Wednesday, December 7, 2016

Syncope Several Times, Complete Heart Block, And a Surprise ECG in the ED!

This was sent by one of our graduates who will remain anonymous.

A 55 year old male with a history of DM and HTN had 2 syncopal episodes, then a third while in the presence of EMS.  There was no drug use.

ECG 1. He was put on the monitor and it showed this:
There is a slow, wide complex.  There are P-waves that are regular but completely dissociated from the QRS.  In fact, they don't ever conduct.
So it is third degree heart block with a ventricular escape.
ECG 2. Within minutes, his heart rate normalized:
Normal sinus rhythm, diffuse non-specific T-wave inversion

ECG 3. He had no complaints on arrival to the ED. This ECG was recorded at 0209:
No obvious abnormalities

ECG 4. At 0416 (2 hours later) he developed "chest burning."  Here is his ECG:
Obvious Inferior Posterior STEMI

ECG 5. His burning quickly resolved, and this ECG was recorded 20 seconds later:
Resolving ST Elevation (That was fast!!)

The patient was "rattled" by this experience, felt as if something very bad had just happened.

ECG 6. 7 minutes later, the burning returned.  Here was the ECG at 0424:
This was the doctor's (my ex-resident's) response:
"He now has ST elevations in a different distribution.  Was inferior before, now lateral What the heck?  I had been considering coronary vasospasm, but the changing distribution seems to make that less likely."

He thought it might be vasospasm of two different coronary arteries.

ECG 7. At 0428 the burning persisted and this was recorded:
Now they are inferior again!!

7 minutes later the burning was gone and this ECG was recorded at 0435:
All STE has resolved again.

The Cath Lab was activated.  Here is the last ECG before he left for the cath lab at 0449:
There are now inferior reperfusion T-waves (inferior Wellens' waves!)
This supports some degree of infarction.
The troponin will be elevated, but not by much as these occlusions were brief.


The cath did not show an occlusion or a definite culprit, but some diffuse non-occlusive disease.  No PCI was performed.

I do not have the subsequent troponin.

Subsequent Echo was showed LVH and evidence of hypertrophic cardiomyopathy, without a wall motion abnormality.  EF was 65%.

The caregivers (emergency physician and cardiologists) were perplexed about what happened.

What happened?

Why the change in location of ST Elevation??? (There are two explanations below)

Look closely at ECGs 4, 6, and 7:

This was my explanation, which Haim Katalan shows was incorrect (his is below mine)

In 4. and 7., which have inferior  ST elevation, the QRS is positive in II, III, and aVF, but negative in aVL (5. also has this QRS axis)

In 6. which has lateral ST elevation, the QRS is negative in lead III, isoelectric in aVF and positive in aVL.

Thus, the limb lead placement was inadvertantly reversed between ECG 5. and 6.  And it was inadvertantly reversed back for ECG 7.

So this was a transient inferior STEMI.

Haim Katalan explanation

I looked carefully at ECG 6-7 and the first ECG with inferior STE. I don't think limb leads was misplaced. i) the chest leads looks different in ECG 6 from 7.  That can not be accounted for by limb lead swap. ii) Also in ECG 6 the STE in I & aVL have an action potential shape completely different from the STD in ECG 7 . iii) also no P wave axis change as would expected in lead swap. 

So my impression is that it was multi vessel spasm.

Transient STEMI is usually due to brief thrombotic occlusion that then lyses.  This occlusion happened several times.  The first time it did not result in chest pain but did result in complete heart block.  In Acute Coronary Syndrome, a thrombotic event, a culprit is not always found.  And the coronary disease may be mild in such cases: the thrombosis just happens at a minimally stenotic, but vulnerable lesion.  It is even possible to have thrombosis with a completely normal angiogram, though in less than 1% of cases.  In such cases, all the the atherosclerosis is outside the lumen, in the wall of the vessel. So you cannot see it on an angiogram, which is a "lumenogram."  You can see this with intravascular ultrasound, which very well images the thickness of the vessel wall.

Of course vasospasm is usually blamed for these transient ST elevation events, but unseen thrombosis is more common.

The good news is that transient STEMI has a better prognosis than non-transient STEMI, AND ACS with a non-obstructive angiogram has a better prognosis than those with tight stenoses or large thrombus burden.

Learning Points:

1.  Always check lead placement when things do not seem right!
2.  Beware of Transient STEMI
3.  Beware that ACS may have minimal findings on angiogram.


  1. Great educational post!

  2. Do you think it could have been embolic? Any history of malignancy or hypercoagulability?

    1. Emboli are organized and well formed and much less likely to reperfuse than fresh in situ thrombus

  3. Thanks for posting Dr. Smith.

    In EKG #6 does the different pattern of STD in V3 and V4 as well as the new STE in V6 mean anything then? The limb leads may have been misplaced but that shouldn't affect the precordial leads right?


    1. That's correct. Read it again as my initial interpretation may have been incorrect and there is a different opinion written now

  4. I will cnalenge this theory by claiming rhat STE shape in the latetal leads is completely different from the STD in the so caled sweached leads. Coronary spasm also no P wave axis change as would expected in leads reversal.

    1. Good for you. Yes. See that I already changed it due to comments.

  5. Steve...

    After reviewing all the ECGs I would suspect involvement of a single vessel - the LCx. Momentary occlusions - whether due to vasospasm or transient thrombi - first in the distal segment of the LCx could give the pattern of an acute epicardial ischemia of the inferoposterior circulation. Then, after that resolved, a temporary occlusion more proximally could give the (more impressive) pattern of a basal-lateral acute ischemia with extension more posterolaterally.

    The inferior wall epicardial ischemia pattern is not as impressive as the basal-lateral pattern, probably helped by collateral circulation from either the RCA (which could be weakly co-dominant) or the LAD.

    1. Jerry,
      Here is the entire cath report. It was right dominant, but your theory is possible if you consider all of your comments as applying to the RCA.

      FINDINGS: A. Hemodynamics. Heart rate is 80 beats per minute. Aortic
      pressure is 94/60 with a mean of 73. Left ventricular systolic pressure is
      90. LVEDP is 16.
      B. Left ventriculography: The left ventricular cavity fills diffusely with
      contrast. The ventricle is not dilated. There is almost complete
      obliteration of the apical segment of his LV in a hyperdynamic ventricle
      that almost appears to have the appearance of hypertrophic myopathy with
      apical button. There was no mitral regurgitation seen. There is ascending
      aorta and aortic root are normal in size. No gradient was seen across the
      aortic valve on pullback.
      C. Coronary cineangiography.
      1. The left main coronary artery is a moderate length vessel. It appears
      to be diffusely narrowed, but no high grade narrowing, perhaps 20% to
      30% diffuse left main narrowing. It is relatively small caliber in the
      left main, felt to be perhaps no more than 2.5 mm diameter.
      2. The left anterior descending coronary artery is also relatively small
      in caliber, 2.5 mm diameter vessel. The vessel has no obvious
      3. There is a ramus intermedius branch that is a large vessel that is free
      of disease.
      4. The circumflex coronary artery is large, but nondominant giving rise to
      two obtuse marginal branches. The circumflex and its branches are free
      of any disease angiographically.
      5. The right coronary artery is a large dominant vessel that gives rise to
      the posterior descending artery and approximately four posterolateral
      branches. The two most distal are quite large. The posterior
      descending artery is also quite large. The proximal right coronary
      artery has some modest 10% plaque, but there is no significant
      narrowing there. The main body of the right coronary artery is also
      widely patent with no significant narrowing. The posterior descending
      artery has some mild diffuse midvessel tubular narrowing of 20% to 30%
      at most. The posterolateral branches appear to be free of disease.

      1. Minor nonobstructive coronary artery disease is seen with 20-30%
      diffuse left main narrowing and 10% proximal right coronary artery
      narrowing and 20% to 30% mid PDA narrowing.
      2. Hyperdynamic left ventricle with LVEF greater than 75%. No wall
      motion abnormalities are noted. We would consider hypertrophic
      myopathy and echocardiography should be done.

    2. Steve...

      Thanks for the cath report. I still feel that the LCx would have to be involved because of the ST-T changes in ECG #6 UNLESS the RCA is actually a "super-dominant RCA": "The right coronary artery is a large dominant vessel that gives rise to the posterior descending artery and approximately FOUR posterolateral branches. The two most distal are QUITE LARGE." (Caps are mine.)

      I suppose a problem in a distal RCA with such large posterolateral branches could result at times in an acute inferior subepicardial ischemia and an at other times in an impressive acute posterolateral subepicardial ischemia as seen in ECG #6. However, I've never seen a "super-dominant RCA" cause such elevation in Leads I and aVL (but I've seen it in V1 - V6).

    3. Jerry,
      Yes, I was agreeing with you on your assessment, but just pointing out that in this case if your theory is correct it would be the RCA and not circ. Normally proximal occlusions occur first, then embolize to more distal ones. Your scenario is much less common, but of course whatever happened is indeed quite uncommon, so it is likely correct!

  6. Fantastic case with lots of important lessons to be learned! Astute observations by Haim Katalan. There are a host of lead misplacements that are possible (especially when you consider multiple misplacements of more than a single lead) — but as per Haim, lack of change of either PQRST morphology in lead aVR — with identical P wave morphology in leads I,II,III (ie, upright P in lead II that remains greater than P wave amplitude in lead I) — together with the change he notes that DOES occur in the chest leads between these 2 tracings (ST elevation seen in V6 in ECG #6 in which ST segments are up in I,aVL — but no ST elevation in V6 for ECG #7) combine to tell us that there was no lead misplacement here!

    Interesting comment below by Jerry Jones! THANKS to Dr. Stephen Smith for presenting this fascinating case!

  7. Given the differential of Transient Stemi, could the rhythm in ecg 1 in lead 2 be AIVR ?

    1. @ AKS — This wasn’t my case — so I’m commenting on just what I see. The rhythm strip for the 1st ECG in lead II is short, as we only see 8 beats. I believe P waves ARE regular (a P wave occurs just at the beginning of beat #6). The QRS is wide — and although it looks like P waves are not related to neighboring QRS complexes — I believe this rhythm strip is TOO SHORT to know that for certain. This is especially because beat #7 occurs early — and whenever you see early beats like this — you have to wonder if they might be conducted! The problem is that QRS morphology of beat #7 is similar but definitely NOT the same in these 2 leads — so I don’t know if this is arising from the same or a different ventricular focus … But I believe it also IS possible that the reason this beat occurs early — is that the P wave that occurs just at the onset of the 6th beat might be conducting (!!!) — with QRS widening being the result of aberrant conduction. So, this isn’t “AIVR” (which is your question) — because we DO see sinus P waves. At the least this appears to be high-grade 2nd-degree AV block — because a number of P waves that should conduct do not conduct. But in my opinion, a LONGER RHYTHM STRIP is need to really know what this rhythm is — :)

  8. Tks Ken. I was looking at the Vent rate. What I calculated is above 50 and as I know Vent escape would go up to 40.

    1. @ AKS — You are correct that the usual rate of ventricular escape rhythms in adults is between 20-40/minute — so IF you had a ventricular rhythm at ~50/minute or faster — but slower than ~110-120/minute — AND — you didn't have P waves — then this would be AIVR ( = Accelerated IdioVentricular Rhythm). But since there are P waves in this 1st ECG rhythm — and especially since it is possible that the early beat toward the end of the tracing may be conducted — it's better to describe this as a manifestation of AV block (in which a slightly accelerated ventricular rhythm arises when P waves are non-conducted) — :)


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