Wednesday, June 3, 2015

Wide Complex Tachycardia Refractory to Anti-dysrhythmics and Cardioversion.

This was contributed by Rebecca Kornas, MD, one of our EM Residents.  Edited and commented upon by Smith.

A middle-aged male with a history of CAD and two vessel CABG and ischemic cardiomyopathy (EF 20%) presented to the emergency department (ED) after an out-of-hospital cardiac arrest.  Paramedics found him in ventricular fibrillation and started mechanical CPR via the LUCAS device, five rounds of epinephrine, and delivered six unsuccessful defibrillation attempts before arriving in the ED. 


He was defibrillated into a wide complex rhythm.  There was no pulse.  Chest compressions were continued.

His initial beside echo showed moderate cardiac activity, but there were no pulses palpated initially and chest compressions were continued. 2 grams magnesium sulfate were administered, 2 50 ml ampules of 50% bicarbonate, and 3 grams of calcium gluconate were given for possible hyperkalemia. Additionally, 300 mg of amiodarone and then a single bolus of 100 mg of lidocaine were administered.

Comment on lidocaine dosing: Lidocaine, to be effective, must be loaded in several boluses.  For an 80 kg individual, give 100 mg, then give 50 mg every 5 minutes for 3 doses (total, 250 mg over 15 minutes), then start a drip at 2-4 mg/min. 
In mg/kg: 1-1.5 mg/kg, followed by 0.5 to 0.75 mg/kg to a maximum total dose of about 3mg/kg.


Clinical course continued:

His second bedside echo showed more robust activity and radial and femoral pulses were palpated. 
As femoral access was obtained to cool the patient, the first 12-lead ECG was obtained: 
What do you think?

One should err on the side of treating wide complex tachycardia as the most dangerous possible rhythm: ventricular tachycardia. Especially, in middle-aged or older patients, especially with a history of cardiomyopathy, and especially with sternotomy scars suggesting ischemic heart disease. 

The exact rhythm was not completely clear to the providers. 

However, there are several indications that the patient was in ventricular tachycardia. 

Analysis of first ECG:

There is a wide complex tachycardia at a rate of 125, with LBBB configuration (small initial r-wave in right precordial leads, deep S-wave, and upright R-wave in V6). 


Is it a true LBBB morphology?  No!  Note RS of 120 ms in V4 (black arrow below), with onset to nadir of S-wave at greater than 100 ms (all too long for normal LBBB).  Importantly, there were several fusion beats noted in lead II (see blue arrows below).  


The beats that are not fusion beats in V1 and V2 have an LBBB duration of 180 ms. Typically LBBB duration is not greater than 170 ms unless there is hyperkalemia.


Same (first) ECG Annotated with arrows:
Blue arrows point to fusion beats, which are nearly diagnostic of VT.  Black arrow points out that the QRS duration is 180 ms.


Clinical Course:

Potassium was 2.9 mEq/L, but this was not noticed.  (Comment: This may well be the etiology of the tachycardia; in refractory VT, K should be normalized to between 4.0 and 4.5 mEq/L)

The patient’s heart rate then increased to 148-152 bpm and his rhythm appeared slightly different. 

Another ECG was obtained. 
Wide complex tachycardia w/ sharp septal activation in leads V1/V2 which could suggest supra-ventricular origin. RS in V4 is still greater than 120 ms.  The entire QRS is still very wide.  From peak of r-wave in right precordial leads to nadir of S-wave is about 60 ms (equivocal).  Normal LBBB is about 50 ms.

This looks almost identical to the initial ECG, but at a different rate and with slightly narrower intervals.  Is it flutter with LBBB?  SVT with LBBB?  Or is it still VT?  Why would this VT rate be different?

Patient had BPs in 140s/90s and was perfusing. There was a discussion as to whether this was atrial flutter with LBBB, or VT. 

In an attempt to break a potential SVT, adenosine was administered via fast push: 6mg, then 12 mg, then 18 mg with no blocked p-waves or termination of tachycardia noted on rhythm strip.  Nor was flutter revealed.

Synchronized cardioversion was attempted with 150 joules —then 200 joules — then 200 joules w/ optimized placement of cardiac pads. The patient remained in this wide complex tachycardia but did have one capture beat noted transiently just after he was shocked.  

Patient was taken to the catheterization lab. 

In the cath lab, the patient was found to have patent grafts and no new lesion in his circumflex. His native RCA was 100% occluded which indicates likely scar-mediated focus of his re-entrant ventricular tachyarrhythmia. 

While in the cath lab he was given additional lidocaine and Potassium was optimized. It was around this time that overdrive pacing in the 240s was delivered, at which time the patient converted to normal sinus rhythm.  The patient was maintained on lidocaine drip in the MICU and transitioned to digoxin, carvedilol and mexiletine.

ECG after conversion to sinus rhythm. 
This is clearly sinus rhythm, and has nearly the same morphology as the 2nd tachycardia.  This suggests that the 2nd tachycardia was also supraventricular.  It is not entirely clear, but the electrophysiologist was quite certain that the tachycardias were VT.  He was not certain whether it was terminated by the lidocaine or by overdrive pacing.


The patient had an ICD placed.  He did well.

Sasaki's Rule for Diagnosing VT: 
This case does not meet all of the criteria, however, this is an interesting rule (not yet validated) to review.

1. Initial R in aVR?  If so, then VT, if not, go to 2.
2. Longest RS in precordial leads greater than 100 ms?  
                     If so (as it is in this case), then VT.  If not, go to 3.
3. Initial r- or q- in any lead greater than 40 ms?  If yes, then VT.  If no, then SVT with aberrancy.

This rule is probably too simple, and not yet validated. But it's simplicity is a virtue, too.

Learning points
1. If RS is greater than 100 ms in any lead, think VT 
2. Appreciate fusion beats. Among wide complex tachycardia, they almost exclusively (with exceptions) occur in VT.  
3. LBBB duration is typically between 120-170 ms. Longer than that should increase suspicion for possible VT or hyperkalemia.
4. Lidocaine must be given with serial boluses
5. VT that is refractory to all other treatments may be converted with overdrive pacing, which is listed in the ACC/AHA guidelines as class IIb for incessant VT.  
6.  I cannot find reports of overdrive pacing by a transcutaneous pacer, but I do not see why that would not work as well.

Other interesting VT cases: 


Wide complex tachycardia in a 36 year old


Wide Complex tachycardia: VT or SVT with aberrancy?




VT vs. SVT with aberrany: here is the sequence of analysis I (Smith) use:

Consider in the context of clinical scenario.  
(None of this applies to fascicular VT or RV outflow VT, which are associated with normal heart structure and originate in or near conducting fibers.  However, these are rare exceptions):

a. VT is more common than SVT among WCT
b. Older patients are more likely still to have VT
c. Any history of cardiomyopathy, MI, structural heart disease, or coronary disease makes VT much more likely

And then consider the ECG.  

The unifying principle of most VT (not "idiopathic" fascicular VT) is that the first part of the QRS is initiated in myocardium, NOT in conducting fibers, and thus it conducts slowly.  Therefore, the initial part of the QRS changes its voltage SLOWLY (wide).  This is what I look for to diagnose VT:

1. The longer the QRS, the more likely it is VT.  A QRS duration greater than 140 ms is likely VT, though it is not a terribly reliable differentiator.  However, a QRS duration of 200 ms is almost always VT or aberrancy with hyperkalemia.  This case is thus very likely to be VT.
2. Obvious AV dissociation?  Then VT, if not:
3. Obvious fusion beats?  If so (as in this case), then VT, if not:
4. Leads V1-V6 unidirectional (no RS or SR) and "concordant" (in the same direction)?  Then VT
5. If there are RS complexes in precordial leads (i.e., they are not concordant): is there any precordial RS that has a duration from onset of R- to nadir of S- that is greater than 100 ms?  Then VT (as in this case).
6. Abnormal LBBB or RBBB pattern (see this link for a figure from the Brugada paper):
----a normal RBBB or LBBB pattern makes SVT very likely: both have a rapid initial deflection, the r-wave in LBBB and the rS in RBBB, followed by a slowly conducting latter part of the QRS.
     a.  If there is LBBB pattern, is the initial r-wave greater than 50 ms?  Or is the onset of the QRS to nadir of the S-wave in V1-V3 greater than 60-70 ms?  If so, this is not true LBBB.  VT.  In this case, it is 100 ms.
     b. If there is RBBB pattern, is there a monophasic R-wave?  Or is the first R of the Rsr' larger than the second one?  Then VT.
7. Initial R-wave in aVR (not an r-wave, not preceded by q-wave)?  Then VT
8.  If the initial deflection in aVR is an r-wave or q-wave, is it greater than 40 ms?  If so, then VT

11 comments:

  1. Thank you for your interesting case. There was recently published paper about new diagnostic algorithm for diagnosing ventricular tachycardia called VT Score. Link: http://dx.doi.org/10.1093/europace/euv118
    According to it first ECG gets 1 point for Lead II RWPT ≥ 50 ms and 2 for AV dissociation. 3 points is diagnostic for VT with 99.2% accuracy.

    ReplyDelete
    Replies
    1. Dexter,
      Thanks for calling my attention to this. Interesting paper!
      Steve

      Delete
  2. This could be bundle branch reentrant VT?

    ReplyDelete
    Replies
    1. Maybe, but that would not explain why it is so wide. If BBB VT, then all conduction is through conducting fibers and QRS is only as wide as a normal BBB.

      Delete
  3. Hi Dr Smith,

    Very interesting case, as the VT here was virtually refractory to every mean the care team would have in their hands !

    As an aside, is there any possible explanation as to why Amiodarone and Lidocaine, respectively of class III and class Ib of the Vaughan-Williams classification were ineffective in the course of this event ? Specifically for Amiodarone as at least one of its numerous properties - beta-blocker effect, Na+ channel blocker, K+ channel blocker or even Ca2+ blocker - would have been thought to stop the arrhythmia ?

    Best regards,

    Olivier.

    ReplyDelete
    Replies
    1. Olivier,
      the lidocaine was underdosed. As for amio, it just does not always work. There is no 100% therapy for any dysrhythmia, so one has to have a "armamentarium" to draw upon. A variety of options.
      Thanks,
      Steve

      Delete
  4. Could the 3rd beat from the right also be a fusion beat? it looks different from the rest of the morphologies.

    ReplyDelete
    Replies
    1. Adrian,
      It certainly could be, and probably is.
      Steve

      Delete
  5. Hi Prof
    I came up with this ABCDEF approach VT vs SVT with aberrancy
    A: AV dissociation
    B: Brugada sign & BBB absent
    C: Concordance (+ or -), monophasic, and Capture beats
    D: Dilated QRS > 160 msec [Josephson sign]
    E: Extreme axis deviation (NW axis): Vereckei algorithm, Ear rabbit taller Left (Marriot sign)
    F: Fusion beats


    ReplyDelete

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