Saturday, October 14, 2017

Cardiogenic shock with wide complex tachycardia and poor LV function in a young woman

A 30-something woman presented with CP and SOB.  She was hypoxic and intubated.  She had very poor LV systolic function on bedside echo.  There were no B-lines and the RV was normal.

The following ECG was recorded:
Wide complex regular tachycardia at a rate of 140, no P-waves
What do you think?
What do you want to do?

This ECG was texted to me on my iPhone without any clinical information, with the question: "VT or SVT with aberrancy?"

Here was my response:

"Tough one, as they always are.  Looks like SVT with LBBB (LBBB morphology strongly supports SVT).  Lead  aVR is all negative.  I am going to say SVT and I would try adenosine."

Alternatively, it is sinus tachycardia with LBBB and P-waves are not visible.  Always consider Lewis leads when this is a possibility, as they are likely to exaggerate and uncover otherwise hidden P-waves.

Further analysis, with magnification of V2 and V3:
This is typical LBBB morphology.

When VT has its origin in the RV, it can have an LBBB-like morphology, but there are differences.  Except in the case of fascicular VT, VT starts in the myocardium (not in conducting tissue) and therefore the initial part of the QRS is not rapid (it is slow).   Thus, when it is VT with LBBB morphology, the onset of the LBBB-like QRS is more prolonged. 

Thus, if it were VT
1) the R-wave in right precordial leads would typically be greater than 30 ms.
Here it is about 20 ms

2) the onset of the R-wave to the nadir of the S-wave would be greater than 70 ms.  In fact, it would usually be greater than 100 ms.
Here it is about 60 ms

Thus, this is very likely SVT with aberrancy (or with baseline LBBB), and the SVT is possibly sinus tachycardia with P-waves that can't be discerned.

If the rate varies over time, sinus becomes more likely.

If it is paroxysmal SVT, Adenosine may convert it.

All ECG findings aside, severely decreased LV systolic function does make VT more likely.  But these ECG findings are pretty convincing.

Case Continued

The physians thought they were dealing with ventricular tachycardia (VT)
--Cardioversion at 200 J biphasic was attempted without success.
--K was slightly low, so K and Mg were given.
--Amiodarone was given, 150 mg x 2.
--Cardioversion x 3 was apparently unsuccessful

    Comment: Cardioversion would usually be effective whether SVT or VT.  The question in my mind would be this: was the patient converted to sinus tachycardia (still with LBBB), at a similar rate, such that it that looked nearly identical to the SVT and the providers were unaware that the cardioversion actually worked?

--Lidocaine was given, after which patient became hypotensive.
--CXR showed pulmonary edema.
--Cardiac function on echo was very poor, prompting initiation of chest compressions.
--After 3 minutes of CPR, and 1 mg of Epi, there was ROSC with hypertension and improved cardiac function.
--The wide complex continued, but rate was down to 120, suggesting that the rhythm had indeed converted to sinus tach, but there was uncertainty as to the presence of P-waves at this point.
--A trans-esophageal echo (TEE) probe was placed by the emergency physicians in the ED.  This revealed coordinated atrial followed by ventricular contraction at a rate of 120, suggesting sinus tachycardia.  (Not proving it, as SVT could have atrial before ventricular contraction)

The patient remained in cardiogenic shock due to severely decreased LV systolic function.  The remainder of the management is beyond the scope of this blog.

Later in the day, this ECG was recorded:
Sinus with LBBB.
So the LBBB is definitely baseline.  This is the same morphology that she had while in tachycardia, proving that the rhythm was supraventricular.

The patient recovered neurologically, but with a persistently very low ejection fraction (20%, due to new cardiomyopathy).  She also had very frequent ventricular ectopy, with short runs of VT.    In order to protect against dysrhythmic sudden death, she was discharged on a "Life Vest". (2)

The diagnosis in retrospect was SVT with aberrancy in the setting of severe cardiomyopathy and acute decompensated heart failure, with later runs of ventricular tachycardia.

Learning Points:

1. If it looks just like LBBB or RBBB, it is probably supraventricular.

2. In a regular wide complex tachycardia, use adenosine if you think it is SVT.  If you're wrong and it is VT, adenosine is safe.

3. VT can have a morphology similar to LBBB, but in VT the initial part of the QRS should be prolonged, such that the septal R-wave is wider than 30 ms and/or the onset of the R- to nadir of the S-wave is greater than 70 ms.(1)

4. In a critically ill intubated patient in shock, ED transesophageal echo (TEE) can help to guide management in many ways.  It can especially help to continuously monitor LV function during a resuscitation.  In this case it also helped to verify sinus tachycardia.

5.  A "Life Vest" (Wearable External Cardioverter Defibrillator) can be used for those who only temporarily need such a device, or as a bridge to a later implantable defibrillator (see full text article below for details, if interested).

References with links to full text

1.  Wellens Hein JJ.  Ventricular tachycardia: diagnosis of broad QRS complex tachycardia.  Heart 2001;86:579–585

2.  Zishiri ET.  Chung MK.  The Role of the Wearable Cardioverter-Defibrillator in Contemporary Clinical Practice.   The Journal of Innovations in Cardiac Rhythm Management.  May 2011.


  1. I thought that extreme right axis deviation must be present for vtach or at least rule out SVT vs VT. Correct me if I am wrong but isn't extreme right axis deviation determined by a larger negative deflection in leads I,II,III?

    1. Northwest axis is common for VT, but not necessary. Axis here is directly lateral (zero degrees).

  2. "The remainder of the management is beyond the scope of this blog." - I'm super curious as to what happened, if you have the time to share! Thanks!

    1. I can't share it because the case is too recognizable. Thanks for your interest, though!

  3. Nicely discussed case! My comments relate to assessment of QRS morpholgoy of the wide tachycardia. While true that a regular wide tachycardia should always be assumed to be VT until proven otherwise — QRS morphology here is strongly suggestive of a supraventricular etiology with LBBB. That because: i) there is a typical upright complex in all left-sided leads (leads I, aVL and V6); and ii) the S wave in several leads (here in leads V3,V4) is exceedingly steep. Of note, there appears to be a small and narrow initial negative deflection (q wave) in leads I and aVL. This suggests prior scar, since “typical” LBBB should not manifest any q wave at all in any left-sided lead. That said, the appearance of the QRS complex in left-sided leads here is much more suggestive of a supraventricular than ventricular etiology. Otherwise — the exceedingly steep S waves that are almost vertical in leads V3 and V4 is also far more suggestive of a supraventricular than ventricular etiology — though of course nothing is 100% ... Thanks to Dr. Smith for his discussion of this case.

  4. I would like to know about T axis its normal range and if abnormal what it indicates?

  5. Excelent case! is adenosine safe with patients with history of cardiomyopathy and reduced EF?

  6. I am sorry, is there any possibility that the tachycardia is a 2:1 flutter?

    1. Benny,
      It is possible, but I don't see any evidence of it.
      Steve Smith

  7. John Israel, NRP, CCPOctober 17, 2017 at 11:14 PM

    Was this case somehow related to toxicology? The age with signs of cardiomyopathy made me suspicious from the start. I heavily considered the rhythem to be Sinus Tachycardia with LBBB, and thought of cocaine overdose. My suspicion was even stronger once lidocaine was used with a worsened outcome.

    It seems like the providers immediately thought cardiology etiology and not tox or metabolic. What would about the case caused this?

    1. John,
      No. It was not tox. I wish I could tell you what it was, but that would compromise confidentiality.

  8. John Israel, NRP, CCPOctober 18, 2017 at 10:46 AM

    I'm curious why the providers immediately jumped to a cardiac etiology for the patients condition. What was it about the presentation and history that made them believe that a dysrhythmia was the primary pathology?

    Personally I read the age and gender and thought toxicology or other metabolic disturbance. To me the ECG apprared to be Sinus Tachycardia with LBBB. While reading through this I thought of amphetamine overdose (namely cocaine). Then when reading that lidocaine made the symptoms worse I was even more suspicious.

    Maybe I have an unfounded bias, but I don't immediately think cardiac eitology on severely sick 30 year old females. Please help my bias.

    1. same answer as above. Your approach is reasonable, but you don't have all the information!

  9. In this clearly unstable wide complex tachycardic patient, it seems to me the first step is always cardioversion; regardless if the rhythm is VT or SVT. In practice, I would never consider mulling over adenosine in someone like this. That being said, knowing the rhythm was actually SVT with LBBB would have been helpful by helping to identify a successful cardioversion. But it looks like the providers did the right thing with cardioversion, and even amio, even though their initial rhythm diagnosis was wrong

    1. I only agree with you in intubated patients. When I received the text, I did not know the patient was intubated. But in awake patients, it is much more monkey business, and risk, to deal with sedation in a sick patient than to give adenosine.


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