Weak, SOB, "DKA", Chest Pain, and Wide Complex Tachycardia: Is there STEMI?

This case was sent by a reader:

A 60 year old man presented with "DKA," Weakness, Dyspnea, and Chest pain with vomiting.  He denied fever or abdominal pain.

Heart rate was  in 150's, systolic BP in 90's, RR 30's, and pulse oximetry in the 90's.

He "looked gray".  His K was 5.2 and glucose 740 mg/dL.

He was acidotic: pH = 7.00, pCO2 = 25, pO2 of 78.

Here is his initial ECG:

There is a wide complex tachycardia.  If you look at V1, there is a narrow r-wave followed by a deep S-wave, typical of LBBB.  However, there are 4 narrow complex beats interspersed (see black arrows in image below).  Are these capture beats in the midst of VT?  If they were, they should come early, but they do not.  So is it VT or SVT with aberrancy?  That is a tough question.  If it is SVT with aberrancy or sinus with aberrancy, all I can surmise is that most of the time the left bundle is refractory at this fast rate, but in 4 instances it recovered in time to avoid LBBB.  The QRS duration is best seen in V1, where it appears to be only 120 ms. 

There have been a lot of interesting comments  on this ECG.  One is how V2 does not seem to fit between V1 and V3 and may be a misplaced lead.  Another points out the notch in descending limb of V1, which is one of Brugada's criteria for VT of the LBBB morhology type (see Brugada types below).  I am not 100% convinced of VT because of the apparently short QRS at 120 ms and I initially favored sinus with aberrancy and obscured p-waves, but have received some contrary feedback which you can read below in the comments section.  The bottom line is I am not certain if it is VT or not.

Brugada criteria for regular wide complex rhythm:
In Brugada's derivation sample, the sensitivity and specificity were 99% and 97%, but subsequent validation studies have not confirmed this. As an example, Vereckei et al. compared Brugada to his two algorithms and found Brugada's to be 86% accurate compared to 91% accuracy for the two Vereckei algorithms.


1. Is there absence of RS complex in all leads V1-V6? (concordance)
--If yes, then VT
2. Is interval from onset of R-wave to nadir of the S > 100 msec in any precordial leads?
--If yes, then rhythn is VT. If no, step 3
3. Is there AV dissociation?
--If yes, then VT, If no, step 4
4. Are morphology criteria foor VT present (see image below)?
--if yes, then VT.


Here are the Brugada morphologies of VT:

Next you need to determine whether there is ST segment elevation or depression. 

I have annotated the same ECG here:

The black arrows are the interspersed narrow complex beats.  It is easy to find the onset of the QRS in V1.  From V1, I draw black lines up to demonstrate the onset of the QRS in the other leads.  The red lines are the end of the QRS.  As you can see, there is concordant ST elevation or excessively discordant ST elevation in several leads.  II, III, and aVF have massive excessively discordant STE, diagnosing inferior STEMI.  There is excessively discordant reciprocal ST depression in leads I and aVL, confirming this.  V2 has concordant ST depression, diagnosing posterior STEMI.  V3 through V6 have excessively discordant STE or concordant STE, diagnosing anterior STEMI as well.

How could there be both inferoposterior and anterior STEMI?  There are three possibilities:

1) this is an LAD with a "wraparound" Type III LAD that feeds the inferior wall
2) there is either an LAD or RCA occlusion, but shock is so severe that the other wall has severe demand ischemia with ST elevation.
3) there is no acute thrombotic occlusion, rather there is only severe demand ischemia from shock, extreme tachycardia, and fixed coronary stenoses.

The second ECG was similar but without the few narrow complexes:

Then the patient rolled over, vomited, and became unresponsive.  He was cardioverted, intubated, had a bradycardic arrest, chest compressions, and epinephrine, and was resuscitated.

Some time during this, this ECG was obtained:

The rate is 220 and it is very wide.  This is clearly ventricular tachycardia.

After resuscitation, this ECG was obtained:

Now there is a narrow complex. There is only inferoposterior STEMI now, with additional ST elevation in V4 and ST depression in V5 and V6.  The rate is 164.  It is hard to say whether this is sinus.  The upright p-wave in V1 suggests atrial flutter with 2:1 block and the second flutter wave hidden in the QRS, but it is difficult to correlate that in lead II.

The cath showed a proximal RCA occlusion and severe 3 vessel  disease.  Unfortunately, he expired the next day.


Here is the VT discussion:

Vince D, Mar 18, 2012 02:26 PM


While I'm very tempted to take opinion of Dr. K. Wang as inherently correct, I still get the sense that those are fusion beats of some sort in tracing #1. Here's what's spinning around in my head at the moment:

1)The initial deflection of each narrow complex matches that of its wide brethren, common for fusion.

2) Although it is an extremely regular tachycardia, and it's true that the narrow beats don't arrive early, the complex immediately following a narrow beat is consistently just a little ahead of schedule, with the following beats shifting forward in time accordingly. This suggests that the entire mechanism of the tachycardia is affected by each fusion.

3) There seems to be a relationship between the narrowness of the complexes and how early the next beat arrives. I'm far from an expert at such things, but points 2 and 3 have me leaning towards some sort of re-entry for the underlying mechanism. It's not just a single early beat following the "event" as in enhanced conductivity. I've only looked at a couple of cases of V-Tach with fusion beats, but this pattern seems to match. I haven't taken the time to compare it to other automatic or re-entrant arrhythmias.

4) Although the morphology is a bit different, the QRS axis of the apparent V-Tach in tracing #3 very closely matches tracings 1 and 2 in both the frontal and precordial planes.

5) In most leads with clear R or S waves, they are slow to reach their peak or nadir.

At the beginning of this comment I was very skeptical of the initial tracings being V-Tach and just meant to bring up my a point of dissonance for me. At this point, however, I have a pretty strong suspicion that V-Tach is actually the diagnosis. Thoughts, or am I off-base?


I will note that my initial suspicions revolved around the idea of the narrow beats being the fusion of LV PVCs in the face of a supra-ventricular rhythm with LBBB, but I just couldn't rectify that with the other findings. I especially wanted it to be a parasystolic LV rhythm, but the irregularity of their appearance nixed that idea early.



Reply
Steve Smith, Mar 18, 2012 04:09 PM

Vince, you're not at all off base.

Your arguments are sound and it very well could be VT. I don't think it's a slam dunk either way.

One argument against a rate-related LBBB is that the rate is yet faster in the last ECG, but there is no BBB.

One argument against VT is that you would have to say there are two different VT morphologies in this patient (the first and third EKGs). You thought they are similar morphologies? To me they look very different.

If these are fusion beats, and I understand your arguments in favor, then on all 4 the supraventricualar beat arrives at exactly the same time as the ventricular beat. This is possible but very unusual. It is unusual to see even one fusion beat in VT, much less 4, but then this is in any case an unusual ECG.

I tried applying some of the rules, for instance, Sasaki (not validated, and none of the rules are really excellent):

Step 1: Initial R in aVR?

This means is there a large single (upright) R-wave (not a small r-wave) in aVR. This indicates that the beats originate and propagate from the apex to the base, so that it must be coming from the ventricle, hence VT.

--If yes, then rhythm is VT. If no, step 2.

Here the answer is NO.

Step 2: In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100 msec (0.10 sec)?
--If yes, then rhythm is VT. If no, step 3.

Here I get a maximum of 80 ms. So NO.

Step 3: Initial r or q ≥ 40 ms in any lead?

If there is, this means that, for the first 40 or more milliseconds, conduction is slow as would occur through myocardium (left ventricle, VT), not through conducting fibers, as would occur in SVT)

--If yes, then it is VT. If no, then it is SVT. "No" here, therefore it is SVT

I see only one lead where there is an initial r- or q-wave of about 40 ms, and that is aVR. So the answer here is also NO.

Then you have to figure in the low pH, which can alter conduction.

In any case, whether VT or not, the STEMI is evident. And when in doubt, shock a fast rhythm in an unstable patient.

Steve Smith