Wide complex tachycardia, resistant to cardioversion. Some fascinating features here.

An elderly dialysis patient presented with chest pain.

She has poor LV function.

Previous echo 4 months ago (confirmed with ED bedside echo):

The estimated left ventricular ejection fraction is 30%.   Severely decreased LV function.

Regional wall motion abnormality-inferior, inferolateral, septum, anterolateral, anterior and apex, lateral.

Here is her ECG:

Regular Wide Complex Tachycardia.  

What do you think?

What do you want to do?

See note from our electrophysiologist at the bottom of the post.

--Regular means it can't be atrial fibrillation

--Most regular wide complex tachcardia are VT, especially if the patient has poor LV function, as in this case.

--Giving adenosine is not contraindicated, but the surest way to fix the problem is with synchronized cardioversion.  It could be slow VT or some SVT with RBBB and LPFB.  Either way, electricity should do the job.

Electrically cardiovert!

Sedation, then 200 J --> would not cardiovert

Repeat --> would not convert again

So this required some more thought.  Did it fail to convert because it is occult sinus tach?

Was it definitely VT?  It is very slow for VT.  

She was not on any medication that could cause this. 

Could it be flutter with slow ventricular response?  There is no indication of flutter waves.

Could it be sinus with RBBB and LPFB aberrancy?

Could it be atrial tachycardia with RBBB and LPFB aberrancy?

QRS analysis: The best way to differentiate SVT from VT is to look at the rapidity of the initial part of depolarization (QRS onset).  There appears to be a rapid depolarization (upstroke of the main part of R-wave, or downstroke of main part of S-wave, but I think that is deceptive.  If you look closely, there is some low voltage deflections prior to those up- or downstrokes.  This is the electrical impulse making its way through myocardium that is not specialized for conducting (impulse starts in myocardium and slowly makes its way to a Purkinje fiber, in this cases the anterior fascicle, and so it has the appearance of RBBB + LPFB)

Is there an old ECG for comparison?

She had an ECG done yesterday!!  Here it is:

There is sinus with normal conduction, very different from her tachycardia.

Could she have sinus tach with rate related BBB?

Let's try to see P-waves better.  If they are present and upright before the QRS, then it is sinus tach with hidden P-waves.  If they are after the QRS and inverted, then it is VT.

So we applied Lewis Leads.

How do we place Lewis Leads? -- Use the monitor leads (not the 12-lead ECG):

1. Place the Right Arm electrode on the patient's manubrium.
2. Place the Left Arm electrode on the 5th intercostal space, right sternal border.
1. Place the Left Leg electrode on the right lower costal margin.
3. Monitor Lead I. 

Here is the result:

What do you think?

You can see RETROGRADE P-waves easily.  This makes the diagnosis of VT easy.

But there is another very interesting feature that is present in the 12-lead but seen even more easily in the Lewis leads!!  

Ventriculo-Atrial VA block (2nd degree Mobitz I block--Wenckebach)  Notice that there is progressive prolongation of the RP interval and then it is completely blocked!

White arrows show where it is blocked:

If you look at the top ECG, you can also see the retrograde P-waves:

The black arrows show inverted P-waves in lead II after the QRS. The blue arrows show down-up biphasic retrograde P-waves.  Normally, in sinus, they are biphasic up-down, but the reverse is down-up!

The patient was diagnosed with VT and given IV amiodarone, whereupon she quickly converted:

Sinus with multiple PVCs

Our electrophysiologist, Rehan Karim, just sent this comment after I posted:

"I just saw your post about the slow ventricular tachycardia. It’s a very interesting ECG I saw yesterday. The retrograde P waves are very obvious in lead V1 and in fact there is Mobitz type-1 second degree VA block in 5:4 Wenckebach pattern. Morphology is consistent with VT also."

Amiodarone or Procainamide? --The eternal question.

The below discussion of this choice comes from this post:

An asymptomatic man in his 50s with heart rate in the 160s - what is the diagnosis? How will you manage this?

Procainamide is a class 1A sodium channel blocker, meaning it slows action potential propagation from cell to cell, reducing speed of conduction and prolonging the QRS and QT. Despite poor overall literature base, procainamide is typically considered the drug of choice for stable monomorphic VT after the results of the Procamio Study, which compared procainamide with amiodarone in the setting of stable monomorphic VT, and favored procainamide, showing roughly double the efficacy with half the adverse effects. Relative contraindications to both include a known prolonged QT, especially if the dysrhythmia is believed to be caused by prolonged QT.  

Another benefit: Procainamide is very effective at terminating SVT.  So if you are incorrect about your diagnosis, it might convert with procainamide anyway!

Check out RebelEM's post and podcast on the PROCAMIO trial for more:

Procainamide dosing:

IV loading dose is 10 to 17 mg/kg, typically administered at a rate of 20-50 mg/min.

Alternative dosing strategy is 100 mg every 5 minutes in adult patients until max dose of 17 mg/kg.

Another alternative dosing regimen was used in the Ottawa Aggressive Protocol (for chemical cardioversion of atrial fibrillation): 1 gm over 60 minutes.

The loading dose is given until the tachydysrhythmia is terminated, or the patient experiences hypotension, or QRS prolongation greater than 50% of baseline, or the max dose of 17 mg/kg has been given.

After the desired clinical effect is achieved, a maintenance dose is typically started at a rate of 1-4 mg/min.