Friday, July 27, 2012

Synchronized Cardioversion: What Happened?

EMS was dispatched for a 62 year old male with an altered mental status. Upon their arrival they found the patient to be non-communicative, responsive to verbal stimuli, in moderate respiratory distress, with pale, diaphoretic skin, and weakly palpable radial pulses. The patient was placed on the monitor during their initial assessment:

Wide complex tachycardia of unknown etiology.
A blood pressure was unobtainable, however a pulse of 150 was palpable at the carotid. Labored respirations were present, with clear breath sounds bilaterally. The patient had an extensive cardiac history, renal failure, and insulin dependent diabetes mellitus. The patient's blood sugar was 300 mg/dL.

A 12-Lead was obtained and interpreted as presumed ventricular tachycardia:

Wide complex tachycardia, interpreted as presumed ventricular tachycardia.
Differentials of a wide complex tachycardia at 150 bpm include: ventricular tachycardia, SVT with aberrancy, sinus tachycardia with aberrancy, and 2:1 atrial flutter with aberrancy. No previous 12-Lead was available for comparison.

Given the presence of a WCT with hemodynamic instability the patient was prepped for synchronized cardioversion. Combo-pads were placed anterio-laterally, the Sync button was pressed, and sync markers were noted with each QRS complex.

The patient was then synchronized cardioverted at 100J biphasic:

100J synchronized cardioversion.
A rhythm change was noted on the monitor:

Ventricular fibrillation post cardioversion.
With ventricular fibrillation present, the paramedic disabled synchronization and delivered a 200J biphasic shock:

200J defibrillation of ventricular fibrillation.
After defibrillation, the patient regained consciousness and palpable radial pulses were present. Emergency transport was initiated. During transport, a sustained run of ventricular tachycardia occurred and the patient was given 100 mg lidocaine IV with a subsequent conversion of a sinus rhythm (not captured). The patient experienced multiple episodes of non-sustained ventricular ectopy during transport.

In this case the paramedic did not appreciate that oversensing was present from the cardiac monitor's display. It was not until after the summary printed that the ineffective synchronization was discovered.

Oversensing during synchronized cardioversion--highlighted in red--resulting in therapy delivery during the vulnerable period.
As the ventricular myocardium repolarizes, it may not do so homogeonously. This window of non-uniformity, with both absolutely and relatively refractory myocardium present is known as the Vulnerable Period. Electrical stimulation during the vulnerable period of ventricular repolarization may result in ventricular tachyarrhythmias.

Illustration of the vulnerable period of ventricular repolarization. Adapted from Reilly et al. 1998 pp 188 Fig 5.19.
This is best appreciated during episodes of a prolonged QT interval. An early-cycle premature ventricular contraction may result in the so called "R-on-T" phenomenon initiating Torsades de Pointes.

A prolonged QT interval and an "R-on-T" PVC resulting in Torsades de Pointes. Used with permission from Dr. Ken Grauer's ECG Web Brain.
In this case, the electrical stimulation was provided by inappropriately synchronized biphasic shock. By default the synchronization used Lead II, which featured proportionately smaller negative complexes when compared to their T-waves. Sometimes atrial tachyarrhythmias, such as atrial flutter or atrial fibrillation, may produce deflections sufficient to trigger R-wave deflection as well.

Oversensing of atrial fibrillation. Adapted from Resuscitation 82 (2011):135-136,Fig.1.
Appropriate lead section is important when performing synchronized cardioversion in order to avoid delivering the therapy while the myocardium is vulnerable. If synchronization is not accurate the operator of the cardiac monitor should switch leads, increase the gain, or change pad placement.


  • Reilly J. Patrick. Applied Bioelectricity: From Electrical Stimulation to Electropathology. Springer-Verlag: New York (1998); pp 188.
  • Dr. Ken Grauer's ECG Web Brain. Accessed online 26 July 2012. [https://www.kg-ekgpress.com/]
  • Sodeck GH, Huber J, Stollberger C. Letter to the Editor: Electrical cardioversion - Misinterpretation of the R-wave. Resuscitation 82 (2011): 135-136. [PubMed]

12 comments:

Anonymous said...

Sorry if this is a more simple question, but I have always had trouble distinguishing V-Tac with Sinus Tac when it looks similar to Lead II or Lead III on this EKG http://2.bp.blogspot.com/-HcrJVpS1vJE/UBGsPx00grI/AAAAAAAAB6c/HKiy-jDJwdM/s1600/62yom-VT-rhythm.jpg

Why would one not call the small upward deflections p-waves? This keeps coming up again and again for me. I wish I had more EKG examples to demonstrate how they can look similar, especially on the monitor screens with ECG simulators.

Any tips for a new paramedic who wants to get this figured out before going out in the field...?

Brooks Walsh said...

First off, this is a great illustration of why the sensing features turns off after each synchronized cardioversion. Very instructive case for folks learning electrical therapy, as well as a warning against complacency for the more experienced crowd!

Unknown said...

Excellent case.

Is there any outcome information available? Obviously the main thing to learn here has to do with recognizing inappropriate R-wave markers for the synchronized cardioversion. However, I am curious if that was the appropriate therapy to begin with. Yes, wide-compex tachycardia of unknown origin is V-Tach until proven otherwise, and this patient was unstable. That said...

Seems to me with a hx of renal failure, hemodynamic instability and symmetrical peaked T waves in V2-V3, I would be highly suspicious of hyperkalemia as the cause of the widened QRS. The STE also seems significant in II and aVF.

When sinus rhythm was restored from V-Fib, was it the same morphology as the first EKG? What was the rate?

Thanks for posting this case!

Christopher said...

Anonymous 1,

A case can be made for sinus tachycardia and a 1st degree AV-Block. A case can be made for Atrial Flutter with 2:1 conduction. A case can be made for VT.

I wish I could tell you definitively why this ECG represents one and not the other, but I lack sufficient details.

My tip for new paramedics is to apply a stepwise approach to your interpretation and to never exclude likely rhythms (e.g. VT). Use adenosine as a diagnostic measurement with regular wide complex tachycardias.

Lastly, find a book or series of books which contains hundreds of ECG's for you to interpret. They usually will contain lots of tough wide complex tachycardia examples. This will help you get comfortable making decisions in the field.

Christopher said...

Unknown,

I wish I had more. Apparently the patient received treatment for "ventricular arrhythmias" in the ED, but who knows if they were right as well!

I think a really strong case could be made for electrolyte/volume problems and this simply being sinus tachycardia. This would lead you down the path of inappropriate cardioversion for certain.

As for the post-VF rhythm, it was documented as sinus tachycardia and a 12-Lead was obtained, but it was not submitted to me. The rate was documented as ~80 bpm.

I wish I had the answers!

ECG Interpretation said...

Excellent case - albeit one without definitive answers ... (sometimes some of the best cases don't have definitive answers .... ) - but NICELY POSTED by Christopher!

I agree with all that is said - and I too have questions and some uncertainty about what the WCT truly is. That said - I think you HAVE to presume it is VT. The QRS is VERY wide - there is almost uniform negativity (except for some small r waves) in all precordial leads - there is delay down-to-nadir in many leads - and the QRS axis is VERY markedly leftward. Hard to tell what it is we see midway between the R-R in V1 (could it be retrograde 1:1 VA conduction....?) - but from what I see - unstable patient in regular WCT like this - I agree with synchronized cardioversion.

I do not think the QRS in the one lead we see post conversion (presumably lead II) is the same as during the WCT (there seems to be an initial small r in lead II during WCT, and the downslope of the negative complex is different=slower than with sinus rhythm) - so I do NOT believe the initial WCT was supraventricular - but can't prove it without the other 11 post-conversion leads ....

For anyone interested - ALL you might want to know about differentiation between VT vs SVT at: https://www.kg-ekgpress.com/acls_comments-_issue_11/

Bottom Line: Excellent interesting post by Christopher (albeit we don't know the answers for sure .... ).

Jarvik 7 said...

A nuanced and excellently presented case (as usual).

Obviously a prior or post 12-lead for morphological comparison would be interesting in re VT vs ST, as would an adenosine trial; but even then, if the VT was sensitive this might not be as informative as one might hope.

Either Orman or Wiengart talks about being lead down the path of SVT rather than compensatory ST and how insidiously this can happen. I have seen a patient with DTs receive three rounds of adenosine... I have always feared this. Inappropriate cardioversion concerns me less than loading beta and calcium channel blockers for a "refractory cardiac etiology," only to find their H and H come back critical low...

Vince D said...

Great point Jarvik 7. On the flip side I've also seen at least two or three patients spend 4-6 hours in the ED and get admitted for SOB, and then when I stumbled across the ECG the next day it turns out that they were in 2:1 flutter the whole time. Still, I'd probably prefer that to the over-treatment cases you describe.

Jesse said...

If you are able to spare some time for an email, I have some synch cardioversion questions and would greatly appreciate your input.

jcookems@yahoo.com

Thanks Chris!

-Jesse

Erin said...

HI Christopher,

Great blog, very interesting case.

My question has to do with the vulnerable period of ventricular depolarisation.

I can find multiple sources (reputable) stating the vulnerable period of the T wave is on the later portion (apex onwards) however there are equally as many sources stating it is from the beginning of the T wave to the apex.

Your appropriated diagram suggests the the later. Do you know if there is a definitive agreement on where the vulnerable period lies?

(The majority texts I have found state post the apex).


Thanks!

Erin

Christopher said...

Erin,

Great question!

In normal ventricular myocardium the vulnerable period is maximal just prior to the apex, however, this period is lengthened during ischemia when you have a larger non-uniformity in repolarization. However, as you note many texts and papers reference Tpeak as the most vulnerable time[1,2].

I also agree that the diagram does not present the optimal zone of vulnerability, as studies focusing on induction of VF have shown a period of around -40ms to +20ms of Tpeak to be maximally vulnerable[3,4].

Therefore the simple answer is the surface ECG does not necessarily present an optimal view of the "zone of heterogeneous repolarization" which can give rise to triggered VT/VF. Any short-coupled stimulus falling just before or after Tpeak is suspect!

Thank you again for your question.

References
1. Conover MB. Understanding Electrocardiography. 8th Ed. Mosby, Inc: Missouri. 2003. pp. 21-22.
2. Swerdlow C, Shivkumar K, Zhang J. Determination of the Upper Limit of Vulnerability Using Implantable Cardioverter-Defibrillator Electrograms. Circ 2003;107:3028-3033. [FullText]
3. Swerdlow CD, Martin DJ, Kass RM, et al. The zone of vulnerability to T wave shocks in humans. J Cardiovasc Electrophysiol 1997;8(2):145-54. [PubMed]
4. Shepard RK, Wood MA, Dan D, et al. Induction of Ventricular Fibrillation by T Wave Shocks: Observations from Monophasic Action Potential Recordings. J Interven Cardiac Electrophisiol 1999;3(4):335-340. [PubMed]

Erin said...

Thanks for the prompt reply Chris, I'll follow up with the listed references - cheers!
Erin