Saturday, November 6, 2021

Agitation, Confusion, and Unusual Wide Complex Tachycardia. What is it, why did it occur, and how to treat?

A 50-something male ran a 10 mile race, after which he complained of a headache.  The next day, he collapsed and had a witnessed seizure.

He arrived agitated and the monitor showed a wide complex tachycardia.  He was very hypertensive and tachycardic.

A 12-lead ECG was obtained:

What is it?  What therapy?

There are wide complex QRS's with 2 different morphologies:

1. RBBB configuration with an axis of about 135 degrees (lower right axis toward III)

2. IVCD (neither RBBB nor LBBB) with a "Northwest" (upper right) axis toward aVR

There appear to be 3 possible P-waves, but they are not consistent and not definitely associated with any QRS.

Thus, I thought that this is probably Bidirectional Ventricular Tachycardia.

I sent it to Ken Grauer, and he drew some lines and gave his thoughts:


Hi Steve. TRULY interesting — and I’m NOT sure what is going on. My thoughts:
  • I don’t see sinus P waves
  • The ventricular rhythm looks quite regular. The QRS is wide — and looks to be of ventricular etiology.
  • Against this being bidirectional VT — is that there is a deflection (RED vertical lines that I drew in V1, V4) that continues precisely on time! I suspect this may reflect retrograde P waves — and I wouldn’t expect this to continue if this was bidirectional VT with 2 different ventricular foci …
  • I know with VT that the pathway of VT reentry may vary — that at times part of the pathway may contain one of the bundle branches — and I suspect that may be what is intermittently happening here ...
  • P.S. — As in the case of pleomorphic VT that I presented (in the June 1, 2020 post in Dr. Smith's ECG Blog) — among potential mechanisms for explaining variation between a limited number of QRS morphologies during VT include: i) A single VT circuit with more than a single exit site; ii) More than a single VT circuit; and/or, iii) Shifting conduction properties that alter the activation sequence (Liu & JosephsonCirc Arrhythm Electrophysiol 4:2-4, 2011). — Ken Grauer, MD —


With the combination of headache after exertion, followed by sudden collapse with altered mental status, in a previously healthy patient, subarachnoid hemorrhage was strongly suspected.  SAH often causes a catecholamine burst and this can result in stress cardiomyopathy (takotsubo), and/or ischemia, with associated VT.   

The patient was intubated for his mental status and additionally so that he could be put on a propofol infusion in order to blunt the catecholamine surge, after which the rhythm stabilized.

Sinus tachycardia with some ST depression consistent with subendocardial ischemia

He had a CT scan of the head:

Aneurysmal subarachnoid hemorrhage

Later, a formal echo was done:

The estimated left ventricular ejection fraction is 59%.

Normal estimated left ventricular ejection fraction

Left ventricular hypertrophy concentric


Regional wall motion abnormality-lateral akinetic

Regional wall motion abnormality-anterior akinetic




There is definite akinesis of the mid-lateral and basal anterior segments.

(The etiology--i.e. coronary vs noncoronary mechanisms---is unclear on this study). 


In combination with elevated troponins (250 ng/mL -- NOT high sensitivity), these findings were thought to be due to stress cardiomyopathy (takotsubo).

Learning Points:

1.  Learn to recognize Bidirectional VT.  See a 2nd case below.

2.  Stress cardiomyopathy can be caused by a catecholamine surge, which has many etiologies including Subarachnoid hemorrhage

3. VT can be caused by catecholamine surge in an otherwise relatively healthy heart

4.  Propofol has been reported as a treatment for VT caused by catecholamine surge.  See search here.

Another case of Bidirectional Ventricular Tachycardia

A Southeast Asian with Tachycardia and Hypotension after taking a dangerous herbal medication (Bidirectional Ventricular Tachycardia from Aconite Poisoning)

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