Thursday, November 3, 2016

I saw this on the computer. Most physicians, at first glance, get this wrong. What is it?

I was reading ECGs on the system, and saw this:
I immediately recognized it like I recognize a friend's face.  (OK, I'm unusual, I'll admit it)
What is it?



















When I showed this to residents, they uniformly thought it was Left Bundle Branch Block (LBBB).  Look again.  

What QRS morphology is necessary for LBBB?
LBBB morphology requires an upright R-wave in V6.  The QRS here is all negative, depolarizing from left to right.  In LBBB, the ventricle is depolarized in the opposite direction: from right to left, not left to right.
Thus, this is very unlikely to be a supraventricular rhythm (e.g., accelerated junctional) with LBBB.

Then look again at the rhythm.  What is it? 

I always ask these questions about rhythm:
1. Is it regular, regularly irregular, or irregularly irregular?
2. Is it wide or narrow?
3. What is the rate?
4. Are there P-waves?
5. [difficult to assess on one ECG: does the rate stay always the same (re-entrant rhythm), or does it vary from minute to minute? (automatic rhythm, such as sinus or escapes)]    


Although beats 4-16 are pathognomonic once you recognize them, it is also helpful to see the first 3 beats of lead II across the bottom:
1. The 1st is narrow complex and preceded by a P-wave.
2. The 2nd and 3rd have a P-wave with a short PR interval and a wider QRS
3. 4-16 comprise a 1) regular, 2) wide complex rhythm at 3) a rate of 96 4) without P-waves.

A paced rhythm has this appearance on precordial leads, as the right ventricular pacing lead is usually in the RV apex and depolarization then proceeds from the apex to the base (from leads II and V6 towards the right shoulder).   The computer does a good job of finding pacing spikes, even when they are invisible to the human eye.  The computer did not detect pacing spikes here.  This patient's heart is NOT being paced.

Therefore, this rhythm originates in the ventricle and propagates to the "northwest."  Ventricular tachycardia looks like this, but VT is much faster, usually at least 120 beats per minute.

So what is this?

Accelerated idioventricular rhythm (AIVR).  It is an automatic rhythm originating in the ventricles.  It is frequently associated with reperfusion of STEMI.  Some studies dispute whether it is really more common in reperfusion than otherwise in acute MI.

Now, look at beats 7-15 across the bottom (lead II).  Immediately after the J-point there is a retrograde P-wave that distorts the ST segment with a slight negative deflection.  This helps to confirm AIVR, and good retrograde AV conduction.

Now that we have the rhythm and QRS (AIVR), what about the ST-T?  Is there ischemia?

I believe, due to its similarity to LBBB, that the (Smith-) modified Sgarbossa rule (SMSR) can be applied to AIVR (and also to paced rhythm), though I do not have data to support that.  Does this ECG above meet the criteria of the SMSR?  Look at lead V2: there is 1.5-2.0 mm of ST Elevation following a 6 mm S-wave, so this is consistent with anterior MI.

My interpretation before looking at the patient's chart:

AIVR (with retrograde P-waves) following reperfusion of an anterior STEMI, with ST elevation that is out of proportion due to residual ischemia.  The first beat is sinus, then the AIVR speeds up and takes over the sinus rhythm.  The second and third beats are fusion beats in which the impulse from the sinus node and the impulse from the AIVR meet so that it is wide, but not very wide.  Remaining beats activate the atrium from below, with a negative P-wave.  Thus, the ventricle is outpacing the atrium.

Let's now look at the case, the presenting ECG, and the management:





















The patient had presented with chest pain and had this ED ECG:
Obvious anterior STEMI

The cath lab had been activated and a mid LAD occlusion opened and stented.

After stenting, the patient became more hypotensive with a wide complex rhythm and the ECG we have been discussing was recorded.  He was no longer having chest pain at this point in time.

Here it is again for you:
Why was he hypotensive? 

First, in AIVR, the ventricle does not get the advantage of the filling pressure that atrial contraction normally provides (there is no "atrial kick").  In fact, the atrium is contracting during ventricular contraction and propelling blood backwards.

This patient was noted to acutely have about a ~30 mmHg drop in blood pressure while in the ventricular rhythm thought to be secondary to this loss of atrial kick and preload.

BP immediately improved after conversion to sinus rhythm. He cycled between the two rhythms fairly frequently.

How would you manage this?

One good way is to just speed up the sinus node and let it take over from the ventricle.  Atropine would help.

Antidysrhythmics should not be given.

Recommendations of the ACC/AHA, in the 2004 STEMI guidelines (there is no comment in subsequent versions):
"7.7.1.4. Accelerated Idioventricular Rhythms and Accelerated Junctional Rhythms
Class III
1. Antiarrhythmic therapy is not indicated for AIVR. (Level of Evidence: C)
2. Antiarrhythmic therapy is not indicated for accelerated junctional rhythm. (Level of Evidence: C)

"Accelerated idioventricular rhythms are characterized by a wide QRS complex, with a regular rate higher than the atrial rate and lower than 100 bpm. The appearance of an idioventricular rhythm is an inexact indicator of reperfusion.  Treatment of idioventricular rhythm is not indicated, and suppression of the rhythm may lead to hemodynamic compromise."



3 hours after the AIVR:
This shows well-developed Q-waves of anterior MI, with excellent ST resolution and shallow T-wave inversion.
This has the appearance of "LV aneurysm" morphology, though it is too early to call it this.

Next Day:
T-wave inversion, typical of reperfusion T-waves 


Outcome
The rhythm cycled between sinus and AIVR, but eventually settled on sinus
Peak Troponin I was 195 ng/mL (very high)!
However, formal echo had EF of 60%.  Good outcome.




Learning Points

1. AIVR is commonly seen in situations of reperfusion of STEMI.  Although studies do not uniformly confirm this, I can say that in my experience, I have seen this dozens of times and every one was after reperfusion.
2. AIVR is normally well tolerated and self-limited and rarely requires treatment.
3. Occasionally, patients may not tolerate AIVR due to loss of atrioventricular synchrony, as above. Atropine can be used to increase the underlying sinus rate so that it inhibits the AIVR.
4. Antidysrhythmics are not indicated and will not help: this is not a re-entrant rhythm; rather it is an automatic rhythm.
5. If it is not a situation of reperfusion, consider other causes: digoxin toxicity and other structure heart diseases. 

12 comments:

  1. Would you say that AIVR can be seen in NonSTEMI also? I happen to have a case of AIVR where there was no ST elevation while the patient were in sinus rhythm (and no obvious reperfusion T waves / "Wellens"), and hs-TnT that went from 59 to 358 ng/L (<15) where coronary angiography the following day showed three vessel disease (with Cx as the probable culprit)

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    Replies
    1. Peter, sure, any ischemia can cause it!
      Steve

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  2. The first thought that struck me after I looked at the upgoing QRS in avR was, are leads properly attached.

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  3. fantastic teaching case. thank you.

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  4. Really great case. Learnt some incredibly interesting gems of new information there, thank you!

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  5. Excellent case!! I am resident in cardiology in Germany and I have never seen a AIVR after reperfusion in STEMI patients, but I will keep this in mind. In Switzerland I had a patient with AIVR but with hyperkalemia and CKD.

    Greetings from Switzerland and I love your blog!!

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    Replies
    1. Thanks, Stephani. Ich liebe Deutschland und die Schweiz. Grusse!

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  6. Amplitudes of qrs complexes alternate, it's clearly seen on the rhythm strip. Does this mean something?

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    Replies
    1. Good observation. I don't think it is significant. There was no effusion.

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