the VT well, so Lidocaine 0.75mg/kg.

  • Billy says:

    This is of course VT until proven otherwise. With the patient's history of MI the prevalence of VT usually increases, but I feel that there is clear AV association in the precordial leads, which makes me think this is a supraventricular tachycardia with a BBB. This would suggest a bifascicular block, which I'm not sure why you think is unlikely Tom?I'm not sure what to make of the heart sounds found upon physical assessment. Is this typical of VT?As far as treatment goes, frankly I would transmit this and consult with medical control because I'm really not sure about this one. Amiodorone wouldn't be a bad choice for this stable patient if you're convinced this is VT, but with these types of difficult wide complex tachycardias I'm more prone for sedation and cardioversion rather than administering a cardiotoxin.

  • Christopher says:

    Some interesting points I found researching SVT v. VT:- "From these observations, we concluded that the absence of an RS complex in all precordial leads or an RS interval of more than 100 msec in any precordial lead when an RS complex was present were each 100% specific for the diagnosis of VT." [1]- "Atrioventricular dissociation was not present in any SVT, however; although 100% specific for the diagnosis of VT, it was seen in only 21% of the VTs." [1]- History of MI: 98% positive predictive value for VT (66%/95% sens/spef) [2]- Age >35 years: 85% positive predictive value for VT (92%/54% sens/spef) [2]- Male: 78% positive predictive value for VT (90%/27% sens/spef) [2][1] Brugada, et al. A New Approach to the Differential Diagnosis of a Regular Tachycardia With a Wide QRS Complex. Circulation 1991. 83:1649-1659).[2] Baerman, et al. Differentiation of Ventricular Tachycardia from Supraventricular Tachycardia with Aberration: Value of the Clinical History. Annals of Emergency Medicine 16:1 Jan 1987, 40-44.

  • Jesse says:

    "or an RS interval of more than 100 msec in any precordial lead when an RS complex was present were each 100% specific for the diagnosis of VT."-C.Watford, Im not sure what you mean by RS interval. Would you elaborate on this please?If you mean duration, then Im confused. Because I thought by definition a BBB has to be over 100 msec, so Im not sure how it can be 100% specific for VT.If you mean interval, like an R2R, or P2P, then in a regular rhythm, the only thing a "greater than" value would imply is a heart rate. Atleast, by my limited knowledge. Hence the polite request for further explanation =)

  • Christopher says:

    Sure, the RS interval is the, "length of the longest interval in any precordial lead from the beginning of the R wave to the deepest part of the S wave when an RS complex [is] present" (from the same paper). Conceptually I see this as the time it takes for the depolarization to spread through the ventricles. My understanding is that ectopic pacemakers in the ventricles take longer to spread through the ventricular myocardium than would an impulse from the atria or through an accessory pathway. Hence the increased duration of the QRS complex (and if present the RS complex). Tom or Adam could probably elucidate this point more than I can!

  • Tom B says:

    Christopher -Be careful with rules like precordial concordance! While it's true that it favors a dx of VT, it's not a particularly senstive finding! So it's not true that VT should be all positive or all negative in the precordial leads.That's the danger of using morphology to differentiate between SVT and VT. Failure to rule-in VT does not rule out VT! That's why it should always be your default dx for a wide complex rhythm.The burden of proof is on the person who says a wide complex rhythm is supraventricular!Tom

  • Tom B says:

    Billy -Be careful, because AV association does not rule out VT! At fast rates, 1:1 VA conduction can't be differentiated from 1:1 AV conduction.Tom

  • Tom B says:

    Christopher – You have defined the RS interval correctly. Just remember that failure to rule in VT does not rule out VT! That's what it means to make VT your default dx. It doesn't need to be ruled in (although it's obviously not dangerous to rule it in). It needs to be ruled out! Tom

  • Tom B says:

    Billy -Sorry, I missed your point about bifascicular block.The fact that it technically shows a bifascicular morphology does not make it SVT, because a VT originating in the left anterior fascicle of the left ventricle can be expected to mimic RBBB/LPFB.In addition, it's not a typical-looking RBBB. Even if it were, it would not rule out VT, IMHO.Tom

  • Christopher says:

    Tom,Before reading those papers the only V-tach's I had seen were fairly "classical". It was a big help to see that all of the morphology rules you acquire through visual repetition aren't at all the law.I'm not exactly sure I'd be able to blurt out Brugada's rules in the field to make the SVT call with any degree of certainty at this point and would of course defer to the Dx of VT!Thanks again, I enjoy the critical thinking exercises.

  • Tom B says:

    Christopher -Even if a patient seemed to fall into the SVT category using Wellens or Brugadas (or any other classification system that uses morphology) I hope you would refrain from using a calcium channel blocker! It's just not worth the risk, IMO.Tom

  • Christopher says:

    I'm with you on that one, additionally I don't believe our protocols permit Ca-channel blockers in the face of a wide-complex tachycardia!

  • Tom B says:

    That seems wise to me!Tom

  • Billy says:

    Tom–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 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?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.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 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?

  • Tom B says:

    Billy -You've raised several excellent points. I'll address them in the update to the case.Thanks,Tom

  • Anonymous says:

    One of two things could have happened to him in my system/state. He would have died, or been transported with 02/IV monitor (12 lead could go either way, probably not) and nothing else. I'm glad these types of calls have a tendency to happen in places where people actually know what they hell they're doing.

  • Beth says:

    In lead II you can clearly see AV dissociation. I am going with a dx of VT on this one. 150 mg of Amiodarone over 10 for him providing his BP could handle it.

  • Chris T says:

    I go with ACLS wide complex tachycardia with pulse. It may have or origines or abbarencies. I would not be considering Adensine. I would also Not yet considering pacing though im prepared. I would call the doc on the phone and discuss this patient. I had one simmilar and was granted my requet for 150mg Amiodarone in 50D5W over 10 mine. Rate 200 pre drip. &6 on arrival of ED. 02 and other suportive measure of coure:-)

  • john says:

    atrial tachycardia with acute inferoseptal MI, BBB, most likely induced by concentric LVH and RVH

  • Paul says:

    I’m going with presumed VT, but personally leaning more toward a supraventricular tachycardia of unknown type with widened QRS. I would start a 16G IV either RAC or REJ, and push 6/12mg of Adenosine to see if there is any effect, or if any better rhythm determination can be made. Some RVOT VTs will convert with Adenosine, so it’s worth a go in my opinion since he’s clearly stable. Failing that, I would go with Procainamide as its useful for aborting VT’s and SVT’s. Failing all of that, I would sedate with Etomidate and Ketamine and cardiovert. I’m not giving Amiodarone because of its organ toxicity combined with his age. I would however, give it if he arrested.

  • Paul says:

    I forgot to add, I would also run in 2 grams of magnesium somewhere along the way as it has been shown to be of benefit in patients with difficult to convert arrhythmias. Given how wide his QRS is, his QT is clearly prolonged anyway.

  • Bernard Deruyter says:

    I would first try carotide sinus massage for vagal stimulation 
    i do think this would reveal right atriales Flutter, counterclock isthodependant. 

  • Paul says:

    I would not recommend carotid sinus massage for anyone who is 75 years old. The risk of them having carotid bruits and you dislodging one of them(thus causing an embolic stroke) is too high to chance it when there are other treatment options available.

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